med surg 2 exam 3

Common Causes and Risk Factors for Heart Failure

Hypertension • Coronary artery disease • Cardiomyopathy • Substance abuse (alcohol and illicit/prescribed drugs) • Valvular disease • Congenital defects • Cardiac infections and inflammations • Dysrhythmias • Diabetes mellitus • Smoking/tobacco use • Family history • Obesity • Severe lung disease • Sleep apnea • Hyperkinetic conditions (e.g., hyperthyroidism)

Cor Pulmonale

Hypoxia and hypoxemia • Increasing dyspnea • Fatigue • Enlarged and tender liver • Warm, cyanotic hands and feet, with bounding pulses • Cyanotic lips • Distended neck veins • Right ventricular enlargement (hypertrophy) • Visible pulsations below the sternum • GI disturbances such as nausea or anorexia • Dependent edema • Metabolic and respiratory acidosis • Pulmonary hypertension

Pulmonary Function Tests

(PFTs) using spirometry. Baseline PFTs are obtained for all patients diagnosed with asthma. The most important PFTs for a patient with asthma are the forced vital capacity (FVC), the forced expiratory volume in the first second (FEV1), and the peak expiratory flow (PEF), sometimes called peak expiratory rate flow (PERF). Definitions of PFTs are listed in Chapter 24. A decrease in either the FEV1 or the PEF (PERF) of 15% to 20% below the expected value for age, gender, and size is common for the patient with asthma (Durham et al., 2017). Asthma is diagnosed when these values increase by 12% or more after treatment with bronchodilators. Airway responsiveness is tested by measuring the PEF and FEV1 before and after the patient inhales the drug methacholine, which induces bronchospasm in susceptible adults.

Myocardial hypertrophy

(enlargement of the myocardium), compensatory mechanism. The walls of the heart thicken to provide more muscle mass, which results in more forceful contractions, further increasing CO. However, cardiac muscle may hypertrophy more rapidly than collateral circulation can provide adequate blood supply to the muscle. Often a hypertrophied heart is slightly oxygen deprived. All the compensatory mechanisms contribute to an increase in the consumption of myocardial oxygen. When the demand for oxygen increases and the myocardial reserve has been exhausted, signs and symptoms of HF develop.

Epistaxis

(nosebleed) is a common problem because of the many capillaries within the nose. Nosebleeds occur as a result of loss of tissue integrity from trauma to the nasal mucosa, hypertension, blood dyscrasia (e.g., leukemia), inflammation, tumor, decreased humidity, nose blowing, nose picking, chronic cocaine use, and procedures such as nasogastric (NG) suctioning. Older adults tend to bleed most often from the posterior portion of the nose.

Infective Endocarditis patho

(previously called bacterial endocarditis) is a microbial infection (e.g., viruses, bacteria, fungi) of the endocardium. The most common infective organism is Streptococcus viridans or Staphylococcus aureus. Infective endocarditis occurs primarily in patients with injection drug use (IDU) and those who have had valve replacements, have experienced systemic alterations in immunity, or have structural cardiac defects. It is important to note that the incidence of infective endocarditis is rising in conjunction with the opioid epidemic in the United States. (See Chapter 5 for more on the opioid epidemic). With a cardiac defect, blood may flow rapidly from a high-pressure area to a low-pressure zone, eroding a section of endocardium. Platelets and fibrin adhere to the denuded endocardium, forming a vegetative lesion. During bacteremia, bacteria become trapped in the low-pressure "sinkhole" and are deposited in the vegetation. Additional platelets and fibrin are deposited, causing the vegetative lesion to grow. The endocardium and valve are destroyed. Valvular insufficiency may result when the lesion interferes with normal alignment of the valve. If vegetations become so large that blood flow through the valve is obstructed, the valve appears stenotic and then is very likely to embolize (i.e., cause the emboli to be released into the systemic circulation) (McCance & Huether, 2019). Possible ports of entry for infecting organisms include: • The oral cavity (especially if dental procedures have been performed) • Skin rashes, lesions, or abscesses • Infections (cutaneous, genitourinary, GI, systemic) • Surgery or invasive procedures, including IV line placement

Tracheotomy

. Local anesthesia is used if there is concern that the airway will be lost during the induction of anesthesia. A tracheotomy is reserved for the patient who cannot be easily intubated with an endotracheal tube. An emergency tracheotomy can establish an airway in less than 2 minutes. Patients receiving mechanical ventilation for upper airway obstruction or respiratory failure may require a tracheostomy after 7 or more days of continuous endotracheal intubation. In such cases, a tracheotomy is performed to prevent laryngeal injury and loss of tissue integrity by the endotracheal tube

ecg

A lead provides one view of the heart's electrical activity. Multiple leads, or views, can be obtained. Electrode placement is the same for male and female patients. Lead systems are made up of a positive pole and a negative pole. An imaginary line joining these two poles is called the lead axis. The direction of electrical current flow in the heart is the cardiac axis. The relationship between the cardiac axis, and the lead axis is responsible for the deflections seen on the ECG pattern: • The baseline is the isoelectric line. It occurs when there is no current flow in the heart after complete depolarization and also after complete repolarization. Positive deflections occur above this line, and negative deflections occur below it. Deflections represent depolarization and repolarization of cells. • If the direction of electrical current flow in the heart (cardiac axis) is toward the positive pole, a positive deflection (above the baseline) is viewed (Fig. 31.2A). • If the direction of electrical current flow in the heart (cardiac axis) is moving away from the positive pole toward the negative pole, a negative deflection (below the baseline) is viewed (Fig. 31.2B). • If the cardiac axis is moving neither toward nor away from the positive pole, a biphasic complex (both above and below baseline) will resul

Acute Respiratory Failure

A near match in the lungs between air movement or ventilation ( ) and blood flow or perfusion ( ) is needed for adequate pulmonary gas exchange. When either ventilation or perfusion is mismatched with the other in a lung or lung area, gas exchange is reduced, and respiratory failure can result (McCance et al., 2019; Lamba et al., 2016). Acute respiratory failure (ARF) can be ventilatory failure, oxygenation ( gas exchange ) failure, or a combination of bo ventilatory and oxygenation failure and is classified by abnormal blood gas values. The critical values are: • Partial pressure of arterial oxygen (PaO 2) less than 60 mm Hg (hypoxemic/oxygenation failure) • or Partial pressure of arterial carbon dioxide (PaCO 2) more than 45 mm Hg occurring with acidemia (pH <7.35) (hypercapnia/ventilatory failure) • and Arterial oxygen saturation (SaO 2) less than 90% in both cases Whatever the underlying problem, the patient in ARF is always hypoxemic (has low arterial blood oxygen levels).

Pandemic Influenza

A pandemic respiratory viral infection is one that has the potential to spread globally because the virus has previously infected only birds or other animals, so no human ancestral immunity is present. Most bird and animal viruses cannot be transmitted to humans. A few notable exceptions have occurred when these viruses mutated and became highly infectious to humans, causing pandemics. Example pandemics include the 1918 "Spanish" influenza and the 2009 H1N1 influenza A.

valve diseases assessment

A patient with valvular disease may suddenly become ill or slowly develop symptoms over many years. Collect information about the patient's family health history, including valvular or other forms of heart disease to which he or she may be genetically predisposed. Ask about attacks of rheumatic fever and infective endocarditis, the specific dates when these occurred, and the use of antibiotics to prevent recurrence of these diseases. Also ask the patient about a history of IV drug misuse, a common cause of infective endocarditis. Discuss fatigue and tolerated activity levels, the presence of angina or dyspnea, and the occurrence of palpitations, if present. As part of the physical assessment, obtain vital signs, inspect for signs of edema, palpate and auscultate the heart and lungs, and palpate the peripheral pulses. Assessment findings are summarized in the Key Features: Valvular Heart Disease box. Echocardiography is the noninvasive diagnostic procedure of choice to visualize the structure and movement of the heart. The more invasive transesophageal echocardiography (TEE) or transthoracic echocardiography (TTE) is also performed to assess most valve problems. Exercise tolerance testing (ETT) and stress echocardiography are sometimes done to evaluate symptomatic response and assess functional capacity. With either mitral or aortic stenosis, cardiac catheterization may be indicated to assess the severity of the stenosis and its other effects on the heart. In patients with mitral stenosis, the chest x-ray shows left atrial enlargement, prominent pulmonary arteries, and an enlarged right ventricle. In those with mitral regurgitation (insufficiency), the chest x-ray reveals an increased cardiac shadow, indicating left ventricular and left atrial enlargement. In the later stages of aortic stenosis, the chest x-ray may show left ventricular enlargement and pulmonary congestion. Left atrial and left ventricular dilation appear on the chest x-ray of patients with aortic regurgitation (insufficiency). If HF is present, pulmonary venous congestion is also evident. An ECG can be used to evaluate rhythm status in patients with mitral stenosis. Atrial fibrillation is a common finding in both mitral stenosis and mitral regurgitation and may develop in aortic stenosis because of left atrial dilation. Interventions: Take Action Management of valvular heart disease depends on which valve is affected and the degree of valve impairment. Some patients can be managed with annual monitoring and drug therapy, whereas others require invasive procedures or heart surgery (Nishimura et al., 2017). Nonsurgical Management Nonsurgical management focuses on drug therapy and rest. During the course of valvular disease, left ventricular failure with pulmonary or systemic congestion may develop. Drug Therapy Diuretics, beta blockers, ACE inhibitors, digoxin, and oxygen are often administered to improve the symptoms of HF. Nitrates are administered cautiously to patients with aortic stenosis because of the potential for syncope associated with a reduction in left ventricular volume (preload). Vasodilators such as calcium channel blockers may be used to reduce the regurgitant flow for patients with aortic or mitral stenosis. Nursing Safety Priority Drug Alert Teach patients with valve disease the importance of prophylactic antibiotic therapy before any invasive dental or oral procedure. This includes patients with a previous history of endocarditis and cardiac transplant or valve recipients. Have patients demonstrate appropriate oral hygiene because optimal oral health is the best intervention to prevent endocarditis. Prophylactic antibiotics are not recommended before GI procedures such as upper GI endoscopy, colonoscopy, or procedures requiring genitourinary instrumentation. A major concern in valvular heart disease is maintaining cardiac output (CO) if atrial fibrillation develops. With mitral valvular disease, left ventricular filling is especially dependent on atrial contraction. When atrial fibrillation develops, there is no longer a single coordinated atrial contraction. CO can decrease, and HF may occur. Ineffective atrial contraction may also lead to the stasis of blood and thrombi in the left atrium. Monitor the patient for the development of an irregular rhythm and notify the primary care provider if it develops. (See Chapter 31 for a detailed explanation of atrial fibrillation.) The primary care provider usually starts drug therapy first to control the heart rate (HR) and maintain CO (HR < 100 is considered a controlled ventricular response). After these outcomes are met, drugs are used in an attempt to restore normal sinus rhythm (NSR). In some cases, the provider elects to convert a patient from atrial fibrillation to sinus rhythm using IV diltiazem or amiodarone. Monitor the patient on a unit where both cardiac rhythm and BP can be assessed closely. Synchronized countershock (cardioversion) may be attempted if atrial fibrillation is rapid, the patient's condition worsens, and the rhythm is unresponsive to medical treatment (see Chapter 31). If the patient remains in atrial fibrillation, low-dose amiodarone is often prescribed to slow ventricular rate. Procainamide hydrochloride may be added to the regimen. A beta-blocking agent (e.g., metoprolol) may also be considered to slow the ventricular response. For valvular heart disease and chronic atrial fibrillation, anticoagulation with warfarin is usually a part of the plan of care to prevent thrombus formation. Thrombi (clots) may form in the atria or on defective valve segments, resulting in systemic emboli. If a portion breaks off and travels to the brain, one or more strokes may occur. Assess the patient's baseline neurologic status and monitor for changes. A transesophageal echocardiography (TEE) is often done before synchronized cardioversion to ensure that thrombi that could embolize when this therapy is administered are not present. Direct oral anticoagulants (DOACs) rivaroxaban, dabigatran, apixaban, and edoxaban are not recommended to anticoagulate patients with atrial fibrillation related to valvular disease. Rest is often an important part of treatment. Activity may be limited because CO cannot meet increased metabolic demands and angina or HF can result. A balance of rest and exercise is needed to prevent skeletal muscle atrophy and fatigue. Nonsurgical Heart Valve Reparative Procedures Reparative procedures are becoming more popular because of continuing problems with thrombi, endocarditis, and left ventricular dysfunction after valve replacement. Reparative procedures do not result in a normal valve, but they usually "turn back the clock," resulting in a more functional valve and an improvement in CO. Turbulent blood flow through the valve may persist, and degeneration of the repaired valve is possible. Balloon valvuloplasty, an invasive nonsurgical procedure, is possible for stenotic mitral and aortic valves; however, careful selection of patients is needed. It may be the initial treatment of choice for people with noncalcified, mobile mitral valves. Patients selected for aortic valvuloplasty are usually older and are at high risk for surgical complications. The benefits of this procedure for aortic stenosis tend to be short lived, rarely lasting longer than 6 months. Aortic valvuloplasty may be beneficial as a bridge to either surgical or percutaneous aortic valve replacement. When performing mitral valvuloplasty, the physician passes a balloon catheter from the femoral vein, through the atrial septum, and to the mitral valve. The balloon is inflated to enlarge the mitral orifice. For aortic valvuloplasty, the physician inserts the catheter through the femoral artery and advances it to the aortic valve, where it is inflated to enlarge the orifice. The procedure usually offers immediate relief of symptoms because the balloon has dilated the orifice and improved leaflet mobility. The results are comparable with those of surgical commissurotomy for appropriately selected patients. Minimally invasive techniques have expanded. For patients who are not surgical candidates, transcatheter aortic valve replacement (TAVR) is an alternate option for treatment of aortic stenosis (Fig. 32.4). Interprofessional collaboration with the cardiologist, surgeon, patient, and the patient's family is often used to determine the best approach. A bioprosthetic valve is placed percutaneously over the damaged valve. This procedure is usually performed through a small incision in the groin allowing for bilateral transfemoral access (Karycki, 2019). One access is used to place the prosthetic valve while the other is used to place a temporary transvenous pacemaker. After initial balloon aortic valvuloplasty, the new valve is wrapped around a balloon on a large catheter that is inserted via the femoral artery (see Fig. 32.4A-B). The patient is then transvenously paced temporarily at a rate of about 200 beats/min to reduce cardiac output and cardiac motion. The balloon is then inflated, and the valve is deployed (see Fig. 32.4C-D). This procedure is performed by a heart valve team consisting of interventional cardiologists and cardiovascular surgeons. The team must be prepared to convert to an open or surgical aortic valve replacement (SAVR) if necessary. If SAVR is required, care of the patient is similar to that of the patient undergoing coronary artery bypass graft (CABG) (see Chapter 35). After the TAVR, patients remain on bedrest for 6 hours and are monitored overnight for complications (Karycki, 2019). This patient population requires antiplatelet therapy with lifelong daily aspirin and clopidogrel for the first 6 months (Karycki, 2019). FIG. 32.4 Transcatheter aortic valve replacement (TAVR) procedure. A, Balloon aortic valvuloplasty. B, New valve placed around balloon. C, Balloon inflated, deploying valve. D, Catheter removed, valve in place. The pulmonary valve can also be replaced percutaneously by a device using a similar procedure to the TAVR. Transcatheter mitral valve repair is also available (Al-Lawati & Cheung, 2016). The MitraClip is used to repair the mitral valve in patients with mitral regurgitation. Under general anesthesia, access is gained percutaneously via the femoral vein, and the catheter and Mitraclip are advanced in the atria and then the left ventricle. The Mitraclip is then retracted and deployed to hold the leaflets of the valve together. Additional devices are currently in clinical trial. Nursing Safety Priority Action Alert After valvuloplasty, observe the patient closely for bleeding from the catheter insertion site and institute postangiogram precautions. Bleeding is likely because of the large size of the catheter. Assess for signs of a regurgitant valve by closely monitoring heart sounds, CO, and heart rhythm. Because vegetations (thrombi) may have been dislodged from the valve, observe for any indication of systemic emboli (see the Infective Endocarditis section in this chapter). Surgical Management Surgeries for patients with valvular heart disease include invasive reparative procedures and replacement. These procedures are performed after symptoms of left ventricular failure have developed but before irreversible dysfunction occurs. Surgical therapy is the only definitive treatment of aortic stenosis and is recommended when angina, syncope, or dyspnea on exertion develops. Heart Valve Reparative Procedures Direct (open) commissurotomy is accomplished with cardiopulmonary bypass during open-heart surgery. The surgeon visualizes the valve, removes thrombi from the atria, incises the fused commissures (leaflets), and débrides calcium from the leaflets, widening the orifice. Mitral valve annuloplasty (reconstruction) is the reparative procedure of choice for most patients with acquired mitral insufficiency. To make the annulus (the valve ring that attaches to and supports the leaflets) smaller, the surgeon may suture the leaflets to an annuloplasty ring or take tucks in the patient's annulus. Leaflet repair is often performed at the same time. Elongated leaflets may be shortened, and shortened leaflets may be repaired by lengthening the chordae that bind them in place. Perforated leaflets may be patched with synthetic grafts. Annuloplasty and leaflet repair result in an annulus of the appropriate size and leaflets that can close completely. Thus regurgitation is eliminated or markedly reduced. Heart Valve Replacement Procedures The development of a wide variety of prosthetic (synthetic) and biologic (tissue) valves has improved the surgical therapy and prognosis of valvular heart disease. Each type has advantages and disadvantages. An aortic valve can be replaced only with a prosthetic valve for symptomatic adults with aortic stenosis and aortic insufficiency. A biologic valve cannot be used because of the high pressure within the aorta. Biologic valve replacements may be xenograft (from other species), such as a porcine valve (from a pig) (Fig. 32.5) or a bovine valve (from a cow). Because tissue valves are associated with little risk for clot formation, long-term anticoagulation is not indicated. Xenografts are not as durable as prosthetic valves and usually must be replaced every 7 to 10 years. The durability of the graft is related to the age of the recipient. Calcium in the blood, which is present in larger quantities in younger patients, breaks down the valves. The older the patient, the longer the xenograft will last. Valves donated from human cadavers and pulmonary autographs (relocation of the patient's own pulmonary valve to the aortic position) are also used for valve replacement. FIG. 32.5 Examples of biologic (tissue) heart valves. A, Freestyle, a stentless pig valve with no frame. B, Hancock II, a stented pig valve. C, Carpentier-Edwards pericardial bioprosthesis. A and B courtesy Medtronic, Inc., Minneapolis, MN; C courtesy Baxter Healthcare Corporation, Edwards CVS Division, Santa Ana, CA. Patients having a valve replacement have open-heart surgery similar to the procedure for a CABG (see Chapter 35). Ideally surgery is an elective and planned procedure. Patients need to have a preoperative dental examination. If dental caries or periodontal disease is present, these problems must be resolved before valve replacement. Teach patients receiving oral anticoagulants to stop taking them before surgery, usually at least 72 hours before the procedure. Inform the patient and family about the management of postoperative pain, incision care, and strategies to prevent infection and respiratory complications. Postoperative nursing interventions for patients with valve replacement are similar to those for a CABG (see Chapter 35). Nursing Safety Priority Critical Rescue Patients with mitral stenosis often have pulmonary hypertension and stiff lungs. Therefore monitor respiratory status closely during weaning from the ventilator. Be especially alert for bleeding in those with aortic valve replacements because of a higher risk for postoperative hemorrhage. If heart rate or blood pressure decreases, call the Rapid Response Team or other health care provider immediately! Patients with valve replacements are also more likely to have significant reductions in cardiac output (CO) after surgery, especially those with aortic stenosis or left ventricular failure from mitral valve disease. Carefully monitor CO and assess for indications of heart failure. Report any indications of HF to the surgeon immediately, and prepare for collaborative management (see earlier discussion on HF in this chapter). When a patient has a mechanical valve, lifelong anticoagulant therapy with warfarin is required. Teach the patient that the international normalized ratio (INR) will need to be monitored frequently. The therapeutic goal for patients with mechanical heart valves is 3.0 to 4.0 (Pagana & Pagana, 2018). However, therapy must be individualized to each patient. Low-dose aspirin is also recommended. Direct oral anticoagulants (DOACs) are not recommended in patients with valve replacement. Teach patients the signs and symptoms of bleeding and to report these symptoms to the primary health care provider.

Pneumothorax and Hemothorax

A pneumothorax is air in the pleural space causing a loss of negative pressure in the chest cavity, a rise in chest pressure, and a reduction in vital capacity, which can lead to lung collapse (Arsbad et al., 2016). It is often caused by blunt chest trauma and may occur with some degree of hemothorax, which is bleeding into the chest cavity. It can also occur as a complication of medical procedures. (A simple hemothorax is a blood loss of less than 1000 mL into the chest cavity; a massive hemothorax is a blood loss of more than 1000 mL.) The pneumothorax can be open (pleural cavity is exposed to outside air, as through an open wound in the chest wall) or closed (such as when a patient with chronic obstructive pulmonary disease has a spontaneous pneumothorax). A tension pneumothorax is a life-threatening complication of pneumothorax in which air continues to enter the pleural space during inspiration and does not exit during expiration (Shay, 2017). As a result, air collects under pressure, completely collapsing the lung and compressing blood vessels, which limits blood return. This process leads to decreased filling of the heart and reduced cardiac output. If not promptly detected and treated, tension pneumothorax is quickly fatal.

Premature Atrial Complexes

A premature atrial complex (contraction) (PAC) occurs when atrial tissue becomes irritable. This ectopic focus fires an impulse before the next sinus impulse is due. The premature P wave may not always be clearly visible because it can be hidden in the preceding T wave. Examine the T wave closely for any change in shape and compare with other T waves. A PAC is usually followed by a pause. The causes of atrial irritability include: • Stress • Fatigue • Anxiety • Inflammation • Infection • Caffeine, nicotine, or alcohol • Drugs such as epinephrine, sympathomimetics, amphetamines, digoxin, or anesthetic agents PACs may also result from myocardial ischemia, hypermetabolic states, electrolyte imbalance, or atrial stretch. Atrial stretch can result from congestive heart failure, valvular disease, and pulmonary hypertension with cor pulmonale. The patient usually has no symptoms except for possible heart palpitations. No intervention is needed except to treat causes such as heart failure. If PACs occur frequently, they may lead to more serious atrial tachydysrhythmias and therefore may need treatment. Administration of prescribed antidysrhythmic drugs may be necessary (see the Common Examples of Drug Therapy: Antidysrhythmic Medication box). Teach the patient measures to manage stress and substances to avoid, such as caffeine and alcohol, that are known to increase atrial irritability.

NYHA system categorizes patients as:

A. Patients at high risk for developing heart failure (Class I NYHA) B. Patients with cardiac structural abnormalities or remodeling who have not developed HF symptoms (Class I NYHA) C. Patients with current or prior symptoms of heart failure (Class II or III NYHA) D. Patients with refractory end-stage heart failure (Class IV NYHA)

risk of ards

ALI leading to ARDS has many causes (Table 29.4), but sepsis is the most common (Mitchell & Seckel, 2018). Some causes result in direct injury to lung tissue; other causes do not directly involve the lungs. As a result of sepsis, pancreatitis, trauma, and other conditions, inflammatory mediators spread to the lungs, causing damage (McCance et al., 2019), another instance of "cytokine storm." ARDS also can occur from direct lung injury. Aspiration of acidic gastric contents, pneumonia, near-drowning, or inhaling toxic fumes are examples of conditions causing direct lung injury. With such events, surfactant production is impaired and the remaining surfactant is diluted. This situation leads to atelectasis, decreased lung compliance, and shunting (movement of blood in the lungs without gas exchange and oxygenation

self management osa

AP therapy for OSA management is appropriate maintenance of the compressor and the mask/tubular system. Keeping the system clean is critical to prevent infection and maintain tissue integrity . With humidification, fungal infections are possible. Most setups require the use of distilled water in the humidifier. The mask device or pillows must be cleaned daily using agents recommended by the specific manufacturer. Instruct the patient to not share the mask, pillows, or tubing with other people to reduce the risk for infection. Teach patients who had surgical interventions for OSA to assess the oropharynx for bleeding, swelling, or indications of infection. A small amount of blood mixed with saliva or mucus, particularly after coughing, is normal. However, new-onset bleeding, large clots, or bright red blood may indicate serious problems. Instruct the patient to notify the surgeon immediately or go to the emergency department if this should occur. Teach the patient how to examine his or her throat with a mirror twice daily and assess its internal size (often by comparing it to coin sizes). A narrowing of the throat or an inability to swallow (with or without pain), and the presence of drooling are indicators of swelling that may obstruct the airway. Instruct the patient to go to the emergency room should these occur. Pain is expected to decrease daily and swallowing should become increasingly more comfortable. Drinking cool liquids, keeping the environment humidified, gargling frequently with warm salt water, and eating soft foods can help reduce pain. Instruct the patient to report an increase in pain or increasingly greater difficulty swallowing to the surgeon. Teach the patient the indications of infection and to notify the surgeon if they occur. Infection indications include an increase in swelling, the presence of pus in any area of the oropharynx, a change in color of the mucous membrane to a "beefy red," an increase in pain, the presence of fever, taste changes, and the presence of bad breath. Activity restriction varies depending on the exact nature of the procedure performed. Obtain a list of surgeon-directed activity restrictions and educate the patient about why each restriction has been prescribed. The most common restrictions include lifting and performing the Valsalva maneuver (holding the breath and bearing down).

arrhythmia

Abnormal heart rhythm

pericarditis

Acute pericarditis is an inflammation or alteration of the pericardium (the membranous sac that encloses the heart). The problem may be fibrous, serous, hemorrhagic, purulent, or neoplastic. Acute pericarditis is most commonly associated with: • Infective organisms (bacteria, viruses, or fungi) (usually respiratory) • Post-myocardial infarction (MI) syndrome (Dressler syndrome) • Postpericardiotomy syndrome • Acute exacerbations of systemic connective tissue disease Chronic constrictive pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium. It is caused by tuberculosis, radiation therapy, trauma, renal failure, or metastatic cancer. In chronic constrictive pericarditis, the pericardium becomes rigid, preventing adequate filling of the ventricles and eventually resulting in cardiac failure.

Targeted Therapy and Immunotherapy of Lung Cancer

AgentsApproved ForTargeted Therapy AgentsAfatinibEGFR-positive metastatic NSCLCAlectinibALK-positive metastatic NSCLCCrizotinibALK-positive metastatic NSCLCErlotinibEGFR-positive metastatic NSCLCImmunotherapy AgentsAtezolizumabStage IV NSCLCDurvalumabStage III NSCLCNivolumabStage III or IV NSCLC and SCLCPembrolizumabStage IV NSCLC

Endotracheal Tube

An ET tube is a long polyvinyl chloride tube that is passed through the mouth or nose and into the trachea (Fig. 29.1). When properly positioned, the tip of the ET tube rests about 2 cm above the carina (the point at which the trachea divides into the right and left mainstem bronchi). Oral intubation is a fast and easy way to establish an airway and is often performed as an emergency procedure. The nasal route is used for oral surgeries and when oral intubation is not possible, but is avoided with midface trauma or possible basilar skull fracture and is not used if the patient has a bleeding problem. An anesthesiologist, nurse anesthetist, or respiratory therapist usually performs the intubation. When intubating a patient with COVID-19, all personnel involved must wear full protective gear, including eye protection, because this procedure has the highest risk for dispersion of infectious droplets. It is recommended that the intubation take place in an airborne infection isolation room (AIIR) (CDC, 2020). The shaft of the tube has a radiopaque line running the length of the tube. This line shows on x-ray and is used to determine correct tube placement. Short horizontal lines (depth markings) are used to place the tube correctly at the naris or mouth (at the incisor tooth) and to identify how far the tube has been inserted. The cuff at the distal end of the tube is inflated after placement and creates a seal between the trachea and the tube. The seal ensures delivery of a set tidal volume when mechanical ventilation is used. The cuff is inflated using a minimal-leak technique; when the cuff is inflated to an adequate sealing volume, a minimal amount of air can pass around it to the vocal cords, nose, or mouth. The patient cannot talk when the cuff is inflated. The pilot balloon with a one-way valve permits air to be inserted into the cuff and prevents air from escaping. This balloon is a guide for determining whether air is present in the cuff, but it does not show how much or how little air is present, nor does it indicate how much pressure is exerted on the trachea from the cuff balloon. The adapter connects the ET tube to the ventilator tubing or an oxygen delivery system. The ET tube size is listed on the shaft of the tube. Adult tube sizes range from 7 to 9 mm. Tube size selected is based on the size of the patient.

hay fever

An allergic response usually to outdoor airborne allergens such as pollen or sometimes indoor allergens such as dust mites or pet dander; also called allergic rhinitis.

Commonly Used Drug Classifications for Patients With Systolic Heart Failure

Angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) Diuretics: • Loop • Potassium-sparing Nitrates Inotropics: • Beta-adrenergic agonists • Phosphodiesterase inhibitors • Calcium sensitizers • Digoxin Beta-adrenergic blockers Angiotensin receptor neprilysin inhibitor (ARNI): • Sacubitril/valsartan Aldosterone antagonist HCN channel blocker: • Ivabradine

Anti-inflammatory Agents

Anti-inflammatory agents decrease airway inflammation . The inhaled forms have fewer systemic side effects than those taken systemically. All of the anti-inflammatory drugs, whether inhaled or taken orally, are controller drugs only. Anti-inflammatory drug therapy for asthma is for prevention or control of asthma. They are not effective in reversing symptoms during an asthma attack and should not be used alone as reliever drugs. Teach patients to take anti-inflammatory asthma drugs on a scheduled basis, even when no symptoms are present.

Pandemic Influenza

Antiviral drugs such as oseltamivir are stockpiled in the event of a pandemic influenza. They can be used for prevention or to shorten the duration of the infection . Distribution for treatment is made on a case-by-case basis, as the drug must be started within 48 hours of symptom onset. Infected patients in the hospital setting should be placed on Droplet Precautions for 7 days and placed in a private room.

psychosocial and lab

Anxiety and frustration are common. Symptoms such as dyspnea increase the patient's anxiety level high risk for depression Electrolyte imbalance may occur from complications of HF or as side effects of drug therapy, especially diuretic therapy. Regular evaluations of a patient's serum electrolytes, including sodium, potassium, magnesium, calcium, and chloride, are essential. Any impairment of renal function resulting from inadequate perfusion causes elevated blood urea nitrogen and serum creatinine and decreased creatinine clearance levels. Hemoglobin and hematocrit tests should be performed to identify HF resulting from anemia. If the patient has fluid volume excess, the hematocrit levels may be low as a result of hemodilution. B-type natriuretic peptide (BNP) is used for diagnosing HF (in particular, diastolic HF) in patients with acute dyspnea. As discussed earlier, it is part of the body's response to decreased cardiac output (CO) from either left or right ventricular dysfunction. An absence of elevation in BNP, in conjunction with history and physical, rules out HF as the cause of acute dyspnea and points to a primary lung dysfunction (Pagana & Pagana, 2018). In the ambulatory care setting, BNP trends may be used over time to guide ambulatory care treatment (Colucci & Chen, 2017). Urinalysis may reveal proteinuria and high specific gravity. Microalbuminuria is an early indicator of decreased compliance of the heart and occurs before the BNP rises. It serves as an "early warning detector" that lets the primary health care provider know that the heart is experiencing early signs of decreased compliance long before symptoms occur. Patient-Centered Care: Older Adult Considerations Thyroxine (T4) and thyroid-stimulating hormone (TSH) levels should be assessed in patients who are older than 65 years, have atrial fibrillation, or have evidence of thyroid disease. Heart failure (HF) may be caused or aggravated by hypothyroidism or hyperthyroidism. Arterial blood gas (ABG) values often reveal hypoxemia (low blood oxygen level) because oxygen does not diffuse easily through fluid-filled alveoli. Respiratory alkalosis may occur because of hyperventilation; respiratory acidosis may occur because of carbon dioxide retention. Metabolic acidosis may indicate an accumulation of lactic acid. Chest x-rays can be helpful in diagnosing left ventricular failure. Typically the heart is enlarged (cardiomegaly), representing hypertrophy or dilation. Pleural effusions develop less often and generally reflect biventricular failure. Echocardiography is considered the best tool in diagnosing heart failure. Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy can be diagnosed with this noninvasive technique. The test can also be used to determine ejection fraction. Radionuclide studies (thallium imaging or technetium pyrophosphate scanning) can also indicate the presence and cause of HF. Multigated acquisition (MUGA) scans, also called multigated blood pool scans, provide information about left ventricular ejection fraction and velocity, which are typically low in patients with HF. These tests are discussed in Chapter 30. Other Diagnostic Assessment An electrocardiogram (ECG) is also performed. It may show ventricular hypertrophy, dysrhythmias, and any degree of myocardial ischemia, injury, or infarction. However, it is not helpful in determining the presence or extent of HF. Invasive hemodynamic monitoring allows the direct assessment of cardiac function and volume status in acutely ill patients. Although medical-surgical nurses do not manage these systems on general hospital units, they should be familiar with the interpretation of some of the major hemodynamic pressures as they relate to patient assessment. These measurements can confirm the diagnosis and guide the management of HF. For example, right atrial pressure is either normal or elevated in left ventricular failure and elevated in right ventricular failure. Pulmonary artery pressure (PAP) and pulmonary artery occlusion pressure (PAOP) are elevated in left-sided HF because volumes and pressures are increased in the left ventricle. Hemodynamic monitoring is

Endemic/Geographic Respiratory Infection

Any organism can cause a pulmonary infection if the exposure is high enough, if the adult has little or no acquired immunity to it, or if the adult's general immune responses are reduced by age, drugs, or other health problems. A variety of respiratory infections are endemic , meaning that the causative organism is much more common within a geographic location, but even then the incidence of the infection is relatively low. Adults living in these areas have often developed some immunity to the organism over time and usually only develop the infection if they come into contact with large numbers of the organism or have a severely reduced immune response. Most commonly, the organisms are spore-forming fungi, although some viral infections also have endemic tendencies. Table 28.4 lists common endemic respiratory infections in North America. These organisms are part of the environment. Healthy adults in endemic areas who are most susceptible to infection are those who have intense exposures. For soil-borne organisms, adults who dig in the soil, farm, or work in construction in which soil is disturbed can be heavily exposed. Everyone can be exposed when the soil is disturbed by dust storms, tornados, flooding, and other types of natural disasters. Working and living in buildings in which demolition and/or reconstruction are occurring can release spores trapped within walls that then become airborne. Working with or camping in areas with organisms that live in soil or decomposing wood and leaves can result in significant exposures. All of these respiratory infections resemble influenza or pneumonia with fever, cough, headache, muscle aches, chest pain, and night sweats and are often misdiagnosed. Also, these infections are not contagious from person to person. Identification of the specific organism is important for specific treatment and prevention of complications. Always ask anyone with respiratory infection symptoms whether they have visited endemic regions to help identify possible sources, expected courses, and appropriate management strategies. Depending on the health and immunity of the infected person and the number of spores present in the respiratory tract, the resulting infection can be mild, moderate, severe, or widely disseminated to other major organs. Special populations, such as older adults, pregnant women, and others who are immunocompromised are at greater risk for more severe disease. With fungal infections, a chronic infection state is possible. Fungal infections are difficult to eradicate. With moderate severity, oral antifungal agents may be prescribed for weeks to months. For more severe disease, IV antifungal agents, including amphotericin, may be needed initially and followed by long-term oral agents. Supportive care is similar to that provided for patients with influenza and pneumonia.

aortic stenosis

Aortic stenosis is the most common cardiac valve dysfunction in the United States and is often considered a disease of "wear and tear." In aortic stenosis, the aortic valve orifice narrows and obstructs left ventricular outflow during systole. This increased resistance to ejection or afterload results in ventricular hypertrophy. As stenosis worsens, cardiac output becomes fixed and cannot increase to meet the demands of the body during exertion. Symptoms then develop. Eventually the left ventricle fails, blood backs up in the left atrium, and the pulmonary system becomes congested. Right-sided HF can occur late in the disease. When the surface area of the valve becomes 1 cm or less, surgery is indicated on an urgent basis! Congenital bicuspid or unicuspid aortic valves are the primary causes for aortic stenosis in many patients. Rheumatic aortic stenosis occurs with rheumatic disease of the mitral valve and develops in young and middle-age adults. Atherosclerosis and degenerative calcification of the aortic valve are the major causative factors in older adults. Aortic stenosis has become the most common valvular disorder in all countries with aging populations. The classic symptoms of aortic stenosis result from fixed cardiac output: dyspnea, angina, and syncope occurring on exertion. When cardiac output falls in the late stages of the disease, the patient experiences marked fatigue, debilitation, and peripheral cyanosis. A narrow pulse pressure is noted when the BP is measured. A diamond-shaped, systolic crescendo-decrescendo murmur is usually noted on auscultation.

Management of Pulmonary Embolism

Apply oxygen by nasal cannula or mask. • Reassure patient that the correct measures are being taken. • Place patient in high-Fowler position. • Apply telemetry monitoring equipment. • Obtain venous access. • Assess oxygenation continuously with pulse oximetry. • Assess respiratory status at least every 30 minutes by: • Listening to lung sounds • Measuring the rate, rhythm, and ease of respirations • Checking skin color and capillary refill • Checking position of trachea • Assess cardiac status by: • Comparing blood pressures in right and left arms • Checking pulse quality • Checking cardiac monitor for dysrhythmias • Checking for distention of neck veins • Ensure that prescribed chest imaging and laboratory tests are obtained immediately (may include complete blood count [CBC] with differential, platelet count, prothrombin time, partial thromboplastin time, D-dimer level, arterial blood gases). • Examine the chest for presence of petechiae. • Give prescribed anticoagulants. • Assess for bleeding. • Handle patient gently. • Institute Bleeding Precautions.

labs asthma

Arterial blood gas (ABG) levels show the effectiveness of gas exchange (see Chapter 14 for discussion of ABGs). The arterial oxygen level (PaO 2) may decrease during an asthma attack. Early in the attack, the arterial carbon dioxide level (PaCO 2) may be decreased as the patient increases the breathing rate and depth. Later in an asthma episode, PaCO 2 rises, as does the end-tidal carbon dioxide level, indicating carbon dioxide retention. Allergic asthma often occurs with elevated serum eosinophil counts and immunoglobulin E (IgE) levels. The sputum may contain eosinophils and mucus plugs with shed epithelial cells (Curschmann spirals).

lung cancer history and signs and symptoms

Ask the patient about risk factors, including smoking, hazards in the workplace, and warning signals (Table 27.5). Calculate the pack-year smoking history as described in Chapter 24. Ask about the presence of lung cancer symptoms, such as hoarseness, cough, sputum production, hemoptysis, shortness of breath, or change in endurance. Symptoms often have been present for years. Ask the patient to describe any recent symptom changes or if position affects them. Assess for chest pain or discomfort, which can occur at any stage of tumor development. Chest pain may be localized or on just one side and can range from mild to severe. Ask about any sensation of fullness, tightness, or pressure in the chest, which may suggest obstruction. A piercing chest pain or pleuritic pain may occur on inspiration. Pain radiating to the arm results from tumor invasion of nerve plexuses in advanced disease. Physical Assessment/Signs and Symptoms—Pulmonary Symptoms of lung cancer are often nonspecific and appear late in the disease. Specific symptoms depend on tumor location. Chills, fever, and cough may be related to pneumonitis or bronchitis that occurs with obstruction. Assess sputum quantity and character. Blood-tinged sputum may occur with bleeding from a tumor. Hemoptysis is a later finding in the course of the disease. If infection or necrosis is present, sputum may be purulent and copious. Breathing may be labored or painful. Obstructive breathing may occur as prolonged exhalation alternating with periods of shallow breathing. Rapid, shallow breathing occurs with pleuritic chest pain and an elevated diaphragm. Look for and document abnormal retractions, the use of accessory muscles, flared nares, stridor, and asymmetric diaphragmatic movement on inspiration. Dyspnea and wheezing may be present with airway obstruction. Ask about dyspnea severity at rest, with activity, and in the supine position. Assess how much the dyspnea interferes with the patient's participation in ADLs, work, recreational activities, and family responsibilities. Increased vibrations felt on the chest wall when the patient speaks (fremitus) indicate areas of the lung where air spaces are replaced with tumor or fluid. Fremitus is decreased or absent when the bronchus is obstructed. The trachea may be displaced from midline if a mass is present in the area. Breath sounds may change with the presence of a tumor. Wheezes indicate partial obstruction of airflow in passages narrowed by tumors. Decreased or absent breath sounds indicate complete obstruction of an airway by a tumor or fluid. A pleural friction rub may be heard when inflammation is present. Physical Assessment/Signs and Symptoms—Nonpulmonary Many other systems can be affected by lung cancer and have changes at the time of diagnosis. Heart sounds may be muffled by a tumor or fluid around the heart (cardiac tamponade). Dysrhythmias may occur as a result of hypoxemia or direct pressure of the tumor on the heart. Cyanosis of the lips and fingertips or clubbing of the fingers may be present (see Fig. 27.8). Bones lose density with tumor invasion and break easily with little pressure and without trauma. The patient may have bone pain or fragility fractures. Late symptoms of lung cancer usually include fatigue, weight loss, anorexia, dysphagia, and nausea and vomiting. Superior vena cava syndrome may result from tumor pressure in or around the vena cava. This syndrome is an emergency (see Chapter 20 ) and requires immediate intervention. The patient may have confusion or personality changes from brain metastasis.

The Patient Recovering From Pneumonia

Ask whether the patient has had any of these problems: • New-onset confusion • Chills and fever • Persistent cough • Dyspnea • Wheezing • Hemoptysis • Increased sputum production • Chest discomfort • Increasing fatigue • Any other symptoms that have failed to resolve Assess the patient for: • Fever • Diaphoresis • Cyanosis, especially around the mouth or conjunctiva • Dyspnea, tachypnea, or tachycardia • Adventitious or abnormal breath sounds • Weakness

The Patient With Heart Failure

Assess for signs of heart failure, including: • Changes in vital signs (heart rate >100 beats/min at rest, new atrial fibrillation, blood pressure <90 or >150 systolic) • Indications of poor tissue perfusion: • Fatigue • Angina • Activity intolerance • Changes in mental status • Pallor or cyanosis • Cool extremities • Indications of congestion: • Presence of cough or dyspnea • Weight gain • Jugular venous distention and peripheral edema Assess functional ability, including: • Performance of ADLs • Mobility and ambulation (review frequency and duration of walking, development of symptoms, and pulse rate) • Cognitive ability Assess nutritional status, including: • Food and fluid intake • Intake of sodium-rich foods • Alcohol consumption • Skin turgor Assess home environment, including: • Safety hazards, especially related to oxygen therapy • Structural barriers affecting functional ability • Social support (family, home health services) Assess the patient's adherence and understanding of illness and its treatment, including: • Signs and symptoms to report to primary health care provider • Dosages, effects, and side or toxic effects of medications • When to report for laboratory and health care provider visits • Ability to accurately weigh self on scale • Presence of advance directive • Use of home oxygen, if appropriate Assess patient and caregiver coping skills.

asess pnuemonia and history

Assess for the risk factors for respiratory infection (see Table 28.1). Document age; living, work, or school environment; diet, exercise, and sleep routines; swallowing problems; presence of a nasogastric tube; tobacco and alcohol use; and past and current use of or addiction to "street" drugs. Remember that often aspiration is "silent" with no signs or symptoms. Ask about past respiratory illnesses and whether the patient has been exposed to influenza or pneumonia or has had a recent viral infection. Using the I PREPARE model listed in Chapter 24, assess the patient for particulate matter exposure (PME). Even noninfectious exposures can result in respiratory inflammation , which increases the risk for pneumonia development. If the patient has chronic respiratory problems, ask whether respiratory equipment is used in the home. Assess whether the patient's cleaning routine for the equipment is adequate to prevent infection. Ask when he or she received the last influenza or pneumococcal vaccine. Ask family members whether they have noticed a change in the patient's cognition . Physical Assessment/Signs and Symptoms Observe the general appearance. Many patients with pneumonia have flushed cheeks and an anxious expression. The patient may have chest pain or discomfort, myalgia, headache, chills, fever, cough, tachycardia, dyspnea, tachypnea, hemoptysis (bloody sputum), and sputum production. Severe chest muscle weakness may also be present from sustained coughing. Observe the patient's breathing pattern, position, and use of accessory muscles. The patient with hypoxia and reduced gas exchange may be uncomfortable in a lying position and will sit upright, balancing with the hands ("tripod position"). Assess the cough and the amount, color, consistency, and odor of sputum produced. Crackles are heard on auscultation when fluid is in interstitial and alveolar areas, and breath sounds may be diminished. Wheezing may be heard if inflammation or exudate narrows the airways. Bronchial breath sounds are heard over areas of density or consolidation. Fremitus is increased over areas of pneumonia, and percussion is dulled. Chest expansion may be diminished or unequal on inspiration. In evaluating vital signs, compare the results with baseline values. A patient with pneumonia, especially an older adult, is often hypotensive with orthostatic changes because of vasodilation and dehydration. A rapid, weak pulse may indicate hypoxemia, dehydration, or impending sepsis and shock. Dysrhythmias may occur from cardiac tissue hypoxia. Common pneumonia signs and symptoms and their causes are listed in Table 28.3. The primary health care provider uses one of several evidence-based pneumonia severity scales to determine whether the patient can be managed in the community or requires hospitalization. When pneumonia is uncomplicated by other health problems, it is often managed in the community. The older adult with pneumonia has weakness, fatigue (which can lead to falls), lethargy, confusion, and poor appetite. Fever and cough may be absent, but hypoxemia is often present. The most common symptom of pneumonia in the older-adult patient is a change in cognition with acute confusion from hypoxia. The WBC count may not be elevated until the infection is severe. Waiting to treat the disease until more typical symptoms appear greatly increases the risk for sepsis and death (Touhy & Jett, 2020).

The Patient With Chronic Obstructive Pulmonary Disease

Assess respiratory status and adequacy of gas exchange: • Measure rate, depth, and rhythm of respirations. • Examine mucous membranes and nail beds for evidence of hypoxia. • Determine use of accessory muscles. • Examine chest and abdomen for paradoxical breathing. • Count number of words patient can speak between breaths. • Determine need and use of supplemental oxygen. (How many liters per minute is the patient using?) • Determine level of consciousness and presence/absence of confusion. • Auscultate lungs for abnormal breath sounds. • Measure oxygen saturation by pulse oximetry. • Determine sputum production, color, and amount. • Ask about activity level. • Observe general hygiene. • Measure body temperature. Assess cardiac status for adequate perfusion: • Measure rate, quality, and rhythm of pulse. • Check dependent areas for edema. • Check neck veins for distention with the patient in a sitting position. • Measure capillary refill. Assess nutrition status: • Check weight maintenance, loss, or gain. • Determine food and fluid intake. • Determine use of nutritional supplements. • Observe general condition of the skin. Assess the patient's and caregiver's understanding of disease and adherence to management, including: • Correct use of supplemental oxygen • Correct technique and dosing schedule for use of inhalers • Symptoms to report to the primary health care provider indicating the need for acute care • Increasing severity of resting dyspnea • Increasing severity of usual symptoms • Development of new symptoms associated with poor gas exchange • Respiratory infection • Failure to obtain the usual degree of relief with prescribed therapies • Use of pursed-lip and diaphragmatic breathing techniques • Scheduling of rest periods and priority activities • Participation in rehabilitation activities

Assessment of Patients Recovering from Pulmonary Embolism

Assess respiratory status: • Observe rate and depth of ventilation. • Auscultate lungs. • Examine nail beds and mucous membranes for evidence of reduced gas exchange. • Take a pulse oximetry reading. • Ask the patient if chest pain or shortness of breath is experienced in any position. • Ask the patient about the presence of sputum and its color and character. Assess cardiovascular status: • Take vital signs, including apical pulse, pulse pressure; assess for presence or absence of orthostatic hypotension and quality and rhythm of peripheral pulses. • Note presence or absence of peripheral edema. • Examine neck vein filling in the recumbent and sitting positions. Assess lower extremities for deep vein thrombosis (DVT): • Examine lower legs and compare with each other for: • General edema and calf swelling • Surface temperature • Presence of red streaks or cordlike, palpable structure Assess for evidence of bleeding: • Examine the mouth and gums for oozing or frank bleeding. • Examine all skin areas, especially old puncture sites and wounds, for bleeding, bruising, or petechiae. Assess cognition and mental status: • Check level of consciousness (LOC) and orientation. Assess the patient's understanding and adherence to management: • Symptoms to report to the primary health care provider. • Drug therapy plan (correct timing and dose, adverse effects). • Bleeding Precautions. • Prevention of venous thromboembolism (VTE).

assess ards

Assess the breathing of any patient at increased risk for ARDS. Determine whether increased work of breathing is present, as indicated by hyperpnea, noisy respiration, cyanosis, pallor, and retraction intercostally (between the ribs) or substernally (beneath the ribs and sternum). Document sweating, respiratory effort, and any change in mental status. Abnormal lung sounds are not heard on auscultation because the edema occurs first in the interstitial spaces and not in the airways. Assess vital signs at least hourly for hypotension, tachycardia, and dysrhythmias. Diagnostic Assessment The diagnosis of ARDS is established by a lowered partial pressure of arterial oxygen (PaO 2) value (decreased gas exchange and oxygenation), determined by arterial blood gas (ABG) measurements. Because a widening alveolar oxygen gradient (i.e., increased fraction of inspired oxygen [FiO 2] does not lead to increased PaO 2 levels) develops with increased shunting of blood, the patient has a progressive need for higher levels of oxygen. Another characteristic of ARDS is a P/F ratio (PaO 2 divided by FiO 2) of less than 200 mm Hg. The patient develops refractory hypoxemia and often needs intubation and mechanical ventilation. Sputum cultures obtained by bronchoscopy and transtracheal aspiration are used to determine if a lung infection also is present. The chest x-ray may show diffuse haziness or a "whited-out" (ground-glass) appearance of the lung. An ECG rules out cardiac problems and usually shows no specific changes.

Care of the Patient With Pericarditis

Assess the nature of the patient's chest discomfort. (Pericardial pain is typically substernal. It is worse on inspiration and decreases when the patient leans forward.) • Auscultate for a pericardial friction rub. • Assist the patient to a position of comfort. • Provide anti-inflammatory agents as prescribed. • Explain that anti-inflammatory agents usually decrease pain within 48 hours. • Avoid the administration of aspirin and anticoagulants because these may increase the possibility of tamponade. • Auscultate the blood pressure carefully to detect paradoxical blood pressure (pulsus paradoxus), a sign of tamponade: • Palpate the blood pressure and inflate the cuff above the systolic pressure. • Deflate the cuff gradually and note when sounds are first audible on expiration. • Identify when sounds are also audible on inspiration. • Subtract the inspiratory pressure from the expiratory pressure to determine the amount of pulsus paradoxus (>10 mm Hg is an indication of tamponade). • Inspect for other indications of tamponade, including jugular venous distention with clear lungs, muffled heart sounds, and decreased cardiac output. • Notify the health care provider if tamponade is suspected.

Care of the Patient With Dysrhythmias

Assess vital signs at least every 4 hours and as needed. • Monitor patient for cardiac dysrhythmias. • Evaluate and document the patient's response to dysrhythmias. • Encourage the patient to notify the nurse when chest pain occurs. • Assess chest pain (e.g., location, intensity, duration, radiation, precipitating and alleviating factors). • Assess peripheral circulation (e.g., palpate for presence of peripheral pulses, edema, capillary refill, color, temperature of extremity). • Provide antidysrhythmic therapy according to unit policy (e.g., antidysrhythmic medication, cardioversion, defibrillation), as appropriate. • Monitor and document patient's response to antidysrhythmic medications or interventions. • Monitor appropriate laboratory values (e.g., cardiac enzymes, electrolyte levels). • Monitor the patient's activity tolerance and schedule exercise/rest periods to avoid fatigue. • Observe for respiratory difficulty (e.g., shortness of breath, rapid breathing, labored respirations). • Promote stress reduction. • Offer spiritual support to the patient and/or family (e.g., contact clergy), as appropriate.

assess pnuemothora

Assessment findings for any type of pneumothorax commonly include: • Reduced (or absent) breath sounds of the affected side on auscultation • Hyperresonance on percussion • Prominence of the involved side of the chest, which moves poorly with respirations • When severe, deviation of the trachea away from the midline and side of injury toward the unaffected side (indicating pushing of tissues to the unaffected side [a mediastinal shift] from increasing pressure within the injured side) For tension pneumothorax, additional assessment findings also may include: • Extreme respiratory distress and cyanosis • Distended neck veins • Hemodynamic instability With a hemothorax, percussion on the involved side produces a dull sound. In addition to symptoms, chest x-rays, CT scans, or ultrasonography may be used for diagnosis of any type of pneumothorax or hemothorax.

assess pericarditis

Assessment findings for patients with acute pericarditis include substernal precordial pain that radiates to the left side of the neck, the shoulder, or the back. The pain is classically grating and oppressive and is aggravated by breathing (mainly on inspiration), coughing, and swallowing. The pain is worse when the patient is in the supine position and may be relieved by sitting up and leaning forward. Ask specific questions to evaluate chest discomfort to differentiate it from the pain associated with an acute MI (see :hapter 35). A pericardial friction rub may be heard with the diaphragm of the stethoscope positioned at the left lower sternal border. This scratchy, high-pitched sound is produced when the inflamed, roughened pericardial layers create friction as their surfaces rub together. Patients with acute pericarditis may have an elevated white blood cell count and usually have a fever. Therefore blood culture and sensitivity may be analyzed in the laboratory. The ECG usually shows ST elevation in all leads, which returns to baseline with treatment. Atrial fibrillation is also common. Echocardiograms may be used to determine a pericardial effusion. The proposed diagnostic criteria for acute pericarditis are two of the following: • Pericardial chest pain • Presence of pericardial rub • New ST elevation in all ECG leads or PR-segment depression • New or worsening pericardial effusion Patients with chronic constrictive pericarditis (lasting longer than 3 months) have signs of right-sided HF, elevated systemic venous pressure with jugular distention, hepatic engorgement, and dependent edema. Exertional fatigue and dyspnea are common complications. Thickening of the pericardium is seen on echocardiography or a computed tomography (CT) scan. Interventions: Take Action The focus of collaborative management is to relieve pain and treat the cause of pericarditis before severe complications occur. See the Best Practice for Patient Safety & Quality Care box for care of the patient with pericarditis.The health care provider usually prescribes NSAIDs for pain associated with pericarditis. Patients who do not obtain pain relief and who do not have bacterial pericarditis may receive corticosteroid therapy. Help the patient assume positions that promote comfort —usually sitting upright and leaning slightly forward. If the pain is not relieved within 24 to 48 hours, notify the primary health care provider. Colchicine twice a day, orally, for 3 months has been shown to prevent pericarditis recurrence (Campbell et al., 2015). The various causes of pericarditis require specific therapies. For example, bacterial pericarditis (acute) usually requires antibiotics and pericardial drainage. The usual clinical course of acute pericarditis is short term (2 to 6 weeks), but episodes may recur. Chronic pericarditis caused by malignant disease may be treated with radiation or chemotherapy, whereas uremic pericarditis is treated by hemodialysis. The definitive treatment for chronic constrictive pericarditis is surgical excision of the pericardium (pericardiectomy). Monitor all patients for pericardial effusion, which occurs when the space between the parietal and visceral layers of the pericardium fills with fluid. This complication puts the patient at risk for cardiac tamponade, or excessive fluid within the pericardial cavit

Edema is an extremely unreliable sign of HF

Be sure that accurate daily weights are taken to document fluid retention. Assessing weight at the same time of the morning using the same scale is important. Weight is the most reliable indicator of fluid gain and loss!

Bradydysrhythmias

Bradydysrhythmias occur when the heart rate is less than 60 beats/min. These rhythms can also be significant because: • Myocardial oxygen demand is reduced from the slow heart rate, which can be beneficial. • Coronary perfusion time may be adequate because of a prolonged diastole, which is desirable. • Coronary perfusion pressure may decrease if the heart rate is too slow to provide adequate cardiac output and blood pressure; this is a serious consequence. herefore the patient may tolerate the bradydysrhythmia well if the blood pressure is adequate. If the blood pressure is not adequate, symptomatic bradydysrhythmias may lead to myocardial ischemia or infarction, dysrhythmias, hypotension, and heart failure

Bronchodilators

Bronchodilators cause bronchiolar smooth muscle relaxation but have no effect on inflammation . Thus for patients who have airflow obstruction by both bronchospasm and inflammation, at least two types of drug therapy are needed. Bronchodilators include beta2 agonists and cholinergic antagonists. Beta 2 agonists bind to and stimulate the beta2-adrenergic receptors in the same way that epinephrine and norepinephrine do. This causes an increase in smooth muscle relaxation. Short-acting beta2 agonists (SABAs) provide rapid but short-term relief. These inhaled drugs are most useful when an attack begins (as relief) or as premedication when the patient is about to begin an activity that is likely to induce an attack (GINA, 2018). Such agents include albuterol, levalbuterol, and terbutaline. Teach the patient with asthma to always carry the relief drug inhaler with him or her and to ensure that enough drug remains in the inhaler to provide a quick dose when needed.Long-acting beta2 agonists (LABAs) are also delivered by inhaler directly to the site of action—the bronchioles. Proper use of the long-acting agonists decreases the need to use reliever drugs as often. Unlike short-acting agonists, long-acting drugs need time to build up an effect, but the effects are longer lasting. These drugs are useful in preventing an asthma attack but cannot stop an acute attack. Therefore teach patients not to use LABAs alone to relieve symptoms of an attack or when wheezing is getting worse but, instead, to use a SABA. Examples of LABAs include formoterol and salmeterol. Both drugs are associated with increased asthma deaths when used as the only therapy for asthma and carry a black box warning from the Food and Drug Administration (FDA).

psych labs copd

COPD affects all aspects of a patient's life. He or she may be isolated because dyspnea causes fatigue or because of embarrassment from coughing and excessive sputum production. Ask the patient about interests and hobbies to assess whether socialization has decreased or whether hobbies cause exposure to irritants. Ask about home conditions for exposure to smoke or crowded living conditions that promote transmission of respiratory infections. Economic status may be affected by the disease through changes in income and health insurance coverage. Drugs delivered by inhalers are expensive, and many patients with limited incomes may use them only during exacerbations and not as prescribed on a scheduled basis. Anxiety and fear from feelings of breathlessness may reduce the patient's ability to participate in a full life. Work, family, social, and sexual roles can be affected. Encourage the patient and family to express their feelings about disease progression and the limitations on lifestyle. Assess their use of support groups and community services. Arterial blood gas (ABG) values identify abnormal gas exchange , oxygenation, ventilation, and acid-base status. Compare repeated ABG values to assess changes in respiratory status. Once baseline ABG values are obtained, pulse oximetry can gauge treatment response. As COPD worsens, the amount of oxygen in the blood decreases (hypoxemia) and the amount of carbon dioxide increases (hypercapnia, also known as hypercarbia). Chronic respiratory acidosis (increased arterial carbon dioxide [PaCO 2]) then results; metabolic alkalosis (increased arterial bicarbonate) occurs as compensation by kidney retention of bicarbonate. This change is seen on ABGs as an elevation of HCO 3-, although pH remains lower than normal. Not all patients with COPD are CO2 retainers, even when hypoxemia is present, because CO2 diffuses more easily across lung membranes than does oxygen. Hypercapnia is often chronically present in advanced emphysema (because the alveoli are affected) rather than in bronchitis (in which the airways are affected). Acute hypercapnia with rapid rises above the patient's usual CO2 levels represents a serious decline in the patient's condition and can lead to respiratory failure (Dorman, 2016). Sputum samples are obtained for culture from hospitalized patients with an acute respiratory infection. The infection is treated on the basis of symptoms and the common bacterial organisms in the local community. A WBC count helps confirm the presence of infection. Other blood tests include hemoglobin and hematocrit to determine polycythemia (a compensatory increase in red blood cells [RBCs] and iron in the chronically hypoxic patient). Serum electrolyte levels are examined because acidosis can change electrolyte values. Low phosphate, potassium, calcium, and magnesium levels reduce muscle strength. In patients with a family history of COPD, serum AAT levels may be assessed. Chest x-rays are used to rule out other lung diseases and to check the progress of patients with respiratory infections or chronic disease. With advanced emphysema, chest x-rays show hyperinflation with widely spaced ribs and a flattened diaphragm. COPD is classified from mild to very severe on the basis of symptoms and pulmonary function test (PFT) changes (Table 27.2; see Table 24.6). Airflow rates and lung volume measurements help distinguish airway disease (obstructive diseases) from interstitial lung disease (restrictive diseases). PFTs determine lung volumes, flow volume curves, and diffusion capacity. Each test is performed before and after the patient inhales a bronchodilator agent. Explain the preparations for the procedures (if any), whether pain or discomfort will be involved, and any needed follow-up care. Although the severity classification in Table 27.2 can help clinicians determine overall disease severity, it does not predict how well the patient can manage his or her activity on a daily basis and how likely an acute exacerbation could occur. So this classification was modified in 2017 to include the severity indications based on symptom scores obtained with the patient responses to the COPD Assessment Test (CAT) (GOLD, 2019). This 8-item test requires the patient to rate his or her specific symptoms on a 0 (no symptom) to a 5 (worst symptom) scale. Scores can range from 0 to 40, with lower scores indicating less severe problems. As a result, each of the GOLD classes also can contain an ABCD designation for actual symptom severity as an indicator of risk for exacerbation. An A designation indicates a low risk for exacerbation, even when the patient has a GOLD class of 4 (very severe disease), whereas a D designation indicates a high risk for exacerbation (and need for hospitalization), even if the patient meets PFT results associated with a GOLD class of 1 (mild disease). This change in classification is used to recognize when interventions are needed to prevent an acute exacerbation (Kaufman, 2017; O'Dell et al., 2018 ). The lung volumes measured for COPD are vital capacity (VC), residual volume (RV), forced expiratory volume (FEV), and total lung capacity (TLC). Although all volumes and capacities change to some degree in COPD, the RV is most affected, with increases reflecting the trapped, stale air remaining in the lungs. A diagnosis of COPD is based mostly on the FEV1 (the FEV in the first second of exhalation). FEV1 can also be expressed as a percentage of the forced vital capacity (FVC). As the disease progresses, the ratio of FEV1 to FVC becomes smaller. The diffusion test measures how well a test gas (carbon monoxide) diffuses across the alveolar-capillary membrane and combines with hemoglobin. In emphysema, alveolar wall destruction decreases the large surface area for diffusion of gas into the blood, leading to a decreased diffusion capacity. In bronchitis alone, the diffusion capacity is usually normal. The patient with COPD has decreased oxygen saturation, often much lower than 90%. Changes in SpO 2 below the patient's usual saturation require medical attention. Patients who have been managing COPD for a long time often are aware of their usual SpO 2 values. Peak expiratory flow meters are used to monitor the effectiveness of drug therapy to relieve obstruction. Peak flow rates increase as obstruction resolves. Teach the patient to self-monitor the peak expiratory flow rates at home and adjust drugs as needed.

complications asthma

COPD affects gas exchange and the oxygenation of all tissues. Complications include hypoxemia, acidosis, respiratory infection, cardiac failure, dysrhythmias, and respiratory failure. Hypoxemia and acidosis occur because the patient with COPD has reduced gas exchange, leading to decreased oxygenation and increased carbon dioxide levels. These problems reduce cellular function. Respiratory infection risk increases because of the increased mucus and poor gas exchange . Bacterial infections are common and make COPD symptoms worse by increasing inflammation and mucus production and inducing more bronchospasm. Airflow becomes even more limited, the work of breathing increases, and dyspnea results. Cardiac failure, especially cor pulmonale (right-sided heart failure caused by pulmonary disease), occurs with bronchitis or emphysema. Air trapping, airway collapse, and stiff alveolar walls increase the lung tissue pressure and narrow lung blood vessels, making blood flow more difficult. The increased pressure creates a heavy workload on the right side of the heart, which pumps blood into the lungs. To pump blood through the narrowed vessels, the right side of the heart generates high pressures. In response to this heavy workload, the right chambers of the heart enlarge and thicken, causing right-sided heart failure with backup of blood into the general venous system. The Key Features: Cor Pulmonale box lists the symptoms and problems of cor pulmonale. Cardiac dysrhythmias are common in patients with COPD. They result from hypoxemia (from decreased oxygen to the heart muscle), other cardiac disease, drug effects, or acidosis.

Meeting Healthy People 2020 Objectives

Cardiac DiseaseTo reduce hospitalizations of older adults with heart failure as the principal diagnosis: • For patients hospitalized for heart failure, collaborate with the case manager for discharge planning, including adequate support in the community. • Provide a continuing plan of care for patients and their families or other caregivers when the patient is discharged from the hospital. • If the patient is discharged to home, call to check that he or she has no impending signs and symptoms of heart failure (the case manager may make calls). • Teach the patient and family or other caregiver about when to call the health care provider for health changes so that the patient can be treated at home. • Ensure that the interprofessional team provides the patient with follow-up care in the home or nursing home.

hf history

Carefully question the patient about his or her medical history, including hypertension, angina (cardiac pain), MI, rheumatic heart disease, valvular disorders, endocarditis, and pericarditis. Ask about the patient's perception of his or her activity tolerance, breathing pattern, sleeping pattern, urinary pattern, and fluid volume status and his or her knowledge about HF With left ventricular systolic dysfunction, cardiac output (CO) is diminished, leading to impaired tissue perfusion, anaerobic metabolism, and unusual fatigue. Assess activity tolerance by asking whether the patient can perform normal ADLs or climb flights of stairs without fatigue or dyspnea. Many patients with heart failure (HF) experience weakness or fatigue with activity or have a feeling of heaviness in their arms or legs. Ask about their ability to perform simultaneous arm and leg work (e.g., walking while carrying a bag of groceries). Such activity may place an unacceptable demand on the failing heart. Ask the patient to identify his or her most strenuous activity in the past week. Many people unconsciously limit their activities in response to fatigue or dyspnea and may not realize how limited they have become. Perfusion to the myocardium is often impaired as a result of left ventricular failure, especially with cardiac hypertrophy. The patient may report chest pain or may describe palpitations, skipped beats, or a fast heartbeat. As the amount of blood ejected from the left ventricle diminishes, hydrostatic pressure builds in the pulmonary venous system and results in fluid-filled alveoli and pulmonary congestion, which results in a cough. The patient in early HF describes the cough as irritating, nocturnal (at night), and usually nonproductive. As HF becomes very severe, he or she may begin expectorating frothy, pink-tinged sputum—a sign of life-threatening pulmonary edema. Dyspnea also results from increasing pulmonary venous pressure and pulmonary congestion. Carefully question about the presence of dyspnea and how it developed. The patient may refer to dyspnea as "trouble catching my breath," "breathlessness," or "difficulty breathing." As exertional dyspnea develops (also called dyspnea upon or on exertion [DUE/DOE]), the patient often stops previously tolerated levels of activity because of shortness of breath. Dyspnea at rest in the recumbent (lying flat) position is known as orthopnea. Ask how many pillows are used to sleep or whether the patient sleeps in an upright position in a bed, recliner, or other type of chair. Patients who describe sudden awakening with a feeling of breathlessness 2 to 5 hours after falling asleep have paroxysmal nocturnal dyspnea (PND). Sitting upright, dangling the feet, or walking usually relieves this condition. Signs of systemic congestion occur as the right ventricle fails, fluid is retained, and pressure builds in the venous system. Edema develops in the lower legs and may progress to the thighs and abdominal wall. Patients may notice that their shoes fit more tightly, or their shoes or socks may leave indentations on their swollen feet. They may have removed their rings because of swelling in their fingers and hands. Ask about weight gain. An adult may retain 4 to 7 L of fluid (10 to 15 lb [4.5 to 6.8 kg]) before pitting edema occurs. Reports of nausea and anorexia may be a direct consequence of liver engorgement (congestion) resulting from fluid retention. In advanced heart failure (HF), ascites and an increased abdominal girth may develop from severe liver congestion. Another common finding related to fluid retention is diuresis at rest. At rest, fluid in the peripheral tissue is mobilized and excreted, and the patient describes frequent awakening at night to urinate. Obtain a careful nutritional history, questioning about the use of salt and the types of food consumed. Ask about daily fluid intake. Patients with HF may experience increased thirst and drink excessive fluid (4000 to 5000 mL/day) because of sodium retention.

Pulmonary Embolism (PE) Severity and Management Options

CategoryPossible SymptomsManagement OptionsMassive PEMortality may be as high as 65%Severe hypotension (SBP <90 mm Hg for at least 15 minutes)Cardiac arrest/cardiopulmonary collapseSevere bradycardiaShockSevere dyspnea/respiratory distressCPRInotropic and/or vasopressor support; fluidsFibrinolytic therapyTissue plasminogen activator (tPA)AlteplaseUnfractionated heparin initial treatmentSubmassive PENormotensionRV dysfunction on echocardiographyRV dilation on echocardiography or CTRight bundle branch blockST elevation or depressionT-wave inversionElevated BNP or troponinTreatment is controversial; some agents not approved for this groupMust weigh benefits of thrombolytic therapy against risk for bleedingFibrinolytics may be preferred if patient appears to be decompensating or if there is RV dysfunction (hypokinesis) or elevation in BNP or troponinLMWH (preferred agent)FondaparinuxUnfractionated heparinLow-risk PEMortality ranges from 1% to 8%NormotensionNo RV dysfunctionNo elevation in BNP or troponinFibrinolytics not warranted because of risk for bleedingLMWHDirect thrombin inhibitorInpatient hospitalization not usually required

Nursing Interventions for Various Causes of Ventilator Alarms

CauseNursing ActionsHigh-Pressure Alarm (sounds when peak inspiratory pressure reaches the set alarm limit [usually set 10-20 mm Hg above the patient's baseline PIP])An increased amount of secretions or a mucus plug is in the airways.Suction as needed.The patient coughs, gags, or bites on the oral ET tube.Insert oral airway to prevent biting on the ET tube.Provide adequate pain management and sedation as prescribed.The patient is anxious or fights the ventilator.Provide emotional support to decrease anxiety.Increase the flow rate.Explain all procedures to the patient.Provide sedation or paralyzing agent as prescribed.Airway size decreases related to wheezing or bronchospasm.Auscultate breath sounds.Collaborate with respiratory therapy department to provide prescribed bronchodilators.Pneumothorax occurs.Alert the pulmonary health care provider or Rapid Response Team about a new onset of decreased breath sounds or unequal chest excursion, which may be caused by pneumothorax.Auscultate breath sounds.The artificial airway is displaced; the ET tube may have slipped into the right mainstem bronchus.Assess the chest for unequal breath sounds and chest excursion.Obtain a chest x-ray as ordered to evaluate the position of the ET tube.After the proper position is verified, secure the tube in place.Obstruction in tubing occurs because the patient is lying on the tubing or there is water or a kink in the tubing.Assess the system, beginning with the artificial airway and moving toward the ventilator.There is increased PIP associated with deliverance of a sigh.Empty water from the ventilator tubing and remove any kinks.Coordinate with respiratory therapist or pulmonary health care provider to adjust the pressure alarm.Decreased compliance of the lungs is noted; a trend of gradually increasing PIP is noted over several hours or a day.Evaluate the reasons for the decreased compliance of the lungs. Increased PIP occurs in ARDS, pneumonia, or any worsening of pulmonary disease.Low-Exhaled Volume (or Low-Pressure) Alarm (sounds when there is a disconnection or leak in the ventilator circuit or a leak in the patient's artificial airway cuff)A leak in the ventilator circuit prevents breath from being delivered.Assess all connections and all ventilator tubing for disconnection.The patient stops spontaneous breathing in the SIMV or CPAP mode or on pressure support ventilation.Evaluate the patient's tolerance of the mode.Evaluate for overmedication with sedation or pain drugs.A cuff leak occurs in the ET or tracheostomy tube.Evaluate the patient for a cuff leak. A cuff leak is suspected when the patient can talk (air escapes from the mouth) or when the pilot balloon on the artificial airway is flat (see Tracheostomy Tubes section in Chapter 25).

Sustained Tachydysrhythmias and Bradydysrhythmias

Chest discomfort, pressure, or pain, which may radiate to the jaw, back, or arm • Restlessness, anxiety, nervousness, confusion • Dizziness, syncope • Palpitations (in tachydysrhythmias) • Change in pulse strength, rate, and rhythm • Pulse deficit • Shortness of breath, dyspnea • Tachypnea • Pulmonary crackles • Orthopnea • S3 or S4 heart sounds • Jugular venous distention • Weakness, fatigue • Pale, cool, skin; diaphoresis • Nausea, vomiting • Decreased urine output • Delayed capillary refill • Hypotension

chronic bronchits

Chronic bronchitis is an inflammation of the bronchi and bronchioles (bronchiolitis) caused by exposure to irritants, especially cigarette smoke. The irritant triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm. Bronchitis affects only the airways, not the alveoli. Chronic inflammation increases the number and size of mucus-secreting glands, which produce large amounts of thick mucus. The bronchial walls thicken and impair airflow. This thickening, along with excessive mucus, blocks some of the smaller airways and narrows larger ones. The increased mucus provides a breeding ground for organisms and leads to chronic infection. Chronic bronchitis impairs airflow and gas exchange because mucus plugs and inflammation narrow the airways. As a result, the PaO 2 level decreases (hypoxemia), and the arterial carbon dioxide (PaCO 2) level increases (respiratory acidosis).

copd etiology

Cigarette smoking is the greatest risk factor for COPD. The patient with a 20-pack-year history or longer often has early-stage COPD with changes in pulmonary function tests (PFTs). The inhaled smoke triggers the release of excessive proteases in the lungs. These enzymes break down elastin, the major component of alveoli. By impairing the action of cilia, smoking also inhibits the cilia from clearing the bronchi of mucus, cellular debris, and fluid. Alpha 1 -antitrypsin deficiency is a less common but important risk factor for COPD, although it is often underrecognized (Southard et al., 2020). The enzyme alpha1-antitrypsin (AAT) is normally present in the lungs. AAT inhibits excessive protease activity, so the proteases only break down inhaled pollutants and organisms and do not damage lung structures. The production of normal amounts of AAT depends on the inheritance of a pair of normal gene alleles for this protein. The AAT gene is recessive. Thus if one of the pair of alleles is faulty and the other allele is normal, the adult makes enough AAT to prevent COPD unless there is significant exposure to cigarette smoke or other inhalation irritants. However, this adult is a carrier for AAT deficiency. When both alleles are faulty, COPD develops at a fairly young age even when the person is not significantly exposed to cigarette smoke or other irritants. About 100,000 Americans have severe AAT deficiency, and many more have mild to moderate deficiencies (Southard et al., 2020). Although an AAT deficiency also can cause problems in the skin and liver, lung diseases are more common. AAT deficiency is a single gene disorder with many known gene variations, and some increase the risk for emphysema. Different variations result in different levels of AAT deficiency, which is why the disease is more severe for some adults than for others (OMIM, 2019c). The most serious variation for emphysema risk is the Z mutation, although others also increase the risk but to a lesser degree. Table 27.1 shows the most common AAT mutations increasing the risk for emphysema. Urge patients who have any AAT deficiency to avoid smoking and other environmental pollutants. In addition to genetic and environmental factors, asthma also appears to be a risk factor for COPD. The incidence of COPD is reported to be 12 times greater among adults with asthma than among adults without asthma after adjusting for smoking history (GOLD, 2019). Both disorders may be present at the same time, known as asthma-COPD overlap syndrome

Severity Classification for Primary Pulmonary Arterial Hypertension

ClassSymptomsIPulmonary hypertension diagnosed by pulmonary function tests and right-sided cardiac catheterizationNo limitation of physical activityModerate physical activity does not induce dyspnea, fatigue, chest pain, or light-headednessIINo symptoms at restMild-to-moderate physical activity induces dyspnea, fatigue, chest pain, or light-headednessIIINo or slight symptoms at restMild (less than ordinary) activity induces dyspnea, fatigue, chest pain, or light-headednessIVDyspnea and fatigue present at restUnable to carry out any level of physical activity without symptomsSymptoms of right-sided heart failure apparent (dependent edema, engorged neck veins, enlarged liver)

Combined Ventilatory and Oxygenation Failure

Combined ventilatory and oxygenation failure involves hypoventilation (poor respiratory movements). Impaired gas exchange at the alveolar-capillary membrane results in poor diffusion of oxygen into arterial blood and carbon dioxide retention. The condition may or may not include poor lung perfusion. When lung perfusion is not adequate, ( ) mismatch occurs, and both ventilation and perfusion are inadequate. This type of respiratory failure leads to a more profound hypoxemia than either ventilatory failure or oxygenation failure alone. A combination of ventilatory failure and oxygenation (gas exchange ) failure occurs in patients who have abnormal lungs, such as those who have any form of chronic bronchitis, emphysema, or cystic fibrosis, or who are having an asthma attack. The bronchioles and alveoli are diseased (causing oxygenation failure), and the work of breathing increases until the respiratory muscles cannot function effectively, causing ventilatory failure leading to acute respiratory failure (ARF). ARF can also occur in patients who have cardiac failure along with ventilatory failure and is made worse because the cardiac system cannot adapt to the hypoxia by increasing the cardiac output.

Risk Factors for Pneumonia

Community-Acquired Pneumonia • Is an older adult • Has never received the pneumococcal vaccination or received it more than 5 years ago • Did not receive the influenza vaccine in the previous year • Has a chronic health problem or other coexisting condition that reduces immunity • Has recently been exposed to respiratory viral or influenza infection • Uses tobacco or alcohol or is exposed to high amounts of secondhand smoke Health Care-Acquired Pneumonia • Is an older adult • Has a chronic lung disease • Has presence of gram-negative colonization of the mouth, throat, and stomach • Has an altered level of consciousness • Has had a recent aspiration event • Has presence of endotracheal, tracheostomy, or nasogastric tube • Has poor nutritional status • Has reduced immunity (from disease or drug therapy) • Uses drugs that increase gastric pH (histamine [H2] blockers, antacids) or alkaline tube feedings • Is currently receiving mechanical ventilation (ventilator-associated pneumonia [VAP])

care management infective endocarditis

Community-based care for patients with infective endocarditis is essential to resolve the problem, prevent relapse, and avoid complications. Patients and families need to be willing and have the knowledge, physical ability, and resources to administer IV antibiotics at home. Collaborate with the home care nurse to complete health teaching started in the hospital and to monitor patient adherence and health status. In collaboration with the case manager, the home care nurse and pharmacist arrange for appropriate supplies to be available to the patient at home. Supplies include the prepared antibiotic, IV pump with tubing, alcohol wipes, IV access device, normal saline solution, and a saline flush solution drawn up in syringes. A saline lock, peripherally inserted central catheter (PICC) line, or central catheter is positioned at a venous site that is easily accessible to the patient or a family member. Teach the patient and family how to administer the antibiotic and care for the infusion site while maintaining aseptic technique. The patient or family member should demonstrate this technique before the patient is discharged from the hospital. Emphasize the importance of maintaining a blood level of the antibiotic by administering the antibiotics as scheduled. After stabilization at home, the case manager or other nurse contacts the patient every week to determine whether he or she is adhering to the antibiotic therapy and whether any problems have been encountered. Encourage proper oral hygiene. Advise patients to use a soft toothbrush, to brush their teeth at least twice per day, and to rinse the mouth with water after brushing. They should not use irrigation devices or floss the teeth because bacteremia may result. Teach them to clean any open skin areas well and apply an antibiotic ointment. Nursing Safety Priority Action Alert Patients must remind health care providers (including their dentists) of their endocarditis. Guidelines for antibiotic prophylaxis have been revised and are recommended only if the patient with a prosthetic valve, a history of infective endocarditis, or an unrepaired cyanotic congenital heart disease undergoes an invasive dental or oral procedure (Habib et al., 2015). Instruct patients to note any indications of recurring endocarditis such as fever. Remind them to monitor and record their temperature daily for up to 6 weeks. Teach them to report fever, chills, malaise, weight loss, increased fatigue, sudden weight gain, or dyspnea to their primary care provider.

Electrocardiographic Complexes, Segments, and Intervals

Complexes that make up a normal ECG consist of a P wave, a QRS complex, a T wave, and possibly a U wave. Segments include the PR segment, ST segment, and TP segment. Intervals include the PR interval, QRS duration, and QT interval (Fig. 31.6). The P wave is a deflection representing atrial depolarization. The shape of the P wave may be a positive, negative, or biphasic (both positive and negative) deflection, depending on the lead selected. When the electrical impulse is consistently generated from the sinoatrial (SA) node, the P waves have a consistent shape in a given lead. If an impulse is then generated from a different (ectopic) focus, such as atrial tissue, the shape of the P wave changes in that lead, indicating that an ectopic focus has fired. The PR segment is the isoelectric line from the end of the P wave to the beginning of the QRS complex, when the electrical impulse is traveling through the atrioventricular (AV) node, where it is delayed. It then travels through the ventricular conduction system to the Purkinje fibers. The PR interval is measured from the beginning of the P wave to the end of the PR segment. It represents the time required for atrial depolarization, the impulse delay in the AV node, and the travel time to the Purkinje fibers. It normally measures from 0.12 to 0.20 second (five small blocks). The QRS complex represents ventricular depolarization. The shape of the QRS complex depends on the lead selected. The Q wave is the first negative deflection and is not present in all leads. When present, it is small and represents initial ventricular septal depolarization. When the Q wave is abnormally present in a lead, it represents myocardial necrosis (cell death). The R wave is the first positive deflection. It may be small, large, or absent, depending on the lead. The S wave is a negative deflection following the R wave and is not present in all leads. The QRS duration represents the time required for depolarization of both ventricles. It is measured from the beginning of the QRS complex to the J point (the junction where the QRS complex ends and the ST segment begins). It normally measures from 0.06 to 0.10 second (1 ½ to 2 ½ small blocks) (Urden et al., 2018; Prutkin, 2018). The ST segment is normally an isoelectric line and represents early ventricular repolarization. It occurs from the J point to the beginning of the T wave. Its length varies with changes in the heart rate, the administration of medications, and electrolyte disturbances. The T wave follows the ST segment and represents ventricular repolarization. It is usually positive, rounded, and slightly asymmetric. T waves may become tall and peaked, inverted (negative), or flat as a result of myocardial ischemia, potassium or calcium imbalances, medications, or autonomic nervous system effects The U wave, when present, follows the T wave and may result from slow repolarization of ventricular Purkinje fibers. It is of the same polarity as the T wave, although generally it is smaller. It is not normally seen in all leads and is more common in lead V3. An abnormal U wave may suggest an electrolyte abnormality (particularly hypokalemia) or other disturbance. Correct identification is important so that it is not mistaken for a P wave. If in doubt, notify the primary health care provider and request that a potassium level be obtained. The QT interval represents the total time required for ventricular depolarization and repolarization. The QT interval is measured from the beginning of the Q wave to the end of the T wave. This interval varies with the patient's age and gender and changes with the heart rate, lengthening with slower heart rates and shortening with faster rates. It may be prolonged by certain medications, electrolyte disturbances, or subarachnoid hemorrhage. A prolonged QT interval may lead to a unique type of ventricular tachycardia called torsades de pointes. Artifact is interference seen on the monitor or rhythm strip, which may look like a wandering or fuzzy baseline. It can be caused by patient movement, loose or defective electrodes, improper grounding, or faulty ECG equipment such as broken wires or cables. Some artifacts can mimic lethal dysrhythmias such as ventricular tachycardia (with toothbrushing) or ventricular fibrillation (with tapping on the electrode). Assess the patient to differentiate an artifact from actual lethal rhythms! Do not rely only on the ECG monitor. Electrocardiographic Rhythm Analysis Analysis of an ECG rhythm strip requires a systematic approach using an eight-step method facilitated by use of a measurement tool called an ECG caliper (Prutkin, 2018; Palmer, 2011 ): 1. Determine the heart rate. The most common method is to count the number of QRS complexes in 6 seconds and multiply that number by 10 to calculate the rate for a full minute. This is called the 6-second strip method and is a quick method to determine the mean or average heart rate. Normal heart rates fall between 60 and 100 beats/min. A rate less than 60 beats/min is called bradycardia. A rate greater than 100 beats/min is called tachycardia. Current monitoring systems will display a continuous heart rate and print it on the ECG strip. Use caution and confirm that the rate is correct by assessing the patient's heart rate directly. Many factors can incorrectly alter the rate displayed by the monitor. 2. Determine the heart rhythm. Assess for atrial and/or ventricular regularity. Heart rhythms can be either regular or irregular. Irregular rhythms can be regularly irregular, occasionally irregular, or irregularly irregular. Check the regularity of the atrial rhythm by assessing the PP intervals, placing one caliper point on a P wave and the other point on the precise spot on the next P wave. Then move the caliper from P wave to P wave along the entire strip ("walking out" the P waves) to determine the regularity of the rhythm. P waves of a different shape (ectopic waves), if present, create an irregularity and do not walk out with the other P waves. A slight irregularity in the PP intervals, varying no more than three small blocks, is considered essentially regular if the P waves are all of the same shape. This alteration is caused by changes in intrathoracic pressure during the respiratory cycle. Check the regularity of the ventricular rhythm by assessing the RR intervals, placing one caliper point on a portion of the QRS complex (usually the most prominent portion of the deflection) and the other point on the precise spot of the next QRS complex. Move the caliper from QRS complex to QRS complex along the entire strip (walking out the QRS complexes) to determine the regularity of the rhythm. QRS complexes of a different shape (ectopic QRS complexes), if present, create an irregularity and do not walk out with the other QRS complexes. A slight irregularity of no more than three small blocks between intervals is considered essentially regular if the QRS complexes are all of the same shape. 3. Analyze the P waves. Check that the P-wave shape is consistent throughout the strip, indicating that atrial depolarization is occurring from impulses originating from one focus, normally the SA node. Determine whether there is one P wave occurring before each QRS complex, establishing that a relationship exists between the P wave and the QRS complex. This relationship indicates that an impulse from one focus is responsible for both atrial and ventricular depolarization. The nurse may observe more than one P-wave shape, more P waves than QRS complexes, absent P waves, or P waves coming after the QRS, each indicating that a dysrhythmia exists. Ask these five questions when analyzing P waves: • Are P waves present? • Are the P waves occurring regularly? • Is there one P wave for each QRS complex? • Are the P waves smooth, rounded, and upright in appearance or are they inverted? • Do all P waves look similar? 4. Measure the PR interval. Place one caliper point at the beginning of the P wave and the other point at the end of the PR segment. The PR interval normally measures between 0.12 and 0.20 second. The measurement should be constant throughout the strip. The PR interval cannot be determined if there are no P waves or if P waves occur after the QRS complex. Ask these three questions about the PR interval: • Are PR intervals greater than 0.20 second? • Are PR intervals less than 0.12 second? • Are PR intervals constant across the ECG strip? 5. Measure the QRS duration. Place one caliper point at the beginning of the QRS complex and the other at the J point, where the QRS complex ends and the ST segment begins. The QRS duration normally measures between 0.06 and 0.10 second. The measurement should be constant throughout the entire strip. Check that the QRS complexes are consistent throughout the strip. When the QRS is narrow (0.10 second or less), it indicates that the impulse was not formed in the ventricles and is referred to as supraventricular or above the ventricles. When the QRS complex is wide (greater than 0.10 second), it indicates that the impulse is either of ventricular origin or of supraventricular origin with aberrant conduction, meaning deviating from the normal course or pattern. More than one QRS complex pattern or occasionally missing QRS complexes may be observed, indicating a dysrhythmia. Ask these questions to evaluate QRS intervals: • Are QRS intervals less than or greater than 0.10 second? • Are the QRS complexes similar in appearance across the ECG paper? 6. Examine the ST segment. The normal ST segment begins at the isoelectric line. ST elevation or depression is significant if displacement is 1 mm (one small box) or more above or below the line and is seen in two or more leads. ST elevation may indicate problems such as myocardial infarction, pericarditis, and hyperkalemia. ST depression is associated with hypokalemia, myocardial infarction, or ventricular hypertrophy. 7. Assess the T wave. Note the shape and height of the T wave for peaking or inversion. Abnormal T waves may indicate problems such as myocardial infarction and ventricular hypertrophy. 8. Measure the QT interval. A normal QT interval should be equal to or less than one-half the distance of the RR interval. Using steps 1 through 8, you can interpret the cardiac rhythm and differentiate normal and abnormal cardiac rhythms (dysrhythmias). Overview of Normal Cardiac Rhythms Normal sinus rhythm (NSR) is the rhythm originating from the sinoatrial (SA) node (dominant pacemaker) that meets these ECG criteria (Fig. 31.7): • Rate: Atrial and ventricular rates of 60 to 100 beats/min • Rhythm: Atrial and ventricular rhythms regular • P waves: Present, consistent configuration, one P wave before each QRS complex • PR interval: 0.12 to 0.20 second and constant • QRS duration: 0.06 to 0.10 second and constan

imaging pe

Computed tomography pulmonary angiography (CTPA) or helical CT may be used for diagnosis. This type of imaging has the added advantage of revealing other pulmonary abnormalities causing the patient's symptoms. Magnetic resonance arteriography (MRA) is used in place of CTPA in some settings. A chest x-ray may be used to diagnose other conditions that mimic acute PE. Doppler ultrasound may be used to document the presence of VTE.

Review of Cardiac Conduction System

Conduction begins with the sinoatrial (SA) node (also called the sinus node), located close to the surface of the right atrium near its junction with the superior vena cava. The SA node is the heart's primary pacemaker. It can spontaneously and rhythmically generate electrical impulses at a rate of 60 to 100 beats/min and therefore has the greatest degree of automaticity (pacing function). The SA node is richly supplied by the sympathetic and parasympathetic nervous systems, which increase and decrease the rate of discharge of the sinus node, respectively. This process results in changes in the heart rate. Impulses from the sinus node move directly through atrial muscle and lead to atrial depolarization, which is reflected in a P wave on the electrocardiogram (ECG). Atrial muscle contraction should follow. Within the atrial muscle are slow and fast conduction pathways leading to the atrioventricular (AV) node. The atrioventricular (AV) junction consists of a transitional cell zone, the AV node itself, and the bundle of His. The AV node lies just beneath the right atrial endocardium, between the tricuspid valve and the ostium of the coronary sinus. Here T-cells (transitional cells) cause impulses to slow down or be delayed in the AV node before proceeding to the ventricles. This delay is reflected in the PR segment on the ECG. This slow conduction provides a short delay, allowing the atria to contract and the ventricles to fill. The contraction is known as atrial kick and contributes additional blood volume for a greater cardiac output. The AV node is also controlled by both the sympathetic and parasympathetic nervous systems. The bundle of His connects with the distal portion of the AV node and continues through the interventricular septum. The bundle of His extends as a right bundle branch down the right side of the interventricular septum to the apex of the right ventricle. On the left side, it extends as a left bundle branch, which further divides. At the ends of both the right and the left bundle branch systems are the Purkinje fibers. These fibers are an interweaving network located on the endocardial surface of both ventricles, from apex to base. The fibers then partially penetrate into the myocardium. Purkinje cells make up the bundle of His, bundle branches, and terminal Purkinje fibers. These cells are responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction. A few nodal cells in the ventricles also occasionally demonstrate automaticity, giving rise to ventricular beats or rhythms. The cardiac conduction system consists of specialized myocardial cells (Fig. 31.1). The electrophysiologic properties of these cells regulate heart rate and rhythm and possess unique properties: automaticity, excitability, conductivity, and contractility. Automaticity (pacing function) is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively. Normally only the sinoatrial (SA) node can generate an electrical impulse. However, under certain conditions, such as myocardial ischemia (decreased blood flow), electrolyte imbalance, hypoxia, drug toxicity, and infarction (cell death), any cardiac cell may produce electrical impulses independently and create dysrhythmias. Disturbances in automaticity may involve either an increase or a decrease in pacing function. Excitability is the ability of nonpacemaker heart cells to respond to an electrical impulse that begins in pacemaker cells. Depolarization occurs when the normally negatively charged cells within the heart muscle develop a positive charge. Conductivity is the ability to send an electrical stimulus from cell membrane to cell membrane. As a result, excitable cells depolarize in rapid succession from cell to cell until all cells have depolarized. The wave of depolarization causes the deflections in the ECG waveforms that are recognized as the P wave and the QRS complex. Disturbances in conduction result when conduction is too rapid or too slow, when the pathway is totally blocked, or when the electrical impulse travels an abnormal pathway. Contractility is the ability of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, causing sufficient pressure to push blood forward through the heart. In other words, contractility is the mechanical activity of the hear

Cystic Fibrosis

Cystic fibrosis (CF) is an autosomal recessive genetic disease that affects many organs with most impairment occurring to pancreatic and/or lung function. Although CF is present from birth and usually is first seen in early childhood, almost half of patients with CF in the United States are adults (Cystic Fibrosis Foundation [CFF], 2019 ; Lomas & Tran, 2020). The underlying problem of CF is blocked chloride transport in the cell membranes. Poor chloride transport causes the formation of mucus that has little water content and is thick. The thick, sticky mucus causes problems in the lungs, pancreas, liver, salivary glands, and testes. The mucus plugs up the airways in the lungs and the glandular tissues in nonpulmonary organs, causing atrophy and organ dysfunction. Nonpulmonary problems include pancreatic insufficiency, malnutrition, intestinal obstruction, poor growth, male sterility, and cirrhosis of the liver. Additional problems of CF in young adults include osteoporosis and diabetes mellitus. Respiratory failure is the main cause of death. Improved management has increased life expectancy, even among those with severe disease, to about 47 years (CFF, 2019; Loas & Tran, 2020). The pulmonary problems of CF result from the constant presence of thick, sticky mucus and are the most serious complications of the disease. The mucus narrows airways, reducing airflow and interfering with gas exchange . The constant presence of mucus results in chronic respiratory tract infections, chronic bronchitis, and dilation of the bronchioles (bronchiectasis). Lung abscesses are common. Over time the bronchioles distend, and mucus-producing cells have increased numbers (hyperplasia) and increased size (hypertrophy). Complications include pneumothorax, arterial erosion and hemorrhage, and respiratory failure. CF is most common among whites, and about 4% (1 in 29) are carriers (CFF, 2019). It is rarer among Hispanic Americans (1 in 46 are carriers), African Americans (1 in 65 are carriers), and Asian American (1 in 90 are carriers). Males and females are affected equally.

lvf

Decreased Cardiac OutputPulmonary Congestion • Fatigue • Weakness • Oliguria during the day (nocturia at night) • Angina • Confusion, restlessness • Dizziness • Tachycardia, palpitations • Pallor • Weak peripheral pulses • Cool extremities • Hacking cough, worse at night • Dyspnea/breathlessness • Crackles or wheezes in lungs • Frothy, pink-tinged sputum • Tachypnea • S3/S4 summation gallop

Breathing Exercises

Diaphragmatic or Abdominal Breathing • If you can do so comfortably, lie on your back with your knees bent. If you cannot lie comfortably, perform this exercise while sitting in a chair. • Place your hands or a book on your abdomen to create resistance. • Begin breathing from your abdomen while keeping your chest still. You can tell if you are breathing correctly if your hands or the book rises and falls accordingly. Pursed-Lip Breathing • Close your mouth and breathe in through your nose. • Purse your lips as you would to whistle. Breathe out slowly through your mouth, without puffing your cheeks. Spend at least twice the amount of time it took you to breathe in. • Use your abdominal muscles to squeeze out every bit of air you can. • Remember to use pursed-lip breathing during any physical activity. Always inhale before beginning the activity and exhale while performing it. Never hold your breath.

Pathophysiology, Signs and Symptoms, and Treatment of Common Cardiomyopathies

Dilated CardiomyopathyHypertrophic CardiomyopathyNonobstructedObstructedPathophysiologyFibrosis of myocardium and endocardiumDilated chambersMural wall thrombi prevalentHypertrophy of all wallsHypertrophied septumRelatively small chamber sizeSame as for nonobstructed except for obstruction of left ventricular outflow tract associated with the hypertrophied septum and mitral valve incompetenceSigns and SymptomsFatigue and weaknessHeart failure (left side)Dysrhythmias or heart blockSystemic or pulmonary emboliS3 and S4 gallopsModerate to severe cardiomegalyDyspneaAnginaFatigue, syncope, palpitationsMild cardiomegalyS4 gallopVentricular dysrhythmiasSudden death commonHeart failureSame as for nonobstructed except with mitral regurgitation murmurAtrial fibrillationTreatmentSymptomatic treatment of heart failureVasodilatorsControl of dysrhythmiasSurgery: heart transplantFor both:Symptomatic treatmentBeta blockersConversion of atrial fibrillationSurgery: ventriculomyotomy or muscle resection with mitral valve replacementNitrates and other vasodilators contraindicated with the obstructed form

Common Organisms Associated With Endemic Respiratory Infection in North America

Disorder/OrganismSourceGeographic AreaManagement for Moderate to Severe Disease or Special PopulationsHantavirus pulmonary syndrome (HPS)HantavirusUrine, droppings, and saliva of infected rodentsSouthwest United States, Mexico, Central AmericaSupportiveOxygenMechanical ventilation in severe cases (38% fatal)AspergillosisAspergillusCommon mold found indoors and outside in damp areas; may be extensive in older buildings; moist soil and decomposing wood and leavesCan occur in any indoor environment damp enough to support mold growthOutdoor growth in San Francisco, Canada & United States around the Great Lakes; Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugsSurgery may be needed in severe casesBlastomycosis (fungal)BlastomycesMoist soil, decomposing wood and leavesCanada & United States around the Great Lakes; Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugsCoccidioidomycosisCoccidioidesSoilSouthwest, far west United States, Mexico, Central and South AmericaSupportive careProlonged course of antifungal drugsCryptococcosisCryptococcus gattiiTrees and soil beneath treesU.S. Pacific coast regions, mid to southern British ColumbiaSupportive careProlonged course of antifungal drugsHistoplasmosisHistoplasmaSoil containing large amounts of bird and bat droppings; surfaces with bird droppingsCentral and eastern United States, especially areas around the Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugs

collab anthrax

Disorder/OrganismSourceGeographic AreaManagement for Moderate to Severe Disease or Special PopulationsHantavirus pulmonary syndrome (HPS)HantavirusUrine, droppings, and saliva of infected rodentsSouthwest United States, Mexico, Central AmericaSupportiveOxygenMechanical ventilation in severe cases (38% fatal)AspergillosisAspergillusCommon mold found indoors and outside in damp areas; may be extensive in older buildings; moist soil and decomposing wood and leavesCan occur in any indoor environment damp enough to support mold growthOutdoor growth in San Francisco, Canada & United States around the Great Lakes; Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugsSurgery may be needed in severe casesBlastomycosis (fungal)BlastomycesMoist soil, decomposing wood and leavesCanada & United States around the Great Lakes; Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugsCoccidioidomycosisCoccidioidesSoilSouthwest, far west United States, Mexico, Central and South AmericaSupportive careProlonged course of antifungal drugsCryptococcosisCryptococcus gattiiTrees and soil beneath treesU.S. Pacific coast regions, mid to southern British ColumbiaSupportive careProlonged course of antifungal drugsHistoplasmosisHistoplasmaSoil containing large amounts of bird and bat droppings; surfaces with bird droppingsCentral and eastern United States, especially areas around the Ohio and Mississippi River ValleysSupportive careProlonged course of antifungal drugs

assess fractures of the nose

Document any nasal problem, including deviation, malaligned nasal bridge, a change in nasal breathing, crackling of the skin (crepitus) on palpation, bruising, and pain. Blood or clear fluid (cerebrospinal fluid [CSF]) may drain from one or both nares as a result of a simple nasal fracture. This is rare and, if present, indicates a serious injury (e.g., skull fracture). CSF can be differentiated from normal nasal secretions because CSF contains glucose that will test positive with a dipstick test for glucose. When CSF dries on a piece of filter paper, a yellow "halo" appears as a ring at the dried edge of the fluid

Antidysrhythmic Medication

Drug CategorySelected Nursing ImplicationsClass I: Sodium Channel BlockersThere are 3 subgroups of class I drugs.Common examples of sodium channel blockers:Type IA • Disopyramide phosphate Type IB • Lidocaine • Mexiletine hydrochloride Type IC • Flecainide acetate • Propafenone hydrochloride Monitor BP and HR; hypotension and bradycardia can occur. Monitor for arrhythmias; these agents affect conduction patterns, sometimes increasing the frequency or severity of dysrhythmias. Monitor for CNS side effects such as dizziness, anxiety, ataxia, insomnia, confusion, seizures, and GI distress; these side effects may require dose reduction or discontinuation of the drug. Monitor for signs of heart failure; many class I agents can also cause HF. Class II: Beta Blockers Only 4 beta blockers are approved for the treatment of dysrhythmias (Burchum & Rosenthal, 2019). Common examples of beta blockers: • Propranolol • Acebutolol • Esmolol • Sotalol • Sotalol is a class II dysrhythmic and a class III drug because of its effect on the QT interval and delay of repolarization. • Assess ventricular arrhythmias because this drug can have proarrhythmic effects. Monitor HR and BP; bradycardia and decreased BP are expected effects. Assess for wheezing or shortness of breath; beta2-blocking effects on the lungs can cause bronchospasm. Assess for insomnia, fatigue, and dizziness; side effects may require a decrease in dosage or discontinuation of the drug. Class III: Potassium Channel Blockers There are currently 5 class III agents. Each drug works to delay repolarization and prolongs the QT interval. Although their effects are similar, the side effects and mechanism of action vary greatly. Selected examples of drug-specific side effects with associated rationales are listed. • Sotalol • Used for atrial and ventricular dysrhythmias. For all class III potassium channel blockers: • Monitor BP and HR; hypotension and bradycardia can occur. • Monitor for arrhythmias; these agents affect conduction patterns, sometimes increasing the frequency or severity of dysrhythmias. • Amiodarone • Used for atrial and ventricular dysrhythmias. For amiodarone: • Continually monitor ECG rhythm during infusion; bradycardia and AV block can occur. • This drug can cause serious toxicities (lung damage, visual impairment). As a result, approval is limited to use for life-threatening dysrhythmias. However, because of efficacy, use remains very common (Burchum & Rosenthal, 2019). • Corneal pigmentation occurs in most patients, but it generally does not interfere with vision. • Dronedarone • Used for AF and atrial flutter. For dronedarone: • Teach patient to take with meals and to avoid grapefruit juice; this drug is better absorbed with food, and grapefruit juice alters the effect of the drug. • Teach patient to notify provider with signs of HF; this drug is contraindicated for patients with HF. • Ibutilide • Used for AF and atrial flutter. For ibutilide: • Stop infusion as soon as the dysrhythmia is terminated or in the event of VT; this drug may cause potentially fatal dysrhythmias. • Assess potassium and magnesium levels before infusion because electrolyte balance must be corrected prior to and during use. • Dofetilide • Used for AF and atrial flutter. For dofetilide: • Teach patient to change positions slowly; orthostatic hypotension is a common side effect. Class IV: Calcium Channel Blockers Only 2 calcium channel blockers are approved for use in the treatment of dysrhythmias. • Verapamil • Diltiazem For all class IV calcium channel blockers: • Monitor HR and BP; bradycardia and hypotension are common side effects. • Teach patients to change position slowly when receiving oral therapy; orthostatic hypotension can occur until tolerance develops. • Used for AF and atrial flutter. • Teach patients to report dyspnea, orthopnea, distended neck veins, or swelling of the extremities; HF can occur, necessitating a decrease in dosage or discontinuation of drug. Class: Other Other drugs used in the treatment of dysrhythmias fall outside of the previous categories. They are unclassified drugs for dysrhythmia treatment. Common examples of other dysrhythmia medications: • Digoxin • Used for AF and atrial flutter. For digoxin: • Assess apical HR before administration; decreased HR is an expected response. • Atropine sulfate • Used for bradycardia. • Teach patient to report nausea, vomiting, diarrhea, paresthesias, confusion, or visual disturbance; these can indicate digoxin toxicity. • Monitor HR and rhythm after administration; increased heart rate is expected. • Adenosine • Used for paroxysmal SVT. • Have emergency equipment available because a short period of asystole is common after administration; bradycardia and hypotension may occur. • Facial flushing, shortness of breath, and chest pain are common side effects.

First-Line Treatment for Tuberculosis

Drug and ActionNursing ImplicationsIsoniazidKills actively growing mycobacteria outside the cell and inhibits the growth of dormant bacteria inside macrophages and caseating granulomasInstruct patients to avoid antacids and to take the drug on an empty stomach (1 hour before or 2 hours after meals) to prevent slowing of drug absorption in the GI tract.Teach patients to take a daily multiple vitamin that contains the B-complex vitamins while on this drug because the drug can deplete the body of this vitamin.Remind patients to avoid alcoholic beverages while on this drug because the liver-damaging effects of this drug are potentiated by alcohol.Tell patients to report darkening of the urine, a yellow appearance to the skin or whites of the eyes, and an increased tendency to bruise or bleed, which are signs and symptoms of liver toxicity or failure.RifampinKills slower-growing organisms, even those that reside inside macrophages and caseating granulomasWarn patients to expect an orange-reddish staining of the skin and urine and all other secretions to have a reddish-orange tinge; also, soft contact lenses will become permanently stained because knowing the expected side effects decreases anxiety when they appear.Instruct sexually active women using oral contraceptives to use an additional method of contraception while taking this drug and for 1 month after stopping it because this drug reduces the effectiveness of oral contraceptives.Remind patients to avoid alcoholic beverages while on this drug because the liver-damaging effects of this drug are potentiated by alcohol.Tell patients to report darkening of the urine, a yellow appearance to the skin or whites of the eyes, and an increased tendency to bruise or bleed, which are signs and symptoms of liver toxicity or failure.Ask patients about all other drugs in use because this drug interacts with many other drugs.PyrazinamideCan effectively kill organisms residing within the very acidic environment of macrophages (which is where the tuberculosis bacillus sequesters)Available only in combination with other anti-TB drugsAsk patients if they have ever had gout because the drug increases uric acid formation and will make gout worse.Instruct patients to drink at least 8 ounces of water when taking this tablet and to increase fluid intake to prevent uric acid from precipitating, making gout or kidney problems worse.Teach patients to wear protective clothing, a hat, and sunscreen when going outdoors in the sunlight because the drug causes photosensitivity and greatly increases the risk for sunburn.Remind patients to avoid alcoholic beverages while on this drug because the liver-damaging effects of this drug are potentiated by alcohol.Tell patients to report darkening of the urine, a yellow appearance to the skin or whites of the eyes, and an increased tendency to bruise or bleed, which are signs and symptoms of liver toxicity or failure.EthambutolInhibits bacterial RNA synthesis, thus suppressing bacterial growthSlow acting and bacteriostatic rather than bactericidal; thus it must be used in combination with other anti-TB drugsInstruct patients to report any changes in vision, such as reduced color vision, blurred vision, or reduced visual fields, immediately to his or her primary health care provider because the drug can cause optic neuritis, especially at high doses, and can lead to blindness. Minor eye problems are usually reversed when the drug is stopped.Remind patients to avoid alcoholic beverages while on this drug because the drug induces severe nausea and vomiting when alcohol is ingested.Ask patients if they have ever had gout because the drug increases uric acid formation and will make gout worse.Instruct patients to drink at least 8 ounces of water when taking this drug and to increase fluid intake to prevent uric acid from precipitating, making gout or kidney problems worse.

interventions pulmonary artery htn

Drug therapy can reduce pulmonary pressures and slow the development of cor pulmonale by dilating pulmonary vessels and preventing clot formation (related to narrowed vessel lumens). Warfarin is taken daily to achieve an international normalized ratio (INR) of 1.5 to 2.0. Calcium channel blockers have been used to dilate blood vessels. The three classes of drugs that have been shown to be most effective in the treatment of PAH are the endothelin-receptor antagonists, prostacyclin agonists, and guanylate cyclase stimulators when used in combination (Hohsfield, 2018). Drug therapy is usually required until lung transplantation or disease progression to death. Endothelin-receptor antagonists, such as bosentan, induce blood vessel relaxation and decrease pulmonary arterial pressure. However, these agents cause general vessel dilation and some degree of hypotension. Other endothelin receptor antagonist drugs include ambrisentan and macitentan. Teach patients to take the drug with a full glass of water, and teach them not to break, chew, or crush the tablet. All drugs in this class increase the risk for birth defects and are contraindicated for women who are pregnant or breast-feeding. Instruct women who are sexually active and within child-bearing age to use two reliable methods of contraception while taking these drugs. In addition, the drugs are associated with some liver toxicity and patients should avoid drinking alcoholic beverages while taking any of them. Also teach patients the indications of liver problems (e.g., jaundice, nausea, pain or tenderness in the upper right abdominal quadrant, dark urine). Natural and synthetic prostacyclin agonists provide specific dilation of pulmonary blood vessels. Continuous infusion of epoprostenol or treprostinil through a small IV pump reduces pulmonary pressures and increases lung blood flow. Treprostinil can also be delivered by continuous subcutaneous infusion. Continuous infusions of prostacyclin drugs can be performed by the patient at home and in other settings. These drugs are also continued when the patient is hospitalized for any reason. The unusual continuous infusion, the need to keep an IV line dedicated strictly to prostacyclin infusion, and the varied dosages of the different brands of prostacyclins contribute to a high drug error rate when infusing this drug. Newer oral formulations of prostacyclin agonists include selexipag and treprostinil are available (Hohsfield et al., 2018; Noel et al., 2017). Iloprost and treprostinil can be delivered by inhalation. A drug often given along with prostacyclins is oral or IV sildenafil. Guanylate cyclase stimulators (also known as phosphodiesterase 5 inhibitors), trigger endothelial nitric oxide and increase the amount an intracellular substance (cGMP) in endothelial cells, which induces relaxation and vasodilation. Oral agents in this class include sildenafil and tadalafil. Another oral drug, riociguat, also stimulates guanylate cyclase without inhibiting phosphodiesterase. All of these drugs can cause general hypotension and significant postural hypotension. Riociguat is associated with birth defects and is contraindicated for use in pregnant or breast-feeding women. Nursing Safety Priority Action Alert A critical nursing priority for a patient undergoing therapy with IV prostacyclin agents is to ensure that the drug therapy is never interrupted. Deaths have been reported if the drug delivery is interrupted even for a matter of minutes. Teach the patient to always have backup drug cassettes and battery packs. If these are not available or if the line is disrupted, the patient should go to the emergency department immediately. Another critical priority is helping the patient receiving IV prostacyclin agents prevent sepsis. The central line IV setup provides an access for organisms to enter the bloodstream directly. Teach the patient to use strict aseptic technique for all aspects of the drug delivery system. Also teach him or her to notify the pulmonologist at the first sign of any infection. Even when sepsis is diagnosed early and appropriate therapy started, patients with PAH have an overall worse outcome (Tartavoulle, 2017). Oxygen therapy is used when dyspnea is uncomfortable. This therapy improves function and reduces symptoms but does not cure or improve PAH. Surgical management of PAH involves lung transplantation. When cor pulmonale is also present, the patient may need combined heart-lung transplantation.

Asthma Prevention and Treatment

DrugNursing ImplicationsBronchodilatorsInduce rapid bronchodilation through relaxing bronchiolar smooth muscle by binding to and activating pulmonary beta2 receptors.Short-Acting Beta 2 Agonist (SABA)Primarily used as a fast-acting reliever (rescue) drug to be used either during an asthma attack or just before engaging in activity that usually triggers an attack.Albuterol (inhaled drug)Levalbuterol (inhaled drug)Teach patients to carry drug with them at all times because it can stop or reduce life-threatening bronchoconstriction.Teach patient to monitor heart rate because excessive use causes tachycardia and other systemic symptoms.When taking any of these drugs with other inhaled drugs, teach patient to use them at least 5 minutes before the other inhaled drugs to allow the bronchodilation effect to increase the penetration of other inhaled drugs.Teach patient the correct technique for using the MDI or DPI to ensure that the drug reaches the site of action.Long-Acting Beta 2 Agonist (LABA)Causes bronchodilation through relaxing bronchiolar smooth muscle by binding to and activating pulmonary beta2 receptors. Onset of action is slow with a long duration. Primary use is prevention of an asthma attack.Salmeterol (inhaled drug)Indacaterol (COPD only) (inhaled drug)Formoterol Arformoterol (COPD only)Teach patient to not use these drugs as reliever drugs because they have a slow onset of action and do not relieve acute symptoms.Teach patient the correct technique for using the MDI or DPI to ensure that the drug reaches the site of action.Cholinergic AntagonistCauses bronchodilation by inhibiting the parasympathetic nervous system, allowing the sympathetic system to dominate, releasing norepinephrine that activates beta2 receptors. Purpose is to prevent asthma attacks or COPD bronchospasms and improve gas exchange, although some are considered reliever drugs.Aclidinium (inhaled drug for prevention only)Ipratropium (inhaled drug for relief and prevention)Tiotropium (inhaled drug)Umeclidinium (inhaled drug for prevention only)If patient is to use any of these as a reliever drug, teach him or her to carry it at all times because it can stop or reduce life-threatening bronchoconstriction.For drugs delivered by MDI, teach patient to shake the inhaler well before using because the drugs separate easily.Teach patient to increase daily fluid intake because the drugs cause mouth dryness.Teach patient to observe for and report blurred vision, eye pain, headache, nausea, palpitations, tremors, and inability to sleep as these are systemic symptoms of overdose and require intervention.Teach patient the correct technique for using the MDI or DPI to ensure that the drug reaches the site of action.Table Continued DrugNursing ImplicationsAnti-InflammatoriesAll of these drugs help improve bronchiolar airflow and increase gas exchange by decreasing the inflammatory response of the mucous membranes in the airways. They do not cause bronchodilation.CorticosteroidsDisrupt production pathways of inflammatory mediators. The main purpose is to prevent an asthma attack caused by inflammation or allergies (controller drug).Fluticasone (MDI inhaled drug)Beclomethasone (MDI inhaled drug)Budesonide (MDI inhaled drug)Teach patient to use the drug daily, even when no symptoms are present, because maximum effectiveness requires continued use for 48-72 hours and depends on regular use.Teach patient to use good mouth care and to check mouth daily for lesions or drainage because these drugs reduce local immunity and increase the risk for local infections, especially Candida albicans (yeast).Teach patient to not use these drugs as reliever drugs because they have a slow onset of action and do not relieve acute symptoms.Teach patient the correct technique for using the MDI to ensure that the drug reaches the site of action.Prednisone (oral drug)Teach patient about expected side effects because knowing which side effects to expect may reduce anxiety when they appear.Teach patient to avoid anyone who has an upper respiratory infection because the drug reduces all protective inflammatory responses, increasing the risk for infection.Teach patient to avoid activities that lead to injury because blood vessels become more fragile, leading to bruising and petechiae.Teach patient to take drug with food to help reduce the side effect of GI ulceration.Teach patient not to suddenly stop taking the drug for any reason because the drug suppresses adrenal production of corticosteroids, which are essential for life.CromoneStabilizes the membranes of mast cells and prevents the release of inflammatory mediators. Purpose is to prevent asthma attack triggered by inflammation or allergens.Nedocromil (inhaled drug)Teach patient to use the drug daily, even when no symptoms are present, because maximum effectiveness requires continued use for 48-72 hours and depends on regular use.Teach patient to not use this drug as a reliever drug because it has a slow onset of action and does not relieve acute symptoms.Teach patient the correct technique for using the MDI to ensure that the drug reaches the site of action.Leukotriene ModifierBlocks the leukotriene receptor, preventing the inflammatory mediator from stimulating inflammation. Purpose is to prevent asthma attack triggered by inflammation or allergens.Montelukast (oral drug)Teach patient to use the drug daily, even when no symptoms are present, because maximum effectiveness requires continued use for 48-72 hours and depends on regular use.Teach patient not to decrease the dose of or stop taking any other asthma drugs unless instructed by the health care professional because this drug is for long-term asthma control and does not replace other drugs, especially corticosteroids and reliever (rescue) drugs.Monoclonal AntibodiesBind to and block the actions of proinflammatory cytokines (interleukin 5) or cell surface sites of IgE that trigger and maintain asthma attacks.Interleukin antagonists:Benralizumab (subcutaneous injection)Mepolizumab (subcutaneous injection)Reslizumab (slow IV infusion only)Only for use in patients who have eosinophilic asthma because these drugs block the actions of interleukin-5 (IL-5), which activates eosinophils and increases their numbers.Do not administer these drugs as a reliever drug because they do not relieve acute symptoms.Monitor patient for at least 2 hours after injection for indications of severe hypersensitivity and anaphylaxis because these drugs contain a foreign protein that has an increased risk for severe allergic reactions.IgE antagonist:Omalizumab (subcutaneous injection)Used only for patients who have a known allergy that triggers asthma attacks because the drug works by antagonizing IgE.Monitor patient for at least 2 hours after injection for indications of severe hypersensitivity and anaphylaxis because the drug contains a foreign protein that has an increased risk for severe allergic reactions.Do not administer this drug as a reliever drug because it does not relieve acute symptoms.

causes of dysrhythmias

Dysrhythmias occur for many reasons, including myocardial infarction (MI), electrolyte imbalances (especially potassium and magnesium), hypoxia, drug toxicity, and hypovolemia (decreased blood volume). People who use cocaine and illicit inhalants are particularly at risk for potentially fatal dysrhythmias. Stress, fear, anxiety, and caffeine can cause an increased heart rate (tachycardia or premature ventricular contractions). Nicotine and alcohol excess can lead to an abnormal heart rate or heart rhythm such as atrial fibrillation. Specific etiologies are described for each common dysrhythmia discussed in this chapter.

assess tb

Early detection of TB depends on patient reports rather than observable indicators. TB has a slow onset, and patients are often not aware of problems until the disease is advanced. TB is considered for any patient with a persistent cough and other symptoms, such as unintended weight loss, anorexia, night sweats, hemoptysis, shortness of breath, fever, or chills (Johnson et al., 2017). History Assess the patient's past exposure to TB. Ask about his or her country of origin and travel to or from foreign countries where incidence of TB is high (Benkert & Rayford, 2018). It is important to ask about the results of any previous tests for TB. Also ask whether the patient has had bacille Calmette-Guérin (BCG) vaccine (often given in childhood overseas), which contains attenuated tubercle bacilli. Anyone who has received BCG vaccine within the previous 10 years will have a positive skin test that can complicate interpretation for current TB infection . Usually the size of the skin response decreases each year after BCG vaccination. These patients should be evaluated for TB with a chest x-ray or an interferon-gamma release assay (IGRA), such as the QuantiFERON-TB Gold test (CDC, 2018e; WHO, 2019). Physical Assessment/Signs and Symptoms The patient with TB has progressive fatigue, lethargy, nausea, anorexia, weight loss, irregular menses, and a low-grade fever. Symptoms may have been present for weeks or months. Night sweats may occur with the fever. A cough with mucopurulent sputum, often streaked with blood, is present. Chest tightness and a dull, aching chest pain occur with the cough. Ask about, assess for, and document the presence of any of these symptoms to help with diagnosis, establish a baseline, and plan nursing interventions. When assessing the patient, you may note dullness with percussion over the involved lung fields, bronchial breath sounds, crackles, and increased transmission of spoken or whispered sounds. Partial obstruction of a bronchus from the disease or compression by lymph nodes may produce localized wheezing.

Endocrine Paraneoplastic Syndromes Associated With Lung Cancer

Ectopic Hormone SymptomsAdrenocorticotropic hormone (ACTH)Cushing syndromeAntidiuretic hormoneSyndrome of inappropriate antidiuretic hormone (SIADH)Weight gainGeneral edemaDilution of serum electrolytesFollicle-stimulating hormone (FSH)GynecomastiaParathyroid hormoneHypercalcemiaEctopic insulinHypoglycemia

Activity Schedule hf

Encourage patients with HF to stay as active as possible and to develop a regular exercise regimen (e.g., home walking program). However, teach the patient not to overdo it. Patients should be referred to cardiac rehabilitation programs. Medicare and third-party payers are now reimbursing for this service, but patients may need to wait 6 weeks to fully participate in the program. In addition to exercise programs, cardiac rehabilitation provides education on risk factor modification, medication adherence, and diet and weight management. Remind patients with persistent crackles and uncontrolled edema to begin exercise after their condition stabilizes. When exercise is indicated, teach the patient to begin walking 200 to 400 feet per day. At home the patient should try to walk at least three times a week and should slowly increase the amount of time walked over several months. If chest pain or severe dyspnea occurs while exercising or the patient has fatigue the next day, he or she is probably advancing the activity too quickly and should slow down. Encourage the patient to keep a diary that documents the time and duration of each exercise session, heart rate, and any symptoms that occur with exercise.

Assess the oral care needs of the patient with risk factors for thickly crusted secretions daily by

Ensure that assistive personnel who provide oral care understand the importance and the correct techniques for preventing secretion buildup and airway obstruction.

Sinus Bradycardia: Pathophysiology Review

Excessive vagal (parasympathetic) stimulation to the heart causes a decreased rate of sinus node discharge. It may result from carotid sinus massage, vomiting, suctioning, Valsalva maneuvers (e.g., bearing down for a bowel movement or gagging), ocular pressure, or pain. Increased parasympathetic stimuli may also result from hypoxia, inferior wall MI, and the administration of drugs such as beta-adrenergic blocking agents, calcium channel blockers, and digoxin. Lyme disease, electrolyte disturbances, neurologic disorders, and hypothyroidism may also cause bradycardia. The stimuli slow the heart rate and decrease the speed of conduction through the heart. When the sinus node discharge rate is less than 60 beats/min, the rhythm is called sinus bradycardia (Fig. 31.8B) (Kusumoto et al., 2019). Sinus bradycardia increases coronary perfusion time, but it may decrease coronary perfusion pressure. However, myocardial oxygen demand is decreased. Well-conditioned athletes with bradycardia have a hypereffective heart in which the strong heart muscle provides an adequate stroke volume and a low heart rate to achieve a normal cardiac output. Interprofessional Collaborative Care Assessment: Recognize Cues The patient with sinus bradycardia may be asymptomatic except for the decreased pulse rate. In many cases, the cause of sinus bradycardia is unknown. Assess the electronic health record (EHR) to determine if the patient is receiving medications that slow the conduction through the SA or AV node. Assess the patient for: • Syncope ("blackouts" or fainting) • Dizziness and weakness • Confusion • Hypotension • Diaphoresis (excessive sweating) • Shortness of breath • Chest pain If the patient is stable, treatment includes identification and treatment of the underlying cause. If the patient has any of these symptoms and the underlying cause cannot be determined, the treatment is to administer drug therapy with intravenous atropine, increase intravascular volume via IV fluids, and apply oxygen if oxygen saturation is below 94% or the patient is short of air. Drugs suspected of causing the bradycardia are discontinued. If beta-blocker overdose is suspected, administration of glucagon may help by increasing the heart rate and blood pressure. If the heart rate does not increase sufficiently, prepare for transcutaneous or transvenous pacing to increase the heart rate. If treatment of the underlying cause does not restore normal sinus rhythm, the patient will require permanent pacemaker implantation. Temporary pacing is a nonsurgical intervention that provides a timed electrical stimulus to the heart when either the impulse initiation or the conduction system of the heart is defective. The electrical stimulus then spreads throughout the heart to depolarize the cells, which should be followed by contraction and cardiac output. Electrical stimuli may be delivered to the right atrium or right ventricle (single-chamber pacemakers) or to both (dual-chamber pacemakers). Temporary pacing is used for patients with symptomatic bradydysrhythmias who do not respond to atropine or for patients with asystole. There are two types of temporary pacing: transcutaneous and transvenous. Transcutaneous pacing is accomplished through the application of two large external electrodes. The electrodes are attached to an external pulse generator. The generator emits electrical pulses, which are transmitted through the electrodes and then transcutaneously to stimulate ventricular depolarization when the patient's heart rate is slower than the rate set on the pacemaker. Transcutaneous pacing is used as an emergency measure to provide demand ventricular pacing in a profoundly bradycardic or asystolic patient until invasive pacing can be used or the patient's heart rate returns to normal. This method of pacing is painful and may require administration of pain and sedative medications for the patient to tolerate the therapy. Transcutaneous pacing is used only as a temporary measure to maintain heart rate and perfusion until a more permanent method of pacing is used. A temporary transvenous system can be inserted in an emergency as a bridge until a permanent pacemaker can be inserted. This system consists of an external battery-operated pulse generator and pacing electrodes, or lead wire. The wire attaches to the generator on one end and is threaded to the right ventricle via the subclavian or femoral vein (Fig. 31.9). In pacemaker systems, electrical pulses, or stimuli, are emitted from the negative terminal of the generator, flow through a lead wire, and stimulate the cardiac cells to depolarize. The current seeks ground by returning through the other lead wire to the positive terminal of the generator, thus completing a circuit. The intensity of electrical current is set by selecting the appropriate current output, measured in milliamperes. The two major modes of pacing are synchronous (demand) pacing and asynchronous (fixed-rate) pacing. Temporary pacing is usually done in the synchronous (demand) pacing mode. The pacemaker's sensitivity is set to sense the patient's own beats. When the patient's heart rate is above the rate set on the pulse generator, the pacemaker does not fire (inhibits itself). When the patient's heart rate is less than the generator setting, the pacemaker provides electrical impulses (paces). When a pacing stimulus is delivered to the heart, a spike (or pacemaker artifact) is seen on the monitor or ECG strip. The spike should be followed by evidence of depolarization (i.e., a P wave, indicating atrial depolarization, or a QRS complex, indicating ventricular depolarization). This pattern is referred to as capture, indicating that the pacemaker has successfully depolarized, or captured, the chamber. Permanent Pacemaker Permanent pacemaker insertion is performed to treat conduction disorders that are not temporary, including complete heart block. These pacemakers are usually powered by a lithium battery and have an average life span of 10 years. After the battery power is depleted, the generator must be replaced by a procedure done with the patient under local anesthesia. Some pacemakers can be recharged externally. Combination pacemaker/defibrillator devices are also available. A biventricular pacemaker may be used to coordinate contractions between the right and left ventricles. In addition to pacing used in the right side of the heart, an additional lead is placed in the left lateral wall of the left ventricle through the coronary sinus. This procedure allows synchronized depolarization of the ventricles and is used in patients with moderate-to-severe heart failure to improve functional ability. FIG. 31.9 Placement of pacemaker in chest and heart leads. The electrophysiologist implants the pulse generator in a surgically made subcutaneous pocket at the shoulder in the right or left subclavicular area, which may create a visible bulge (see Fig. 31.9). The leads are introduced transvenously via the cephalic or the subclavian vein to the endocardium on the right side of the heart. A leadless pacing system has recently been developed where the pacemaker is a self-contained unit that is placed in the right ventricle via the femoral vein (Urden et al., 2018). Previous attempts with this approach have been associated with high complication rates; however, newer developments are showing promise. Further research regarding long-term use of leadless pacing systems is under way (Hayes, 2018). After the procedure, monitor the ECG rhythm to check that the pacemaker is working correctly. Assess the implantation site for bleeding, swelling, redness, tenderness, and infection. The dressing over the site should remain clean and dry. The patient should be afebrile and have stable vital signs. The health care provider prescribes initial activity restrictions, which are then gradually increased. Complications of permanent pacemakers are similar to those of temporary invasive pacing and include development of pericardial effusion, pericardial tamponade, and diaphragmatic pacing. In diaphragmatic pacing, the patient may report pain at the level of the diaphragm. Observe for muscle contractions over the diaphragm that are synchronous with the heart rate. Pacemaker checks are done on an ambulatory-care basis at regular intervals. Reprogramming may be needed if pacemaker problems develop. The pulse generator is interrogated using an electronic device to determine the pacemaker settings and battery life (Fig. 31.10). In addition, most pacemaker manufacturers offer wireless home transmitter devices. Data are then sent via landline telephone to a database, which is accessed by the device clinic or primary health care provider. Stress the need to keep follow-up appointments for more detailed pacemaker checks and reprogramming, if necessary, and for assessment. Give written and verbal information to patients who have a permanent pacemaker about the type and settings of their pacemaker. Teach the patient to report any pulse rate lower than that set on the pacemaker. Review the proper care of the pacemaker insertion site and the importance of reporting any fever or any redness, swelling, or drainage at the pacemaker insertion site. If the surgical incision is near either shoulder, advise the patient to avoid lifting the arm over the head or lifting more than 10 lb for the next 4 weeks because this could dislodge the pacemaker wire. Encourage the patient that usual arm movement is encouraged to prevent shoulder stiffness. FIG. 31.10 Permanent pacemaker (A) and programmer (B). From Fischell, T. A., et al. [2010]. Initial clinical results using intracardiac electrogram monitoring to detect and alert patients during coronary plaque rupture and ischemia, Journal of the American College of Cardiology, 56[14], 1089−1098. Nursing Safety Priority Action Alert Teach patients who have permanent pacemakers to: • Avoid sources of strong electromagnetic fields, such as magnets and telecommunications transmitters. (These may cause interference and could change the pacemaker settings, causing a malfunction. Magnetic resonance imaging (MRI) is usually contraindicated, depending on the machine's technology.) • Carry a pacemaker identification card provided by the manufacturer and wear a medical alert bracelet at all times Current evidence does not include special precautions with common household appliances (e.g. microwaves), with modern communication devices (e.g. cell phones), or with portable media players (Olshansky & Hayes, 2017). See the Patient and Family Education: Preparing for Self-Management box for care after the insertion of a permanent pacemaker.

implement osa

Far more patients are helped by nonsurgical procedures; surgical management is reserved for anatomic-related causes and severe OSA that remains resistant to nonsurgical approaches. Changes in sleeping position or weight loss may correct mild sleep apnea and improve gas exchange . Position-fixing devices may prevent subluxation of the tongue and reduce obstruction. Use of an oral appliance, called maxillomandibular advancement, can improve airflow by supporting the lower jaw in a more forward position. These devices are especially helpful for adults who have a retracted lower jaw. Noninvasive positive-pressure ventilation (NPPV) via continuous positive airway pressure (CPAP) to hold open the upper airways is the most commonly used form of nonsurgical management for OSA. CPAP delivers a set positive airway pressure continuously during each cycle of inhalation and exhalation with the use of a small electric compressor and some type of delivery device such as a nasal-oral facemask, nasal mask, or nasal pillows (with or without cushioned or gel prongs). new cpap machines, less noisy, less intrusive, etc adherence with the therapy is critical overed by Medicare for older adults if the patient uses it consistently for at least 6 hours daily. Neither sedatives nor stimulants treat the cause of OSA. Surgical intervention is considered when patients are not able to tolerate CPAP or when its use does not improve OSA. Before surgery is planned, patients may first undergo a thorough endoscopic examination under deep sedation to determine which problem or problems cause the OSA. This examination can reveal variation in anatomic structures or changes in anatomic features that result from oral-pharyngeal muscle relaxation. Once a specific cause or problem has been identified, the correct specific surgery can be planned. Implanted stimulators represent a minimally invasive surgery that can help patients with mild-to-moderate sleep apnea. This surgery involves placing an electrode in the neck that can stimulate the hypoglossal nerve (cranial nerve XII). The small battery-powered charge generator is implanted in the chest in a manner similar to a pacemaker. When respiratory effort is slowed during sleep and when apnea occurs, the generator sends signals to the stimulator, which then uses mild electrical shocks to cause contraction of appropriate airway muscles. The stimulatory shocks are of such a low intensity that the patient is not awakened and does not feel pain but are strong enough to keep the airway open. It is not strong enough to keep the airway open in patients whose OSA is caused by complete concentric collapse of the soft palate during sleep. Tracheostomy is a possible but uncommon type of surgery to manage OSA. It is reserved as a last resort for very severe OSA that is not relieved by more moderate interventions. Common minor surgical procedures that can correct some anatomic problems associated with mild-to-moderate OSA include simple tonsillectomy, adenoidectomy, uvulectomy, or repair of a deviated septum. Uvulopalatopharyngoplasty (UPPP) is a collection of procedures that are more complex and intended to resolve OSA by remodeling the entire posterior oropharynx. Older UPPP procedures focused on significant removal of tissue in the oropharyngeal cavity. These older, more extensive procedures often were not successful in correcting OSA, leaving some patients no better off and sometimes worse than before surgery. Immediate complications included severe pain, bleeding, and oropharyngeal swelling. Long-term complications sometimes included permanent taste changes, changes in voice quality, and scar tissue formation. Modified uvulopalatopharyngoplasty (modUPPP) is a more recent reconstructive approach with a variety of procedures that may be performed using conventional, robotic-assisted, or laser surgery techniques. The procedure is individualized by the surgeon for each patient. With modUPPP the focus is less on extensive tissue removal and more on repositioning and reinforcing oropharyngeal support structures to improve oropharyngeal airway flow. Although exact surgical techniques vary, the desired outcome is to change the pull of palatal and oropharyngeal muscles from central and downward to upward and toward the sides of the throat, thus making the oropharynx larger omplications in the immediate period after surgery include edema, infection, and bleeding. Pain and difficulty swallowing are common for the first week after surgery. Maintaining a patent airway in the postoperative period is important because the tissue manipulation during surgery results in some degree of temporary swelling. Observe the patient for respiratory effort and effectiveness of gas exchange based on pulse oximetry or end-tidal carbon dioxide measurement. Assess the size and shape of the oropharynx. Assess whether the patient can swallow effectively, even if it is painful. Note whether he or she can swallow oral secretions or whether drooling is present. Assess voice quality and determine whether stridor or crowing is present; these conditions indicate a partial obstruction of the airway Assess the patient at least every 2 hours during the first 24 hours after surgery for indications of airway narrowing or partial obstruction (e.g., increased respiratory effort, presence of stridor or crowing, drooling or an inability to swallow oral secretions, reduction in the size of the oropharynx, decreasing oxygen saturation, rising end-tidal carbon dioxide level). If any of these signs or symptoms are present, initiate the Rapid Response Team to prevent a partial obstruction from becoming a complete obstruction. Relieving pain after surgery has a high priority because the oropharynx has a rich nerve supply and is extremely sensitive. Usually the patient receives pain control drugs parenterally for the first 24 hours because of the pain involved in swallowing. Aspirin and other NSAIDs are avoided during the first 24 hours to reduce the risk for excessive bleeding prescribe antibiotics in the intraoperative and postoperative periods. This operation cannot be a truly sterile procedure. Assess the oropharynx daily for indicators of infection including the presence of purulent exudate, foul-smelling breath, or a change in color of mucous membranes to beefy red. Document and report any of these changes. The oropharynx and its associated structures have a rich blood supply and have the potential for excessive bleeding during and after surgery. Some bleeding or oozing after surgery is normal. Examine the oropharynx for the amount and color of bleeding from surgical sites every 2 to 4 hours the first day. Darker blood and blood mixed with secretions is considered normal. If the amount of blood increases or becomes bright red, notify the surgeon. Instruct the patient to tell nursing personnel if he or she perceives an increase in bleeding. Assess the patient for excessive swallowing or belching that could indicate blood dripping down the throat. Avoid the use of aspirin or NSAID-containing pain relievers until the risk for bleeding has passed. Instruct the patient to avoid trauma to the area by avoiding toothbrushes and using mouthwash and oral sponges to clean the teeth and gums until the surgeon indicates toothbrushing and flossing are permitted

Infective Endocarditis

Fever associated with chills, night sweats, malaise, and fatigue • Anorexia and weight loss • Cardiac murmur (newly developed or change in existing) • Development of heart failure • Evidence of systemic embolization • Petechiae • Splinter hemorrhages • Osler nodes (on palms of hands and soles of feet) • Janeway lesions (flat, reddened maculae on hands and feet) • Roth spots (hemorrhagic lesions that appear as round or oval spots on the retina) • Positive blood cultures

assess and intervention cardiomyopathy

Findings in cardiomyopathy depend on the structural and functional abnormalities. For example, left ventricular or biventricular failure is characteristic of dilated cardiomyopathy (DCM). Some patients with DCM are asymptomatic for months to years and have left and/or right ventricular dilation confirmed on x-ray examination or echocardiography. Others experience sudden, pronounced symptoms of left ventricular failure, such as progressive dyspnea on exertion, orthopnea, palpitations, and activity intolerance. Right-sided HF develops late in the disease and is associated with a poor prognosis. Atrial fibrillation occurs in some patients and is associated with embolism. The clinical picture of hypertrophic cardiomyopathy (HCM) results from the hypertrophied septum causing a reduced stroke volume (SV) and cardiac output (CO). Most patients are asymptomatic until late adolescence or early adulthood. The primary symptoms of HCM are exertional dyspnea, angina, and syncope. The chest pain is atypical in that it usually occurs at rest, is prolonged, has no relation to exertion, and is not relieved by the administration of nitrates. A high incidence of ventricular dysrhythmias is associated with HCM. Sudden death occurs and may be the first manifestation of the disease (Cao & Zhang, 2017). Echocardiography, radionuclide imaging, and angiocardiography during cardiac catheterization are performed to diagnose and differentiate cardiomyopathies. Interventions: Take Action The treatment of choice for the patient with cardiomyopathy varies with the type of cardiomyopathy and may include both medical and surgical interventions. Nonsurgical Management The care of patients with dilated or restrictive cardiomyopathy is initially the same as that for HF. Drug therapy includes the use of diuretics, vasodilating agents, and cardiac glycosides to increase CO. Because patients are at risk for sudden death, teach them to report any palpitations, dizziness, or fainting, which might indicate a dysrhythmia. Antidysrhythmic drugs or implantable cardiac defibrillators may be used to control life-threatening dysrhythmias. To block inappropriate sympathetic stimulation and tachycardia, beta blockers (e.g., metoprolol) are used. If cardiomyopathy has developed in response to a toxin (such as alcohol), further exposure to that toxin must be avoided. Management of obstructive HCM includes administering negative inotropic agents such as beta-adrenergic blocking agents (carvedilol) and calcium antagonists (verapamil). These drugs decrease the outflow obstruction that accompanies exercise. They also decrease heart rate (HR), resulting in less angina, dyspnea, and syncope. Vasodilators, diuretics, nitrates, and cardiac glycosides are contraindicated in patients with obstructive HCM because vasodilation and positive inotropic effects may worsen the obstruction. Strenuous exercise is also prohibited because it can increase the risk for sudden death. Excess alcohol intake and dehydration should also be avoided. Depending on risk stratification, an implantable cardioverter defibrillator (ICD) may be recommended to prevent sudden cardiac death. Patients with HCM are encouraged to seek genetic counseling. First-degree relatives should be screened for the presence of HCM, and echocardiography should be offered starting at age 12. Surgical Management Myectomy and Ablation The type of surgery performed depends on the type of cardiomyopathy. The most commonly used surgical treatment for obstructive HCM involves excising a portion of the hypertrophied ventricular septum to create a wider outflow tract (ventricular septal myectomy). This procedure results in long-term improvement in activity tolerance for most patients. Percutaneous alcohol septal ablation is another option for patients with HCM. Absolute alcohol is injected into a target septal branch of the left anterior descending coronary artery to produce a small septal infarction. Over time this will result in remodeling of the area, reducing the obstruction. The patient with arrhythmogenic right ventricular cardiomyopathy who does not respond to drug therapy may have a radiofrequency catheter ablation or placement of an implantable defibrillator (see Chapter 31 for discussion of these procedures). Heart Transplantation Heart transplantation (surgical replacement with a donor heart) is the treatment of choice for patients with severe DCM and may be considered for patients with restrictive cardiomyopathy. The procedure may also be done for end-stage heart disease caused by coronary artery disease, valvular disease, or congenital heart disease. Preoperative Care Criteria for candidate selection for heart transplantation include: • Life expectancy less than 1 year • Age generally younger than 65 years • New York Heart Association (NYHA) Class III or IV • Normal or only slightly increased pulmonary vascular resistance • Absence of active infection • Stable psychosocial status • No evidence of current drug or alcohol misuse Once the candidate is eligible and a heart is available, provide preoperative care as described in Chapter 9. Operative Procedures The surgeon transplants a heart from a donor with a comparable body weight and ABO compatibility into a recipient less than 6 hours after procurement. In the most common procedure (bicaval technique), the intact right atrium of the donor heart is preserved by anastomoses at the patient's (recipient's) superior and inferior venae cavae. In the more traditional orthotopic technique, cuffs of the patient's right and left atria are attached to the donor's atria. Anastomoses are made between the recipient and donor atria, aorta, and pulmonary arteries (Fig. 32.7). Because the remaining remnant of the recipient's atria contains the sinoatrial (SA) node, two unrelated P waves are visible on the ECG. Postoperative Care The postoperative care of the heart transplant recipient is similar to that for conventional cardiac surgery (see Chapter 35). However, the nurse must be especially observant to identify occult bleeding into the pericardial sac with the potential for tamponade. The patient's pericardium has usually stretched considerably to accommodate the diseased, hypertrophied heart, predisposing the patient to concealed postoperative bleeding. The transplanted heart is denervated (disconnected from the body's autonomic nervous system) and unresponsive to vagal stimulation. In the early postoperative phase, isoproterenol may be titrated to support the heart rate and maintain cardiac output. Atropine, digoxin, and carotid sinus pressure are not used because they do not have their usual effects on the new heart. Denervation of the heart may cause pronounced orthostatic hypotension in the immediate postoperative phase. Caution the patient to change position slowly to help prevent this complication. Some patients also require a permanent pacemaker that is rate responsive to his or her activity level. The purpose is to increase CO and improve activity tolerance. FIG. 32.7 One technique for heart transplantation. To suppress natural defense mechanisms and prevent transplant rejection, patients require a combination of immunosuppressants for the rest of their lives. Chapter 16 describes transplant rejection and prevention in detail. Nursing Safety Priority Critical Rescue After surgery, perform comprehensive cardiovascular and respiratory assessments frequently according to agency or heart transplant surgical protocol. See the Best Practice for Patient Safety & Quality Care box for the signs and symptoms of rejection that are specific to heart transplant. Report any of these manifestations to the surgeon immediately! To detect rejection, the surgeon performs right endomyocardial biopsies at regularly scheduled intervals and whenever symptoms occur. Be very careful about handwashing and aseptic technique because patients are immunosuppressed from drug therapy. Infection is the major cause of death and usually develops in the immediate post-transplant period or during treatment for acute rejection. The median survival rate for adults following cardiac transplantation is 11 years and rising (Pham, 2018). Over time, many of these surviving patients are developing a form of coronary artery disease (CAD) called cardiac allograft vasculopathy (CAV), which presents as diffuse plaque in the arteries of the donor heart. The cause is thought to involve a combination of immunologic and nonimmunologic processes that result in vascular endothelial injury and an inflammatory response (Pham, 2018). Because the heart is denervated, patients do not usually experience angina. Regularly scheduled exercise tolerance tests and angiography are required to identify CAV. Only a small percentage of patients with CAV benefit from revascularization procedures such as balloon angioplasty or coronary artery bypass surgery. Stents are beginning to show some promise in managing these patients. Retransplantation may be done in select patients. To delay the development of CAV, encourage patients to follow lifestyle changes similar to those with primary CAD (see Chapter 35). The provider may prescribe a calcium channel blocker such as diltiazem to prevent coronary spasm and closure. Stress the importance of strict adherence to nutritional modifications and drug regimens. Teach the patient the importance of participating in a regular exercise program. Collaborate with the physical therapist and the cardiac rehabilitation specialist to plan the most appropriate exercise plan for the patient. Discharge planning involves a collaborative, interdisciplinary approach. Patients require extensive health teaching for self-management and community resources for support. Counseling and support groups can help patients cope with their fear of organ rejection. Drug therapy adherence is crucial to prevent this problem. Continuing community-based care for patients with a heart transplant is similar to that for heart failure discussed earlier in this chapter.

Flail Chest

Flail chest is the result of fractures of three or more adjacent ribs in two or more places causing paradoxical chest wall movement (inward movement of the thorax during inspiration, with outward movement during expiration) (Fig. 29.3). It usually involves one side of the chest and results from blunt chest trauma—often high-speed car crashes. Because the force required to produce a flail chest is great, it is important to assess for other possible underlying injuries. Flail chest can also occur from bilateral separations of the ribs from their cartilage connections to each other anteriorly, without an actual rib fracture. This condition can occur as a complication of cardiopulmonary resuscitation. Other injuries to the lung tissue under the flail segment may be present. Gas exchange , coughing, and clearance of secretions are impaired. Splinting further reduces the patient's ability to exert the extra effort to breathe and may contribute later to failure to wean. Assess the patient with a flail chest for paradoxical chest movement, dyspnea, cyanosis, tachycardia, and hypotension. The patient is often anxious, short of breath, and in pain. Work of breathing is increased from the paradoxical movement of the involved segment of the chest wall. opposite lung during inspiration. Interventions include humidified oxygen, pain management, promotion of lung expansion through deep breathing and positioning, and secretion clearance by coughing and tracheal suction. The patient with a flail chest may be managed with vigilant respiratory care. Mechanical ventilation is needed if respiratory failure or shock occurs. Monitor ABG values and vital capacity closely. With severe hypoxemia and hypercarbia, the patient is intubated and mechanically ventilated with PEEP. With lung contusion or an underlying pulmonary disease, the risk for respiratory failure increases. Usually flail chest is stabilized by positive-pressure ventilation. Surgical stabilization is used only in extreme cases of flail chest. Monitor the patient's vital signs and fluid and electrolyte balance closely so hypovolemia or shock can be managed immediately. If he or she has a lung contusion, provide oxygen as needed and give IV fluids as prescribed. Assess for and relieve pain with prescribed analgesic drugs by IV, epidural, or nerve block route. Give psychosocial support to the anxious patient by explaining all procedures, talking slowly, and allowing time for expression of feelings and concerns.

Permanent Pacemakers

Follow the instructions for pacemaker site skin care that have been specifically prepared for you. Report any fever or redness, swelling, or drainage from the incision site to your physician. • Do not manipulate the pacemaker generator site. Twisting or manipulation of the generator site can cause the leads to shift (lead dislodgement) (Townsend, 2018). • Keep your pacemaker identification card in your wallet and wear a medical alert bracelet. • Take your pulse for 1 full minute at the same time each day and record the rate in your pacemaker diary. Take your pulse any time you feel symptoms of a possible pacemaker failure and report your heart rate and symptoms to your primary health care provider. • Know the rate at which your pacemaker is set and the basic functioning of your pacemaker. Know which rate changes to report to your primary health care provider. • Do not apply pressure over your generator. Avoid tight clothing or belts. • You may take baths or showers without concern for your pacemaker. • Inform all health care providers that you have a pacemaker. Certain tests that they may wish to perform (e.g., magnetic resonance imaging) could affect or damage it. • Know the indications of battery failure for your pacemaker as you were instructed and report these findings to your primary health care provider if they occur. • Do not operate electrical appliances directly over your pacemaker site because this may cause your pacemaker to malfunction. • Do not lean over electrical or gasoline engines or motors. Be sure that electrical appliances or motors are properly grounded. • Avoid all transmitter towers for radio, television, and radar. Radio, television, other home appliances, and antennas do not pose a hazard. • Be aware that antitheft devices in stores may cause temporary pacemaker malfunction. If symptoms develop, move away from the device. • Inform airport personnel of your pacemaker before passing through a metal detector and show them your pacemaker identification card. The metal in your pacemaker will trigger the alarm in the metal detector device. • Stay away from any arc welding equipment. • Be aware that it is safe to operate a microwave oven unless it does not have proper shielding (old microwave ovens) or is defective. • Report any of these symptoms to your primary health care provider if you experience them: difficulty breathing, dizziness, fainting, chest pain, weight gain, and prolonged hiccupping. If you have any of these symptoms, check your pulse rate and call your primary health care provider. • If you feel symptoms when near any device, move 5 to 10 feet away from it and check your pulse. Your pulse rate should return to normal. • Keep all of your health care provider and pacemaker clinic appointments. • Take all medications prescribed for you as instructed. • Follow your prescribed diet. • Follow instructions about restrictions on physical activity, such as no sudden, jerky movement, for 8 weeks to allow the pacemaker to settle in place

interventions pnuemothorax

For a stable patient with a small pneumothorax who has mild symptoms and no continuing air leak, no treatment may be needed. For more severe pneumothorax, tension pneumothorax, and hemothorax, chest tube therapy is essential. Chest tube management is discussed in Chapter 27. Initial management of a tension pneumothorax is an immediate needle thoracostomy, with a large-bore needle inserted by the primary health care provider into the second intercostal space in the midclavicular line of the affected side. This intervention changes a tension pneumothorax to a simple pneumothorax and is only a temporary measure. More definitive treatment is mandatory, with chest tube placement into the fourth intercostal space, and the other end attached to a water seal drainage system until the lung reinflates. Interventions for hemothorax include chest tube placement to remove the blood in the pleural space to normalize breathing and prevent infection. Closely monitor the chest tube drainage. Serial chest x-rays are used to determine treatment effectiveness. Other care includes pain control, pulmonary hygiene, and continued assessment for respiratory failure. An open thoracotomy is needed when there is initial blood loss of 1000 mL from the chest or persistent bleeding at the rate of 150 to 200 mL/hr over 3 to 4 hours. Monitor the vital signs, blood loss, and intake and output. Assess the patient's response to the chest tubes and infuse IV fluids and blood as prescribed. The blood lost through chest drainage can be infused back into the patient after processing if needed.

Continuous Electrocardiographic Monitoring

For continuous ECG monitoring, the electrodes are not placed on the limbs because movement of the extremities causes "noise," or motion artifact, on the ECG signal. Place the electrodes on the trunk, a more stable area, to minimize such artifacts and to obtain a clearer signal. If the monitoring system provides five electrode cables, place the electrodes as follows: • Right arm electrode just below the right clavicle • Left arm electrode just below the left clavicle • Right leg electrode on the lowest palpable rib, on the right midclavicular line • Left leg electrode on the lowest palpable rib, on the left midclavicular line • Fifth electrode placed to obtain one of the six chest leads With this placement, the monitor lead-select control may be changed to provide lead I, II, III, aVR, aVL, aVF, or one chest lead. The monitor automatically alters the polarity of the electrodes to provide the lead selected. The clarity of continuous ECG monitor recordings is affected by skin preparation and electrode quality. To ensure the best signal transmission and decrease skin impedance, clean the skin and clip hairs if needed. Make sure that the area for electrode placement is dry. The gel on each electrode must be moist and fresh. Attach the electrode to the lead cable and then to the contact site. The contact site should be free of any lotion, tincture, or other substance that increases skin impedance. Electrodes cannot be placed on irritated skin or over scar tissue. Electrodes may be applied by assistive personnel (AP), but the nurse determines which lead to select and checks for correct electrode placement. Assess the quality of the ECG rhythm transmission to the monitoring system. The ECG cables can be attached directly to a wall-mounted monitor (a hard-wired system) if the patient's activity is restricted to bedrest and sitting in a chair, as in a critical care unit. For an ambulatory patient, the ECG cable is attached to a battery-operated transmitter (a telemetry system) held in a pouch. The ECG is transmitted to a remote monitor via antennae located in strategic places, usually in the ceiling. Telemetry allows freedom of movement within a certain area without losing transmission of the ECG. Most acute care facilities have monitor technicians (monitor "techs") who are educated in ECG rhythm interpretation and are responsible for: • Watching a bank of monitors on a unit • Printing ECG rhythm strips routinely and as needed • Interpreting rhythms • Reporting the patient's rhythm and significant changes to the nurse The technical support is particularly helpful on a telemetry unit that does not have monitors at the bedside. The nurse is responsible for accurate patient assessment and management. The use of telemetry monitors on medical-surgical units is increasing and nursing assessment is critical to initiate appropriate interventions (Nickasch et al., 2016). Some units have full-disclosure monitors, which continuously store ECG rhythms in memory up to a certain amount of time. This system allows nurses and health care providers to access and print rhythm strips for more thorough patient assessment. Routine strips and any changes in rhythm are printed and documented in the patient's record. The health care provider is responsible for determining when monitoring can be suspended, such as during showering. He or she also determines whether monitoring is needed during off-unit testing procedures and for transportation to other facilities. Clinical alarms, such as those associated with continuous ECG monitoring, have been identified as one of the top 10 technology hazards. National Patient Safety Goal Reduce Harm Associated With Clinical Alarms Clinical alarms, such as those associated with continuous ECG monitoring, were designed to protect patients. These alarms can alert health care providers to a patient problem; however, the alarms are only beneficial if they are used in an effective manner. This is a complex problem, as care units are often filled with numerous types of alarms, making individual alarms hard to distinguish and creating desensitization among the staff (The Joint Commission, 2020). As a result, alarm safety must be recognized as a priority. The National Patient Safety Goal to improve clinical alarm safety asks hospitals to implement specific policy and procedure regarding clinical alarm safety including: • Clinically appropriate settings for alarms • When alarm signals can be disabled • What alarm parameters can be changed • Monitoring and responding to alarm signals Nurses must be proactive in the management of clinical alarms. Think carefully before suspending an alarm or adjusting alarm parameters and be informed regarding organization policy regarding alarm management. Prehospital personnel, such as paramedics and emergency medical technicians (EMTs) with advanced training, frequently monitor ECG rhythms at the scene and on the way to a health care facility. They function under medical direction and protocols but may also be communicating with a nurse in the emergency department. The ECG strip is printed on graph paper (Fig. 31.4), with each small block measuring 1 mm in height and width. ECG recorders and monitors are standardized at a speed of 25 mm/sec. Time is measured on the horizontal axis. At this speed, each small block represents 0.04 second. Five small blocks make up one large block, defined by darker bold lines and representing 0.20 second. Five large blocks represent 1 second, and 30 large blocks represent 6 seconds. Vertical lines in the top margin of the graph paper are usually 15 large blocks apart, representing 3-second segments

signs and symptoms of copd

General appearance can provide clues about respiratory status and energy level. Observe weight in proportion to height, posture, mobility, muscle mass, and overall hygiene. The patient with increasingly severe COPD is thin, with loss of muscle mass in the extremities, although the neck muscles may be enlarged. He or she tends to be slow moving and slightly stooped. The patient often sits in a forward-bending posture with the arms held forward, a position known as the orthopneic or tripod position (Fig. 27.7). When dyspnea becomes severe, activity intolerance may be so great that bathing and general grooming are neglected. Respiratory changes that occur as a result of obstruction include changes in chest size, and fatigue. Inspect the chest and assess the breathing rate and pattern. The patient with respiratory muscle fatigue breathes with rapid, shallow respirations and may have an abnormal breathing pattern in which the abdominal wall is sucked in during inspiration or may use accessory muscles in the abdomen or neck. During an acute exacerbation, the respiratory rate could be as high as 40 to 50 breaths/min and requires immediate medical attention. As respiratory muscles become fatigued, respiratory movement is jerky and appears uncoordinated. Check the patient's chest for retractions and asymmetric chest expansion. The patient with emphysema has limited diaphragmatic movement (excursion) because the diaphragm is flattened and below its usual resting state. Chest vibration (fremitus) is often decreased, and the chest sounds hyperresonant on percussion because of trapped air (Jarvis, 2020). Auscultate the chest to assess the depth of inspiration and any abnormal breath sounds. Wheezes and other abnormal sounds often occur on inspiration and expiration, although crackles are usually not present. Reduced breath sounds are common, especially with emphysema. Note the pitch and location of the sound and the point in the respiratory cycle at which the sound is heard. A silent chest may indicate serious airflow obstruction or pneumothorax. Assess the degree of dyspnea using a Visual Analog Dyspnea Scale (VADS), as shown in Chapter 24, Fig. 24.8. Ask the patient to place a mark on the line to indicate his or her breathing difficulty. Document and use this scale to determine the therapy effectiveness and pace the patient's activities. Examine the patient's chest for the presence of a "barrel chest" (see Fig. 27.3). With a barrel chest, the ratio between the anteroposterior (AP) diameter of the chest and its lateral diameter is 1:1 rather than the normal ratio of 1:1.5, as a result of lung overinflation and diaphragm flattening (Jarvis, 2020). The patient with chronic bronchitis often has a cyanotic, or blue-tinged, dusky appearance and has excessive sputum production. Assess for cyanosis, delayed capillary refill, and finger clubbing (Fig. 27.8), which indicate chronically decreased arterial oxygen levels. Cardiac changes occur as a result of the anatomic changes associated with COPD. Assess the patient's heart rate and rhythm. Check for swelling of the feet and ankles (dependent edema) or other signs of right-sided heart failure. Examine nail beds and oral mucous membranes. In late-stage emphysema the patient may have pallor or cyanosis and is usually underweight.

Head and Neck Cancer

Head and neck cancer is relatively common and its effect can have devastating consequences for gas exchange , eating, facial appearance, self-image, speech, and communication. The care needs for patients with these problems are complex, requiring a coordinated interprofessional team approach. Common team members include an oncologist, surgeon, nurse, registered dietitian nutritionist, speech-language pathologist, dentist, respiratory therapist, social worker, wound care specialist, clergy, occupational and physical therapists, and psychosocial counselors (Janotha & Tamari, 2017). Head and neck cancers are usually squamous cell carcinomas. These slow-growing tumors are curable when diagnosed and treated at an early stage. The prognosis for those who have more advanced disease at diagnosis depends on the extent and location of the tumors. Untreated, these cancers are often fatal within 2 years of diagnosis (ACS, 2020). The cancer begins as a loss of cellular regulation when the mucosa is chronically irritated and becomes tougher and thicker. Eventually genes controlling cell growth are damaged, allowing excessive growth of these abnormal and malignant cells. Initial lesions first appear as white, patchy lesions (leukoplakia) or red, velvety patches (erythroplakia). Head and neck cancer first spreads (metastasizes) into local lymph nodes, muscle, and bone. Later spread is systemic to distant sites, usually to the lungs or liver. Most head and neck cancers arise from the mucous membrane and skin, but they also can start from salivary glands, the thyroid, tonsils, or other structures. Treatment is based on tumor cell type and degree of spread at diagnosis. The two major risk factors for head and neck cancer are tobacco and alcohol use, especially in combination (McCance et al., 2019). Other risk factors include voice abuse, chronic laryngitis, exposure to chemicals or dusts, poor oral hygiene, long-term gastroesophageal reflux disease (GERD), and

The prevention of worldwide respiratory pandemics is the responsibility of everyone.

Health officials at the global, national, and state levels monitor for outbreaks. The recommended approach for any potential or actual pandemic is early recognition of cases and implementation of community and personal quarantine. Social-distancing behaviors help to reduce viral exposure. When a cluster of cases is discovered in an area, stockpiled vaccines are made available for immunization. Nonessential public activities in the area should be stopped, such as public gatherings, attendance at schools, religious services, shopping, and many types of employment. Adults should stay home and use the food, water, and medications they have stockpiled to last at least 2 weeks per person for disaster preparedness as described in Chapter 12. Travel to and from this area should be stopped.

Self-Management Education hf

Health teaching is essential for promoting self-management (also called self-care). Many patients are re-admitted to hospitals because they do not maintain their prescribed treatment plan, including lifestyle changes. Because of the need for extensive discharge instructions, most hospitals are using teaching packets with videos, CDs, and easy-to-read information about the importance of adhering to specific self-management strategies at home. One standardized and commonly used self-management plan called MAWDS is outlined in Table 32.4. Medication reconciliation is also important to be sure that similar drugs are not being prescribed and that patients meet the Core Measure requirements for HF. It is important to perform a learning needs assessment and tailor education to the patient's particular need to see changes in behavior and improved outcomes. Ambulatory care clinics for HF patients are also becoming increasingly common. Their purpose is to offer assessments, drug therapy, and health teaching. Some nurses specialize in caring for patients with health failure.

Common Causes of Oxygenation Failure

High altitudes, closed spaces, smoke inhalation, carbon monoxide poisoning • Pneumonia • Congestive heart failure with pulmonary edema • Pulmonary embolism (PE) • Acute respiratory distress syndrome (ARDS) • Interstitial pneumonitis-fibrosis • Methemoglobinemia • Hypovolemic shock • Hypoventilation

histroy copd

Identifying patients with early-stage COPD is important in starting the appropriate management. Initiation of drug management together with reducing particulate matter exposures can help delay the pathologic consequences of the disorder and increase the patient's functional activity (GOLD, 2019; O'Dell et al., 2018). Although pulmonary function testing is needed for confirmation of COPD presence, the disorder should be suspected in any patient who has dyspnea, chronic cough or sputum production, recurrent lower respiratory infections, and/or a history of particulate matter exposures (GOLD, 2019). Ask about risk factors such as age, gender, and occupational history. COPD is seen more often in older men. Some types of emphysema occur in families, especially those with alpha1-antitrypsin (AAT) deficiency (Southard et al., 2020). Obtain a thorough smoking history because tobacco use is a major risk factor. Ask about the length of time the patient has smoked and the number of packs smoked daily. Use these data to determine the pack-year smoking history. Also ask about the use of electronic cigarettes or vaping, including the type of product inhaled and the duration of the habit. Ask the patient to describe the breathing problems and assess whether he or she has any difficulty breathing while talking. Does he or she speak in complete sentences, or is it necessary to take a breath between every one or two words? Ask about the presence, duration, or worsening of wheezing, coughing, and shortness of breath. Determine which activities trigger these problems. Assess any cough, and ask whether sputum is clear or colored and how much is produced each day. Ask about the time of day when sputum production is greatest. Smokers often have a productive cough when they get up in the morning; nonsmokers generally do not. Ask the patient to compare the activity level and shortness of breath now with those of a month ago and a year ago. Ask about any difficulty with eating and sleeping. Many patients sleep in a semisitting position because breathlessness is worse when lying down (orthopnea). Ask about any difficulty with ADLs or sexual activity. Document this assessment to personalize the intervention plan. Weigh the patient and compare this weight with previous weights. Unplanned weight loss is likely when COPD severity increases, because the work of breathing increases metabolic needs. Dyspnea and mucus production often result in poor food intake and inadequate nutrition. Ask the patient to recall a typical day's meals and fluid intake. When heart failure is present with COPD, general edema with weight gain may occur.

Idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis is a common restrictive lung disease. The patient is usually an older adult with a history of cigarette smoking, chronic exposure to inhalation irritants, or exposure to the drugs amiodarone or ambrisentan. Most patients have progressive disease with few remission periods. Even with proper treatment, most patients usually survive only 2 to 3 years after diagnosis (Vega-Olivo & Criner, 2018). Pulmonary fibrosis is an example of excessive wound healing with loss of cellular regulation . Once lung injury occurs, inflammation begins tissue repair. The inflammation continues beyond normal healing time, causing fibrosis and scarring. These changes thicken alveolar tissues, making gas exchange difficult. The onset is slow, with early symptoms of mild dyspnea on exertion. Pulmonary function tests show decreased forced vital capacity (FVC). High-resolution computed tomography (HRCT) shows a "honeycomb" pattern in affected lung tissue. As the fibrosis progresses, the patient becomes more dyspneic and hypoxemia becomes severe. Eventually he or she needs high levels of oxygen and is often still hypoxemic. Respirations are rapid and shallow. Therapy focuses on slowing the fibrotic process and managing dyspnea. Drug therapy with nintedanib, a tyrosine kinase inhibitor, or pirfenidone, an antifibrotic agent, can help improve cellular regulation of fibrous cell growth and delay progression (Vega-Olivo & Criner, 2018). Immunosuppressant drugs include corticosteroids and cytotoxic drugs such as cyclophosphamide, azathioprine, chlorambucil, or methotrexate but have many side effects and shown limited benefit. Starting any drug therapy early is critical, even though not all patients respond to therapy. Even among those who have a response to therapy, the disease eventually continues to progress and leads to death by respiratory failure. Lung transplantation is a curative therapy; however, the selection criteria, cost, and availability of organs make this option unlikely for most patients. The patient and family need support and help with community resources. Nursing care focuses on helping the patient and family understand the disease process and maintaining hope for fibrosis control. It is important to prevent respiratory infections. Teach the patient and family about the symptoms of infection and to avoid respiratory irritants, crowds, and people who are ill. Home oxygen is needed by the time the patient has dyspnea because significant fibrosis has already occurred and gas exchange is reduced. Teach about oxygen use as a continuous therapy. Fatigue is a major problem. Teach the patient and family about energy conservation measures (see the discussion of activity intolerance in the Chronic Obstructive Pulmonary Disease section). These measures and rest help reduce the work of breathing and oxygen consumption. Encourage the patient to pace activities and accept assistance as needed. In the later stages of the disease, the focus is to reduce the sensation of dyspnea. This is often accomplished with the use of oral, parenteral, or nebulized morphine. Provide information about hospice, which supports and coordinates resources to meet the needs of the patient and family when the prognosis for survival is less than 6 months

Fractures of the Nose

If the bone or cartilage is not displaced and no complications are present, treatment may not be needed. However, displacement of either the bone or cartilage can cause airway obstruction or cosmetic deformity and is a potential source of infection.

The Patient With COPD

In addition to primary health care providers and nurses, other professionals important to ensuring optimal management include registered dietitian nutritionists, pharmacists, respiratory therapists, occupational therapists, physical therapists, social workers, patient navigators, community health workers, and mental health practitioners.

Oxygenation (Gas Exchange) Failure

In oxygenation (gas exchange ) failure, chest pressure changes are normal, and air moves in and out without difficulty but does not oxygenate the pulmonary blood sufficiently. It occurs in the type of ( ) mismatch in which air movement and oxygen intake (ventilation) are normal but lung blood flow (perfusion ) is decreased. Many lung disorders can cause oxygenation failure. Problems include impaired diffusion of oxygen at the alveolar level, right-to-left shunting of blood in the pulmonary vessels, ( ) mismatch, breathing air with a low oxygen level, and abnormal hemoglobin that fails to bind oxygen. In one type of ( ) mismatch, areas of the lungs still have perfusion, but gas exchange does not occur, which leads to hypoxemia. An extreme example of ( ) mismatch is when systemic venous blood (oxygen poor) passes through the lungs without being oxygenated and is "shunted" to the left side of the heart and into the systemic arterial system. Normally, less than 5% of cardiac output contains venous blood that has bypassed oxygenation. With poor oxygenation in the lungs or a shunt that allows venous blood to bypass the lungs, even more arterial blood is not oxygenated, and applying 100% oxygen does not correct the problem. A classic cause of such a ( ) mismatch is acute respiratory distress syndrome (ARDS), which is discussed later in the chapter. Table 29.3 lists specific causes of oxygenation failure.

Atrial Dysrhythmias

In patients with atrial dysrhythmias, the focus of impulse generation shifts away from the sinus node to the atrial tissues. The shift changes the axis (direction) of atrial depolarization, resulting in a P-wave shape that differs from normal P waves. The most common atrial dysrhythmias are: • Premature atrial complexes • Supraventricular tachycardia • Atrial fibrillation

pnuemonia etiology

Infectious pneumonia develops when a patient's immunity cannot overcome the invading organisms (Arsbad et al., 2016). Organisms from the environment (especially after natural disasters), invasive devices, equipment, and supplies or other people can invade the body. Risk factors are listed in Table 28.1. Pneumonia can be caused by any organism such as bacteria, viruses, mycoplasmas, fungi, rickettsiae, protozoa, and helminths (worms). Noninfectious causes of pneumonia include inhalation of toxic gases, chemical fumes, and smoke; and aspiration of water, food, fluid (including saliva), and vomitus. Infectious pneumonia can be categorized as community acquired (CAP), hospital acquired (HAP), health care acquired (HCAP) or ventilator-associated (VAP)

Inhalation Anthrax

Inhalation anthrax (respiratory anthrax) is a bacterial infection caused by the gram-positive organism Bacillus anthracis. This organism lives as a spore in soil where grass-eating animals live and graze. Most naturally occurring cases of anthrax are on the skin (cutaneous). Inhalation anthrax accounts for only about 5% of cases and is not spread by person-to-person contact. When infection occurs through the lungs, the disease is nearly 100% fatal without treatment (CDC, 2017). Although inhalation anthrax is an occupational hazard of veterinarians, farmers, and others who frequently contact animal wool, hides, bone meal, and skin, any occurrence in other adults is considered an intentional act of bioterrorism. Nursing Safety Priority Action Alert Inhalation anthrax is rare; thus any occurrence in a person who does not have an occupational risk is considered an intentional act of bioterrorism. Report the presence of symptoms consistent with inhalation anthrax to hospital authorities immediately. This organism first forms a spore (i.e., an encapsulated organism that is inactive). When many spores are inhaled deeply into the lungs, they enter white blood cells (WBCs), leave their capsules, and replicate. The active bacteria produce toxins that are released into the infected tissues and into the blood, making the infection worse. Massive edema occurs along with hemorrhage and destruction of lung cells. Infected WBCs spread the organisms rapidly to the lymph nodes and blood, causing bacteremia, sepsis, and meningitis. Lethal toxins produced by the bacteria are the most common cause of death. Inhalation anthrax has two stages: prodromal (or incubation period) and fulminant (with active disease). Symptoms (listed in the Key Features: Inhalation Anthrax box) may take up to 8 weeks to develop after exposure. The prodromal stage is early and difficult to distinguish from influenza or pneumonia. Symptoms include low-grade fever, fatigue, mild chest pain, and a dry, harsh cough. A special feature of inhalation anthrax is that it is not accompanied by upper respiratory symptoms of sore throat or rhinitis. Usually the patient starts to feel better and symptoms improve in 2 to 4 days. If the diagnosis is made and the patient begins appropriate antibiotic therapy at this stage, the likelihood of survival is high. The fulminant stage begins after the patient feels a little better. Usually there is a sudden onset of severe illness, including respiratory distress, hematemesis (bloody vomit), dyspnea, diaphoresis, stridor, chest pain, and cyanosis. High fever, hemorrhagic mediastinitis, and pleural effusions develop. As the infection spreads through the blood, septic shock and hemorrhagic meningitis develop. Death often occurs within 24 to 36 hours even if antibiotics are started in this stage.

interventions pnuemonia

Interventions Interventions to improve gas exchange are similar to those for the patient with asthma or chronic obstructive pulmonary disease (see Chapter 27). Nursing priorities include delivery of oxygen therapy and assisting the patient with bronchial hygiene. Oxygen therapy is usually delivered by nasal cannula or mask unless the hypoxemia does not improve with these devices. The patient who is confused may not tolerate a facemask. Check the skin under the device and under the elastic band, especially around the ears, for areas of redness or skin breakdown. Actions for oxygen therapy are listed in the Best Practice for Patient Safety & Quality Care: Oxygen Therapy box in Chapter 25. Incentive spirometry is used to improve inspiratory muscle action and to prevent or reverse atelectasis (alveolar collapse). Instruct the patient to sit up if possible, exhale fully, place the mouthpiece in his or her mouth; take a long, slow, deep breath, raising the piston as high as possible, and then hold the breath for 2 to 4 seconds before slowly exhaling. Evaluate technique and record the volume of air inspired. Teach the patient to perform 5 to 10 breaths per session every hour while awake. This intervention may not be helpful to patients who are very fatigued and/or have severe dyspnea. Preventing Airway Obstruction Planning: Expected Outcomes The patient with pneumonia is expected to maintain a patent airway. Interventions Interventions to improve gas exchange by avoiding airway obstruction in pneumonia are similar to those for chronic obstructive pulmonary disease (COPD) or asthma. Because of fatigue, muscle weakness, chest discomfort, and excessive secretions, the patient often has difficulty clearing secretions. Help him or her cough and deep breathe at least every 2 hours. The alert patient may use an incentive spirometer to facilitate deep breathing and stimulate coughing. Encourage the alert patient to drink at least 2 L of fluid daily to prevent dehydration and to thin secretions unless another health problem requires fluid restriction. Monitor intake and output, oral mucus membranes, and skin turgor to assess hydration status, especially when fever and tachypnea are present. Bronchodilators, especially beta2 agonists (see the Common Examples of Drug Therapy: Asthma Prevention and Treatment box in Chapter 27), are prescribed when bronchospasm is present. They can be given by nebulizer or metered-dose inhaler. Inhaled or IV steroids are used with acute pneumonia when inflammation and airway swelling are present. Expectorants such as guaifenesin may be used. Preventing Sepsis Planning: Expected Outcomes The patient with pneumonia is expected to be free of the invading organism and to return to a pre-pneumonia health status. Interventions Eliminating the infecting organism is key to treating pneumonia and preventing sepsis. When sepsis occurs with pneumonia, the risk for death is high. Anti-infectives are given for all types of pneumonias except those caused by viruses. Selection of drugs and route of delivery is based on how the pneumonia was acquired (i.e., CAP, HAP, or HCAP), how ill the patient is, which organism is involved, and whether the patient has conditions that increase the risk for complications, especially reduced immunity. The primary health care provider must consider drug resistance in the specific geographic area and in that hospital setting. Drug resistance is becoming increasingly common, especially for infection with Streptococcus pneumoniae (drug resistant S. pneumoniae [DRSP]). Usually anti-infectives are used for 5 to 7 days for a patient with uncomplicated CAP and up to 21 days for a patient with severely impaired immunity or one with HAP (Connor, 2018; Esden, 2020 ). For pneumonia caused by aspiration of food or stomach contents, interventions focus on preventing lung damage and treating the infection. Aspiration of acidic stomach contents can cause widespread inflammation , leading to acute respiratory distress syndrome (ARDS) and permanent lung damage. See Chapter 29 for a discussion of ARDS. Managing Empyema When pulmonary empyema occurs as a result of pneumonia, further interventions are needed. Pulmonary empyema is a collection of pus in the pleural space most commonly caused by pulmonary infection . When empyema is present, gas exchange can be impaired by both reduced lung diffusion and reduced effective ventilation. Empyema is suspected when chest wall motion is reduced, fremitus is reduced or absent, percussion is flat, and breath sounds are decreased. Abnormal breath sounds, including bronchial breath sounds, egophony, and whispered pectoriloquy, Systems Thinking And Quality Improvement Can 30-Day Hospital Readmissions Be Reduced for Patients Recovering From Pneumonia? Goering, L. (2018). Pneumonia recovery: A plan can help. MEDSURG Nursing, 27(5), 305−309, 330. Hospital re-admissions within 30 days after discharge for treatment of pneumonia, especially among older adults, are relatively high. Many of the problems and complications responsible for re-admission are preventable with appropriate transitional care, patient and family education, and consistent implementation of evidence-based interprofessional care interventions. One Midwestern hospital group developed a written interprofessional plan, known as the Pneumonia Recovery Plan (PRP), targeted to patients admitted for pneumonia. This tool for patients and families, which used both sides of a single sheet of paper, was given to patients on the first day of admission. It listed specific patient actions needed at admission and throughout the hospital stay, as well as for the weeks after discharge. Nurses were the primary explainers of the PRP for patients both initially and daily through discharge. Discharge planners and other interprofessional team members routinely reinforced the proscribed patient actions. No new interventions were introduced nor was nursing workload increased, just more consistent implementation of current evidence-based practices. Outcome measures for evaluation were reduction of length of stay (LOS), reduction of 20% for 30-day re-admission, and improvement of patient satisfaction to the 95th percentile in all categories. As a result of this quality improvement project, LOS for patients with pneumonia was reduced an average of 1.29 days and re-admission rates dropped from 33.3% to 7.4%. Although patient satisfaction did not improve to the 95th percentile in all categories, patients indicated a high degree of satisfaction with the PRP and the communication of needed patient actions and medication information. Eventually, the PRP was a part of electronic medical records and successfully instituted at another hospital. Commentary: Implications for Research and Practice This project started with identifying where gaps in care for hospitalized patients with pneumonia were likely contributing to the need for re-admission within 30 days. The emphasis of making the patient a full partner in pneumonia recovery care and ensuring consistent actions recognized as important by all members of the interprofessional team contributed heavily to successful transitional care for patient benefit. Nurses were key to consistent implementation of the plan. This plan and its collaborative development processes could serve as a model to improve transitional care and promote an uncomplicated return to health for other common disorders. may also be present. Diagnosis is made by chest x-ray or CT scan and a sample of the pleural fluid (obtained via thoracentesis). Empyema fluid is thick, opaque, exudative, and foul smelling. Treatment includes draining the empyema cavity, re-expanding the lung, and controlling the infection . Appropriate antibiotics are prescribed. A chest tube(s) to closed-chest drainage is used to promote lung expansion and drainage. The tube is removed when the lung is fully expanded and the infection is under control. Chest surgery may be needed for thick pus or excessive pleural thickening. Nursing interventions are similar to those for patients with a pleural effusion, pneumothorax, or infection. Chapters 27and 29 discuss these interventions in more detail.

interventions lung cancer

Interventions for the patient with lung cancer can have the purposes of curing the disease, increasing survival time, and enhancing quality of life through palliation. Both nonsurgical and surgical interventions are used to achieve these purposes. Cure is most likely for patients who undergo treatment for stage I or II disease. Cure is rare for patients who undergo treatment for stage III or IV disease, although survival time is increasing. Chemotherapy is often the treatment of choice for lung cancers, especially small cell lung cancer (SCLC). It may be used alone or as adjuvant (add-on) therapy in combination with surgery for non-small cell lung cancer (NSCLC). The combination of drugs used depends on tumor response and the overall health of the patient; however, most include platinum-based agents. Side effects of cancer chemotherapy include chemotherapy-induced nausea and vomiting (CINV), alopecia (hair loss), open sores on mucous membranes (mucositis), immunosuppression with neutropenia, anemia, decreased numbers of platelets, and peripheral neuropathy. Consult Chapter 20 for discussion of the nursing care needs for patients who have these side effects. Immunosuppression with neutropenia, which greatly increases the risk for infection, is the major dose-limiting side effect of chemotherapy for lung cancer. It can be managed by the use of growth factors to stimulate bone marrow production of immune system cells. Teach the patient and family about precautions to take to reduce the patient's risk for infection (see Chapter 20 for information about chemotherapy and associated nursing care). Targeted therapy is common in the treatment of non−small cell lung cancer (NSCLC). These agents take advantage of one or more differences in cancer cell growth or metabolism that is either not present or only slightly present in normal cells. For lung cancer, usually these differences are identified as variations in two different genes, EGFR (which codes for epidermal growth factor receptors) and ALK (which codes for ALK receptor tyrosine kinases). Agents used as targeted therapies work to disrupt cancer cell division in one of several ways. However, these agents only work when the cancer cell has the particular target or specific genetic mutation. Therefore testing of the cancer cells is needed before therapy begins, and not all cancers of the same type express the target. These agents are increasing survival time for patients with NSCLC but do not lead to a cure. The Common Examples of Drug Therapy: Targeted Therapy and Immunotherapy of Lung Cancer box lists some targeted agents used in lung cancer therapy mmunotherapy for lung cancer is a type of targeted therapy designed to allow the patient's own immune system to better recognize and attack his or her cancer cells. Normally, certain immune system cells including T-cells, B-cells, monocytes, and natural killer (NK) cells recognize and attack foreign cells and unhealthy self cells. Many "checkpoints" are in place to ensure that these cells do not "go rogue" and attack normal healthy self cells. One type of checkpoint is activation of the PD-1 receptor on these cells. PD stands for "programmed death." When the PD-1 receptors are activated, the immune system cell stops dividing, stops its seek-and-destroy actions, and may die. Some lung cancer cells are able to evade detection as unhealthy self cells by having their cell surface proteins known as PD-L1 and PD-L2 bind to and activate the PD-1 receptors on immune system cells. (PD-L stands for programmed death ligand.) When the PD-1 receptors are activated by cancer cell PD-L proteins, the immune system cells' activity is suppressed and they fail to recognize the cancer cells and take no action against them. The immunotherapy drugs for lung cancer prevent the suppressive interaction between the cancer cells' PD-L1 or PD-L2 proteins and the immune system cells' PD-1 receptors. Some drugs do this by binding and covering the PD-L proteins so that they cannot interact with immune system cells' PD-1 receptors and other drugs essentially hide the PD-1 receptors. Either way, the result is that immune system cells remain active and able to seek and destroy cancer cells. At present, immunotherapy does not replace traditional chemotherapy or radiation for first-line lung cancer treatment and is not used for cure. It may be used in combination with chemotherapy or as monotherapy for later-stage (III or IV) lung cancers. Use of immunotherapy, when lung cancer cells have large amounts of PD-L1 or PD-L2 on their surfaces, has significantly extended the lives of patients with NSCLC. One is also being used with later-stage small cell lung cancer. All are monoclonal antibodies administered by intravenous infusion. The Common Examples of Drug Therapy: Targeted Therapy and Immunotherapy of Lung Cancer box lists the most common approved immunotherapies for lung cancer. Radiation therapy can be an effective treatment for locally advanced lung cancers confined to the chest. Best results are seen when radiation is used in addition to surgery or chemotherapy. Radiation may be performed before surgery to shrink the tumor and make resection easier. Only the areas thought to have cancer are positioned in the radiation path. The immediate side effects of this treatment are skin irritation and peeling at the radiation site, fatigue, nausea, and taste changes. Some patients have esophagitis during therapy, making nutrition more difficult. Collaborate with a registered dietitian nutritionist to teach patients to eat foods that are soft, bland, and high in calories. Skin care in the radiation-treated area can be difficult, and consultation with a wound care specialist may be needed. Because skin in the radiation path is more sensitive to sun damage, advise patients to avoid direct skin exposure to the sun during treatment and for at least 1 year after radiation is completed. See Chapter 20 for other nursing care issues associated with radiation therapy. Photodynamic therapy (PDT) may be used to remove small bronchial tumors when they are accessible by bronchoscopy. This therapy first involves injecting the patient with an agent that sensitizes cells to light and remains in cancer cells longer than normal cells. After 48 to 72 hours, most of the drug has accumulated in the cancer cells. A laser light is focused on the tumor with the patient intubated and under anesthesia. The light activates a reaction that causes irreversible damage and death to cells retaining the sensitizing drug. Surgical Management Surgery is the main treatment for stage I and stage II NSCLC. Total tumor removal may result in a cure. If complete resection is not possible, the surgeon removes the bulk of the tumor. The specific surgery depends on the stage of the cancer and the patient's overall health. Lung cancer surgery may involve removal of the tumor only, removal of a lung segment, removal of a lobe (lobectomy), or removal of the entire lung (pneumonectomy). These procedures can be performed by open thoracotomy or by minimally invasive surgery in select patients. Preoperative care is focused on relieving anxiety and promoting the patient's participation (see Chapter 9 for routine preoperative care). Reinforce the surgeon's explanation of the procedure, and provide education related to what is expected after surgery. Teach about the probable placement of the chest tube and drainage system (except after pneumonectomy). Operative procedures for lung cancer may consist of a lobectomy, pneumonectomy, segmental resection, or wedge resection. A segmental resection is a lung resection that includes the bronchus, pulmonary artery and vein, and tissue of the involved lung segment or segments of a lobe. A wedge resection is removal of the peripheral portion of small, localized areas of disease. A lobe or entire lung can be removed through video-assisted thoracoscopic surgery (VATS), which is minimally invasive, in select patients. The procedure involves making small incisions in the chest for placement of the instruments. The lung, section, or lobe is then isolated from its airway, which is surgically closed. The lobe or lung is closed off from the rest of the lung and sealed in a bag to prevent leakage of tumor tissue and possible seeding of the cancer. The bagged lung is then removed whole through one of the small incisions. Postoperative care for patients who have undergone thoracotomy (except for pneumonectomy) requires closed-chest drainage to drain air and blood that collect in the pleural space. A chest tube drain placed in the pleural space allows lung re-expansion and prevents air and fluid from returning to the chest (Fig. 27.10). The drainage system consists of one or more chest tubes or drains, a collection container placed below the chest level, and a water seal to keep air from entering the chest. The drainage system may be a stationary, disposable, self-contained system (Fig. 27.11) or a smaller, portable, disposable, self-contained system that requires no connection to a vacuum source (Fig. 27.12). The nursing care priorities for the patient with a chest tube are to ensure the integrity of the system, promote comfort, ensure chest tube patency, and prevent complications (Sasa, 2019). Chest Tube Placement and Care The tip of the tube used to drain air is placed near the front lung apex (see Fig. 27.10). The tube that drains liquid is placed on the side near the base of the lung. The wounds are covered with airtight dressings, most commonly silicone foam dressings (Wood et al., 2019). The chest tube is connected by about 6 feet of tubing to a collection device placed below the chest, allowing gravity to drain the pleural space while the patient can turn and move without pulling on the chest tube. When two chest tubes are inserted, they are joined by a Y-connector close to the patient and the 6 feet of tubing is attached to the Y-connector. Stationary chest tube drainage systems, such as the Pleur-evac system, use a water-seal mechanism that acts as a one-way valve to prevent air or liquid from moving back into the chest cavity. Disposable system use a one-piece disposable plastic unit with three chambers. The three chambers are connected to one another. The tube(s) from the patient is (are) connected to the first chamber in the series of three, which is the drainage collection container. The second chamber is the water seal to prevent air from moving back up the tubing system and into the chest. The third chamber, when suction is applied, is the suction regulator. Tubing from the patient penetrates chamber one shallowly, as does the tube connecting chamber one with chamber two. The fluid in chamber one collected from the patient is measured hourly during the first 24 hours. This drainage fluid must never fill to the point that it comes into contact with any tubes! If the tubing from the patient enters the fluid, drainage stops and can lead to a tension pneumothorax. Chamber two is the water seal that prevents air from re-entering the patient's pleural space. As the trapped air leaves the pleural space, it will pass through chamber one (collection chamber) before entering chamber two (the water-seal chamber), which should always contain at least 2 cm of water to prevent air from returning to the patient. As trapped air from the patient's pleural space passes through the water seal, which serves as a one-way valve, the water will bubble. Once all the air has been evacuated from the pleural space, bubbling of the water seal stops. Nursing Safety Priority Action Alert For a water-seal chest tube drainage system, 2 cm of water is the minimum needed in the water seal to prevent air from flowing backward into the patient. Check the water level every shift and add sterile water to this chamber to the level marked on the indicator (specified by the manufacturer of the drainage system). Bubbling of water in the water-seal chamber indicates air drainage from the patient. Bubbling is seen when intrathoracic pressure is greater than atmospheric pressure, such as when the patient exhales, coughs, or sneezes. When the air in the pleural space has been removed, bubbling stops. A blocked or kinked chest tube can also cause bubbling to stop. Excessive bubbling in the water-seal chamber may indicate an air leak. The water in the water-seal chamber column normally rises 2 to 4 inches during inhalation and falls during exhalation, a process called tidaling. Absence of tidaling may mean that the lung has fully re-expanded or that there is an obstruction in the chest tube. Chamber three is the suction control of the system. There are different types of suction, most commonly wet or dry. With wet suction, the fluid level in chamber three is prescribed by the surgeon. The chamber is connected to wall suction, which is turned up until there is gentle bubbling in the chamber. With dry suction, the prescribed suction is dialed in on the device. When connected to wall suction, the regulator is set to the amount indicated by the device's manufacturer. Check hourly to ensure the sterility and patency of the drainage system. Keep sterile gauze at the bedside to cover and occlude the insertion site immediately if the chest tube becomes dislodged. Also keep padded clamps at the bedside for use if the drainage system is interrupted. Check the water-seal chamber for unexpected bubbling created by an air leak in the system. Bubbling is normal during forceful expiration or coughing because air in the chest is being expelled. Continuous bubbling indicates an air leak (Sasa, 2019 ). Notify the surgeon if bubbling occurs continuously in the water-seal chamber. See the Best Practice for Patient Safety & Quality Care: Management of Chest Tube Drainage System box for additional evidence-based actions to use when caring for a patient with a water-seal chest tube drainage system. Mobile or portable chest tube drainage systems are "dry" chest drainage systems without a water seal to prevent air from re-entering the patient's lung through the chest tube. Instead, these lightweight devices use a dynamic control "flutter" valve that prevents backflow of air. When the patient exhales, air is forced from the chest cavity into the chest tube under pressure, the soft flutter valve opens, and air moves into the harder surrounding tube shell, where it is vented. Portable units allow the patient to ambulate and even go home with chest tubes still in placeChest tube removal is performed when drainage is minimal and lung expansion is stable. Usually the surgeon removes the chest tube at the bedside, which causes a short period of procedural pain. After removal, the site is dressed and sealed with an occlusive dressing and observed for drainage. Assess the patient hourly for respiratory distress for the first few hours after chest tube removal. Respiratory distress may signal lung collapse and the need for chest tube reinsertion. Pain control measures are needed regardless of whether surgery is performed as an open procedure or with minimally invasive techniques. Give the prescribed drugs for pain and assess the patient's responses to them. Teach patients using patient-controlled analgesia (PCA) devices to self-administer the drug before pain intensity becomes too severe. Monitor vital signs before and after giving opioid analgesics, especially for the patient who is not being mechanically ventilated. Respiratory Management Immediately after surgery the patient is mechanically ventilated. See Chapter 29 for nursing care of the patient receiving mechanical ventilation. Once the patient is breathing on his or her own, the priorities are to maintain a patent airway, ensure adequate ventilation, and prevent complications. Assess the patient at least every 2 hours for adequacy of ventilation and gas exchange . Check the alignment of the trachea. Assess oxygen saturation and the rate and depth of respiration. Listen to breath sounds on the nonoperative side, particularly noting the presence of crackles. Perform oral suctioning only as needed. Usually the patient receives oxygen by mask or nasal cannula for the first 2 days after surgery. Assist the patient to a semi-Fowler position or up in a chair as soon as possible. Encourage him or her to use the incentive spirometer every hour while awake. If coughing is permitted, help him or her cough by splinting any incision and ensuring that the chest tube does not pull with movement. Specially designed walkers that support the patient and all equipment for early ambulation with chest tubes in place are available (Grondell et al., 2018). Preventing Complications Complications of a pneumonectomy include empyema (purulent material in the pleural space) and development of a bronchopleural fistula (an abnormal duct that develops between the bronchial tree and the pleura). Positioning of the patient after pneumonectomy varies according to surgeon preference and the patient's comfort. Some surgeons want the patient placed on the nonoperative side immediately after a pneumonectomy to reduce stress on the bronchial stump incision. Others prefer to place the patient on the operative side to allow fluids to fill in the now empty space. Interventions for Palliation Oxygen therapy is prescribed when the patient is hypoxemic and helps relieve dyspnea and anxiety. (See Chapter 25 for issues related to home oxygen therapy.) Radiation therapy can help relieve hemoptysis, obstruction of the bronchi and great veins (superior vena cava syndrome), difficulty swallowing from esophageal compression, and pain from bone metastasis. Radiation for palliation uses higher doses for shorter periods. Thoracentesis is performed when pleural effusion is a problem for the patient with lung cancer. The excess fluid increases dyspnea, discomfort, and the risk for infection. The purpose of treatment is to remove pleural fluid and prevent its formation. Thoracentesis is a procedure for fluid removal by suction after the placement of a large needle or catheter into the intrapleural space. Fluid removal temporarily relieves hypoxia; however, the fluid can rapidly re-form in the pleural space. When fluid development is continuous and uncomfortable, a tunneled pleural catheter that continuously drains may be placed into the intrapleural space to collect the fluid (Miller et al., 2018). Dyspnea management is needed because the patient with lung cancer tires easily and is often most comfortable resting in a semi-Fowler position. Dyspnea is reduced with oxygen, use of a continuous morphine infusion, and positioning for comfort. The severely dyspneic patient may be most comfortable sitting and sleeping in a lounge chair or reclining chair. Pain management is usually to help the patient be as pain free and comfortable as possible. Pharmacologic management with opioid drugs as oral, parenteral, or transdermal preparations is needed. Analgesics are most effective when given around the clock with additional PRN analgesics used for breakthrough pain. Hospice care can be beneficial for the patient in the terminal phase of lung cancer. Hospice programs provide support to the terminally ill patient and the family, meet physical and psychosocial needs, adjust the palliative care regimen as needed, make home visits, and provide volunteers for errands and respite care. (See Chapter 8 for a more complete discussion of end-of-life issues.)

psychosocial osha

Irritability and personality changes are common in adults with persistent OSA, including depression, as is a general loss of interest in social activities. n determining the presence of these psychosocial changes. Ask the patient about problems with recall, concentration, perceived energy level, and the ability to stay on task when working or studying

Preparing for Intubation

Know the proper procedure for summoning intubation personnel in the facility to the bedside in an emergency situation. Explain the procedure to the patient as clearly as possible. Basic life-support measures, such as obtaining a patent airway and delivering 100% oxygen by a manual resuscitation bag with a facemask, are crucial to survival until help arrives. During intubation, the nurse coordinates the rescue response and continuously monitors the patient for changes in vital signs, signs of hypoxia or hypoxemia, dysrhythmias, and aspiration. Ensure that each intubation attempt lasts no longer than 30 seconds, preferably less than 15 seconds. After 30 seconds, provide oxygen by means of a mask and manual resuscitation bag to prevent hypoxia and cardiac arrest. Suction as necessary.

Preventing Pneumonia

Know your risk for pneumonia (older than 65 years, have a chronic health problem [especially a respiratory problem], or have limited mobility and are confined to a bed or chair during your waking hours). • Have the annual influenza vaccination after discussing appropriate timing of the immunization with your primary health care provider. • Discuss the pneumococcal vaccine with your primary health care provider and have the vaccination as recommended. • Avoid crowded public areas during flu seasons. • If you have a mobility problem, cough, turn, move about as much as possible, and perform deep-breathing exercises. • If you are using respiratory equipment at home, clean the equipment as you have been instructed by the manufacturer. • Avoid indoor pollutants, such as dust, secondhand (passive) smoke, and aerosols. • If you do not smoke, vape, or use tobacco in any form, do not start. • If you smoke or vape, seek professional help on how to stop (or at least decrease) your habit. • Get enough rest and sleep on a daily basis. • Eat a healthy, balanced diet. • Drink at least 3 L (quarts) of nonalcoholic fluids each day (unless fluid restrictions are needed because of another health problem).

signs and symptoms hf

Left-Sided Heart Failure Left ventricular failure is associated with decreased cardiac output and elevated pulmonary venous pressure. It may appear clinically as: • Weakness • Fatigue • Dizziness • Acute confusion • Pulmonary congestion • Breathlessness • Oliguria (scant urine output) Decreased blood flow to the major body organs can cause dysfunction, especially renal failure. Nocturia may occur when the patient is at rest. The pulse may be tachycardic, or it may alternate in strength (pulsus alternans). Take the apical pulse for a full minute, noting any irregularity in heart rhythm. An irregular heart rhythm resulting from premature atrial contractions (PACs), premature ventricular contractions (PVCs), or atrial fibrillation (AF) is common in HF (see Chapter 31). The sudden development of an irregular rhythm may further compromise CO. Carefully monitor the patient's respiratory rate, rhythm, and character, as well as oxygen saturation. The respiratory rate typically exceeds 20 breaths/min. Assess whether the patient is oriented to person, place, and time. A short mental status examination may be used if there are concerns about orientation. Objective assessment is important because many people are skillful at covering up memory loss. Older adults are frequently disoriented or confused when the heart fails as a result of brain hypoxia (decreased oxygen). Increased heart size is common with a displacement of the apical impulse to the left. A third heart sound, S3 gallop, is an early diastolic filling sound indicating an increase in left ventricular pressure. This sound is often the first sign of HF. A fourth heart sound (S4) can also occur; it is not a sign of failure but rather a reflection of decreased ventricular compliance. Auscultate for crackles and wheezes of the lungs. Late inspiratory crackles and fine profuse crackles that repeat themselves from breath to breath and do not diminish with coughing indicate HF. Crackles are produced by intra-alveolar fluid and are often noted first in the bases of the lungs and spread upward as the condition worsens. Wheezes indicate a narrowing of the bronchial lumen caused by engorged pulmonary vessels. Identify the precise location of crackles and wheezes and whether the wheezes are heard on inspiration, expiration, or both. Right-Sided Heart Failure Right ventricular failure is associated with increased systemic venous pressures and congestion. On inspection, assess the neck veins for distention and measure abdominal girth. Hepatomegaly (liver engorgement), hepatojugular reflux, and ascites may also be assessed. Abdominal fluid can reach volumes of more than 10 L. When the fluid accumulates in the abdomen, pressure is placed on the stomach and intestines. This pressure can lead to early satiety and malnutrition. Assess for dependent edema. In ambulatory patients, edema commonly presents in the ankles and legs. When patients are restricted to bedrest, the sacrum is dependent and fluid accumulates there.

lung cancer

Lung cancer is a leading cause of cancer-related deaths worldwide in affluent and less affluent countries. In North America, more deaths from lung cancer occur each year than from prostate cancer, breast cancer, and colon cancer combined, although the incidence has been decreasing somewhat for the past decade. In the United States, more than 228,000 new cases are diagnosed each year and more than 135,000 deaths occur from lung cancer annually (American Cancer Society [ACS], 2020). In Canada, more than 29,300 new cases are diagnosed each year and more than 21,000 deaths from lung cancer occur annually (Canadian Cancer Society, 2019). The overall 5-year survival for all patients with lung cancer is only about 19%. This poor long-term survival is because most lung cancers are diagnosed at a late stage, when metastasis is present. Only 15% of patients have small tumors and localized disease at the time of diagnosis. The 5-year survival rate for this population is 56% (ACS, 2020). The prognosis for advanced lung cancer remains poor. Treatment often focuses on relieving symptoms or increasing survival time (palliation) rather than cure. Most primary lung cancers arise as a result of failure of cellular regulation in the bronchial epithelium. Chapter 19 discusses the general mechanisms and processes of cancer development. Lung cancers are collectively called bronchogenic carcinomas and are classified as small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC has several subtypes that are managed in the same ways, although causes and locations in the lungs differ. Metastasis (spread) of lung cancer occurs by direct extension, through the blood, and by invading lymph glands and vessels. Tumors in the lungs can grow and obstruct the bronchus partially or completely, interfering with gas exchange . Tumors in other areas of lung tissue can grow so large that they can compress and obstruct the airway. Compression of the alveoli, nerves, blood vessels, and lymph vessels can occur and also interfere with gas exchange . Lung cancer can spread to the lung lymph nodes, distant lymph nodes, and other tissues including bone, liver, brain, and adrenal glands. Additional symptoms, known as paraneoplastic syndromes, complicate certain lung cancers. The paraneoplastic syndromes are caused by hormones secreted by tumor cells and occur most commonly with SCLC. Table 27.4 lists the endocrine paraneoplastic syndromes that may occur. Staging of lung cancer is performed to assess the size and extent of the disease using the standard TNM system described in Chapter 19. Higher numbers represent later stages and less chance for cure or long-term survival.

lung cancers etiology

Lung cancers occur as a result of repeated exposure to inhaled substances that cause chronic tissue irritation or inflammation interfering with cellular regulation of cell growth. Cigarette smoking is the major risk factor and is responsible for 81% of all lung cancer deaths (ACS, 2020). Etiology and Genetic Risk Nonsmokers exposed to "secondhand" or "thirdhand" smoke also have a greater risk for lung cancer than do nonsmokers who are minimally exposed to cigarette smoke. See Chapter 24 for a discussion of passive smoking risks. Other lung cancer risk factors include chronic exposure to asbestos, beryllium, chromium, coal distillates, cobalt, iron oxide, mustard gas, petroleum distillates, radiation, tar, nickel, and uranium. Air pollution with benzopyrenes and hydrocarbons also increases the risk for lung cancer. Lung cancer, especially the adenocarcinoma form of NSCLC, does occur in adults who are "never smokers" (Sherry, 2017), particularly among women. Possible contributing factors for lung cancer in this population include exposure to environmental carcinogens, second-hand smoke exposure, genetic differences, familial predisposition, and advancing age.

MONA acronym for mi

M-morphine O-oxygen N-nitrates A-aspirin

etiology tb

M. tuberculosis is a slow-growing, acid-fast rod transmitted via the airborne route. Adults most often infected are those having repeated close contact with an infectious person who has not yet been diagnosed with TB. The risk for infection transmission is reduced after an adult with active TB has received proper drug therapy for 2 to 3 weeks, clinical improvement occurs, and acid-fast bacilli (AFB) in the sputum are reduced.

interventions pe

Managing Hypoxemia When a patient has a sudden onset of dyspnea and chest pain, or other symptoms of respiratory impairment, immediately initiate the Rapid Response Team. Apply oxygen, reassure the patient, and elevate the head of the bed. Prepare for blood gas analysis while continuing to monitor and assess for other changes. Planning: Expected Outcomes The patient with PE is expected to have adequate tissue perfusion in all major organs. Interventions Nonsurgical management of PE is most common. In some cases invasive procedures also may be needed. Nursing management involves using the care practices listed in the Best Practice for Patient Safety & Quality Care: Management of Pulmonary Embolism box. Rapid categorization of PE severity and prompt management are required (Table 29.1). Nonsurgical Management Management activities for PE focus on increasing gas exchange and oxygenation, improving lung perfusion , reducing risk for further clot formation, and preventing complications. Priority nursing interventions include implementing oxygen therapy, administering anticoagulation or fibrinolytic therapy to improve tissue perfusion, monitoring the patient's responses to the interventions, and providing psychosocial support. Oxygen therapy is critical for the patient with PE. The severely hypoxemic patient may need mechanical ventilation and close monitoring with ABG studies. In less severe cases oxygen may be applied by nasal cannula or mask. Use pulse oximetry to monitor oxygen saturation and hypoxemia. See Chapter 25 for a detailed discussion of oxygen therapy. Monitor the patient continually for any changes in status. Check vital signs, lung sounds, and cardiac and respiratory status at least every 1 to 2 hours. Document increasing dyspnea, dysrhythmias, distended neck veins, and pedal or sacral edema. Assess for crackles and other abnormal lung sounds along with cyanosis of the lips, conjunctiva, oral mucosa, and nail beds. Drug therapy begins immediately with anticoagulants to prevent embolus enlargement and more clotting (Brien, 2019). Unfractionated heparin, low-molecular-weight heparin, or fondaparinux is used unless the PE is massive or occurs with hemodynamic instability. Review the patient's partial thromboplastin time (PTT)—also called activated partial thromboplastin time (aPTT)—before therapy is started and thereafter according to facility policy. Therapeutic PTT values usually range between 1.5 and 2.5 times the control value for this health problem. Factor anti-Xa levels may be used instead of PTT or aPTT if the response to unfractionated heparin is insufficient or inappropriate. (Heparin primarily acts on Factor Xa, making the anti-Xa assay more useful to guide treatment in some situations.) Fibrinolytic drugs, such as alteplase, are used for treatment of PE when specific criteria are met such as shock, hemodynamic collapse, or instability. Fibrinolytic drugs are used to break up the existing clot. Both heparin and fibrinolytic drugs are high-alert drugs. These drugs have an increased risk to cause harm if given at too high a dose, at too low a dose, or to the wrong patient. Because of the high risk for bleeding, patients receiving fibrinolytic therapy are monitored in an ICU setting. eparin comes in a variety of concentrations in vials that have differing amounts, which contributes to possible drug errors. In accordance with The Joint Commission's National Patient Safety Goals (NPSGs), check the prescribed dose carefully and ensure that the correct concentration is being used to prevent overdosing or underdosing. Heparin therapy usually continues for 5 to 10 days. Most patients are started on an oral anticoagulant, such as warfarin, on day 1 or 2 of heparin therapy. Therapy with both heparin and warfarin continues until the international normalized ratio (INR) reaches 2.0 to 3.0. Heparin is usually infused for at least 5 days and continues for 24 hours after the INR is greater than 2. Monitor the platelet count and INR during this time. A low-molecular-weight heparin (e.g., dalteparin, enoxaparin) or a direct thrombin inhibitor (e.g., apixaban, dabigatran, rivaroxaban) is often used instead of warfarin. Oral anticoagulant use continues for 3 to 6 weeks, but patients at continuing risk for PE may take it indefinitely. Anticoagulation and fibrinolytic therapy can lead to excessive bleeding. The antidote for heparin is protamine sulfate; the antidote for warfarin is vitamin K1, which is available as an injectable drug, phytonadione. Antidotes for fibrinolytic therapy include clotting factors, fresh-frozen plasma, and aminocaproic acid. Antidotes to anticoagulant drugs and fibrinolytic drugs should be readily available on the unit, from the pharmacy, or from the blood bank for patients undergoing these therapies. Surgical Management Two surgical procedures for the management of PE are embolectomy and inferior vena cava (IVC) filtration. Embolectomy is the surgical or percutaneous removal of the embolus. It may be performed when fibrinolytic therapy cannot be used for a patient who has massive or multiple large pulmonary emboli with shock or bleeding complications. Inferior vena cava filtration with placement of a retrievable vena cava filter prevents further emboli from reaching the lungs in patients with ongoing risk for PE. Patients for whom filter placement is considered less risky than drug therapy include those with recurrent or major bleeding while receiving anticoagulants, those with septic PE, and those undergoing pulmonary embolectomy. Placement of a vena cava filter is detailed in Chapter 33. Managing Hypotension Planning: Expected Outcomes The patient with PE is expected to have adequate circulation and tissue perfusion . Interventions In addition to the interventions used for hypoxemia, IV fluid therapy and drug therapy are used to increase cardiac output and maintain blood pressure. IV fluid therapy involves giving crystalloid solutions to restore plasma volume and prevent shock (see Chapter 34). Continuously monitor the ECG and pulmonary artery and central venous/right atrial pressures of the patient receiving IV fluids because increased fluids can worsen pulmonary hypertension and lead to right-sided heart failure. Also monitor indicators of fluid adequacy, including urine output, skin turgor, and moisture of mucous membranes. Drug therapy with vasopressors is used when hypotension persists despite fluid resuscitation. Commonly used agents include norepinephrine, epinephrine, or dopamine. Agents that increase myocardial contractility (positive inotropic agents), including milrinone and dobutamine, may be used. Vasodilators, such as nitroprusside, may be used to decrease pulmonary artery pressure if it is impeding cardiac contractility. Assess the patient's cardiac status hourly during therapy with any of these drugs. Minimizing Bleeding Planning: Expected Outcomes The patient with PE is expected to have appropriate clotting and remain free from bleeding. Interventions Drug therapy that disrupts clots or prevents their formation impairs the patient's ability to start and continue the blood clotting cascade when injured, increasing the risk for bleeding. Priority nursing actions are ensuring that specific antidotes are present on the nursing unit, protecting the patient from situations that could lead to bleeding, ensuring correct dosage and timing of drug therapy, assessing laboratory values, and monitoring the amount of bleeding that occurs. Assess for evidence of bleeding (e.g., oozing around puncture sites or the gums, bruises that cluster, petechiae, or purpura) at least every 2 hours. Examine all stools, urine, drainage, and vomitus for gross blood, and test for occult blood. Measure any blood loss as accurately as possible. Assess the patient's abdomen for increasing distention or firmness. Consider measuring the abdominal girth every 8 hours (increasing girth can indicate internal bleeding). Monitor laboratory values daily. Review the complete blood count (CBC) to determine the risk for impaired clotting and whether any blood loss has occurred. If the patient has severe blood loss, packed red blood cells and/or fresh-frozen plasma may be prescribed (see Transfusion Therapy in Chapter 37). Monitor the platelet count. A decreasing count may indicate ongoing clotting or heparin-induced thrombocytopenia (HIT) caused by the formation of anti-heparin antibodies. A platelet transfusion may be indicated. Minimizing Anxiety Planning: Expected Outcomes The patient with PE is usually anxious and fearful as a result of the life-threatening nature of the problem and cerebral hypoxia. He or she is expected to have anxiety reduced to an acceptable level. Interventions The patient with PE is anxious and fearful and often has pain. Interventions for reducing anxiety in those with PE include oxygen therapy (see Interventions discussion in the Managing Hypoxemia section), communication, and drug therapy. Communication is critical in allaying anxiety. Acknowledge the anxiety and the patient's perception of a life-threatening situation. Stay with him or her and speak calmly and clearly, providing assurances that appropriate measures are being taken. Explain the rationale and share information when giving drugs, changing position, taking vital signs, or assessing the patient. Coordinate with pastoral care to help provide spiritual comfort. Drug therapy with an antianxiety drug may be prescribed if the patient's anxiety interferes with diagnostic testing, management, or adequate rest. Unless he or she is mechanically ventilated, sedating agents are avoided to reduce the risk for hypoventilation and to reduce the risk for worsening delirium with older patients. Pharmacologic therapy is used for pain management. Care is taken to avoid suppressing the respiratory response.

Ventilator Controls and Settings

Manufacturers of positive pressure ventilators may have various accessories and different terminology, but the basic settings are generally similar (Fig. 29.2). The pulmonologist, intensivist, or respiratory health care provider prescribes the ventilator settings, and usually the ventilator is readied or set up by the respiratory therapy department. The nurse assists in connecting the patient to the ventilator and monitors the ventilator settings in conjunction with respiratory therapy. Tidal volume (VT) is the volume of air the patient receives with each breath, as measured on either inspiration or expiration. The average prescribed VT ranges between 6 and 8 mL/kg of body weight, based on ideal body weight (IBW) and an accurate measure of patient height. Rate, or breaths/min, is the number of ventilator breaths delivered per minute. The rate is usually set between 10 and 14 breaths/min. Patient condition and ventilator mode can be factors in setting a rate above or below this range. Fraction of inspired oxygen (FiO 2) is the oxygen level delivered to the patient. The prescribed FiO 2 is based on the ABG values and the patient's condition. The range is 21% to 100% oxygen. The oxygen delivered to the patient is warmed to body temperature (98.6°F [37°C]) and humidified to 100%. This is needed because upper air passages of the respiratory tree, which normally warm and humidify air, are bypassed. Humidifying and warming prevent mucosal damage. Peak airway (inspiratory) pressure (PIP) is the pressure used by the ventilator to deliver a set tidal volume at a given lung compliance. The PIP value appears on the display of the ventilator. It is the highest pressure reached during inspiration. Trends in PIP reflect changes in resistance of the lungs and resistance in the ventilator. An increased PIP reading means increased airway resistance in the patient or the ventilator tubing (bronchospasm or pinched tubing, patient biting the ET tube), increased secretions, pulmonary edema, or decreased pulmonary compliance (the lungs or chest wall is "stiffer" and harder to inflate). An upper pressure limit is set to prevent barotrauma. When the limit is reached, the high-pressure alarm sounds, and the remaining volume is not given. Positive end-expiratory pressure (PEEP) is positive pressure exerted during expiration. PEEP improves oxygenation by enhancing gas exchange and preventing atelectasis. Most patients on mechanical ventilation will have a set PEEP of 5 to 6 cm H2O in order to prevent alveolar collapse and improve arterial oxygenation. PEEP may be increased to 15 cm H2O or greater when the arterial oxygen pressure (PaO 2) remains low despite increasing the FiO 2. The need for increased PEEP indicates a severe gas exchange problem. It is important to lower the FiO 2 delivered whenever possible because prolonged use of a high FiO 2 can damage lungs from the toxic effects of oxygen. PEEP prevents alveoli from collapsing because the lungs are kept partially inflated so alveolar-capillary gas exchange is promoted throughout the ventilatory cycle. The effect should be an increase in arterial blood oxygenation so the FiO 2 can be decreased. Flow rate is how fast each breath is delivered and the range is usually set between 40 and 60 L/min. If a patient is agitated or restless, has a widely fluctuating inspiratory pressure reading, or has other signs of air hunger, the flow may be set too low. Increasing the flow should be tried before using chemical restraints. Other settings may be used depending on the mode of ventilation and patient condition. These settings may include waveform, plateau, pressure-volume loop, trigger sensitivity, and alarm settings.

Indications of Worsening or Recurrent Heart Failure

Many patients who are re-admitted to hospitals for treatment of HF fail to seek medical attention promptly when symptoms recur. Teach the patient and caregiver to immediately report to the primary health care provider the occurrence of any of these symptoms, which could indicate worsening or recurrent heart failure: • Rapid weight gain (3 lb in a week or 1 to 2 lb overnight) • Decrease in exercise tolerance lasting 2 to 3 days • Cold symptoms (cough) lasting more than 3 to 5 days • Excessive awakening at night to urinate • Development of dyspnea or angina at rest or worsening angina • Increased swelling in the feet, ankles, or hands Drug Therapy Provide oral, written, and video instructions about the drug regimen. Teach the caregiver and patient how to count a pulse rate, especially if the patient is taking digoxin, beta blockers, or ivabradine. See the Patient and Family Education: Preparing for Self-Management: Beta Blocker/Digoxin Therapy box for instructions for the patient taking beta blockers and digoxin. Advise the patient taking diuretics to take them in the morning to avoid waking during the night for voiding. After determining whether he or she has a weight scale and can use it, emphasize the importance of weighing each morning at the same time. Daily weights indicate whether the patient is losing or retaining fluid. Some patients are taught to use a sliding scale to adjust their daily diuretic dose, depending on their daily weight, similar to the way a patient with diabetes adjusts an insulin dose based on the capillary glucose level. Teach patients taking ACEIs, ARBs, or sacubitril/valsartan to move slowly when changing positions, especially from a lying to a sitting position. Remind them to report dizziness, light-headedness, and cough to the health care provider. Serum potassium level and renal function are monitored at least every few months for patients taking diuretics and ACE inhibitors, ARBs, or sacubitril/valsartan. Diuretics, especially loop diuretics such as furosemide and bumetanide, deplete potassium and often cause hypokalemia. Conversely, ACE inhibitors, ARBs, sacubitril/valsartan, or potassium-sparing diuretics may result in potassium retention. If serum potassium levels drop below 4 mEq/L, the health care provider may prescribe potassium supplements or add a potassium-sparing diuretic such as spironolactone or eplerenone. Provide information about potassium-rich foods to include in the diet for patients at risk for hypokalemia (see Chapter 13). Nutrition Therapy Remind patients with chronic HF to restrict their dietary sodium. In collaboration with the home care nurse or dietitian, provide written instructions on low- or restricted-sodium diets. A 3-g sodium diet is recommended for mild-to-moderate disease. Remind the patient to avoid salty foods and table salt. Patients usually find this diet acceptable and fairly easy to follow. Teach patients how to read food labels, specifically ingredients that include sodium. A 2-g sodium diet may be needed for patients with severe HF. They should not add salt during or after meal preparation, avoid milk and milk products, use few canned or prepared foods, and read food labels to determine sodium content. This diet is not easily tolerated by many patients, and the cost of low-sodium foods can be a financial burden. Commercial salt substitutes typically contain potassium. Teach patients that their renal status and serum potassium level must be evaluated while using these products. Suggest that patients try lemon, spices, and herbs to enhance the flavor of low-salt foods.

Mechanical Ventilation

Mechanical ventilation to support and maintain gas exchange is used in many settings, not just in critical care units. The nurse plays a pivotal role in the coordination of care and prevention of problems. The Best Practice for Patient Safety & Quality Care box: Care of the Patient Receiving Mechanical Ventilation box lists essential nursing care actions during mechanical ventilation. The purposes of mechanical ventilation are to improve gas exchange and decrease the work needed for effective breathing. It is used to support the patient until lung function is adequate or until the acute episode has passed. A ventilator does not cure diseased lungs; it provides ventilation until the patient can resume the process of breathing on his or her own. Remember why the patient is using the ventilator so your management efforts also can focus on correcting the causes of the respiratory failure. If normal gas exchange with oxygenation, ventilation, and respiratory muscle strength is achieved, mechanical ventilation can be discontinued.

Heart Failure Self-Management Health Teaching (MAWDS)

Medications: • Take medications as prescribed and do not run out. • Know the purpose and side effects of each drug. • Avoid NSAIDs to prevent sodium and fluid retention. Activity: • Stay as active as possible but don't overdo it. • Know your limits. • Be able to carry on a conversation while exercising. Weight: • Weigh each day at the same time on the same scale to monitor for fluid retention. Diet: • Limit daily sodium intake to 2 to 3 g as prescribed. • Limit daily fluid intake to 2 L. Symptoms: • Note any new or worsening symptoms and notify the health care provider immediately.

Valvular Heart Disease

Mitral StenosisMitral RegurgitationMitral Valve ProlapseAortic StenosisAortic RegurgitationFatigueDyspnea on exertionOrthopneaParoxysmal nocturnal dyspneaHemoptysisHepatomegalyNeck vein distentionPitting edemaAtrial fibrillationRumbling, apical diastolic murmurFatigueDyspnea on exertionOrthopneaPalpitationsAtrial fibrillationNeck vein distentionPitting edemaHigh-pitched holosystolic murmurAtypical chest painDizziness, syncopePalpitationsAtrial tachycardiaVentricular tachycardiaSystolic clickDyspnea on exertionAnginaSyncope on exertionFatigueOrthopneaParoxysmal nocturnal dyspneaHarsh, systolic crescendo- decrescendo murmurPalpitationsDyspneaOrthopneaParoxysmal nocturnal dyspneaFatigueAnginaSinus tachycardiaBlowing, decrescendo diastolic murmur

diagnosis lung cancer

Most commonly, lung lesions are first identified on chest x-rays. CT scans are then used to identify the lesions more clearly and guide biopsy procedures. The definitive diagnosis of lung cancer is made by examination of cancer cells from biopsy or from pleural effusion fluid (if present). A thoracoscopy to directly view lung tissue may be performed through a video-assisted thoracoscope entering the chest cavity via small incisions through the chest wall. Other diagnostic studies may be needed to determine how widely the cancer has spread. Such tests include MRI and radionuclide scans of the liver, spleen, brain, and bone help. Positron emission tomography (PET) scanning is a thorough way to locate metastases. These tests help determine the extent of the cancer and the best methods to treat it.

infective endocarditis assess and intervene

Most patients have recurrent fevers from 99°F to 103°F (37.2°C to 39.4°C). However, as a result of physiologic changes associated with aging, older adults may be afebrile. The severity of symptoms may depend on the virulence of the infecting organism. Assess the patient's cardiovascular status. Almost all patients with infective endocarditis develop murmurs. Carefully auscultate the precordium, noting and documenting any new murmurs (usually regurgitant in nature) or any changes in the intensity or quality of an old murmur. An S3 or S4 heart sound also may be heard. HF is the most common complication of infective endocarditis. Assess for right-sided HF (as evidenced by peripheral edema, weight gain, and anorexia) and left-sided HF (as evidenced by fatigue, shortness of breath, and crackles on auscultation of breath sounds). See the discussion of HF earlier in this chapter. Arterial embolization is a major complication in up to half of patients with infective endocarditis. Fragments of vegetation (clots) break loose and travel randomly through the circulation. When the left side of the heart is involved, vegetation fragments are carried to the spleen, kidneys, GI tract, brain, and extremities. When the right side of the heart is involved, emboli enter the pulmonary circulation. Splenic infarction with sudden abdominal pain and radiation to the left shoulder can also occur. When performing an abdominal assessment, note rebound tenderness on palpation. The classic symptom with renal infarction is flank pain that radiates to the groin and is accompanied by hematuria (red blood cells in the urine) or pyuria (white blood cells in the urine). Mesenteric emboli cause diffuse abdominal pain, often after eating, and abdominal distention. About a third of patients have neurologic changes; others have signs and symptoms of pulmonary problems. Emboli to the central nervous system cause either transient ischemic attacks (TIAs) or a stroke. Confusion, reduced concentration, and aphasia or dysphagia may occur. Pleuritic chest pain, dyspnea, and cough are symptoms of pulmonary infarction related to embolization. Petechiae (pinpoint red spots) occur in many patients with endocarditis. Examine the mucous membranes, the palate, the conjunctivae, and the skin above the clavicles for small, red, flat lesions. Assess the distal third of the nail bed for splinter hemorrhages (Fig. 32.6), which appear as black longitudinal lines or small red streaks. he major component of treatment for endocarditis is drug therapy. Other interventions help prevent the life-threatening complications of the disease. Antimicrobials are the main treatment, with the choice of drug depending on the specific organism involved. Because vegetations surround and protect the offending microorganism, an appropriate drug must be given in a sufficiently high dose to ensure its destruction. Antimicrobials are usually given IV, with the course of treatment lasting 4 to 6 weeks. For most bacterial cases, the ideal antibiotic is one of the penicillins or cephalosporins. Patients may be hospitalized for several days to institute IV therapy and then are discharged for continued IV therapy at home. After hospitalization, most patients who respond to therapy may continue it at home when they become afebrile, have negative blood cultures, and have no signs of HF or embolization. Anticoagulants do not prevent embolization from vegetations. Because they may result in bleeding, these drugs are avoided unless they are required to prevent thrombus formation (clotting) on a prosthetic valve. The patient's activities are balanced with adequate rest. Consistently use appropriate aseptic technique to protect the patient from contact with potentially infective organisms. Continue to assess for signs of HF (e.g., rapid pulse, fatigue, cough, dyspnea) throughout the antimicrobial regimen and report significant changes. Surgical Management The cardiac surgeon may be consulted if antibiotic therapy is ineffective in sterilizing a valve, if refractory HF develops secondary to a defective valve, if large valvular vegetations are present, or if multiple embolic events occur. Current surgical interventions for infective endocarditis include: • Removing the infected valve (either biologic or prosthetic) • Repairing or removing congenital shunts • Repairing injured valves and chordae tendineae • Draining abscesses in the heart Preoperative and postoperative care of patients having surgery involving the valves is similar to that described earlier in this chapter for valve replacement.

interventions copd

Most patients with COPD use nonsurgical management to improve or maintain gas exchange . Surgical management requires that the patient meet strict criteria. Nursing care is most successful with helping the patient become a partner in COPD management by participating in all therapies to improve gas exchange . Thus priority nursing management for patients with COPD focuses on ensuring consistent use of prescribed drug therapy and on airway maintenance, monitoring, breathing techniques, positioning, effective coughing, oxygen therapy, exercise conditioning, suctioning, and hydration. Before any intervention, assess the breathing rate, rhythm, depth, and use of accessory muscles. The accessory muscles are less efficient than the diaphragm, and the work of breathing increases. Determine whether any factors are contributing to the increased work of breathing, such as respiratory infection. Airway maintenance is the most important focus of interventions to improve gas exchange . Drug Therapy Drug therapy is recommended at all levels of disease to delay progression and promote continued activity tolerance (GOLD, 2019; O'Dell et al., 2018). Drugs used to manage COPD are the same drugs as for asthma and include beta-adrenergic agents, cholinergic antagonists, xanthines, corticosteroids, and cromones (see the Common Examples of Drug Therapy: Asthma Prevention and Treatment box in the Asthma section). The focus is on long-term control therapy with longer-acting drugs, such as arformoterol, indacaterol, tiotropium, aclidinium bromide, olodaterol, and the combination drugs, such as fluticasone/vilanterol (e.g., BREO ELLIPTA), olodaterol/tiotropium, vilanterol/umeclidinium (e.g., ANORO ELLIPTA), and a newer triple combination of fluticasone/umeclidinium/vilanterol (e.g., TRELEGY ELLIPTA). Just as for asthma management, a key issue for successful drug therapy for COPD management is the correct technique for inhaler use. Have the patient demonstrate or fully describe exactly how he or she uses the inhaler(s) at every new outpatient interaction. Reinforce correct technique use and apply a variety of interventions that can help the patient acquire the knowledge and skills needed to use the inhaler correctly (see the Systems Thinking and Quality Improvement: Reducing Critical Errors in Patient Inhaler Use box). The patient with COPD is more likely to be taking systemic agents in addition to inhaled drugs. Another drug class for COPD is the mucolytics, which thin the thick secretions, making them easier to cough up and expel. Nebulizer treatments with normal saline or a mucolytic agent such as acetylcysteine or dornase alfa and normal saline help thin secretions. Guaifenesin is a systemic mucolytic that is taken orally. A combination of guaifenesin and dextromethorphan also raises the cough threshold. Stepped therapy, which adds drugs as COPD progresses, is recommended for patients with chronic bronchitis or emphysema, although the patient's response to drug therapy is the best indicator of when drugs or their dosages need changing. Ideally the patient notices changes and participates in management strategies. Drugs are "stepped" up with disease exacerbations and decreased when the patient's symptoms return to his or her stable level. If the patient's symptoms decrease over time and remain stable, drug therapy can be "stepped down" to the lowest level that allows the disease severity to remain stable (O'Dell et al., 2018). Monitoring Monitoring for changes in respiratory status is key to providing prompt interventions to reduce complications. Assess the hospitalized patient with COPD at least every 2 hours, even when the purpose of hospitalization is not COPD management. Apply prescribed oxygen, assess the patient's response to therapy, and prevent complications. If the patient's condition worsens, as evidenced by a sudden sharp rise in CO2 or severe decrease in Pao2, more aggressive therapy is needed. Noninvasive ventilation (NIV) may be useful for patients with stable, very severe COPD and daytime hypercapnia (Dorman, 2016; GOLD, 2019 ). Intubation and mechanical ventilation may be needed for patients in respiratory failure. Breathing Techniques Diaphragmatic or abdominal and pursed-lip breathing may be helpful for managing dyspneic episodes. Teach the patient to use these techniques, shown in the Patient and Family Education: Preparing for Self-Management: Breathing Exercises box, during all activities to reduce the amount of stale air in the lungs and manage dyspnea. Teach these techniques when the patient has less dyspnea. In diaphragmatic breathing, the patient consciously increases movement of the diaphragm. Lying on the back allows the abdomen to relax. Breathing through pursed lips creates mild resistance, which prolongs exhalation and increases airway pressure. This technique delays airway compression and reduces air trapping. Positioning Having the patient remain in an upright position with the head of the bed elevated can help alleviate dyspnea by increasing chest expansion and keeping the diaphragm in the proper position to contract. This position conserves energy by supporting the patient's arms and upper body. Help the patient who can tolerate sitting in a chair get out of bed for 1-hour periods two to three times a day. Effective Coughing Coughing effectively can improve gas exchange by helping increase airflow in the larger airways. The patient with COPD has difficulty removing secretions, which results in poor gas exchange. Excessive mucus increases the risk for infections. Controlled coughing is helpful in removing excessive mucus. Teach the patient to cough on arising in the morning to eliminate mucus that collected during the night. Coughing to clear mucus before mealtimes may make meals more pleasant. Coughing before bedtime may help clear lungs for a less interrupted night's sleep. For effective coughing, teach the patient to sit in a chair or on the side of a bed with feet placed firmly on the floor. Instruct him or her to turn the shoulders inward and to bend the head slightly downward, hugging a pillow against the stomach. The patient then takes a few breaths, attempting to exhale more fully. After the third to fifth breath (in through the nose, out through pursed lips), instruct him or her to take a deeper breath and bend forward slowly while coughing two or three times ("mini" coughs) from the same breath. On return to a sitting position, the patient takes a comfortably deep breath. The entire coughing procedure is repeated at least twice. Oxygen Therapy Oxygen is prescribed for relief of hypoxemia and hypoxia. The need for oxygen therapy and its effectiveness can be determined by arterial blood gas (ABG) values and oxygen saturation. The patient with COPD may need an oxygen flow of 2 to 4 L/min via nasal cannula or up to 40% via Venturi mask. Ensure that there are no open flames in rooms in which oxygen is in use. See Chapter 25 for information on oxygen therapy. In the past, the patient with COPD was thought to be at risk for extreme hypoventilation with oxygen therapy because of a decreased drive to breathe as blood oxygen levels rose. However, this concern has not been shown to be evidence based and has been responsible for ineffective management of hypoxia in patients with COPD. All hypoxic patients, even those with COPD and hypercarbia, should receive oxygen therapy at rates appropriate to reduce hypoxia and bring Sp O 2 levels up between 88% and 92%. Exercise Conditioning Exercise for conditioning and pulmonary rehabilitation can improve function and endurance in patients with COPD. Patients often respond to the dyspnea of COPD by limiting their activity, even basic ADLs (Lee et al., 2018). Over time, the muscles used in breathing weaken, resulting in increased dyspnea with lower activity levels. Pulmonary rehabilitation involves education and exercise training to prevent muscle deconditioning. Each patient's exercise program is personalized to his or her current limitations and planned outcomes. The simplest plan is having the patient walk (indoors or outdoors) daily at a self-paced rate until symptoms limit further walking, followed by a rest period, and then continue walking until 20 minutes of actual walking has been accomplished. As the time during rest periods decreases, the patient can add 5 more minutes of walking time. Teach patients whose symptoms are severe to modify the exercise by using a walker with wheels or, if needed, to use oxygen while exercising. Exercise needs to be performed at least two or three times weekly for best improvement. Formal pulmonary rehabilitation programs can be beneficial even for patients who are severely impaired. Additional exercise techniques to retrain ventilatory muscles include isocapneic hyperventilation and resistive breathing. Isocapneic hyperventilation, in which the patient hyperventilates into a machine that controls the levels of oxygen and carbon dioxide, increases endurance. In resistive breathing the patient breathes against a set resistance. Resistive breathing increases respiratory muscle strength and endurance. Suctioning Perform suctioning only when needed—not routinely. Nasotracheal suction is used only for patients with a weak cough, weak pulmonary muscles, and inability to expectorate effectively. Assess for dyspnea, tachycardia, and dysrhythmias during the procedure. Assess for improved breath sounds after suctioning. Suctioning is discussed in detail in Chapter 25. Hydration Maintaining hydration may thin the thick, tenacious (sticky) secretions, making them easier to remove by coughing. Unless hydration needs to be avoided for other health problems, teach the patient with COPD to drink at least 2 L/day. Humidifiers may be useful for those living in a dry climate or those who use dry heat during the winter. Surgical Management Lung transplantation and lung volume reduction surgery (LVRS) can improve gas exchange in the patient with COPD. Transplantation is a less common procedure because of cost and the scarce availability of donor lungs. The more common surgical procedure for patients with emphysema is LVRS. The purpose of LVRS is to improve gas exchange through removal of hyperinflated lung tissues that are filled with stagnant air containing little, if any, oxygen. The level of carbon dioxide is the same as that in the capillary, and no gas exchange occurs. Successful lung volume reduction results in increased forced expiratory volume and decreased total lung capacity and residual volume. Activity tolerance increases, and oxygen therapy may no longer be needed. Preoperative care involves careful patient selection and testing to determine which areas of the lungs should be reduced. Patients who are selected for this procedure have end-stage emphysema, minimal chronic bronchitis, and stable cardiac function. They also must be ambulatory; not ventilator dependent; free of pulmonary fibrosis, asthma, or cancer; and not have smoked for at least 6 months. The patient must be rehabilitated to the stage that he or she is able to walk, without stopping, for 30 minutes at 1 mile/hr and maintain a 90% or better oxygen saturation level. In addition to standard preoperative testing, tests to determine the location of greatest lung hyperinflation and poorest lung blood flow are performed. These tests include pulmonary plethysmography, gas dilution, and perfusion scans. Operative procedures for lung reduction are usually performed on both lungs, most often by the minimally invasive surgical technique of video-assisted thoracoscopic surgery (VATS) (GOLD, 2019). Each lung is examined for areas of hyperinflation. The surgeon removes as much of the hyperinflated tissue as possible. Postoperative care after LVRS involves close patient monitoring for continuing respiratory problems, as well as for usual postoperative complications. Bronchodilator and mucolytic therapies are maintained. Pulmonary hygiene includes incentive spirometry 10 times per hour while awake, chest physiotherapy starting on the first day after surgery, and hourly pulmonary assessment. Preventing Weight Loss Planning: Expected Outcomes The patient with COPD is expected to achieve and maintain a body weight within 10% of ideal. Interventions The patient with COPD often has nausea, early satiety (feeling too "full" to eat), poor appetite, and meal-related dyspnea. The work of breathing raises calorie and protein needs, which can lead to protein-calorie malnutrition. Malnourished patients lose muscle mass and strength, lung elasticity, and alveolar-capillary surface area, all of which reduce gas exchange. Identify patients at risk for or who have this complication and collaborate with a registered dietitian nutritionist (RDN) to perform a nutrition assessment. Monitor weight and other indicators of nutrition, such as serum prealbumin levels. Dyspnea management is needed because shortness of breath interferes with eating. Teach the patient to plan the biggest meal of the day for the time when he or she is most hungry and well rested. Four to six small meals a day may be preferred to three larger ones. Remind patients to use pursed-lip and abdominal breathing and to use the prescribed bronchodilator 30 minutes before the meal to reduce bronchospasm. Food selection can help prevent weight loss. Abdominal bloating and a feeling of fullness often prevent the patient from eating a complete meal. Collaborate with the RDN to teach about foods that are easy to chew and not gas forming. Advise the patient to avoid dry foods that stimulate coughing and caffeine-containing drinks that increase urine output and may lead to dehydration. Urge the patient to eat high-calorie, high-protein foods. Some supplements are formulated for patients with COPD and provide nutrition with reduced carbon dioxide production. If early satiety is a problem, advise him or her to avoid drinking fluids before and during the meal and to eat smaller, more frequent meals. Minimizing Anxiety Planning: Expected Outcomes The patient with COPD is expected to have decreased anxiety. Interventions Patients with COPD become anxious during acute dyspneic episodes, especially when excessive secretions are present. Anxiety also may cause dyspnea. Help the patient understand that anxiety can increase dyspnea and have a plan for dealing with anxiety. Together with the patient, develop a written plan that states exactly what he or she should do if symptoms flare. Having a plan provides confidence and control in knowing what to do, which often helps reduce anxiety. Stress the use of pursed-lip and diaphragmatic breathing techniques during periods of anxiety or panic. Family, friends, and support groups can be helpful. Recommend professional counseling, if needed, as a positive suggestion. Stress that talking with a counselor can help identify techniques to maintain control over dyspnea and panic. Explore other approaches to help the patient manage dyspneic episodes and panic attacks, such as progressive relaxation, hypnosis therapy, and biofeedback. For some patients, antianxiety drug therapy may be needed for severe anxiety. Improving Endurance Planning: Expected Outcomes The patient with COPD is expected to increase activity to a level acceptable to him or her. Interventions The patient with COPD often has chronic fatigue. During acute exacerbations, he or she may need extensive help with the ADLs of eating, bathing, and grooming. As the acute problem resolves, encourage the patient to pace activities and perform as much self-care as possible. Teach him or her to not rush through morning activities because rushing increases dyspnea, fatigue, and hypoxemia. As activity gradually increases, assess the patient's response by noting skin color changes, pulse rate and regularity, oxygen saturation, and work of breathing. Suggest the use of oxygen during periods of high energy use such as bathing or walking. Energy conservation is the planning and pacing of activities for best tolerance and minimum discomfort. Ask the patient to describe a typical daily schedule. Help him or her divide each activity into its smaller parts to determine whether that task can be performed in a different way or at a different time. Teach about planning and pacing daily activities with rest periods between activities. Help the patient develop a chart outlining the day's activities and planned rest periods. Encourage the patient to avoid working with the arms raised. Activities involving the arms decrease exercise tolerance because the accessory muscles are used to stabilize the arms and shoulders rather than to assist breathing. Many activities involving the arms can be done sitting at a table leaning on the elbows. Teach the patient to adjust work heights to reduce back strain and fatigue. Remind him or her to keep arm motions smooth and flowing to prevent jerky motions that waste energy. Work with the occupational therapist to teach about the use of adaptive tools for housework, such as long-handled dustpans, sponges, and dusters, to reduce bending and reaching. Suggest organizing work spaces so that items used most often are within easy reach. Measures such as dividing laundry or groceries into small parcels that can be handled easily, using disposable plates to save washing time, and letting dishes dry in the rack also conserve energy. Teach the patient to not talk when engaged in other activities that require energy, such as walking. In addition, teach him or her to avoid breath holding while performing any activity. Preventing Respiratory Infection Planning: Expected Outcomes The patient with COPD is expected to avoid serious respiratory infection. Interventions Pneumonia is a common complication ofCOPD, especially among older adults. Patients who have excessive secretions are at increased risk for respiratory tract infections. Teach patients to avoid crowds, and stress the importance of receiving a pneumonia vaccination and a yearly influenza vaccine. NCLEX Examination Challenge 27.2 Health Promotion and Maintenance A client with COPD has just been reclassified for disease severity from a GOLD 2 to a GOLD 3. Which client statement about changes in management or lifestyle indicate to the nurse that more teaching is needed to prevent harm? A. "This year I will get the pneumonia vaccination in addition to a flu shot." B. "Now I will try to rest as much as possible and avoid any unnecessary exercise." C. "Maybe drinking a supplement will help me retain weight and have more energy." D. "Perhaps using a spacer with my metered dose inhaler will make the drug work better." Care Coordination and Transition Management Sustained transition to home or community management of COPD following acute exacerbation management can be difficult. Readmission within 30 to 60 days after discharge from acute care is high, and intensive care coordination is needed to reduce it (Saunier, 2017). Home Care Management Most patients with COPD are managed in the ambulatory care setting and cared for at home. When pneumonia or a severe exacerbation develops, the patient often returns home after hospitalization. For those with advanced disease, 24-hour care may be needed for ADLs and monitoring. If home care is not possible, placement in a long-term care setting may be needed. Patients with hypoxemia may use oxygen at home either as needed or continually. Continuous, long-term oxygen therapy can reverse tissue hypoxia and improve cognition and well-being. For more information on home oxygen therapy, see Chapter 25. Collaborate with the case manager to obtain the equipment needed for care at home. Patient needs may include oxygen therapy, a hospital-type bed, a nebulizer, a tub transfer bench or shower chair, and scheduled visits from a home care nurse for monitoring and evaluation. The patient with COPD faces a lifelong disease with remissions and exacerbations. Explain to the patient and family that he or she may have periods of anxiety, depression, and ineffective coping. Instruct them to identify and avoid stressors that can worsen the disease. Reinforce the techniques of pursed-lip breathing, diaphragmatic breathing, positioning, relaxation therapy, energy conservation, and coughing and deep breathing. Teaching about all of the needed topics may require coordination with the home care or clinic staf

self tb

Most patients with TB are managed outside the hospital; however, patients may be diagnosed with TB while in the hospital for another problem. Discharge may be delayed if the living situation is high risk or if nonadherence to prescribed drug therapy is likely. Ensure collaboration with other members of the interprofessional team, including the case manager or social service worker in the hospital or the community health nursing agency, to ensure that the patient is discharged to the appropriate environment with continued supervision. Self-Management Education Teach the patient to follow the drug regimen exactly as prescribed and always to have a supply on hand. Teach about side effects and ways of reducing them to promote adherence. Remind him or her that the disease is usually no longer contagious after drugs have been taken for 2 to 3 consecutive weeks and clinical improvement is seen; however, he or she must continue with the prescribed drugs for 6 months or longer as prescribed. Directly observed therapy, in which a health care professional watches the patient swallow the drugs, may be indicated in some situations. This practice leads to more treatment successes, fewer relapses, and less drug resistance. More recently, DOT has been successfully performed using a video format (VDOT) in which patients use a phone or other real-time electronic device to demonstrate compliance with the drug regimen. This method helps patients "live their lives" without having to physically come to a place for DOT. Drawbacks to this method include whether the patient is willing and able to use such a device and how good the connectivity is for both the patient's device and the nurse's access to the video (Ingram, 2018). The patient who has weight loss and severe lethargy should gradually resume usual activities. Proper nutrition is needed to prevent infection recurrence. Provide the patient with information about how TB can be spread to others. A key to preventing infection transmission is identifying those in close contact with the infected person so that they can be tested and treated if needed. Multidrug therapy may be indicated to prevent TB in heavily exposed adults or for those who have other health problems that reduce immunity. Health Care Resources Teach the patient to receive follow-up care by a primary health care provider for at least 1 year after active treatment. The American Lung Association (ALA) can provide free information to the patient about the disease and its treatment. In addition, Alcoholics Anonymous (AA) and other health care resources for patients with alcoholism are available if needed. Inform patients who smoke or vape that smoking and vaping further reduce breathing effectiveness. Use the suggestions and interventions discussed in Chapter 24 to help the patient quit or reduce cigarette smoking. Assist the patient who uses illicit drugs to locate a drug-treatment program.

Characteristics Associated With the Most Common Alpha1-Antitrypsin Gene Mutations

Mutation GenotypeLevel of Serum Alpha1-Antitrypsin (% of Normal)Disease SeverityM/S80%No detectable diseaseS/S50%-60%Minimal to no disease expressionM/Z50%-55%Minimal to no disease expressionS/Z30%-35%Pulmonary disease, early ageZ/Z10%-15%Severe COPD, extrapulmonary involvement

triad disease

Nasal polyps Asthma ASA allergy

interventions acute resp failure

Oxygen therapy is appropriate for any patient with acute hypoxemia. It is used in ARF to keep the arterial oxygen (PaO 2) level above 60 mm Hg while treating the cause of the respiratory failure. Oxygen therapy is discussed in detail in Chapter 25. If oxygen therapy does not maintain acceptable PaO 2 levels indicating adequate gas exchange , mechanical ventilation (invasive or noninvasive) may be needed. Drugs given systemically, by nebulizer, or by metered dose inhaler (MDI) may be prescribed to dilate the bronchioles and decrease inflammation to promote gas exchange . Corticosteroids may be used, but their benefit has not been demonstrated conclusively. Analgesics are needed if the patient has pain. If the patient requires mechanical ventilation, he or she may need neuromuscular blockade drugs for optimal ventilator effect. Other management strategies depend on the underlying condition(s) that predisposed the patient to ARF development, which may include diuretic therapy or antibiotic therapy. Help the patient find a position of comfort that allows easier breathing (i.e., usually a more upright position). To decrease the anxiety occurring with dyspnea, help him or her to use relaxation, diversion, and guided imagery. Start energy-conserving measures, such as minimal self-care and no unnecessary procedures. Encourage deep breathing and other breathing exercises.

pulmonary embolism

PE) is a collection of particulate matter (solids, liquids, or air) that enters venous circulation and lodges in the pulmonary vessels. (An embolism is a blood clot [thrombus] or other object [e.g., air, fatty deposit] that is carried in the bloodstream and lodges in another area.) Large emboli in the lung vessels obstruct pulmonary blood flow, leading to reduced gas exchange , reduced oxygenation, pulmonary tissue hypoxia, decreased perfusion , and potential death. Any substance can cause an embolism, but a blood clot is the most common (McCance et al., 2019; Moore, 2019). PE is common and may account for as many as 100,000 deaths each year in the United States (Centers for Disease Control and Prevention [CDC], 2018). It may be the most common cause of preventable death in hospitalized patients, but because symptoms can be vague it may be misdiagnosed, and patients at risk may not receive appropriate initial care. Most often, a PE occurs when inappropriate blood clotting forms a venous thromboembolism (VTE) (or deep vein thrombosis [DVT]) in a vein in the legs or the pelvis and a clot breaks off and travels to the right side of the heart. The clot then lodges in the pulmonary artery or within one or more of its branches, obstructing the alveolar perfusion and outflow, which results in increased alveolar dead space and creating a ventilation-perfusion ( ) mismatch. Platelets collect on the embolus, triggering the release of substances that cause blood vessel constriction. Widespread pulmonary vessel constriction and pulmonary hypertension impair gas exchange and tissue perfusion . Deoxygenated blood moves into arterial circulation, causing hypoxemia (low arterial blood oxygen level), although some patients with PE do not have hypoxemia. Major risk factors for VTE leading to PE are: • Prolonged immobility • Central venous catheters • Surgery • Pregnancy • Obesity • Advancing age • General and genetic conditions that increase blood clotting • History of thromboembolism Smoking, estrogen therapy, heart failure, stroke, cancer (particularly lung or prostate), and trauma also increase the risk for VTE and PE (McCance et al., 2019). Fat, oil, air, tumor cells, amniotic fluid and fetal debris, foreign objects (e.g., broken IV catheters), injected particles, and infected clots can enter a vein and cause PE. Fat emboli can occur with fracture of the femur, and oil emboli from diagnostic procedures. These have a mortality rate of about 10% (Fukumoto & Fukumoto, 2018; Moore, 2016). Fat emboli cause injury to pulmonary vessels and cause acute respiratory distress syndrome (ARDS) (discussed as a disorder later in this chapter) rather than directly disrupting blood flow. Septic clots may develop from a pelvic abscess, an infected IV catheter, and injections of illegal drugs. VTE and PE are also associated with heparin-induced thrombocytopenia (HIT Prevention of conditions, especially venous stasis, that lead to VTE and PE is a major nursing concern. Preventive actions are outlined in the Best Practice for Patient Safety & Quality Care: Prevention of Pulmonary Embolism box. Lifestyle changes can help reduce the risk for PE. Tobacco use and nicotine in any form narrow blood vessels and increase the risk for clot formation. Hormone-based contraceptives also increase blood clotting. Urge patients to stop smoking cigarettes, especially women who use hormone-based contraceptives. Reducing weight and becoming more physically active can reduce risk for PE. Teach patients who are traveling for long periods to drink plenty of water, change positions often, avoid crossing their legs, and get up from the sitting position at least 5 minutes out of every hour to prevent stasis and clot formation. For patients known to be at risk for PE, small doses of heparin or low-molecular-weight heparin, or an indirect thrombin inhibitor, may be prescribed. Oral direct thrombin inhibitors may be used instead of heparin for VTE prevention in patients who have nonvalvular atrial fibrillation (Burchum & Rosenthal, 2019). For adults who have an ongoing risk for VTE and PE, prevention may include preoperative placement of a retrievable inferior vena cava (IVC) filter. This placement occurs before any surgery in which the patient is expected to be confined to bed for more than just a few days, and the filter is retrieved when the patient is fully ambulatory.

assessing airway obstruction partial vs complete obstruction

Partial obstruction produces-diaphoresis, tachycardia, anxiety, and elevated blood pressure. Diagnostic procedures include chest or neck x-rays, laryngoscopic examination, and CT. PROGRESSING OBSTRUCTION-hypoxia and hypercarbia, restlessness, increasing anxiety, sternal retractions, a "seesawing" chest motion, abdominal movements, or a feeling of impending doom from air hunger. Use pulse oximetry or end-tidal carbon dioxide (EtCO 2 or PEtCO 2) assess for stridor, cyanosis, and changes in level of consciousness.

Home Care Management hf

Patients with chronic HF need to make many adjustments in their lifestyles. They must adhere to the collaborative plan of care that includes dietary restrictions, activity, prescriptions, and drug therapy. They need careful, concise explanations of the self-management plan. The community-based nurse in any setting encourages the patient to verbalize fears and concerns about his or her illness and helps to explore coping skills. Patient participation in self-management can help alleviate and control symptoms.

Peritonsillar Abscess

Peritonsillar abscess (PTA) is a rare complication of acute bacterial tonsillitis. Infection spreads from the tonsil to the surrounding tissue and forms an abscess that can become large enough to obstruct the airway. Signs and symptoms include a collection of pus behind the tonsil causing swelling on one side of the throat, pushing the uvula toward the unaffected side. The patient may have severe throat pain radiating to the ear or teeth, a muffled voice, fever, and difficulty swallowing. He or she may also have spasms and pain of the muscles used in chewing (trismus) and difficulty breathing. Bad breath is present, and lymph nodes on the affected side are swollen. Most patients can be treated as outpatients with antibiotics, although some may need steroids to reduce the swelling. Drainage of the abscess may be needed. Stress the importance of completing the antibiotic regimen and coming to the emergency department quickly if symptoms of obstruction (drooling and stridor) appear.

Pneumonia

Pneumonia is a common disorder with many causes that reduce gas exchange . Although all pneumonias have excess fluid in the lungs from an inflammatory process, pneumonia from respiratory infection is associated with the formation of thick exudate containing proteins and other particles that seriously reduce gas exchange. Inflammation causing pneumonia can be triggered by infectious organisms and by inhaling irritating agents. Inflammation, which is the syndrome of normal tissue responses to cellular injury, allergy, or the invasion of pathogens, occurs in the interstitial spaces, the alveoli, and often the bronchioles. The process begins when pathogens penetrate the airway mucosa and multiply in the alveolar spaces. White blood cells (WBCs) move into the area of infection, causing local capillary leak, edema, and formation of exudates. The exudates collect in and around the alveoli, and the alveolar walls thicken. Both events seriously reduce gas exchange by interfering with diffusion in the lungs leading to hypoxemia, which can cause death. Red blood cells (RBCs) and fibrin move into the alveoli, and capillary leak spreads the infection to other lung areas. If organisms move into the bloodstream, septicemia and sepsis results (Giuliano & Baker, 2020). If the infection extends into the pleural cavity, empyema (a collection of pus in the pleural cavity) results. The fibrin and edema stiffen the lung tissue, reducing compliance and decreasing the vital capacity. Alveolar collapse (atelectasis) reduces gas exchange even more. As a result, arterial oxygen levels fall, causing hypoxemia. Pneumonia may occur as lobar pneumonia with consolidation (an abnormal solidification with lack of air spaces) in a segment or an entire lobe of the lung or as bronchopneumonia with diffusely scattered patches around the bronchi. The extent of lung involvement depends on the host defenses. Bacteria multiply quickly in a person whose immune system is compromised. Tissue necrosis results when an abscess forms and perforates the bronchial wall.

Premature Ventricular Complexes

Premature ventricular complexes (PVCs), also called premature ventricular contractions, result from increased irritability of ventricular cells and are seen as early ventricular complexes followed by a pause. When multiple PVCs are present, the QRS complexes may be unifocal or uniform, meaning that they are of the same shape (Fig. 31.12A), or multifocal or multiform, meaning that they are of different shapes (Fig. 31.12B). PVCs frequently occur in repetitive rhythms, such as bigeminy (two), trigeminy (three), and quadrigeminy (four). Two sequential PVCs are a pair, or couplet. Three or more successive PVCs are usually called nonsustained ventricular tachycardia (NSVT). Premature ventricular contractions are common, and their frequency increases with age. They may be insignificant or may occur with problems such as myocardial infarction, chronic heart failure, chronic obstructive pulmonary disease (COPD), and anemia. PVCs may also be present in patients with hypokalemia or hypomagnesemia. Sympathomimetic agents, anesthesia drugs, stress, nicotine, caffeine, alcohol, infection, or surgery can also cause PVCs, especially in older adults. Postmenopausal women often find that caffeine causes palpitations and PVCs. The patient may be asymptomatic or experience palpitations or chest discomfort caused by increased stroke volume of the normal beat after the pause. Peripheral pulses may be diminished or absent with the PVCs themselves because the decreased stroke volume of the premature beats may decrease peripheral perfusion. Nursing Safety Priority Action Alert Because other dysrhythmias can cause widened QRS complexes, assess whether the premature complexes perfuse to the extremities. Palpate the carotid, brachial, or femoral arteries while observing the monitor for widened complexes or auscultating apical heart sounds. With acute MI, PVCs may be considered a warning, possibly triggering life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF). If there is no underlying heart disease, PVCs are not usually treated other than by eliminating or managing any contributing cause (e.g., caffeine, stress). Potassium or magnesium is given for replacement therapy if hypokalemia or hypomagnesemia is the cause. If the number of PVCs in a 24-hour period is excessive, the patient may be placed on beta-adrenergic blocking agents (beta blockers) (see the Common Examples of Drug Therapy: Antidysrhythmic Medication box)

Surgical Procedures for Laryngeal Cancer and Their Effect on Voice Quality

ProcedureDescriptionResulting Voice QualityLaser surgeryTumor reduced or destroyed by laser beam through laryngoscopeNormal or hoarseTransoral cordectomyTumor (early lesion) resected through laryngoscopeNormal or hoarse (high cure rate)LaryngofissureNo cord removed (early lesion)Normal (high cure rate)Supraglottic partial laryngectomyHyoid bone, false cords, and epiglottis removedNeck dissection on affected side performed if nodes involvedNormal or hoarseHemilaryngectomy or vertical laryngectomyOne true cord, one false cord, and one half of thyroid cartilage removedHoarseTotal laryngectomyEntire larynx, hyoid bone, strap muscles, one or two tracheal rings removedNodal neck dissection if nodes involvedNo natural voice

Inhalation Anthrax

Prodromal Stage (Early)Fulminant Stage (Late) • Fever • Fatigue • Mild chest pain • Dry cough • No indications of upper respiratory infection • Mediastinal "widening" on chest x-ray • Diaphoresis • Stridor on inhalation and exhalation • Hypoxia • High fever • Mediastinitis • Pleural effusion • Hypotension • Septic shock

interventions tb

Promoting Airway Clearance Planning: Expected Outcomes The patient with TB is expected to maintain a patent and adequate airway. Interventions Interventions to maintain a patent airway are similar to those for pneumonia and COPD. Instruct the patient to drink plenty of fluids unless another condition requires restriction. Teach him or her to take a deep breath before coughing. An incentive spirometer may facilitate effective coughing. Reducing Drug-Resistance and Infection Spread Planning: Expected Outcomes The patient with TB is expected to become free of active disease and not spread the disease to others. Interventions Interventions to help the patient become free of active disease are focused on antimicrobial therapy and infection control measures. Combination drug therapy is the most effective method of treating active TB and preventing transmission (Burchum & Rosenthal, 2019). Therapy continues until the disease is under control. Multiple-drug regimens kill or suppress the growth of organisms as quickly as possible and reduce the emergence of drug-resistant organisms. First-line therapy for non-drug-resistant (drug-susceptible) TB is listed in the Common Examples of Drug Therapy: First-Line Treatment for Tuberculosis box and uses isoniazid, rifampin, pyrazinamide, and ethambutol for the first 8 weeks (initial treatment phase). The continuation phase for most patients lasts another 18 weeks for drug-susceptible TB, and the patient takes isoniazid and rifampin either daily or twice a week (CDC, 2018e). (Some of the same drugs are also used for shorter time periods to treat latent TB infections.) Patients who remain culture positive after 8 weeks and those who are HIV positive but not taking antiretroviral therapy may require 7 months of continuation therapy. These drugs are now available in two- or three-drug combinations. Variations of the first-line drugs along with other drug types, such as fluoroquinolone and aminoglycoside antibiotics, are used when the patient does not tolerate the standard first-line therapy. Nursing interventions focus on patient teaching for drug therapy adherence and infection control. Strict adherence to the prescribed drug regimen is crucial for suppressing the disease. Adherence is difficult because of the long duration of treatment. (Duration of therapy is often 26 weeks but can be as long as 2 years for multidrug-resistant [MDR] TB.) Thus your major role is educating the patient about drug therapy and stressing the importance of taking each drug regularly, exactly as prescribed, for as long as it is prescribed. Provide accurate information in multiple formats, such as pamphlets, videos, and drug-schedule worksheets. To determine whether the patient understands how to take the drugs, ask him or her to describe the treatment regimen, side effects, and when to call the health care agency and primary health care provider. The patient with TB often has concerns about the disease prognosis. Offer a positive outlook for the patient who adheres to the drug regimen. However, with current resistant strains of TB, emphasize that not taking the drugs as prescribed could lead to a drug-resistant infection . Nursing Safety Priority Drug Alert The first-line drugs used as therapy for TB all can damage the liver. Warn the patient to not drink any alcoholic beverages for the entire duration of TB therapy. Some multidrug-resistant TB (MDR TB) strains are emerging as extensively drug-resistant (XDR TB). MDR TB is an infection that resists INH and rifampin. XDR TB is resistant not only to the first-line antituberculosis drugs but also to the second-line antibiotics, including the fluoroquinolones and at least one of the aminoglycosides. The WHO estimates that 4% to 5% of all TB cases are drug resistant (WHO, 2019). The most common cause of MDR TB and XDR TB is mismanagement of drug therapy, either from inappropriate selection or use of antibiotics. Patients with acquired immune deficiency syndrome (AIDS; HIV-III) also often have MDR TB (WHO, 2018). Patients who contract TB from a person with a resistant strain will also have a resistant strain of TB. So teaching patients to adhere to their drug regimens will also help them prevent the spread of the disease in both forms. Drug therapy for MDR TB and XDR TB is limited and requires higher doses for longer periods. Bedaquiline is specifically targeted to multidrug-resistant TB. Side effects of this drug can be life threatening, so it is not used when other drugs will work. It should be given through directly observed therapy Bedaquiline can prolong the QT interval, cause ventricular dysrhythmias, and lead to sudden death. Patients on this drug need to have regular ECGs and serum electrolyte evaluations. Nursing Safety Priority Action Alert Warn patients with extensively drug-resistant TB that absolute adherence to therapy is critical for survival and cure of the disease. These patients should receive directly observed therapy (DOT) (described under the "Self-Management Education" section (DOT). The drug delamanid has been approved by WHO and the regulatory bodies for other countries for use alone, in combination with bedaquiline, or following bedaquiline therapy with multidrug-resistant TB. It is currently in clinical trials with the U.S. Food and Drug Administration (FDA). The hospitalized patient with active TB is placed on Airborne Precautions (see Chapter 21) in a well-ventilated room that has at least six exchanges of fresh air per minute. All health care workers must use a personal respirator when caring for the patient. Use Standard Precautions with appropriate protection as with all patients. Airborne Precautions are discontinued when the patient is no longer contagious. Other care issues for the patient with TB include teaching about infection prevention and what to expect about disease monitoring and participating in activities. TB is often treated outside the acute care setting, with the patient convalescing at home. Airborne Precautions are not necessary in this setting because family members have already been exposed; however, all members of the household need to undergo TB testing. Teach the patient to cover the mouth and nose with a tissue when coughing or sneezing, to place used tissues in plastic bags, to wear a mask when in contact with crowds, and to use social distancing until the drugs suppress infection. Tell the patient that sputum specimens are needed about every 4 weeks once drug therapy is initiated. When the results of three consecutive sputum cultures are negative, the patient is no longer infectious (contagious) and may return to former activities. Remind him or her to avoid exposure to any inhalation irritants because these can cause further lung damage. Improving Nutrition Planning: Expected Outcomes The patient with TB is expected to have improved nutrition. Interventions The patient with TB often has a long-standing history of malnutrition. Conduct a nutrition assessment using an evidence-based tool. Determine patient likes/dislikes, the ability to buy healthy food, condition of teeth or dentures, weight and body mass index, and history of substance use. When inadequate nutrition is a problem, be sure to include a registered dietitian nutritionist (RDN) as part of the interprofessional team. Drugs to treat TB often cause nausea. If this happens, instruct the patient to take once-a-day drugs at night. Antiemetics can also be prescribed. If food doesn't interfere with the drug absorption (check the label), taking pills with a small snack of simple carbohydrates may help. Refer the patient to Meals on Wheels or other meal-delivery service. Instruct him or her about good oral hygiene, which makes food taste better. Monitor weight weekly and document trends to determine the effectiveness of nutrition interventions. For best healing, the patient needs a diet with quality proteins; iron; vitamins A, B, C, and E; and abundant fresh produce. Educate him or her about nutrition in collaboration with an RDN. Tell the patient to avoid alcohol. Alcohol can cause liver damage, and so can most of the antituberculosis drugs. Alcohol is also a source of "empty calories," and adults who drink alcohol to excess are often malnourished. An adult who gets a large number of calories from alcohol will not feel hungry. A special problem for this group of patients is lack of phosphorus, which is part of the cellular energy compound ATP. With low phosphorus, the patient will lack energy. Refer the patient to support groups if alcoholism or other substance abuse is present. Improved nutrition will help improve immunity . Managing Fatigue Planning: Expected Outcomes The patient with TB is expected to have improved stamina and less fatigue. Interventions Many of the interventions for fatigue will be the same as those for improving nutrition. Poor nutrition can lead directly to fatigue. Encourage the patient to resume activities slowly and get plenty of rest. Reassure him or her that the fatigue will improve as therapy progresses and the disease is controlled. Assess the patient's sleep-wake habits and encourage a full night's sleep with short daytime naps. Help him or her develop a healthy bedtime ritual if needed. Mental stamina may be decreased as a result of the lengthy convalescence. Reassure the patient that, by taking drugs as directed, the disease will be cured and energy levels will increase.

Pulmonary Contusion

Pulmonary contusion, a potentially lethal injury, is a common chest injury and occurs most often by rapid deceleration during car crashes. After a contusion, respiratory failure can develop immediately or over time. Hemorrhage and edema occur in and between the alveoli, reducing both lung movement and the area available for gas exchange . Local inflammation can cause further damage. The patient becomes hypoxemic and dyspneic. Patients may be asymptomatic at first and can later develop various degrees of respiratory failure and possibly pneumonia. These patients often have decreased breath sounds or crackles and wheezes over the affected area. Other symptoms include bruising over the injury, dry cough, tachycardia, tachypnea, and dullness to percussion. If there is no disruption of the parenchyma, bruise resorption often occurs without treatment. Management includes maintenance of ventilation and oxygenation. Provide oxygen, give IV fluids as prescribed, and place the patient in a moderate-Fowler position. If a high FiO 2 is needed, oxygen may be administered using a high-flow nasal cannula (HFNC). When side-lying, the "good lung down" position may be helpful. The patient in obvious respiratory distress may need noninvasive positive-pressure ventilation (NIPPV) or mechanical ventilation with positive end-expiratory pressure (PEEP) to inflate the lungs. A vicious cycle occurs in which more muscle effort is needed for ventilating a lung with a contusion and the patient becomes progressively hypoxemic. This situation causes him or her to tire easily, have reduced gas exchange , and become more fatigued and more hypoxemic. This condition often leads to acute respiratory distress syndrome (ARDS).

pulmonary arterial htn

Pulmonary hypertension is the chronic increase in pulmonary vascular pressures above 25 mm Hg, which makes the right side of the heart work much harder for lung perfusion to support proper gas exchange . Normally the pulmonary vascular pressures are low, 15 to 18 mm Hg, allowing the pressures generated by the contraction of the less-muscled right ventricle to easily overcome them and move blood into the pulmonary artery (McCance et al., 2019). Over time, the higher lung vascular pressures lead to right-sided heart failure (cor pulmonale) that can be fatal. Many lung problems, such as chronic obstructive pulmonary disease and pulmonary fibrosis, can secondarily cause increased pulmonary pressures. For secondary pulmonary hypertension, good control of the condition causing it can delay or prevent cor pulmonale. Primary pulmonary artery hypertension (PAH), also known as idiopathic pulmonary artery hypertension, is a condition in which pulmonary vessels and often other lung tissues undergo growth changes that greatly increase pressure in the lung circulatory system for unknown reasons. Just as with secondary pulmonary hypertension, PAH progresses and leads to cor pulmonale with reduced perfusion and gas exchange . The absolute cause of PAH is unknown, and it is diagnosed in the absence of other lung disorders (McCance et al., 2019). Genetic and environmental factors working together may increase the risk. For example, although it is a relatively rare problem, exposure to some drugs, such as fenfluramine/phentermine or dasatinib, increases the risk. The disorder occurs mostly in women between the ages of 20 and 40 years and occurs more often within some families, suggesting a possible genetic susceptibility. The familial PAH form appears to be transmitted in an autosomal dominant pattern with reduced penetrance (OMIM, 2018). Without treatment, death usually occurs within 2 years after diagnosis, most often from profound heart failure. The pathologic problem in PAH is blood vessel constriction with increasing vascular resistance in the lung. The events that lead up to increasing resistance may include an imbalance between those factors that increase vascular resistance and those that induce blood vessel relaxation. Intrinsic agents that increases vascular resistance are endothelin-1, a very powerful vasoconstrictor that works by binding to endothelin receptors on vascular smooth muscle, and thromboxane, which induces arterial vasoconstriction and enhances clotting by activating platelets. Intrinsic factors that promote vascular relaxation are nitric oxide (NO) and prostacyclin-1. Many adults with primary PAH have a deficiency of prostacyclin 1. Often PAH is not diagnosed until late in the disease process when the lungs and heart have already been damaged significantly (McCance et al., 2019). Teach adults, especially women, who have a first-degree relative (parent or sibling) with PAH to have regular health checks and to consult a primary health care provider whenever pulmonary problems are present.

activation of the renin-angiotensin system (RAS).

Reduced blood flow to the kidneys, Vasoconstriction becomes more pronounced in response to angiotensin II, and aldosterone secretion causes sodium and water retention. Preload and afterload increase. Angiotensin II contributes to ventricular remodeling, resulting in progressive myocyte (myocardial cell) contractile dysfunction over time

exercise activity asthma

Regular exercise is a recommended part of asthma therapy to maintain cardiac health, strengthen muscles, and promote gas exchange and perfusion . Teach patients to examine the conditions that trigger an attack and adjust the exercise routine as needed. Some may need to use an inhaled SABA before beginning activity. For others, adjusting the environment may be needed (e.g., changing from outdoor ice-skating in cold, dry air to indoor ice-skating).

Pandemic Respiratory Infections

Respiratory viral infections are common among humans and vary from mild colds to severe seasonal influenza that can lead to pneumonia, other complications, and death. These infections are considered human disorders and are not usually found in other animals. Respiratory infections caused by viruses are usually self-limiting because humans are able to mount some degree of an immunity response against the invading viruses. Part of adaptive immunity develops as a result of generations of ancestral exposures to common viral families such as rhinoviruses, respiratory syncytial viruses (RSV), and coronaviruses, among others. However, this immunity is not perfect. These viral strains change slightly every year so that the antibodies an adult makes against a specific strain one year are not completely effective against exposure to other strains of that same viral family later that year or another year. This is why adults can have several colds in the same year. It is also why influenza vaccinations are needed yearly to increase protection, as discussed in the Seasonal Influenza section.

assess rheumatic carditis

Rheumatic carditis is one of the major indicators of rheumatic fever. The common signs and symptoms are: • Tachycardia • Cardiomegaly (enlarged heart) • Development of a new murmur or a change in an existing murmur • Pericardial friction rub • Precordial pain • Electrocardiogram (ECG) changes (prolonged P-R interval) • Indications of HF • Evidence of an existing streptococcal infection Primary prevention is extremely important. Teach all patients to remind their primary health care providers to provide appropriate antibiotic therapy if they develop the indications of streptococcal pharyngitis: • Moderate-to-high fever • Abrupt onset of a sore throat • Reddened throat with exudate • Enlarged and tender lymph nodes Interventions: Take Action Penicillin is the antibiotic of choice for treatment. Erythromycin is the alternative for penicillin-sensitive patients. Once a diagnosis of rheumatic fever is made, antibiotic therapy is started immediately. Teach the patient to continue the antibiotic administration for the full 10 days to prevent reinfection. Suggest ways to manage fever, such as maintaining hydration and taking antipyretics. Encourage the patient to get adequate rest. Explain to the patient and family that a recurrence of rheumatic carditis is most likely the result of reinfection by Streptococcus. Antibiotic prophylaxis is necessary for the rest of the patient's life to prevent infective endocarditis discussed earlier in this chapter

rheumatic carditis patho

Rheumatic carditis, also called rheumatic endocarditis, is a sensitivity response that develops after an upper respiratory tract infection with group A beta-hemolytic Streptococci. It occurs in almost half of patients with rheumatic fever. The precise mechanism by which the infection causes inflammatory lesions in the heart is not established; however, inflammation is evident in all layers of the heart. The inflammation results in impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage. Rheumatic carditis is characterized by the formation of Aschoff bodies (small nodules in the myocardium that are replaced by scar tissue). A diffuse cellular infiltrate also develops and may be responsible for the resulting heart failure (HF). The pericardium becomes thickened and covered with exudate, and a serosanguineous pleural effusion may develop. The most serious damage occurs to the endocardium, with inflammation of the valve leaflets developing. Hemorrhagic and fibrous lesions form along the inflamed surfaces of the valves, resulting in stenosis or regurgitation of the mitral and aortic valves

Rib Fracture

Rib fractures are a common injury to the chest wall, often resulting from direct blunt trauma to the chest. The force applied to the ribs fractures them and drives the bone ends into the chest. Thus there is a risk for deep chest injury such as pulmonary contusion, pneumothorax, and hemothorax. The patient has pain on movement and splints the chest defensively. Splinting reduces breathing depth and clearance of secretions. If the patient has pre-existing lung disease, the risk for atelectasis and pneumonia increases. Those with injuries to the first or second ribs, flail chest, seven or more fractured ribs, or expired volumes of less than 15 mL/kg often have a deep chest injury and a poor prognosis. Management of uncomplicated rib fractures is simple because the fractured ribs reunite spontaneously. The chest is usually not splinted by tape or other materials. The main focus is to decrease pain so adequate ventilation is maintained. An intercostal nerve block may be used if pain is severe. Opioids are effective analgesics that allow for coughing and effective incentive spirometry use; however, they can cause respiratory depression. NSAIDs, epidural anesthesia, and patient-controlled analgesia (PCA) are other available options.

Seasonal Influenza

Seasonal influenza, or "flu," is a highly contagious acute viral respiratory infection that can occur at any age (Cannon et al., 2018). Influenza may be caused by different strains of one of several virus families, referred to as A, B, and C. Epidemics are common and lead to complications of pneumonia or death, especially in older adults, those with heart failure or chronic lung disorders, and immunocompromised patients. Most patients are treated at home, but hospitalization may be needed when symptoms are severe or the patient develops complications such as pneumonia. During the 2017−2018 influenza season, more than 30,000 patients were hospitalized for the infection with about 60% of these being older than 65 years (Centers for Disease Control and Prevention [CDC], 2018d). The patient with influenza often has a rapid onset of severe headache, muscle aches, fever, chills, fatigue, and weakness. Adults are contagious 24 hours before symptoms occur and up to 5 days after they begin. Sore throat, cough, and watery nasal discharge can also occur. Infection with influenza strain B can lead to nausea, vomiting, and diarrhea. Most patients feel fatigued for 1 to 2 weeks after the acute episode has resolved. Seasonal influenza can be prevented or its severity reduced when adults receive an annual influenza vaccination. The vaccine is changed every year based on which specific viral strains are most likely to cause illness during the influenza season (i.e., late fall and winter in the Northern Hemisphere). Usually the vaccines contain antigens for the three (trivalent) or four (quadrivalent) viral strains expected to be prevalent that season. The recommended influenza vaccination for all adults is an IM injection. For adults age over 65 years, a new formulation is available, known as a "senior flu shot." This injection is a higher dose, trivalent or quadrivalent vaccine designed for more effective protection for adults with age-related reduced immunity . For adults under age 50 years, a new formulation of a quadrivalent nasal mist using live attenuated viruses has been approved (Pfeifer, 2018). Although annual vaccination is not 100% effective at preventing influenza, it is especially important for adults who: • Are older than 50 years • Have chronic illness or immune compromise • Reside in institutions • Live with or care for others with health problems that put them at risk for severe complications of influenza • Are health care personnel providing direct care to patients (CDC, 2018a) Nurses have an opportunity to urge vaccination in the community and can show support for this action by receiving annual vaccinations themselves. This action not only helps practicing nurses avoid becoming infected, but it also reduces the risk for infection transmission from health care professional to patient. The influenza vaccination rate among health care personnel during the 2017−2018 flu season was 78% (by self-report) (Black et al., 2018). National Patient Safety Goals Vaccinations for the prevention of influenza are widely available and are recommended for adults by The Joint Commission's National Patient Safety Goals. Teach the patient who is sick to reduce the risk for spreading the flu by thoroughly washing hands, especially after nose blowing, sneezing, coughing, rubbing the eyes, or touching the face. Other precautions include staying home from work, school, or crowded places; covering the mouth and nose with a tissue when sneezing or coughing; disposing properly of used tissues immediately; and avoiding close contact with other people (social distancing) (CDC, 2018a). Although handwashing is a good way to prevent transmitting the virus, many people cannot wash their hands immediately after sneezing. The technique recommended by the CDC for controlling flu spread is to sneeze or cough into the upper sleeve rather than into the hand (CDC, 2018c). (Respiratory droplets on the hands can contaminate surfaces and be transmitted to others.) Interprofessional Collaborative Care Tests for influenza are available; however, in a community that already has cases of the disease, the diagnosis is usually based on the patient's reported symptoms. The rapid influenza diagnostic test (RIDT) is common but has high false-negative rates, and the patient should be treated if influenza is suspected even if the RIDT is negative. Other tests, including cultures, are usually recommended only in specific situations. Viral infections do not respond to antibiotic therapy. Neuraminidase inhibitor (NAI) antiviral drugs such as oseltamivir, zanamivir, and peramivir have been effective in the prevention and treatment of some strains of influenza A and B. They can be given to adults at high risk for complications who have been exposed to influenza but have not yet been vaccinated. These drugs also shorten the duration of influenza. The drugs prevent viral spread in the respiratory tract by inhibiting a viral enzyme that allows the virus to penetrate respiratory cells. To be most effective as treatment rather than for prevention, they must be taken within 24 to 48 hours after symptoms begin. Peramivir is only available as an IV drug. A newly approved antiviral drug with a different mechanism of action is baloxavir. This oral drug taken once daily prevents influenza viral gene transcription and reproduction. Patients older than 65 years should be treated with antiviral drugs as soon as possible to reduce their risks for hospitalization, complications, and disability (CDC, 2018a). Instruct the patient to rest for several days and increase fluid intake unless another problem requires fluid restriction. Saline gargles may ease sore throat pain. Antihistamines may reduce the rhinorrhea. Other supportive measures are the same as those for rhinosinusitis.

Common Causes of Acute Lung Injury

Shock • Trauma • Serious nervous system injury • Pancreatitis • Fat and amniotic fluid emboli • Pulmonary infections • Sepsis • Excessive inflammation from COVID-19 pneumonia • Inhalation of toxic gases (smoke, oxygen) • Pulmonary aspiration (especially of stomach contents) • Drug ingestion (e.g., heroin, opioids, aspirin) • Hemolytic disorders • Multiple blood transfusions • Cardiopulmonary bypass • Submersion in water with water aspiration (especially in fresh water)

Assessing for Signs and Symptoms of Heart Transplant Rejection

Shortness of breath • Fatigue • Fluid gain (edema, increased weight) • Abdominal bloating • New bradycardia • Hypotension • Atrial fibrillation or flutter • Decreased activity tolerance • Decreased ejection fraction (late sign)

Pathophysiology of Common Signs and Symptoms of Pneumonia

Sign or SymptomPathophysiologyIncreased respiratory rate/dyspneaStimulation of chemoreceptorsIncreased work of breathing as a result of decreased lung complianceStimulation of J receptorsAnxietyPainHypoxemiaAlveolar consolidationPulmonary capillary shuntingCoughFluid accumulation in receptors of the trachea, bronchi, and bronchiolesPurulent, blood-tinged, or rust-colored sputumA result of the inflammatory process in which fluid from the pulmonary capillaries and red blood cells moves into the alveoliFeverPhagocytes release pyrogens that cause the hypothalamus to increase body temperaturePleuritic chest discomfortInflammation of the parietal pleura causes pain on inspiration

labs pnuemonia

Sputum is obtained and examined by Gram stain, culture, and sensitivity testing; however, the responsible organism is often not identified. A sputum sample is easily obtained from the patient who can cough into a specimen container. Extremely ill patients may need suctioning to obtain a sputum specimen. In these situations, a specimen is obtained by sputum trap (Fig. 28.1) during suctioning. A complete blood count (CBC) is obtained to assess for an elevated WBC count, which is a common finding except in older adults. Blood cultures may be performed to determine whether the organism has entered the bloodstream. In severely ill patients, arterial blood gases (ABGs) may be assessed to determine baseline arterial oxygen and carbon dioxide levels and to help identify a need for supplemental oxygen. Serum electrolyte, blood urea nitrogen (BUN), and creatinine levels are also assessed. A high BUN level may occur as a result of dehydration. Hypernatremia (high blood sodium levels) occurs with dehydration. A lactate level may be performed to help assess for sepsis. Because CAP often follows or is present with influenza, recommend that adults with CAP also have influenza testing (Esden, 2020). Imaging Assessment Chest x-ray is the most common diagnostic test for pneumonia but may not show changes until 2 or more days after symptoms are present. Pneumonia usually appears on chest x-ray as an area of increased density. It may involve a lung segment, a lobe, one lung, or both lungs. In the older adult, the chest x-ray is essential for early diagnosis because other pneumonia symptoms are often vague (Touhy & Jett, 2020). Other Diagnostic Assessments Pulse oximetry is used to assess for hypoxemia. Thoracentesis is used in patients who have an accompanying pleural effusion.

Prevention of Pulmonary Embolism

Start passive and active range-of-motion exercises for the extremities of immobilized and postoperative patients. • Ambulate patients as soon as possible after surgery. • Use pneumatic compression devices after surgery as prescribed. • Evaluate patient for criteria indicating the need for anticoagulant therapy. • Give prescribed prophylactic low-dose anticoagulant or antiplatelet drugs after specific surgical procedures as soon as surgical bleeding risk has subsided. • Teach patients to avoid the use of tight garters, girdles, and constricting clothing. • Prevent pressure under the popliteal space (e.g., do not place a pillow under the knee; instead, use an alternating pressure mattress). • Perform a comprehensive assessment of peripheral circulation every 8 hours. • Elevate the affected limb 20 degrees or more above the level of the heart to improve venous return, as appropriate. • Change patient position every 2 hours or ambulate as tolerated. • Refrain from massaging leg muscles. • Instruct patients not to cross their legs. • Teach the patient and family about precautions. • Encourage smoking cessation.

The Step System for Medication Use in Asthma Control

Step 1Step 2Step 3Step 4Step 5As-needed rapid-acting beta2 agonist (relief inhaler)As-needed rapid-acting beta2 agonist (relief inhaler)As-needed rapid-acting beta2 agonist (relief inhaler)As-needed rapid-acting beta2 agonist (relief inhaler)As-needed rapid-acting beta2 agonist (relief inhaler)No daily drugs neededDaily treatment with the use of one of these two options:Daily treatment with the use of one of these four options:Daily treatment with Step 3 option that provided best control and tolerance along with one or more of these two options:Daily treatment with Step 4 option(s) that provided best control and tolerance along with either of these two options:Low-dose ICSLow-dose ICS and long-acting beta2 agonistMedium-dose or high-dose ICS and long-acting beta2 agonistOral glucocorticosteroid (lowest dose)Leukotriene modifieraMedium-dose or high-dose ICSLow-dose ICS and leukotriene modifierLow-dose ICS and sustained-release theophyllineLeukotriene modifier and sustained-release theophyllineIgEb antagonistInterleukin-5 antagonistInterleukin-17 antagonist

02 and status asthmaticus

Supplemental oxygen by mask or nasal cannula is often used during an acute asthma attack. High-flow delivery may be needed when bronchospasms are severe and limit flow of oxygen through the bronchiole tubes (see Chapter 25 for high-flow delivery systems). Ensure that no open flames (e.g., smoking, fireplaces, burning candles) or other combustion hazards are in rooms where oxygen is in use Status asthmaticus is a severe, life-threatening acute episode of airway obstruction that intensifies once it begins and often does not respond to usual therapy. The patient arrives in the emergency department with extremely labored breathing and wheezing. Use of accessory muscles for breathing and distention of neck veins are observed. If the condition is not reversed, the patient may develop pneumothorax and cardiac or respiratory arrest. IV fluids, potent systemic bronchodilators, steroids, epinephrine, and oxygen are given immediately to reverse the condition. Magnesium sulfate also may be used, although this practice is controversial. Prepare for emergency intubation. Sudden absence of wheezing along with a low oxygen saturation indicates complete airway obstruction and requires a tracheotomy. When breathing improves, management is similar to that for any patient with asthma.

Supraventricular Tachycardia: Pathophysiology Review

Supraventricular tachycardia (SVT) involves the rapid stimulation of atrial tissue at a rate of 100 to 280 beats/min in adults. During SVT, P waves may not be visible, especially if there is a 1:1 conduction with rapid rates, because the P waves are embedded in the preceding T wave. SVT may occur in healthy young people, especially women. SVT is usually caused by a re-entry mechanism in which one impulse circulates repeatedly throughout the atrial pathway, restimulating the atrial tissue at a rapid rate. The term paroxysmal supraventricular tachycardia (PSVT) is used when the rhythm is intermittent. It is initiated suddenly by a premature complex such as a PAC and terminated suddenly with or without intervention. Interprofessional Collaborative Care Signs and symptoms depend on the duration of the SVT and the rate of the ventricular response. In patients with a sustained rapid ventricular response, assess for palpitations, chest pain, weakness, fatigue, shortness of breath, nervousness, anxiety, hypotension, and syncope. Cardiovascular deterioration may occur if the rate does not sustain adequate blood pressure. In that case, SVT can result in angina, heart failure, and cardiogenic shock. With a nonsustained or slower ventricular response, the patient may be asymptomatic except for occasional palpitations. If SVT occurs in a healthy person and stops on its own, no intervention may be needed other than eliminating identified causes. If it continues, the patient should be studied in the electrophysiology study (EPS) laboratory. The preferred treatment for recurrent SVT is radiofrequency catheter ablation, described later in this chapter with treatment of atrial fibrillation. In sustained SVT with a rapid ventricular response, the desired outcomes of treatment are to decrease the ventricular response, convert the dysrhythmia to a sinus rhythm, and treat the cause. Vagal maneuvers induce vagal stimulation of the cardiac conduction system, specifically the SA and AV nodes. Although not as common today, vagal maneuvers may be attempted to treat supraventricular tachydysrhythmias and include carotid sinus massage and Valsalva maneuvers. However, the results of these interventions are often temporary and may cause "rebound" tachycardia or severe bradycardia. Further therapy must be initiated. In carotid sinus massage, the health care provider massages over one carotid artery for a few seconds, observing for a change in cardiac rhythm. This intervention causes vagal stimulation, slowing SA and AV nodal conduction. Prepare the patient for the procedure. Instruct him or her to turn the head slightly away from the side to be massaged and observe the cardiac monitor for a change in rhythm. An ECG rhythm strip is recorded before, during, and after the procedure. After the procedure, assess vital signs and the level of consciousness. Complications include bradydysrhythmias, asystole, ventricular fibrillation (VF), and cerebral damage. Because of these risks, carotid massage is not commonly performed. A defibrillator and resuscitative equipment must be immediately available during the procedure. To stimulate a vagal reflex, the health care provider instructs the patient to bear down as if straining to have a bowel movement. Assess the patient's heart rate, heart rhythm, and blood pressure. Observe the cardiac monitor and record an ECG rhythm strip before, during, and after the procedure to determine the effect of therapy. Drug therapy is prescribed for some patients to convert SVT to a normal sinus rhythm (NSR). Adenosine is used to terminate the acute episode and is given rapidly (over several seconds) followed by a normal saline bolus. Nursing Safety Priority Drug Alert Side effects of adenosine include significant bradycardia with pauses, nausea, and vomiting. When administering adenosine, be sure to have emergency equipment readily available! AV nodal blocking agents, such as beta and calcium channel blockers, are also given to treat SVT. The Common Examples of Drug Therapy: Antidysrhythmic Medication box lists medications that may be used for SVT. If symptoms of poor perfusion are severe and persistent, the patient may require synchronized cardioversion to immediately terminate the SVT. For long-term treatment, patients are referred to an electrophysiologist for radiofrequency catheter ablation. Synchronized cardioversion and catheter ablation are discussed later in this chapter with treatment of atrial fibrillation.

Major compensatory mechanisms include:

Sympathetic nervous system stimulation • Renin-angiotensin system (RAS) activation (also called renin-angiotensin-aldosterone [RAAS] activation) • Other chemical responses • Myocardial hypertrophy Stimulation of the adrenergic receptors causes an increase in heart rate (beta adrenergic) and blood pressure from vasoconstriction (alpha adrenergic)

Sinus Tachycardia: Pathophysiology Review

Sympathetic nervous system stimulation or vagal (parasympathetic) inhibition results in an increased rate of SA node discharge, which increases the heart rate. When the rate of SA node discharge is more than 100 beats/min, the rhythm is called sinus tachycardia (Fig. 31.8A). From age 10 years to adulthood, the heart rate normally does not exceed 100 beats/min except in response to activity and then usually does not exceed 160 beats/min. Rarely does the heart rate reach 180 beats/min. Sinus tachycardia initially increases cardiac output and blood pressure. However, continued increases in heart rate decrease coronary perfusion time, diastolic filling time, and coronary perfusion pressure while increasing myocardial oxygen demand. Increased sympathetic stimulation is a normal response to physical activity but may also be caused by anxiety, pain, stress, fever, anemia, hypoxemia, and hyperthyroidism. Drugs such as epinephrine, atropine, caffeine, alcohol, nicotine, cocaine, aminophylline, and thyroid medications may also increase the heart rate. In some cases, sinus tachycardia is a compensatory response to decreased cardiac output or blood pressure, as occurs in dehydration, hypovolemic shock, myocardial infarction (MI), infection, and heart failure. Assess patients for signs and symptoms of hypovolemia and dehydration, including increased pulse rate, decreased urinary output, decreased blood pressure, and dry skin and mucous membranes. Interprofessional Collaborative Care The patient may be asymptomatic except for an increased pulse rate. However, if the rhythm is not well tolerated, he or she may have symptoms of instability. Nursing Safety Priority Action Alert For patients with sinus tachycardia, assess for fatigue, weakness, shortness of breath, orthopnea, decreased oxygen saturation, increased pulse rate, and decreased blood pressure. Also assess for restlessness and anxiety from decreased cerebral perfusion and for decreased urine output from impaired renal perfusion. The patient may also have anginal pain and palpitations. The ECG pattern may show T-wave inversion or ST-segment elevation or depression in response to myocardial ischemia. The desired outcome is to decrease the heart rate to normal levels by treating the underlying cause. Remind the patient to remain on bedrest if the tachycardia is causing hypotension or weakness. Teach the patient to avoid substances that increase cardiac rate, including caffeine, alcohol, and nicotine. Help patients develop stress-management strategies or refer the patient to a mental health professional.

arterial vasoconstriction.

Sympathetic stimulation also results Vasoconstriction has the benefit of maintaining blood pressure and improving tissue perfusion in low-output states. However, constriction of the arteries increases afterload, the resistance against which the heart must pump. Afterload is the major determinant of myocardial oxygen requirements. As it increases, the left ventricle requires more energy to eject its contents and SV may decline.

Stroke volume

Sympathetic stimulation increases venous return to the heart, which further stretches the myocardial fibers causing dilation. results in more forceful contraction. More forceful contractions increase SV and CO. After a critical point is reached within the cardiac muscle, further volume and stretch reduce the force of contraction and cardiac output.

Asthma Symptoms and Control Level

Symptoms • Daytime symptoms of wheezing, dyspnea, coughing present more than twice weekly • Waking from night sleep with symptoms of wheezing, dyspnea, coughing • Reliever (rescue) drug needed more than twice weekly • Activity limited or stopped by symptoms more than twice weekly Control Level Controlled: None of the above symptoms Partly Controlled: 1 or 2 of the above symptoms Uncontrolled: 3 to 4 of the above symptoms

Weaning Methods

Synchronous Intermittent Mandatory Ventilation • The patient breathes between the machine's preset breaths/min rate. • The machine is initially set on an SIMV rate of 12, meaning that the patient receives a minimum of 12 breaths/min by the ventilator. • The patient's respiratory rate will be a combination of ventilator breaths and spontaneous breaths. • As the weaning process ensues, the pulmonary health care provider prescribes gradual decreases in the SIMV rate, usually at a decrease of 1 to 2 breaths/min. T -Piece Technique • The patient is removed from the ventilator for short periods (initially 5 to 10 minutes) and allowed to breathe spontaneously. • The ventilator is replaced with a T-piece (see Chapter 25) or CPAP, which delivers humidified oxygen. • The prescribed FiO 2 may be higher for the patient on the T-piece than on the ventilator. • Weaning progresses as the patient can tolerate progressively longer periods off the ventilator. • Nighttime weaning is not usually attempted until the patient can maintain spontaneous respirations for most of the day. Pressure Support Ventilation • The patient's respiratory rate and tidal volume are their own. • PSV allows the patient's respiratory effort to be augmented by a predetermined pressure assist from the ventilator. • As the weaning process ensues, the amount of pressure applied to inspiration is gradually decreased. Daily Spontaneous Breathing Trials • The patient remains on PSV but the PEEP and pressure support (PS) are both decreased. • In some trials, the PEEP is decreased to 5 cm H2O and the PS is decreased to 0. • The patient's hemodynamic status is monitored as well as pulmonary status. • After 30 to 60 minutes ABGs are obtained for analysis. • SBT should be attempted daily to assess for readiness to liberate from mechanical ventilation.

diagnostic tb

TB infection can be tested by methods. In addition to chest x-ray, sputum cultures of blood or respiratory secretions can be tested. Many fully automated nucleic acid amplification tests (NAATs) for TB are used on respiratory secretions. Results of these tests are available in less than 2 hours; however, they have limitations. Tuberculin skin testing (TST), also known as the Mantoux test, is the most commonly used reliable screening test for TB. A small amount (0.1 mL) of purified protein derivative (PPD) is placed intradermally in the forearm. The test is "read" in 48 to 72 hours. An area of induration (localized swelling with hardness of soft tissue), not just redness, measuring 10 mm or greater in diameter, indicates exposure to and possible infection with TB (Fig. 28.3). In adults with reduced immunity , induration of 5 mm is a positive result. If possible, the site is re-evaluated after 72 hours because false-negative readings occur more often after only 48 hours. A positive reaction indicates exposure to TB or the presence of inactive (dormant) disease, not active disease. A reduced skin reaction or a negative skin test does not rule out TB disease or infection of the very old or anyone who has severely reduced immunity . Failure to have a skin response because of reduced immunity when infection is present is called anergy. Blood analysis can be done with interferon-gamma release assays, or IGRAs. The first IGRA was the QuantiFERON-TB Gold In-Tube test. IGRAs show how the patient's immune system responds to the TB bacterium. A positive result means that the person is infected with TB but does not indicate whether the infection is latent or active. Another blood test, the Xpert MTB/RIF Ultra, which can detect drug-resistant strains of TB and is also recommended for testing people with HIV infection, has been approved by both the CDC and WHO. Sputum culture confirms the diagnosis and is also used to evaluate treatment effectiveness. Enhanced TB cultures take up to 4 weeks for a valid result. After drug therapy is started, sputum samples are obtained at specified intervals. Cultures are usually negative after 3 months of effective treatment. Annual screening is needed for anyone who comes into contact with people who may be infected with TB, including some health care workers. Screening is very important for foreign-born adults and migrant workers. Participation in screening programs is higher when programs are delivered in a culturally sensitive and nonthreatening manner. Urge anyone who is considered high risk to have an annual TB screening test. Imaging Assessment Once a person's skin test is positive for TB, a chest x-ray is used to detect active TB or old, healed lesions. Calcifications usually indicate old, healed lesions. Caseation and inflammation may be seen on the x-ray if the disease is active (McCance et al., 2019). The chest x-rays of HIV-infected patients may be normal or may show infiltrates in any lung zone and lymph node enlargement.

Tachydysrhythmias

Tachydysrhythmias are heart rates greater than 100 beats/min. They are a major concern in the adult patient with coronary artery disease (CAD). Coronary artery blood flow occurs mostly during diastole when the aortic valve is closed and is determined by diastolic time and blood pressure in the root of the aorta. Tachydysrhythmias are serious because they: • Shorten the diastolic time and therefore the coronary perfusion time (the amount of time available for blood to flow through the coronary arteries to the myocardium) • Initially increase cardiac output and blood pressure (However, a continued rise in heart rate decreases the ventricular filling time because of a shortened diastole, decreasing the stroke volume. Consequently, cardiac output and blood pressure will begin to decrease, reducing aortic pressure and therefore coronary perfusion pressure.) • Increase the work of the heart, increasing myocardial oxygen demand The patient with a tachydysrhythmia may have: • Palpitations • Chest discomfort (pressure or pain from myocardial ischemia or infarction) • Restlessness and anxiety • Pale, cool skin • Syncope ("blackout") from hypotension Tachydysrhythmias may also lead to heart failure. Presenting symptoms of heart failure may include dyspnea, lung crackles, distended neck veins, fatigue, and weakness (see Chapter 32). See the Key Features box for signs and symptoms of sustained bradydysrhythmias and tachydysrhythmias.

Automated External Defibrillation

The American Heart Association promotes the use of automated external defibrillators (AEDs) for use by laypersons and health care professionals responding to cardiac arrest emergencies (Fig. 31.15). These devices are found in many public places such as malls, airports, and commercial jets. The patient in cardiac arrest must be on a firm, dry surface. The rescuer places two large adhesive-patch electrodes on the patient's chest in the same positions as for defibrillator electrodes. The rescuer stops CPR and commands anyone present to move away, ensuring that no one is touching the patient. This measure eliminates motion artifact when the machine analyzes the rhythm. The rescuer presses the "analyze" button on the machine. After rhythm analysis, which may take up to 30 seconds, the machine advises that a shock is either necessary or not indicated. Shocks are recommended for VF or pulseless VT only. If a shock is indicated, issue a command to clear all contact with the patient and press the charge button. Once the AED is charged, press the shock button and the shock will be delivered. The shock is delivered through the patches, so it is hands-off defibrillation, which is safer for the rescuer. The rescuer then resumes CPR until the AED instructs to "stop CPR" to analyze the rhythm. If the rhythm is VF or VT and another shock is indicated, the AED will instruct the rescuer to charge and deliver another shock. Newer AEDs perform rhythm analysis and defibrillation without the need for a rescuer to press a button to analyze or shock the victim. It is essential that Advanced Cardiac Life Support (ACLS) be provided as soon as possible. Use of AEDs allows for earlier defibrillation. Therefore there is a greater chance of successful rhythm conversion and patient survival.

COVID-19 Infection

The coronavirus family, in addition to causing the common cold in humans, includes bird and animal strains that have caused severe respiratory influenzas. In 2002 and 2003, the coronavirus COVID-2 jumped species and was responsible for SARS (severe acute respiratory syndrome). In 2012 another coronavirus mutation was responsible for MERS-Cov (Middle East respiratory syndrome), which had a high but demographically confined mortality rate. In December 2019 extending into 2020, the world experienced a coronavirus pandemic, COVID-19 (CO = coronavirus; VI = virus; D = disease; 19 = 2019). This strain of virus was first reported to have infected humans and rapidly spread in the fall of 2019 (McIntosh, 2020). Evidence shows that COVID-19 is spread via droplet transmission (CDC, 2020b; Palmore, 2020; WHO, 2020). It can also be transmitted during medical procedures that generate aerosols (WHO, 2020). Researchers continue to investigate whether airborne transmission can occur in the absence of a medical procedure, such as in poorly ventilated indoor settings (WHO, 2020). By the middle of September 2020 it infected almost 28 million people in 188 countries and territories, resulting in 905,181 deaths (Johns Hopkins University, 2020). At this same time in Canada, 136,565 cases were reported with 9208 deaths; in the United States 6.3 million people were infected, with 191,248 deaths (reflecting a death rate of 3%) (Johns Hopkins University, 2020). In comparison, 35.5 million people in the United States contracted seasonal influenza in the 2018-2019 influenza season, resulting in 34,200 deaths (death rate of about 0.1%) (CDC, 2019). COVID-19 statistics continue to change with increased testing and better understanding of care based upon evolving evidence. Some patients who develop COVID-19 are asymptomatic or experience minimal symptoms. Others experience minor respiratory symptoms similar to a common cold, and recover with no apparent long-term effects. Others, particularly older adults and individuals with pre-existing chronic conditions, can develop a viral pneumonia that can lead to severe acute respiratory distress syndrome. See the Key Features: COVID-19 box for symptoms that are currently associated with the infection. Typically, symptoms appear 2 to 14 days after exposure to the virus. Key Features

interventions hf

The expected outcome is that the patient will have an optimal spontaneous breathing pattern that increases gas exchange and maintains a serum carbon dioxide level that is within normal limits. Interventions The purpose of collaborative care is to help promote gas exchange. Ventilation assistance may be needed because the oxygen content of the blood is often decreased in patients who have pulmonary congestion. Monitor the patient's respiratory rate, rhythm, and quality every 1 to 4 hours. Auscultate breath sounds every 4 to 8 hours. Nursing Safety Priority Action Alert Provide the necessary amount of supplemental oxygen within a range prescribed by the health care provider to maintain oxygen saturation at 90% or greater. If the patient has dyspnea, place in a high-Fowler's position with pillows under each arm to maximize chest expansion and improve gas exchange. Repositioning and performing coughing and deep-breathing exercises every 2 hours helps to improve gas exchange and prevents atelectasis. Interprofessional collaboration with the respiratory therapist is important to plan the most effective methods for assisting with ventilation. Increasing Perfusion Planning: Expected Outcomes The expected outcome is that the patient will have increased perfusion with adequate cardiac output. Interventions Collaborative care begins with nonsurgical interventions, but the patient may need surgery if these are not successful in meeting optimal outcomes. Nonsurgical Management Nonsurgical management relies primarily on a variety of drugs (Table 32.3). If drug therapy is ineffective, other nonsurgical options are available. Drugs to improve stroke volume include those that reduce afterload, reduce preload, and improve cardiac muscle contractility. A major role of the nurse is to administer medications as prescribed, monitor for their therapeutic and adverse effects, and teach the patient and family about drug therapy. Drugs that reduce afterload. By relaxing the arterioles, arterial vasodilators can reduce the resistance to left ventricular ejection (afterload) and improve cardiac output (CO). These drugs do not cause excessive vasodilation but reverse some of the inappropriate or excessive vasoconstriction common in HF. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers. Patients with even mild heart failure (HF) resulting from left ventricular dysfunction are given a trial of angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs). Both ACE inhibitors (e.g., enalapril and captopril) and ARBs (e.g., valsartan, irbesartan, and losartan) improve function and quality of life for patients with HF. Because of the significant clinical experience with ACE inhibitors, this drug class is the drug of choice in the treatment of HF (Burchum & Rosenthal, 2019). ARBs are also effective and can be used as an initial agent for those who do not tolerate ACE inhibitors, usually due to a nagging dry cough. For patients with acute HF, the health care provider may prescribe an IV-push ACE inhibitor such as Vasotec IV. The ACE inhibitors and ARBs suppress the renin-angiotensin system (RAS), which is activated in response to decreased renal blood flow. ACE inhibitors prevent conversion of angiotensin I to angiotensin II, resulting in arterial dilation and increased stroke volume. ARBs block the effect of angiotensin II receptors and thus decrease arterial resistance and arterial dilation. In addition, these drugs block aldosterone, which prevents sodium and water retention, thus decreasing fluid overload. Both ACEIs and ARBs work more effectively for Euro-Americans than for African-American populations (Paul & Page, 2016). Volume-depleted patients should receive a low starting dose, or the fluid volume should be restored before beginning the prescribed drug as the principle adverse effects of these drugs is hypotension. Monitor for hyperkalemia, a potential adverse drug effect in patients who have renal dysfunction. Be aware that there is a risk of angioedema as well; although the risk is low, angioedema is a potentially lethal side effect (Burchum & Rosenthal, 2019; Yancy et al., 2017). Angiotensin receptor neprilysin inhibitor (ARNI). A newer combination drug, sacubitril/valsartan, has demonstrated a reduction in death and hospitalization in patients with chronic Class II to IV heart failure with a decreased ejection fraction. Valsartan is an ARB that is combined with sacubitril, which inhibits neprilysin. Together these drugs increase natriuretic peptides while suppressing the RAAS (Burchum & Rosenthal, 2019). Sucubitril/valsartan is used in place of an ACE inhibitor or ARB and should not be given within 36 hours of the last dose of an ACE inhibitor or in patients with a history of angioedema (Drazner, 2018; Yancy et al., 2017). Other side effects are similar to those of ACE inhibitors and include hypotension, hyperkalemia, cough, dizziness, and renal failure. Assess for orthostatic hypotension, acute confusion, poor peripheral perfusion, and reduced urine output in patients with low systolic blood pressure. Monitor serum potassium and creatinine levels to determine renal dysfunction CEIs and ARBs are started slowly and cautiously. The first dose may be associated with a rapid drop in blood pressure (BP). Patients at risk for hypotension usually have an initial systolic BP less than 100 mm Hg, are older than 75 years, have a serum sodium level less than 135 mEq/L, or are volume depleted. Monitor BP every hour for several hours after the initial dose and each time the dose is increased. Immediately report to the health care provider and document a systolic blood pressure of less than 90 mm Hg (or designated protocol level). If this problem occurs, place the patient flat and elevate legs to increase cerebral perfusion and promote venous return. Interventions that reduce preload. Ventricular fibers contract less forcefully when they are overstretched, such as in a failing heart. Interventions aimed at reducing preload attempt to decrease volume and pressure in the left ventricle, increasing ventricular muscle stretch and contraction. Preload reduction is appropriate for HF accompanied by congestion with total body sodium and water overload. Nutrition therapy. In HF, nutrition therapy is aimed at reducing sodium and water retention to decrease the workload of the heart. The primary care provider may restrict sodium intake in an attempt to decrease fluid retention. Many patients need to omit table salt (no added salt) from their diet, thus reducing sodium intake to about 3 g daily. If salt intake must be reduced further, the patient may need to eliminate high-sodium foods (e.g., ham, bacon, pickles) and all salt in cooking, thus reducing sodium intake to 2 g daily. If needed, collaborate with the dietitian to help the patient select foods that meet a restricted therapeutic diet. There is no strong evidence to suggest that less than 2 g of sodium daily is helpful; in fact, it may be harmful (Horwitz & Krumholz, 2018). Few patients are placed on severe fluid restrictions. However, patients with excessive aldosterone secretion may experience thirst and drink 3 to 5 L of fluid each day. As a result, their fluid intake may be limited to a more normal 2 L daily. Supervise assistive personnel (AP) to ensure that they limit the prescribed intake and accurately record intake and output. Weigh the patient daily or delegate this activity to UAP and supervise that it is done. Keep in mind that 1 kg of weight gain or loss equals 1 L of retained or lost fluid. The same scale should be used every morning before breakfast for the most accurate assessment of weight. Monitor for an expected decrease in weight because excess fluid is excreted from the body. Drug therapy. Common drugs prescribed to reduce preload are diuretics and venous vasodilators. Morphine sulfate is also given for patients in acute HF to reduce anxiety, decrease preload and afterload, slow respirations, and reduce pain associated with a myocardial infarction (MI). The primary health care provider adds diuretics to the regimen when diet and fluid restrictions have not been effective in managing the symptoms of HF. Diuretics are the first-line drug of choice in older adults with HF and fluid overload. These drugs enhance the renal excretion of sodium and water by reducing circulating blood volume, decreasing preload, and reducing systemic and pulmonary congestion. The type and dosage of diuretic prescribed depend on the severity of HF and renal function. Loop diuretics such as furosemide, torsemide, and bumetanide are most effective for treating fluid volume overload. For patients with acute HF, furosemide or bumetanide can be administered by IV push (IVP). Patient-Centered Care: Older Adult Considerations Loop diuretics continue to work even after excess fluid is removed. As a result, some patients, especially older adults, can become dehydrated. Observe for signs of dehydration in the older adult, especially acute confusion, decreased urinary output, and dizziness. Provide evidence-based interventions to reduce the risk for falls, as discussed in Chapter 4. The health care provider may initially prescribe a thiazide diuretic, such as hydrochlorothiazide (HCTZ), for older adults with mild volume overload. Unlike loop diuretics, the action of thiazides is self-limiting (i.e., diuresis decreases after edema fluid is lost). Therefore the dehydration that may occur with loop diuretics is not common with these drugs. Patients also prefer thiazides because of the gradual onset of diuresis. As HF progresses, many patients develop diuretic resistance with refractory edema. The health care provider may choose to manage this problem by prescribing both types of diuretics. Other strategies include IV continuous infusion of furosemide or bumetanide or rotating loop diuretics. Monitor for and prevent potassium deficiency (hypokalemia) from diuretic therapy. The primary signs of hypokalemia are nonspecific neurologic and muscular symptoms, such as generalized weakness, depressed reflexes, and irregular heart rate. A potassium supplement may be prescribed for some patients. Other health care providers prescribe a potassium-sparing diuretic, such as spironolactone, for patients at risk for dysrhythmias from hypokalemia. Although not as effective as other diuretics, spironolactone helps retain potassium, which decreases the risk for ventricular dysrhythmias, and is usually used in stage III/IV heart failure. Monitor for hyperkalemia and renal failure and anticipate stopping the medication if potassium or creatinine levels rise. Patients being managed with ACE inhibitors or ARBs and diuretics at the same time may not experience hypokalemia. However, if their kidneys are not functioning well, they may develop hyperkalemia (elevated serum potassium level). Review the patient's serum creatinine level. If the creatinine is greater than 1.8 mg/dL, notify the health care provider before administering supplemental potassium. The health care provider may prescribe venous vasodilators (e.g., nitrates) for the patient with HF who has persistent dyspnea. Significant constriction of venous and arterial blood vessels occurs to compensate for reduced CO. Constriction reduces the volume of fluid that the vascular bed can hold and increases preload. Venous vasodilators may benefit by: • Returning venous vasculature to a more normal capacity • Decreasing the volume of blood returning to the heart • Improving left ventricular function Nitrates may be administered IV, orally, or topically. IV nitrates are used most often for acute HF. These drugs cause primarily venous vasodilation but also a significant amount of arteriolar vasodilation. Monitor the patient's blood pressure when starting nitrate therapy or increasing the dosage. Patients may initially report headache, but assure them that they will develop a tolerance to this effect and that the headache will cease or diminish. Acetaminophen can be given to help relieve discomfort. Unfortunately, tolerance to the vasodilating effects develops when nitrates are given around the clock. To prevent this tolerance, the health care provider may prescribe at least one 12-hour nitrate-free period out of every 24 hours (usually overnight). Nitrates such as isosorbide are prescribed to provide nitrate-free periods and reduce the problem of tolerance. Chapter 35 discusses nitrates in more detail. Drugs that enhance contractility. Contractility of the heart can also be enhanced with drug therapy. Positive inotropic drugs are most commonly used, but vasodilators and beta-adrenergic blockers may also be administered. For chronic HF, low-dose beta blockers are most commonly used. Digoxin may be prescribed to improve symptoms, thereby decreasing dyspnea and improving functional activity. Digoxin. Although not as commonly used today, digoxin, a cardiac glycoside, has been demonstrated to provide symptomatic benefits for patients in chronic heart failure (HF) with sinus rhythm and atrial fibrillation. Digoxin (sometimes called dig) therapy reduces exacerbations of HF and hospitalizations when added to a regimen of ACE inhibitors or ARBs, beta blockers, and diuretics. However, it may increase mortality as a result of drug toxicity, especially in older adults. As a result, digoxin is considered a second-line agent (Burchum & Rosenthal, 2019). The potential benefits of digoxin include: • Increased contractility • Reduced heart rate (HR) • Slowing of conduction through the atrioventricular node • Inhibition of sympathetic activity while enhancing parasympathetic activity Digoxin is absorbed from the GI tract erratically. Many drugs, especially antacids, interfere with its absorption. It is eliminated primarily by renal excretion. Older patients, those with impaired renal function, and those with low lean body mass should be maintained on lower doses of the drug (McIlvennan & Page, 2016). ncreased cardiac automaticity occurs with toxic digoxin levels or in the presence of hypokalemia, resulting in ectopic beats (e.g., premature ventricular contractions [PVCs]). Changes in potassium level, especially a decrease, cause patients to be more sensitive to the drug and cause toxicity. The signs and symptoms of digoxin toxicity are often vague and nonspecific and include anorexia, fatigue, blurred vision, and changes in mental status, especially in older adults. Toxicity may cause nearly any dysrhythmia, but PVCs are most commonly noted. Assess for early signs of toxicity such as bradycardia, heart block, and loss of the P wave on the ECG. Carefully monitor the apical pulse rate and heart rhythm of patients receiving digoxin. The health care provider determines the desirable heart rate (HR) to achieve. Current evidence indicates that a heart rate greater than 70 beats/min is a risk factor for increased morality and has negative clinical effects (see Fig. 32.2) (Prasun & Albert, 2018). Report the development of either an irregular rhythm in a patient with a previously regular rhythm or a regular rhythm in a patient with a previously irregular one. Monitor serum digoxin and potassium levels (hypokalemia potentiates digoxin toxicity) to identify toxicity. Older adults are more likely than other patients to become toxic because of decreased renal excretion. Any drug that increases the workload of the failing heart also increases its oxygen requirement. Be alert for the possibility that the patient may experience angina (chest pain) in response to digoxin. Other inotropic drugs. Patients experiencing acute heart failure are candidates for IV drugs that increase contractility. For example, beta-adrenergic agonists, such as dobutamine, are used for short-term treatment of acute episodes of HF. Dobutamine improves cardiac contractility and thus cardiac output and myocardial-systemic perfusion. A more potent drug used for acute HF, milrinone, functions as a vasodilator/inotropic agent with phosphodiesterase activity. Also known as a phosphodiesterase inhibitor, this drug increases cyclic adenosine monophosphate (cAMP), which enhances the entry of calcium into myocardial cells to increase contractile function. Like the beta-adrenergic agonists, milrinone is given IV. Chapter 35 discusses inotropic drugs in more detail. Beta-adrenergic blockers. Beta-adrenergic blockers (commonly referred to as beta blockers) improve the condition of some patients in HF. Prolonged exposure to increased levels of sympathetic stimulation and catecholamines worsens cardiac function. Beta-adrenergic blockade reverses this effect, improving morbidity, mortality, and quality of life for patients in HF. Beta blockers must be started slowly for HF. Carvedilol, extended-release metoprolol succinate, and bisoprolol are approved for treatment of HF (Burchum & Rosenthal, 2019). Do not confuse metoprolol tartrate with metoprolol succinate. The first dose is extremely low. Monitor the patient in either the hospital or primary health care provider's office to assess for bradycardia or hypotension after the first dose is given. Do not stop taking beta blockers abruptly as this can cause an increased risk of clinical decompensation (McIlvennan & Page, 2016). Instruct the patient to weigh daily and report any signs of worsening HF immediately. The primary health care provider gradually increases the drug dose if HF worsens. The patient is evaluated at least weekly for changes in BP, pulse, activity tolerance, and orthopnea. A modest drop in BP is acceptable if he or she remains asymptomatic and can stand without experiencing dizziness or a further drop in BP. The resting heart rate (HR) should remain between 55 and 60 and increase slightly with exercise. Activity tolerance improves, and less orthopnea is experienced. Most patients with mild and moderate HF demonstrate improved ejection fraction, decreased hospital admissions, and improvement in symptoms when beta blockers are added to their treatment regimens. The benefits of this therapy are seen over a long period rather than immediately. Aldosterone antagonists. Aldosterone antagonists (spironolactone or eplerenone) can reduce symptoms associated with HF and may be added to HF therapy in patients who remain symptomatic while taking an ACE inhibitor and a beta blocker (Burchum & Rosenthal, 2019). As a potassium-sparing diuretic, aldosterone antagonists decrease the risk for dysrhythmias from hypokalemia. Aldosterone antagonists also block the effect of aldosterone, which decreases the amount of water and sodium retained. Monitor the patient for hyperkalemia and renal failure and anticipate stopping the medication if potassium or creatinine levels rise. Every-other-day dosing is an alternative for patients at risk of developing hyperkalemia. HCN channel blocker. In 2015, ivabradine was approved by the Food and Drug Administration (FDA) for the treatment of symptomatic stabilized chronic heart failure. This medication is a first-in-class, hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker, which slows the heart rate by inhibiting a specific channel in the sinus node. It has been shown to reduce the risk of hospitalization rate in HF patients. Ivabradine is used for HF patients who have an ejection fraction (EF) less than 35% who are in sinus rhythm with a resting heart rate of 70 beats/min or greater. This medication is used for patients who are on the maximally tolerated dose of beta-blocker therapy or have a contraindication to beta-blocker therapy. Side effects of ivabradine include bradycardia, hypertension, atrial fibrillation, and luminous phenomena (visual brightness) (Colucci, 2018). Advise the patient to take this medication with meals. Teach the patient how to check radial pulse and to report low heart rate or irregularity to the health care provider. Advise that visual changes associated with light may occur with initial treatment. These visual changes are usually transient and will disappear with time (Colucci, 2018). Patients should use caution when driving or using machines in situations where light intensity may change abruptly. For patients with diastolic HF, drug therapy has not been as effective. Calcium channel blockers, ACE inhibitors, and beta blockers have been used with various degrees of success. Other nonsurgical options. In addition to drug therapy, other nonsurgical options, both noninvasive and invasive, may be used and include: • Continuous positive airway pressure (CPAP) • Cardiac resynchronization therapy (CRT) • CardioMEMS implantable monitoring system • Investigative gene therapy Continuous positive airway pressure (CPAP) is a respiratory treatment that improves obstructive sleep apnea in patients with HF. It also improves cardiac output (CO) and ejection fraction (EF) by decreasing afterload and preload, blood pressure (BP), and dysrhythmias. Sleep apnea is directly correlated with coronary artery disease as a result of diminished oxygen supply to the heart during apneic episodes. This respiratory problem is discussed in detail in Chapter 26. Cardiac resynchronization therapy (CRT), also called biventricular pacing, uses a permanent pacemaker alone or is combined with an implantable cardioverter/defibrillator. Electrical stimulation causes more synchronous ventricular contractions to improve EF, CO, and mean arterial pressure. This modality is indicated for patients with Class III or IV HF, an EF of less than 35%, and presence of a left bundle branch block. CRT improves the patient's ability to perform ADLs. Chapter 31 discusses pacing in more detail. A CardioMems implantable monitoring system inserted into the pulmonary artery allows the patient to take a daily reading of the pulmonary artery pressure. These data are transmitted to the provider's office and allow for management and adjustment of medications. The device, about the size of the quarter, is implanted during a right heart catheterization and is permanent. The patient is provided a special pillow with an antenna and portable electronic unit. He or she turns the system on, places the pillow on the bed, and lies on top of the pillow. The device will advise if the position needs to be changed and when reading is complete. The CardioMEMS device can detect increases in pulmonary pressures, indicating fluid retention before the patient demonstrates symptoms. Therapy can be adjusted before symptoms, which may prevent readmission to the hospital and improve quality of life. Gene therapy may be indicated for patients in end-stage HF who are not candidates for heart transplantation. This therapy replaces damaged genes with normal or modified genes by a series of injections of growth factor into the left ventricle. Although still investigative, this therapy may result in improved exercise tolerance and regrowth of cardiac cells. Surgical Management Heart transplantation is the most definitive surgical option for patients with refractory end-stage HF (see the Heart Transplantation section). However, donor availability is limited, and candidacy for heart transplantation is often complicated by comorbidities that exist in the HF patient. Several surgical procedures are available to improve CO in patients who are not candidates for a transplant or are awaiting transplant. Ventricular assist devices. Patients with debilitating end-stage heart failure are often sent home on drug therapy and referred to hospice. However, ventricular assist devices (VADs) can dramatically improve the lives of many patients. In this procedure, a mechanical pump is implanted to work with the patient's own heart (Fig. 32.3). Both left and right VADs are available, depending on the type of HF the patient has. Those with end-stage kidney disease, severe chronic lung disease, clotting disorders, and infections that do not respond to antibiotics are not candidates for this surgery. Postoperative complications include bleeding, infective endocarditis, ventricular dysrhythmias, and stroke. Nursing care is similar to that described for cardiac surgery in Chapter 35. VADs can be used in the short term while awaiting heart transplantation (a "bridge-to-transplant" procedure) or long term (destination therapy) (Broglio et al., 2015). Most patients survive with a VAD until a transplant is available. Other surgical therapies. HF causes ventricular remodeling, or dilation, which worsens as the disease progresses. Left ventricular surgical reconstruction can be done as an alternative to cardiac transplantation in an attempt to improve function of the left ventricle. However, potential impact and long-term survival rates have not been established (Fang, 2015). For example, in endoventricular circular patch cardioplasty, the surgeon removes portions of the cardiac septum and left ventricular wall and grafts a circular patch (synthetic or autologous) into the opening. This procedure provides a more normal shape to the left ventricle to improve the heart's ejection fraction (EF) and cardiac output (CO). Perioperative care is similar to that for the patient having a coronary artery bypass graft (CABG) (see Chapter 35). Preventing or Managing Pulmonary Edema Planning: Expected Outcomes The most desirable outcome is that the patient will not develop pulmonary edema as a result of heart failure (HF). However, if the patient progresses to pulmonary edema, the expected outcome is that he or she will recover from this complication without other problems. Interventions Monitor for signs of acute pulmonary edema, a life-threatening event that can result from severe HF (with fluid overload), acute myocardial infarction (MI), mitral valve disease, and possibly dysrhythmias. In pulmonary edema, the left ventricle fails to eject sufficient blood and pressure increases in the lungs as a result. The increased pressure causes fluid to leak across the pulmonary capillaries and into the lung airways and tissues. Nursing Safety Priority Critical Rescue Assess for and report early symptoms, such as crackles in the lung bases, dyspnea at rest, disorientation, and confusion, especially in older patients. Document the precise location of the crackles because the level of the fluid progresses from the bases to higher levels in the lungs as the condition worsens. The patient in acute pulmonary edema is typically extremely anxious, tachycardic, and struggling for air. As pulmonary edema becomes more severe, he or she may have a moist cough productive of frothy, blood-tinged sputum; and his or her skin may be cold, clammy, or cyanotic (see the Key Features: Pulmonary Edema box). If the patient is not hypotensive, place in a sitting (high-Fowler's) position with the legs down to decrease venous return to the heart. The priority nursing action is to administer oxygen therapy at 5 to 12 L/min by simple facemask or at 6 to 10 L/min by nonrebreathing mask with reservoir (which may deliver up to 100% oxygen) to promote gas exchange and perfusion (Urden et al., 2018). Apply a pulse oximeter and titrate the oxygen flow to keep the patient's oxygen saturation above 90%. If supplemental oxygen does not resolve the patient's respiratory distress, collaborate with the respiratory therapist, physician, advanced practice nurse, or physician assistant for more aggressive therapy, such as continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) ventilation. Intubation and mechanical ventilation may be needed for some patients. The patient diagnosed with pulmonary edema is admitted to the acute care hospital, often in a critical care unit. Reassure the patient and family that his or her distress will decrease with proper management. If the patient's systolic blood pressure is above 100, administer sublingual nitroglycerin (NTG) as prescribed to decrease afterload and preload every 5 minutes for three doses while establishing IV access for additional drug therapy. The health care provider prescribes rapid-acting diuretics, such as furosemide or bumetanide. Give furosemide IV push (IVP) over 1 to 2 minutes to avoid ototoxicity (Burchum & Rosenthal, 2019). Bumetanide may be administered IVP over 1 to 2 minutes to avoid ototoxicity or as a continuous infusion to provide consistent fluid removal over 24 hours. Monitor vital signs frequently, at least every 30 to 60 minutes. If the patient's blood pressure is adequate, IV morphine sulfate may be prescribed to reduce venous return (preload), decrease anxiety, and reduce the work of breathing. Monitor respiratory rate and BP closely. Other drugs, such as IV NTG and drugs to treat HF, may be administered. Monitor the patient's vital signs closely (especially BP) while these drugs are being given. In severe cases of fluid overload and renal dysfunction or diuretic resistance, ultrafiltration may be used. See Chapter 63 for a complete discussion of this procedure and nursing implications. The benefits of ultrafiltration include: • Decrease in cardiac filling pressures • Decrease in pulmonary arterial pressure • Increase in cardiac index • Reduction in norepinephrine, renin, and aldosterone posthospital week) and follow-up with the health care provider within 1 week of discharge (Murtaugh et al., 2017). As the nurse is planning for discharge, it is critical that care transmission records are used to provide critical information to the home care agency. When reviewing discharge instructions, the nurse should go over the follow-up appointment and include verbal and written information including the date, time, and location

Afterload

The force or resistance against which the heart pumps.

labs pe

The hyperventilation triggered by hypoxia and pain first leads to respiratory alkalosis, indicated by low partial pressure of arterial carbon dioxide (PaCO 2) on arterial blood gas (ABG) analysis. The PaO 2/FiO 2 (fraction of inspired oxygen) ratio falls as a result of "shunting" of blood from the right side of the heart to the left without picking up oxygen from the lungs. Shunting causes the PaCO 2 level to rise, resulting in respiratory acidosis. Later, metabolic acidosis results from buildup of lactic acid caused by tissue hypoxia. (See Chapter 14 for a more detailed discussion of acidosis.) Even if ABG studies and pulse oximetry show hypoxemia, these results alone are not sufficient for the diagnosis of PE (McCance et al., 2019; Moore, 2019). A patient with a small embolus may not be hypoxemic, and PE is not the only cause of hypoxemia. Other laboratory studies performed when PE is suspected include a general metabolic panel, troponin, brain natriuretic peptide (BNP), and D-dimer levels. The D-dimer rises with fibrinolysis. When the value is normal or low, it can rule out a PE (McCance et al., 2019). However, even if the value is high, other diagnostic testing is needed to determine whether a PE has occurred (Pagana & Pagana, 2018).

Implantable Cardioverter/Defibrillator

The implantable cardioverter/defibrillator (ICD) is indicated for patients who have experienced one or more episodes of spontaneous sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) not caused by a myocardial infarction (MI). Collaborate with the physician and the electrophysiology nurse to prepare the patient for this procedure. A psychological profile is done to determine whether the patient can cope with the discomfort and fear associated with internal defibrillation from the ICD. Many patients report anxiety, depression, and decreased quality of life, which improves for the majority of patients after 12 months. Two types of lead systems are available: transvenous and subcutaneous. In the traditional transvenous system, the leads are introduced via the subclavian vein and the generator is implanted in the left pectoral area, similar to a permanent pacemaker insertion. In the subcutaneous ICD, the leads are tunneled underneath the skin and placed to the left of the sternum to form a right angle just below the xiphoid, where they attach to the generator. The generator is implanted in the left midaxillary chest wall. The subcutaneous ICD is recommended for younger patients (<40 years), patients without venous access, and patients who do not require concomitant pacemaker therapy. This procedure is performed in the electrophysiology laboratory. If the patient experiences a VT or VF episode after ICD placement and the ICD therapies are not successful, the qualified nurse or health care provider promptly externally defibrillates and initiates high-quality CPR. Some patients use a lightweight, automated wearable cardioverter/defibrillator (WCD). This external vestlike device is worn 24 hours a day except when the patient showers or bathes. One popular brand is the Zoll Lifecore LifeVest, which is programmed to monitor for VT and VF. A family member must be present to call 911 and initiate CPR if the patient experiences pulseless VT or VF while in the shower. If the patient is conscious while experiencing VT, he or she can press a button to prevent a shock. This precaution is an advantage over implantable devices because ICDs are programmed to always deliver a shock when VT or VF occurs. The generator may be activated or deactivated by the provider placing a magnet over the implantation site for a few moments. The patient requires close monitoring in the postoperative period for dysrhythmias and complications such as bleeding and cardiac tamponade. The nurse must know whether the ICD is activated or deactivated. Care of the patient is similar to that after implantation of a permanent pacemaker, discussed earlier in this chapter. If the device was implanted following sudden cardiac arrest, driving is usually restricted for 6 months (Brady & MacLeod, 2018). See the Patient and Family Education: Preparing for Self-Management: Implantable Cardioverter/Defibrillator box for the important points for health teaching. Patient and Family Education: Preparing for Self-Management Implantable Cardioverter/Defibrillator • Follow the instructions for implantable cardioverter/defibrillator (ICD) site skin care that have been specifically prepared for you. • Report to your primary health care provider any fever or redness, swelling, soreness, or drainage from your incision site. • Do not wear tight clothing or belts that could cause irritation over the ICD generator. • Do not manipulate your generator site. • Avoid activities that involve rough contact with the ICD implantation site. Activity more vigorous than bowling or golf should be avoided (Brady & MacLeod, 2018). • Keep your ICD identification card in your wallet and consider wearing a medical alert bracelet. • Know the basic functioning of your ICD device, its rate cutoff, and the number of consecutive shocks it can deliver. • Avoid magnets directly over your ICD because they can inactivate the device. If beeping tones are coming from the ICD, move away from the electromagnetic field immediately (within 30 seconds) before the inactivation sequence is completed and notify your primary health care provider. • Inform all health care providers caring for you that you have an ICD implanted, because certain diagnostic tests and procedures must be avoided to prevent ICD malfunction. These include diathermy, electrocautery, and nuclear magnetic resonance tests. • Avoid other sources of electromagnetic interference, such as devices emitting microwaves (not microwave ovens); transformers; radio, television, and radar transmitters; large electrical generators; metal detectors, including handheld security devices at airports; antitheft devices; arc welding equipment; and sources of 60-cycle (Hz) interference. Also avoid leaning directly over the alternator of a running motor of a car or boat. • Most modern wireless communication devices do not interfere with ICD function; however, cell phones should be used on the opposite side from the ICD (Brady & MacLeod, 2018). • Report to your primary health care provider symptoms such as fainting, nausea, weakness, blackout, and rapid pulse rates. • Take all medications prescribed as instructed. • Follow instructions on restrictions on physical activity, such as not swimming, driving motor vehicles, or operating dangerous equipment. Driving is typically restricted for 1 week to allow for healing. • Keep all health care provider and ICD clinic appointments. • Sit or lie down immediately if you feel dizzy or faint to avoid falling if the ICD discharges. • Know how to contact the local emergency medical services (EMS) in your community. Inform them in advance that you have an ICD so that they can be prepared if they need to respond to an emergency call for you. • Encourage family members to learn how to perform CPR. Family members should know that if they touch you when the device discharges, they may feel a slight but not harmful shock. • Follow instructions on what to do if the ICD successfully discharges. This may include maintaining a diary of the date, the time, activity preceding the shock, symptoms, the number of shocks delivered, and how you feel after the shock. The health care provider may want to be notified each time the device discharges. • Avoid strenuous activities that may cause your heart rate to meet or exceed the rate cutoff of your ICD because this causes the device to discharge inappropriately. • Notify your primary health care provider for information regarding access to health care if you are leaving town or relocating.

Modes of Ventilation

The mode of ventilation is the way in which the patient receives breaths from the ventilator. The most common modes of ventilation—assist-control (AC) ventilation, synchronized intermittent mandatory ventilation (SIMV), and pressure support (PS) ventilation—are based on either the volume mode or pressure mode of gas delivery. Assist-control (AC) ventilation is a full support mode. The ventilator takes over the work of breathing for the patient. The tidal volume and ventilatory rate are preset and referred to as mandatory breaths. If the patient does not trigger spontaneous breaths, a ventilatory pattern is established by the ventilator. This mode of ventilation can be used with either a pressure-regulated mode or a volume-regulated mode of gas delivery. It is programmed to respond to the patient's inspiratory effort if he or she begins a breath. In this case, the ventilator delivers the preset tidal volume whether the breath is mandatory or patient initiated. This mode allows the patient to increase the rate of breathing above the set rate. A disadvantage of the AC mode is that the ventilator continues to deliver a preset tidal volume even when the patient's spontaneous breathing rate increases. This can cause hyperventilation and respiratory alkalosis. Investigate and correct causes of hyperventilation, such as pain, anxiety, or acid-base imbalances. Although AC is considered a full support mode, it is possible for the patient to be weaned directly from AC to a spontaneous mode such as pressure support ventilation. Synchronized intermittent mandatory ventilation (SIMV) is similar to AC ventilation in that tidal volume and ventilatory rate are preset. This type of ventilation can be used in either pressure- or volume-regulated mode. If the patient does not breathe, a ventilatory pattern is established by the ventilator. Unlike the AC mode, SIMV allows spontaneous breathing at the patient's own rate and tidal volume between the ventilator breaths. It can be used as a main ventilatory mode or as a weaning mode. When used for weaning, the number of mechanical breaths (SIMV breaths) is gradually decreased (e.g., from 12 to 2) as the patient resumes spontaneous breathing. The mandatory ventilator breaths are delivered when the patient is ready to inspire. This action coordinates breathing between the ventilator and the patient. Pressure support ventilation is used for spontaneously breathing patients. No tidal volume is set. It delivers the patient's own breath with assistance from a set airway pressure and PEEP. It is used as a step in the weaning process. Continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP) are noninvasive pressure support modes of ventilation (NIPPV) used for spontaneously breathing patients. They require the use of a nasal mask or facemask. CPAP applies positive airway pressure throughout the entire respiratory cycle, keeps the alveoli open during inspiration, and prevents alveolar collapse during expiration. This process increases functional residual capacity (FRC) and improves gas exchange and oxygenation. Normal levels of CPAP are 5 to 15 cm H2O. BiPAP provides two levels of pressure: a higher inspiratory (IPAP) pressure, typically 10 to 20 cm H2O, and a lower expiratory (EPAP) pressure, typically 4 to 8 cm H2O, which make exhalation easier and improve gas exchange . Both machines can be used to treat patients with sleep apnea, but BiPAP may also be used for patients with chronic obstructive pulmonary disease (COPD), heart failure, respiratory muscle fatigue, or impending respiratory failure to avoid more invasive ventilation methods. Other modes of ventilation, such as airway pressure release ventilation (APRV), proportional assist ventilation (PAV), and high-frequency oscillatory ventilation (HFOV), are alternative modes of ventilation for patients with severe hypoxemia, those needing improved ventilator synchrony, or those needing rescue therapy.

assess pulmonary artery htn

The most common early symptoms are dyspnea and fatigue in an otherwise healthy adult. Some patients also have angina-like chest pain. Table 27.3 lists the classification of PAH. Diagnosis is made from the results of right-sided heart catheterization showing elevated pulmonary pressures. Other test results suggesting PAH include abnormal ventilation-perfusion scans, pulmonary function tests (PFTs) showing reduced functional pulmonary volumes with reduced diffusion capacity, and an abnormal appearance on CT.

infective endocarditis diagnosis

The most reliable criteria for diagnosing endocarditis include positive blood cultures, a new regurgitant murmur, and evidence of endocardial involvement by echocardiography. A positive blood culture is a prime diagnostic test. Both aerobic and anaerobic specimens are obtained for culture. Some slow-growing organisms may take 3 weeks and require a specialized medium to isolate. Low hemoglobin and hematocrit levels may also be present. Echocardiography has improved the ability to diagnose infective endocarditis accurately. Transesophageal echocardiography (TEE) allows visualization of cardiac structures that are difficult to see with transthoracic echocardiography (TTE) (see Chapter 30) (Baddour et al., 2015).

ventilation older adult considerations

The older patient, especially one who has smoked or who has a chronic lung problem such as COPD, is at risk for ventilator dependence and failure to wean. Age-related changes, such as chest wall stiffness, reduced ventilatory muscle strength, and decreased lung elasticity, reduce the likelihood of weaning. The usual symptoms of ventilatory failure—hypoxemia and hypercarbia—may be less obvious in the older adult. Use other clinical measures of gas exchange and oxygenation, such as a change in mental status, to determine breathing effectiveness

self manage pnuemonia

The patient needs to continue the anti-infective drugs as prescribed. An important nursing role is to reinforce, clarify, and provide information to the patient and family as needed. Unfortunately, the re-admission rate within 30 days after discharge is relatively high, especially among older adults (Goering, 2018). See the accompanying Systems Thinking and Quality Improvement box focusing on one group's successful method of reducing preventable re-admissions. Home Care Management No special changes are needed in the home. If the home has a second story, the patient may prefer to stay on one floor for a few weeks, because stair climbing can be tiring. Toileting needs may be met by using a bedside commode if a bathroom is not located on the level the patient is using. Home care needs depend on the patient's level of fatigue, dyspnea, and family and social support. The long recovery phase, especially in the older adult, can be frustrating. Fatigue, weakness, and a residual cough can last for weeks. Some patients fear they will never return to a "normal" level of functioning. Prepare them for the disease course and offer reassurance that complete recovery will occur. After discharge a home nursing assessment may be helpful. Specific issues to assess for a patient recovering from pneumonia are presented in the Focused Assessment box. Self-Management Education Review all drugs with the patient and family and emphasize the importance of completing anti-infective therapy. Instruct the patient to notify the primary health care provider if chills, fever, persistent cough, dyspnea, wheezing, hemoptysis, increased sputum production, chest discomfort, or increasing fatigue returns or fails to go away completely. Instruct him or her to get plenty of rest and increase activity gradually. An important aspect of education for the patient and family is avoiding upper respiratory tract infection and viruses. Teach him or her to avoid crowds (especially in the fall and winter when viruses are prevalent), people who have a cold or flu, and exposure to irritants such as smoke. A balanced diet and adequate fluid intake are essential.

endotracheal intubation

The patient who needs mechanical ventilation must have an artificial airway. The most common type of airway for a short-term basis is the endotracheal (ET) tube. Although there is no exact time frame, a tracheostomy is considered if an artificial airway is needed for longer than 10 to 14 days in order to reduce tracheal and vocal cord damage (see Chapter 25). Tracheostomy also is considered when a patient requires more than one intubation for respiratory failure. The expectations of intubation are to maintain a patent airway, provide a means to remove secretions, and provide ventilation and oxygen.

interventions cf

The patient with CF needs daily therapy to slow disease progress and enhance gas exchange . There is no cure for CF. Nonsurgical Management The management of the patient with CF is complex and lifelong. Nutrition management focuses on weight maintenance, vitamin supplementation, diabetes management, and pancreatic enzyme replacement (Razga & Handu, 2019). Pulmonary management focuses on preventive maintenance and management of exacerbations. Priority nursing interventions focus on teaching about drug therapy, infection prevention, pulmonary hygiene, nutrition, and vitamin supplementation. Preventive/maintenance therapy involves the use of positive expiratory pressure, active cycle of breathing technique, and an individualized exercise program. Daily chest physiotherapy with postural drainage is beneficial for the patient with CF. This therapy uses chest percussion, chest vibration, and dependent drainage to loosen secretions and promote drainage. Increasingly, the use of a chest physiotherapy (CPT) vest is recommended (Fig. 27.9), although no specific evidence supports its use as superior to any other type of chest physiotherapy (Wilson, 2018). This system uses an inflatable vest that rapidly fills and deflates, gently compressing and releasing the chest wall up to 25 times per second, a process called high-frequency chest wall oscillation (HFCWO). The action creates minicoughs that dislodge mucus from the bronchial walls, increase mobilization, and move it toward central airways, where it can be removed by coughing or suctioning. HFCWO also thins secretions, making them easier to clear. Pulmonary function tests are monitored regularly. Daily drugs include bronchodilators, anti-inflammatories, mucolytics, and antibiotics. Exacerbation therapy is needed when the patient with CF has increased chest congestion, reduced activity tolerance, increased or new-onset crackles, and a 10% decrease in FEV1. Other symptoms include increased sputum production with bloody or purulent sputum, increased coughing, decreased appetite, weight loss, fatigue, decreased SpO 2, and chest muscle retractions. Often infection is present, with fever, increased lung infiltrate on x-ray, and an elevated white blood cell count. Every attempt is made to avoid mechanical ventilation for the patient with CF. Bi-level positive airway pressure (BiPAP) may be a part of daily therapy for the patient with advanced disease (see Chapters 25 and 29 for information on BiPAP). Management focuses on airway clearance, increased gas exchange , and antibiotic therapy. Supplemental oxygen is prescribed on the basis of SpO 2 levels. The respiratory therapist initiates airway clearance techniques four times a day. Bronchodilator and mucolytic therapies are intensified. Steroidal agents are started or increased. Depending on the severity of the exacerbation, a 14- to 21-day course of oral antibiotics may be prescribed. Antibiotic choice is based on which bacteria are found in the patient's sputum. If antibiotics are not effective or if the exacerbation is very severe, IV antibiotics are used, usually an aminoglycoside such as tobramycin and colistin or meropenem. The most common respiratory infection for patients with CF is Pseudomonas aeruginosa (CFF, 2019). Another serious bacterial infection for patients with CF is Burkholderia cepacia. The organism lives in the respiratory tracts of patients with CF and is often resistant to antibiotic therapy. It is spread by casual contact from one CF patient to another. It is possible for B. cepacia to be transmitted to a CF patient during clinic and hospital visits; thus special infection control measures that limit close contact between adults with CF are needed. These measures include separating infected CF patients from noninfected CF patients on hospital units and seeing them in the clinic on different days. Strict CFF-approved procedures are used to clean clinic rooms and respiratory therapy equipment. Drug therapy for this infection usually includes co-trimoxazole (a combination of trimethoprim and sulfamethoxazole) along with the usual drugs used for exacerbation therapy. Teach patients about protecting themselves by not routinely shaking hands or kissing in social settings. Handwashing is critical because the organism also can be acquired indirectly from contaminated surfaces such as sinks and tissues. As life span increases for patients with CF, other problems, such as bronchiole bleeding from lung arteries, may develop. Interventional radiology may be needed to embolize the bleeding arterial branches. Patients with CF may undergo this procedure repeatedly to control hemoptysis. Other problems that occur with CF over time include severe gastroesophageal reflux disease (GERD), osteoporosis, and sensory hearing loss. Osteoporosis increases the risk for bone fractures. Gene therapy for CF is available for use in patients with specific gene mutations. The drug ivacaftor, known as a CFTR modulator or potentiator, has been found to be of value to patients with CF who are heterozygous for any one of about 35 specific mutations in the CFTR gene alleles. It is of no benefit to patients who are homozygous for the mutations (Coulthard, 2018). This drug helps improve chloride transport by increasing the time that the ion channels are open. The combination drug ivacaftor/lumacaftor is effective as therapy for patients whose CF is caused by the F508del (also known as the Phe508del) mutation, the most common mutation involved in CF, even in patients who are homozygous for the mutation with both alleles being affected. This oral drug combination is considered a "corrector" rather than a modulator, by moving the activated CFTR to the membrane surface for improved function. Another newly approved corrector oral drug, tezacaftor, when combined with ivacaftor has some effect for patients with the Phe508del mutation and appears to have fewer adverse respiratory events than the other combination, although decreases in liver function have been found with the use of all of these drugs. The successful outcome for these agents is increased movement of chloride ions across epithelial membranes, resulting in reduced sodium and fluid absorption so that mucus is less thick and sticky. These drugs have no effect in patients whose CFTR gene does not have the specific mutations. A significant drawback to these therapies is the cost, which is about $250,000/year of treatment (Coulthard, 2018). Surgical Management Surgical management of the patient with CF is lung transplantation. The patient has greatly reduced symptoms but is at continuing risk for lethal pulmonary infections, especially with antirejection drug therapy. Nonpulmonary problems are not helped by this treatment. Transplantation extends life for 1 to 15 years with an average of 7 years, but the transplant rejection rate is high, possibly caused by poor GI absorption of antirejection drugs (CFF, 2019). Fewer lung transplants are performed compared with transplantation of other solid organs because of the scarcity of available lungs. In addition, many patients who could benefit from lung transplantation have serious problems in other organs that make the procedure even more dangerous. Lung transplant procedures include two lobes or a single lung transplantation, as well as double-lung transplantation. The type of procedure is determined by the patient's overall condition and the life expectancy after transplantation. Usually the patient with CF has a bilateral lobe transplant from either a cadaver donor or a living-related donor. Preoperative Care Many factors are considered before lung transplantation surgery. Recipient and donor criteria vary from one program to another, but some criteria are universal. Recipient criteria for the patient with CF include that he or she must have severe, irreversible lung damage and still be well enough to survive the surgery. Common exclusion criteria include a cancer diagnosis, systemic infection, HIV/AIDS, and irreversible heart, kidney, or liver disease. Donor criteria, regardless of whether the lung tissue is obtained from a cadaver or from a living-related donor, include that the donor be infection free and cancer free, have healthy lung tissue, be a close tissue match with the recipient, and have the same blood type as the recipient. When the donor is a living relative, additional criteria include an age restriction and that he or she has healthy organs and has not had previous chest surgery. The two nursing priorities before surgery are teaching the patient the expected regimen of pulmonary hygiene to be used in the period immediately after surgery and assisting him or her in a pulmonary muscle strengthening/conditioning regimen. Operative Procedure The patient may or may not need to be placed on cardiopulmonary bypass, depending on the exact procedure. Those having single-lung or lobe transplantation usually do not need bypass; those having double-lung transplantation usually do. The most common incision used for lung transplantation is a transverse thoracotomy ("clamshell"). The diseased lung or lungs are removed. The new lobes, lung, or lungs are placed in the chest cavity with proper connections made to the trachea, bronchi, and blood vessels. Usually lung transplantation surgery is completed within 4 to 6 hours. Postoperative Care The patient is usually intubated for at least 48 hours, and chest tubes and arterial lines are in place. The care needed is the same as that for any thoracic surgery. Major problems after lung transplantation are bleeding, infection, and transplant rejection. The patient usually remains in the ICU for several days after transplantation. Postoperative chest physiotherapy often is performed with high-frequency chest wall oscillation (HFCWO) at this time. Antirejection drug regimens are started immediately after surgery, which increases the risk for infection. Combination therapy with the antirejection drugs is used for the rest of the patient's life. Corticosteroids are avoided in the first 10 to 14 days after surgery because of their negative impact on the healing process. After transplantation, patients have more energy and usually feel very good. The drug regimen for nonpulmonary CF problems is continued for the rest of the patient's life or until after a pancreatic transplant is performed. Exercise is gradually increased, and some patients even participate in intense activities, such as jogging, running, skiing, skating, swimming, etc.

history and assess asthma

The patient with asthma usually has a pattern of intermittent episodes of dyspnea (perceived shortness of breath), chest tightness, coughing, wheezing, and increased mucus production. Ask whether the symptoms occur continuously, seasonally, in association with specific activities or exposures, at work, or more frequently at night. Some patients have symptoms for 4 to 8 weeks after a cold or other upper respiratory infection. The patient with atopic (allergic) asthma also may have other allergic problems. Ask whether any family members have asthma or respiratory problems. Ask about current or previous smoking habits. If the patient smokes, use this opportunity to teach him or her about smoking cessation (see Chapter 24). Wheezing in nonsmokers is important in the diagnosis of asthma The patient with mild to moderate asthma may have no symptoms between asthma attacks. During an acute episode, common symptoms are an audible wheeze and increased respiratory rate. At first the wheeze is louder on exhalation. When inflammation occurs with asthma, coughing may increase. The patient may use accessory muscles to help breathe during an attack. Observe for muscle retraction at the sternum and the suprasternal notch and between the ribs. The patient with long-standing, severe asthma may have a "barrel chest," caused by air trapping (Fig. 27.3). The anteroposterior (AP) diameter (diameter between the front and the back of the chest) increases with air trapping, giving the chest a rounded rather than an oval shape. The normal chest is about 1.5 times as wide as it is deep. In severe, chronic asthma, the AP diameter may equal or exceed the lateral diameter (Jarvis, 2020). Compare the chest AP diameter with the lateral diameter. Chronic air trapping also flattens the diaphragm and increases the space between the ribs. Along with an audible wheeze, the breathing cycle is longer, with prolonged exhalation, and requires more effort. The patient may be unable to speak more than a few words between breaths. Hypoxia occurs with severe attacks. Pulse oximetry shows hypoxemia (poor blood oxygen levels). Examine the oral mucosa and nail beds for cyanosis. Other indicators of hypoxemia include changes in the level of cognition or consciousness and tachycardia

interventions facial trauma

The priority action is to establish and maintain an airway for adequate gas exchange . Anticipate the need for emergency intubation, tracheotomy, or cricothyroidotomy (creation of a temporary airway by making a small opening in the throat between the thyroid cartilage and the cricoid cartilage). Care at first focuses on establishing an airway, controlling hemorrhage, and assessing for the extent of injury. Stabilizing the fractured jaw allows the teeth to heal in proper alignment and involves fixed occlusion (wiring the jaws together with the mouth in a closed position). The patient remains in fixed occlusion for 6 to 10 weeks. Treatment delay, tooth infection, or poor oral care may cause jaw bone infection. This condition may then require surgical removal of dead tissue, IV antibiotic therapy, and a longer period with the jaws in a fixed position. Extensive jaw fractures may require open reduction with internal fixation (ORIF) procedures. Compression plates and reconstruction plates with screws may be applied. Plates may be made of stainless steel, titanium, or a metal alloy. Usually these plates are permanent. Depending on the metal used, they may or may not interfere with MRI studies. Facial fractures may be repaired with microplating surgical systems that involve bone substitutes or commercial bone graft material. Shaping plates hold the bone fragments in place until new bone growth occurs. The plates may remain in place permanently or may be removed after healing. With inner maxillary fixation (IMF), the bones are realigned and then wired in place with the bite closed. Nondisplaced aligned fractures can be repaired in a clinic or office using local dental anesthesia. General anesthesia is used to repair displaced or complex fractures or fractures that occur with other facial bone fractures. After surgery, teach the patient about oral care with an irrigating device such as a Water-Pik or Sonicare. If the patient has IMF, teach self-management with wires in place, including a dental liquid diet. If the patient vomits, watch for aspiration because of the patient's inability to open the jaws to allow ejection of the emesis. Teach him or her how to cut the wires if vomiting occurs to maintain gas exchange . If the wires are cut, instruct the patient to return to the surgeon for rewiring as soon as possible to reinstitute fixation. Nutrition is important and difficult for a patient with fractures because of oral fixation. Collaborate with the registered dietitian nutritionist for patient teaching and support.

facial trauma assess

The priority action when caring for a patient with facial trauma is airway assessment for gas exchange. Signs of airway obstruction are stridor, shortness of breath, dyspnea, anxiety, restlessness, hypoxia, decreased oxygen saturation, cyanosis, and loss of consciousness. After establishing the airway, assess the trauma site for bleeding and obvious fractures. Check for soft-tissue edema, facial asymmetry, pain, or leakage of spinal fluid through the ears or nose, indicating a skull fracture. Assess vision and eye movement because orbital and maxillary fractures can entrap the eye nerves and muscles. Check behind the ears (mastoid area) for extensive bruising, known as the "battle sign," which is often associated with skull fracture and brain trauma. Because facial trauma can occur with spinal trauma and skull fractures, cranial CT, facial series, and cervical spine x-rays are obtained.

Sinus Dysrhythmias

The sinoatrial (SA) node in the right atrium is the pacemaker in all sinus dysrhythmias. Innervation from sympathetic and parasympathetic nerves is normally in balance to ensure a normal sinus rhythm (NSR). An imbalance increases or decreases the rate of SA node discharge either as a normal response to activityor physiologic changes or as a pathologic response to disease. Sinus tachycardia and sinus bradycardia are the two most common types of sinus dysrhythmias.

Llead systems

The standard 12-lead ECG consists of 12 leads (or views) of the heart's electrical activity. Six of the leads are called limb leads because the electrodes are placed on the four extremities in the frontal plane. The remaining six leads are called chest (precordial) leads because the electrodes are placed on the chest in the horizontal plane. FIG. 31.3 Electrode positions for 12-lead ECG. Standard bipolar limb leads consist of three leads (I, II, and III) that each measure the electrical activity between two points and a fourth lead (right leg) that acts as a ground electrode. Of the three measuring leads, the right arm is always negative, the left leg is always positive, and the left arm can be either positive or negative. Other lead systems include the 18-lead ECG, which adds six leads placed on the horizontal plane on the right side of the chest to view the right side of the heart. This is sometimes referred to as a right-sided ECG. The extra leads are sometimes placed on the back. Unipolar limb leads consist of a positive electrode only. The unipolar limb leads are aVR, aVL, and aVF, with a meaning augmented; V is a designation for a unipolar lead. The third letter denotes the positive electrode placement: R for right arm, L for left arm, and F for foot (left leg). The positive electrode is at one end of the lead axis. The other end is the center of the electrical field, at about the center of the heart. There are six unipolar (or V) chest leads, determined by the placement of the chest electrode. The four limb electrodes are placed on the extremities, as designated on each electrode (right arm, left arm, right leg, and left leg). The fifth (chest) electrode on a monitor system is the positive, or exploring, electrode and is placed in one of six designated positions to obtain the desired chest lead. With a 12-lead ECG, four leads are placed on the limbs and six are placed on the chest, eliminating the need to move any electrodes about the chest (Fig. 31.3). Positioning of the electrodes is crucial in obtaining an accurate ECG. Comparisons of ECGs taken at different times will be valid only when electrode placement is accurate and identical at each test. Positioning is particularly important when working with patients with chest deformities or large breasts. Patients may be asked to move the breasts to ensure proper electrode placement. For serial ECGs, a surgical marker may be used to mark the electrode placement site to allow for accurate placement. It is important to remove the electrodes following the ECG because skin breakdown can occur. While obtaining a 12-lead ECG, remind the patient to be as still as possible in a semireclined position, breathing normally. Any repetitive movement will cause an artifact and could lead to inaccurate interpretation of the ECG. Nurses are sometimes responsible for obtaining 12-lead ECGs, but more commonly, technicians are trained to perform this skill. Remind the technician to notify the nurse or primary health care provider of any suspected abnormality. A nurse may direct a technician to take a 12-lead ECG on a patient experiencing chest pain to observe for diagnostic changes, but it is ultimately the primary health care provider's responsibility to definitively interpret the ECG.

assess respiratory failure

The symptoms of ARF are related to the systemic effects of hypoxia, hypercapnia, and acidosis. Assess for dyspnea (perceived difficulty breathing)—the hallmark of respiratory failure. Evaluate dyspnea on the basis of how breathless the patient becomes while performing common tasks. Depending on the nature of the underlying problem, the patient might not be aware of changes in the work of breathing. Dyspnea is more intense when it develops rapidly. Slowly progressive respiratory failure may first be noticed as dyspnea on exertion (DOE) or when lying down. The patient may have orthopnea, finding it easier to breathe in an upright position. With chronic respiratory problems, a minor increase in dyspnea may represent severe gas exchange problems. Assess for a change in the patient's respiratory rate or pattern and changes in lung sounds. Pulse oximetry (SpO 2) may show decreased oxygen saturation, but end-tidal CO2 (EtCO 2 or PEtCO 2) monitoring may be more valuable for monitoring the patient with ARF. Pulse oximetry may show adequate oxygen saturation, but because of increased EtCO 2 the patient may be close to respiratory failure. Review arterial blood gas (ABG) values to accurately identify the degree of hypoxia and hypercarbia. Other symptoms of hypoxic respiratory failure include restlessness, irritability or agitation, confusion, and tachycardia. Symptoms of hypercapnic failure may include decreased level of consciousness (LOC), headache, drowsiness, lethargy, and seizures. The effects of acidosis may lead to decreased LOC, drowsiness, confusion, hypotension, bradycardia, and weak peripheral pulses.

valve diseases self

The teaching plan for the patient with valvular heart disease includes: • The disease process and the possibility of HF • Drug therapy, including diuretics, vasodilators, beta blockers, calcium channel blockers, antibiotics, and anticoagulants • The prophylactic use of antibiotics • A plan of activity and rest to conserve energy Because patients with defective or repaired valves are at risk for infective endocarditis, teach them to adhere to the precautions described for endocarditis. Remind them to inform all health care providers of the valvular heart disease history. Tell providers that they require antibiotic administration before all invasive dental procedures. See the Patient and Family Education: Preparing for Self-Management: Valvular Heart Disease box for a summary of health teaching. Patients who have had valve replacements with prosthetic valves require lifetime prophylactic anticoagulation therapy to prevent thrombus formation. Teach patients taking anticoagulants how to manage their drug therapy successfully, including nutritional considerations (if taking warfarin) and the prevention of bleeding. For example, the patient should be taught to avoid foods high in vitamin K, especially dark green leafy vegetables, and to use an electric razor to avoid skin cuts. In addition, teach him or her to report any bleeding or excessive bruising to the primary health care provider. For patients who have surgery, reinforce how to care for the sternal incision and instruct them to watch for and report any fever, drainage, or redness at the site. Most patients can usually return to normal activity after 6 weeks but should avoid heavy physical activity involving their upper extremities for 3 to 6 months to allow the incision to heal. Those who have had valvular surgery should also avoid invasive dental procedures for 6 months because of the potential for endocarditis. Those with prosthetic valves need to avoid any procedure using magnetic resonance unless the newest technology is available. Remind patients to obtain a medical alert bracelet, card, or necklace to indicate that they have a valve replacement and are taking anticoagulants. Patients with valvular heart disease may have complicated medication schedules that can potentially lead to inadequate self-management. Provide clear, concise instructions about drug therapy and discuss the risks associated with nonadherence. Patients with a failed valve or those who do not follow the treatment plan are at high risk for heart failure. Teach them to report any changes in cardiovascular status, such as dyspnea, syncope, dizziness, edema, and palpitations. The psychological response to valve surgery is similar to that after coronary artery bypass surgery. Patients may experience an altered self-image as a result of the required lifestyle changes or the visible medial sternotomy incision. In addition, those with prosthetic valves may need to adjust to a soft but audible clicking sound of the valve. Encourage patients to verbalize their feelings about the prosthetic heart valve. They may display a variety of emotions after surgery, especially after hospital discharge.

Heart failure is a common problem among older adults

The use of certain drugs can contribute to the development or exacerbation of the problem in this population. For example, long-term use of NSAIDs for arthritis and other persistent (chronic) pain can cause fluid and sodium retention. NSAIDs may cause peripheral vasoconstriction and increase the toxicity of diuretics and angiotensin-converting enzyme inhibitors (ACEIs). Thiazolidinediones (TZDs) (e.g., pioglitazone used for patients with diabetes) also cause fluid and sodium retention.

Ventilation: Nursing Management

The use of mechanical ventilation involves a collaborative and complex decision-making process for the patient, family, and interprofessional care team. Long-term use and its discontinuance has both ethical and legal consequences. Address the physical and psychological concerns of the patient and family because the mechanical ventilator often causes them anxiety. Explain the purpose of the ventilator and acknowledge the patient's and family's feelings. Encourage the patient and family to express their concerns. Act as the coach to help and support them through this experience. Patients undergoing mechanical ventilation in ICUs often experience delirium, or "ICU psychosis." These patients need frequent, repeated explanations and reassurance. When caring for a ventilated patient, be concerned with the patient first and the ventilator second. If the ventilator alarm sounds, examine the patient for breathing, color, and oxygen saturation before assessing the ventilator. It is vital to understand why mechanical ventilation is needed. Some problems requiring ventilation, such as excessive secretions, sepsis, and trauma, require different interventions to successfully wean from the ventilator. Chronic health problems (e.g., COPD, left-sided heart failure, anemia, malnutrition) may slow weaning from mechanical ventilation and require close monitoring and intervention. The nursing priorities in caring for the patient during mechanical ventilation are monitoring and evaluating patient responses, managing the ventilator system safely, and preventing complications. Monitoring the Patient's Response Monitor, evaluate, and document the patient's response to the ventilator. Assess vital signs and listen to breath sounds every 30 to 60 minutes at first. Monitor respiratory parameters (e.g., capnography, pulse oximetry) and check ABG values. Monitoring provides information to guide the patient's activities, such as weaning, physical or occupational therapy, and self-care. Pace activities to ensure effective ventilation with adequate gas exchange and oxygenation. Interpret ABG values to evaluate the effectiveness of ventilation and determine whether ventilator settings need to be changed. Assess the breathing pattern in relation to the ventilatory cycle to determine whether the patient is tolerating or fighting the ventilator. Patient asynchrony with mechanical ventilation has many causes and reduces the effectiveness of gas exchange . Assess and record breath sounds, and confirm that breath sounds are equal bilaterally to ensure proper endotracheal (ET) tube placement. Determine the need for suctioning by observing secretions for type, color, and amount. The most common indicator of the need for suctioning is the presence of coarse crackles over the trachea. Assess the area around the ET tube or tracheostomy site at least every 4 hours for color, tenderness, skin irritation, and drainage, and document the findings. The nurse spends the most time with the patient and is most likely to be the first person to recognize changes in vital signs or ABG values, fatigue, or distress. If the patient's condition does not respond to current intervention, promptly coordinate with the respiratory health care provider and respiratory therapist. The respiratory health care provider may change the prescribed management plan to prevent the patient's condition from deteriorating. The respiratory therapist can most accurately assess the function of the ventilation equipment and make appropriate adjustments or replacements. Nursing Safety Priority Critical Rescue Always assess patients being mechanically ventilated for indications of respiratory distress and poor gas exchange . When symptoms of respiratory distress develop during mechanical ventilation, respond by immediately removing the ventilator and providing ventilation with a bag-valve-mask device. This action allows quick determination of whether the problem is with the ventilator or the patient. If no ventilator problem is identified, reconnect the patient to the ventilator and request respiratory therapy assistance. Serve as a resource for the psychological needs of the patient and family. Anxiety can reduce tolerance for mechanical ventilation. Skilled and sensitive nursing care promotes emotional well-being and synchrony with the ventilator. The patient cannot speak, and communication can be frustrating and produce anxiety. The patient and family may panic because they believe that the voice has been lost. Reassure them that the ET tube prevents speech only temporarily. Plan methods of communication to meet the patient's needs, such as a picture board, pen and paper, alphabet board, electronic tablet computer, or programmable speech-generating device. Some patients who are alert are able to use text messaging on smart phones for communication with staff, relatives, and friends. Finding a successful means for communication is important because the patient often feels isolated by the inability to speak. Anticipate his or her needs, and provide easy access to frequently used belongings. The observation of facial expressions in noncommunicative patients may indicate pain, especially during suctioning. Visits from family, friends, and pets and keeping a call light within reach are some ways of giving patients a sense of control over the environment. Urge them to participate in self-care. Managing the Ventilator System Ventilator settings are prescribed by the respiratory health care provider in conjunction with the respiratory therapist. Settings include tidal volume, respiratory rate, fraction of inspired oxygen (FiO 2), and mode of ventilation (assist-control [AC] ventilation, synchronized intermittent mandatory ventilation [SIMV], and adjunctive therapies such as positive end-expiratory pressure [PEEP] or pressure support). Perform and document ventilator checks according to the standards of the unit or facility (in many facilities this function is performed by respiratory therapists). Respond promptly to alarms. During a ventilator check, compare the prescribed ventilator settings with the actual settings and confirm these findings with the respiratory therapist. Check the level of water in the humidifier and the temperature of the humidifying system to ensure that they are not too high. Temperature extremes damage the airway mucosa. Remove any condensation in the ventilator tubing by draining water into drainage collection receptacles, and empty them every shift. Nursing Safety Priority Action Alert To prevent bacterial contamination, do not allow moisture and water in the ventilator tubing to enter the humidifier. Mechanical ventilators have alarm systems that warn of a problem with either the patient or the ventilator. Alarms should never be turned off or ignored during mechanical ventilation. The major alarms on a ventilator indicate either a high pressure or a low exhaled volume. Table 29.5 lists interventions for causes of ventilator alarms. Assess and care for the ET or tracheostomy tube. Maintain a patent airway by suctioning when any of these conditions are present: • Secretions • Increased peak airway (inspiratory) pressure (PIP) • Rhonchi • Decreased breath sounds Proper care of the ET or tracheostomy tube also ensures a patent airway. Assess tube position at least every 2 hours, especially when the airway is attached to heavy ventilator tubing that may pull on the tube. Position the ventilator tubing so the patient can move without pulling on the ET or tracheostomy tube, possibly dislodging it. To detect changes in tube position, mark it where the tube touches the patient's teeth or nose. Give oral care per facility policy. Standardized oral care performed at least every 12 hours has been shown to reduce ventilator-associated pneumonia (VAP), although the exact solution remains controversial (Boltey et al., 2017; Parisi et al., 2016; Warren et al., 2019). Special attention is needed for the patient being transported while receiving mechanical ventilation. Monitor SpO 2 during transport to assess adequacy of ventilation. Assess lung sounds each time the patient is moved, transferred, or turned. Consider the use of end-tidal carbon dioxide (EtCO 2) monitoring, if available. Preventing Complications A wide variety of complications, now known as ventilator-associated events (VAEs), are conditions that result in a sustained decrease in oxygenation (Baird, 2016). Specific indicators include greater than 20% increase in the daily minimum fraction of inspired oxygen or an increase of at least 3 cm H2O in the daily minimum positive end-expiratory pressure (PEEP) to maintain oxygenation. Table 29.6 lists the tiers of VAEs. Other complications affecting many body systems are related to positive pressure from the ventilator. Cardiac problems from mechanical ventilation include hypotension and fluid retention. Hypotension is caused by positive pressure that increases chest pressure and inhibits blood return to the heart. The decreased blood return reduces cardiac output, causing hypotension, especially in patients who are dehydrated or need high PIP for ventilation. Teach the patient to avoid a Valsalva maneuver (bearing down while holding the breath). Fluid is retained because of decreased cardiac output. The kidneys receive less blood flow, which stimulates the renin-angiotensin-aldosterone system (RAAS) to retain fluid. Humidified air in the ventilator system contributes to fluid retention. Monitor the patient's fluid intake and output, weight, hydration status, and indications of hypovolemia. Lung problems from mechanical ventilation include: • Barotrauma (damage to the lungs by positive pressure) • Volutrauma (damage to the lung by excess volume delivered to one lung over the other) • Atelectrauma (shear injury to alveoli from opening and closing) • Biotrauma (inflammatory response-mediated damage to alveoli) • Ventilator-associated lung injury/ventilator-induced lung injury (VALI/VILI) (damage from prolonged ventilation causing loss of surfactant, increased inflammation, fluid leakage, and noncardiac pulmonary edema) • Acid-base imbalance Barotrauma includes pneumothorax, subcutaneous emphysema, and pneumomediastinum. Patients at highest risk for barotrauma have chronic airflow limitation (CAL), have blebs or bullae, are on PEEP, have dynamic hyperinflation, or require high pressures to ventilate the lungs (because of "stiff" lungs, as seen in acute respiratory distress syndrome [ARDS]). Ventilator-induced lung injury can be prevented by using low tidal volumes combined with moderate levels of PEEP, especially in patients with acute lung injury (ALI) or ARDS. Blood gas problems can be corrected by ventilator changes and adjustment of fluid and electrolyte imbalances GI and nutrition problems result from the stress of mechanical ventilation. Stress ulcers occur in many patients receiving mechanical ventilation. These ulcers complicate the nutrition status and, because the mucosa is not intact, increase the risk for systemic infection. Antacids and histamine blockers such as cimetidine or proton pump inhibitors such as esomeprazole may be prescribed as soon as the patient is intubated. Because many other acute or life-threatening events occur at the same time, nutrition is often neglected. Malnutrition is an extreme problem for these patients and is a cause of failing to wean from the ventilator. In malnutrition, the respiratory muscles lose mass and strength. The diaphragm, the major muscle of inspiration, is affected early. When it and other respiratory muscles are weak, ineffective breathing results, fatigue occurs, and the patient cannot be weaned. Balanced nutrition, whether by diet, enteral feedings, or parenteral feeding, is essential during ventilation and is often started within 48 hours of intubation in consultation with a registered dietitian nutritionist. Nutrition for the patient with chronic obstructive pulmonary disease (COPD) is more complicated because it requires a reduction of dietary carbohydrates. During metabolism, carbohydrates are broken down to glucose, which then produces energy, carbon dioxide, and water. Excessive carbohydrate loads increase carbon dioxide production, which the patient with COPD may be unable to exhale. Hypercarbic respiratory failure may result. Nutrition formulas with a higher fat content (e.g., Pulmocare, Nutren Pulmonary) are calorie sources to combat this problem. Electrolyte replacement is also important because electrolytes influence muscle function. Monitor potassium, calcium, magnesium, and phosphate levels and replace them as prescribed. Infections are part of two tiers of ventilator-associated events (VAEs) and are a threat for the patient using a ventilator, especially ventilator-associated pneumonia (VAP). The ET or tracheostomy tube bypasses the body's filtering process and provides direct access for bacteria to enter the lower respiratory system. The artificial airway is colonized with bacteria within 48 hours, which promotes pneumonia development and increases morbidity. Aspiration of colonized fluid from the mouth or stomach can be a source of infection. Infection prevention through strict adherence to infection control, especially handwashing during suctioning and care of the tracheostomy or ET tube, is essential, as is meticulous oral care (Warren et al., 2019). To prevent VAP, implement "ventilator bundle" order sets, which typically include these actions (Parisi et al., 2016; Warren et al., 2019): • Keeping the head of the bed elevated at least 30 degrees • Performing oral care per agency policy (usually brushing teeth with a suction toothbrush at least every 12 hours and antimicrobial rinse) • Ulcer prophylaxis • Preventing aspiration • Pulmonary hygiene, including chest physiotherapy, postural drainage, and turning and positioning Using the ventilator bundle has greatly reduced the overall incidence of VAP. Vigilant oral care using a suction toothbrush is a key component of the VAP prevention strategy, although actual practice varies regarding timing, products used, and specific application methods (Wong et al., 2016). Additional information on pneumonia can be found in Chapter 28. Most patients requiring mechanical ventilation, except those with ARDS, are placed in a supine position with the head of the bed elevated to at least 30 degrees. This backrest elevation does not appear to be associated with an increase in sacral skin breakdown when other skin protection practices are in place (Grap et al., 2018). Muscle deconditioning and weakness can occur because of immobility. Getting the patient out of bed and having him or her ambulate with help and perform exercises not only improve muscle strength and help prevent pneumonia but also boost morale, enhance gas exchange , and promote oxygen delivery to all muscles. Early progressive mobility decreases ventilator days and ICU stays, although it is an underused intervention, possible because of staff misconceptions. The Systems Thinking and Quality Improvement box demonstrates how education and engagement can help increase the implementation of this evidence-based intervention (Castro et al., 2015). Early passive exercise also may be beneficial. Ventilator dependence is the inability to wean off the ventilator and can have both a physiologic and a psychological basis. The longer a patient uses a ventilator, the more difficult the weaning process is because the respiratory muscles fatigue and cannot assume breathing. Special units and facilities can maximize the rehabilitation and weaning of ventilator-dependent patients. The health care team uses every method of weaning before a patient is declared "unweanable." Long-term ventilator use and the decision to terminate ventilator use even when respiratory independence has not been achieved have both ethical and legal implications for the patient, family, and health care professionals. Some of these issues are presented in the Ethical/Legal Considerations box. Weaning Weaning is the process of going from ventilatory dependence to spontaneous breathing. The process is prolonged by complications. Many problems can be avoided with appropriate nursing care. For example, turning and positioning the patient not only promote comfort and prevent skin breakdown but also improve gas exchange and prevent pneumonia and atelectasis. Table 29.7 lists various weaning techniques. Extubation Extubation is the removal of the endotracheal (ET) tube. The tube is removed when the need for intubation has been resolved. Before removal, explain the procedure. Set up the prescribed oxygen delivery system at the bedside and bring in the equipment for emergency reintubation. Hyperoxygenate the patient and thoroughly suction both the ET tube and the oral cavity. Instruct the patient to inhale deeply and then rapidly deflate the cuff of the ET tube and remove the tube during exhalation. Immediately instruct the patient to cough. It is normal for large amounts of oral secretions to collect. Give oxygen by facemask or nasal cannula. The fraction of inspired oxygen (FiO 2) is usually prescribed at 10% higher than the level used while the ET tube was in place. Monitor vital signs after extubation every 5 minutes at first and assess the ventilatory pattern for signs of respiratory distress. It is common for patients to be hoarse and have a sore throat for a few days after extubation. Teach the patient to sit in a semi-Fowler position, take deep breaths every half-hour, use an incentive spirometer every 2 hours, and limit speaking. These measures help improve gas exchange , decrease laryngeal edema, and reduce vocal cord irritation. Observe closely for respiratory fatigue and airway obstruction. Early symptoms of obstruction are mild dyspnea, coughing, and the inability to expectorate secretions. Stridor is a high-pitched, crowing noise during inspiration caused by laryngospasm or edema around the glottis. It is a late sign of a narrowed airway Nursing Safety Priority Critical Rescue Monitor the patient frequently to recognize symptoms of obstruction. When stridor or other symptoms of obstruction occur after extubation, respond by immediately initiating the Rapid Response Team before the airway becomes completely obstructed. and requires prompt attention. Racemic epinephrine, a topical aerosol vasoconstrictor, is given, and reintubation may be needed.

Dysrhythmias may also be classified by their site of origin in the heart.

These include common sinus, atrial, and ventricular dysrhythmias. Although many specific dysrhythmias can occur, general assessment and interventions for patient care may be similar (see the Best Practice for Patient Safety & Quality Care: Care of the Patient With Dysrhythmias box). Assess the patient's apical and radial pulses for a full minute for any irregularity, which may occur with premature beats or atrial fibrillation. If the apical pulse differs from the radial pulse rate, a pulse deficit exists and indicates that the heart is not pumping adequately to achieve optimal perfusion to the body. Dysrhythmias are often managed with antidysrhythmic drug therapy. Specific drugs and other treatments for common dysrhythmias are discussed later in this chapter.

inspissated secretions

This condition often is caused by poor oral hygiene with thickened and hardened oral secretions that can completely block the airway and lead to dea ususally have altered loc and are dehydrated, unable to cough

Tiers of Ventilator-Associated Events

TierCharacteristics 1. Ventilator-associated condition (VAC) Patient develops hypoxemia for a sustained period of more than 2 days, regardless of its etiology. 2. Infection-related ventilator-associated complication (IVAC) Hypoxemia develops in the setting of generalized infection or inflammation, and antibiotics are instituted for a minimum of 4 days. 3. Ventilator-associated pneumonia (VAP) There is additional laboratory evidence of white blood cells or Gram stain of material from a respiratory secretion specimen of acceptable quality and/or presence of respiratory pathogens on quantitative cultures from patients with IVAC.

Cancer of the Nose and Sinuses

Tumors of the nasal cavities and sinuses result from the loss of cellular regulation. Malignant tumors are rare and are more common among adults with chronic exposure to wood dusts, dusts from textiles, leather dusts, flour, nickel and chromium dust, mustard gas, and radium. Cigarette smoking along with these exposures increases the risk (American Cancer Society [ACS], 2020). The onset of sinus cancer is slow, and symptoms resemble sinusitis. These include persistent nasal obstruction, drainage, bloody discharge, and pain that persists after treatment of sinusitis. Lymph node enlargement often occurs on the side with tumor mass. Tumor location is identified with x-ray, CT, or MRI. A biopsy is performed to confirm the diagnosis. Surgical removal of all or part of the tumor is the main treatment for nasopharyngeal cancers and often is combined with radiation therapy. Chemotherapy may be used in conjunction with surgery and radiation for some tumors. Problems after surgery include a change in body image or speech and changes in taste and smell. Provide general postoperative care as described in Chapter 9, including maintaining a patent airway, monitoring for hemorrhage, providing wound care, assessing nutrition status, and performing tracheostomy care (if needed). (See Chapter 25 for tracheostomy care.) Perform careful mouth and sinus cavity care with saline irrigations using an electronic irrigation system (e.g., Water-Pik, Sonicare) or a syringe. Assess the patient for pain and infection.

Types of Pneumonia

Type of PneumoniaDefinitionManagement ConsiderationsCommunity-acquiredContracted outside a health care setting; acquired in the communityMost common bacterial agents: Streptococcus pneumoniae, Haemophilus influenzaeMost common viral agents: influenza, respiratory syncytial virus (RSV)Antibiotics are often empirical based on multiple patient and environmental factorsTreatment length: minimum of 5 daysPrompt initiation of antibiotics required; in ED setting, first dose given before patient leaves unit for inpatient bed or within 6 hr of presentation to the EDHealth care-associatedOnset/diagnosis of pneumonia occurs <48 hr after admission in patient with specific risk factors: • In hospital for >48 hr in the past 90 days • Living in nursing home or assisted-living facility • Received IV therapy, wound care, antibiotics, chemotherapy in the past 30 days • Seen at a hospital or dialysis clinic within the past 30 days May have multidrug-resistant organisms Hand hygiene critical Hospital-acquiredOnset/diagnosis of pneumonia >48 hr after admission to hospitalEncourage pulmonary hygiene and progressive ambulationProvide adequate hydrationAssess risk for aspiration using an evidence-based toolMonitor for early signs of sepsisHands hygiene is criticalProvide vigorous oral careVentilator-associatedOnset/diagnosis of pneumonia within 48-72 hr after endotracheal intubationPresence of ET tube increases risk for pneumonia by bypassing protective airway mechanisms and allowing aspiration of secretions from the oropharynx and stomach; dental plaque also increases riskInitiate ventilator bundle order set, including: • Elevate HOB at least 30 degrees • Daily sedation "vacation" and weaning assessment • DVT prophylaxis • Oral care regimen • Stress ulcer prophylaxis • Suctioning, either as needed or continuous subglottal suction Hand hygiene is critical

Chest Trauma

Unintentional traumatic injuries accounted for 161,371 deaths in the United States during 2016, with chest trauma as a contributing factor in about 50% of those deaths (CDC, 2019). Many of the injured die before arriving at the hospital. Few types of chest injuries require thoracotomy. Most can be treated with basic resuscitation, intubation, or chest tube placement. The first emergency approach to all chest injuries is ABC ( a irway, b reathing, c irculation), a rapid assessment and treatment of life-threatening conditions. See Chapter 10 for more information on care of the trauma patien

Interprofessional Collaborative Care pandemic

Until the specific type of potentially pandemic influenza is identified and its routes of transmission are known, patients must be isolated, and Airborne, Droplet, and Contact Precautions must be used. Rapid influenza diagnostic tests are available. Treatment for influenza is often supportive in nature. Patients who are stable are instructed to recover at home and to avoid exposure to other individuals. Rest and fluids should be encouraged. If fever or myalgias are present, acetaminophen can be taken. The health care provider may prescribe an antiviral medication such as oseltamivir to be started within 48 hours of symptom onset. For influenzas with no effective treatment, interventions are supportive to allow the patient's own immune system to fight the infection . Oxygen is given when hypoxia, breathlessness, or a change in cognition occurs. Respiratory treatments to dilate the bronchioles and move respiratory secretions are used. If hypoxemia is not improved with oxygen therapy, intubation and mechanical ventilation may be needed. Antibiotics are used to treat a bacterial pneumonia that may occur with influenza. COVID-19 Infection Viral and antibody tests for COVID-19 became available in summer 2020. Viral tests indicate if a person has the active (current) COVID-19 infection; the antibody test might indicate if the person previously had COVID-19 (CDC, 2020c). People who should be tested include those with symptoms, those who have been within 6 feet of an infected person for at least 15 minutes, and those referred by a health care provider or state health department. Depending on the severity of symptoms, management ranges from supportive measures to critical care. Patients who are asymptomatic or have only mild symptoms must be taught to quarantine for 14 days. For severe cases, management may include noninvasive ventilation, intubation with mechanical ventilation, and extracorporeal membrane oxygenation (ECMO). A trial of self-proning may be recommended by the health care provider before intubation (Anesi, 2020). Trials of hyperbaric oxygen therapy (HBO) continue. As of September 2020, no specific drug had received full approval for treatment. One new and not yet approved drug, the IV antiviral agent remdesivir, received emergency use authorization by the U.S. Food and Drug Administration (FDA, 2020). Mixed results have arisen regarding treatment with certain drugs used for other disorders; true and reliable efficacy cannot be determined without large, randomized, and controlled clinical trials. Current evidence shows that dexamethasone, other glucocorticoids, convalescent plasma, and other antibody-based therapies are used in treatment. Other new and existing antiviral drugs are in early-phase trials to measure activity against replication of COVID-19. The highly contagious nature of the disease and the need for the use of techniques/interventions that more easily disperse droplets to others (e.g., suctioning, intubation) requires extraordinary containment measures during all aspects of care. When caring for a patient with COVID-19, it is critical that health care providers wear an N95 respirator mask (with a face shield whenever possible), gowns, shoe covers, gloves, and goggles (if no face shield is available). Inhaled medications should be delivered by metered dose inhalers with spacer devices versus given by nebulizer to avoid aerosolization of COVID-19. Physical distancing between patients and among health care providers, when not providing direct care, is recommended (CDC, 2020b). Teach family members to monitor themselves for illness, especially respiratory infection, for at least 2 weeks after the last contact with the patient. Nursing Safety Priority Action Alert When performing procedures that induce coughing or promote aerosolization of particles (e.g., suctioning, using a positive-pressure facemask, obtaining a sputum culture, or giving aerosolized treatments) for the patient with a potentially pandemic respiratory infection, protect yourself and other health care workers. Wear a gown, N95 mask, face shield, and protective eyewear during the procedures. Keep the door to the patient's room closed. Avoid touching your face. Wash your hands after removing personal protective equipment (PPE) and when you leave the patient's room. Wear gloves when disinfecting contaminated surfaces or equipment.

health promotion pnuemonia

Vaccination can help prevent pneumonia. Currently, there are two pneumonia vaccines: pneumococcal polysaccharide vaccine (PPSV23) and pneumococcal conjugate vaccine (PCV13) for prevention of pneumonia (Phillips & Swanson, 2016). The CDC recommends that adults older than 65 years be vaccinated with both, first with PCV13 followed by PPSV23 about 12 months later. Adults who have already received the PPSV23 should have PCV13 about a year or more later. These recommendations also apply to adults between 19 and 64 years of age who have specific risk factors such as chronic illnesses (CDC, 2018b). Because pneumonia often follows influenza, especially among older adults, urge all adults to receive the seasonal vaccination annually. Patient education about vaccination and other means of pneumonia prevention is important. Teaching points are presented in the Patient and Family Education: Preparing for Self-Management: Preventing Pneumonia box. National Patient Safety Goals The Joint Commission recommends that nurses especially encourage adults older than 65 years and those with a chronic health problem to receive immunization against pneumonia. For inpatients admitted for any condition, The Joint Commission recommends checking the pneumonia vaccination status and, if needed, offer the vaccination during the inpatient stay. Other pneumonia prevention techniques include strict handwashing to avoid spreading organisms and avoiding crowds during cold and flu season. Teach the patient who has a cold or the flu to see his or her primary health care provider if fever lasts more than 24 hours, the problem lasts longer than 1 week, or symptoms worsen. Respiratory therapy equipment must be well maintained and decontaminated or changed as recommended. Use sterile water rather than tap water in GI tubes and institute Aspiration Precautions as indicated, including screening patients for aspiration risk (Meehan & McKenna, 2020). VAP is on the rise, but the risk can be reduced with conscientious assessment and meticulous nursing care. The preventive care for VAP is discussed in Chapter 29 and is listed in Table 28.2. Nursing Safety Priority Action Alert Because pneumonia is a frequent cause of sepsis, use a sepsis screening tool to monitor patients who have pneumonia (see Chapter 34). For patients with pneumonia, always check oxygen saturation with vital signs.

COVID-19 Infection

Vaccines for the prevention of COVID-19 are currently in phase 3 clinical trials. Teach all people the need to properly wear a mask, engage in frequent handwashing, and practice social distancing to prevent the spread of COVID-19. Nonintubated patients should wear a mask while hospitalized and should be placed in a standard, single-patient room with a private bathroom. The door to the room should be closed at all times. Those having aerosolized-generating interventions should be placed in an airborne infection isolation room (AIIR) (CDC, 2020b). Most inpatient agencies have designated certain wings or floors reserved for patients with COVID-19. Patient-Centered Care: Cultural/Spiritual Considerations Although the effects of COVID-19 on the health of racial and ethnic minority groups are still emerging, current data indicate a disproportionate and substantially higher incidence of illness and a greater death rate among black and Hispanic adults (CDC, 2020a). The report also suggests that these disease differences appear to be more socioeconomic in origin rather than the result of an increased genetic or racial risk.

Types of Ventilators

Ventilators are available in two types. The most commonly used ventilators are positive-pressure ventilators. During inspiration, a pressure is generated that drives gas flow to push air into the lungs and expand the chest. Usually an endotracheal (ET) tube or tracheostomy is needed. Noninvasive positive-pressure ventilation systems use a mask or nasal prongs to deliver the gas flow. The nomenclature varies among ventilator manufacturers and sometimes between clinical areas (e.g., ICU, operating room). In general, ventilator settings are based on three components: trigger, gas delivery, and breath termination. Inspiratory trigger is the initiation of the ventilator breath from the effort of the patient or as a set, timed breath from the ventilator. Gas delivery is achieved by setting the tidal volume, which is a specific target volume of gas, or setting a target pressure that delivers a variable volume of gas. Breath termination is the transition between inspiration and expiration. The inspiratory breath is terminated by a set volume, pressure, time, or flow. Volume-cycled ventilation pushes air into the lungs until a preset volume is delivered. A constant tidal volume is delivered, regardless of the pressure needed to deliver the tidal volume. However, a set pressure limit prevents excessive pressure from being exerted on the lungs. The advantage of this mode is that a constant tidal volume is delivered regardless of changes in lung or chest wall compliance or airway resistance. Pressure-cycled ventilation pushes air into the lungs until a preset airway pressure is reached. Tidal volumes and inspiratory time vary. Time-cycled ventilations push air into the lungs until a preset time has elapsed. Tidal volume and pressure vary. Flow-cycled ventilatio is used with pressure support ventilation. It will terminate the breath when it reaches a preset flow rate derived as a percentage of the patient's maximum inspiratory flow

Ventilatory Failure

Ventilatory failure is a problem in oxygen intake (air movement or ventilation) and blood flow (perfusion ) that causes a ventilation-perfusion ( ) mismatch in which blood flow (perfusion) is normal but air movement (ventilation) is inadequate. It occurs when the chest pressure does not change enough to permit air movement into and out of the lungs. As a result, too little oxygen reaches the alveoli, and carbon dioxide is retained. Perfusion is wasted in this area of no air movement from either inadequate oxygen intake or excessive carbon dioxide retention, leading to poor gas exchange and hypoxemia. Ventilatory failure usually results from any of these problems: a physical problem of the lungs or chest wall; a defect in the respiratory control center in the brain; or poor function of the respiratory muscles, especially the diaphragm. The problem is defined by a PaCO 2 level above 45 mm Hg plus acidosis (pH below 7.35) in patients who have otherwise healthy lungs. Many disorders can result in ventilatory failure. Causes are either extrapulmonary (involving nonpulmonary tissues but affecting respiratory function) or intrapulmonary (disorders of the respiratory tract). Table 29.2 lists causes of ventilatory failure.

Ventricular Dysrhythmias

Ventricular dysrhythmias are potentially more life threatening than atrial dysrhythmias because the left ventricle pumps oxygenated blood throughout the body to perfuse vital organs and other tissues. The most common or life-threatening ventricular dysrhythmias include (Al-Khatib et al., 2018): • Premature ventricular complexes • Ventricular tachycardia • Ventricular fibrillation • Ventricular asystole

Abdominal thrust maneuver is performed on an unconscious patient instead of chest compressions only when

a known obstruction is present and the patient has a palpable pulse. If no obstruction has been observed in an unconscious person, chest compressions are started instead of abdominal thrusts because many more unconscious adults have cardiac problems than have airway obstruction.

epistaxis interventions

a nasal plug that contains an agent to promote blood clotting and expands on contact with blood to compress mucosal blood vessel critical cases of nosebleeds- packed. Anterior packing controls bleeding from the anterior nasal cavity. Posterior nasal bleeding is an emergency because it cannot be easily reached and the patient may lose a lot of blood quickly. Posterior packing, epistaxis catheters (nasal pressure tubes), or gel tampons are placed through the nose within the posterior nasal region to stop the bleeding. Placement of these devices is uncomfortable; and the airway may be obstructed with reduced gas exchange if the pack slips (Schreiber, 2020). Observe the patient for respiratory distress and for tolerance of the devices. Humidity, oxygen, bedrest, and antibiotics may be prescribed. Opioid drugs may be prescribed for pain. Assess patients receiving opioids at least hourly for gag and cough reflexes. Use pulse oximetry to monitor for hypoxemia. The tubes or packing is usually removed after 1 to 3 days. For posterior bleeding that does not respond to packing or tubes, additional options include cauterizing or ligating the blood vessels or performing an embolization of the bleeding artery with interventional radiology. Potential complications of embolization include facial pain, loss of tissue integrity with necrosis of skin or nasal mucosa, facial nerve paralysis, and blindness. After the tubes or packing has been removed, teach the patient and family these interventions to use at home for comfort and safety: • Apply petroleum jelly sparingly to the nares for comfort. • Use saline nasal sprays after healing to add moisture and prevent rebleeding. • Avoid vigorous nose blowing, the use of aspirin or other NSAIDs, and strenuous activities such as heavy lifting for at least 1 month.

acute hf can be caused by

acute coronary disease, structural or functional problems

stridor

airway obstruction

difference between emphysema and chronic bronchitis

alot of sputum in cb and pronounced dyspnea cb- productive cough emphysema- structural changesmoreco2

Cholinergic antagonists,

also called anticholinergic drugs or long-acting muscarinic antagonists (LAMAs), are similar to atropine and block the parasympathetic nervous system. This action increases bronchodilation and decreases pulmonary secretions. The most common drug in this class is ipratropium inhalant. Some cholinergic antagonists are short acting and are used several times a day. Long-acting agents such as tiotropium are used once daily.

Lung and airway changes as a part of aging make breathing problems more serious in the older adult,

and asthma-related deaths are highest in adults over age 65 years (Touhy & Jett, 2020). Another problem related to aging is a decrease in the sensitivity of beta-adrenergic receptors. When stimulated, these receptors relax smooth muscle and cause bronchodilation. As these receptors become less sensitive, they no longer respond as quickly or as strongly to agonists and beta-adrenergic drugs, which are often used as rescue therapy during an acute asthma attack. Thus teaching older patients how to avoid asthma attacks and how to correctly use preventive drug therapy is a nursing priority.

Monoclonal antibodies

are newer drugs specifically for the management of eosinophilic asthma and include benralizumab, mepolizumab, and reslizumab. All of these drugs block the activity of IL-5. They are used as "add-on" drugs for patients whose eosinophilic asthma has not responded well to more standard therapies

Leukotriene modifiers

are oral drugs that work in several ways to control asthma when taken on a scheduled basis. Montelukast and zafirlukast block the leukotriene receptor. Zileuton prevents leukotriene synthesis

Cricothyroidotomy

as a stab wound through the cricothyroid membrane between the thyroid cartilage and the cricoid cartilage Any hollow tube—but preferably a tracheostomy tube—can be placed through the opening to hold this airway open until a tracheotomy can be performed. This procedure is used when it is the only way to secure an airway. Another emergency procedure to bypass an obstruction is the insertion of a 14-gauge needle or a very small endotracheal tube directly into the cricoid space to allow airflow into and out from the lungs.

Instruct the patient to keep wire cutters with him or her at all times to preven

aspiration if vomiting occurs.

interventions airway obstruction

assess causee, when caused by tongue falling back / excessive secretions- extend the patients head and neck and insert a nasal or an oral airay , suction IF by foreign body- perform abdominal thrusts Upper airway obstruction may require emergency procedures such as- cricothyroidotomy or tracheotomy IF object cant be removed quickly if not by foreign object- endotracheal intubation may be needed. Laryngoscopy may be performed to determine the cause of obstruction or to remove foreign bodies

albuterol is a rescue med

asthma ANXIETY RELATED- MONITOR VITALS- 15-20 over normal contact provider

rinse mouth after adminstering steroids for

asthma dexamethasone

home care pe

atients with extensive lung damage may have activity intolerance from reduced gas exchange and become fatigued easily. The living arrangements may need to be modified so patients can spend most of the time on one floor and avoid climbing stairs. Depending on the degree of impairment, patients may require varying amounts of assistance with ADLs. Coordinate with members of the interprofessional team as described earlier under the Interprofessional Collaborative Care section to ensure optimal patient function. The patient with a PE may continue anticoagulation therapy for weeks, months, or years after discharge, depending on the risks for PE, and have impaired clotting . Teach him or her and the family about Bleeding Precautions, activities to reduce the risk for VTE and recurrence of PE, complications, and the need for follow-up care as described i s. Enoxaparin and newer anticoagulation agents (dabigatran, rivaroxaban, and apixaban) do not require laboratory monitoring. Patients with severe dyspnea may need home oxygen therapy. Respiratory therapy treatments can be performed in the home. The nurse or case manager coordinates arrangements for oxygen and other respiratory therapy equipment to be available if needed at home. This person also helps ensure continuing follow-up with the variety of specialists and laboratory monitoring needed based on the degree of the patient's continuing health problems

what is the difference between arrhythmia and dysrhythmia

bad rhythm and witout rhythm

osa diagnosis

beginning assessment includes having the patient complete a questionnaire regarding perceived sleep quality and extent of daytime sleepiness STOP-Bang Sleep Apnea the Epworth Sleepiness Scale, the Pittsburgh Sleep Quality Index, and the Multiple Sleep Latency Test, among others. If the results of a questionnaire suggest OSA, the patient may then undergo a less intrusive "at-home" sleep study. The patient sleeps in his or her own bed with electronic monitoring of respiratory rate, heart rate, chest movement, eye movements, and other muscle activity. If results indicate a sleep apnea problem, the patient is referred for a more definitive overnight sleep study known as polysomnography in which he or she is directly observed during a full sleep time while wearing a variety of monitoring equipment to evaluate depth of sleep, type of sleep, respiratory effort, oxygen saturation, carbon dioxide exhalation, and muscle movement. Monitoring methods include an electroencephalogram (EEG), an electrocardiogram (ECG), pulse oximetry, and electromyography (EMG).

The most common cause of OSA is upper airway obstructio

by the soft palate or tongue. Contributing factors include obesity, a large uvula, a short neck, smoking, enlarged tonsils or adenoids, and oropharyngeal edema. Adults with congenital variation in oral cavity structures, the pharynx, or the neck also are at increased risk for OSA.

High-output heart failure

can occur when cardiac output remains normal or above normal, unlike left- and right-sided heart failure, which are typically low-output states. High-output failure is caused by increased metabolic needs or hyperkinetic conditions, such as septicemia, high fever, anemia, and hyperthyroidism. This type of heart failure is not as common as other types. High-output heart failure occurs when the normally functioning heart cannot keep up with an unusually high demand for blood to one or more organs in the body. The heart may be working well otherwise, but it cannot pump out enough blood to keep up with this extra need.

pulsus paradoxus in

cardiac tamponade

heart failure leads to

cardiomyo

airway obstruction - heimleck maneuver

check breathing, start cpr HEAR STRIDOR

COPD is an umbrella term for what 2 diseases?

chronic bronchitis and emphysema

copd signs

clubbing , barrel chest

things that can trigger asthma

cold smoking, cockroaches, carpet

pleural friction rub

continuous, dry grating sound caused by inflammation of pleural surfaces and loss of lubricating pleural fluid

Corticosteroids

decrease inflammation in many ways, including by reducing the production of inflammatory chemicals. Inhaled corticosteroids (ICSs) can be helpful in controlling asthma symptoms and have overall fewer serious side effects than systemic corticosteroids (Penkalski, 2019). High-potency steroid inhalers, such as fluticasone, budesonide, and mometasone, may be used once per day for maintenance. Some drugs for asthma control include those that are combinations of an inhaled corticosteroid and an inhaled beta2 agonist, such as Breo Elipta. This combination comes in different strengths and is used once daily. Systemic corticosteroids, because of severe side effects, are avoided for mild-to-moderate intermittent asthma and are used on a short-term basis for moderate asthma. For some patients with severe asthma, daily oral corticosteroids may be needed.

what indicates left sided ventricular failure

decreased tissue perfusion from poor cardiac output and pulmonary congestion from increased pressure in pulmonary vessels

cf can be at risk to develop

diabetes mucus invades pancreas

Laryngeal trauma and damage occur with a crushing or

direct-blow injury, fracture, or prolonged endotracheal intubation Symptoms include difficulty breathing, inability to produce sound (aphonia), hoarseness, and subcutaneous emphysema (air present in the subcutaneous tissue). Bleeding from the airway (hemoptysis) may occur, depending on the location of the trauma. The primary health care provider performs a direct visual examination of the larynx by laryngoscopy or fiberoptic laryngoscopy to determine the extent of the injury. Management of patients with laryngeal injuries consists of assessing the effectiveness of gas exchange and monitoring vital signs (including respiratory status and pulse oximetry) every 15 to 30 minutes. Maintaining a patent airway is a priority. Apply oxygen and humidification as prescribed to maintain adequate oxygen saturation. Surgical intervention is needed for lacerations of the mucous membranes, cartilage exposure, and cord paralysis. Laryngeal repair is performed as soon as possible to prevent laryngeal stenosis and to cover any exposed cartilage. An artificial airway may be needed temporarily.

copd suggestion

drink alot of fluids

Cardiac dysrhythmias are abnormal rhythms of the heart's

electrical system that can affect its ability to effectively pump oxygenated blood throughout the body

interventions ards

eneral management of the patient with ARDS focuses on the three phases of ARDS. Timing of the phases varies from patient to patient. Exudative phase. This phase includes early changes of dyspnea and tachypnea resulting from the alveoli becoming fluid filled and from pulmonary shunting and atelectasis. Early interventions focus on supporting the patient and providing oxygen. Fibrosing alveolitis phase. Increased lung injury leads to pulmonary hypertension and fibrosis. The body attempts to repair the damage, and increasing lung involvement reduces gas exchange and oxygenation. Multiple organ dysfunction syndrome (MODS) can occur. Interventions focus on delivering adequate oxygen, preventing complications, and supporting the lungs. Resolution phase. Usually occurring after 14 days, resolution of the injury is possible; if not, the patient either dies or has chronic disease. Fibrosis may or may not occur. Patients surviving ARDS often have neuropsychologic deficits. Specific Management The patient with ARDS often needs intubation and mechanical ventilation with positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP). Best practice involves using "open lung" and lung protective ventilation strategies. Low tidal volumes (6 mL/kg of body weight) have been shown to prevent lung injury. PEEP is started at 5 cm H2O and increased to keep oxygen saturation adequate. PEEP levels may need to be high. Pressure-controlled ventilation is preferred over volume-controlled ventilation to promote the nonfunctional alveoli to participate in gas exchange . Because one of the side effects of PEEP is tension pneumothorax, assess lung sounds hourly and suction as often as needed to maintain a patent airway. Airway pressure release ventilation (APRV) and high-frequency oscillatory ventilation (HFOV) are alternative modes of mechanical ventilation that improve gas exchange with oxygenation and ventilation in patients with moderate-to-severe ARDS. The airway pressure with both APRV and HFOV is significantly higher than with conventional mechanical ventilation. Sedation and paralysis may be needed for adequate ventilation and to reduce tissue oxygen needs, especially with HFOV. Sedation and paralysis are not required with APRV but may be needed to prevent patient disruption of mechanical ventilation. This method can allow for spontaneous breathing between mandatory breaths (see the section Modes of Ventilation). Positioning may be important in promoting gas exchange , but the exact position is controversial. Some patients do better in the prone position, especially if it is started early in the disease course (Arias et al., 2017; Mitchell & Seckel, 2018; Schreiber, 2018) (see the Evidence-Based Practice box). Prone positioning may be achieved using a mechanical turning device, although the turning equipment is awkward and care in the prone position is more difficult. Automated kinetic beds are available to assist with turning. Manually turning the patient every 2 hours has been shown to improve perfusion ; however, this intervention often is not performed as frequently as needed. Early progressive mobility also has demonstrated benefit in reducing ventilator needs, days on the ventilator, and mortality. Automatic turning appears to have a slight advantage of decreasing some pulmonary complications but has not yet shown secondary benefits such as decreased lengths of stay, reduced ICU mortality, or decreased ventilator days. For severe ARDS, extracorporeal membrane oxygenation (ECMO) using heart-lung bypass equipment has been a successful life-support technique when the patient does not improve with more traditional management Patients with severe COVID-19 infection may also be treated with ECMO if all other treatment methods fail (Fitzsimons & Crowley, 2020). However, the proper timing of ECMO and standardization of this therapy for best outcomes have not been established, and survival is more likely in younger patients who have no other health problems (Sahetya et al., 2018). In addition, it is often not available in many community hospitals. Drug and Fluid Therapy Antibiotics are used to treat infections when organisms are identified. Other drugs are used to manage any underlying cause. Currently no treatments reverse the pathologic changes in the lungs, although many interventions that modify the inflammatory responses and reduce oxidative stress are under investigation. These agents include vitamins C and E, N-acetylcysteine, and nitric oxide (Zhang et al., 2017). Research shows that patients with ARDS who receive conservative fluid therapy have improved lung function and a shorter duration of mechanical ventilation and ICU length of stay compared with those who receive more liberal fluid therapy. Conservative fluid therapy involves infusing smaller amounts of IV fluid and using diuretics to maintain fluid balance, whereas liberal fluid therapy often results in an increasingly positive fluid balance and more edema. For those critically ill patients who are at risk for ARDS as a result of trauma, fluid management that involves slight hypotension is thought to help prevent ARDS (Kolarik & Roberts, 2017). Nutrition Therapy The patient with ARDS is at risk for malnutrition, which further reduces respiratory muscle function and the immune response. The interprofessional team must include a registered dietitian nutritionist. Enteral nutrition (tube feeding) or parenteral nutrition is started as soon as possible.

ssessing how often the patient swallows after nasal surgery is a priority because

epeated swallowing may indicate posterior nasal bleeding. Use a penlight to examine the throat for bleeding and notify the surgeon if bleeding is present

oxygen is a prescription

follow physician order

he nursing priority in the prevention of ARDS is early recognition of patients at high risk

for the syndrome. Because patients who aspirate gastric contents are at great risk, closely assess and monitor those receiving tube feedings (because the tube keeps the gastric sphincter open) and those with problems that impair swallowing and gag reflexes. To help prevent ARDS, follow meticulous infection control guidelines, including handwashing, invasive catheter and wound care, and Contact Precautions. Teach assistive personnel the importance of always adhering to infection control guidelines. Carefully observe patients who are being treated for any health problem associated with ARDS. For patients with swallowing problems or a poor gag reflex, use a suction toothbrush when providing oral care

The nursing priority for patients with disorders of the upper respiratory tract is to promote

gas exchange by ensuring a continuously patent airway.

osha signs and symptoms

general appearance including height and weight. Many adults with OSA are overweight, which can both cause OSA and be caused by this disorder. Examine the jaw, external neck, and chin. OSA is associated with a retracted lower jaw, smaller chin, and shorter neck. Examine the oral cavity and throat for size and shape of the pharynx, size and shape of the uvula, and tongue thickness and position, and determine whether other structures (e.g., tonsils, adenoids, pillars, soft palate) are swollen or enlarged. Chronic OSA is associated with cardiovascular changes, especially hypertension that may not respond as expected to prescribed drug therapy. Assess the patient's blood pressure and heart rate and rhythm, as well as pulse oximetry. If the patient is being treated for hypertension, ask which drug(s) and drug dosages are used for its management. If the patient is not being treated for hypertension but blood pressure is elevated on assessment, retake the blood pressure later during the examination. Document persistent elevations.

assess pe

h. It is important to remember that many patients with PE do not have the "classic" signs and symptoms, which often leads to PEs being overlooked. Respiratory symptoms are outlined in the Key Features: Pulmonary Embolism (Classic Signs and Symptoms) box and are mostly related to decreased gas exchange (McCance et al., 2019). Assess the patient for dyspnea and pleuritic chest pain (sharp, stabbing-type pain on inspiration). Other symptoms vary depending on the size and type of embolism. Breath sounds may be normal or include crackles, wheezes, or a pleural friction rub. A dry or productive cough may be present; hemoptysis (bloody sputum) may result from pulmonary infarction but is not present in all patients. Cardiac symptoms related to decreased tissue perfusion include tachycardia, distended neck veins, syncope (fainting or loss of consciousness), cyanosis, and hypotension. Systemic hypotension results from acute pulmonary hypertension and reduced forward blood flow. Abnormal heart sounds, such as an S3 or S4, may occur. ECG changes are nonspecific and transient. T-wave and ST-segment changes may occur, as may left-axis or right-axis deviations. Right ventricular dysfunction and failure are extreme complications. The patient may have cardiac arrest or frank shock. Nursing Safety Priority Critical Rescue Monitor patients at risk to recognize signs and symptoms of PE (e.g., shortness of breath, chest pain, and/or hypotension without an obvious cause). If symptoms are present, respond by initiating the Rapid Response Team. If PE is strongly suspected, prompt categorization and management strategies are started before diagnostic studies have been completed.

Advance Directives

he family should be prepared to act in agreement with the patient's wishes in the event of cardiac arrest. If resuscitation is desired, be sure that the family knows how to activate the emergency medical system (EMS) and how to provide cardiopulmonary resuscitation (CPR) until an ambulance arrives. If CPR is not desired, the patient, family, and nurse plan how the family will respond.

interventions head and neck cancer

he focus of treatment is to remove or eradicate the cancer while preserving as much function as possible. Surgery, radiation, chemotherapy, or biotherapy may be used alone or in combination, depending on the stage of the disease; the patient's general health, nutrition status, and age; and the patient's personal choice. Treatment for laryngeal cancer may range from radiation therapy (for a small specific area or tumor) to total laryngopharyngectomy with bilateral neck dissections followed by radiation therapy, depending on the extent and location of the lesion. Nursing care focuses on preoperative preparation, optimal in-hospital care, discharge planning and teaching, and extensive outpatient rehabilitation. Radiation therapy for treatment of small cancers in specific locations has a cure rate of at least 40%. Radiation, particularly proton beam therapy (PBT) may be used alone or in combination with surgery and chemotherapy, and may be performed before or after surgery (see Chapter 20). Most patients have hoarseness, sore throat, dysphagia, skin problems, impaired taste, and dry mouth for weeks after radiation (NCCN, 2019). The skin at the site of irradiation becomes red and tender and may peel during therapy. Instruct the patient to avoid exposing this area to sun, heat, cold, and abrasive actions such as shaving. Teach the patient to wear protective clothing made of soft cotton and to wash this area gently daily with a mild soap. Using appropriate skin care products (approved by the radiation oncology department) can reduce the intensity of skin reactions. If the salivary glands are in the irradiation path, the mouth becomes dry (xerostomia). This effect is long-term and may be permanent (Cullen et al., 2018). A dental consultation is needed because the risk for cavities is increased by both the radiation and the dry mouth. Moisturizing sprays, increased water intake, and humidification can help ease the discomfort. Chemotherapy can be used alone or in addition to surgery or radiation for head and neck cancer. Chemotherapy and radiation therapy (chemoradiation) are often used at the same time. Although the exact drugs used may vary, depending on cancer cell features, most chemotherapy regimens for head and neck cancers include cisplatin (or another platinum-based drug) in combination with 5-FU. Chapter 20 discusses care needs of patients receiving chemotherapy. Biotherapy (targeted therapy) with an epidermal growth factor receptor inhibitor (EGFRI) such as cetuximab is used for those patients whose tumors overexpress the receptor. Although it is a targeted therapy, this drug blocks epidermal growth factor receptors (EGFRs) in normal tissues as well as those in the tumor. As a result, severe skin reactions are common and difficult for the patient. Other biotherapies for head and neck cancer include some that are more specific for cancer caused by HPV types 16, 18, 31, and 33. These may include nivolumab and pembrolizumab (NCCN, 2019). Surgical intervention is determined by tumor size, node number, and metastasis location. Very small, early-stage tumors may be removed with laser therapy or photodynamic therapy; however, most head and neck cancers require extensive traditional surgery. Examples of possible surgical procedures include laryngectomy (total and partial), tracheotomy, and oropharyngeal cancer resections. The major types of surgery for laryngeal cancer include cord stripping, removal of a vocal cord (cordectomy), partial laryngectomy, and total laryngectomy. If cancer is in the lymph nodes in the neck, the surgeon performs a nodal neck dissection along with removal of the primary tumor ("radical neck"). Preoperative Care Teach the patient and family about the tumor. Explain about self-management of the airway, suctioning, pain-control methods, the critical care environment (including ventilators and critical care routines), nutrition support, feeding tubes, and plans for discharge. The patient will need to learn new methods of speech, at least during the time that mechanical ventilation is used and, depending on surgery type, perhaps forever. Along with the SLP, help the patient prepare for this change before surgery and practice the use of the selected form of communication. Operative Procedures Table 26.2 lists specific information about the various surgical procedures for laryngeal cancer. When a partial or complete laryngectomy is performed a tracheostomy is needed. With a partial laryngectomy, the tracheostomy is temporary. With a total laryngectomy, the upper airway is separated from the throat and esophagus, and a permanent laryngectomy stoma in the neck is created. Neck dissection includes the removal of lymph nodes, the sternocleidomastoid muscle, the jugular vein, the 11th cranial nerve, and surrounding soft tissue. Shoulder drop is expected after extensive surgery. Postoperative Care Head and neck surgery often lasts 8 hours or longer, and the patient spends the immediate period after surgery in an ICU. Monitor airway patency, vital signs, hemodynamic status, and comfort level. Take vital signs and monitor for hemorrhage and other general complication of anesthesia and surgery hourly for the first 24 hours and then according to agency policy until the patient is stable. Complications after surgery include airway obstruction, hemorrhage, wound breakdown, and tumor recurrence. The first priorities after head and neck surgery are airway maintenance and ensuring gas exchange. Maintaining the Airway and Gas Exchange Immediately after surgery, the patient may need mechanical ventilation. During weaning, the patient usually uses a tracheostomy collar (over the artificial airway or open stoma) with oxygen and humidity to help move mucus secretions. Secretions may remain blood-tinged for 1 to 2 days. Use Standard Precautions, and report any increase in bleeding to the surgeon. A laryngectomy tube is used for patients who have undergone a total laryngectomy and need an appliance to prevent scar tissue shrinkage of the skin-tracheal border. This tube is similar to a tracheostomy tube but is shorter and wider with a larger lumen. Care is similar to tracheostomy tube care (see Chapter 25) except that the patient can change the laryngectomy tube daily or as needed. A laryngectomy button is similar to a laryngectomy tube but is softer, has a single lumen, and is very short. Provide alternative communication techniques because the patient cannot speak. Managing the Wound Stoma care after a total laryngectomy is a combination of wound care and airway care. Inspect the stoma and clean the suture line with sterile saline (or a prescribed solution) to prevent secretions from forming crusts and obstructing the airway. Perform suture line care every 1 to 2 hours during the first few days after surgery and then every 4 hours. The mucosa of the stoma and trachea should be bright pink and shiny and without crusts, similar to the appearance of the oral mucosa. Tissue "flaps" may be used to close the wound and improve appearance. Flaps are skin, subcutaneous tissue, and sometimes muscle, taken from other body areas and used for reconstruction after head and neck resection. The first 24 hours after surgery are critical. Evaluate all grafts and flaps hourly for the first 72 hours. Monitor capillary refill, color, drainage, and Doppler activity of the major blood vessel to the area. Report changes to the surgeon immediately because surgical intervention may be needed. Position the patient so the surgical flaps are not dependent. Wound breakdown with loss of tissue integrity is a common complication in patients after head and neck surgery, especially if radiation therapy occurred before surgery. Manage wound breakdown with packing and local care as prescribed to keep the wound clean and stimulate the growth of healthy granulation tissue. Wounds may be extensive, and the carotid artery may be exposed, which increases the risk for rupture and hemorrhage. Nursing Safety Priority Critical Rescue Assess the patient hourly for the first several days after head and neck surgery to recognize a carotid artery leak. If you suspect a leak, respond by initiating the Rapid Response Team and do not touch the area because additional pressure could cause an immediate rupture. If the carotid artery actually ruptures because of drying or infection, immediately place constant pressure over the site and secure the airway. Maintain direct manual, continuous pressure on the carotid artery and immediately transport the patient to surgery for carotid resection. Do not leave the patient. Carotid artery rupture has a high risk for stroke and death. Managing Pain Pain after surgery has many causes and should be managed while still allowing the patient to be able to participate in care. Morphine often is given IV by a patient-controlled analgesia (PCA) pump for the first 1 to 2 days after surgery. As the patient progresses, liquid opioid analgesics can be given by feeding tube. Oral drugs for pain and discomfort are started only after the patient can tolerate oral intake. Maintaining Nutrition All patients are at risk for malnutrition during treatment for head and neck cancer. A nasogastric (NG), gastrostomy, or jejunostomy tube is placed during surgery for nutrition support while the head and neck heal and may remain in place for 7 to 10 days. It is removed when the patient is able to swallow safely. Aspiration cannot occur after a total laryngectomy because the airway is completely separated from the esophagus. Promoting Communication The patient's voice quality and speech are altered after surgery. This problem has enormous effects on the patient's social interactions, continued employment, and quality of life. In collaboration with an SLP, work with the patient and family toward developing an acceptable communication method during the inpatient period. Speech production varies with patient practice, amount of tissue removed, and radiation effects but can be very understandable. The speech rehabilitation plan for patients who have a total laryngectomy at first consists of writing, using a picture board, smart phone, or computer. The patient then uses an artificial larynx and may eventually learn esophageal speech. He or she needs encouragement and support from the SLP, hospital team, and family while relearning to speak. Having a laryngectomee (an adult who has had a laryngectomy) from one of the local self-help organizations, such as the ACS Visitor Program or the International Association of Laryngectomees, visit the patient and family is often beneficial. FIG. 26.4 An electrolarynx to generate speech after a laryngectomy. Esophageal speech is attempted by most patients who have a total laryngectomy. Sound can be produced this way by "burping" the air swallowed or injected into the esophageal pharynx and shaping the words in the mouth. Mechanical devices, called electrolarynges, may be used for communication. Most are battery-powered devices placed against the side of the neck or cheek (Fig. 26.4). The air inside the mouth and throat is vibrated, and the patient moves his or her lips and tongue as usual. The quality of speech generated with mechanical devices is robotlike. Tracheoesophageal puncture (TEP) may be used if esophageal speech is ineffective and if the patient meets strict criteria. A small surgical puncture is created between the trachea and the esophagus using a special catheter. After the puncture heals, a silicone prosthetic voice device is inserted in place of the catheter. The patient covers the stoma and the opening of the prosthesis with a finger or with a special valve to divert air from the lungs, through the trachea, into the esophagus, and out of the mouth where lip and tongue movement produces speech. Preventing Aspiration The surgical changes in the upper respiratory tract and altered swallowing mechanisms increase the patient's risk for aspiration. Aspiration can result in pneumonia, weight loss, and prolonged hospitalization. A nasogastric (NG) feeding tube increases the risk for aspiration because it keeps the lower esophageal sphincter partially open. Most patients who need enteral feeding supplementation have a percutaneous endoscopic gastrostomy (PEG) tube placed rather than an NG tube. See Chapter 55 for care of patients receiving enteral nutrition by NG or PEG tube. Swallowing can be a problem for the patient who has a tracheostomy tube. It can be normal if the cranial nerves and anatomic structures are intact. In a normal swallow, the larynx rises and moves forward to protect itself from the passing stream of food and saliva. The tracheostomy tube may fix the larynx in place, Patient and Family Education: Preparing for Self-Management The Supraglottic Method of Swallowing 1. Sit in an upright, preferably out-of-bed, position. 2. Clear your throat. 3. Take a deep breath. 4. Place ½ to 1 teaspoon of food into your mouth. 5. Hold your breath or "bear down" (Valsalva maneuver). 6. Swallow twice. 7. Release your breath and clear your throat. 8. Swallow twice again. 9. Breathe normally. resulting in difficulty swallowing. An inflated tracheostomy tube cuff can balloon backward into the esophagus and interfere with the passage of food. The wall between the posterior trachea and the esophagus is very thin, which allows this pushing action. The patient who is cognitively intact may adapt to eating normal food when the tracheostomy tube is small and the cuff is not inflated. The patient who has had a partial vertical or supraglottic laryngectomy must be observed for aspiration. It is critical to teach the patient to use alternate methods of swallowing without aspirating. The "supraglottic" method of swallowing, as listed in the Patient and Family Education: Preparing for Self-Management box, is used after a swallowing study has determined it is safe for the patient and is especially effective after a partial laryngectomy or base-of-tongue resection. This method exaggerates the normal protective mechanisms of cessation of respiration during the swallow. The double swallow helps clear food that may be pooling in the pharynx or throat structures. Supporting Self-Esteem The patient with head and neck cancer usually has a change in self-concept and self-image resulting from issues such as the presence of a stoma or artificial airway, speech changes, and a change in the method of eating. Psychosocial issues may include guilt, regret, and uncertainty. He or she may not be able to speak at all or may have permanent speech deficits. Help the patient set realistic goals, starting with involvement in self-care. Reinforce the alternative communication methods suggested by the SLP so the patient can communicate in the hospital and after discharge. After surgery, the patient may feel socially isolated because of the change in voice and facial appearance. Loose-fitting, high-collar shirts or sweaters, scarves, and jewelry can be worn to cover the laryngectomy stoma, tracheostomy tube, and other changes related to surgery. Cosmetics may aid in covering any facial or neck disfigurement. Care Coordination and Transition Management If no complications occur, the patient is usually discharged home or to an extended-care facility within 2 weeks. At the time of discharge, he or she or a family member should be able to perform tracheostomy or stoma care and participate in nutrition, wound care, and communication methods. Often the patient and family need referrals to support groups or a community health agency familiar with the care of patients recovering from head and neck cancer. Coordinate the efforts of Patient and Family Education: Preparing for Self-Management Home Laryngectomy Care • Avoid swimming and use care when showering or shaving. • Lean slightly forward and cover the stoma when coughing or sneezing. • Wear a stoma guard or loose clothing to cover the stoma. • Clean the stoma with mild soap and water. Lubricate the stoma with a non-oil-based ointment as needed. • Increase humidity by using saline in the stoma as instructed, a bedside humidifier, pans of water, and houseplants. • Obtain and wear a MedicAlert bracelet and emergency care card for life-threatening situations. the interprofessional team in assessing the specific discharge needs and making the appropriate referrals to home care agencies. Home Care Management Extensive home care preparation is needed after a laryngectomy for cancer. The convalescence period is long, and airway management is complicated. For the patient with severe respiratory problems, home changes to allow for one-floor living may be needed. Increased humidity is needed. A humidifier add-on to a forced-air furnace can be obtained, or a room humidifier or vaporizer may be used. Be sure to stress that meticulous cleaning of these items is needed to prevent spread of mold or other sources of infection. A home care nurse is often an important resource for the patient and family. This nurse assesses the patient and home situation for problems in self-care, complications, adjustment, and adherence to the medical regimen. Self-Management Education Teach the patient and family how to care for the stoma or tracheostomy or laryngectomy tube, depending on the type of surgery performed, using the actions listed in the Patient and Family Education: Preparing for Self-Management: Home Laryngectomy Care box. Stoma care teaching is focused on protection, which is needed as a result of the anatomic changes resulting from surgery. Instruct the patient to use a shower shield over the tube or stoma when bathing to prevent water from entering the airway. Suggest that the patient wear a protective cover or stoma guard to protect the stoma during the day. Communication involves having the patient continue the selected communication method that began in the hospital. Instruct him or her to wear a medical alert (MedicAlert) bracelet and carry a special identification card. For patients with a laryngectomy, this card is available from the local chapters of the International Association of Laryngectomees. The card instructs the reader about providing an emergency airway or resuscitating someone who has a stoma. Psychosocial Preparation The many changes resulting from a laryngectomy influence physical, social, and emotional functioning for both the patient and his or her significant other (Sterba et al., 2016). The patient with a permanent stoma, tracheostomy tube, NG or PEG tube, and wounds has an altered body image. Stress the importance of returning to as normal a lifestyle as possible. Most patients can resume many of their usual activities within 4 to 6 weeks after surgery. The patient with a total laryngectomy cannot produce sounds during laughing and crying. Mucus secretions may appear unexpectedly when these emotions arise or when coughing or sneezing occurs. The mucus can be embarrassing, and the patient needs to be prepared to cover the stoma with a handkerchief or gauze. The patient who has undergone composite resections has difficulty with speech and swallowing. He or she may need to deal with tracheostomy and feeding tubes in public places.

cardiomyopathy

heart enlarged 3 types treatment- all failed is heart transplant- OUTCOME- HEART FAILURE IF LEFT UNTREATED

in those who have had an MI,

heart muscle cell injury causes an immune response. Proinflammatory cytokines, such as tumor necrosis factor (TNF) and interleukins (IL-1 and IL-6), are released, especially with left-sided HF. These substances contribute to ventricular remodeling.

Asthma

hronic disease in which reversible acute airway obstruction occurs intermittently, reducing airflow (Fig. 27.1). Airway obstruction occurs by both inflammation and airway tissue sensitivity (hyperresponsiveness) with bronchoconstriction. Inflammation obstructs the airway lumens (i.e., the hollow insides) (Fig. 27.2). Airway hyperresponsiveness and constriction of bronchial smooth muscle narrow the tubular structure of the airways. Airway inflammation and sensitivity can trigger bronchiolar constriction

causes of left sided ventricular hf

htn, cad, valvular disease

Heart failure (HF) is caused by systemic

hypertension in most cases. Some patients experiencing myocardial infarction (MI, "heart attack") also develop HF. he next most common cause is structural heart changes, such as valvular dysfunction, particularly pulmonic or aortic stenosis, which leads to pressure or volume overload on the heart.

patients with an ejection fraction of less than 30% are considered candidates for an

implantable cardioverter/defibrillator

Sleep apnea

including dysfunction in central nervous system control over ventilation, poor circulation and oxygenation, and airway obstruction.

petechiae murmur fever

infective endocarditis

Mitral Regurgitation (Insufficiency)

insufficiency) prevent the mitral valve from closing completely during systole. Incomplete closure of the valve allows the backflow of blood into the left atrium when the left ventricle contracts. During diastole, regurgitant output again flows from the left atrium to the left ventricle along with the normal blood flow. The increased volume must be ejected during the next systole. To compensate for the increased volume and pressure, the left atrium and ventricle dilate and hypertrophy. The causes of primary mitral regurgitation are mitral valve prolapse, rheumatic heart disease, infective endocarditis, myocardial infarction (MI), connective tissue diseases such as Marfan syndrome, and dilated cardiomyopathy. (McCance & Huether, 2019). Secondary causes include ischemic and nonischemic heart disease that damage the valve. Rheumatic heart disease is the number-one cause in developing nations. When it results from rheumatic heart disease, it usually coexists with some degree of mitral stenosis. Mitral regurgitation usually progresses slowly; patients may remain symptom free for decades. Symptoms begin to occur when the left ventricle fails in response to chronic blood volume overload. Symptoms include fatigue and chronic weakness as a result of reduced CO. Dyspnea on exertion and orthopnea develop later. A significant number of patients report anxiety, atypical chest pains, and palpitations. Assessment may reveal normal BP, atrial fibrillation, or changes in respirations characteristic of left ventricular failure. When right-sided HF develops, the neck veins become distended, the liver enlarges (hepatomegaly), and pitting edema develops. A high-pitched systolic murmur at the apex, with radiation to the left axilla, is heard on auscultation. Severe regurgitation often exhibits a third heart sound (S3).

copd

is a collection of lower airway disorders that interfere with airflow and gas exchange . These disorders include emphysema and chronic bronchitis. Although these are separate disorders with different pathologic processes, many patients with emphysema also have chronic bronchitis

Emphysema

is a destructive problem of lung elastic tissue that reduces its ability to recoil after stretching, leading to hyperinflation of the lung (see Fig. 27.1). These changes result in dyspnea with reduced gas exchange and the need for an increased respiratory rate. In the healthy lung, enzymes called proteases are present to destroy and eliminate particulates inhaled during breathing. Cigarette smoking triggers increased synthesis of these enzymes to higher-than-normal levels, which then damage the alveoli and small airways by breaking down elastin. Over time, alveolar sacs lose their elasticity (recoil) and the small airways collapse or narrow. Some alveoli are destroyed, and others become large and flabby, with less area for gas exchange. An increased amount of air is trapped in the lungs. Causes of air trapping are loss of elastic recoil in the alveolar walls, overstretching and enlargement of the alveoli into air-filled spaces called bullae, and collapse of small bronchioles. These changes greatly increase the work of breathing and interfere with airflow to the lungs. The hyperinflated lung flattens the diaphragm (Fig. 27.6), weakening the effectiveness of this muscle. As a result, the patient with emphysema needs to use accessory muscles in the neck, chest wall, and abdomen to inhale and exhale. This increased effort increases the need for oxygen, making the patient have an "air hunger" sensation. Inhalation starts before exhalation is completed, resulting in an uncoordinated breathing pattern. Gas exchange is affected by the increased work of breathing and the loss of alveolar tissue. Although some alveoli enlarge, the functional area available for gas exchange is decreased. Often the patient adjusts by increasing the respiratory rate, so arterial blood gas (ABG) values may not show gas exchange problems until the patient has advanced disease. Then carbon dioxide is produced faster than it can be eliminated, resulting in carbon dioxide retention and chronic respiratory acidosis (see Chapter 14). The patient with late-stage emphysema also has a low arterial oxygen (PaO 2) level because it is difficult for oxygen to move from diseased alveoli into the blood. Emphysema is classified as panlobular, centrilobular, or paraseptal, depending on the pattern of destruction and dilation of the gas-exchanging units (acini) (see Fig. 27.1). Each type can occur alone or in combination in the same lung. Most are associated with tobacco smoking (e.g., cigarettes, cigars, pipes), marijuana smoking, or other chronic inhaled particulate matter exposures (PME) such as wood smoke and biomass fuels

Tuberculosis (

is a highly communicable disease caused by infection with Mycobacterium tuberculosis. It is one of the most common bacterial infections worldwide and one of the top 10 causes of death (World Health Organization [WHO], 2019). The organism is transmitted via aerosolization (i.e., an airborne route) (Fig. 28.2). When a person with active TB coughs, laughs, sneezes, whistles, or sings, infected respiratory droplets become airborne and may be inhaled by others. Not all TB infections actually develop into active TB (American Lung Association [ALA], 2018). This is because the normal protection of immunity prevents full development of TB in the healthy person (McCance et al., 2019). (Immunity is the protection from illness or disease that is maintained by the body's physiologic defense mechanisms.) The bacillus multiplies freely when it reaches a susceptible site (bronchi or alveoli). An inflammation and exudative response occurs, causing pneumonitis. With the development of acquired immunity to TB, further growth of bacilli is controlled in most cases. The lesions usually resolve and leave little or no residual bacilli. Only a small percentage of adults infected with the bacillus ever develop active TB. Cell-mediated immunity against TB develops 2 to 10 weeks after initial infection and is manifested by a positive reaction to a tuberculin test. The primary infection may be so small that it does not appear on a chest x-ray. The process of TB infection occurs in this order: 1. The granulomatous inflammation created by the TB bacillus in the lung becomes surrounded by collagen, fibroblasts, and lymphocytes. 2. Caseation necrosis, which is necrotic tissue being turned into a granular mass, occurs in the center of the lesion. If this area shows on x-ray, it is the primary lesion. Areas of caseation then undergo resorption, degeneration, and fibrosis. These necrotic areas may calcify (calcification) or liquefy (liquefaction). If liquefaction occurs, this material then empties into a bronchus and the emptied area becomes a cavity (cavitation). Bacilli continue to grow in the necrotic cavity wall and spread the infection through the lymph channels into new areas of the lung. A lesion also may grow by direct extension if bacilli multiply rapidly during inflammation . The lesions can extend through the pleura, resulting in pleural or pericardial effusion. Miliary or hematogenous TB is the spread of TB throughout the body when a large number of organisms enter the blood. Many tiny nodules scattered throughout the lung are seen on chest x-ray. Other body areas can become infected as a result of this spread. Initial infection is seen more often in the upper lobes of the lung. The local lymph nodes are infected and enlarged. An asymptomatic period usually follows the primary infection and can last for years or decades before clinical symptoms develop. This is called latent TB. An infected person is not contagious to others until symptoms of disease occur. Secondary TB is a reactivation of the disease in a previously infected person. It is more likely to occur when immunity is reduced, especially among older adults, those with chronic diseases, and those with HIV disease.

cardiomyopathy patho

is a subacute or chronic disease of cardiac muscle, and the cause may be unknown. Cardiomyopathies are classified into four categories on the basis of abnormalities in structure and function: dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy (Table 32.5). Dilated cardiomyopathy (DCM) is the structural abnormality most commonly seen. DCM involves extensive damage to the myofibrils and interference with myocardial metabolism. Ventricular wall thickness is normal, but both ventricles are dilated (left ventricle is usually worse) and systolic function is impaired. Causes may include alcohol abuse, chemotherapy, infection, inflammation, and poor nutrition. Decreased CO from inadequate pumping of the heart causes the patient to experience dyspnea on exertion (DOE), decreased exercise capacity, fatigue, and palpitations. The cardinal features of hypertrophic cardiomyopathy (HCM) are asymmetric ventricular hypertrophy and disarray of the myocardial fibers. Left ventricular hypertrophy leads to a stiff left ventricle, which results in diastolic filling abnormalities. Obstruction in the left ventricular outflow tract is seen in most patients with HCM. Mitral valve structural abnormalities are commonly associated with HCM and contribute to the obstruction in ventricular outflow (Larkin et al., 2019). HCM is transmitted as a single-gene autosomal-dominant trait occurring in 1 in 500 people (McCance & Huether, 2019). Some patients die without any symptoms, whereas others have DOE, syncope, dizziness, and palpitations. Many athletes who die suddenly probably had hypertrophic cardiomyopathy. Restrictive cardiomyopathy, the rarest of the cardiomyopathies, is characterized by stiff ventricles that restrict filling during diastole. Symptoms are similar to those of left or right HF or both. The disease can be primary or caused by endocardial or myocardial disease such as sarcoidosis or amyloidosis. The prognosis for this type of cardiomyopathy is poor. Arrhythmogenic right ventricular cardiomyopathy (dysplasia) results from replacement of myocardial tissue with fibrous and fatty tissue. Although the name implies right ventricle disease, about a third of patients also have left ventricle (LV) involvement. This disease has a familial association and most often affects young adults. Some patients have symptoms, and others do not.

Sinus arrhythmia

is a variant of NSR. It results from changes in intrathoracic pressure during breathing. In this context, the term arrhythmia does not mean an absence of rhythm, as the term suggests. Instead, the heart rate increases slightly during inspiration and decreases slightly during exhalation. This irregular rhythm is frequently observed in healthy adults. Sinus arrhythmia has all the characteristics of NSR except for its irregularity. The PP and RR intervals vary, with the difference between the shortest and the longest intervals being greater than 0.12 second (three small blocks): • Rate: Atrial and ventricular rates between 60 and 100 beats/min • Rhythm: Atrial and ventricular rhythms irregular, with the shortest PP or RR interval varying at least 0.12 second from the longest PP or RR interval • P waves: One P wave before each QRS complex; consistent configuration • PR interval: Normal, constant • QRS duration: Normal, constant Sinus arrhythmias are occasionally due to nonrespiratory causes such as digoxin or morphine. These drugs enhance vagal tone and cause decreased heart rate and irregularity unrelated to the respiratory cycle.

Acute respiratory distress syndrome (ARDS)

is acute respiratory failure (ARF) with these features: • Hypoxemia that persists even when 100% oxygen is given (refractory hypoxemia, a cardinal feature) • Decreased pulmonary compliance • Dyspnea • Non-cardiac-associated bilateral pulmonary edema • Dense pulmonary infiltrates on x-ray (ground-glass appearance) Often ARDS occurs after an acute lung injury (ALI) in people who have no pulmonary disease as a result of other conditions such as sepsis, burns, pancreatitis, trauma, and transfusion. Other terms for ARDS include adult respiratory distress syndrome, "stiff lungs," shock lung, and acute respiratory dysfunction syndrome Despite different causes of ALI in ARDS, the trigger is a systemic inflammatory response that activates a variety of pro-inflammatory cytokines that maintain a continuing inflammation in the alveoli and pulmonary vasculature. This response is known as a "cytokine storm" and, when prolonged, results in thick, swollen tissues that hinder gas exchange and promote the formation of scar tissue. As a result, ARDS symptoms are similar regardless of the cause. The main site of injury in the lung is the alveolar-capillary membrane, which normally is permeable only to small molecules. It can be injured during sepsis, pulmonary embolism, shock, aspiration, severe inflammation from COVID-19 infection, or inhalation injury (Mitchell & Seckel, 2018). When injured, this membrane becomes more permeable to large molecules, which allows debris, proteins, and fluid into the alveoli. Lung tissue normally remains relatively dry, but in patients with ARDS lung fluid increases and contains more proteins. In ARDS associated with COVID-19, the thick exudate inhibits gas exchange. Other changes occur in the alveoli and respiratory bronchioles. Normally the type II pneumocytes produce surfactant, a substance that increases lung compliance (elasticity and recoil of lung tissue) and prevents alveolar collapse. Surfactant activity is reduced in ARDS because type II pneumocytes are damaged and because the surfactant is diluted by excess lung fluids. As a result, the alveoli become unstable and tend to collapse. These collapsed or fluid-filled alveoli cannot participate in gas exchange . Edema then forms around terminal airways, which are compressed and closed and can be destroyed. Lung volume and compliance are further reduced. As fluid continues to leak in more lung areas, fluid, protein, and blood cells collect in the alveoli and in the spaces between the alveoli. Lymph channels are compressed, and more fluid collects. Poorly inflated alveoli receive blood but cannot oxygenate it, increasing the shunt. Hypoxemia and ventilation-perfusion ( ) mismatch result. Transfusion-related acute lung injury (TRALI) is the sudden onset (within 6 hours of a transfusion) of hypoxemic lung disease along with infiltrates on x-ray without cardiac problems. TRALI is associated with the activation of the inflammatory response caused by a recent transfusion of plasma-containing blood products such as packed red blood cells (PRBCs), platelets, and fresh-frozen plasma. Other lung complications of transfusion include transfusion-associated circulatory overload (TACO) and transfusion-related immunomodulation (TRIM). T

Rhinosinusitis

is an inflammation of the mucous membranes of one or more of the sinuses and is usually seen with rhinitis, especially the common cold (coryza). Anything that interferes with sinus drainage (e.g., deviated nasal septum, nasal polyps or tumors, inhaled air pollutants or cocaine, allergies, facial trauma, and dental infection) can lead to rhinosinusitis. Even when the problem starts with a noninfectious cause such as seasonal allergies, swelling and inflammation block the flow of secretions from the sinuses, which may then become infected. Most episodes of rhinosinusitis are caused by viral infection and usually develop in the maxillary and frontal sinuses, although bacterial infection can also occur. Complications include cellulitis, abscess, and meningitis. Interprofessional Collaborative Care Rhinosinusitis is usually managed as an outpatient problem. Even when sinus surgery is needed, it usually takes place in an ambulatory surgical setting. Assess for signs and symptoms of rhinosinusitis, which include pain over the cheek radiating to the teeth, tenderness to percussion over the sinuses, referred pain to the temple or back of the head, and general facial pain that is worse when bending forward. In bacterial infection , purulent nasal drainage with postnasal drip, sore throat, fever, erythema, swelling, fatigue, dental pain, and ear pressure may be present. Management focuses on symptom relief and patient education. Teach him or her about correct use of the drug therapy prescribed. Also teach the patient to use the techniques described for reducing the transmission of influenza infection. Drug therapy includes decongestants, antihistamines, and intranasal steroid spray to block or reduce the amount of chemical mediators in nasal and sinus tissues and relieve local inflammation . Antipyretics are given for fever, and analgesics may be given for pain. Patient-Centered Care: Older Adult Considerations First-generation antihistamines may not be appropriate drugs for older adults because these patients often have reduced drug clearance, higher risk for confusion, and anticholinergic effects such as dry mouth and constipation. Common drugs to avoid in this category include chlorpheniramine, diphenhydramine, and hydroxyzine. Teach older adults why they should not self-medicate with these drugs. Treatment for bacterial rhinosinusitis includes broad-spectrum antibiotics, decongestants, and antipyretics. In some cases, nasal steroids or systemic steroids may be prescribed. Nursing Safety Priority Action Alert Instruct patients with any bacterial infection to complete the entire antibiotic prescription, even when symptoms improve or subside. This action will help eradicate the organism and prevent development of resistant bacterial strains. Supportive therapy such as humidification, nasal irrigation, and applying hot wet packs over the sinus area can increase the patient's comfort and help prevent spread of the infection . Instruct the patient about the importance of rest and increased fluid intake. Sleeping with the head of the bed elevated and avoiding cigarette smoke may reduce discomfort.

Endotracheal intubation

is performed by inserting a tube into the trachea via the nose (nasotracheal) or mouth (orotracheal) by a physician, anesthesia provider, or other specially trained personnel. When pharyngeal or laryngeal edema formation is expected or likely, an endotracheal tube is placed before swelling is severe enough to make insertion impossible.

assess cf

is sweat chloride analysis (Pagana & Pagana, 2018). The sweat chloride test is positive for CF when the chloride level in the sweat ranges between 60 and 200 mEq/L (mmol/L), compared with the normal value of less than 40 mEq/L (mmol/L) (CFF, 2019). Values of 40 to 59 mEq/L (mmol/L) are considered borderline. Genetic testing can be performed to determine which specific mutation an adult may have. Different mutations result in different degrees of disease severity. Nonpulmonary symptoms include abdominal distention, gastroesophageal reflux, rectal prolapse, foul-smelling stools, and steatorrhea (excessive fat in stools). The patient is often malnourished and has many vitamin deficiencies, especially of the fat-soluble vitamins (e.g., vitamins A, D, E, K). As pancreatic function decreases, diabetes mellitus develops with loss of insulin production. Diabetes is present in more than 50% of adults with CF (Frost et al., 2018). The adult with severe CF is usually smaller and thinner than average. Another problem seen in adults with CF is the early onset of osteoporosis and osteopenia, with a greatly increased risk for bone fracture (CFF, 2019). Pulmonary symptoms caused by CF are progressive (McCance et al., 2019). Respiratory infections are frequent or chronic with exacerbations. Patients usually have chest congestion, limited exercise tolerance, cough, sputum production, use of accessory muscles, and decreased pulmonary function (especially forced vital capacity [FVC] and forced expiratory volume in the first second of exhalation [ FEV1]). Chest x-rays show infiltrate and an increased anteroposterior (AP) diameter. During an acute exacerbation or when the disease progresses to end stage, the patient has increased chest congestion, reduced activity tolerance, increased crackles, increased cough, increased sputum production (often with hemoptysis), and severe dyspnea with fatigue. Arterial blood gas (ABG) studies show acidosis (low pH), greatly reduced arterial oxygen (PaO 2) levels, increased arterial carbon dioxide (PaCO 2) levels, and increased bicarbonate levels. With infection, the patient has fever, an elevated white blood cell count, and decreased oxygen saturation. Other symptoms of infection include tachypnea, tachycardia, intercostal retractions, weight loss, and increased fatigue. Interventions: Take Action

Upper airway obstruction

is the interruption of airflow through nose, mouth, pharynx, or larynx.

Atrial fibrillation

is the most common dysrhythmia seen in clinical practice. AF can be encountered and treated in the ambulatory and acute care settings. It can impair quality of life and cause considerable morbidity and mortality, largely related to clotting concerns such as embolic stroke, deep venous thrombosis (DVT), or pulmonary embolism (PE). Pathophysiology Review In patients with AF, multiple rapid impulses from many atrial foci depolarize the atria in a totally disorganized manner at a rate of 350 to 600 times per minute; ventricular response is usually 120 to 200 beats/min. The result is a chaotic rhythm with no clear P waves, no atrial contractions, loss of atrial kick, and an irregular ventricular response (Fig. 31.11). The atria merely quiver in fibrillation (commonly called A fib). Often the ventricles beat with a rapid rate in response to the numerous atrial impulses. The rapid and irregular ventricular rate decreases ventricular filling and reduces cardiac output. This alteration in cardiac function allows for blood to pool, placing the patient at risk for clotting concerns such as DVT or PE. AF is frequently associated with underlying cardiovascular disease (Urden et al., 2018). Etiology and Genetic Risk AF is associated with atrial fibrosis and loss of muscle mass. These structural changes are common in heart diseases such as hypertension, heart failure, and coronary artery disease. For those without an underlying disorder leading to the development of AF, as many as 30 genetic mutations have been identified as the potential cause (Palatinus & Das, 2015). Investigation continues in the development of genetic testing to identify patients at risk and targeted treatment (Palatinus & Das, 2015). As AF progresses, cardiac output decreases by as much as 20% to 30%. Incidence and Prevalence Atrial fibrillation (AF) is the most common dysrhythmia in the developed world, currently affecting 2.7 to 6.1 million people in the United States (January et al., 2014; January et al., 2019). The incidence of AF increases with age. As such, it is predicted that this number will double in the next 25 years (Morillo et al., 2017). Atrial fibrillation causes serious problems in older people, leading to stroke and/or heart failure. Risk factors include hypertension (HTN), previous ischemic stroke, transient ischemic attack (TIA) or other thromboembolic event, coronary heart disease, diabetes mellitus, heart failure, obesity, hyperthyroidism, chronic kidney disease, excessive alcohol use, and mitral valve disease. Interprofessional Collaborative Care Assessment: Recognize Cues History When obtaining a history, assess for prior history of AF or other dysrhythmias. Recurrence of AF is common, and assessment of previous conduction issues can be helpful in developing the plan of care. Assess for history of cardiovascular disease. The risk of AF is much higher in patients with a history of hypertension, heart failure, obesity, or acute coronary syndrome (Urden et al., 2018). Physical Assessment/Signs and Symptoms On physical examination, the apical pulse may be irregular. Symptoms depend on the ventricular rate. Because of the loss of atrial kick, the patient in uncontrolled AF is at greater risk for inadequate cardiac output. Signs of poor perfusion may be observed. Assess the patient for fatigue, weakness, shortness of breath, dizziness, anxiety, syncope, palpitations, chest discomfort or pain, and hypotension. Some patients may be asymptomatic. Psychosocial Assessment Patients with AF, especially those with a high ventricular rate, can feel very anxious. With increased heart rate, cardiac output decreases, which can create dyspnea, contributing to feelings of anxiety. Assess patients who have chronic atrial fibrillation for methods of coping with a long-term conduction issue. Patients with chronic AF may have anxiety related to anticoagulation medications and the potential for emboli development. Other Diagnostic Assessment Definitive diagnosis occurs by obtaining a 12-lead ECG. AF is classified into five categories based on length of time in the rhythm: paroxysmal, persistent, long-standing persistent, permanent, and nonvalvular. AF is termed paroxysmal when the patient experiences an episode within 7 days that converts back to sinus rhythm. Episode lengths vary but do not continue beyond a week. Persistent AF is experienced as episodes that occur for longer than 7 days. AF sustained for more than 12 months is categorized as long-standing persistent. Permanent AF is defined as patients who remain in AF, and a decision is made not to restore or maintain sinus rhythm by either medical or surgical intervention. Nonvalvular AF occurs in the absence of mitral valve disease or repair. Preventing Embolus Formation Planning: Expected Outcomes The expected outcome is that the patient will remain free of embolus formation by restoring regular cardiac conduction. Interventions The purpose of collaborative care is to restore regular blood flow through the atrium when possible. Correcting the rhythm and controlling the rate of the rhythm restore blood flow, which helps prevent embolus formation and increases cardiac output. Drug therapy is often effective for treating AF. Nursing Safety Priority Action Alert The loss of coordinated atrial contractions in AF can lead to pooling of blood, resulting in clotting. The patient is at high risk for pulmonary embolism! Thrombi may form within the right atrium and then move through the right ventricle to the lungs. If pulmonary embolism is suspected, remain with the patient and monitor for shortness of breath, chest pain, and/or hypotension. Initiate the Rapid Response Team and notify the provider. In addition, the patient is at risk for systemic emboli, particularly an embolic stroke, which may cause severe neurologic impairment or death. Monitor patients carefully for signs of stroke. Initiate Rapid Response Team if stroke is suspected to facilitate timely diagnosis. Patients with AF who have valvular disease are particularly at risk for venous thromboembolism (VTE). In VTE, the patient may report lower extremity pain and swelling. Anticipate ultrasound of vasculature and initiation of systemic anticoagulation. Traditional interventions for AF include antidysrhythmic drugs to slow the ventricular conduction or to convert the AF to normal sinus rhythm (NSR). Examples of drugs to slow conduction are calcium channel blockers such as diltiazem or, for more difficult-to-control AF, amiodarone. Dronedarone is a medication similar to amiodarone, yet better tolerated by patients, for maintenance of sinus rhythm after cardioversion. However, dronedarone should not be used in patients with heart failure because it can cause an exacerbation of cardiac symptoms or with permanent AF because it increases the risk of stroke, myocardial infarction, or cardiovascular death. Beta blockers, such as metoprolol and esmolol, may also be used to slow ventricular response. Digoxin is given for patients with heart failure and AF. It is useful in controlling the rate of ventricular response. However, it does not convert AF to sinus rhythm. Carefully monitor the pulse rate of patients taking these drugs. Medications used for rhythm control of AF include flecainide, dofetilide, propafenone, and ibutilide. These medications are usually started within the acute care setting because of the risk of developing prolonged QT intervals and bradycardia. Continuous cardiac monitoring and frequent 12-lead ECGs are needed. Amiodarone is also used but does not require an acute care stay. If permanent AF is present, rhythm control antiarrhythmic medications should not be used. The medications used for rate and rhythm control are further discussed in the Common Examples of Drug Therapy: Antidysrhythmic Medication box. Although the goal is to convert the patient from AF to SR, that may not be possible for many older adults (Urden et al., 2018). As such, these patients require long-term anticoagulation to prevent stroke and thrombus formation. See Chapter 33 for more on anticoagulant therapy. Because of the unpredictable drug response and many food-drug interactions, laboratory test monitoring (e.g., international normalized ratio [INR]) is required when a patient is taking warfarin. Teach patients the importance of avoiding foods high in vitamin K and to avoid herbs such as ginger, ginseng, goldenseal, Ginkgo biloba, and St. John's wort, which could interfere with the drug's action. Because of the problems associated with warfarin, direct oral anticoagulants (DOACs) such as dabigatran, rivaroxaban, apixaban, or edoxaban may be given on a long-term basis to prevent strokes associated with nonvalvular AF. Because these drugs achieve a steady state, there is no need for laboratory test monitoring. Prothrombin time (PT) and INR are not accurate predictors of bleeding time when DOACs are used. Although the risk of bleeding is lower with DOACs, it is important to be aware of the reversal agents for these medications. Initially, dabigatran was the only DOAC with a reversal agent. Idarucizumab, an intravenous monoclonal antibody, binds to dabigatran, thereby preventing dabigatran from inhibiting thrombin. Side effects of idarucizumab include hypokalemia, confusion, constipation, fever, and pneumonia. Recently, the FDA has approved andexanet alfa as the reversal agent for rivaroxaban and apixaban (Garcia & Crowther, 2018). However, use of these reversal agents significantly increases the risk of clotting and stroke and should only be used in the event of life-threatening bleeding. Nursing Safety Priority Drug Alert Teach patients taking any type of anticoagulant drug to report bruising, bleeding nose or gums, and other signs of bleeding to their primary health care provider immediately. Preventing Heart Failure Planning: Expected Outcomes The expected outcome is that the patient will remain free of heart failure by restoration of normal conduction with a controlled ventricular rate. Interventions Collaborative care to prevent heart failure and improve cardiac output generally begins with drug therapy; however, the patient may require other nonsurgical or surgical interventions if medication is not successful in meeting optimal outcomes. Nonsurgical Interventions Nonsurgical interventions most commonly include electrical cardioversion, left atrial appendage closure, radiofrequency catheter ablation, and pacing. Electrical cardioversion. Electrical cardioversion is a synchronized countershock that may be performed to restore normal conduction in a hospitalized patient with new-onset AF. A cardioversion can also be scheduled electively for stable AF that is resistant to medical therapy. When the onset of AF is greater than 48 hours, the patient must take anticoagulants for at least 3 weeks (or until the INR is 2 to 3) before the procedure to prevent clots from moving from the heart to the brain or lungs (Urden et al., 2018). If the onset of AF is uncertain, a transesophageal echocardiogram (TEE) may be performed to assess for clot formation in the left atrium. The shock depolarizes a large amount of myocardium during the cardiac depolarization. It is intended to stop the re-entry circuit and allow the sinus node to regain control of the heart. Emergency equipment must be available during the procedure. The physician, advanced practice nurse, or other qualified nurse explains the procedure to the patient and family. Help the patient sign a consent form unless the procedure is an emergency for a life-threatening dysrhythmia. Because he or she is usually conscious, a short-acting anesthetic agent is administered for sedation. One electrode is placed to the left of the precordium, and the other is placed on the right next to the sternum and below the clavicle. The defibrillator should be set in the synchronized mode. A dot or line will be indicated over each QRS complex, confirming the synchronized mode. This avoids discharging the shock during the T wave, which may increase ventricular irritability, causing ventricular fibrillation (VF). Charge the defibrillator to the energy level requested, usually starting at a low rate of 120 to 200 joules for biphasic machines. Nursing Safety Priority Critical Rescue For safety before cardioversion, turn oxygen off and remove from patient; fire could result. Shout "CLEAR" before shock delivery for electrical safety! After cardioversion, assess the patient's response and heart rhythm. Therapy is repeated, if necessary, until the desired result is obtained or alternative therapies are considered. If the patient's condition deteriorates into VF after cardioversion, check to see that the synchronizer is turned off so immediate defibrillation can be administered. Nursing care after cardioversion includes: • Maintaining a patent airway • Administering oxygen • Assessing vital signs and the level of consciousness • Administering antidysrhythmic drug therapy, as prescribed • Monitoring for dysrhythmias • Assessing for chest burns from electrodes • Providing emotional support • Documenting the results of cardioversion Left atrial appendage closure. For patients who are at high risk for stroke and who are not candidates for long-term anticoagulation, the left atrial appendage (LAA) occlusion device may be an option (Hijazi & Saw, 2018; January et al., 2019). The LAA is a small sac in the wall of the left atrium. For those with nonvalvular AF, the LAA is the most common site of blood clot development leading to the risk of stroke. Inserted percutaneously via the femoral vein, a device to occlude the LAA is delivered via a transseptal puncture. In the United States, the Watchman (nitinol frame with fenestrated fabric) is the only device approved for use in atrial fibrillation patients. After insertion, anticoagulation with aspirin and warfarin is required. A repeat TEE is performed approximately 45 days after insertion to assess for leaks around the device. If no leak is detected, the warfarin is stopped and antiplatelet therapy is continued. Complications are similar to those for undergoing cardiac ablation procedure. Radiofrequency catheter ablation.Radiofrequency catheter ablation (RCA) is an invasive procedure that may be used to destroy an irritable focus in atrial or ventricular conduction. The patient must first undergo electrophysiologic studies and mapping procedures to locate the focus. Then radiofrequency waves are delivered to abolish the irritable focus. When ablation is performed in the AV nodal or His bundle area, damage may also occur to the normal conduction system, causing heart blocks and requiring implantation of a permanent pacemaker. In AF, pulmonary vein isolation and ablation create scar tissue that blocks impulses and disconnects the pathway of the abnormal rhythm. Patients with AF with a rapid ventricular rate not responsive to drug therapy may have AV nodal ablation performed to totally disconnect the conduction from the atria to the ventricles, which requires implantation of a permanent pacemaker. AF ablation should not be performed if long-term anticoagulation is contraindicated. Biventricular pacing. This type of pacing may be another alternative for patients with heart failure and conduction disorders. Biatrial pacing, antitachycardia pacing, and implantable atrial defibrillators are other methods used to suppress or resolve AF. (See full pacing discussion earlier in this chapter.) Surgical Interventions Patients in AF with heart failure (discussed in Chapter 32) may benefit from the surgical maze procedure, an open-chest surgical technique often performed with coronary artery bypass grafting (CABG). Before this procedure, electrophysiologic mapping studies are done to confirm the diagnosis of AF. The surgeon places a maze of sutures in strategic places in the atrial myocardium, pulmonary artery, and possibly the superior vena cava to prevent electrical circuits from developing and continuing AF. Sinus impulses can then depolarize the atria before reaching the AV node and preserve the atrial kick. Postoperative care is similar to that after other open-heart surgical procedures (see Chapter 35). The surgical MAZE procedure is being replaced by catheter procedures using a minimally invasive form. The catheter maze procedure is done by inserting a catheter through a leg vein into the atria and dragging a heated ablating catheter along the atria to create lines (scars) of conduction block. Patients having this minimally invasive form of the procedure have fewer complications, less pain, and a quicker recovery than those with the open, surgical maze procedure. Patient-Centered Care: Older Adult Considerations Older adults are at increased risk for dysrhythmias because of normal physiologic changes in their cardiac conduction system. The sinoatrial node has fewer pacemaker cells. There is a loss of fibers in the bundle branch system. Therefore older adults are at risk for sinus node dysfunction and may require pacemaker therapy. The most common dysrhythmias are premature atrial contractions, premature ventricular contractions, and atrial fibrillation. Dysrhythmias tend to be more serious in older patients because of underlying heart disease, causing cardiac decompensation. Consequently, blood flow to organs that may already be decreased because of the aging process may be further compromised, leading to multisystem organ dysfunction. See the Patient-Centered Care: Older Adult Considerations: Dysrhythmias box for special considerations for older adults receiving antidysrhythmic therapy. Patient-Centered Care: Older Adult Considerations Dysrhythmias Special nursing considerations for the older patient with dysrhythmias are: • Evaluate the patient with dysrhythmias immediately for the presence of a life-threatening dysrhythmia or hemodynamic deterioration. • Assess the patient with a dysrhythmia for angina, hypotension, heart failure, and decreased cerebral and renal perfusion. • Consider these causes of dysrhythmias when taking the patient's history: hypoxia, drug toxicity, electrolyte imbalances, heart failure, and myocardial ischemia or infarction. • Assess the patient's level of education, hearing, learning style, and ability to understand and recall instructions to determine the best approaches for teaching. • Assess the patient's ability to read written instructions. • Teach the patient the generic and trade names of prescribed antidysrhythmic drugs and their purposes, dosage, side effects, and special instructions for use. • Provide clear written instructions in basic language and easy-to-read print. • Provide a written drug dosage schedule for the patient, considering all the drugs the patient is taking and possible drug interactions. • Assess the patient for possible side effects or adverse reactions to drugs, considering age and health status. • Teach the patient to take his or her pulse and to report significant changes in heart rate or rhythm to the primary health care provider. • Inform the patient of available resources for blood pressure and pulse checks, such as blood pressure clinics, home health agencies, and cardiac rehabilitation programs. • Instruct the patient about the importance of keeping follow-up appointments with the primary health care provider and reporting symptoms promptly. • Include the patient's family members or significant other in all teaching whenever possible. • Teach the patient to avoid drinking caffeinated beverages, stop smoking, drink alcohol only in moderation, and follow his or her prescribed diet. Care Coordination and Transition Management Home Care Patients discharged from the hospital may have considerable needs, often more related to their underlying chronic diseases than to their dysrhythmia. A case manager or care coordinator can assess the need for health care resources and coordinate access to services. The focus of home care is often nursing assessment and health teaching. The community-based nurse provides the patient and family members with an opportunity to verbalize their concerns and fears. Provide emotional support and referrals for ongoing care in the community. Assess the patient for possible side effects of antidysrhythmic agents or anticoagulation therapy. Self-Management Education Patients and their families must have a thorough understanding of the prescribed medication therapy, including antidysrhythmic and anticoagulant agents. Pharmacies provide written instructions with filled prescriptions. Teach patients and families the generic and trade names of their drugs and the drugs' purposes, using basic terms that are easily understood. Clear instructions regarding dosage schedules and common side effects are important (see the Common Examples of Drug Therapy: Antidysrhythmic Medication box). Emphasize the importance of reporting these side effects and any dizziness, nausea, vomiting, chest discomfort, or shortness of breath to the primary care provider. Be sure to include education that medication should not be stopped abruptly unless instructed by the primary health care provider. Teach the patient the signs and symptoms of bleeding. Advise patients to call the provider if any signs of bleeding are identified. Teach all patients and their family members how to take a pulse and blood pressure. Some patients may want to use technology to calculate and record their pulse rate. Several applications (apps) for handheld mobile devices (such as the iPhone) are available, but their accuracy varies. "Instant Heart Rate" and "Quick Heart Rate" are examples of apps used to calculate pulse rate. Recently, Apple released an update to the Apple watch that includes an ECG app specifically designed to detect atrial fibrillation. The device is FDA cleared for over-the-counter use to help identify (not diagnose) atrial fibrillation (U.S. Food and Drug Administration, 2018). Remind patients to report any signs of a change in heart rhythm, such as a significant decrease in pulse rate, a rate more than 100 beats/min, or increased rhythm irregularity. Smart Blood Pressure (SmartBP) is a blood pressure and pulse-management system that records, tracks, and analyzes data to share via an iPhone or iPad. The patient can send these readings to his or her primary health care provider as needed to maintain frequent vital sign monitoring. See the Patient and Family Education: Preparing for Self-Management: How to Prevent or Decrease Dysrhythmias box for patient and family education. Patient and Family Education: Preparing for Self-Management How to Prevent or Decrease Dysrhythmias For Patients at Risk for Vasovagal Attacks Causing Bradydysrhythmias • Avoid doing things that stimulate the vagus nerve, such as raising your arms above your head, applying pressure over your carotid artery, applying pressure on your eyes, bearing down or straining during a bowel movement, and stimulating a gag reflex when brushing your teeth or putting objects in your mouth. For Patients With Premature Beats and Ectopic Rhythms • Take the medications that have been prescribed for you and report any adverse effects to your health care provider. • Stop smoking, avoid caffeinated beverages and energy drinks as much as possible, and drink alcohol only in moderation. • Learn ways to manage stress and avoid getting too tired. For Patients With Ischemic Heart Disease • If you have an angina attack, treat it promptly with rest and nitroglycerin administration as prescribed by your health care provider. This decreases your chances of experiencing a dysrhythmia. • If chest pain is not relieved after taking the amount of nitroglycerin that has been prescribed for you, seek medical attention promptly. Also seek prompt medical attention if the pain becomes more severe or you experience other symptoms, such as sweating, nausea, weakness, and palpitations. For Patients at Risk for Potassium Imbalance • Know the symptoms of decreased potassium levels, such as muscle weakness and cardiac irregularity. • Eat foods high in potassium, such as tomatoes, beans, prunes, avocados, bananas, strawberries, and lettuce. • Take the potassium supplements that have been prescribed for you.

he Patient Requiring Intubation and Ventilation

ith mechanical ventilation, the patient who has severe problems of gas exchange may be supported until the underlying problem improves or resolves. Usually mechanical ventilation is a temporary life-support technique. The need for this support may be lifelong for those with severe restrictive lung disease or chronic progressive neuromuscular disease that reduces ventilation. Mechanical ventilation is most often used for patients with hypoxemia and progressive alveolar hypoventilation with respiratory acidosis. The hypoxemia is usually caused by pulmonary shunting of blood when other methods of oxygen delivery do not provide a sufficiently high fraction of inspired oxygen (FiO 2). Mechanical ventilation may be used for patients who need temporary ventilatory support after surgery, those who expend too much energy with breathing and barely maintain adequate gas exchange , or those who receive general anesthesia or heavy sedation. Assess the patient to be intubated in the same way as for other breathing problems. Once mechanical ventilation has been started, assess the respiratory system on an ongoing basis. Monitor and assess for problems related to the artificial airway or ventilator.

Cromones

ither inhaled or taken orally, are useful as controller asthma therapy when taken on a scheduled basis. These agents reduce airway inflammation by either inhibiting the release of inflammatory chemicals (nedocromil) or preventing mast cell membranes from opening when an allergen binds to IgE (cromolyn sodium)

types of hf

left sided, right sided high output failure

diastolic heart failure preserved left ventricular function

left ventricle cannot relax adequately during diastole. Inadequate relaxation or "stiffening" prevents the ventricle from filling with sufficient blood to ensure an adequate cardiac output. Although ejection fraction is more than 40%, the ventricle becomes less compliant over time because more pressure is needed to move the same amount of volume compared with a healthy heart. igns and symptoms and management of diastolic failure are similar to those of systolic dysfunction (

most hfs begin with failure of the

lv and then failure of both ventricles

Right-sided heart (ventricular) failure

may be caused by left ventricular failure, right ventricular myocardial infarction (MI), or pulmonary hypertension. In this type of heart failure (HF), the right ventricle cannot empty completely. Increased volume and pressure develop in the venous system, and peripheral edema results.

Acute cardiac tamponade

may occur when small volumes (20 to 50 mL) of fluid accumulate rapidly in the pericardium and cause a sudden decrease in cardiac output (CO). If the fluid accumulates slowly, the pericardium may stretch to accommodate several hundred milliliters of fluid. Cardiac tamponade can occur with pericarditis, as well as other conditions such as ventricular wall rupture from acute MI, cancer, aortic dissection, and as a complication from invasive cardiac (York et al., 2018). Report any suspicion of this complication to the health care provider immediately. Findings of cardiac tamponade include (Kaplow & Iyere, 2017): • Jugular venous distention • Paradoxical pulse, also known as pulsus paradoxus. See the earlier box, Best Practice for Patient Safety & Quality Care: Care of the Patient With Pericarditis, for more information on paradoxical pulse assessment. • Tachycardia • Muffled heart sounds • Hypotension Cardiac tamponade is an emergency! The health care provider may initially manage the decreased CO with increased fluid volume administration while awaiting an echocardiogram or x-ray to confirm the diagnosis. Unfortunately, these tests are not always helpful because the fluid volume around the heart may be too small to visualize. Hemodynamic monitoring in a specialized critical care unit usually demonstrates compression of the heart, with all pressures (right atrial, pulmonary artery, and wedge) being similar and elevated (plateau pressures). The health care provider may elect to perform a pericardiocentesis to remove fluid and relieve the pressure on the heart. Under echocardiographic or fluoroscopic and hemodynamic monitoring, the cardiologist inserts an 8-inch (20.3-cm), 16- or 18-gauge pericardial needle into the pericardial space. When the needle is positioned properly, a catheter is inserted and all available pericardial fluid is withdrawn. A pericardial drain may be placed temporarily. Monitor the pulmonary artery, wedge, and right atrial pressures during the procedure. The pressures should return to normal as the fluid compressing the heart is removed, and the signs and symptoms of tamponade should resolve. In situations in which the cause of the tamponade is unknown, pericardial fluid specimens may be sent to the laboratory for culture and sensitivity tests and cytology. Nursing Safety Priority Action Alert After the pericardiocentesis, closely monitor the patient for the recurrence of tamponade. Pericardiocentesis alone often does not resolve acute tamponade. Be prepared to provide adequate fluid volumes to increase CO and to prepare the patient for surgical intervention if tamponade recurs. If the patient has a recurrence of tamponade or recurrent effusions or adhesions from chronic pericarditis, a portion or all of the pericardium may need to be removed to allow adequate ventricular filling and contraction. The surgeon may create a pericardial window, which involves removing a portion of the pericardium to permit excessive pericardial fluid to drain into the pleural space. In more severe cases, removal of the toughened encasing pericardium (pericardiectomy) may be necessary.

Verifying Tube Placement

mmediately after an ET tube is inserted, placement is verified by checking end-tidal carbon dioxide levels and by chest x-ray (Barton et al., 2016). Assess for breath sounds bilaterally, sounds over the gastric area, symmetric chest movement, and air emerging from the ET tube. If breath sounds and chest wall movement are absent on the left side, the tube may be in the right mainstem bronchus. The respiratory health care provider intubating the patient should be able to reposition the tube without repeating the entire intubation procedure. If the tube is in the stomach or esophagus, the abdomen may be distended and end-tidal carbon dioxide (EtCO 2) monitoring would indicate the absence of carbon dioxide. In such a case, reintubation is necessary and the stomach must be decompressed with a nasogastric (NG) tube after the ET tube is properly placed. Monitor chest wall movement and breath sounds until tube placement is verified by chest x-ray. Stabilizing the Tube The nurse, respiratory therapist, or anesthesia provider stabilizes the ET tube at the mouth or nose. The tube is marked at the level where it touches the incisor tooth or naris. Two people working together use a head halter technique to secure the tube. An oral airway also may be inserted or a commercial bite block placed to keep the patient from biting an oral ET tube. One person stabilizes the tube at the correct position and prevents head movement while a second person applies the tube-holding device. After the procedure is completed, verify and document the presence of bilateral and equal breath sounds and the level of the tube. Nursing Care The priority nursing action when caring for an intubated patient is maintaining a patent airway. Assess tube placement, cuff leak, breath sounds, indications of adequate gas exchange and oxygenation, and chest wall movement regularly. Nursing Safety Priority Critical Rescue Assess intubated patients to recognize indications of decreased gas exchange (cyanosis, decreased oxygen saturation, increased end-tidal CO2, anxiety). When these indications are present, respond by checking for DOPE: displaced tube, obstructed tube (most often with secretions), pneumothorax, and equipment problems. Prevent the patient from pulling or tugging on the tube to avoid tube dislodgment, and check the pilot balloon to ensure that the cuff is inflated. The most common causes of unplanned extubation in adults are confusion and agitation (Rojo et al., 2020). Monitor the pressure within the cuff to ensure that it is maintained between 20 to 30 cm H2O to stabilize the tube without causing tracheal injury. Suctioning, coughing, and speaking can cause dislodgment. Neck flexion, neck extension, and rotation of the head also can cause the tube to move. In addition, cuff pressures may be affected by patient position changes and may require more frequent monitoring. Tongue movement also can change the tube's position. When other measures fail, obtain a prescription for soft wrist restraints and apply these for the patient who is pulling on the tube. Restraints are used only as a last resort to prevent accidental extubation. Complications of an ET or nasotracheal tube can occur during placement, while in place, during extubation, or after extubation (either early or late). Common complications include tube obstruction, tube dislodgment, pneumothorax, tracheal tears, bleeding, and infection. Trauma and other problems can occur to the face; eye; nasal and paranasal areas; oral, pharyngeal, bronchial, tracheal, and pulmonary areas; esophageal and gastric areas; and cardiovascular, musculoskeletal, and neurologic systems.

wheezes sound like

musical hisses

patho of asthma

narrowing inflamation airway obstruction coughing short of breath

Natriuretic peptides

neurohormones that work to promote vasodilation and diuresis through sodium loss in the renal tubules. The B-type natriuretic peptide (BNP) is produced and released by the ventricles as they stretch in response to fluid overload from HF. BNP levels increase with age and are generally higher in healthy women than healthy men (Pagana & Pagana, 2018).

structures of the upper respiratory tract

nose, sinus oropharynx, larynx and trachea

assess head andneck cancer

obacco and alcohol use, history of acute or chronic laryngitis or pharyngitis, oral sores, swallowing difficulty, and lumps in the neck. Calculate the patient's pack-years of smoking history (see Chapter 24). Ask about alcohol intake (how many drinks per day and for how many years). Also ask about oral exposure to HPV (Schiech, 2016), which has been recognized as an increasing cause of head and neck cancer. Table 26.1 lists the warning signs of head and neck cancer. With laryngeal cancer, painless hoarseness may occur because of tumor size and an inability of the vocal cords to come together for normal speech. Any adult who has a history of hoarseness, mouth sores, or a lump in the neck for 3 to 4 weeks should be evaluated for laryngeal cancer. Many types of imaging studies, including x-rays of the skull, sinuses, neck, and chest, are useful in diagnosing cancer spread and the extent of tumor invasion. Studies commonly included in diagnosis are CT with contrast medium; MRI; nuclear imaging, single-photon emission computed tomography (SPECT), and fluorodeoxyglucose positron emission tomography/CT (FDG-PET/CT) scans to locate metastatic sites (National Comprehensive Cancer Network [NCCN], 2019). Endoscopic examination under anesthesia may be used to define the extent of the tumor. Biopsy tissues taken at the time of endoscopy confirm the diagnosis, tumor type, cell features, location, and stage (see Chapter 19).

people at risk for sleep apnea

obese ppl may be on cpap= positive air pressure

Monitor patients at risk for airway

obstruction and impaired ventilation. When you recognize the need for emergency intubation and ventilation, respond by bringing the code (or "crash") cart, airway equipment box, and suction equipment (often already on the code cart) to the bedside. Maintain a patent airway through positioning (head-tilt, chin-lift) and the insertion of an oral or nasopharyngeal airway until the patient is intubated. Delivering manual breaths with a bag-valve-mask may also be required.

Mitral valve prolapse (MVP)

occurs because the valvular leaflets enlarge and prolapse into the left atrium during systole. This abnormality is usually benign but may progress to pronounced mitral regurgitation in some patients. The etiology of MVP is variable and has been associated with conditions such as Marfan syndrome and other congenital cardiac defects. MVP also has a familial tendency. Usually, however, no other cardiac abnormality is found. Most patients with MVP are asymptomatic. However, some may report chest pain, palpitations, or exercise intolerance. Chest pain is usually atypical, with patients describing a sharp pain localized to the left side of the chest. Dizziness, syncope, and palpitations may be associated with atrial or ventricular dysrhythmias. A normal heart rate and BP are usually found on physical examination. A midsystolic click and a late systolic murmur may be heard at the apex of the heart. The intensity of the murmur is not related to the severity of the prolapse.

The lower respiratory tract is the tubular system

of the trachea (below the larynx), two mainstem bronchi, five secondary bronchi, thousands of branching bronchi and bronchioles, and the alveolar ducts, which connect to the final portions of the tract, the alveoli. Air must flow through the entire tubular system for needed oxygen to reach the alveolar ducts and alveoli where primary gas exchange occurs. When the function of any of these structures is reduced, both gas exchange and systemic perfusion are impaired. Many lower airway problems are chronic and progressive, requiring changes in lifestyle, especially for older adults (Touhy & Jett, 2020). The Patient-Centered Care: Older Adult Considerations box lists nursing accommodations to make when caring for an older patient with a respiratory problem.

interventions asthma

ontrol and prevent episodes, improve airflow and gas exchange , and relieve symptoms. Priority nursing actions focus on patient education about using his or her personal asthma action plan, which includes drug therapy and lifestyle management strategies to help him or her understand the disease and its management

drugs asthma

ontrol therapy drugs are used to reduce airway sensitivity (responsiveness) to prevent asthma attacks from occurring and maintain gas exchange . They are used every day, regardless of symptoms. Reliever drugs (also called rescue drugs) are used to actually stop an attack once it has started. Some patients may need drug therapy only during an asthma episode. For others, daily drugs are needed to keep asthma episodic rather than a more frequent problem. Therapy involves the use of bronchodilators and various drug types to reduce inflammation. Some drugs reduce the asthma response, and other drugs actualldrugs are two or more agents from different classes combined together for better response. With step therapy, drug therapy is prescribed at different levels, starting with step 1 and progressing up (stepping up), until acceptable control is achieved. When the patient achieves control and maintains it for 3 months, the respiratory health care provider adjusts the drug regimen down a step (stepping down) at a time to reach and maintain a goal of good control at the lowest possible drug dosages.Currently three types of inhalers are available: metered dose inhalers (MDIs), which deliver drugs as a fine liquid spray; dry powder inhalers (DPIs), which deliver drugs as a fine powder; and soft mist inhalers (SMIs), which deliver drugs as a very fine soft mist. The MDIs require a propellant to form an aerosol spray and may be used with a spacer (preferred) or without a spacer. DPIs rely on the negative pressure of inhalation to pull the drug into the respiratory tract. SMIs have a mechanical spring-loaded device that creates an aerosol cloud or mist, which is then pulled into the respiratory tract by patient inhalation. Neither DPIs nor SMIs use a spacer for drug delivery. An advantage of SMIs over MDIs and DPIs is that the speed of the drug particles within the mist increases the distance they travel, which increases the likelihood of reaching the lower airways (Burchum & Rosenthal, 2019). Many patients do not get the full benefit of inhaled drugs because of incorrect device use. Often the inhaled drug stays in the mouth and throat or exits through the nose without ever reaching the lower airways. Ensuring that drug dosages reach the site of action requires strict attention to correct technique regardless of which type of inhaler is used

vasopressin

osterior pituitary gland secretes vasopressin (antidiuretic hormone [ADH]). The hormone causes vasoconstriction and fluid retention, which worsen HF. Endothelin is secreted by endothelial cells when they are stretched. As the myocardial fibers are stretched in patients with HF, this potent vasoconstrictor is released, which increases peripheral resistance and hypertension. HF worsens as a result of these actions.

interventions fractures of the nose

performs a simple closed reduction (moving the bones by palpation to realign them) of the nasal fracture using local or general anesthesia within the first 24 hours after injury. After 24 hours the fracture is more difficult to reduce because of edema and scar formation. Then reduction may be delayed for several days until edema is gone. Management focuses on pain relief and cold compresses to decrease swelling. Reduction and surgery may be needed for severe fractures or for those that do not heal properly. Rhinoplasty is a surgical reconstruction of the nose performed to repair a fractured nose and also to change the shape of the nose for improved function or appearance. The patient returns from surgery with packing in both nostrils, which prevents bleeding and provides support for the reconstructed nose. As long as the packing is in place, the patient cannot breathe through the nose. A "moustache" dressing (or drip pad), often a folded 2 × 2 gauze pad, is usually placed under the nose (Fig. 26.3). A splint or cast may cover the nose for better alignment and protection. Change or teach the patient to change the drip pad as necessary. After surgery, observe for edema and bleeding from loss of tissue integrity . The patient with uncomplicated rhinoplasty usually is discharged the day of surgery. Instruct him or her and the family about the routine care described in the following paragraphs. Instruct the patient to stay in a semi-Fowler position and to move slowly. Suggest that he or she rest and use cool compresses on the nose, eyes, and face to help reduce swelling and bruising. After the gag reflex has returned, urge the patient to drink at least 2500 mL/day. To prevent bleeding, teach the patient to avoid forceful coughing or straining during a bowel movement, not to sniff upward or blow the nose, and not to sneeze with the mouth closed for the first few days after the packing is removed. Instruct him or her to avoid aspirin and other NSAIDs to prevent bleeding. Antibiotics may be prescribed to prevent infection. Explain that because of edema the final surgical result may require 6 to 12 months. asoseptoplasty, or submucous resection (SMR), may be needed to straighten a deviated septum when chronic symptoms or discomfort occurs. The deviated section of cartilage and bone is removed or reshaped as an ambulatory surgical procedure. Nursing care is similar to that for a rhinoplasty.

self manage education asthma

plan is tailored to meet the patient's personal triggers, asthma symptoms, and drug responses. It includes: • The prescribed daily controller drug(s) schedule and prescribed reliever drug directions • Patient-specific daily asthma control assessment questions • Directions for adjusting the daily controller drug schedule • When to contact the primary health care provider (in addition to regularly scheduled visits) • Emergency actions to take when asthma is not responding to controller and reliever drugs ach the patient to keep a symptom and intervention diary to learn specific triggers of asthma, early cues for impending attacks, and personal response to drugs. Stress the importance of proper use of his or her personal asthma action plan for any severity of asthma,

Right-sided HF in the absence of left-sided HF is usually the result of

pulmonary problems such as chronic obstructive pulmonary disease (COPD) or pulmonary hypertension. Acute respiratory distress syndrome (ARDS) may also cause right-sided HF. These problems are discussed elsewhere in this text.

afib

quivers- clots- at risk for stroke and heart attack WARFARIN- PT AND INR- every 3 days

premature complexes

remature complexes are early rhythm complexes. They occur when a cardiac cell or cell group, other than the sinoatrial (SA) node, becomes irritable and fires an impulse before the next sinus impulse is produced. The abnormal focus is called an ectopic focus and may be generated by atrial, junctional, or ventricular tissue. After the premature complex, there is a pause before the next normal complex, creating an irregularity in the rhythm. The patient with premature complexes may be unaware of them or may feel palpitations or a "skipping" of the heartbeat. If premature complexes, especially those that are ventricular, become more frequent, the patient may experience symptoms of decreased cardiac output. Premature complexes may occur repetitively in a rhythmic fashion: • Bigeminy exists when normal complexes and premature complexes occur alternately in a repetitive two-beat pattern, with a pause occurring after each premature complex, so complexes occur in pairs. • Trigeminy is a repeated three-beat pattern, usually occurring as two sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in triplets. • Quadrigeminy is a repeated four-beat pattern, usually occurring as three sequential normal complexes followed by a premature complex and a pause, with the same pattern repeating itself in a four-beat pattern.

Facial trauma

s described by the specific bones (e.g., mandibular, maxillary, orbital, nasal fractures) and the side of the face involved. Mandibular (lower jaw) fractures are the most common. Le Fort I is a nasoethmoid complex fracture. Le Fort II is a maxillary and nasoethmoid complex fracture. Le Fort III combines I and II plus an orbital-zygoma fracture, called craniofacial disjunction because the midface has no connection to the skull. The rich facial blood supply results in extensive bleeding and bruising with loss of tissue integrity .

Mitral stenosis

s usually results from rheumatic carditis, which can cause valve thickening by fibrosis and calcification. Rheumatic fever is the most common cause of the problem. In mitral stenosis, the valve leaflets fuse and become stiff and the chordae tendineae contract and shorten. The valve opening narrows, preventing normal blood flow from the left atrium to the left ventricle. As a result of these changes, left atrial pressure rises, the left atrium dilates, pulmonary artery pressures increase, and the right ventricle hypertrophies. Pulmonary congestion and right-sided heart failure occur first. Later, when the left ventricle receives insufficient blood volume, preload is decreased and cardiac output (CO) falls. People with mild mitral stenosis are usually asymptomatic. As the valvular orifice narrows and pressure in the lungs increases, the patient experiences dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea (sudden dyspnea at night), palpitations, and dry cough. Hemoptysis (coughing up blood) and pulmonary edema occur as pulmonary hypertension and congestion progress. Right-sided HF can cause hepatomegaly (enlarged liver), neck vein distention, and pitting dependent edema late in the disorder. On palpation, the pulse may be normal, rapid, or irregular (as in atrial fibrillation). Because the development of atrial fibrillation indicates that the patient may decompensate, the health care provider should be notified immediately of changes to the heart rhythm. A rumbling, apical diastolic murmur is noted on auscultation.

cf

salty tasting skin

risk factor for copd

smoking

Ventricular Fibrillation:

sometimes called V fib, is the result of electrical chaos in the ventricles and is life threatening! Impulses from many irritable foci fire in a totally disorganized manner, so ventricular contraction cannot occur. There are no recognizable ECG deflections (Fig. 31.14A). The ventricles merely quiver, consuming a tremendous amount of oxygen. There is no cardiac output or pulse and therefore no cerebral, myocardial, or systemic perfusion. This rhythm is rapidly fatal if not successfully ended within 3 to 5 minutes. VF may be the first manifestation of coronary artery disease (CAD). Patients with myocardial infarction (MI) are at great risk for VF. It may also occur in those with hypokalemia, hypomagnesemia, hemorrhage, drug therapy, rapid supraventricular tachycardia (SVT), or shock. Surgery or trauma may also cause VF. Interprofessional Collaborative Care Emergency care for VF is critical for survival. When VF begins, the patient becomes faint, immediately loses consciousness, and becomes pulseless and apneic (no breathing). There is no blood pressure, and heart sounds are absent. Respiratory and metabolic acidosis develop. Seizures may occur. Within minutes, the pupils become fixed and dilated, and the skin becomes cold and mottled. Death results without prompt intervention. The desired outcomes of collaborative care are to resolve VF promptly and convert it to an organized rhythm. Therefore the priority is to defibrillate the patient immediately according to ACLS protocol. If a defibrillator is not readily available, high-quality CPR must be initiated and continued until the defibrillator arrives. An automated external defibrillator (AED) is frequently used because it is simple for both medical and lay personnel. Defibrillation is discussed with cardiopulmonary resuscitation later in this chapter. Drug therapy is used when dysrhythmias are sustained and/or life threatening. Drug therapy from one or more classes of antidysrhythmic agents is often used (see the Common Examples of Drug Therapy: Antidysrhythmic Medication box). The Vaughn-Williams classification is commonly used to categorize drugs according to their effects on the action potential of cardiac cells (classes I through IV). Other drugs also have antidysrhythmic effects but do not fit the Vaughn-Williams classification. Class I antidysrhythmics are membrane-stabilizing agents used to decrease automaticity. The three subclassifications in this group include type IA drugs, which moderately slow conduction and prolong repolarization, prolonging the QT interval. These drugs are used to treat or prevent supraventricular and ventricular premature beats and tachydysrhythmias, but they are not as commonly used as other drugs. An example is procainamide hydrochloride. Type IB drugs shorten repolarization. These drugs are used to treat or prevent ventricular premature beats, ventricular tachycardia (VT), and ventricular fibrillation (VF). Examples include lidocaine and mexiletine hydrochloride. Type IC drugs markedly slow conduction and widen the QRS complex. These agents are used primarily to treat or prevent recurrent, life-threatening ventricular premature beats, VT, and VF. Examples include flecainide acetate and propafenone hydrochloride. FIG. 31.14 Ventricular dysrhythmias. A, Coarse ventricular fibrillation. B, Ventricular asystole with one idioventricular complex. Class II antidysrhythmics control dysrhythmias associated with excessive beta-adrenergic stimulation by competing for receptor sites, thereby decreasing heart rate and conduction velocity. Beta-adrenergic blocking agents, such as propranolol and esmolol hydrochloride, are class II drugs. They are used to treat or prevent supraventricular and ventricular premature beats and tachydysrhythmias. Sotalol hydrochloride is an antidysrhythmic agent with both noncardioselective beta-adrenergic blocking effects (class II) and action potential duration prolongation properties (class III). It is an oral agent that may be used for the treatment of documented ventricular dysrhythmias, such as VT, that are life threatening. Class III antidysrhythmics lengthen the absolute refractory period and prolong repolarization and the action potential duration of ischemic cells. Class III drugs include amiodarone and ibutilide and are used to treat or prevent ventricular premature beats, VT, and VF. Class IV antidysrhythmics slow the flow of calcium into the cell during depolarization, thereby depressing the automaticity of the sinoatrial (SA) and atrioventricular (AV) nodes, decreasing the heart rate, and prolonging the AV nodal refractory period and conduction. Calcium channel blockers, such as verapamil hydrochloride and diltiazem hydrochloride, are class IV drugs. They are used to treat supraventricular tachycardia (SVT) and atrial fibrillation (AF) to slow the ventricular response. Magnesium sulfate is an electrolyte administered to treat refractory VT or VF because these patients may be hypomagnesemic, with increased ventricular irritability. The drug is also used for a life-threatening VT called torsades de pointes, which can result from certain antidysrhythmics such as amiodarone.

Ventricular asystole,

sometimes called ventricular standstill, is the complete absence of any ventricular rhythm (Fig. 31.14B). There are no electrical impulses in the ventricles and therefore no ventricular depolarization, no QRS complex, no contraction, no cardiac output, and no perfusion to the rest of the body. The patient in ventricular asystole has no pulse, respirations, or blood pressure. The patient is in full cardiac arrest. In some cases, the sinoatrial (SA) node may continue to fire and depolarize the atria, with only P waves seen on the ECG. However, the sinus impulses do not conduct to the ventricles, and QRS complexes remain absent. In most cases, the entire conduction system is electrically silent, with no P waves seen on the ECG. Ventricular asystole usually results from myocardial hypoxia, which may be a consequence of advanced heart failure. It may also be caused by severe hyperkalemia and acidosis. If P waves are seen, asystole is likely because of severe ventricular conduction blocks. Interventions: Take Action When cardiac arrest occurs, cardiac output stops. The underlying rhythm is usually ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole. Without cardiac output, the patient is pulseless and becomes unconscious because of inadequate cerebral perfusion and gas exchange. Shortly after cardiac arrest, respiratory arrest occurs. Therefore cardiopulmonary resuscitation is essential to prevent brain damage and death. Cardiopulmonary Resuscitation and Defibrillation Cardiopulmonary resuscitation (CPR), also known as Basic Cardiac Life Support (BCLS), must be initiated immediately when asystole occurs. When finding an unresponsive patient, confirm unresponsiveness and call 911 (in community or long-term care setting) or the emergency response team (in the hospital). Gather the AED or defibrillator before initiating CPR. Guidelines for CPR have changed from an ABC (airway-breathing-compressions) approach to the initial priorities of CAB(compressions-airway-breathing) (AHA, 2017; Craig-Brangan & Day, 2019). • Check for a carotid pulse for 5 to 10 seconds. • If carotid pulse is absent, start chest compressions of 100 to 120 compressions per minute and a compression depth of at least 2 inches with no more than 2.4 inches. Push hard and fast! Avoid leaning into the chest after each compression to allow for full chest wall recoil. • Maintain a patent airway. • Ventilate (breathing) with a mouth-to-mask device. Give rescue breaths at a rate of 10 to 12 breaths/min. If an advanced airway is in place, one breath should be given every 6 to 8 seconds (8 to 10 breaths/min). • Ventilation-to-compression ratio should be maintained at 30 compressions to 2 breaths if advanced airway is not in place. • Limit interruptions to compressions to less than 10 seconds. • When possible, compressors should be changed every 2 minutes to maintain effective compressions. Be sure to use Standard Precautions when administering CPR. Be aware that complications of CPR include: • Rib fractures • Fracture of the sternum • Costochondral separation • Lacerations of the liver and spleen • Pneumothorax • Hemothorax • Cardiac tamponade • Lung contusions • Fat emboli As soon as help arrives, place a board under the patient who is not on a firm surface. To make room for the resuscitation team and the crash cart, ask that the area be cleared of movable items and unnecessary personnel. When the AED or defibrillator arrives, do not stop chest compressions while the defibrillator is being set up. If trained to use the AED or defibrillator, apply hands-off defibrillator pads to the patient's chest and turn on the monitor. If the patient is in VF or pulseless VT, the immediate priority is to defibrillate! Defibrillation, an asynchronous countershock, depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit, allowing the sinus node to regain control of the heart. After defibrillation, CPR is resumed. CPR must continue at all times except during defibrillation. Nursing Safety Priority Critical Rescue Early defibrillation is critical in resolving pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF). It must not be delayed for any reason after the equipment and skilled personnel are present. The earlier defibrillation is performed, the greater the chance of survival! Do not defibrillate ventricular asystole. The purpose of defibrillation is disruption of the chaotic rhythm. allowing the SA node signals to restart. In ventricular asystole, no electrical impulses are present to disrupt. Before defibrillation, loudly and clearly command all personnel to clear contact with the patient and the bed and check to see they are clear before the shock is delivered. Deliver shock and immediately resume CPR for 5 cycles or about 2 minutes. Reassess the rhythm every 2 minutes and if indicated. Charge the defibrillator to deliver an additional shock at the same energy level previously used. During the 2-minute intervals while high-quality CPR is being delivered, the Advanced Cardiac Life Support (ACLS) team administers medications and performs interventions to try and restore an organized cardiac rhythm (AHA, 2018). Discussion of ACLS protocol is beyond the scope of this tex After the ACLS team initiates interventions, the role of the medical-surgical nurse is to provide information about the patient. Specific nursing responsibilities include providing a brief summary of the patient's medical condition and the events that occurred up until the time of cardiac arrest. Report the patient's initial cardiac rhythm. Remain in the room to answer questions, document the event, and assist with compressions. If family is present, provide emotional support and explanation of events in the room. An emerging clinical practice is allowing or encouraging family presence at resuscitation attempts. This can be a positive experience for family members and significant others because it promotes closure after the death of a loved one. Although there may be staff resistance and some limits to family presence, overall it is a beneficial practice that should be considered in all resuscitation attempts. When spontaneous circulation resumes, the patient is transported to the intensive care unit. Be ready to hand off a report to the ICU nurse using SBAR communication or another agency system and assist with patient transport.

Ventricular tachycardia

sometimes referred to as V tach, occurs with repetitive firing of an irritable ventricular ectopic focus, usually at a rate of 140 to 180 beats/min or more (Fig. 31.13). VT may result from increased automaticity or a re-entry mechanism. It may be intermittent (nonsustained VT) or sustained, lasting longer than 15 to 30 seconds. The sinus node may continue to discharge independently, depolarizing the atria but not the ventricles, although P waves are seldom seen in sustained VT. Interprofessional Collaborative Care Ventricular tachycardia may occur in patients with ischemic heart disease, MI, cardiomyopathy, hypokalemia, hypomagnesemia, valvular heart disease, heart failure, drug toxicity (e.g., steroids), or hypotension. Patients who use cocaine or illicit inhalants are at a high risk for VT. In patients who go into cardiac arrest, VT is commonly the initial rhythm before deterioration into ventricular fibrillation (VF) as the terminal rhythm! FIG. 31.13 Sustained ventricular tachycardia at a rate of 166 beats/min. Signs and symptoms of sustained VT partially depend on the ventricular rate. Slower rates are better tolerated. Nursing Safety Priority Critical Rescue In some patients, VT causes cardiac arrest. Assess the patient's circulation and airway, breathing, level of consciousness, and oxygenation level. For the stable patient with sustained VT, administer oxygen and confirm the rhythm via a 12-lead ECG. Amiodarone or lidocaine may be prescribed. Current Advanced Cardiac Life Support (ACLS) guidelines state that elective cardioversion is highly recommended for stable VT. The primary health care provider may prescribe an oral antidysrhythmic agent to prevent further occurrences. If the patient has been taking digoxin, the drug is withheld for up to 48 hours before an elective cardioversion. Digoxin increases ventricular irritability and puts the patient at risk for VF after the countershock. Patients who persist with episodes of stable VT may require radiofrequency catheter ablation. Unstable VT without a pulse is treated the same way as ventricular fibrillation, as described in the following paragraphs.

Assess the patient for signs of respiratory difficulty (tachypnea, nasal flaring, anxiety, sternal retraction, shortness of breath, restlessness, decreased oxygen saturation, decreased level of consciousness, stridor). If any signs are present, respond by

staying with the patient and instructing other trauma team members or the Rapid Response Team to prepare for an emergency intubation or tracheotomy.

key signs of asthma attack

sternal retractions and nasal flaring

Xanthines

such as theophylline and aminophylline are used rarely, only when all other types of management are ineffective. These drugs are given systemically, and the dosage that is effective is close to the dosage that produces many dangerous side effects. Blood levels must be monitored closely to ensure that the drug level is within the therapeutic range.

left sided heart failure divided into two types

systolic and diastolic

aortic regurgitation,

the aortic valve leaflets do not close properly during diastole; and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed. This allows flow of blood from the aorta back into the left ventricle during diastole. The left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies. Aortic insufficiency usually results from nonrheumatic conditions such as infective endocarditis, congenital anatomic aortic valvular abnormalities, hypertension, and Marfan syndrome (a rare, generalized, systemic connective tissue disease). Patients with aortic regurgitation remain asymptomatic for many years because of the compensatory mechanisms of the left ventricle. As the disease progresses and left ventricular failure occurs, the major symptoms are exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Palpitations may be noted with severe disease, especially when the patient lies on the left side. Nocturnal angina with diaphoresis often occurs. On palpation, the nurse notes a "bounding" arterial pulse. The pulse pressure is usually widened, with an elevated systolic pressure and diminished diastolic pressure. The classic auscultatory finding is a high-pitched, blowing, decrescendo diastolic

Heart failure

the inability of the heart to work effectively as a pump

systolic heart failure (hf with reduced ejection fraction)

the inability of the heart to work effectively as a pump preload increases with low contraction afterload increases bc of increased peripheral resistance

ejection fraction

the percentage of blood ejected from the heart during systole) drops from a normal of 50% to 70% to below 40% with ventricular dilation. As it decreases, tissue perfusion diminishes and blood accumulates in the pulmonary vessels. Manifestations of systolic dysfunction may include symptoms of inadequate tissue perfusion or pulmonary and systemic congestion. Systolic heart failure is often called forward failure because cardiac output is decreased and fluid backs up into the pulmonary system.

LABAs should never be prescribed as the only drug t

therapy for asthma and are not to be used during an acute asthma attack or bronchospasm. Teach the patient to use these control drugs daily as prescribed, even when no symptoms are present, and to use a SABA to relieve acute symptoms. Any patient using these drugs must be monitored closely.

One preventable cause of airway obstruction

thickly crusted oral and nasopharyngeal secretions,

Obstructive sleep apnea

type of breathing pattern disruption during sleep that lasts at least 10 seconds and occurs a minimum of five times in an hour OSA usually occurs with sleep time hypopnea (lower-than-normal respiratory rate and depth insufficient for effective gas exchange ). During sleep the head and neck muscles relax, allowing the tongue, soft palate, and neck structures to be displaced. As a result, the upper airway is obstructed, but neural control of chest movement is unimpaired. The apnea decreases gas exchange , increases blood carbon dioxide levels, and decreases the pH. These blood gas changes then stimulate neural centers. The sleeper awakens after 10 seconds or longer of apnea and corrects the obstruction, and respiration resumes. After he or she goes back to sleep, the cycle begins again, sometimes as often as every 5 minutes. This cyclic pattern of disrupted sleep and fragmented sleep prevents the deep sleep needed for best physiologic restoration. The apnea period can result in arterial blood oxygen saturation levels of significantly less than 80%. The adult with OSA usually has chronic excessive daytime sleepiness, an inability to concentrate, morning headache, and irritability. Long-term effects of chronic OSA include increased risk for hypertension, stroke, cognitive deficits, weight gain, diabetes, and pulmonary and cardiovascular disease (Senaratna et al., 2017). Hormonal energy balance regulation can lead to serious metabolic issues

Preload

volume of blood in ventricles at end of diastole

OSHA History

who has persistent daytime sleepiness or reports "waking up tired," particularly if he or she also snores heavily. Ask about sensations of daytime sleepiness or falling asleep while performing tasks such as using the computer, reading, or driving. In extreme cases, patients may fall asleep while eating or any time they sit down. Ask whether the patient can recall ever being awakened by his or her own snoring and whether family members have noticed heavy snoring. Ask about the frequency of nightmares, which are associated with OSA. Also ask whether family members have ever observed the patient to have a disturbed breathing pattern while sleeping. A common pattern consists of breaths that become further apart followed by a period of no breathing (apnea), which is then followed by chest and abdominal movements that lead to gasping and snorting with partial awakening to correct the obstruction temporarily. Also ask patients who may have OSA whether they have tried to induce a deeper sleep with over-the-counter sleep aids or increased evening alcohol consumption. Many patients with OSA develop some degree of gastroesophageal reflux disease (GERD) at night. Possible causes include strong abdominal and chest movements during an apnea episode, overeating, eating or drinking close to bedtime, and lying flat while sleeping. Ask the patient whether he or she is awakened often with "heartburn," stomach contents in the mouth, or a burning, choking sensation with coughing. Determine the frequency of such episodes.

Common Causes of Ventilatory Failure

xtrapulmonary CausesIntrapulmonary Causes • Neuromuscular disorders • Myasthenia gravis • Guillain-Barré syndrome • Poliomyelitis • Spinal cord injuries affecting nerves to intercostal muscles • Central nervous system dysfunction • Stroke • Increased intracranial pressure • Meningitis • Chemical depression • Opioid analgesics, sedatives, anesthetics • Kyphoscoliosis • Massive obesity • Sleep apnea • External obstruction or constriction • Airway disease • Chronic obstructive pulmonary disease (COPD), asthma • Ventilation-perfusion ( ) mismatch • Pulmonary embolism • Pneumothorax • Acute respiratory distress syndrome (ARDS) • Amyloidosis • Pulmonary edema • Interstitial fibrosis

Care of the Patient Receiving Mechanical Ventilation

• Assess the patient's respiratory status and gas exchange at least every 4 hours for the first 24 hours and then as needed: • Take vital signs every 4 hours including oxygen saturation and lung auscultation (assess hourly or more often for patients in an ICU). • Be alert for the possibility of unintended extubation or self-extubation. If the patient requires sedation or restraints, follow institution guidelines for patient safety. • Assess color around the lips and nail beds, and observe for bilateral chest expansion. • Assess the placement of the endotracheal tube. • Evaluate ABGs as available. • Maintain head of the bed more than 30 degrees when patient is supine to decrease the risk for aspiration and ventilator-associated pneumonia. • Review ventilator settings at least every 8 hours, including alarm settings, with the respiratory therapist (RT). • Review the patient information on the ventilator display to confirm that the patient is receiving the prescribed set tidal volume and that peak pressures are not elevated (indicator of obstruction or decreased lung compliance). • Empty ventilator tubings when moisture collects. • Be sure the cuff is adequately inflated to ensure tidal volume. If there is a concern for overinflation, have the RT check the cuff pressure. • Assess the need for suctioning every 2 hours and suction only as needed (being sure to preoxygenate the patient before suctioning). • Assess the patient's mouth around the ET tube for pressure injuries. • Perform mouth care at least every 12 hours using standard ventilator bundles. • Perform tracheostomy care at least every 8 hours, changing the ET tube holder or tape as needed, and moving the oral ET tube to the opposite side of the mouth daily to prevent ulcers. • Assess ventilated patients for GI distress (diarrhea, constipation, tarry stools). • Turn the patient at least every 2 hours and get him or her out of bed as prescribed to prevent complications of immobility. • Monitor the patient's progress on current ventilator settings and promptly relay any concerns to the respiratory health care provider or RT. • Monitor for adverse effects of mechanical ventilation: infection, barotrauma, reduced cardiac output. • Position the patient to facilitate ventilation-perfusion ( ) matching ("good lung down"), as appropriate. • Monitor the effects of ventilator changes on gas exchange, the patient's subjective responses, and readiness to wean. • Provide a method of communication. Request consultation with a speech-language pathologist for assistance, if necessary. • Administer muscle-paralyzing agents, sedatives, and narcotic analgesics, as prescribed, using the lowest possible dose to achieve patient comfort without oversedation. • Include the patient and family whenever possible (especially during suctioning and tracheostomy care).

Asthma Management

• Avoid potential environmental asthma triggers, such as smoke, fireplaces, dust, mold, and weather changes of warm to cold. • Avoid drugs that trigger your asthma (e.g., aspirin, NSAIDs, beta blockers). • Avoid food that has been prepared with monosodium glutamate (MSG) or metabisulfite. • If you have exercise-induced asthma, use your reliever bronchodilator inhaler 30 minutes before exercise to prevent or reduce bronchospasm. • Be sure that you know the proper technique and correct sequence when you use metered dose inhalers. • Get adequate rest and sleep. • Reduce stress and anxiety; learn relaxation techniques; adopt coping mechanisms that have worked for you in the past. • Wash all bedding with hot water to destroy dust mites. • Seek immediate emergency care if you experience any of these: • Gray or blue fingertips or lips • Difficulty breathing, walking, or talking • Retractions of the neck, chest, or ribs • Nasal flaring • Failure of drugs to control worsening symptoms

Pulmonary Edema

• Crackles • Dyspnea at rest • Disorientation or acute confusion (especially in older adults as early symptom) • Tachycardia • Hypertension or hypotension • Reduced urinary output • Cough with frothy, pink-tinged sputum • Premature ventricular contractions and other dysrhythmias • Anxiety • Restlessness • Lethargy

eval osa

• Does not remain hypertensive or has hypertension that can be controlled with appropriate therapy • Is adherent with prescribed nonsurgical interventions • Has fewer sleep-time apnea periods of 10 seconds or longer • Has improved gas exchange with greater duration of restorative sleep • Reports less daytime sleepiness and has more energy • Has an uneventful recovery from surgical intervention

Management of Chest Tube Drainage System

• Ensure that the dressing on the chest around the tube is tight and intact. Depending on agency policy and the surgeon's preference, reinforce or change loose dressings. • Assess for difficulty breathing. • Assess breathing effectiveness by pulse oximetry. • Listen to breath sounds for each lung. • Check alignment of trachea. • Check tube insertion site for condition of the skin. Palpate area for puffiness or crackling that may indicate subcutaneous emphysema. • Observe site for signs of infection (redness, purulent drainage) or excessive bleeding. • Check to see if tube "eyelets" are visible (they should not be visible). • Assess for pain and its location and intensity and administer drugs for pain as prescribed. • Assist patient to deep breathe, cough, perform maximal sustained inhalations, and use incentive spirometry. • Reposition the patient who reports a "burning" pain in the chest. Drainage System • Do not "strip" the chest tube; use a hand-over-hand "milking" motion. • Keep drainage system lower than the level of the patient's chest. • Keep the chest tube as straight as possible from the bed to the suction unit, avoiding kinks and dependent loops. Extra tubing can be loosely coiled on the bed. • Ensure that the chest tube is securely taped to the connector and that the connector is taped to the tubing going into the collection chamber. • Assess bubbling in the water-seal chamber; should be gentle bubbling on patient's exhalation, forceful cough, position changes. • Assess for "tidaling" (rise and fall of water in chamber two with breathing). • Check water level in the water-seal chamber and keep at the level recommended by the manufacturer. • Check water level in the suction control chamber and keep at the level prescribed by the surgeon (unless dry suction system is used). • Clamp the chest tube only for brief periods to change the drainage system or when checking for air leaks. • Check and document amount, color, and characteristics of fluid in the collection chamber as often as needed according to the patient's condition and agency policy. • Empty collection chamber or change the system before the drainage makes contact with the bottom of the tube. • When a sample of drainage is needed for culture or other laboratory test, obtain it from the chest tube; after cleaning the chest tube, use a 20-gauge (or smaller) needle and draw up specimen into a syringe. Immediately Notify Surgeon or Rapid Response Team for: • Tracheal deviation from midline • Sudden onset or increased intensity of dyspnea • Oxygen saturation less than 90% • Drainage greater than 70 mL/hr • Visible eyelets on chest tube • Chest tube falls out of the patient's chest (first, cover the area with dry, sterile gauze) • Chest tube disconnects from the drainage system (first, put end of tube in a container of sterile water and keep below the level of the patient's chest) • Drainage in tube stops (in the first 24 hours

Beta Blocker/Digoxin Therapy

• Establish same time of day to take this medication every day. • Continue taking this medication unless your health care provider tells you to stop. • Do not take digoxin at the same time as antacids or cathartics (laxatives). • Take your pulse rate before taking each dose of digoxin. Notify your health care provider of a change in pulse rate (60 to 100 beats/min is typically normal, depending on your baseline pulse rate) or rhythm and increasing fatigue, muscle weakness, confusion, or loss of appetite (signs of digoxin toxicity). • If you forget to take a dose, it may be delayed a few hours. However, if you do not remember it until the next day, you should take only your usual daily dose. • Report for scheduled laboratory tests (e.g., potassium and digoxin levels). • If potassium supplements are prescribed, continue the dose until told to stop by your health care provider.

Warning Signals Associated With Lung Cancer

• Hoarseness • Change in respiratory pattern • Persistent cough or change in cough • Blood-streaked sputum • Rust-colored or purulent sputum • Frank hemoptysis • Chest pain or chest tightness • Shoulder, arm, or chest wall pain • Recurring episodes of pleural effusion, pneumonia, or bronchitis • Dyspnea • Fever associated with one or two other signs • Wheezing • Weight loss • Clubbing of the fingers

mergency Care for a Patient With an Anterior Nosebleed

• Maintain Standard Precautions or Body Substance Precautions. • Position the patient upright and leaning forward to prevent blood from entering the larynx and possible aspiration. • Reassure the patient and attempt to keep him or her quiet to reduce anxiety and blood pressure. • Apply direct lateral pressure to the nose for 10 minutes and apply ice or cool compresses to the nose and face if possible. • If nasal packing is necessary, loosely pack both nares with gauze or nasal tampons. • To prevent rebleeding from dislodging clots, instruct the patient to not blow the nose for 24 hours after the bleeding stops. • Instruct the patient to seek medical assistance if these measures are ineffective or if the bleeding occurs frequently.

Valvular Heart Disease

• Notify all your health care providers that you have a defective heart valve. • Remind the health care provider of your valvular problem when you have any invasive dental work (e.g., extraction). • Request antibiotic prophylaxis before and after these procedures if the health care provider does not offer it. • Clean all wounds and apply antibiotic ointment to prevent infection. • Notify your primary health care provider immediately if you experience fever, petechiae (pinpoint red dots on your skin), or shortness of breath.

Warning Signs of Head and Neck Cancer

• Pain • Lump in the mouth, throat, or neck • Difficulty swallowing • Color changes in the mouth or tongue to red, white, gray, dark brown, or black • Oral lesion or sore that does not heal in 2 weeks • Persistent or unexplained oral bleeding • Numbness of the mouth, lips, or face • Change in the fit of dentures • Burning sensation when drinking citrus juices or hot liquids • Persistent, unilateral ear pain • Hoarseness or change in voice quality • Persistent or recurrent sore throat • Shortness of breath • Anorexia and weight loss

Nursing Accommodations for an Older Adult With a Respiratory Problem

• Provide rest periods between activities such as bathing, meals, and ambulation. • Have the patient sit in an upright position for meals to prevent aspiration. • Encourage nutritional fluid intake after the meal to prevent an early sensation of fullness and promote increased calorie intake. • Schedule drugs around routine activities to increase adherence to drug therapy. • Arrange chairs in strategic locations to allow the patient with dyspnea to stop and rest while walking. • Urge the patient to notify the primary health care provider promptly for any symptoms of infection. • Encourage the patient to receive the pneumococcal vaccines and to have an annual influenza vaccination. • For patients who are prescribed home oxygen, instruct them to keep tubing coiled when walking to reduce the risk for tripping

Pulmonary Embolism (Classic Signs and Symptoms)

• Sudden onset of dyspnea • Sharp, stabbing chest pain • Apprehension, restlessness • Feeling of impending doom • Cough • Hemoptysis • Diaphoresis • Increased respiratory rate • Crackles • Pleural friction rub • Tachycardia • S3 or S4 heart sound • Fever, low grade • Petechiae over chest and axillae (usually only associated with fat embolism syndrome [FES]) • Decreased arterial oxygen saturation (SaO 2)

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• Systemic congestion • Jugular (neck vein) distention • Enlarged liver and spleen • Anorexia and nausea • Dependent edema (legs and sacrum) • Distended abdomen • Swollen hands and fingers • Polyuria at night • Weight gain • Increased blood pressure (from excess volume) or decreased blood pressure (from failure)

incidence tb and health promotion

• Those in constant, frequent contact with an untreated infected person • Those who have reduced immunity or HIV disease • Adults who live in crowded areas such as long-term care facilities, prisons, homeless shelters, and mental health facilities • Older homeless adults • Users of injection drugs or alcohol • Lower socioeconomic groups • Foreign immigrants from less affluent countries Health Promotion and Maintenance Many adults who acquire TB have risk factors such as homelessness, living in very crowded conditions, or substance use with malnutrition. These risk factors are best managed on a societal level. Communities need to work toward providing adequate housing, substance-use programs that are accessible, and feeding centers or food banks for those in need. On a personal level, many health conditions make it more likely to contract TB if exposed. Adults with these health conditions should avoid people who are ill, stay well nourished, and practice good handwashing and social distancing. Any adult who works with people at high risk of having TB should be screened yearly

Causes of upper airway obstruction include:

• Tongue edema (surgery, trauma, angioedema as an allergic response to a drug) • Tongue occlusion (e.g., loss of gag reflex, loss of muscle tone, unconsciousness, coma) • Laryngeal edema from any cause (e.g., smoke or toxin inhalation, local or generalized inflammation, allergic reactions, anaphylaxis) • Peritonsillar and pharyngeal abscess • Head and neck cancer • Thick secretions • Stroke and cerebral edema • Facial, tracheal, or laryngeal trauma or burns • Foreign-body aspiration