Adult Exam 1

acute respiratory failure

ARF caused by failure to adequately ventilate and or oxygenate ventilatory failure = due to mechanical abnormality of lungs or chest wall, impaired muscle function (diaphragm) or malfunction in the resp control center of the brain o2 failure = from lack of perfuson to pul cap bed (pul embolism) or condtion that alters gas exchange (pul edema or pneumonia) both inadequate cent and oxygenation can happen if diseased lungs (asthma, emphysema, CF) criteria based on ABGs

LOWER RESPIRATORY TRACT INFECTIONS

Acute Bronchitis • Acute bronchitis is an inflammation of the bronchi. • It is a self-limiting condition; treatment is supportive. • Cough, the primary symptom, may last up to 3 weeks. Pertussis • Pertussis is a highly contagious infection of the respiratory tract. • Despite improved immunization in the United States, incidence rates are rising in the adult population. • Pertussis is characterized by uncontrollable, violent coughing. • Treatment consists of antibiotics and supportive care. Pneumonia • Pneumonia is an acute inflammation of the lung parenchyma. • It can be classified according to the causative microorganism, such as bacteria, viruses, Mycoplasma, fungi, parasites, and chemicals. • A clinically effective way to classify pneumonia: • ♣ Community-acquired pneumonia (CAP) is a lower respiratory tract infection of the lung parenchyma with onset in the community or during the first 2 days of hospitalization. • ♣ Hospital-acquired pneumonia (HAP) begins 48 hours or longer after admission to a hospital and was not present at the time of admission. • ♣ Classifying pneumonia is important because of the differences in the most likely causative organisms and the selection of appropriate antimicrobial therapy. • Aspiration pneumonia refers to the sequelae occurring from abnormal entry of secretions or substances into the lower airway. • Necrotizing pneumonia is a complication of bacterial lung infection and may produce cavitation within the lung parenchyma • Opportunistic pneumonia occurs in certain patients with altered immune responses who are highly susceptible to respiratory infections. • Specific pathophysiologic changes related to pneumonia vary according to the type of offending organism. The majority of organisms trigger an inflammatory response in the lung. Complications, such as pleural effusion, abscess, and acute respiratory failure, develop more frequently in those with underlying chronic conditions. • Treatment with antibiotics is necessary for bacterial pneumonia; all patients require supportive measures. Tuberculosis • Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis, a gram-positive, acid-fast bacillus that is usually spread from person to person via airborne droplets. • Historically there was a decline in TB nationwide. Then there was a resurgence of TB in those with HIV infection and an emergence of multidrug-resistant strains of M. tuberculosis. The number of TB cases has decreased again. • Types of TB include: • ♣ Primary TB: Bacteria inhaled, and patient is contagious to others • ♣ Secondary TB: TB bacilli are not active, and there is no risk of transmission of the disease to others • The tuberculin skin test (TST), using purified protein derivative (PPD), and interferon-γ release assays (IGRAs) are used to screen high-risk people for M. tuberculosis infection. • Drug therapy is used to treat an individual with active TB disease. For therapy to be maximally effective, four drugs are used for the initial 3-month phase or longer. • Patients with latent TB infection (LTBI) are of primary concern. These individuals are treated with antitubercular drugs to prevent active disease and decrease the number of TB carriers in the community. • Patients strongly suspected of having TB should be placed on airborne isolation, receive appropriate drug therapy, and receive an immediate medical workup, including chest x-ray, sputum smear, and culture. • Nursing care for a patient with TB revolves around the nursing diagnoses of ineffective breathing pattern, imbalanced nutrition, noncompliance, and activity intolerance. Atypical Mycobacteria • Atypical mycobacteria cause disease that resembles TB, both in manifestations and treatment. • Disease typically occurs in those who are immunosuppressed or have chronic pulmonary disease. • Treatment is similar to that for TB. Pulmonary Fungal Infections • Pulmonary fungal infections are caused by the inhalation of spores. Exposure is common, but most persons are asymptomatic or develop a mild nonspecific respiratory illness. • A more severe and sometimes life-threatening pneumonia can occur in seriously ill patients being treated with corticosteroids, antineoplastic and immunosuppressive drugs, and in patients with HIV and cystic fibrosis. • Since these infections are not transmitted from person to person, the patient does not have to be placed in isolation. • Amphotericin B (an antifungal medication) is the mainstay of treatment. Lung Abscess • A lung abscess is a pus-containing lesion of the lung. • Causes may include IV drug use, malignancy, TB, and parasitic and fungal diseases. • The onset of a lung abscess is usually insidious, especially if anaerobic organisms are the primary cause. A more acute onset occurs with aerobic organisms. • Prolonged antibiotic therapy (2 to 4 months) is the primary method of treatment. Environmental Lung Diseases • Environmental or occupational lung diseases are caused or aggravated by workplace or environmental exposure and are preventable. • Pneumoconiosis is a general term for a group of lung diseases caused by inhalation and retention of mineral or metal dust particles. • The best approach to management of environmental lung diseases is to try to prevent or decrease environmental and occupational risks. CHEST TRAUMA AND THORACIC INJURIES Pneumothorax • Pneumothorax is air in the pleural space resulting in a partial or complete collapse of the lung. There are several types: • ♣ A spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled blisters) located on the surface of the lung. These blebs can occur in healthy, young individuals or as a result of lung disease such as COPD, asthma, cystic fibrosis, and pneumonia. • ♣ Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures. • ♣ A tension pneumothorax occurs when there is a rapid accumulation of air in the pleural space, causing severely high intrapleural pressures with resultant tension on the heart and great vessels. • ♣ Pneumothorax can occur from either nonpenetrating (closed) or penetrating (open) chest trauma • ♣ Treatment depends on the severity of the pneumothorax and hemodynamic stability of the patient. • Hemothorax is an accumulation of blood in the intrapleural space. • Chylothorax is lymphatic fluid in the pleural space caused by a leak in the thoracic duct. Causes of both include trauma, surgical procedures, and malignancy. Fractured Ribs • Rib fractures are the most common type of chest injury resulting from blunt trauma. • Clinical manifestations include pain at the site, especially with inspiration and coughing. • The main treatment goal is to decrease pain to promote effective breathing. Patients also need to be taught deep breathing, coughing, and use of incentive spirometry. Flail Chest • Flail chest results from multiple rib fractures, causing an unstable chest wall. The diagnosis of flail chest is based on the fracture of two or more ribs, in two or more separate locations, causing an unstable segment. • Initial therapy consists of airway management, adequate ventilation, supplemental O2 therapy, and pain control. • The goal of therapy is to reexpand the lung and ensure adequate oxygenation. Chest Tubes and Pleural Drainage • The purpose of chest tubes and pleural drainage is to remove the air, fluid, and/or blood from the pleural space and to restore normal intrapleural pressure so that the lungs can re-expand. • Routine monitoring is done to assess adequate functioning of the chest tube unit. This involves observing for tidaling and bubbling in the water-seal chamber, assessing for subcutaneous emphysema, listening for breath sounds over the lung fields, and measuring the amount of fluid drainage. Chest Surgery • A thoracotomy, or the surgical opening into the thoracic cavity, is considered major surgery because the incision is large, cutting into bone, muscle, and cartilage. The two types of thoracic incisions are median sternotomy, performed by splitting the sternum, and lateral thoracotomy. • Video-assisted thoracic surgery (VATS) is a minimally invasive thorascopic surgical procedure that in many cases can avoid the impact of a full thoracotomy. RESTRICTIVE RESPIRATORY DISORDERS Pleural Effusion • Pleural effusion is a collection of fluid in the pleural space. It is not a disease but rather an indication of another disease. • Pleural effusion is frequently classified as transudative or exudative according to whether the protein content of the effusion is low or high, respectively. • ♣ A transudative effusion occurs primarily in noninflammatory conditions and is an accumulation of protein-poor, cell-poor fluid. • ♣ An exudative effusion is an accumulation of fluid and cells in an area of inflammation. • ♣ An empyema is a pleural effusion that contains pus. • The type of pleural effusion can be determined by a sample of pleural fluid obtained via thoracentesis (a procedure done to remove fluid from the pleural space). • The main goal of management of pleural effusions is to treat the underlying cause. Pleurisy • Pleurisy, or pleuritis, is an inflammation of the pleura. The most common causes are pneumonia, TB, chest trauma, pulmonary infarctions, and neoplasms. • Treatment of pleurisy is aimed at treating the underlying disease and providing pain relief. Atelectasis • Atelectasis is a condition of the lungs characterized by collapsed, airless alveoli. • The most common cause of atelectasis is airway obstruction that results from retained exudates and secretions. This is frequently observed in the postoperative patient. INTERSTITIAL LUNG DISEASES Idiopathic Pulmonary Fibrosis • Idiopathic pulmonary fibrosis is characterized by scar tissue in the connective tissue of the lungs as a sequela to inflammation or irritation. • The clinical course is variable and the prognosis poor, with a 5-year survival rate of 30% to 50% after diagnosis. • The current guidelines for IPF treatment do not find sufficient evidence to support the routine use of any specific drug therapy. Guidelines support the use of O2 therapy and lung transplantation for patients who meet the criteria. Sarcoidosis • Sarcoidosis is a chronic, multisystem granulomatous disease of unknown cause that primarily affects the lungs. The disease may also involve the skin, eyes, liver, kidney, heart, and lymph nodes. • Treatment is supportive and aimed at suppressing the inflammatory response VASCULAR LUNG DISORDERS Pulmonary Edema • Pulmonary edema is an abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs. • In severe circumstances, it may be considered a life-threatening medical emergency. • The most common cause of pulmonary edema is left-sided heart failure. Pulmonary Embolism • Pulmonary embolism is the blockage of pulmonary arteries by a thrombus, fat, or air emboli, or tumor tissue. • Most pulmonary embolisms arise from thrombi in the deep veins of the legs. • The most common risk factors for pulmonary embolism are immobility or reduced mobility, surgery within the last 3 months, history of deep vein thrombosis, and malignancy. • Pulmonary infarction (death of lung tissue) and pulmonary hypertension are complications of pulmonary embolism. • Pulmonary embolism may be diagnosed by spiral CT scan, V/Q scan, and/or pulmonary angiography. • The objectives of treatment are to prevent further growth or extension of thrombi in the lower extremities, prevent embolization from the upper or lower extremities to the pulmonary vascular system, and provide cardiopulmonary support if indicated. Pulmonary Hypertension • Pulmonary hypertension can occur as a primary disease (idiopathic pulmonary arterial hypertension [IPAH]) or as a secondary complication of a respiratory, cardiac, autoimmune, hepatic, or connective tissue disorder (secondary pulmonary arterial hypertension [SPAH]). • IPAH is a severe and progressive disease. It is characterized by mean pulmonary arterial pressure greater than 25 mm Hg at rest (normal 12 to 16 mm Hg) or greater than 30 mm Hg with exercise. • IPAH is a diagnosis of exclusion. All other conditions must be ruled out. • Although there is no cure for IPAH, treatment can relieve symptoms, increase quality of life, and prolong life. • SPAH occurs when a primary disease causes a chronic increase in pulmonary artery pressures. SPAH can develop as a result of parenchymal lung disease, left ventricular dysfunction, intracardiac shunts, chronic pulmonary thromboembolism, or systemic connective tissue disease. Cor Pulmonale • Cor pulmonale is enlargement of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is usually a preexisting condition in the individual with cor pulmonale. • The most common cause of cor pulmonale is COPD. • The primary management of cor pulmonale is directed at treating the underlying pulmonary problem that precipitated the heart problem. Lung Transplantation • There are four types of transplant procedures available: single lung transplant, bilateral lung transplant, heart-lung transplant, and transplant of lobes from living related donor. • Lung transplant recipients are at high risk for noninfectious and infectious complications. • ♣ Noninfectious complications: VTE, diaphragm dysfunction, and malignancy. • ♣ Infectious complications: bacterial, viral, fungal, and protozoal infections. Infections are the leading cause of death after transplant. • Immunosuppressive therapy usually includes a three-drug regimen of cyclosporine or tacrolimus, mycophenolate mofetil (CellCept), and prednisone.

what is pneumonia

Acute infection of lung parenchyma tx with macrolides, doxycycline, fluoroquinolones NOT penicillin Associated with significant morbidity and mortality rates Pneumonia and influenza are 8th leading cause of death in the U.S. Pneumonia is an acute infection of the lung parenchyma. Until 1936, pneumonia was the leading cause of death in the United States. The discovery of sulfa drugs and penicillin was pivotal in the treatment of pneumonia. Since that time, there has been remarkable progress in the development of antibiotics to treat pneumonia. However, despite newer antimicrobial agents, pneumonia is still associated with significant morbidity and mortality rates.

Nursing ManagementAcute Coronary Syndrome

Ambulatory Care Cardiac rehabilitation Patient and caregiver teaching Physical activity METs scale Monitor heart rate Low-level stress test before discharge Isometric versus isotonic activities Cardiac rehabilitation is the restoration of a person to an optimal state of function in six areas: physiologic, psychologic, mental, spiritual, economic, and vocational. Many persons recover from ACS physically, yet they may never attain psychologic well-being. All patients (ACS, chronic stable angina, and cardiac surgery) need to be referred to a cardiac rehabilitation program. Patient teaching needs to occur at every stage of the patient's hospitalization and recovery (e.g., ED, telemetry unit, home care). Limit your use of medical terminology. For example, explain that the heart, a four-chambered pump, is a muscle that needs oxygen like all other muscles in order to work properly. When blood vessels supplying the heart with oxygen are blocked by plaque, less oxygen is available to the heart muscle. As a result, the heart cannot pump normally. It helps to have a model of the heart or to sketch a picture of what you are explaining. Literature written for a nonmedical audience is available through the AHA. Anticipatory guidance involves preparing the patient and caregiver for what to expect in the course of recovery and rehabilitation. By learning what to expect during treatment and recovery, the patient gains a sense of control over his or her life. Physical activity, an integral part of rehabilitation, is necessary for optimal physiologic functioning and psychologic well-being. One method used to identify levels of physical activity is by using metabolic equivalent (MET) units: 1 MET is the amount of oxygen needed by the body at rest. The MET determines the energy costs of various exercises. In the hospital, the activity level is gradually increased so that by the time of discharge the patient can tolerate moderate-energy activities of 3 to 6 METs. Many HCPs order low-level exercise stress tests before discharge to assess readiness for discharge, optimal HR for an exercise program, and potential for ischemia or reinfarction. Because of the short hospital stay, it is critical to give the patient specific guidelines for physical activity so that overexertion will not occur. Tell the patient to "listen to what your body is saying"—the most important aspect of recovery. Teach patients to check their HR. The patient should know the limits within which to exercise. Tell the patient the maximum HR that should be present at any point. If the HR exceeds this level or does not return to the resting HR within a few minutes, tell the patient to stop and rest. Also tell the patient to stop exercising and rest if chest pain or shortness of breath occurs. The basic categories of physical activity are isometric (static) and isotonic (dynamic). Most daily activities are a mixture of the two. Isometric activities involve the development of tension during muscular contraction but produce little or no change in muscle length or joint movement. Lifting, carrying, and pushing heavy objects are isometric activities. Because the HR and BP change rapidly during isometric work, isometric exercises should be limited. Isotonic activities involve changes in muscle length and joint movement with rhythmic contractions at relatively low muscular tension. Walking, jogging, swimming, bicycling, and jumping rope are examples of activities that are mostly isotonic. Isotonic exercise can put a safe, steady load on the heart and lungs and improve the circulation in many organs.

Abdominal Aortic Aneurysm

Angiography demonstrating fusiform abdominal aortic aneurysm. Note calcification of the aortic wall (arrows) and extension of the aneurysm into the common iliac arteries.

The nurse is caring for a patient who survived a sudden cardiac death. What should the nurse include in the discharge instructions? "Because you responded well to CPR, you will not need an implanted defibrillator." "The most common way to prevent another arrest is to take your prescribed drugs." "Your family members should learn how to perform CPR and practice these skills regularly." "Since there was no evidence of a heart attack, you do not need to worry about another episode."

Answer: C Rationale: Rapid cardiopulmonary resuscitation, prompt defibrillation (with an automated external defibrillator), and early advanced cardiac life support can produce high long-term survival rates for a witnessed arrest.

Classification of Aortic Dissection

Aortic dissection is classified based on location of dissection and duration of onset Type A dissection affects the ascending aorta and arch Type B dissection begins in the descending aorta

ARDS Clinical Manifestations

As ARDS progresses, profound respiratory distress requires endotracheal intubation and PPV See next slide for figure of x-ray. Pleural effusions may also be present. Severe hypoxemia, hypercapnia, and metabolic acidosis, as well as manifestations of target organ dysfunction, may develop if therapy is not started promptly. Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs Leaves few recognizable air spaces

Aortic DissectionComplications- Cardiac tamponade

Cardiac tamponade Severe, life-threatening complication Occurs when blood escapes from dissection into pericardial sac Clinical manifestations include: Hypotension Narrowed pulse pressure Distended neck veins Muffled heart sounds Pulsus paradoxus

Clinical Manifestations of ACS Myocardial Infarction - Catecholamine

Catecholamine release and stimulation of SNS Release of glycogen Diaphoresis Increased HR and BP Vasoconstriction of peripheral blood vessels Skin: ashen, clammy, and/or cool to touch During the initial phase of MI, the ischemic heart cells release catecholamines (norepinephrine and epinephrine) that are normally found in these cells. This results in release of glycogen, diaphoresis, increased HR and BP, and vasoconstriction of peripheral blood vessels. On physical examination, the patient's skin may be ashen, clammy, and cool to touch.

Sudden Cardiac Death Nursing/Interprofessional Care

Diagnostic workup to rule out or confirm MI Cardiac biomarkers ECGs Treat accordingly Cardiac catheterization PCI or CABG People who survive an episode of SCD require a diagnostic workup to determine whether they have had an MI. Serial analysis of cardiac biomarkers and ECGs are done, and the patient is treated accordingly. In addition, because most persons with SCD have CAD, cardiac catheterization is done to determine the possible location and extent of coronary artery occlusion. PCI or CABG surgery may be indicated. 24-hour Holter monitoring Exercise stress testing Signal-averaged ECG Electrophysiologic study (EPS) Implantable cardioverter-defibrillator (ICD) Antidysrhythmic drugs LifeVest Most SCD patients have a lethal ventricular dysrhythmia that is associated with a high incidence of recurrence. It is useful to know when those persons are most likely to have a recurrence and what drug therapy is the most effective treatment. Assessment of dysrhythmias in these patients includes 24-hour Holter monitoring or other type of event recorder, exercise stress testing, signal-averaged ECG, and electrophysiologic study (EPS). EPS is performed under fluoroscopy. Pacing electrodes are placed in various intracardiac areas and stimuli are selectively used in an attempt to produce dysrhythmias. The patient's response to various antidysrhythmic drugs is determined and monitored in a controlled environment. The most common approach to preventing a recurrence is the use of an implantable cardioverter-defibrillator (ICD). It has been shown that an ICD improves survival compared with drug therapy alone. Drug therapy with amiodarone (Cordarone) may be used in conjunction with an ICD to decrease episodes of ventricular dysrhythmias. Some patients at risk for SCD may consider using a LifeVest as a bridge to ICD or heart transplantation. A LifeVest is a personal external defibrillator that has two main parts: a garment and monitor. The garment is worn under clothing and has electrodes that continuously record the patient's ECG. The monitor is worn around the waist or from a shoulder strap. If the patient has ventricular tachycardia or ventricular fibrillation, the device sounds an alarm to confirm that the patient is unresponsive. If the patient is conscious, the patient can press two buttons to stop the shock. If the patient does not respond, the device warns bystanders that a shock is about to be delivered. If the dysrhythmia continues and the patient still does not respond, a treatment shock is delivered through the electrodes. Patient teaching Psychosocial adaptation "Brush with death" "Time bomb" mentality Additional issues Driving restrictions Role reversal Change in occupation Teaching people about the symptoms of impending cardiac arrest and the actions to take can save lives. Rapid cardiopulmonary resuscitation (CPR) and defibrillation with an automated external defibrillator (AED), combined with early advanced cardiac life support, has high long-term survival rates for a witnessed arrest. When caring for these patients, be alert to the patient's psychosocial adaptation to this sudden "brush with death." Many of these patients develop a "time bomb" mentality. They fear the recurrence of cardiac arrest and may become anxious, angry, and depressed. Their caregivers are likely to experience the same feelings. Patients and caregivers may also need to deal with additional issues such as possible driving restrictions, role reversal, and change in occupation.

ARDS Etiology and Pathophysiology

Neutrophils are attracted and release mediators, producing changes in lungs ↑ Pulmonary capillary membrane permeability Destruction of elastin and collagen Formation of pulmonary microemboli Pulmonary artery vasoconstriction The pathophysiologic changes in ARDS are divided into three phases: (1) injury or exudative phase, (2) reparative or proliferative phase, and (3) fibrotic phase. Injury or exudative phase 1-7 days after initial lung injury or host insult Neutrophils adhere to pulmonary microcirculation Damage to vascular endothelium ↑ Capillary permeability Injury or exudative phase Engorgement of peribronchial and perivascular interstitial space Fluid crosses into alveolar space Intrapulmonary shunt develops as alveoli fill with fluid, and blood passing through cannot be oxygenated Initially, engorgement of the peribronchial and perivascular interstitial space produces interstitial edema. Next, fluid from the interstitial space crosses the alveolar membrane and enters the alveolar space. Intrapulmonary shunt develops because the alveoli fill with fluid, and blood passing through them cannot be oxygenated (Figs. 67-4 and 67-9). Injury or exudative phase Alveolar cells type 1 and 2 are damaged Surfactant dysfunction → atelectasis Hyaline membranes line alveoli Contribute to fibrosis and atelectasis Leads to decreased gas exchange capability and lung compliance The function of surfactant is to maintain alveolar stability by decreasing alveolar surface tension and preventing alveolar collapse. Decreased synthesis of surfactant and inactivation of existing surfactant cause the alveoli to become unstable and collapse (atelectasis). In addition, during this stage, necrotic cells, protein, and fibrin form hyaline membranes that line the alveoli. Hyaline membranes contribute to the development of fibrosis and atelectasis, leading to a decrease in gas exchange capability and lung compliance. Injury or exudative phase Interstitial and alveolar edema and atelectasis Severe V/Q mismatch and shunting of pulmonary capillary blood result in refractory hypoxemia Unresponsive to increasing O2 concentrations Lungs become less compliant Higher airway pressures must be generated The primary pathophysiologic changes that describe the injury or exudative phase of ARDS are interstitial and alveolar edema and atelectasis. As the lungs become less compliant because of decreased surfactant, pulmonary edema, and atelectasis, the patient must generate higher airway pressures to inflate "stiff" lungs. At this stage, ventilator management will often include a "pressure-control" type of ventilation. Pressure control ventilation will help keep the inspiratory and plateau pressures from becoming too high. This prevents alveolar over-distention and rupture. By reducing the amount of pressure going into the stiff, noncompliant lungs, further lung injury may be prevented. Injury or exudative phase ↑ Work of breathing (WOB) ↑ Respiratory rate ↓ Tidal volume Produces respiratory alkalosis from increase in CO2 removal ↓ CO2 and tissue perfusion Hypoxemia and the stimulation of juxtacapillary receptors in the stiff lung parenchyma (J reflex) initially cause an increase in respiratory rate and a decrease in tidal volume. CO increases in response to hypoxemia, a compensatory effort to increase pulmonary blood flow. However, as atelectasis, pulmonary edema, and pulmonary shunt increase, compensation fails, and hypoventilation, decreased CO, and decreased tissue O2 perfusion eventually occur. Reparative or proliferative phase 1-2 weeks after initial lung injury Influx of neutrophils, monocytes, and lymphocytes Fibroblast proliferation Lung becomes dense and fibrous Lung compliance continues to ↓ Increased pulmonary vascular resistance and pulmonary hypertension may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature. Lung compliance continues to decrease as a result of interstitial fibrosis. Reparative or proliferative phase Hypoxemia worsens Thickened alveolar membrane Diffusion limitation and shunting If reparative phase persists, widespread fibrosis results If phase is stopped, lesions will resolve Fibrotic or chronic/late phase 2-3 weeks after initial lung injury Lung is completely remodeled by collagenous and fibrous tissues Fibrotic or chronic/late phase ↓ Lung compliance ↓ Area for gas exchange Hypoxemia continues Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis The diffuse scarring and fibrosis result in decreased lung compliance.

Rhythms you should know...

Normal Sinus Rhythms Sinus Brady Sinus Tachycardia Premature Ventricular Contractions Supraventricular Tachycardia Atrial Flutter Atrial Fibrillation Artifact The P wave represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction). The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It represents the time taken for the impulse to spread through the atria, AV node, and bundle of His; the bundle branches; and Purkinje fibers to a point immediately preceding ventricular contraction. The QRS complex consists of three distinct waves. The Q wave is the first negative (downward) deflection after the P wave, short and narrow, and not present in several leads. The R wave is the first positive (upward) deflection in the QRS complex, and the S wave is the first negative (downward) deflection after the R wave. The QRS interval is measured from the beginning to the end of the QRS complex. It represents the time taken for depolarization (contraction) of both ventricles (systole). The ST segment is measured from the S wave of the QRS complex to the beginning of the T wave. It represents the time between ventricular depolarization and repolarization (diastole). It should be isoelectric (flat). The T wave represents the time for ventricular repolarization. It should be upright. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. It represents the time taken for entire electrical depolarization and repolarization of the ventricles. Typically, an ECG consists of 12 leads (or views) of the heart's activity. A lead consists of a positive and a negative electrode, with the positive electrode being the "seeing eye." Activity coming toward the positive electrode produces an upward deflection on the EKG paper, and one going away from the seeing eye produces a downward deflection (this is the reason for lead tracings looking different). Six of the leads measure electrical forces in the frontal plane. These are bipolar (positive and negative) leads I, II, and III (left column of tracings); and unipolar (positive) leads aVr, aVl, and aVf. The remaining six unipolar leads (V1 through V6) measure the electrical forces in the horizontal plane (precordial leads). The 12-lead ECG may show changes suggesting structural changes, conduction disturbances, damage (e.g., ischemia, infarction), electrolyte imbalance, or drug toxicity. Obtaining 12 ECG views of the heart is also helpful in the assessment of dysrhythmias. Accurate interpretation of an ECG depends on the correct placement of the leads on the patient. A. Limb leads I, II, and III. Leads are located on the extremities. Illustrated are the angles from which these leads view the heart. B. Lead placement for limb leads aVR, aVL, and aVF. These unipolar leads use the center of the heart as their negative electrode. C. Lead placement for the chest electrodes: V1, fourth intercostal space at the right sternal border; V2, fourth intercostal space at the left sternal border; V3, halfway between V2 and V4; V4, fifth intercostal space at the left midclavicular line; V5, fifth intercostal space at the anterior axillary line; V6, fifth intercostal space at the midaxillary line. One or more ECG leads can be used to continuously monitor a patient's ECG. The leads most commonly selected are leads II and V1. MCL1 is a modified chest lead that is similar to V1 and is used when only three leads are available for monitoring. A. Lead placement for MCL, using a three-lead system. B. Lead placement for V1 or V6, using a five-lead system. C. Typical electrocardiogram tracing in lead MCL1. C, Chest; LA, left arm; LL, left leg; MCL1, modified chest lead; RA, right arm; RL, right leg P wave Atrial rate and rhythm PR interval Ventricular rate and rhythm QRS complex ST segment QT interval T wave When assessing a cardiac rhythm, use a consistent and systematic approach. One such approach includes the following: 1. Look for the presence of the P wave. Is it upright or inverted? Is there one for every QRS complex or more than one? Are there atrial fibrillatory or flutter waves present? 2. Evaluate the atrial rhythm. Is it regular or irregular? 3. Calculate the atrial rate. 4. Measure the duration of the PR interval. Is it normal duration or prolonged? 5. Evaluate the ventricular rhythm. Is it regular or irregular? 6. Calculate the ventricular rate. 7. Measure the duration of the QRS complex. Is it normal duration or prolonged? 8. Assess the ST segment. Is it isoelectric (flat), elevated, or depressed? 9. Measure the duration of the QT interval. Is it normal duration or prolonged? 10. Note the T wave. Is it upright or inverted? Additional questions to consider include the following: 1. What is the dominant or underlying rhythm and/or dysrhythmia? 2. What is the clinical significance of your findings? 3. What is the treatment for the particular rhythm?

Aortic AneurysmClinical Manifestations - Thoracic aorta aneurysm (TAA)

Often asymptomatic Most common manifestation: Deep diffuse chest pain Pain may extend to interscapular area

pericarditis Complications

Pericardial Effusion Cardiac Tamponade

Nursing Management chest tubes

Prepare drainage unit by adding water to water-seal chamber and suction control chamber as indicated Maintain patency of drainage system, Keep tubing loosely coiled, Tape connections Prepare CDU: Wet suction: add sterile water to 2-cm mark in water-seal chamber and to 20-cm mark (or as ordered) in suction control chamber. Dry suction: add sterile water to the fill line of the air leak meter. Attach suction tubing and increase suction until the bellows-like float moves across the display window. Keep all tubing loosely coiled below chest level. Tubing should drop straight from bed or chair to drainage unit. Do not let it be compressed. Keep all connections between chest tubes, drainage tubing, and the drainage collector tight and tape at connections. Observe tidaling Observe for air leak (bubbling in water-seal chamber) Observe fluid levels in water-seal chamber Observe for air fluctuations (tidaling) and bubbling in the water-seal chamber. If no tidaling is observed (rising with inspiration and falling with expiration in the spontaneously breathing patient) = drainage system is blocked, the lungs are reexpanded, or the system is attached to suction If the chest tube is connected to suction, disconnect from wall suction to check for tidaling. Observe for air leak in water-seal chamber. If bubbling increases, there may be an air leak in the drainage system or a leak from the patient (bronchopleural leak). Suspect a system leak when bubbling is continuous. If leak persists, briefly clamp the chest tube at the patient's chest. If the leak stops, then the air is coming from the patient. If the air leak persists, briefly and methodically move the clamps down the tubing away from the patient until the air leak stops. The leak will then be present between the last two clamp points. If the air leak persists all the way to the drainage unit, replace the unit. Observe fluid levels in water-seal chamber. High fluid levels in the water-seal indicate residual negative pressure. The chest system may need to be vented by using the high-negativity release valve available on the drainage system to release residual pressure from the system. Do not lower water-seal column when wall suction is not operating or when patient is on gravity drainage. Assess patient's clinical status Vital signs, lung sounds, pain Drainage amount Drainage site infection Subcutaneous emphysema Encourage deep breathing, ROM exercises, incentive spirometry Assess for manifestations of reaccumulation of air and fluid in the chest (↓ or absent breath sounds), significant bleeding (>100 mL/hr), chest drainage site infection (drainage, erythema, fever, ↑ WBC), or poor wound healing. Notify physician for management plan. Evaluate for subcutaneous emphysema at chest tube site. Encourage the patient to breathe deeply periodically to facilitate lung expansion and encourage range-of-motion exercises to the shoulder on the affected side. Encourage use of incentive spirometry every hour while awake to prevent atelectasis or pneumonia. NO - Milking or stripping chest tube = incr intrapleural pressures and damage lungs Position tubing so that drainage flows freely to negate need for milking or stripping Monitor for complications Reexpansion pulmonary edema Vasovagal response Subcutaneous emphysema Dressing care Sterile occlusive dressing Closely monitor the patient for complications associated with chest tube placement and drainage. If 1 to 1.5 L of fluid and/or blood are removed rapidly, reexpansion pulmonary edema severe symptomatic hypotension can occur. Subcutaneous emphysema can occur from air leaking into the tissue surrounding the chest tube insertion site. A 'crackling' sensation will be felt when palpating the skin. A small amount of subcutaneous air is harmless and will be reabsorbed. However, severe subcutaneous emphysema can cause drastic swelling of the head and neck with potential airway compromise. Meticulous sterile technique during dressing changes can reduce the incidence of infected sites. Change dressing according to unit protocol and physician preference. Remove old dressing carefully to avoid removing unsecured chest tube. Assess the site and culture site as indicated. Cleanse the site according to protocol, maintaining asepsis. Redress with occlusive dressing (e.g., Opsite or gauze with occlusive tape). Most physicians prefer the use of petroleum gauze dressing around the tube to prevent air leak. Date the dressing and document dressing change. Monitor integrity of chest tube system If the following occur within the first hour, notify HCP at once: Drainage > 200 mL, Subcutaneous emphysema, Respiratory distress Monitor color and amount of drainage Monitor integrity of the chest tube system. Monitor the color and amount of drainage hourly in the first few hours post-chest tube insertion. Drainage greater than 200 mL in the first hour, development of subcutaneous emphysema, or any signs and symptoms of respiratory distress should be reported to the appropriate HCP at once. Do not elevate system above chest Change when full Measure fluid level Report > 100 mL/hr If unit overturned, have patient exhale and cough Do NOT clamp If break in system, place distal end in sterile water to maintain water seal Never elevate the drainage system to the level of the patient's chest because this will cause fluid to drain back into the lungs. Secure the unit to the drainage stand. Change the unit if the collection chamber is full. Do not try to empty it. Mark the time of measurement and the fluid level on the drainage unit according to the unit standards. Report any change in the quantity or characteristics of drainage (e.g., clear yellow to bloody) to the physician and record the change. Notify physician if >100 mL/hr drainage. Check the position of the chest drainage container. If the drainage system is overturned and the water-seal is disrupted, return it to an upright position and encourage the patient to take a few deep breaths, followed by forced exhalations and cough maneuvers. Clamping of chest tubes during transport or when the tube is accidentally disconnected is no longer advocated. The danger of rapid accumulation of air in the pleural space, causing tension pneumothorax, is far greater than that of a small amount of atmospheric air that enters the pleural space. If chest tube becomes disconnected, the immediate priority is to reestablish the water-seal system. In some hospitals, when disconnection occurs, the chest tube is immersed in sterile water (about 2 cm) until the system can be reestablished. It is important to know the unit protocol, individual clinical situation (whether an air leak exists), and HCP preference before any chest tube clamping occurs. Appearance of a new air leak warrants assessment of the drainage system to identify if the air leak is coming from the patient or the system.

Ventricular Tachycardia

QRS takes over everything 3 or more PVCs can make you go into this hills to the vallys of death - if dont fix go into Afib? Monomorphic, polymorphic, sustained, and nonsustained Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation Ventricular tachycardia occurs when an ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker. Different forms of VT exist, depending on QRS configuration. Monomorphic VT has QRS complexes that are the same in shape, size, and direction. Polymorphic VT occurs when the QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats. VT may be sustained (longer than 30 seconds) or nonsustained (less than 30 seconds). The development of VT is an ominous sign. It is a life-threatening dysrhythmia because of decreased CO and the possibility of development of ventricular fibrillation, which is a lethal dysrhythmia. A run of three or more PVCs defines ventricular tachycardia (VT). Ventricular rate is 150 to 250 beats/minute. Rhythm may be regular or irregular. AV dissociation may be present, with P waves occurring independently of the QRS complex. The atria may be depolarized by the ventricles in a retrograde fashion. The P wave is usually buried in the QRS complex, and the PR interval is not measurable. The QRS complex is distorted in appearance and wide (greater than 0.12 second in duration). The T wave is in the opposite direction of the QRS complex. Associated with heart disease, electrolyte imbalances, drugs, CNS disorder Can be stable (patient has a pulse) or unstable (pulseless) Sustained VT causes severe decrease in CO Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest VT is associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, long QT syndrome, drug toxicity, and central nervous system disorders. This dysrhythmia can be seen in patients who have no evidence of heart disease. Sustained VT causes a severe decrease in CO because of decreased ventricular diastolic filling times and loss of atrial contraction. This results in hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest. The dysrhythmia must be treated quickly, even if it occurs only briefly and stops abruptly. Episodes may recur if prophylactic treatment is not started. Ventricular fibrillation may also develop. Precipitating causes must be identified and treated (e.g., hypoxia) VT with pulse (stable) treated with antidysrhythmics or cardioversion(give them sedation) Pulseless VT treated with CPR and rapid defibrillation If the VT is monomorphic and the patient is hemodynamically stable (i.e., pulse is present) and has preserved left ventricular function, IV procainamide, sotalol, or amiodarone is used. If the VT is polymorphic with a normal baseline QT interval, any one of the following drugs is used: β-adrenergic blockers, amiodarone, procainamide, or sotalol. Polymorphic VT with a prolonged baseline QT interval is treated with IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing (discussed later in chapter). Drugs that prolong the QT interval (e.g., dofetilide [Tikosyn]) should be discontinued. Cardioversion is used if drug therapy is ineffective. VT without a pulse is a life-threatening situation. Cardiopulmonary resuscitation (CPR) and rapid defibrillation are the first lines of treatment, vasopressors (e.g., epinephrine) and antidysrhythmics (e.g., amiodarone)

Chest X-Ray of Person with ARDS

The x-ray shows new, bilateral, diffuse, homogeneous pulmonary infiltrates without cardiac failure, fluid overload, chest infection, or chronic lung disease.

Inferior Vena Cava Filters

These pictures depict some of the different types of inferior vena cava filters. A, Greenfield filter; B, Bird's nest filter; D, Vena Tech LP filter.

HEPA Mask

This is a picture of a high-efficiency particulate air (HEPA) mask. Because many different types of HEPA masks are currently available, health care professionals should be "fit tested" each time a different brand or model of mask is used to ensure proper mask size. Otherwise, the CDC recommends that yearly mask "fit testing" is acceptable. To be effective, the mask must be molded to fit tightly around the nose and mouth.

Chest Trauma

Traumatic injuries to chest contribute to majority of all traumatic deaths Range of injuries Simple rib fractures → life-threatening organ rupture Thoracic injuries range from simple rib fractures to complex life-threatening rupture of organs. From = Blunt, Shearing and compression injuries of thoracic structures minor --> life threatening Penetrating = Open wound through pleural space two categories: blunt trauma and penetrating trauma. Blunt trauma = chest strikes or is struck by an object. can cause shearing and compression of thoracic structures. high-velocity impact = shearing forces can result in laceration or tearing of the aorta. Compression of the chest may result in contusion, crush injury, and organ rupture. Penetrating trauma is an injury in which a foreign object impales or passes through the body tissues, creating an open wound. Examples include knife wounds, gunshot wounds, and injuries with other sharp objects. Severity depends on location of penetration and affected organs/vessels.

Aortic AneurysmsClassification

Two basic classifications True - fusiform/sacculated False - pseudoaneurysm/aortic dissection

Acute Kidney InjuryClinical ManifestationsOliguric phase

Urinary output less than 400 mL/day Occurs w/i 1 to 7 days after injury Lasts 10 to 14 days Urinary changes: most common initial manifestation = oliguria If cause ischemia = oliguria occurs w/i 24 hours. longer oliguric phase lasts, poorer prognosis for complete recovery of kidney function. About 50% of patients will not be oliguric = dx more difficult. Changes in urine output generally do not correspond to changes in GFR. changes in urine output are often helpful in differentiating etiology of AKI. For example, anuria (no urine output) seen w/ urinary tract obstruction, oliguria is commonly seen w/ prerenal causes, and nonoliguric AKI is seen with acute interstitial nephritis and ATN. UA = show casts, RBCs, and white blood cells (WBCs). casts = mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules. Urinary specific gravity = measure of the concentration of solutes in the urine normally 1.003-1.030. Urine osmolality = measure # of dissolved particles in urine. range is 300-1300 mOsm/kg. urine concentration, it is more accurate than specific gravity. Oliguric phase: Fluid volume Hypovolemia may exacerbate AKI Decr urine output fluid retention Neck veins distended Bounding pulse Edema HNT Fluid overload --> HF, pulmonary edema, pericardial, pleural effusions Fluid volume: Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI, especially prerenal causes. When urinary output decr, fluid retention occurs. The severity of the manifestations depends on the extent of the fluid overload. reduced urine output (anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and hypertension may develop. Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions. Metabolic acidosis: Impaired kidney cannot excrete hydrogen ions Serum bicarbonate production is decr Severe acidosis develops Kussmaul respirations normal kidney = excess hydrogen ions are excreted to maintain a physiologic balance of the blood pH. The impaired kidneys cannot excrete hydrogen ions or the acid products of metabolism. Serum bicarbonate production is decreased because of defective reabsorption and regeneration of bicarbonate ions. Serum bicarbonate is depleted through buffering of acidic hydrogen ions and metabolic end products. The patient with severe acidosis may develop Kussmaul respirations (rapid, deep respirations) in an effort to compensate by incr the exhalation of CO2. Sodium balance: Incr excretion of sodium Hyponatremia can lead to cerebral edema K excess Impaired ability of kidneys to excrete K Incr risk with massive tissue trauma Usually asymptomatic ECG changes Sodium balance: Damaged tubules cannot conserve sodium. urinary excretion of Na may incr, resulting in normal or below-normal levels of serum Na. Excessive intake of sodium should be avoided because it can lead to volume expansion, HNT, and HF . Uncontrolled hyponatremia or water excess can lead to cerebral edema. Potassium excess: The kidneys normally excrete 80% to 90% of the body's potassium. In AKI the serum potassium level incr hc kidney's normal ability to excrete k is impaired. Hyperkalemia risk is incr if AKI caused by massive tissue trauma bc damaged cells release additional K into extracellular fluid. Bleeding and blood transfusions may cause cellular destruction, releasing more K into extracellular fluid. Metabolic acidosis worsens hyperkalemia as hydrogen ions enter cells and K is driven out of the cells into extracellular fluid. pt w/ hyperkalemia are asymptomatic, complain of weakness w/ severe hyperkalemia. bc cardiac muscle is intolerant of acute incr in K, emergency tx of hyperkalemia needed. Acute or rapid development of hyperkalemia may result in clinical signs that are apparent on electrocardiogram (ECG). peaked T waves, widening QRS complex, ST segment depression. Progressive changes in the ECG that are related to incr K Hematologic disorders= Leukocytosis Waste product accumulation = incr BUN, serum creatinine Neurologic disorders = Fatigue and difficulty concentrating, Seizures, stupor, coma Hematologic disorders: Hospital-acquired AKI often occurs in patients who have multiorgan failure. Leukocytosis is often present with AKI. most common cause of death is infection. most common site of infection = urinary, respiratory systems. Waste product accumulation: kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). incr BUN level caused by dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury, or GI bleeding. The best serum indicator of AKI is creatinine because it is not significantly altered by other factors. Neurologic disorders: Neurologic changes can occur as the nitrogenous waste products accumulate in the brain, other nervous tissue. manifestations = fatigue, difficulty concentrating, seizures, stupor, coma.

resp failure dx

abgs cxray bicarb pH pulse ox CT - pul embo arterial pressure

chest tube insertion

arm above head on affected side to expose midaxillary area elevate bed to 30-60 degrees = to lower diaphragm and decr risk on injury cxray to confirm local anesthetic, small incision over ribs, adv up and over the rib to avoid intercostal nerves and blood vessles tube is secured/sutured in place wound is covered with occulsive dressing/petroeum (airtight) gauze

dialysis

bruit and thrill watch for infection

pneumonia dx

cxray: consolidation (solidifcation density) of lung tissue, might be -for a few days pulse ox - usually under 95%

chest should have ____ pressure

negative

what dressing to put on if tube fallsout

occlusive vaseline gauze attached on 3 sides

tb labs

positive intradermal within 2-10wks of infection quantiFERON-TB Gold - blood test for interferon gamma (INF-g)

what happens when you clamp a chest tube

tension pneumothorax

acute resp failure etiology - hypoxemic

vent perfusion shunt diffusion limitation alveolar hypoventilation

Endovascular graft procedureBenefits

↓ Anesthesia and operative time Smaller operative blood loss ↓ Morbidity and mortality More rapid resumption of physical activity Shortened hospital stay Quicker recovery Higher patient satisfaction Reduction in overall costs

Pericardial Effusion

Build up of fluid in the pericardium May start to compress nearby structures Pulmonary Tissue Laryngeal Nerve Heart Pericardial Effusions can occur rapidly (e.g., chest trauma) or slowly (e.g., tuberculosis pericarditis). Large effusions may compress nearby structures. Pulmonary tissue compression can cause cough, dyspnea, and tachypnea. Phrenic nerve compression can cause hiccups, and compression of the laryngeal nerve may result in hoarseness. Heart sounds are generally distant and muffled, although BP is usually maintained.

ECG Finding With Anterolateral Wall MI

ECG findings with anterolateral wall myocardial infarction. Normally, leads I, aVL, and V1 to V3 have positive R wave. Note the pathologic Q waves in these leads and the ST-segment elevation in leads V2 to V5 (arrows). what part of the wall what part of the heart was effected by this

Aortic AneurysmsDefinition

Outpouching or dilation of arterial wall Common problems involving aorta men > women and whites >African Americans Incidence ↑ with age Aneurysms may occur in more than one location. Peripheral artery aneurysms can also develop but are not common.

resp failure s/s

min-->hrs or day --> days hypoxia = dypnea, tachypnea, prolonged exhale, nasal flaring, intercostal muscles retation, paradoxic chest, cyanosis (late) hypercapnia - dyspnea, tripod, pursed lip, decr resp dat, shallow breathes, decr tidal volume, decr minute vent WOB = work of breathing lay down, rather sit, has to sit up

worst case scenario of acute pharyngitis - peritonsillar abscess

mostly caused by hemolytic streptococci s/s - pain, swelling, blockage of throat, high fever, incr wbc count, chills, hard to swallow, muffled voice tx - iv antibiotics, needle aspiration or incision and drainage of abscess laryngeal polyps - develop on the vocal cords from vocal cords from vocal abuse - talking or singing or irritation, like smoking s/s = hoarsness rest/hydration, surgery to remove large ones = risk of dysphagia, dyspnea, stridor, can become malignant

pneumonia patient care

high fowlers breathing treatments/meds/O2 coughing/suctioning skin break down from O2 device physical limitations = rest periods incr breathing = incr kcals 2-3L a day

Pertussis

highly contagious, gram- bacillus - bordetella pertussis bacteria attaches to cilia of resp track and release toxins to damage cilia = inflam/swelling DPT (diphtheria, pertussis, tetanus) vaccine may diminish over time allowing milder infection if 19 and over get Tdap (tetanus, diphtheria, pertussis) stage 1 - catarrhal, first 2 wks of infections, mild URI, low grade/no fever, runny nose, watery eyes, mild nonproductive cough stage 2 - paroxysmal stage - 2-10th wk paroxysms of cough stage 3 - convalescent - 2-3wks, less severe cough, weakness hallmark characteristic = violent coughing, whooping cound when trying to breath in against obstructed glottis no whoop in teens/adults, vaccinated ppl cough more @night tx - antibiotics, macrolides (erthromycin), decr s/s and decr spread infections from - 5 days after antibiotics or from cartarrhal phase to 3rd wk NO - cough suppresents or antihistamines - more coughing NO - corticosteriods, bronchodilators

consequences of hypoexia and hypoxia

hypozemia --> hypoxia aerobic --> anaerobic metabolism creastes lactic acid = hard to get rid of bp and CO decr metabolic acidosis/cell death/brain death

chest tube nursing management

if tube becomes disconnected = reestablish water seal system/ immerse in sterile water DO NOT clamp chest tube for transport if 1-1.5L removed = becareful of reexpansion pulmonary edema or severe, symptomatic hypotension subQ emphysema from air leaking into tissue = cracking sensation = can cause swelling of head and neck meticulous sterile techniquw used during dressing changes report to HCP = drainage over 200mls in 1st hr, s/s resp distress, subQ emphy

Pericarditis Etiology and Pathophysiology

in the patient with an MI may be described as two distinct syndromes. first is acute pericarditis, which may occur within the first 48 to 72 hours after an MI. second is Dressler syndrome (late pericarditis), which occurs 4 to 6 weeks after an MI

rhinitis

inflam of nasal mucosa and mucosa os sinuses caused by infection - viral/bacterial common cold (coryza) - virus, spread person to person, droplets coexst with other disorders - asthma, allergies, chronic or acute, allergic allergin = incr histamine release and WBC in masal mucosa = mediators blind to blood vessles receptors causing cap leakakce = local edema/swelling findings: drainage (rhinorrhea), purulent, sneezing, pruritus of nose, throat, ears, itchy watery eyes, sore throat, red/inflamed nasal mucosa, low grade fever tx - rest (8-10hrs a day), incr fluids, humidifier meds - antihistamines (brompheniramine) leukotriene inhibitors (montelukast) mast cell stabilizers (cromolyn) used to block release of chemicals form WBC that bind with receptors in nasal tissues = prevent itching/edema, decongestants - phenylephrine - constric blood vessles = decr edema = ONLY 3-4 days bc rebound nasal congestion intranasal glucocorticoid spray - most effective, seasonal and perennial antipyretics and antibiotics AE = vertigo, HNT, urinary retention dx - allergy testing echinacea, vit C, zinc

tb complications

military tb headaches, neck stiffness, tired life threatening pericarditis - dyspnea, swollen neck veins, pleuritic pain, hypotension - bc heart doesnt have room to pump treat like tb pleural TB extrapulmonary, cheast pain, cough, gever, unilateral pleural effusion

chest tubes

20 inches long size 12F - 40F (over 36F = drain blood, med = drain fluid, small = air) pig tail = small and curved = keep them in place

The nurse is caring for a patient with pneumonia. If a pleural effusion is developing, the nurse would expect which finding? Barrel-shaped chest Paradoxical respirations Hyperresonance on percussion Localized decreased breath sounds

Answer: D Rationale: Clinical manifestations of pleural effusion include diminished breath sounds over the affected area, decreased movement of the chest on the affected side, dullness to percussion, dyspnea, cough, and occasional sharp and nonradiating chest pain that is worse on inhalation.

Nursing ManagementAcute Coronary Syndrome -Complications related to CPB

Bleeding and anemia from damage to RBCs and platelets Fluid and electrolyte imbalances Hypothermia as blood is cooled as it passes through the bypass machine Infections

Pacemakers - ECG monitoring for malfunction

Causes inappropriate firing Lack of pacing when needed leads to bradycardia or asystole Pacemaker malfunction primarily involves a failure to sense or a failure to capture. Failure to sense occurs when the pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately. This can result in the pacemaker firing during the excitable period of the cardiac cycle resulting in VT. Failure to sense is caused by fibrosis around the tip of the pacing lead, battery failure, sensing set too high, or dislodgement of the electrode. Failure to capture occurs when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction. This can result in serious bradycardia or asystole. Failure to capture is caused by pacer lead damage, battery failure, dislodgement of the electrode, electrical charge set too low, or fibrosis at the electrode tip.

Pneumonia Outcomes

Clear breath sounds Normal breathing patterns No signs of hypoxia Normal chest x-ray Normal WBC count Absence of complications related to pneumonia

latent tb meds

isoniazid and rifapentine 9months of meds

resp failure care

FIO2, ventiuri mask mobilize secretions cough/positioning augmenedted coughing = quad coughing = hands on anterolateral base of patients lungs, pt inhales and exhale push up on lungs = cough huffing cough = cough while say huff staged cough = sitting position, breath 3-4 times in and out by mouth, cough forward w/ pillow against diaphragm good lung down position hydration - 2-3 L a day humidification chest PT - if more 30 ml of sputum a day airway suction positive pressure ventilation - use if ventialtion and oygenation still low, use invasive or NIPPV (Bipap, cpap)

PE Important but not diagnostic

Important but not diagnostic Arterial blood gases Chest x-ray Electrocardiogram Troponin levels b-type natriuretic peptide ABG analysis is important, but not diagnostic. The PaO2 may be low because of inadequate oxygenation secondary to occluded pulmonary vasculature preventing matching of perfusion to ventilation. The pH is often normal unless respiratory alkalosis develops as a result of prolonged hyperventilation or to compensate for lactic acidosis caused by shock. Abnormal findings are usually identified on the chest x-ray (atelectasis, pleural effusion) and the ECG (ST segment and T wave changes), but they are not diagnostic for PE. Serum troponin levels and b-type natriuretic peptide (BNP) levels are frequently elevated but not diagnostic.

Aortic DissectionInterprofessional Care

Initial goal HR and BP control ↓ BP and myocardial contractility to diminish pulsatile forces within aorta Pain management

PE Interprofessional Care

Prevention—the key! Sequential compression devices Early ambulation Prophylactic anticoagulation

Thoracic endovascular aortic repair

TEVAR Standard to treat acute and chronic Type B aortic dissections with complications Similar to EVAR temporary lumbar drain = inserted for cerebrospinal fluid removal to reduce spinal cord edema and prevent paralysis. lumbar drain is used = strict aseptic techniques = avoid introducing infection.

tb dx

mantouz test 48-72 hours intradermal palpable, raised, harden area, 10mm or greater 5mm for immunocompromised if received calmette guerin vaccine in last 10 years = false + --> get cxray or quantiferon tb gold cxray - dected active lesions acid-fast bacilli smear and culture - suggests active infection, 3 early morning sputum samples, in negative airflow room

RotoProne Bed

The RotoProne Delta Therapy System allows clinicians to place patients in the prone position, safely and effectively. This product is not specifically indicated for the treatment of ARDS or VAP.

Changes Associated With Myocardial Ischemia

The isoelectric line is flat and represents those normal times in the cardiac cycle when the ECG is not recording any electrical activity in the heart. These times are as follows: (1) from the end of the P wave to the start of the QRS complex, (2) during the entire ST segment, and (3) from the end of the T wave to the start of the next P wave. Note the changes in the above visual. ST segment is depressed on left (note normal flat ST segment at same level of isoelectric line on right). ECG on right depicts T wave inversion. Patients with ischemia may display one or both changes.

resp failure dx

cxray = pul edema, cardiomegaly, diffuse infiltrates, infiltrates ECG = rule out cardiac involvement hemodynamic monitoring = pul cap wedge pressure with ARDs is low or normal (4-12mmhg)

pneumo vs hemo throax

air rises pneumo is higher up than hemo

bronchoscopy

to see larynx, trachea, bronchi NPO 4-8hrs before cough and deep breathing for elders Q2 complications laryngospasm - contraction of vocal cords = cant inhale pneumothroax aspiration

pneumonia education

use resp, nutrition, rehab continue meds, rest periods, hand hygein, no crowds, recovery is long, stop smoking, flu shot

Aortic AneurysmsGenetic Link

Bicuspid aortic valve Coarctation of aorta Turner's syndrome Autosomal dominant polycystic kidney disease Ehlers-Danlos syndrome Loeys-Dietz syndrome Marfan's syndrome The familial tendency is related to a number of congenital anomalies. specific collagen defects (e.g., Ehlers-Danlos syndrome) premature breakdown of vascular elastic tissue (e.g., Loeys-Dietz syndrome, Marfan's syndrome).

ADHF drug therapy

Diuretics Decrease volume overload (preload) Loop diuretics - Furosemide (Lasix) Vasodilators Reduce circulating blood volume and improve coronary artery circulation IV nitroglycerin Sodium nitroprusside Nesiritide (Natrecor) Morphine Reduces preload and afterload Relieves dyspnea and anxiety Positive inotropes β-agonists (dopamine, dobutamine, norepinephrine [Levophed]) Phosphodiesterase inhibitor (milrinone) Digitalis Morphine Morphine sulfate reduces preload and afterload. It is frequently used in the treatment of HF and acute coronary syndrome (see Chapter 33). It dilates both pulmonary and systemic blood vessels. When morphine is used, the patient often experiences relief from dyspnea and, consequently, the anxiety often associated with dyspnea. Use morphine cautiously in patients with ADHF. Morphine is related to more adverse events, including a greater need for mechanical ventilation, more ICU admissions, prolonged hospitalization, and higher mortality rates in these patients. Positive inotropes Inotropic therapy increases myocardial contractility. Drugs include β-agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], norepinephrine [Levophed]), the phosphodiesterase inhibitor milrinone (Primacor), and digitalis. The β-agonists are only used as a short-term treatment of ADHF. Milrinone is a phosphodiesterase inhibitor that has been called an inodilator. It increases myocardial contractility (inotropic effect) and promotes peripheral vasodilation. Inhibition of phosphodiesterase increases cyclic adenosine monophosphate (cAMP). This enhances calcium entry into the cell and improves myocardial contractility. Milrinone increases CO and reduces BP (decrease afterload). Like dopamine and dobutamine, this drug is available only for IV use. Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity. Digitalis is a positive inotrope that improves LV function. Digitalis increases contractility but also increases myocardial oxygen consumption. Because digitalis requires a loading dose and time to work, it is not recommended for the initial treatment of ADHF. Currently, inotropic therapy is only recommended for use in the short-term management of patients with ADHF who have not responded to conventional drug therapy (e.g., diuretics, vasodilators, morphine). Diuretics They act to decrease sodium reabsorption at various sites within the nephrons, thereby enhancing sodium and water loss. Loop diuretics (e.g., furosemide [Lasix]) can be given by IV push and act rapidly in the kidneys. Vasodilators IV nitroglycerin is a vasodilator that reduces circulating blood volume. It also improves coronary artery blood flow by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. When titrating IV nitroglycerin, monitor BP frequently (every 5 to 10 minutes) to avoid hypotension. Sodium nitroprusside (Nipride) is a potent IV vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. Complications of IV sodium nitroprusside include hypotension and thiocyanate toxicity, which can develop after 48 hours of use. Sodium nitroprusside is given in an ICU, since symptomatic hypotension is the main adverse effect. Nesiritide, given IV, is a recombinant form of BNP. It causes both arterial and venous dilation. The main hemodynamic effects of nesiritide include (1) a reduction in PAWP and (2) a decrease in systemic BP. Although classified as a vasodilator, nesiritide is also a neurohormonal blocking agent. It can be used for short-term treatment of ADHF. Nesiritide does not require titration after the initial IV bolus. Because the main adverse effect of nesiritide is symptomatic hypotension, monitor BP closely.

12-Lead ECG

each show a different point of the heart

thoracentesis

surgical perforation of the chest wall and pleural space with large bore hole needle dx - HF, inflam, infection, empyema, pneumonia, chest injuries check cell count, protein and glucose, enzymes, LDH, amylase, abnormal cells, culture use xray to find pleural effusion fluid is limited to 1L at a time to prevent reexpansion pulmonary edam complication mediastinal shift pneumothorax nleeding infection

VATS

video assisted thoracic surgery minimally invasive surgery real time 2 dimernional video image of insisde chest cavity dx and tx - disease of pleura, pul masses, nodules, mediastinal masses, interstial lung disease less discomfort, faster healing, decr LOS

A patient is admitted to the coronary care unit following a cardiac arrest and successful cardiopulmonary resuscitation. When reviewing the health care provider's admission orders, which order should the nurse question? Oxygen at 4 L/min per nasal cannula Morphine sulfate 2 mg IV every 10 minutes until the pain is relieved Tissue plasminogen activator (tPA) 100 mg IV infused over 3 hours IV nitroglycerin at 5 mcg/minute and increase 5 mcg/minute every 3 to 5 minutes

Answer: C Rationale: Traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation is a relative contraindication for the administration of fibrinolytic therapy.

Ambulatory Care aorta

Encourage patient to express concerns Instruct patient to gradually increase activities No heavy lifting Teach about signs and symptoms of complications Infection Neurovascular changes Fatigue, poor appetite, and irregular bowel habits are common. Any redness, swelling, increased pain, drainage from incisions, or fever greater than 100° F (37.8° C) should be reported to a HCP. Sexual dysfunction in male patients is common after aortic surgery. A referral to a urologist may be useful if erectile dysfunction occurs.

Aorta Nursing ManagementPlanning

Normal tissue perfusion Intact motor and sensory function No complications related to surgical repair Thrombosis Infection Rupture

Nursing Implementation Evaluation AKI

Regain and maintain normal fluid and electrolyte balance Adhere to the tx Experience no complications Have complete recovery

sinusitis

aka rhinosinusitis inflam of mucous membrane of one or more sinues usually maxillary or frontal swelling of mucosa can block drainage of secetions = sinus infection often occures after rhinitis associated with deviated septum, nasal polyps, inhaled air pollutions/cocaine, facial trauma, dental infection, loss of immune finction findings: nasal congestion, headache, facial pressure, worse when tilt head forward, cough, bloody drainage, tenderness of papitations, low grade fever dx - ct scan or xray, endoscopuc sinus cavity lavage or sugery to relieve obstruction humidification, saline spary, hot wet packs, incr fluids, incr rest, no air travel, swimming or diving, no ovaco meds: nasal decongestion - phenylephrine = decr swelling (rebound nasal congestion) broad spectrum antibiotics - amoxicillin NSAIDs, acetominophen, asprin contact provider if - severe headache, neck stiffness (nuchal rigidity), high fever complications = meningitics, encephalitis

resp failure care

mechanical vent with positive end expiratory pressure (PEEP) or positive airway pressure (CPAP) suction assess suputum color/amount/consistancy PEEP = can cause pneumothroax position for good ventilation oral care Q2 daily weights, I&O feedings 35-45 degrees alternative communication - pen/paper

AAA resections - renal issues

If extends above renal arteries or if cross-clamp must be applied above renal arteries Check adequate renal perfusion after clamp removal and before closure of incision Risk of postop renal complications ↑ significantly when repair is above renal arteries The risk of postoperative renal complications such as acute renal injury increases significantly in patients who have surgical repair of AAAs above the level of the renal arteries.

Pneumonia Complications

Complications develop more frequently in older individuals and those with underlying chronic diseases. Potential complications include the following: • Atelectasis (collapsed, airless alveoli) of one or part of one lobe may occur. These areas may clear with effective deep breathing and coughing, flutter device, spurometry • Pleurisy (inflammation of the pleura) may occur. • Pleural effusion (fluid in the pleural space) can occur. In most cases, the effusion is sterile and is reabsorbed in 1 to 2 weeks. Occasionally, effusions require aspiration by thoracentesis. • Bacteremia =Streptococcus pneumoniae and Haemophilus influenzae. • Pneumothorax can occur when air collects in the pleura space, causing the lungs to collapse. • Meningitis can be caused by Streptococcus pneumoniae. The patient with pneumonia who is disoriented, confused, or drowsy may have a lumbar puncture to evaluate the possibility of meningitis. • Acute respiratory failure is one of the leading causes of = pneumonia damages the lungs' ability to facilitate the exchange of oxygen and carbon dioxide across the alveolar-capillary membrane. • Sepsis/septic shock = can lead to shock and multisystem organ dysfunction syndrome (MODS) Lung abscess is not a common may occur with S. aureus -gram • Empyema = accumulation of purulent exudate in the pleural, requires antibiotic therapy and drainage of the exudate by a chest tube or open surgical drainage. atelectasis - airway inflammation and edema = aveolar collapse and incr risk of hypoxemia, SOB, diminished/no breath sounds, cxray bactermia - sepsis - pathogen into blood stream acute respiratory distress syndrome - hypoxemia, dyspnea worsens as bilateral pulmonary edema from noncardia prob, cxray shows ground glass appearance, glood gases show high arterial blood levels of CO2 (hypercarbia), O2 stat is low

Pneumonia Evaluation

Effective respiratory rate, rhythm, and depth of respirations Lungs clear to auscultation Reports pain control SpO2 ≥ 95 Free of adventitious breath sounds Clear sputum from airway

Pneumonia Ambulatory Care

Emphasize need to take full course of medication(s) Drug-drug and drug-food interactions Adequate rest, hydration (6-10 glasses) Avoid alcohol and smoking Cool mist humidifier Chest x-ray (6-8wks), vaccinations

RH Planning

Goals: Normal or Baseline heart function Resumption of daily activities without joint pain Verbalization of ability to manage the disease sequelae

Aorta

Largest artery Responsible for supplying oxygenated blood to essentially all vital organs

Nursing ManagementWhat is your nursing assessment?

Past health history: Previous history of CAD, chest pain/angina, MI, valve disease (e.g., aortic stenosis), heart failure, or cardiomyopathy; hypertension, diabetes, anemia, lung disease; hyperlipidemia Drugs: Use of antiplatelets/anticoagulants, nitrates, angiotensin-converting enzyme inhibitors, β-adrenergic blockers, calcium channel blockers; antihypertensive drugs; lipid-lowering drugs; over-the-counter drugs (e.g., vitamin and herbal supplements) History of present illness: Description of events related to current illness, including any self-treatments and response.

Acute Respiratory Distress Syndrome (ARDS)

Sudden progressive form of acute respiratory failure Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid Alveoli fill with fluid ARDS exists on a continuum. One way to assess the degree of impairment in gas exchange is to measure the PaO2/FIO2 (P/F) ratio. Under normal circumstances (e.g., PaO2 85 to 100 mm Hg; FIO2 0.21 [room air]), the P/F ratio would be greater than 400 (e.g., 95/0.21 = 452). With the onset and progression of lung injury and impairment in O2 delivery through the alveolar-capillary membrane, the PaO2 may remain lower than expected despite increased FIO2. The P/F ratio differentiates between mild, moderate, and severe ARDS.

Aorta PostopRenal perfusion status

Urinary output Fluid intake Daily weight CVP/PA pressure Blood urea nitrogen/creatinine In the immediate postoperative period, record hourly urine outputs. Decr renal perfusion = embolization of the aortic thrombus/plaque to one or both of the renal arteries. = ischemia of one or both kidneys. Hypotension, dehydration, prolonged aortic clamping during surgery, or blood loss can also lead to decreased renal perfusion.

fractured ribs

most common type of chest injury from blunt trauma 5-9 usually fractured bc least protected by chest muscles if splintered of displaces = can damage pleura, lungs, other organs pain during inspiration, shallow breathes, atelectasis, pneumoia bc decr chest wall movement and retained secretions tx - decr pain, strapping chest with tape or binder is NOT recommended bc limits chest expansion = atelectasis, NSAIDs, opioids, nevere blocks, deep breathing/coughing, spirometry

TB

mycobacterium tuberculosis airborne - min to hrs body encases the TB bacillus with collagen and other cells appear as Ghon tubercle on chest xray - hallmark classify - presentation (primary, latent, reactivated) and pulmonary or extrapulmonary

tidaling

normal fluctuation of the water within the water deal chamber is called disappears as lung expands bubbling middle chamber, air leak

Multidrug-resistant (MDR)

organisms are major problem in treatment Staphylococcus aureus, Gram-negative bacilli Risk factors = Advanced age, Immunosuppression, History of antibiotic use, Prolonged mechanical ventilation Primary culprits include MRSA and gram- negative bacilli. Antibiotic susceptibility tests can identify MDR organisms. The virulence of these organisms can severely limit the available and appropriate antimicrobial therapy. MDR organisms can also increase the morbidity and mortality risks associated with pneumonia.

resp failure labs

ABGs PaO2 = less 60 and sat less 90% on room air PaCO2 = over 45 pH = less 7.35 resp acidosis

Pneumonia Nursing Implementation

Health Promotion Teach hygiene, nutrition, rest, regular exercise to maintain natural resistance Cough or sneeze into elbow, not hands Avoid cigarette smoke Prompt treatment of URIs (rest/fluids, s/s over 7 days = medical care) Influenza and pneumococcal vaccination avoid exposure to people with URIs. Proper positioning to prevent aspiration Reposition patient every 2 hours - lung expansion, mobilize secretions In ICU Strict adherence to ventilator bundle (a group of interventions aimed at reducing the risk of VAP ) to prevent VAP altered LOC (e.g., side-lying, upright) that will prevent or minimize the risk of aspiration. Elevate head-of-bed 30 degrees and have sit up for all meals Assist with eating, drinking, taking meds as needed Assess for gag reflex Early mobilization Incentive spirometry Twice-daily oral hygiene orogastric or nasogastric tubes are small, any interruption in the integrity of the lower esophageal sphincter can allow reflux of gastric contents. Check skin for signs of breakdown. Prevent pneumonia in at risk patients: Pain management Strict medical asepsis Hand hygiene Respiratory devices Suctioning Avoid unnecessary antibiotic usage Use strict sterile aseptic technique when suctioning the trachea of a patient and use caution when handling ventilator circuits, tracheostomy tubing, and nebulizer circuits that can become contaminated from patient secretions. Acute Care Frequent assessments Prompt initiation of antibiotics Oxygen therapy Hydration Nutritional support Interprofessional collaboration Respiratory therapists Physical therapists Acute Intervention Breathing exercises Early ambulation Therapeutic positioning Pain management Position to minimize respiratory efforts (e.g., elevate the head of the bed and provide overbed table for patient to lean on) to reduce oxygen needs. slow deep breathing, turning, coughing respiratory muscle fatigue incentive spirometer as appropriate to promote alveolar ventilation. Collaboration with respiratory therapy for postural drainage and chest percussion is important. Perform a comprehensive assessment of pain to include location, characteristics, onset/duration, frequency, quality, intensity or severity of pain, and precipitating factors to determine appropriate interventions. Encourage patient to monitor own pain and to intervene appropriately to allow independence and prepare for discharge. Teach use of nonpharmacologic techniques (e.g., relaxation, guided imagery, music therapy, distraction, and massage) before, after, and, if possible, during painful activities; before pain occurs or increases; and along with other pain relief measures to relieve pain and reduce the need for analgesia. Use pain control measures before pain becomes severe because mild to moderate pain is controlled more quickly. Medicate before an activity to increase participation but evaluate the hazard of sedation to help minimize pain that will be experienced.

Interprofessional CareAcute Coronary Syndrome - Initial interventions

12-lead ECG Upright position Oxygen - keep O2 sat > 93% IV access Nitroglycerin (SL) and ASA (chewable) Statin Morphine It is extremely important to quickly diagnose and treat a patient with ACS to preserve heart muscle. Obtain a 12-lead ECG and start continuous ECG monitoring. Position the patient in an upright position unless contraindicated and initiate oxygen by nasal cannula to keep oxygen saturation above 93%. Establish an IV route to provide an access for emergency drug therapy. Give sublingual NTG and 162-325 mg of aspirin (chewable) if not given before arrival at the ED. A high-dose statin (atorvastatin [Lipitor]) is started if not already taking prior to the hospitalization. Morphine sulfate is given for pain unrelieved by NTG.

pleural drainage

1st compartment - receives fluid and air from pleural or mediastinal space, fluid stays here while expelled air vents to the secondary compartment 2nd compartment - water seal chamber contains 2 cm of water, one way valve, incoming air enters from collection chamber and bubbles up through the water, water prevents back flow of air into the patient 3rd compartment - suction control chamed, 2 types water and dry, water = used column of water to control the amound of suction, chambed filled with 20cm of water, amont of suction is generated by amount of water dry = no water, visual alter that says if its working amont of bubbling doesnt incr suction brisk bubbles = pneumothorac initially interm bubbles = exhale, coughing, sneezing no bubbles = lung is healed or occulded tube

Atypical myobacteria

30 kinds that do not cause TB, but do cause pulmonary disease, lymphadenitis, skin or shoft tissue disease, disseminated disease different from tb clinically and radiologically, but can be differentiated by bacteriologic culture not airborne, not droplets found in tap water, soil, feces, house dust (3rd world country) Mycobacterium avium - MAC - aerosols, from baths, hot spas, swinning pools, and is a cause of atypical myobacteria pulmonary infections, but only a small number get MAC people immunosuppressed (HIV/AIDS) or chronic pulmonary disease are at risk treatment is like TB - depends on bacteria, more antibiotics than normal

Hospital-Acquired Pneumonia (HAP)

48 hours or longer after hospitalization and not present at time of admission VAP: 48 hours after endotracheal intubation Associated with longer hospital stays, increased costs, sicker patients, and increased risk of morbidity and mortality HAP, previously known as nosocomial pneumonia, is a pneumonia in a nonintubated Ventilator-associated pneumonia (VAP), also a type of HAP, refers to pneumonia that occurs more than 48 hours after endotracheal intubation Once the dx of HAP or VAP is made, treatment of pneumonia is initiated based on known risk factors, early versus late onset, and probable organism. Antibiotic therapy adjusted once the results of sputum cultures identify the exact pathogen.

Aortic AneurysmInterprofessional Care threshold

5.5 cm is threshold for repair Intervention at >5 cm in women with AAA Surgical intervention may occur sooner if the patient has a genetic disorder (e.g., Marfan's, Ehlers-Danlos syndrome), the aneurysm expands rapidly, if it becomes symptomatic, or if the risk of rupture is high. A careful review of body systems is necessary to identify any co-morbidities, especially of the lungs, heart, or kidneys, Correction of existing carotid and/or coronary artery blockages may be needed before the aneurysm is repaired. If ruptured, emergent surgical intervention required 90% mortality with ruptured AAAs

Temporary Transvenous Pacemaker

A transvenous pacemaker consists of a lead or leads that are threaded transvenously to the right atrium and/or right ventricle and attached to the external power source Most temporary transvenous pacemakers are inserted in emergency departments and critical care units in emergency situations. They provide a bridge to insertion of a permanent pacemaker or until the underlying cause of the dysrhythmia is resolved.

Stages of Edema Formation in ARDS

A, Normal alveolus and pulmonary capillary. B, Interstitial edema occurs with increased flow of fluid into the interstitial space. C, Alveolar edema occurs when fluid crosses the blood-gas barrier.

Proning

A, Turning patient prone on Vollman Prone Positioner. B, Patient lying prone on Vollman Prone Positioner.

acute decompensated HF clinical manifestations

ADHF sudden onset of s/s of HF EMERGENCY pulmonary and systemic congestion due to incr left sided and right sided filling pressures early = incr pulmonary venous pressure = incr RR = decr PaO2 later = interstilial edema = tachypnea further = alveolar edema = resp acidemia can look like pulmonary edema life threatening situation = alveoli fill w/ fluid most common w/ left sided HF Acute decompensated HF (ADHF) is defined as the sudden onset of signs and symptoms of HF, requiring urgent medical care. The universal finding in ADHF is pulmonary and systemic congestion due to elevated left-sided and right-sided filling pressures. In acute decompensated HF (ADHF), the pulmonary venous pressure increases caused by failure of the LV. This results in engorgement of the pulmonary vascular system. As a result, the lungs become less compliant, and there is increased resistance in the small airways. To help compensate, the lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (Pao2). If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove. Interstitial edema occurs at this point. Tachypnea develops and the patient becomes symptomatic (e.g., short of breath). If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema). As the disruption becomes worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid. This is accompanied by a worsening of the arterial blood gas values (i.e., lower Pao2 and possible increased partial pressure of carbon dioxide in arterial blood [Paco2] and progressive respiratory acidemia). ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid. The most common cause of pulmonary edema is left-sided HF secondary to CAD.

Ventricular TachycardiaTorsades de Pointes

Torsades de pointes (French for "twisting of the points") is polymorphic VT associated with a prolonged QT interval of the underlying rhythm. all over the place

acute resp distress syndrome

ARDS acute resp failure with mortality rate of 60% systematic inflam responce injuries the alveolar cap membrane becomes permeable to large molecules and lung space is fliied with fluid reduction of surfactant weakens alveoli = collpase or filling w/ fluid = worse edema risk: lung damage, aspiration, emboli, pnuemonia, sepsis, near drowning, truama, transfusion, CNS damage, smoke, gas, drugs/overdoses dyspnea, bilateral noncardiogenic pulm edema, decr lung compliance, dense patchy bilateral pul infiltraces, severe hypoezmia (despite admin of 100% O2)

Aortic AneurysmsDefinition

Abdominal aortic aneurysms (AAA) ¾ occur in abdominal aorta ¼ occur in thoracic aorta Most occur below renal arteries The larger aneurysm, the greater risk of rupture

Tension pneumothorax

Accumulation of air in pleural space that does not escape Causes mediastinal shift and hemodynamic instability Can occur with open or closed pneumothorax continued accumulation of air in the pleural space = compression of the lung on the affected side and pressure on the heart and great vessels, pushing them away from the affected side. mediastinum shifts toward the unaffected side, compressing the 'good' lung, which further compromises oxygenation. pressure increases, venous return is decreased, and cardiac output falls. Tension pneumothorax may result from either an open or a closed pneumothorax. In an open chest wound, a flap may act as a one-way valve. Thus air can enter on inspiration but cannot escape. can occur with mechanical ventilation and resuscitative efforts. It can also occur if chest tubes are clamped or become blocked in a patient with a pneumothorax. Unclamping the tube or relief of the obstruction may correct this situation. Tension pneumothorax is a medical emergency, with both the respiratory and cardiovascular systems affected. Manifestations include dyspnea, marked tachycardia, tracheal deviation, decreased or absent breath sounds on the affected side, neck vein distention, cyanosis, and profuse diaphoresis. If the tension in the pleural space is not relieved, the patient is likely to die from inadequate cardiac output or severe hypoxemia. Treat with needle decompression and chest tube insertion (will discuss further later in this PowerPoint presentation).

Comparison of AKI with CKD

Acute kidney injury (AKI) is the term used to encompass the entire range of the syndrome, very slight deterioration in kidney function to severe impairment. AKI = rapid loss of kidney function, rise in serum creatinine level and/or a decr urine output. severity of dysfunction can range from a small incr in serum creatinine or decr in urine output to the development of azotemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood). AKI can develop over hours or days with progressive incr blood urea nitrogen (BUN), creatinine, K, w/ or w/o decr in urine output. aki = sudden, death from infection ckd = gradula and death from cardio

Pneumonia Nutritional Therapy

Adequate hydration Prevent dehydration Thin and loosen secretions Adjust for older adults, patients with heart failure, those with preexisting respiratory conditions High calorie, small, frequent meals Monitor for weight loss

PE Evaluation

Adequate tissue perfusion and respiratory function Adequate cardiac output Increased level of comfort Prevention of further recurrence of PE

RH Nursing Implementation

Adequate treatment of streptococcal pharyngitis prevents initial attacks of RF tx = oral penicillin V (Penicillin VK) or amoxicillin (Moxatag) 10 days if allergic to penicillin = narrow-spectrum cephalosporin (e.g., cephalexin [Keflex]), clindamycin (Cleocin), azithromycin (Zithromax) is used Therapy requires strict adherence to the full course of treatment. Give salicylates, NSAIDs, and corticosteroids as ordered and monitor fluid intake as appropriate. rest relief of joint pain Apply heat = joint pain. symptoms have subsided = the patient without carditis can walk. patient has carditis with HF = bed rest

Aortic AneurysmsRisk Factors

Age Male gender High BP Coronary artery disease Family history High cholesterol Lower extremity PAD Carotid artery disease Previous stroke Tobacco use is the most important modifiable risk factor. Being overweight or obese

Health Promotion Aorta

Alert for opportunities to teach health promotion to patients and their caregivers Encourage patient to reduce cardiovascular risk factors These measures help ensure graft patency after surgery Examples of risk factors include BP control, smoking cessation (see Chapter 10), increasing physical activity, and maintaining normal body weight and serum lipid levels.

Aortic AneurysmsClassification - False aneurysm

Also called pseudoaneurysm Not an aneurysm Disruption of all layers of arterial wall = Results in bleeding contained by surrounding structures False aneurysms may result from trauma or infection, or may occur after peripheral artery bypass graft surgery at the site of the graft-to-artery anastomosis. result from arterial leakage after removal of cannulae (e.g., lower extremity arterial catheters, intraaortic balloon pump devices).

Locations and Patterns of Angina and MI

Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms. Many people with angina complain of indigestion or a burning sensation in the epigastric region. The sensation may also be felt between the shoulder blades. Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as not being heart related. Some patients, especially women and older adults, report atypical symptoms of angina including dyspnea, nausea, and/or fatigue. This is referred to as angina equivalent.

Aortic AneurysmClinical Manifestations - Ascending aorta/aortic arch

Angina Transient ischemic attacks Coughing SOB Hoarseness and/or dysphagia If presses on superior vena cava Decr venous return = Distend neck veins = edema of face and arms Ascending aorta and aortic arch aneurysms can cause (1) angina from decreased blood flow to the coronary arteries (2) transient ischemic attacks from decreased blood flow to the carotid arteries (3) coughing, SOB, hoarseness, dysphagia = pressure on laryngeal nerve.

A patient's ABG results include pH 7.31, Paco2 50 mm Hg, Pao2 51 mm Hg, and HCO3 24 mEq/L. Oxygen is administered at 2 L/min, and the patient is placed in high-Fowler's position. An hour later, the ABGs are repeated with results of pH 7.36, Paco2 40 mm Hg, Pao2 60 mm Hg, and HCO3 24 mEq/L. What is most important for the nurse to do? Increase the oxygen flow rate to 4 L/min. Document the findings in the patient's record. Reposition the patient in a semi-Fowler's position. Prepare the patient for endotracheal intubation and mechanical ventilation.

Answer: A Rationale: The initial arterial blood gas (ABG) report indicates partially compensated respiratory acidosis with moderate hypoxemia. The next ABG results indicate improvement, but the hypoxemia continues (Pao2 remains low). The patient should receive a higher concentration of oxygen to treat hypoxemia.

A 56-year-old normally healthy patient at the clinic is diagnosed with bacterial community-acquired pneumonia. Before treatment is prescribed, the nurse asks the patient about an allergy to amoxicillin erythromycin sulfonamides cephalosporins

Answer: B macrolides (erythromycin) or doxycycline. If the patient is allergic to macrolides, doxycycline would be prescribed.

A patient in the coronary care unit develops ventricular fibrillation. The first action the nurse should take is to Perform defibrillation. Initiate cardiopulmonary resuscitation. Prepare for synchronized cardioversion. Administer IV antidysrhythmic drugs per protocol.

Answer: B Rationale: Immediate treatment for ventricular fibrillation is the initiation of cardiopulmonary resuscitation, followed by the use of defibrillation and definitive drug therapy according to advanced cardiac life support guidelines.

The most significant factor in long-term survival of a patient with sudden cardiac death is Absence of underlying heart disease. Rapid institution of emergency services and procedures. Performance of perfect technique in resuscitation procedures. Maintenance of 50% of normal cardiac output during resuscitation efforts.

Answer: B Rationale: Rapid cardiopulmonary resuscitation and prompt defibrillation (with an automated external defibrillator) and early advanced cardiac life support can produce high long-term survival rates for a witnessed arrest.

A patient with severe chronic lung disease is hospitalized with respiratory distress. Which finding would suggest to the nurse that the patient has developed rapid decompensation? An SpO2 of 86% A blood pH of 7.33 Agitation or confusion PaCO2 increases from 48 to 55 mm Hg

Answer: C Rationale: It is especially important to monitor specific and nonspecific signs of respiratory failure in patients with chronic lung disease because a small change can cause significant decompensation. Immediately report any change in mental status, such as agitation, combative behavior, confusion, or decreased level of consciousness.

When assessing a patient with sepsis, which finding would alert the nurse to the onset of acute respiratory distress syndrome (ARDS)? SpO2 of 80% Use of accessory muscles of respiration Fine, scattered crackles on auscultation of the chest ABGs of pH 7.33, Paco2 48 mm Hg, and Pao2 80 mm Hg

Answer: C Rationale: The initial presentation of acute respiratory distress syndrome is often subtle. At the time of the initial injury, and for several hours to 1 to 2 days afterward, the patient may not experience respiratory symptoms, or the patient may exhibit only dyspnea, tachypnea, cough, and restlessness. Chest auscultation may be normal or may reveal fine, scattered crackles.

Following an aortic aneurysm repair, the patient suddenly develops severe pain in the right lower extremity. The right pedal pulse is decreased and the right foot is cool and pale. Which complication should the nurse suspect? Hypothermia Wound infection Bleeding from the graft site Embolization or graft occlusion

Answer: D Rationale: A decreased or absent pulse together with a cool, pale, mottled, or painful extremity may indicate embolization or graft occlusion.

The nurse would interpret an induration of 5 mm resulting from tuberculin skin testing as a positive finding in which patient? A patient with a history of illegal IV drug use A patient with diabetes and end-stage kidney disease A patient who immigrated from India 3 months ago A patient who is human immunodeficiency virus- infected

Answer: D Rationale: Induration of 5 mm in an HIV-infected person is considered a positive reaction.

Which assessment would indicate to the nurse that a patient has oliguria related to an intrarenal acute kidney injury? Urinary sodium levels are low. The serum creatinine level is normal. Oliguria is relieved after fluid replacement. Urine testing reveals a specific gravity of 1.010.

Answer: D Rationale: The urine specific gravity in oliguria of intrarenal acute kidney injury will be fixed at 1.010. This value reflects tubular damage with loss of concentrating ability by the kidneys. The serum creatinine level is above normal in oliguria of intrarenal acute kidney injury. Urinary secretion of sodium increases with oliguria of intrarenal acute kidney injury. Prerenal oliguria related to hypovolemia will usually respond to fluid replacement.

aorta Infection

Antibiotic administration Assessment of body temperature Monitoring of WBC Adequate nutrition Observe surgical incision for signs of infection All IV, arterial, and CVP or PA catheter insertion sites should be cared for by using strict aseptic technique because they are ports of entry for bacteria. Meticulous perineal care for the patient with an indwelling urinary catheter is essential to minimize the risk of urinary tract infection. Keep surgical incisions clean and dry. An adequate BP is important to maintain graft patency. Prolonged low BP may result in graft thrombosis. Drug therapy for severe hypertension consists of IV diuretics (e.g., furosemide [Lasix]) or IV antihypertensive agents (e.g., nitroprusside [Nipride], esmolol [Brevibloc], labetalol [Normodyne]).

pneumonia Three ways organisms reach lungs:

Aspiration from nasopharynx or oropharynx Inhalation of microbes present in air Hematogenous spread from primary infection elsewhere in body

PE Drug Therapy

Anticoagulation Low-molecular-weight heparin (LMWH) Unfractionated IV heparin Warfarin (Coumadin) Fibrinolytic agents Tissue plasminogen activator (tPA) Alteplase (Activase) Immediate anticoagulation is required for patients with PE. Subcutaneous administration of low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox]) or fondaparinux has been found to be safer and more effective than unfractionated heparin. It is the recommended choice of treatment for patients with acute PE, administered once daily. Advantages of LMWH over unfractionated heparin include greater bioavailability, can be administered subcutaneously, longer duration of therapeutic effect, and monitoring the aPTT is not necessary or useful. Unfractionated IV heparin can be as effective but is more difficult to titrate to therapeutic levels. Warfarin (Coumadin), an oral anticoagulant, should also be initiated at time of diagnosis. Warfarin should be administered for at least 3 months, and then reevaluated. Alternatives to warfarin include apixaban (Eliquis), dabigitran (Pradaxa), and endoxaban (Savaysa). Anticoagulant therapy may be contraindicated if the patient has complicating factors such as blood dyscrasias, hepatic dysfunction causing alterations in the clotting, overt bleeding, a history of hemorrhagic stroke, or heparin-induced thrombocytopenia (HIT). Although not common, some HCPs use direct thrombin inhibitors in the treatment of PE. Similarly, fibrinolytic agents, such as tissue plasminogen activator (tPA) or alteplase (Activase), may help dissolve the pulmonary embolus and the source of the thrombus in the pelvis or deep leg veins, thereby decreasing the likelihood of recurrent emboli.

Aortic DissectionComplications

Aorta may rupture Results in exsanguination and death Hemorrhage in mediastinal, pleural, or abdominal cavities Occlusion of arterial supply to vital organs Symptoms of spinal cord ischemia range from weakness and decr sensation and rarely to complete lower extremity paralysis. Renal ischemia can lead to renal failure. Manifestations of abdominal (mesenteric) ischemia = abdominal pain, decr bowel sounds, altered bowel function, and bowel necrosis.

Implantable Cardioverter-Defibrillator (ICD)

Appropriate for patients who: survived SCD spontaneous sustained VT syncope with inducible ventricular tachycardia/fibrillation during EPS high risk for future life-threatening dysrhythmias -cardiomyopathy decr heart mortality rates in these patients. Consists of a lead system placed via subclavian vein to the endocardium Sensing system monitors HR and rhythm - delivering 25 joules or less to heart when detects lethal dysrhythmia A battery-powered pulse generator is implanted subcutaneously, over pectoral muscle, patient's nondominant side. similar in size to a pacemaker. The ICD sensing system monitors the HR and rhythm, and identifies VT or VF. After the sensing system detects a lethal dysrhythmia, the device delivers a 25-joule or less shock to the patient's heart. If the first shock is unsuccessful, the device recycles and can continue to deliver shocks. Overdrive pacing for tachycardias Backup pacing for bradycardias S-ICD In addition to defibrillation capabilities, ICDs are equipped with antitachycardia and antibradycardia pacing capabilities. These devices use algorithms that detect dysrhythmias and determine the appropriate response. They can initiate overdrive pacing of supraventricular and ventricular tachycardias, sparing the patient painful defibrillator shocks. They also provide backup pacing for bradydysrhythmias that may occur after defibrillation discharges. Preprocedure and postprocedure for ICD = permanent pacemaker The S-ICD pulse generator is placed under the skin on the left side of the chest and the electrode is placed under the skin above the sternum. The system delivers a shock when VT or VF is detected. Since the S-ICD does not have any electrodes implanted in the heart, it has no pacing capability. body image, recurrent dysrhythmias, pain, anxiety expectation of pain with ICD discharge (described as a feeling of a blow to the chest)

Pulmonary Edema

As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the alveolar-capillary interface. A. Normal relationship. B. Increased pulmonary capillary hydrostatic pressure causes fluid to move from the vascular space into the pulmonary interstitial space. C. Lymphatic flow increases in an attempt to pull fluid back into the vascular or lymphatic space. D. Failure of lymphatic flow and worsening of left heart failure result in further movement of fluid into the interstitial space and into the alveoli.

First-Degree AV Block

Associated with disease states and certain drugs Typically not serious Patients asymptomatic No treatment Monitor for changes in heart rhythm longer than 0.20 P-R First-degree AV block is associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (e.g., hypokalemia), vagal stimulation, digoxin, β-blockers, CCC, and flecainide. usually not serious but can be a sign of higher degrees of AV block. First-degree AV block is a type of AV block in which every impulse is conducted to the ventricles but the time of AV conduction is prolonged. After the impulse moves through the AV node, the ventricles usually respond normally. HR is normal and rhythm is regular. The P wave is normal, the PR interval is prolonged (greater than 0.20 second), and the QRS complex usually has a normal shape and duration.

TB Drug Therapy - Vaccine

Bacille-Calmette-Guérin (BCG) vaccine to prevent TB is currently in use in many parts of world In United States, not recommended except for very select individuals Can result in positive PPD reaction Bacille-Calmette-Guérin (BCG) vaccine is a live, attenuated strain of Mycobacterium bovis. The vaccine is given to infants in parts of the world where there is a high prevalence of TB. The BCG vaccine should be considered only for very select individuals who meet specific criteria (e.g., health care workers continually exposed to patients with MDR-TB and infection control precautions are not successful). BCG = false-positive TST. IGRA = not affected.

RH Evaluation

Be able to perform ADLs with minimal fatigue and pain Adhere to treatment regimen Express confidence in managing disease Use measures to prevent complications

EVAR

Bifurcated (two branched) endovascular stent grafting of an aneurysm. A, The insertion of a woven polyester tube (graft) covered by a tubular metal web (stent). B, The stent graft is inserted through a large blood vessel (e.g., femoral artery) using a delivery catheter. The catheter is positioned below the renal arteries in the area of the aneurysm. C, The stent graft is slowly released (deployed) into the blood vessel. When the stent comes in contact with the blood vessel, it expands to a preset size. D, A second stent graft can be inserted in the contralateral (opposite) vessel if necessary. E, Fully deployed bifurcated stent graft.

Pulmonary Embolism

Blockage of one or more pulmonary arteries by thrombus, fat or air embolus, or tumor tissue Obstructs alveolar perfusion Most commonly affects lower lobes Pulmonary embolism (PE) is the blockage of one or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue. The word embolus derives from a Greek word meaning "plug" or "stopper." Emboli are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system. A pulmonary embolus consists of material that gains access to the venous system and then to the pulmonary circulation. The embolus travels with the blood flow through ever-smaller blood vessels until it lodges and obstructs perfusion of the alveoli. Approximately 10% of patients with massive PE die within the first hour. Treatment with anticoagulants significantly reduces mortality. Describe the figures—the one on the left demonstrates decreased perfusion beyond the embolus location as the pulmonary embolus blocks blood flow. The lung is ventilated, but gas exchange is decreased as there is no blood supply to the ventilated alveoli. The picture on the right depicts a large pulmonary embolus located within a pulmonary vessel.

Nursing ManagementAcute Coronary Syndrome

CABG: postoperative nursing care Assess patient for bleeding Monitor hemodynamic status Assess fluid status Replace blood and electrolytes PRN Restore temperature Monitor for atrial fibrillation (which is common) Assessing the patient for bleeding (e.g., chest tube drainage, incision sites) Hemodynamic monitoring Checking fluid status Replacing electrolytes as needed Restoring temperature (e.g., warming blankets) Postoperative dysrhythmias, specifically atrial dysrhythmias, are common in the first 3 days after CABG surgery. Β-Blockers should be restarted as soon as possible after surgery (unless contraindicated) to reduce the incidence of AF. CABG: postoperative nursing care Surgical site care Radial artery harvest site Leg incisions Chest incision Pain management DVT prevention Pulmonary hygiene Cognitive dysfunction Nursing care for the patient with a CABG involves caring for the surgical sites (e.g., chest, arm, leg). Care of the leg incision is minimal since endoscopy is used to harvest the vein. Chest incisions are usually closed with Dermabond and do not require dressings. Management of the chest wound, which involves a sternotomy, is similar to that of other chest surgeries. Care of the radial artery harvest site includes monitoring sensory and motor function of the hand. The patient with radial artery harvest should be on a calcium channel blocker for approximately 3 months to reduce the incidence of arterial spasm at the arm or anastomosis site. Other interventions include strategies to manage pain and prevent venous thromboembolism (e.g., early ambulation, sequential compression device) and respiratory complications (e.g., use of incentive spirometer, splinting during coughing and deep-breathing exercises). Postoperatively, patients may experience some cognitive dysfunction. This includes impairment of memory, concentration, language comprehension, and social integration. Patients may inexplicably cry or become teary. Postoperative cognitive dysfunction (POCD) can manifest days to weeks after surgery and may remain a permanent disorder.

Pulseless Electrical Activity treatment

CPR followed by intubation and IV epinephrine Treatment is directed toward correction of the underlying cause

Rib Fractures

Can damage pleura, lungs, and internal organs S/S = Pain, Splinting, Shallow respirations, Atelectasis and pneumonia dilaudid and morphine IV most common type of chest injury resulting from blunt trauma. Ribs 5 through 9 are most commonly fractured because they are the least protected by chest muscles. fractured rib is splintered or displaced = damage pleura, lungs, and other internal organs. Atelectasis and pneumonia = bc of decreased chest wall movement and retained secretions. Treatment NO strapping or binding chest USE NSAIDs, opioids, nerve blocks Deep breathing and coughing Incentive spirometry decr pain so that the pt can breathe adequately and clear secretions. Strapping/thoracic binder not recommended = limits chest expansion and predisposes the individual to atelectasis. Nonsteroidal antiinflammatory drugs, opioids, and thoracic nerve blocks can be used to reduce pain and aid with deep breathing and coughing.

TB Ambulatory Care, Nursing Implementation

Can go home even if cultures positive Monthly sputum cultures Teach patient how to minimize exposure to others Ensure that patient can adhere to treatment Negative cultures are needed to declare the patient not infectious Patients who have responded clinically are discharged home (even with positive cultures) if their household contacts have already been exposed and the patient is not posing a risk to others. A sputum specimen for AFB smear and culture should be obtained at a minimum of monthly intervals until two consecutive specimens are negative on culture. More frequent AFB smears may be useful to assess the early response to treatment and to provide an indication of infectiousness. Teach patient how to minimize exposure to close contacts and household members. Homes should be well-ventilated, especially the areas where the infected person spends a lot of time. While still infectious, the patient should sleep alone, spend as much time as possible outdoors, and minimize time in congregate settings or public transportation. Teach the patient and caregiver about compliance with the prescribed regimen. This is very important as most treatment failures occur because the patient neglects to take the drug, discontinues it prematurely, or takes it irregularly. Strategies to improve adherence to drug therapy include teaching and counseling, reminder systems, incentives or rewards, contracts and DOT. Notify health department Teach symptoms of recurrence Instruct about factors that could reactivate TB Smoking cessation Notification of the public health department is required. The public health nurse will be responsible for follow-up on household contacts and assessment of the patient for compliance. If compliance is an issue, the public health agency may be responsible for DOT. Most individuals can be considered adequately treated when the therapy regimen has been completed and there is evidence of negative cultures, clinical improvement, and improvement on chest x-ray. Because about 5% of individuals experience relapses, teach the patient to recognize the symptoms that indicate recurrence of TB. If these symptoms occur, the patient should seek immediate medical attention. Instruct the patient about certain factors that could reactivate TB, such as immunosuppressive therapy, malignancy, and prolonged debilitating illness. If the patient experiences any of these events, the HCP must be told so that TB can be closely monitored for reactivation. In some situations, it is necessary to put the patient on anti-TB therapy. Because smoking is associated with poor outcomes in TB, patients should be encouraged to quit. Provide patients with teaching and resources to help them stop smoking.

Clinical Manifestations RH

Carditis 1. Heart murmur or murmurs (Mitral or Aortic regurgitation or Mitral Stenosis) 2. Heart Enlargement/Heart failure secondary to myocarditis 3. Pericarditis resulting in muffled heart sounds, chest pain, pericardial friction rub, or signs of effusion. Monoarthritis or Polyarthritis Sydenhams Chorea Erythema Subcutaneous Nodules Monoarthritis or polyarthritis is the most common finding in RF = knees, ankles, elbows, and wrists Sydenham's chorea is the major CNS manifestation of RF. It is often a delayed sign occurring several months after the initial infection = involuntary movements, especially of the face and limbs; muscle weakness; and disturbances of speech and gait. Erythema marginatum lesions are a less common feature of RF. The bright pink, nonpruritic, maplike macular lesions occur mainly on the trunk and proximal extremities and may be exacerbated by heat (e.g., warm bath). Subcutaneous nodules, usually associated with severe carditis, are firm, small, hard, painless swellings located over extensor surfaces of joints, particularly the knees, wrists, and elbows.

Pneumothorax

Caused by air entering pleural cavity Positive pressure in cavity = lung to partially or fully collapse suspected after any trauma to chest wall Normally, negative subatmospheric pressure exists between the visceral pleura (surrounding the lung) and the parietal pleura (lining the thoracic cavity), known as the pleural space. This space contains a few milliliters of lubricating fluid to reduce friction when the tissues move. When air enters this space, the change to positive pressure causes a partial or complete lung collapse. As the volume of air in the pleural space increases, the lung volume decreases. In an open pneumothorax, air enters through an opening in the chest wall and parietal (outer) lining of the pleura. A closed pneumothorax occurs when the visceral (inner) lining of the pleura is disrupted, allowing air to enter the pleural space from the lung. There is no external wound. Clinical manifestations: Variable Mild tachycardia and dyspnea → severe respiratory distress Absent breath sounds over affected area x-rays - air, fluid, decr lung volume if small = mild tachycardia, dyspnea may be the only manifestations. if large area = respiratory distress, shallow, rapid respirations; dyspnea; air hunger; decr oxygen

Acute Kidney InjuryEtiology and PathophysiologyPrerenal

Causes are factors that reduce systemic circulation, causing decr in renal blood flow Severe dehydration, heart failure, ↓ CO decr GFR = Causes oliguria Autoregulatory mechanisms attempt to preserve blood flow prerenal oliguria from the oliguria of intrarenal AKI. In prerenal oliguria there is no damage to the kidney tissue (parenchyma). The oliguria is caused by a decr in circulating blood volume (e.g., severe dehydration, heart failure, decreased cardiac output) is readily reversible w/ tx. With a decr in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone attempt to preserve blood flow to essential organs. Prerenal azotemia results in a reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention, and decreased urine output. Prerenal conditions contribute to intrarenal disease if renal ischemia is prolonged. If decreased perfusion persists for an extended time, the kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage).

Acute Kidney InjuryEtiology and PathophysiologyIntrarenal

Causes include conditions that cause direct damage to kidney tissue Prolonged ischemia, nephrotoxins Hemoglobin released from hemolyzed RBCs Myoglobin released from necrotic muscle cells Nephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules. Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction. Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI. Acute tubular necrosis (ATN) Results from ischemia, nephrotoxins, or sepsis Severe ischemia causes disruption in basement membrane Nephrotoxic agents cause necrosis of tubular epithelial cells Potentially reversible Acute tubular necrosis (ATN) is the most common intrarenal cause of AKI and is primarily the result of ischemia, nephrotoxins, or sepsis Severe kidney ischemia causes a disruption in the basement membrane and patchy destruction of the tubular epithelium. Nephrotoxic agents = necrosis of tubular epithelial cells = slough off and plug tubules. ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates. ATN is the most common cause of AKI for hospitalized patients. Risks = surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, prolonged hypotension, and nephrotoxic agents

Continuous Lateral Rotation

TotalCare Spo2 RT® bed system offers continuous lateral rotation therapy and percussion and vibration therapies. Patients can easily and quickly be repositioned.

Acute Kidney InjuryEtiology and Pathophysiology Postrenal

Causes include mechanical obstruction of outflow Benign prostatic hyperplasia Prostate cancer Calculi Trauma Extrarenal tumors Bilateral ureteral obstruction Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function. most common postrenal causes BPH, prostate cancer, calculi, trauma, extrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive decline in kidney function. If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis. Postrenal causes of AKI account for less than 10% of AKI cases.

Complications of Myocardial Infarction - Papillary muscle dysfunction or rupture

Causes mitral valve regurgitation Aggravates an already compromised LV → rapid clinical deterioration Left ventricular aneurysm Myocardial wall becomes thinned and bulges out during contraction Leads to HF, dysrhythmias, and angina Papillary muscle dysfunction may occur if the infarcted area includes or is near the papillary muscle that attaches to the mitral valve. Papillary muscle rupture is a rare and life-threatening complication. It causes immediate and massive mitral valve regurgitation with no time for the heart to compensate. Dyspnea, pulmonary edema, and decreased CO result from the backup of blood in the left atrium. This condition aggravates an already damaged LV by reducing CO even further. There is rapid clinical decline of the patient. Treatment includes afterload reduction with nitroprusside (Nipride) and/or IABP therapy, and immediate cardiac surgery with mitral valve repair or replacement. Left ventricular aneurysm results when the infarcted heart wall is thin and bulges out during contraction. This can develop within a few days, weeks, or months. It is more common with anterior MIs. The patient with a ventricular aneurysm may experience HF, dysrhythmias, and angina. Besides ventricular rupture, which is usually fatal, ventricular aneurysms can hide thrombi that can lead to an embolic stroke. Anticoagulation therapy is recommended for these patients if not contraindicated.

Cardiac Tamponade: Clinical Manifestations

Chest Pain Confusion Anxious Agitation/Restless Muffled Heart Sounds Narrowed Pulse Pressure Tachypnea Tachycardia Jugular Vein Distention Pulsus Paradoxus The patient with cardiac tamponade may report chest pain and is often confused, anxious, and restless. As the compression of the heart increases, there is decreased cardiac output (CO), muffled heart sounds, and narrowed pulse pressure. The patient develops tachypnea and tachycardia. Neck veins are usually markedly distended because of increased jugular venous pressure. Pulsus paradoxus, which may be present, is a decrease in systolic BP during inspiration that is exaggerated in cardiac tamponade (Measurement of Pulsus Paradoxus Table 36-5). In a patient with a slow onset of a cardiac tamponade, dyspnea may be the only clinical manifestation.

Chest Tubes and Pleural Drainage

Chest drainage unit. This unit has 3 chambers: (1) collection chamber; (2) water-seal chamber; and (3) suction control chamber. Suction control chamber requires a connection to a wall suction source that is dialed up higher than the prescribed suction for the suction to work. In the water suction unit, the suction control chamber controls the wall suction pressure. (From Atrium Medical Corporation, Hudson, N.H.) This is a picture of the Atrium Pleural Drainage unit with water suction control. Use pointer to show three compartments. Dry suction control No water Dial in desired negative pressure Must vent when decreasing pressure The dry suction chest = no water - visual alert that indicates if the suction is working. It uses either a restrictive device or a regulator to dial the desired negative pressure; this is internal in the chest drainage system. To incr the suction pressures, turn the dial on the drainage system. Increasing the vacuum source will not increase the pressure. decr suction, depress the manual vent to reduce excess vacuum to the lower prescribed level.

Complications - Pleural TB

Chest pain, fever, cough, and a unilateral pleural effusion are common Pleural effusion Bacteria in pleural space cause inflammation. Pleural exudates of protein-rich fluid Empyema Large numbers of tubercular organisms in pleural space Pleural TB, a specific type of extrapulmonary TB can result from either primary disease or reactivation of a latent infection. Chest pain, fever, cough, and presence of a unilateral pleural effusion are common. A pleural effusion is caused by bacteria in the pleural space, which trigger an inflammatory reaction and a pleural exudate of protein-rich fluid. Empyema is less common than effusion but may occur from large numbers of tubercular organisms in the pleural space. Diagnosis is confirmed by AFB cultures and a pleural biopsy.

TB dx - cxray

Chest x-ray Cannot make diagnosis solely on x-ray May appear normal in a patient with TB Upper lobe infiltrates, cavitary infiltrates, lymph node involvement, and pleural and/or pericardial effusion suggest TB Other diseases, such as sarcoidosis, can mimic the appearance of TB.

Synchronized Cardioversion

Choice of therapy for VT with a pulse or supraventricular tachydysrhythmias (atrial fibrillation with a rapid ventricular response) Synchronized circuit delivers a countershock on the R wave of the QRS complex of the ECG Procedure similar to defibrillation except sync button turned ON Initial energy lower 70-75 joules (biphasic) 100 joules (monophasic) If patient becomes pulseless, turn sync button off and defibrillate If synchronized cardioversion is done on a nonemergency basis (i.e., the patient is awake and hemodynamically stable), the patient is sedated (e.g., IV midazolam [Versed]) before the procedure. Strict attention to maintaining the patient's airway is critical.

TB Classification grades

Classes 0 = No TB exposure 1 = Exposure, no infection 2 = Latent TB, no disease 3 = TB, clinically active 4 = TB, not clinically active 5 = TB suspected Several systems can be used to classify TB. The American Thoracic Society classifies TB based on development of the disease: Class 0 No TB exposure, not infected (no history of exposure, negative tuberculin skin test) Class 1 TB exposure, no evidence of infection (history of exposure, negative tuberculin skin test) Class 2 Latent TB infection - TB infection without disease (significant reaction to tuberculin skin test, negative bacteriologic studies, no x-ray findings compatible with TB, no clinical evidence of TB) Class 3 TB infection with clinically active disease (positive bacteriologic studies or both a significant reaction to tuberculin skin test and clinical or x-ray evidence of current disease) Class 4 TB, but not clinically active No current disease (history of previous episode of TB or abnormal, stable x-ray findings in a person with a significant reaction to tuberculin skin test; negative bacteriologic studies if done; no clinical or x-ray evidence of current disease) Class 5 TB suspect (diagnosis pending); person should not be in this classification for more than 3 months

Planning AKI

Completely recover without any loss of kidney function Maintain normal fluid and electrolyte balance Have decreased anxiety Adhere to and understand need for careful follow-up care

Cardiovascular statuspost op aorta

Continuous ECG monitoring Electrolyte monitoring Arterial blood gas monitoring Oxygen administration Antidysrhythmic and antihypertensive meds Pain control Resume heart medications MI = in perioperative period bc decr myocardial oxygen supply or incr myocardial oxygen demands. Cardiac dysrhythmias bc electrolyte imbalances, hypoxemia, hypothermia, or myocardial ischemia.

Unstable Angina and MIDiagnostic Studies

Coronary angiography For patients with a STEMI Not for patients with UA or NSTEMI The patient with a STEMI must undergo coronary angiography within 90 minutes of presentation or receive thrombolytic therapy within 30 minutes in agencies without PCI capability. This will open the totally occluded artery and limit the infarction size. The patient with UA or NSTEMI may or may not undergo coronary angiography to evaluate the extent of the disease. Guidelines suggest that it is reasonable to do coronary angiography on stable but high-risk patients with UA or NSTEMI within 12-72 hours after presentation. If appropriate, a PCI is performed at this time. Some patients may be treated only with conservative medical management. Pharmacologic stress testing For patients with abnormal but nondiagnostic ECG and negative biomarkers When the ECG and serum cardiac biomarkers do not confirm MI, other measures for diagnosing CAD are considered. To assess for ischemia or infarction, pharmacologic stress testing may be done when a patient has an abnormal but nondiagnostic ECG and negative biomarkers.

TB Clinical Manifestations

Cough becomes frequent Hemoptysis is not common and is usually associated with advanced disease Dyspnea is unusual Can also present more acutely High fever Chills, generalized flulike symptoms Pleuritic pain Productive cough Crackles and/or adventitious breath sounds Extrapulmonary TB manifestations dependent on organs infected Sometimes TB has a more acute, sudden presentation. The patient may have a high fever, chills, generalized flulike symptoms, pleuritic pain, and a productive cough. Auscultation of the lungs may be normal or reveal crackles, and/or adventitious (such as bronchial) breath sounds. The clinical manifestations of extrapulmonary TB are dependent on the organs infected. For example, renal TB can cause dysuria and hematuria. Bone and joint TB may cause severe pain. Headaches, vomiting, and lympadenopathy may be present with TB meningitis. Immunosuppressed people and older adults are less likely to have fever and other signs of an infection Carefully investigate respiratory problems in HIV patients Rule out opportunistic diseases A change in cognitive function may be the only initial sign of TB in an older person Immunosuppressed (e.g., HIV-infected) people and older adults are less likely to have fever and other signs of an infection. In patients with HIV, classic manifestations of TB such as fever, cough, and weight loss may be wrongly attributed to P. jiroveci pneumonia (PJP) or other HIV-associated opportunistic diseases. Clinical manifestations of respiratory problems in patients with HIV must be carefully investigated to determine the cause. A change in cognitive function may be the only initial presenting sign of TB in an older person.

PE Diagnostic Studies

D-Dimer Elevated with any clot degradation False negatives with small PE Spiral (helical) CT scan Most frequently used diagnostic test Requires IV contrast media Ventilation-perfusion (V/Q) scan Used if patient cannot have contrast Two components Perfusion scanning Ventilation scanning Pulmonary angiography Most sensitive but invasive Arterial blood gases (ABGs) Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation. Ventilation scanning involves inhalation of a radioactive gas such as xenon. Scanning reflects the distribution of gas through the lung. The ventilation component requires the cooperation of the patient and may be impossible to perform in the critically ill patient, particularly if the patient is intubated. Pulmonary angiography is the most sensitive and specific test for PE. However, it is an expensive and invasive procedure that involves the insertion of a catheter through the antecubital or femoral vein, advancement of the catheter to the pulmonary artery, and injection of contrast medium. The accessibility and accuracy of the spiral CT has greatly diminished the need for pulmonary angiography. D-dimer is a laboratory test that measures the amount of cross-linked fibrin fragments. These fragments are the result of clot degradation and are rarely found in healthy individuals. The disadvantage of D-dimer testing is that it is neither specific (many other conditions cause elevation) nor sensitive as up to 50% of patients with small pulmonary emboli have normal results. Patients with suspected PE and an elevated D-dimer level but normal venous ultrasound may need a spiral CT or lung scan. A spiral (helical) CT scan (also known as CT angiography or CTA) is the most frequently used test to diagnose PE. An IV injection of contrast media is required to view the pulmonary blood vessels. The scanner continuously rotates around the patient while obtaining views (slices) of the pulmonary vasculature. This allows visualization of all anatomic regions of the lungs. Computer software reconstructs the data to provide a three-dimensional picture and assist in emboli visualization.

Aortic AneurysmsEtiology and Pathophysiology

Dilated aortic wall becomes lined with thrombi that can embolize Leads to acute ischemic symptoms in distal branches Causes Degenerative Congenital Mechanical = penetrating or blunt trauma Inflammatory Infectious The most common cause of descending AAAs is atherosclerosis . Male gender and tobacco use are the major risk factors for AAAs of atherosclerotic origin. Other risk factors include the presence of coronary or peripheral artery disease, high BP, and high cholesterol.

Pathophysiology of ARDS

Direct lung injury may cause ARDS, or ARDS may develop because of the systemic inflammatory response syndrome (SIRS). ARDS may also develop as a consequence of multiple organ dysfunction syndrome (MODS).

larynx/trachea

from the epiglottis to larynx then trachea larynx - vocal cords trachea - l/r sides at the carina/angle of louis

Case Study

D.F. is a 74-year old female who arrives in the E.D. with complaints of chest pain and shortness of breath. D.F. was recently discharged from rehab after undergoing bilateral knee replacements. She is 5 ft 2 in. tall and weighs 158 lb. Her past medical history is negative except for mitral regurgitation and heart failure. What risk factors does D.F. have for the development of pulmonary embolism? Obesity, orthopedic surgery, immobility, dehydration, heart failure (See next slide for discussion of all risk factors.) You perform a focused assessment on D.F. Her vital signs are BP 100/64, HR 110, Respirations 24, Temp 37. She has bibasilar crackles. Her breathing appears labored. She is somewhat restless and in obvious distress. What clinical manifestations of pulmonary embolism does D.F. demonstrate? Chest pain, dyspnea, tachycardia, tachypnea, restlessness, crackles What diagnostic tests would you expect to teach D.F. about? Serum D-dimer levels, spiral CT scan, chest x-ray, ECG, troponin, b-natriuretic peptide (BNP). If cannot have contrast media for spiral CT scan, then would expect patient to have a ventilation-perfusion (V/Q) scan. D.F.'s D-Dimer is positive. Spiral CT scan confirms the diagnosis of pulmonary emboli. What treatment measures would you expect to implement for D.F.? Anticoagulation therapy (either LMWH or unfractionated heparin), thrombolytics if severe, oxygen therapy. Vasopressors and fluids if becomes hypotensive. Inferior vena cava filter if patient has multiple lower extremity DVT - to prevent embolization to lungs. D.F. is started on a continuous IV drip of unfractionated heparin at 1000 units/hour. Drip will be titrated to therapeutic level using aPTT levels drawn every 6 hours. What nursing interventions would be appropriate in the care of D.F.? Semi-Fowler's position, maintain IV access, titrate oxygen therapy to maintain adequate oxygen saturation, frequent assessment of patient's respiratory and cardiovascular status, monitor aPTT laboratory results and titrate heparin as needed, provide emotional support and reassurance, provide patient education retreatments and long-term anticoagulation.

Case Study pneumonia

D.T. is an 88-year-old woman who lives alone. She has been feeling weaker over past 2 days. Last night became confused and disoriented. Her housekeeper notified her daughter, who brought D.T. to the clinic. She complains of coughing over the past 3 days. She has a history of mild heart failure that is treated medically but has no other significant health disorders. She last saw her health care provider 4 months ago. What are D.T.'s risk factors for pneumonia? What type of pneumonia is D.T. likely exhibiting? Age, limited mobility, chronic heart failure CAP because there is no mention of hospitalization or long-term care facility residency within the last 2 weeks; she last saw her HCP 4 months ago. What clinical manifestations of pneumonia is D.T. displaying? For what other clinical manifestations would you assess D.T. ? What diagnostic tests would you expect the nurse practitioner in the clinic to order? Cough, weakness, confusion Shaking chills; dyspnea; tachypnea; pleuritic chest pain; green, yellow, or rust-colored sputum; rhonchi and rales; bronchial breath sounds; egophony; ↑ fremitus; dullness to percussion if pleural effusion present; nonspecific manifestations including diaphoresis, anorexia, myalgias, headache, and abdominal pain Chest x-ray, sputum for gram stain and culture and sensitivity, CBC with differential, electrolytes, brain natriuretic peptide (BNP) D.T.'s chest x-ray reveals consolidation in her left lower lobe, consistent with pneumonia. Her WBC is 17,000/μL (17 × 109/L) with an increased number of bands. Her electrolytes and BNP are within normal limits. Sputum Gram stain shows gram-positive diplococci and many WBCs. Because of her age and altered mentation, the health care provider admits her to the hospital for treatment. On admission, D.T. has bronchial breath sounds with dullness of the left lower lobe and egophony. Her O2 saturation is 87%. What is your priority of care for D.T.? Monitor pulse oximetry and provide oxygen therapy as needed. Begin antibiotics as soon as possible; individualize rest and activity to D.T.'s tolerance. Maintain fall precautions to prevent injury. Administer analgesics prn to relieve the chest pain and antipyretics such as aspirin or acetaminophen for significantly elevated temperature. Maintain adequate hydration while monitoring for any heart failure. Maintain adequate nutrition with high caloric, small, frequent meals. It has been 4 days since D.T. was admitted for pneumonia. She is hemodynamically stable and neurologically intact. She has been switched from IV antibiotics to oral antibiotics and is ready for discharge. What important teaching should you provide to the patient and family? Teach the importance of rest and fluids while recovering, the importance of finishing the antibiotics, and food or drug interactions with the prescribed antibiotic, avoidance of alcohol and smoking, importance of follow-up chest x-ray, information about yearly influenza vaccinations, and signs and symptoms to watch for in the future.

Sudden Cardiac Death (SCD)

Death from a cardiac cause Majority of SCDs result from ventricular dysrhythmias Ventricular tachycardia Ventricular fibrillation

RH Nursing Diagnosis

Decreased Cardiac Output Activity Intolerance Ineffective Health Management Nursing diagnoses for the patient with RF and rheumatic heart disease may include, but are not limited to, the following: • Decreased CO related to valve dysfunction or HF • Activity intolerance related to arthralgia or arthritis secondary to joint pain, pain from pericarditis, and HF • Ineffective health management related to lack of knowledge concerning possible disease sequelae and the need for long-term prophylactic antibiotic therapy

Nursing Management Chronic Stable Angina and ACS -Nursing Diagnoses

Decreased cardiac output Acute pain Anxiety Activity intolerance Ineffective health management Decreased cardiac output related to altered contractility and altered heart rate and rhythm Acute pain related to an imbalance between myocardial oxygen supply and demand Anxiety related to perceived or actual threat of death, pain, and/or possible lifestyle changes Activity intolerance related to general weakness secondary to decreased cardiac output and poor lung and tissue perfusion Ineffective health management related to lack of knowledge of disease process, risk factor reduction, rehabilitation, home activities, and medications

PE Risk Factors

Deep vein thrombosis Immobility or reduced mobility Surgery History of DVT Malignancy Obesity Oral contraceptives/ hormones Smoking Heart failure Pregnancy/delivery Clotting disorders Atrial fibrillation Central venous catheters Fractured long bones Most pulmonary emboli arise from deep vein thrombosis (DVT) in the deep veins of the legs. Risk factors for PE include immobility or reduced mobility, surgery within the last 3 months (especially pelvic and lower extremity surgery), history of DVT, malignancy, obesity, oral contraceptives, hormone therapy, cigarette smoking, prolonged air travel, heart failure, pregnancy, and clotting disorders. Other sites of origin of PE include femoral or iliac veins, the right side of the heart (atrial fibrillation), and the pelvic veins (especially after surgery or childbirth). Upper extremity DVT occasionally occurs in the presence of central venous catheters or arterial lines. These cases may resolve with the removal of the catheter. A saddle embolus refers to a large thrombus lodged at an arterial bifurcation. Less common causes of PE include fat emboli (from fractured long bones), air emboli (from improperly administered IV therapy), bacterial vegetation on heart valves, amniotic fluid, and tumors.

TB Evaluation

Expected Outcomes Resolution of disease Normal pulmonary function Absence of any complications No further transmission of TB

Aortic DissectionClinical Manifestations

Depend on location of intimal tear and extent of dissection Acute Type A aortic dissection Abrupt onset of excruciating anterior chest pain Acute Type B aortic dissection More likely to report pain located in their back, abdomen, or legs Pain location may overlap between Type A and B dissections. The pain is frequently described as "sharp" and "worst ever," or as "tearing," "ripping," or "stabbing." Pain characterized as Sudden, severe pain in anterior part of chest, or intrascapular pain radiating down spine to abdomen or legs May mimic that of MI Dissection pain can be differentiated from MI pain that is more gradual in onset and has increasing intensity. As the dissection progresses, pain may migrate and follow the path of the dissection. Older patients are less likely to present with abrupt onset of chest or back pain and are more likely to present with hypotension and vague symptoms. Cardiovascular, neurologic, and respiratory signs may be present If aortic arch involved Neurologic deficiencies may be present Type A Disruption of blood flow in coronary arteries and aortic valve insufficiency Neurologic deficits may include altered level of consciousness, weakened or absent carotid and temporal pulses, and dizziness or syncope. The patient may develop angina; MI; and a new high-pitched, heart murmur. In severe cases, these complications can result in left heart failure (e.g., dyspnea, orthopnea, pulmonary edema), cardiogenic shock, and death.

Interprofessional CarePneumothorax

Dependent on severity May resolve spontaneously Treatment Thoracentesis Chest tubes Pleurodesis - more than one/on going issue, make adhesion so pleural space stays intact together Urgent needle decompression for tension pneumothorax tx of a pneumothorax depends on its severity and the nature of the underlying cause. If pt is stable, and has minimal air and/or fluid accumulated in the intrapleural space, no treatment may be necessary as the condition may resolve spontaneously. most definitive and common form of tx of pneumothorax and hemothorax = insert chest tube, connect it to water-seal drainage. Repeated spontaneous pneumothorax = treated surgically by a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another. Tension pneumothorax is a medical emergency, requiring urgent needle decompression followed by chest tube insertion to water-seal drainage. Penetrating chest wound: Sucking chest wound, Air enters pleural space during inspiration A vent dressing is used as emergency treatment Occlusive dressing secured on 3 sides Emergency treatment consists of covering the wound with an occlusive dressing that is secured on three sides (vent dressing). During inspiration, as negative pressure is created in the chest, the dressing pulls against the wound, preventing air from entering the pleural space. During expiration, as the pressure rises in the pleural space, the dressing is pushed out and air escapes through the wound and from under the dressing. If the object that caused the open chest wound is still in place, do not remove it until a HCP is present. Stabilize the impaled object with a bulky dressing.

Unstable Angina and MIDiagnostic Studies

Detailed health history 12-lead ECG Compare to previous ECG Changes in QRS complex, ST segment, and T wave Distinguish between STEMI and NSTEMI Serial ECGs reflect evolution of MI In addition to the patient's history of pain, risk factors, and health history, the primary diagnostic studies used to determine whether a person has UA or an MI include an ECG and serum cardiac biomarkers. The ECG is one of the primary tools to diagnose UA or an MI (STEMI or NSTEMI). Whenever possible, it should be compared to a previous ECG. Changes in the QRS complex, ST-segment, and T-wave caused by ischemia and infarction can develop slowly or quickly with UA and MI. The ECG must be read carefully, since changes can be absent or subtle at first. For this reason, serial 12-lead ECGs are done. For diagnostic and treatment purposes, it is important to distinguish between STEMI and NSTEMI/UA. STEMI patients usually have a complete coronary occlusion. ST elevation is first seen on the 12-lead ECG. Within a few hours to days, T-wave inversion and pathologic Q waves develop. Patients with NSTEMI or UA usually have transient thrombosis or incomplete coronary occlusion. These patients often develop ST depression or T wave inversion on the initial ECG. They usually do not develop pathologic Q waves. Because MI is a dynamic process that evolves over time, serial ECGs are done to show the evolution of ischemia, injury, infarction, and resolution of the infarction.

ARDS Etiology and Pathophysiology

Develops from a variety of direct or indirect lung injuries Most common cause is sepsis Exact cause for damage to alveolar-capillary membrane not known Patients with multiple risk factors are 3 to 4 times more likely to develop ARDS. Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems

Accelerated Idioventricular Rhythm (AIVR)

Develops when the intrinsic pacemaker rate (SA node or AV node) becomes less than that of ventricular ectopic pacemaker Rate is between 40 and 100 beats/minute Atropine if patient symptomatic Temporary pacing Do not suppress rhythm can develop when the intrinsic pacemaker rate (SA node or AV node) becomes less than that of a ventricular ectopic pacemaker. happens from MI or dig tox It is most commonly associated with acute MI and reperfusion of the myocardium after thrombolytic therapy or percutaneous coronary interventions (e.g., angioplasty). It can be seen with digitalis toxicity. In the setting of acute MI, AIVR is usually self-limiting and well tolerated, and it needs no treatment. If the patient becomes symptomatic (e.g., hypotensive, chest pain), atropine can be considered. Temporary pacing may be required. Drugs that suppress ventricular rhythms (e.g., amiodarone) should not be used as these can terminate the ventricular rhythm and further reduce the HR.

TB Drug Therapy - DOT

Directly observed therapy (DOT) Noncompliance is major factor in multidrug resistance and treatment failures Requires watching patient swallow drugs Preferred strategy to ensure adherence May be administered by public health nurses at clinic site DOT is an expensive but essential public health issue. The risk for reactivation of TB and MDR-TB is increased in patients who do not complete the full course of therapy.

Acute Kidney InjuryClinical Manifestations

Diuretic phase: Daily urine output is 1 to 3 L May reach 5 L or more Monitor for hyponatremia, hypokalemia, dehydration Recovery phase: take up to 1yr for kidney function to stabilize Diuretic phase: high urine volume is caused by osmotic diuresis from the high urea concentration in glomerular filtrate, inability of tubules to concentrate urine. In this phase, kidneys have recovered their ability to excrete wastes, but not to concentrate urine. Large losses of fluid, electrolytes require patient be monitored for hyponatremia, hypokalemia, and dehydration. diuretic phase may last 1 to 3 weeks. Near the end of this phase, the patient's acid-base, electrolyte, waste product (BUN, creatinine) values stabalize. Recovery phase: begins when the GFR incr, allowing BUN, serum creatinine levels to decr. Major improvements occur in the first 1 to 2 weeks of this phase, kidney function may take up to 12 months to stabilize. outcome of AKI is influenced by patient's overall health, severity of kidney failure, the #type of complications. Some do not recover, progress to end-stage renal disease. older adult less likely to have complete recovery of kidney function. Patients may have normal kidney function, but remain in early stage of CKD.

Interprofessional CareAcute Coronary Syndrome -Thrombolytic therapy

Draw blood and start 2-3 IV sites Complete invasive procedures prior Administer according to protocol Monitor closely for signs of bleeding Assess for signs of reperfusion Return of ST segment to baseline best sign IV heparin to prevent reocclusion Each hospital has a protocol for giving thrombolytic therapy. However, there are several common factors. Draw blood to obtain baseline laboratory values and start two or three lines for IV therapy. All other invasive procedures are done before the thrombolytic agent is given to reduce the possibility of bleeding in the patient. Depending on the drug selected, therapy is given in one IV bolus or over a period of time (30 to 90 minutes). Evaluate heart rhythm, vital signs, and pulse oximetry, and assess the heart and lungs frequently to evaluate the patient's response to therapy. Regularly assess for changes in neurologic status as this may indicate cerebral bleeding. When reperfusion occurs (i.e., the coronary artery that was blocked is opened and blood flow is restored to the heart muscle), several clinical signs may occur. The most reliable sign is the return of the ST segment to baseline on the ECG. Other signs include a resolution of chest pain, and an early, rapid rise of the cardiac biomarkers within 3 hours of therapy and peaking within 12 hours. These levels increase as the necrotic heart cells release proteins into the circulation after perfusion is restored to the area. The presence of reperfusion dysrhythmias (e.g., accelerated idioventricular rhythm) is a less reliable sign of reperfusion. These dysrhythmias are generally self-limiting and do not require aggressive treatment. A major concern with thrombolytic therapy is reocclusion of the artery. The site of the thrombus is unstable, and another clot may form or spasm of the artery may occur. Therefore, IV heparin therapy is started.

Aortic DissectionEtiology and Pathophysiology

Due to degeneration of the elastic fibers in the arterial wall Chronic hypertension hastens the process Tear in inner layer allows blood to "track" between inner and middle layer Blood surges through this tear into the middle layer of the aorta, causing the inner and middle layers to separate (dissect). If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal. As heart contracts, each systolic pulsation ↑ pressure on damaged area Further ↑ dissection May occlude major branches of aorta Cutting off blood supply to brain, abdominal organs, kidneys, spinal cord, and extremities

Cardiopulmonary Bypass

During CPB, blood is diverted from the patient's heart to a machine where it is oxygenated and returned (via a pump) to the patient. This allows the surgeon to operate on a quiet, nonbeating, bloodless heart while perfusion to vital organs is maintained.

ARDS Clinical Manifestations: Early

Dyspnea, tachypnea, cough, restlessness Chest auscultation = reveal fine, scattered crackles ABGs Mild hypoxemia and respiratory alkalosis caused by hyperventilation initial injury --> 1 to 2 days afterward =no respiratory symptoms. Respiratory alkalosis results from hypoxemia and the stimulation of juxtacapillary receptors. Chest x-ray may be normal or reveal minimal scattered interstitial infiltrates Edema may not show until 30% increase in fluid content in the lungs

Case Study

E.O., a 74-year-old woman, comes to the ED with deep chest pain radiating throughout the chest to the back. She reports that she smoked 1 pack of cigarettes/day for 20 years, quitting 5 years ago. She weighs 212 lb. We will now walk through a case study of a patient with an aortic aneurysm. What risk factors does E.O. present with? What other risk factors would you assess for? (See next slides) Based on E.O.'s symptoms, which type of aneurysm would you suspect? What are the immediate concerns for her? Thoracic aortic aneurysm Concern for potential rupture E.O. has an ECG in the ED that rules out an acute MI. Chest x-ray is suspicious for thoracic aneurysm. She is now scheduled to go to radiology for CT scan of her chest. E.O. returns from CT scan with a diagnosis of a thoracic aortic aneurysm measuring 5.2 cm. A surgical consult is ordered and E.O. is scheduled for surgery in the next hour. E.O.'s assessment findings include Alert and oriented to person and place-disoriented to time BP 158/98, P 92, R 22 Verbalizes pain at 6 on 0-10 scale Bilateral pedal pulses audible by Doppler Discuss the assessment findings and which ones are of concern: Disorientation may be related to hypoxia, anxiety, or age Vital signs elevated related to pain Pedal pulses weak; may indicate poor peripheral perfusion Discuss other important preoperative assessments and rationales. E.O.'s daughter is called and arrives in the E.D. Her daughter is very anxious and has many questions regarding the impending surgery. Have students formulate a teaching statement regarding E.O.'s diagnosis. What information would they convey regarding the preparation for surgery and postoperative recovery period? E.O.'s surgery goes well and she arrives in ICU. What are your priorities in monitoring her in the immediate postoperative period? Have students break into groups with each group discussing assessment of one system: neurologic, respiratory, cardiovascular, GI, renal. E.O. progresses well through the postoperative phase and is scheduled to be discharged. Her daughter is present and they are ready for discharge instructions. Have students outline the important points to convey to E.O. and her daughter for discharge.

Aortic DissectionDiagnostic Studies

ECG to rule out MI Chest x-ray 3-D CT scan MRI Transesophageal echocardiography chest x-ray = widening of the mediastinum and pleural effusion. 3-D CT scanning and transesophageal echocardiography (TEE) (down throat and get a picture) = standard of care for the diagnosis of acute aortic dissection. A CT scan or MRI can provide more detailed information on the severity of the dissection and related complications (e.g., pericardial effusions, carotid dissection) TEE is preferred in very unstable patients or those with contraindications to CT or MRI (e.g., those with metal implants, allergies to contrast material).

pericarditis Diagnostic Tests

EKG Echocardiogram CT Scan MRI CXR Labs: CRP, ESR, Troponin Possibly test HIV and Antinuclear Antibody (ANA) The most sensitive ECG changes include diffuse (widespread) ST segment elevations. This reflects the abnormal repolarization that develops secondary to the pericardial inflammation. You need to differentiate these changes from the ST changes seen in MI. Echocardiographic findings are most useful in determining the presence of a pericardial effusion or cardiac tamponade. Methods such as Doppler imaging and color M-mode assess diastolic function and diagnose constrictive pericarditis (discussed later in the chapter). A CT scan and MRI provide for visualization of the pericardium and pericardial space. Chest x-ray findings are generally normal, but cardiomegaly may be seen in a patient who has a large pericardial effusion Common laboratory findings include leukocytosis and elevation of CRP and ESR. Troponin levels may be elevated in patients with ST segment elevation and acute pericarditis, which could indicate concurrent heart damage. HIV and antinuclear antibody testing may be done. The fluid obtained during pericardiocentesis or the tissue from a pericardial biopsy may be studied to determine the cause of the pericarditis.

Aortic Aneurysm - Endovascular graft procedure

EVAR = Alternative to conventional surgical repair Involves placement of sutureless aortic graft into abdominal aorta inside aneurysm Minimally invasive = Done through femoral artery cutdown The grafts are made of various materials such as a Dacron cylinder consisting of several sections, and are supported with multiple rings of flexible wire, Delivered through sheath to predetermined point Endovascular graft procedure Graft Delivered through a femoral artery catheter Deployed against vessel wall by balloon inflation Anchored to vessel by series of small hooks Endovascular graft procedure Blood then flows through graft, preventing expansion of aneurysm Aneurysm wall will begin to shrink over time Must meet strict eligibility criteria to be a candidate Criteria include iliofemoral vessels that will allow for safe graft insertion and vessels of sufficient length and width to support the graft.

Pulseless Electrical Activity

Electrical activity can be observed on the ECG, but no mechanical activity of the heart is evident, and the patient has no pulse Pulseless electrical activity (PEA) is a situation in which organized, electrical activity is seen on the ECG, but there is no mechanical heart activity and the patient has no pulse. Prognosis is poor unless the underlying cause is quickly identified and treated. electricity shows up but not enough to show a pulse

Aortic DissectionInterprofessional Care - Surgical therapy

Emergency surgery for acute Type A aortic dissection When drug therapy is ineffective or when complications of aortic dissection are present Surgery is delayed to allow edema to decrease and permit clotting of blood Mortality rate is 50% within 48 hours of symptom onset. Involves resection of aortic segment and replacement with synthetic graft material In-hospital mortality and neurologic complications are high Open surgical repair is recommended = chronic dissection that have a connective tissue disorder, and a descending thoracic aortic diameter greater than 5.5 cm. Causes of death = aortic rupture, mesenteric ischemia, MI, sepsis, stroke, multiorgan failure.

Endovascular graft procedurePotential complications

Endoleak Aneurysm growth Aneurysm rupture Aortic dissection Bleeding Stent migration Renal artery occlusion Graft thrombosis Incisional site hematoma Site infection Renal artery occlusion may occur due to stent migration most common complication = endoleak, the seepage of blood back into the old aneurysm = due to an inadequate seal at either graft end, a tear through the graft fabric, or leakage between overlapping graft segments, and may require coil embolization (insertion of beads) for hemostasis.

Nursing Diagnoses and Collaborative Problem AKI

Excess fluid volume Risk for infection Fatigue Anxiety Potential complication: dysrhythmia Excess fluid volume related to kidney failure and fluid retention Risk for infection related to invasive lines, uremic toxins, and altered immune responses secondary to kidney failure Fatigue related to anemia, metabolic acidosis, and uremic toxins Anxiety related to disease processes, therapeutic interventions, and uncertainty of prognosis Potential complication: dysrhythmias related to electrolyte imbalances

Nursing ManagementEvaluation aorta

Expected Outcomes Patent arterial graft with adequate distal perfusion Adequate urine output No signs of infection

Interprofessional CareAcute Coronary Syndrome - Coronary surgical revascularization

Failed medical management Presence of left main coronary artery or three-vessel disease Not a candidate for PCI (e.g., blockages are long or difficult to access) Failed PCI with ongoing chest pain History of diabetes mellitus, LV dysfunction, chronic kidney disease CABG surgery and PCI are considered palliative treatment for CAD and not a cure.

Implantable Cardioverter-Defibrillator (ICD) - steps

Follow-up appointments Incision care Arm restrictions Sexual activity Driving Avoid direct blows Avoid large magnets, MRI 1. Follow up with a HCP for routine checks of the function of the ICD. This is often done by interrogating the device using a telephone. 2. infection, Keep incision dry for 4 days after insertion or as instructed. 3. Avoid lifting arm on ICD side above shoulder until approved. 4. It is usually safe to resume sexual activity once your incision is healed. 5. Avoid driving until cleared 6. Avoid direct blows to ICD site. 7. Avoid large magnets and strong electromagnetic fields, should not have a (MRI) scan unless the ICD is approved Air travel not restricted Avoid antitheft devices Medic Alert ID ICD identification card Caregivers to learn CPR If your ICD fires, call your HCP immediately. If your ICD fires and you feel sick, contact the emergency medical services If your ICD fires more than once, contact EMS.

Pacemakers - Patient and Caregiver Teaching

Follow-up appointments for pacemaker function checks Incision care Arm restrictions Avoid direct blows Avoid high-output generator No MRIs unless pacer approved Microwaves OK Avoid antitheft devices Travel not restricted Monitor pulse Pacemaker ID card Medic Alert ID Include the following instructions when teaching the patient and/or caregiver management of a pacemaker. 1. Maintain follow-up care with your HCP to begin regular pacemaker function checks. This is often done by interrogating the device using a telephone. 2. Report any signs of infection at incision site (e.g., redness, swelling, drainage) or fever to your HCP immediately. 3. Keep incision dry for 4 days after implantation, or as ordered. 4. Avoid lifting arm on pacemaker side above shoulder until approved by your cardiologist. 5. Avoid direct blows to pacemaker site. 6. Avoid close proximity to high-output electric generators as these can interfere with the function of the pacemaker. 7. You should not have a magnetic resonance imaging (MRI) scan unless the pacemaker is approved as MRI safe or there is a protocol in place for patient safety during the procedure. 8. Microwave ovens are safe to use and do not interfere with pacemaker function. 9. Avoid standing near antitheft devices in doorways of department stores and public libraries. You should walk through them at a normal pace. 10. Travel is not restricted. Inform security (e.g., airport, train station, public buildings) of presence of pacemaker because it may set off the metal detector. If hand-held screening wand is used, it should not be placed directly over the pacemaker. Manufacturer information may vary regarding the effect of metal detectors on the function of the pacemaker. 11. Monitor pulse and inform HCP if HR drops below predetermined rate. 12. Carry pacemaker information card and a current list of your drugs at all times. 13. Obtain and wear a Medic Alert ID device at all times. 14. Consider joining a pacemaker support group

ARDS Planning

Following recovery PaO2 within normal limits for age or at baseline on room air SaO2 >90% Resolution of precipitating factor(s) for ARDS Clear lungs on auscultation Patients with moderate to severe ARDS are cared for in critical care units. With appropriate therapy, overall goals for the patient with ARDS include a Pao2 ≥ 60 mm Hg and adequate lung ventilation to maintain normal pH.

Transcutaneous Pacing

For emergency pacing needs Noninvasive Bridge until transvenous pacer can be inserted Use lowest current that will "capture" Patient may need analgesia/sedation A transcutaneous pacemaker (TCP) is used to provide adequate HR and rhythm to the patient in an emergency situation. The TCP consists of a power source and a rate- and voltage-control device that attaches to two large, multifunction electrode pads. Position one pad on the anterior part of the chest, usually on the V4 lead position, and the other pad on the back between the spine and the left scapula at the level of the heart. When programming the TCP, always use the lowest current that results in a ventricular contraction (capture) to minimize patient discomfort. Before starting TCP therapy, it is important to tell the patient what to expect. Explain that the muscle contractions created by the pacemaker when the current passes through the chest wall are uncomfortable. The TCP consists of a power source and a rate- and voltage-control device that attaches to two large, multifunction electrode pads. The pads can be used for both pacing and defibrillation. piece on front and back like when dfib baby

Rheumatic Fever

From group A Stretococcal Pharyngitis Affects the heart, skin, joints and CNS acute inflammatory disease of the heart potentially involving all layers (endocardium, myocardium, and pericardium). RF is a complication that occurs as a delayed result (usually after 2 to 3 weeks) of a group A streptococcal pharyngitis. Manifestations of RF appear to be related to an abnormal immunologic response to group A streptococcal cell membrane antigens. RF has declined in developed countries because of the effective use of antibiotics to treat streptococcal infections.

Aortic AneurysmInterprofessional Care

Goal - prevent aneurysm from rupturing Early detection/treatment imperative Once detected = Studies done to determine size and location A careful review of body systems is necessary to identify any co-morbidities, especially of the lungs, heart, or kidney, Autotransfusion reduces need for blood transfusion during surgery AAA resection Require cross-clamping of aorta proximal and distal to aneurysm Can be completed in 30 to 45 minutes Clamps are removed and blood flow to lower extremities is restored

TB Planning

Goals Comply with therapeutic regimen Have no recurrence of disease Have normal pulmonary function Take appropriate measures to prevent spread of disease The overall goals are that the patient with TB will comply with the therapeutic regimen, have no recurrence of disease, have normal pulmonary function, and take appropriate measures to prevent the spread of the disease.

Endovascular graft procedure

Graft dysfunction may require traditional surgical repair Need for long-term follow-up pt require periodic imaging for the rest of their lives to monitor for an endoleak, document stability of the aneurysm sac, and determine the need for surgical intervention.

TB Health Promotion

Health Promotion Ultimate goal in the United States is eradication Selective screening programs in high-risk groups to detect TB Treatment of LTBI Follow-up positive TST results Reportable diseasw Address social determinants of TB The ultimate goal is to eradicate TB worldwide. Screening programs in known risk groups are of value in detecting individuals with TB. Treatment of LTBI reduces the number of TB carriers in the community. The person with a positive tuberculin skin test should have a chest x-ray to assess for the presence of active TB disease. Individuals with a diagnosis of TB must be reported to the public health authorities for identification and assessment of contacts and risk to the community. Programs to address the social determinants of tuberculosis are necessary to decrease transmission of TB. Reducing poverty, over-crowded living conditions, malnutrition, smoking, and drug/alcohol abuse can help minimize TB infection rates. Improving access to health care and education is also important.

Hemothorax

Hemopneumothorax Chylothorax = Lymphatic fluid in pleural space = Treat conservatively, with meds, surgery, or pleurodesis Hemothorax is an accumulation of blood in the pleural space resulting from injury to the chest wall, diaphragm, lung, blood vessels, or mediastinum. The patient with a traumatic hemothorax requires immediate insertion of a chest tube for evacuation of the blood, which can be recovered and reinfused for a short period of time after the injury. When it occurs with pneumothorax, it is called a hemopneumothorax. Chylothorax is the presence of lymphatic fluid in the pleural space. The thoracic duct is disrupted either traumatically or from a malignancy, and the lymphatic fluid fills the pleural space. This milky white fluid is high in lipids. Normal lymphatic flow through the thoracic duct is 1500 to 2500 mL/day. This amount can be increased up to tenfold after ingestion of fats. Some cases heal with conservative treatment (chest drainage, bowel rest, and dietary modifications). Octreotide has been used to reduce the flow of lymphatic fluid with some success. Surgery (thoracic duct ligation) and pleurodesis (the artificial production of adhesions between the parietal and visceral pleura), may be considered for refractory cases.

Cytomegalovirus (CMV) pneumonia

Herpes virus Asymptomatic and mild to severe disease Life threatening in immunosuppressed person Tx- antiviral medications and high-dose immunoglobulin Cytomegalovirus (CMV), a herpes virus, can cause viral pneumonia. Most CMV infections are asymptomatic or mild, but severe disease can occur in people with an impaired immune response. CMV is the most common life-threatening infectious complication after hematopoietic stem cell transplantation. Antiviral medications (e.g., ganciclovir [Cytovene], foscarnet [Foscavir], cidofovir [Vistide]) and high-dose immunoglobulin are used for treatment.

TB Nursing Assessment

History Physical symptoms Productive cough Night sweats Afternoon temperature elevation Weight loss Pleuritic chest pain Crackles over apices of lungs Sputum collection Ask the patient about a previous history of TB, chronic illness, or any immunosuppressive medications. Obtain social and occupational history to determine risk factors for transmission of TB. Assess the patient for productive cough, night sweats, afternoon temperature elevation, weight loss, pleuritic chest pain, and abnormal lung sounds. If the patient has a productive cough, early morning is the ideal time to collect sputum specimens for an acid-fast bacillus (AFB) smear.

ARDS Nursing Assessment

History of lung disease Exposures to lung toxins Tobacco, alcohol, or drug use Related hospitalizations Thoracic or spinal cord trauma Severe obesity Because ARDS causes acute respiratory failure, the subjective and objective data that you should obtain from a person with ARDS are the same as those for acute respiratory failure (Table 67-3). Some patient information may not be possible to obtain initially due to management priorities of oxygenation and ventilation. Use of O2, inhalers, nebulizers, OTC drugs, immunosuppressant therapy Previous intubation Thoracic or abdominal surgery Exercise Immunizations Eating habits, change in appetite Weight gain/loss Fatigue Dizziness Dyspnea, wheezing, cough, sputum, palpitations, swollen feet Changes in sleep pattern, use of CPAP Headache Chest pain or tightness Anxiety Restlessness, agitation Pale, cool, clammy or warm, flushed skin Peripheral edema or cyanosis Shallow, increasing respiratory rate progressing to decreased rate Use of accessory muscles Asymmetric chest expansion Abnormal breath sounds Pleural friction rub Tachycardia progressing to bradycardia Hypertension progressing to hypotension Pulsus paradoxus, JVD, pedal edema Abdominal distention, ascites Somnolence, confusion, delirium Changes in pH, PaCO2, PaO2, SaO2 Decreased tidal volume, FVC Abnormal x-ray Abnormal central venous or pulmonary artery pressures Initial increased CO As hypoxemia, hypercapnia, and acidosis become more severe, CO will decrease

Tuberculosis (TB)

Infectious disease caused by Mycobacterium tuberculosis Lungs most commonly infected 1/3 of world's population has TB Leading cause of death in patients with HIV/AIDs Tuberculosis (TB) usually involves the lungs, but any organ can be infected including brain, kidneys, and bones. CDC reports that more than 2 billion people are infected with TB. The incidence of TB worldwide declined until the mid-1980s when HIV disease emerged. The major factors that contributed to the resurgence of TB were (1) high rates of TB among patients with HIV infection and (2) the emergence of multidrug-resistant (MDR) strains of M. tuberculosis. Although the prevalence of TB has increased in Europe, it has steadily declined in the United States since reaching a resurgence peak in 1992. Prevalence is decreasing in the United States

Pneumonia dx Tests

History, physical examination, and chest x-ray Chest x-ray - pleural effusions. sputum specimen for culture and Gram stain to identify the organism is obtained before beginning antibiotic therapy. However, antibiotic administration should not be delayed if a specimen cannot be readily obtained. Delays in antibiotic therapy can increase the risk of morbidity and mortality. Leukocytosis = bacterial pneumonia; the white blood cell (WBC) count is usually greater than 15,000/μL (15 × 109/L) with the presence of bands (immature neutrophils). (not always in elders) Arterial blood gases (ABGs) may be obtained to assess for hypoxemia (partial pressure of oxygen in arterial blood [PaO2] less than 80 mm Hg), hypercapnia (partial pressure of carbon dioxide in arterial blood [PaCO2] greater than 45 mm Hg), and acidosis (pH <7.35). Blood cultures are done for patients who are seriously ill. A thoracentesis and/or bronchoscopy with washings may be used to obtain fluid samples from patients not responding to initial therapy. biologic markers of infection to guide clinical decisions for treatment of pneumonia is under investigation. Serum levels of C-reactive protein (CRP) and procalcitonin are currently under investigation in providing information to help guide clinicians in distinguishing pneumonia from other types of cardiac and respiratory failure. sputum culture and sensitivity: b/f starting antibiotic, use suction if unable to cough Blood cultures: to rule out organism in blood Serum electro: cause of dehydration

TB Risk Factors

Homeless Residents of inner-city neighborhoods Foreign-born persons Living or working in institutions (includes health care workers, shelters, prisons, hospitals) IV injecting drug users Poverty, poor access to health care Immunosuppression - . HIV infection, malignancy, long-term corticosteroid use TB occurs disproportionately in the poor, underserved, and minorities.

TB Interprofessional Care

Hospitalization not necessary for most patients Infectious for first 2 weeks after starting treatment if sputum + Drug therapy used to prevent or treat active disease Need to monitor compliance Most patients with TB are treated on an outpatient basis. Many people can continue to work and maintain their lifestyles with few changes. Hospitalization may be needed for the severely ill or debilitated. The mainstay of TB treatment is drug therapy. Promoting and monitoring compliance is critical for treatment to be successful.

Aortic AneurysmSurgical therapy - Preop

Hydration Stabilize electrolytes, coagulation, hematocrit elective surgery = hydrated, electrolyte, coagulation, hematocrit abnormalities = corrected preoperatively. Open aneurysm repair (OAR): Incising diseased segment of aorta Removing intraluminal thrombus or plaque Inserting synthetic graft= Dacron or polytetrafluoroethylene (PTFE) Suturing native aortic wall around graft Acts as protective cover If the iliac arteries are also aneurysmal, a bifurcated graft replaces the entire diseased segment. With saccular aneurysms, it may be possible to excise only the bulbous lesion, repairing the artery by primary closure (suturing the artery together) or by application of an autogenous or synthetic patch graft.

Nursing ManagementAcute Coronary Syndrome - Coronary revascularization: CABG

ICU for first 24-36 hours Pulmonary artery catheter Intraarterial line Pleural/mediastinal chest tubes Continuous ECG ET tube with mechanical ventilation Epicardial pacing wires Urinary catheter NG tube For patients having CABG surgery, care is provided in the ICU for the first 24 to 36 hours. Ongoing and intensive monitoring of the patient's hemodynamic status is critical. The patient will have numerous invasive lines for monitoring cardiac status and other vital organs. These include: A pulmonary artery catheter for hemodynamic monitoring An intraarterial line for continuous BP monitoring Pleural and mediastinal chest tubes for chest drainage Continuous ECG monitoring An endotracheal tube connected to mechanical ventilation Epicardial pacing wires for emergency pacing of the heart A urinary catheter to monitor urine output NG tube for gastric decompression Most patients will be extubated within 6 hours and transferred to a step-down unit within 24 hours for continued monitoring of cardiac status.

Post op aorta

ICU monitoring Arterial line = A-line = uptoday bp Central venous pressure (CVP) or pulmonary artery (PA) catheter - @SVC Mechanical ventilation Peripheral IV lines Urinary catheter - urine and renal/abdominal pressures Postoperatively, aortic surgery patients typically go to an ICU for 24 to 48 hours for close monitoring. ICU monitoring NG tube - decompress abd ECG Pulse ox Pain meds - morphine bc help with sympathetic response

Interprofessional CareAcute Coronary Syndrome - Drug therapy

IV nitroglycerin (NTG) Morphine β-adrenergic blockers ACE inhibitors Antidysrhythmic drugs Lipid-lowering drugs Stool softeners IV NTG (Tridil) is used in the initial treatment of the patient with ACS. The goal of therapy is to reduce anginal pain and improve coronary blood flow. IV NTG decreases preload and afterload while increasing the myocardial oxygen supply. The onset of action is immediate. Titrate NTG to control and stop chest pain. Because hypotension is a common side effect, BP is closely monitored during this time. Patients who do become hypotensive are often volume depleted and can benefit from an IV fluid bolus. Morphine is the drug of choice for chest pain that is unrelieved by NTG. As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility, and decreasing BP and HR. In addition, morphine can help reduce anxiety and fear. In rare situations, morphine can depress respirations. Monitor patients for signs of bradypnea or hypotension, conditions to avoid in myocardial ischemia and infarction. β-Blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility. The use of these drugs in patients who are not at risk for complications of MI (e.g., cardiogenic shock, bradycardia or hypotension) reduces the risk of reinfarction and the occurrence of HF. β-Blockers are continued indefinitely. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers inhibitors should be started within the first 24 hours if the BP is stable and there are no contraindications. They are continued indefinitely in patients recovering from STEMI or NSTEMI, with heart failure, or an EF of 40% or less. The use of ACE inhibitors can help prevent ventricular remodeling and prevent or slow the progression of HF. For patients who cannot tolerate ACE inhibitors (e.g., angioedema, cough), ARBs should be considered. Dysrhythmias are the most common complications after an MI. In general, they are self-limiting and are not treated aggressively unless they are life threatening (e.g., sustained ventricular tachycardia). A lipid panel is obtained on all patients with ACS. All patients with ACS or diagnosed with CAD should receive lipid-lowering drugs indefinitely, unless contraindicated. After an MI, the patient may be predisposed to constipation because of bed rest and opioid administration. Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate bowel movements. This prevents straining and the resultant vagal stimulation from the Valsalva maneuver. Vagal stimulation produces bradycardia and can provoke dysrhythmias.

Aortic DissectionInterprofessional Care - Drug therapy

IV β-adrenergic blocker: Esmolol (Brevibloc) Other antihypertensive agents: Calcium channel blockers Nitroprusside Angiotensin-converting enzyme inhibitors pain: Morphine An IV β-adrenergic blocker (e.g., esmolol [Brevibloc]) = titrated to a target heart rate of 60 beats per minute or less or to a systolic BP between 100-110 mm Hg. Morphine is the preferred analgesic = decreases sympathetic nervous system stimulation as well as relieving pain. A calcium channel blocker (e.g., diltiazem [Cardizem], verapamil [Calan]) = lower HR if a β-adrenergic blocker is contraindicated. IV angiotensin-converting enzyme (ACE) inhibitor (e.g., enalaprilat [Vasotec])

Nursing Implementation Health Promotion AKI

Identify and monitor populations at high risk Control exposure to nephrotoxic drugs and industrial chemicals Prevent prolonged episodes of hypotension and hypovolemia Measure daily weight Monitor intake and output Monitor electrolyte balance Replace significant fluid losses Provide aggressive diuretic therapy for fluid overload Use nephrotoxic drugs sparingly In the hospital, the factors that increase the risk for developing AKI are the presence of preexisting CKD, older age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, and obstetric complications. Careful monitoring of patient's weight, intake and output, fluid balance, and electrolyte balance is essential. Assess and record extrarenal losses of fluid from vomiting, diarrhea, hemorrhage, and increased insensible losses. Prompt replacement of significant fluid losses will help prevent ischemic tubular damage associated with trauma, burns, and extensive surgery. Intake and output records and the patient's weight provide valuable indicators of fluid volume status. Aggressive diuretic therapy for the patient with fluid overload resulting from any cause can lead to a reduction in renal blood flow. Nephrotoxic drugs should be used sparingly in a patient at high risk. When these drugs must be used, they should be given in the smallest effective doses for the shortest possible periods. Caution the patient about abuse of over-the-counter analgesics (especially nonsteroidal antiinflammatory drugs [NSAIDs]) as these may worsen kidney function in the patient with mild CKD. Angiotensin-converting enzyme (ACE) inhibitors can also decrease perfusion pressure and cause hyperkalemia. . If other measures such as diet modification, diuretics, and sodium bicarbonate cannot control the hyperkalemia, ACE inhibitors may need to be reduced or eliminated. However, ACE inhibitors are frequently used to prevent proteinuria and progression of kidney disease, especially in diabetic patients.

pericarditis tx

Identify and treat the underlying problem! Bacterial: Antibiotics and NSAIDS Autoimmune: Corticosteriods and NSAIDS Recurrent Pericarditis: Cochicine Pericardiocentesis Done for Pericardial Effusion with acute cardiac tamponade Pericardial Window Pericardiocentesis: Hemodynamic support = giving volume expanders and inotropic agents (e.g., dopamine) and discontinuing any anticoagulants. guided by echocardiography. A needle is inserted into the pericardial space to remove fluid for analysis and to relieve heart pressure. Complications = dysrhythmias, further cardiac tamponade, pneumomediastinum, pneumothorax, myocardial laceration, coronary artery laceration. Pericardial Window: diagnosis or for drainage of excess fluid. This involves cutting a "window" or portion of the pericardium. This allows the fluid to drain continuously into the peritoneum or chest.

Aortic DissectionInterprofessional Care -Conservative therapy

If no symptoms = Can be treated conservatively for a period of time Pain relief, HR, and BP control CVD risk factor modification Close surveillance with CT or MRI acute or chronic Type B aortic dissection without complications = treated conservatively.

Pneumonia Nursing Diagnoses

Impaired gas exchange Ineffective breathing pattern Acute pain (chest) Activity intolerance

RRT

Indications for renal replacement therapy (RRT) = diaylsis Volume overload Elevated serum potassium level Metabolic acidosis BUN level > 120 mg/dL (43 mmol/L) Significant change in mental status Pericarditis, pericardial effusion, or cardiac tamponade Peritoneal dialysis (PD) Not frequently used Intermittent hemodialysis (HD) Continuous renal replacement therapy (CRRT) Cannulation of artery and vein Intermittent hemodialysis (HD) (e.g., at intervals of 4 hours either daily, every other day, or three to four times per week) is the method of choice when rapid changes are required in a short period of time. Continuous renal replacement therapy (CRRT) = effectively and involves cannulation of an artery and a vein.

ARDS Nursing Diagnoses

Ineffective airway clearance Ineffective breathing pattern Risk for imbalanced fluid volume Anxiety Impaired gas exchange Imbalanced nutrition: less than body requirements Impaired gas exchange related to alveolar hypoventilation, intrapulmonary shunting, V/Q mismatch, and diffusion impairment Ineffective airway clearance related to excessive secretions, decreased level of consciousness, presence of an artificial airway, neuromuscular dysfunction, and pain Ineffective breathing pattern related to neuromuscular impairment of respirations, pain, anxiety, decreased level of consciousness, respiratory muscle fatigue, and bronchospasm

TB Nursing Diagnoses

Ineffective breathing pattern Ineffective airway clearance Risk for infection Noncompliance Ineffective health management Nursing diagnoses for the patient with TB may include, but are not limited to, the following: Ineffective breathing pattern related to decreased lung capacity Ineffective airway clearance related to increased secretions, fatigue, and decreased lung capacity Risk for infection (spread of infection to others) related to cough and sputum production, lack of knowledge of disease process, and social/economic circumstances Noncompliance and ineffective health management related to lack of knowledge of disease process, lack of motivation, and long-term nature of treatment and lack of resources

Pacemakers - Monitor for other complications

Infection Hematoma formation Pneumothorax Atrial or ventricular septum perforation Lead misplacement prophylactic IV antibiotic therapy before and after insertion post-insertion chest x-ray to check lead placement/ rule out pneumothorax continuous ECG monitoring of rhythm.

What is Pericarditis

Inflammation of the pericardial sack The pericardium is composed of the inner serous membrane (visceral pericardium) and the outer fibrous (parietal) layer (Fig. 36-1). The pericardial space is the cavity between these two layers. Normally it contains 10 to 15 mL of serous fluid. The pericardium serves an anchoring function, provides lubrication to decrease friction between heart contractions, and helps to prevent excessive dilation of the heart during diastole. It may be congenitally absent or surgically removed.

Complications of Myocardial Infarction - Acute pericarditis

Inflammation of visceral and/or parietal pericardium Mild to sever chest pain Increases with inspiration, coughing, movement of upper body Relieved by sitting in forward position Pericardial friction rub ECG changes Pericarditis is an inflammation of the visceral and/or parietal pericardium May occur 2 to 3 days after an acute MI. Pericarditis is characterized by mild to severe chest pain that increases with inspiration, coughing, and movement of the upper body. Sitting in a forward position often relieves the pain. Assess the patient with suspected pericarditis for the presence of a friction rub over the pericardium. The sound is best heard with the diaphragm of the stethoscope at the mid to lower left sternal border. It may be persistent or intermittent. Fever may also be present. Diagnosis of pericarditis can be made with serial 12-lead ECGs. Typical ECG changes include diffuse ST-segment elevations. This reflects the inflammation of the pericardium. Treatment includes pain relief with high doses of aspirin (e.g., 650 mg every 4-6 hours).

Interprofessional CareAcute Coronary Syndrome - Nutritional therapy

Initially NPO Progress to Low salt Low saturated fat Low cholesterol Initially, patients may be NPO (nothing by mouth), except for sips of water, until stable (e.g., pain free, nausea resolved). You advance the diet as tolerated to a low-salt, low-saturated fat, and low-cholesterol diet.

Clinical Manifestations of ACS Myocardial Infarction - Cardiovascular

Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO) Crackles Jugular venous distention Abnormal heart sounds S3 or S4 New murmur In response to the release of catecholamines, BP and HR may initially increase. The BP may later drop because of decreased cardiac output (CO). If severe enough, this may result in decreased renal perfusion and urine output. Crackles, if present, may persist for several hours to several days, suggesting LV dysfunction. Jugular venous distention, hepatic engorgement, and peripheral edema may indicate right ventricular dysfunction. Examination may reveal abnormal heart sounds that may seem distant. Other abnormal sounds suggesting LV dysfunction are S3 and S4. In addition, a loud holosystolic murmur may develop. This may indicate a ventricular septal defect, papillary muscle rupture, or valve dysfunction.

Hyperkalemia

Insulin and sodium bicarbonate Calcium carbonate Sodium polystyrene sulfonate (Kayexalate) Hyperkalemia = most serious complications = life-threatening dysrhythmias. Both insulin and sodium bicarbonate serve as a temporary measure for treatment of hyperkalemia = shift of potassium into cells, but potassium will eventually be released. Calcium gluconate raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium. Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually remove potassium from the body. NO if paralytic ileus bc bowel necrosis

TB dx - IGRAs

Interferon-γ gamma release assays (IGRAs) Detects T-cells in response to Mycobacterium tuberculosis Includes QuantiFERON-TB and T-SPOT.TB tests Rapid results Several advantages over TST but more expensive Interferon-γ (INF) gamma release assays (IGRAs) provide another screening tool for TB. IGRAs are blood tests that detect INF-gamma release from T-cells in response to Mycobacterium tuberculosis. Examples of IGRAs include QuantiFERON-TB test and the T-SPOT. Test results are available in a few hours. IGRAs offer several advantages over the TST in that they require only one patient visit, are not subject to reader bias, have no booster phenomenon, and are not affected by prior BCG vaccination. The cost of an IGRA is substantially higher than the TST. Current guidelines suggest that both tests are viable options and that selection should be based on context and reasons for testing. Neither IGRAs or TST can distinguish between LTBI and active TB infection. LTBI can only be diagnosed by excluding active TB.

Aortic AneurysmClinical Manifestations

May mimic pain associated with abdominal or back disorders May cause back pain, epigastric discomfort, altered bowel elimination, intermittent claudication Compression of nearby anatomic structures and nerves may cause symptoms such as back pain, epigastric discomfort, altered bowel elimination, and intermittent claudication. aneurysms spontaneously embolize plaque, causing "blue toe syndrome" (patchy mottling of the feet and toes in the presence of palpable pedal pulses).

Cardiac Tamponade

Occurs with increased Pericardial Effusions Result: Compression of the Heart The speed of fluid accumulation affects the severity of clinical manifestations. Cardiac tamponade can occur acutely (e.g., rupture of heart, trauma) or subacutely (e.g., secondary to renal failure, malignancy).

Case Study

J.K. is a 37-year-old man who fell off the roof of a house he was constructing. He sustained severe lacerations of his face and left leg, with substantial blood loss. Which type of kidney injury is J.K. at risk for? What are the contributing factors for this? What signs and symptoms of renal involvement would you assess for? Which type of kidney injury is J.K. at risk for? Prerenal What are the contributing factors for this? Fluid volume loss from blood loss Leads to decreased cardiac output and decreased renal perfusion What signs and symptoms of renal involvement would you assess for? See next slides. J.K.'s injuries have been repaired, but his urine output has dropped below 350 mL/day. J.K.'s laboratory results reveal BUN 53 mg/dL and serum creatinine 2.7 mg/dL. He complains of fatigue. His BP has risen to 178/98. J.K. is in the oliguric stage of prerenal AKI. What other manifestations should you observe for? What other laboratory results should you monitor? J.K.'s urine output suddenly increases to 2 L overnight. Is this a positive sign? J.K. is in the oliguric stage of prerenal AKI. What other symptoms should you observe for? What other laboratory results should you monitor? J.K.'s urine output suddenly increases to 2 L overnight. Is this a positive sign?

Case Study

J.P., an 82-year-old woman, is brought to the ED from a long-term care facility. 4 days ago she aspirated her lunch. We will now walk through a case study of a patient with ARDS. Have students list initial assessment to be gathered: Level of consciousness Vital sounds Lung sounds Oxygen saturation ECG monitoring See next slide for additional data. The physician on call for the facility diagnosed her with aspiration pneumonia. She was started on antibiotic therapy of azithromycin (Zithromax). We will now walk through a case study of a patient with ARDS. Have students list initial assessment to be gathered: Level of consciousness Vital sounds Lung sounds Oxygen saturation ECG monitoring See next slide for additional data. During the past 24 hours, J.P. has developed progressive dyspnea and restlessness. On admission to the ED, she is confused and agitated. At times she is gasping for air. Chest x-ray shows diffuse infiltrates. What was the cause of J.P.'s respiratory distress? What are her risks for ARDS? What is her priority of care? What was the cause of J.P.'s respiratory distress? Aspiration What are her risks for ARDS? Age Infection What is her priority of care? Airway, breathing, oxygenation J.P. has been in the hospital for 1 week. She has been diagnosed with ARDS. She is on IV antibiotics and oxygen therapy, but continues to struggle to breath. Her O2 is 88% on 6 L via a face mask. What is she experiencing clinically? What is she at risk for in terms of ARDS progression? What is she experiencing clinically? Refractory hypoxemia What is she at risk for in terms of ARDS progression? See next slides. As J.P.'s symptoms worsen, she works hard to breathe. She develops diffuse crackles throughout her lungs. She is pale and diaphoretic. Vital signs: BP 158/98, HR 114, RR 32, O2 sat 84%. What diagnostic tests would be indicated for J.P? What is the next step in treatment for her? What diagnostic tests would be indicated for J.P.? Pulmonary function tests Repeat chest x-ray Arterial blood gases What is the next step in treatment for her? Mechanical ventilation See next slides. J.P.'s daughter arrives to be with her. She shares that her mother had smoked for over 30 years, but quit 20 years ago. She asks you if smoking contributed to her respiratory problems now. Ask students to respond to J.P.'s daughter's question. What other history would they gather from the daughter and J.P.'s long-term care facility chart? See next slides. J.P. is now on mechanical ventilation, sedated to allow her to rest, and beginning to improve slowly. Her O2 saturation is now 92% and her blood gases are slowly returning to normal. Have students identify appropriate nursing diagnoses for J.P. What are her goals for recovery? Have students discuss appropriate collaborative and nursing interventions.

ARDS Respiratory Therapy

Kinetic therapy Patient rotated side-to-side >40 degrees CLRT provides continuous, slow, side-to-side turning of the patient by rotating the actual bed frame <40 degrees. In addition, the bed may contain a vibrator pack that provides chest physical therapy. 18-24hrs

TB Clinical Manifestations

LTBI - asymptomatic Pulmonary TB Constitutional symptoms (fatigue, malaise, anorexia, weight loss, low-grade fever, night sweats) Symptoms of pulmonary TB usually do not develop until 2 to 3 weeks after infection or reactivation. The characteristic pulmonary manifestation is an initial dry cough that frequently becomes productive with mucoid or mucopurulent sputum. Dyspnea is a late symptom that may signify considerable pulmonary disease or a pleural effusion. Hemoptysis, which occurs in less than 10% of patients with TB, is also a late symptom.

Complications - TB pneumonia

Large amounts of bacilli discharged from granulomas into lung or lymph nodes Manifests as bacterial pneumonia Other organ development Spinal destruction Bacterial meningitis Peritonitis Because TB can infect organs throughout the body, various acute and long-term complications can result. TB in the spine (Pott's disease) can lead to destruction of the intervertebral disc and adjacent vertebrae. Central nervous system TB can cause severe bacterial meningitis. Abdominal tuberculosis can lead to peritonitis, especially in HIV-positive patients. The kidneys, adrenal glands, lymph nodes, and urogenital tract may also be affected.

Epicardial Pacing

Leads placed on epicardium during heart surgery Passed through chest wall and attached to external power source as needed Epicardial pacing involves attaching an atrial and ventricular pacing lead to the epicardium during heart surgery. The leads are passed through the chest wall and attached to the external power source. Epicardial pacing leads are placed prophylactically in case any bradydysrhythmias or tachydysrhythmias occur in the early postoperative period.

PostopNeurologic status aorta

Level of consciousness Pupil size and response to light Facial symmetry Speech Ability to move upper extremities Quality of hand grasps when descending aorta is involved = neurovascular assessment of the lower extremities is important. Check skin temperature and color, capillary refill time, and sensation and movement of the extremities.

Prodysrhythmia

Life-threatening dysrhythmia caused by antidysrhythmic drugs Severe LV (bc largest) dysfunction increases risk Digoxin and class IA, IC, and III antidysrhythmia drugs Antidysrhythmia drugs can cause life-threatening dysrhythmias similar to those for which they are given. The patient who has severe left ventricular dysfunction is the most susceptible to prodysrhythmias. first several days of drug therapy = vulnerable period for developing prodysrhythmias. For this reason, many oral antidysrhythmia drug regimens are started in a monitored hospital setting.

Defibrillation

LifePak contains a monitor, defibrillator, and transcutaneous pacemaker. An automatic external defibrillator (AED) is a defibrillator that has rhythm detection capability and the ability to advise the operator to deliver a shock using hands-free defibrillator pads. Proficiency in the use of the AED is a part of the basic life support course for HCPs.

Pneumonia Etiology

Likely to result when defense mechanisms become incompetent or overwhelmed ↓ Cough and epiglottal reflexes may allow aspiration Normally, the airway distal to the larynx is protected from infection by various defense mechanisms. Mechanisms that create a mechanical barrier to microorganisms entering the tracheobronchial tree include air filtration, epiglottis closure over the trachea, cough reflex, mucociliary escalator mechanism, and reflex bronchoconstriction. Immune defense mechanisms include secretion of immunoglobulins A and G and alveolar macrophages. Pneumonia is more likely to occur when defense mechanisms become incompetent or are overwhelmed by the virulence or quantity of infectious agents. Decreased consciousness weakens the cough and epiglottal reflexes, which may allow aspiration of oropharyngeal contents into the lungs. Mucociliary mechanism impaired Pollution Cigarette smoking Upper respiratory infections Tracheal intubation Aging Chronic diseases suppress immune system Air pollution, cigarette smoking, viral upper respiratory infections (URIs), tracheal intubation, and normal changes that occur with aging can impair the mucociliary escalator mechanism. Chronic diseases can suppress the immune system's ability to inhibit bacterial growth. The risk factors for pneumonia are listed in Table 27-1.

Case Study

M. Z. is a 28-year-old male who arrives to the ED following a high-speed motor vehicle accident. He is complaining of severe chest pain, rating it at a 10 on a scale of 0 to 10. You notice that his breathing is labored. Part of his chest wall is moving in the opposite direction of the remainder when he breathes. M.Z.'s BP is 96/50, heart rate 126, respiratory rate 36, temp 37° C, and pulse oximetry 88% on 4L of oxygen. He is alert and oriented and states that his car was "T-boned" on the driver's side where he was sitting. He has no open wounds. How would you classify M.Z.'s trauma? Based on his presentation and the mechanism of injury, what type of injury would you suspect M.Z. to have? Blunt trauma Pneumothorax, fractured ribs with flail chest What potential life-threatening complication of a potential pneumothorax would you need to assess M.Z. for? What would you look for? What would be your priority nursing assessments of M.Z.? What are your priority nursing interventions for M.Z.? M.Z.'s chest x-ray confirms the presence of right-sided fractures in ribs 6-9 in two places each with a free- standing segment. He also has a moderate-sized right hemopneumothorax. ED physician asks to prepare for chest tube insertion. How would you set up a water- suction chest tube drainage system? How would you position him for insertion of chest tube? Put water into water-seal compartment (middle compartment) to the 2 cm mark. Add water to the suction control chamber to the 20 cm level unless otherwise ordered. Attach suction tubing to drainage unit and to wall suction. Position him on left side with right arm raised above the head. Head of bed is elevated to allow diaphragm to fall downward. M.Z. tolerated the chest tube insertion well. The tube is attached to a water-seal drainage unit and to wall suction with -20 cm of water in the suction control chamber. What would be your priority assessments post-insertion? Respiratory and cardiopulmonary status as before, assess for tidaling and bubbling (air leak) in water-seal chamber, monitor drainage amount, assess for subcutaneous emphysema. M.Z. is stabilized and ready for transfer to the progressive care unit. What could the receiving RN delegate to an unlicensed nursing personnel (UAP) in order to optimize time management? Obtain vital signs and report these to the RN. Keep the drainage system and all tubing below chest level. Encourage patient deep breathing to prevent atelectasis. Assist with range-of-motion exercises if they are part of the plan of care. Measure chest tube output as a part of the intake and output and mark the drainage level on the drainage collection unit.

Acute Kidney Injury dx test contraindicated:

MRI with gadolinium contrast medium Magnetic resonance angiography (MRA) w/ gadolinium contrast medium Nephrogenic systemic fibrosis Admin of gadolinium can be potentially fatal. pt w/ kidney failure, CIN can occur when contrast medium for dx studies causes nephrotoxic injury. pt w/ DM receiving metformin, drug should be held for 48 hours prior to and after the use of contrast media to decr risk of lactic acidosis. avoid CIN = avoid exposure to contrast media by using other dx tests such as US.

Nutritional therapy AKI

Maintain caloric intake Primarily carbohydrates and fat Limited protein, sodium Enteral nutrition goal = provide adequate calories to prevent catabolism despite restrictions necessary to prevent electrolyte disorders, fluid disorders, azotemia. Nutritional intake must maintain adequate caloric intake (30 to 35 kcal/kg, 0.8 to 1.0 g of protein per kilogram of body weight) = prevent breakdown of body protein for energy purposes. energy = from carb, fat sources to prevent ketosis from endogenous fat breakdown, gluconeogenesis from muscle protein breakdown. Supplementation of essential amino acids can be given for amino acid replacement. Sodium = restricted = prevent edema, hypertension, HF Dietary fat = increased = 30% to 40% of total calories from fat. cannot maintain oral intake = enteral nutrition . When the gastrointestinal (GI) tract is not functional, parenteral nutrition is necessary to provide adequate nutrition. The patient treated with parenteral nutrition may need daily HD or CRRT to remove the excess fluid.

Maintain graft patencyaorta post op

Maintain graft patency by Normal BP IV fluids blood components CVP or PA pressure monitoring Urinary output monitoring Avoid severe hypertension= Drug therapy may be indicated

ARDS Medical Supportive Therapy

Maintenance of cardiac output and tissue perfusion Hemodynamic monitoring via a central venous or pulmonary artery catheter Monitor CO and BP Sample blood for ABGs CO falls = crystalloid fluids or colloid Use of inotropic drugs such as dobutamine (Dobutrex) or dopamine (Intropin) = incr muscle contrations Packed red blood cells = incr hemoglobin = O2-carrying capacity Controversy exists regarding the optimal hemoglobin level. Some advocate keeping the level around 9 gm/dL (90 g/L) with an SpO2 of 90% or more (when PaO2 is greater than 60 mm Hg). Others recommend hemoglobin levels greater than 7 gm/dL (70 g/L). Enteral or parenteral feedings are started Monitor daily weight, intake and output Increasing pulmonary capillary permeability results in fluid in the lungs and causes pulmonary edema. At the same time, the patient may be volume depleted. This places the patient at risk for hypotension and decreased CO from mechanical ventilation and PEEP. The patient is often placed on fluid restriction, and diuretics are used as necessary.

Acute Kidney Injury Interprofessional Care

Manage signs and symptoms/Prevent complications AKI is potentially reversible, primary goals of tx are to eliminate cause Force fluids Osmotic diuretics (mannitol) monitor I&O during oliguric phase first step = determine adequate intravascular volume and CO to ensure adequate perfusion of the kidneys. Diuretic therapy may be administered and usually includes loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) or osmotic diuretic (e.g., mannitol). If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful. The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g., respiration, diaphoresis).

Nursing ManagementAcute Kidney Injury

Measure VS Measure I&O Examine urine Assess general appearance Observe dialysis access site Mental status/level of consciousness Oral mucosa Lung sounds Heart rhythm Laboratory values Diagnostic test results Daily monitoring of a patient's urine output is essential because this information provides prognostic implications and is crucial in determining therapy and daily fluid volume replacement. Examine the urine for color, specific gravity, glucose, protein, blood, and sediment. Assess the patient's general appearance, including skin color, edema, neck vein distention, and bruises. If a patient is receiving dialysis, observe the access site for signs of inflammation and exudate. Evaluate the patient's mental status and level of consciousness. Examine the oral mucosa for dryness and inflammation. Auscultate the lungs for crackles and rhonchi or diminished breath sounds. Monitor the heart for the presence of an S3 gallop, murmurs, or a pericardial friction rub. Assess ECG readings for the presence or development of dysrhythmias. Review laboratory values and diagnostic test results.

Second-Degree AV Block, Type 2 (Mobitz II)

Middle part shows the blocked/dropped QRS Pwaves will stay the same Pwaves are there but dont lead to QRS Associated with heart disease and drug toxicity Often progressive and results in decr CO Treat with pacemaker Type II AV block is associated with rheumatic heart disease, CAD, anterior MI, drug toxicity . Type II AV block often progresses to third-degree AV block and is associated with a poor prognosis reduced HR = decr CO = hypotension = myocardial ischemia. Type II AV block is an indication for therapy with a permanent pacemaker. Transcutaneous pacing or the insertion of a temporary pacemaker before the insertion of a permanent pacemaker if the patient becomes symptomatic (e.g., hypotension, angina). Atropine NOT an effective drug for this In type II second-degree AV block (Mobitz II heart block), a P wave is nonconducted without progressive PR lengthening. This usually occurs when a block in one of the bundle branches is present. On conducted beats, the PR interval is constant. Atrial rate is usually normal. Ventricular rate depends on the degree of AV block. P wave has a normal shape. PR interval = normal or prolonged in duration and remains constant on conducted beats. QRS greater than 0.12 second bc of bundle branch block.

TB Complications - Miliary TB

Miliary TB Large numbers of organisms spread via the bloodstream to distant organs Fatal if untreated Manifestations progress slowly and vary depending on which organs are infected Fever, cough, and lymphadenopathy occur Can include hepatomegaly and splenomegaly Appropriately treated pulmonary TB typically heals without complications except for scarring and residual cavitation within the lung. Significant pulmonary damage, although rare, can occur in patients who are poorly treated or who do not respond to TB treatment. Miliary TB is the widespread dissemination of the mycobacterium. The bacteria are spread via the bloodstream to several distant organs. The infection is characterized by a large amount of TB bacilli and may be fatal if left untreated. It can occur as a result of primary disease or reactivation of latent infection. Clinical manifestations of miliary TB slowly progress over a period of days, weeks, or even months. Symptoms vary depending on the organs that are affected. Fever, cough, and lymphadenopathy are present. Hepatomegaly and splenomegaly may also occur.

Acute Coronary Syndrome Minimally invasive direct coronary artery bypass (MIDCAB)

Minimally invasive direct coronary artery bypass (MIDCAB) For patients with disease of left anterior descending or right coronary artery Does not involve a sternotomy and CPB Minimally invasive direct coronary artery bypass (MIDCAB) offers patients with disease of the left anterior descending or right coronary artery an approach to surgical treatment that does not involve a sternotomy and CPB. The technique requires several small incisions between the ribs or a mini thoracotomy. A thoracoscope or robotic assistance is used to dissect the IMA from the chest. A mechanical stabilizer immobilizes the operative site. The IMA is then sutured to the left anterior descending or right coronary artery. Some patients undergo hybrid procedures where they have a MIDCAB for the left anterior descending artery and undergo a PCI of a second or third artery at a later time.

Nursing ManagementAcute Coronary Syndrome - Coronary revascularization: PCI

Monitor for recurrent angina Frequent VS, including cardiac rhythm Monitor catheter insertion site for bleeding Neurovascular assessment Bed rest per institutional policy Patients with ACS may undergo coronary revascularization with PCI or CABG surgery. The major nursing responsibilities for the care of the patient following PCI involve: Monitoring for signs of recurrent angina Frequent assessment of vital signs, including HR and rhythm Evaluation of the catheter insertion site for signs of bleeding Neurovascular assessment of the involved extremity Maintenance of bed rest per institution policy.

Gerontologic Considerations AKI

More susceptible to AKI Dehydration Polypharmacy- diuretics, laxatives Illness immobility Hypotension Diuretic therapy Aminoglycoside therapy Obstructive disorders Surgery Infection Dehydration = predisposing factor, tends to occur much more frequently in older adults. Dehydration from = polypharmacy (diuretics, laxatives, drugs that suppress appetite or consciousness), acute febrile illnesses, immobility/bedridden. Other common causes of AKI in elder = hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders (e.g., prostatic hyperplasia), surgery, infection, contrast media. Mortality rates similar for older and younger patients. over 65 years = less likely to recover from AKI. Despite this, a patient's chronologic age is not a barrier to offering renal replacement therapy.

Complications of Myocardial Infarction - Heart failure

Occurs when pumping power of heart has diminished Left-sided HF Mild dyspnea, restlessness, agitation, slight tachycardia initially Right-sided HF Jugular venous distention, hepatic congestion, lower extremity edema Heart failure (HF) is a complication that occurs when the right or left heart's pumping action is reduced. Depending on the severity and extent of the injury, left-sided HF occurs initially with subtle signs such as mild dyspnea, restlessness, agitation, or slight tachycardia. Other signs indicating the onset of left-sided HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds on auscultation of the heart, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea. Signs of right-sided HF include jugular venous distention, hepatic congestion, or lower extremity edema.

Pneumonia Clinical Manifestations

Most common Cough Fever, chills Dyspnea, tachypnea Pleuritic chest pain Green, yellow, or rust-colored sputum Change in mentation for older or debilitated patients Nonspecific manifestations Viral pneumonia may initially present as influenza, with respiratory symptoms appearing and/or worsening 12 to 36 hours after onset. The older or debilitated patient may not have classic symptoms of pneumonia. Confusion or stupor (possibly related to hypoxia) may be the only finding. Hypothermia, rather than fever, may also be noted with the older patient. Nonspecific clinical manifestations include diaphoresis, anorexia, fatigue, myalgias, and headache. Physical examination findings Fine or coarse crackles Bronchial breath sounds Egophony - a change in the sound of the voice of the patient -listen ↑ Fremitus - (vibration of the chest wall produced by vocalization With pleural effusion may exhibit dullness to percussion over the affected area. - feel vibration On physical examination, fine or coarse crackles may be auscultated over the affected region. If consolidation is present, bronchial breath sounds, egophony (a change in the sound of the voice of the patient) and increased fremitus (vibration of the chest wall produced by vocalization) may be noted. Patients with pleural effusion may exhibit dullness to percussion over the affected area.

Complications of Myocardial Infarction - Dysrhythmias

Most common complication Present in 80% to 90% of MI patients Can be caused by ischemia, electrolyte imbalances, or SNS stimulation VT and VF are most common cause of death in prehospitalization period Any condition that affects the heart cells' sensitivity to nerve impulses (e.g., ischemia, electrolyte imbalances, SNS stimulation) can cause dysrhythmias that adversely affect the damaged heart muscle. Bradycardias (e.g., complete heart block) develop when key areas of the conduction system are destroyed. VT or VF most often occur within the first 4 hours after the onset of pain. Premature ventricular contractions (PVCs) may precede VT and VF. Life-threatening ventricular dysrhythmias must be treated immediately. With reperfusion, it is not uncommon to see PVCs, asymptomatic nonsustained VT, and idioventricular rhythms. These rhythms are not associated with an increased risk of sudden cardiac death (SCD) and are not treated unless the patient is symptomatic.

Disorders of the Aorta

Most common vascular problems of aorta Aneurysms Aortoiliac occlusive disease Aortic dissection

Cardiac Tamponade

Muffled, distant heart sounds, Hypotension, Neck vein distention, Incr CVP (central venous pressure) Blood rapidly collects in pericardial sac, compresses myocardium because the pericardium does not stretch, and prevents ventricles from filling. Medical emergency: pericardiocentesis with surgical repair as appropriate

Clinical Manifestations of ACS Myocardial Infarction - n/v/fever

Nausea and vomiting Reflex stimulation of the vomiting center by severe pain Vasovagal reflex Fever Up to 100.4° F (38° C) in first 24-48 hours Systemic inflammatory process caused by heart cell death The temperature may increase to 100.4° F (38° C) within the first 24-48 hours. The temperature elevation may last for as long as 4-5 days. This increase in temperature is due to a systemic inflammatory process caused by the death of heart cells.

Clinical Manifestations of ACS Unstable Angina

New in onset Occurs at rest Increase in frequency, duration, or with less effort Pain lasting > 10 minutes Needs immediate treatment Symptoms in women often under-recognized Unstable angina (UA) is chest pain that is new in onset, occurs at rest, or occurs with increasing frequency, duration, or with less effort than the patient's chronic stable angina pattern. The pain typically lasts 10 minutes or more. Prompt treatment is needed for patients suspected of having UA. The patient with previously diagnosed chronic stable angina will describe a significant change in the pattern of angina. It will occur with increasing frequency and is easily provoked by minimal or no exertion, during sleep, or even at rest. Unlike chronic stable angina, UA is unpredictable and must be treated immediately. Despite efforts to increase awareness, women's symptoms continue to be under-recognized as heart related. These include fatigue, shortness of breath, indigestion, and anxiety. Fatigue is the most prominent symptom. However, all these symptoms can relate to many different diseases and syndromes. It is because of these reasons that women often present with UA before CAD is diagnosed.

ARDS Evaluation

No abnormal breath sounds Effective cough and expectoration Normal respiratory rate, rhythm, and depth Synchronous thoracoabdominal movement Appropriate use of accessory muscles Decreased or absent peripheral edema Normal pulmonary artery or pulmonary artery wedge pressures Decreased anxiety Verbalization of positive attitude toward outcome PaO2 and PaCO2 within normal ranges or at baseline Maintenance of weight or weight gain Serum albumin and protein within normal ranges

Changes Associated With Infarction

Note the deep, wide Q wave, indicating the presence of a myocardial infarction. T wave inversion related to MI occurs within hours following the event and may persist for months. The ECG changes seen in injury and MI reflect electrical disturbances in the myocardial cells caused by a prolonged lack of blood and oxygen leading to necrosis. SLIDE 62 in dysrhy powerpoint

Pacemakers - Postprocedure care

OOB once stable Limit arm and shoulder activity Monitor insertion site for bleeding and infection Patient teaching important After the pacemaker has been inserted, the patient can be out of bed once stable. Have the patient limit arm and shoulder activity on the operative side to prevent dislodging the newly implanted pacing leads. Observe the insertion site for signs of bleeding and check that the incision is intact. Note any temperature elevation or pain at the insertion site and treat as ordered. Most patients are discharged the next day if stable. Provide patient teaching (see next slide).

Complications of Myocardial Infarction - Cardiogenic shock

Occurs because of = Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction Requires aggressive management = Associated with a high death rate Cardiogenic shock occurs when oxygen and nutrients supplied to the tissues are inadequate because of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction. This occurs less often with the early and rapid treatment of STEMI with PCI or thrombolytic therapy. When cardiogenic shock does occur, it is associated with a high death rate. Cardiogenic shock requires aggressive management. This includes control of dysrhythmias, intraaortic balloon pump (IABP) therapy, and support of contractility with vasoactive drugs. Goals of therapy are to maximize oxygen delivery, reduce oxygen demand, and prevent complications (e.g., acute kidney injury).

Interprofessional CareAcute Coronary Syndrome - OPCAB

Off-pump coronary artery bypass (OPCAB) Sternotomy but no CPB Robotic or totally endoscopic coronary artery bypass (TECAB) Transmyocardial laser revascularization Indirect revascularization High-energy laser creates channels in heart to allow blood flow to ischemic areas OPCAB The off-pump coronary artery bypass (OPCAB) procedure uses a median sternotomy to access all coronary vessels. OPCAB is performed on a beating heart (no CPB) using mechanical stabilizers. OPCAB is associated with less blood loss, less renal dysfunction, less postoperative atrial fibrillation, and fewer neurologic complications. It is estimated that less than 20% of CABG procedures are OPCAB procedures. OPCAB is primarily used for patients with multiple comorbidities who should avoid CPB. TECAB This technique uses a robot in performing CABG surgery. This procedure is done without the use of CPB or with the use of CPB using femoral access. TECAB is used for limited bypass grafting. The benefits include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time. Transmyocardial Laser Revascularization Transmyocardial laser revascularization is an indirect revascularization procedure. It is used for patients with advanced CAD who are not candidates for traditional CABG surgery and who have persistent angina despite maximum medical therapy. The procedure involves the use of a high-energy laser to create channels in the heart muscle to allow blood flow to ischemic areas. The procedure can be done using a left thoracotomy approach or in combination with CABG surgery. It is as an adjunctive therapy when bypass grafts cannot be placed.

Aortic AneurysmClinical Manifestations - Abdominal aortic aneurysms (AAA)

Often asymptomatic Frequently detected On routine physical exam - can see pulse when they lay down on abdomen When patient examined for unrelated problem (i.e., CT scan, abdominal x-ray) A pulsatile mass in the periumbilical area slightly to the left of the midline may be present. Bruits may be auscultated over the aneurysm. Physical findings may be more difficult to detect in obese individuals.

Aortic Dissection

Often misnamed "dissecting aneurysm" Not a type of aneurysm Result of a false lumen through which blood flows Aortic dissection results from the creation of a false lumen between the intima (inner lining) and the media (middle layer) of the arterial wall. Aortic dissection is classified based on the location of the dissection and duration of onset. Type A dissection affects the ascending aorta and arch. Type B dissection begins in the descending aorta. Dissections are also classified as acute (first 14 days), sub-acute (14 to 90 days), or chronic (greater than 90 days) based on symptom onset. (See next 2 slides for figures.) Affects men more often than women Occurs most frequently in sixth and seventh decades of life Predisposing factors include age, aortic diseases (e.g., aortitis, coarctation, arch hypoplasia), atherosclerosis, blunt or iatrogenic trauma, tobacco use, cocaine or methamphetamine use, congenital heart disease (e.g., bicuspid aortic valve), connective tissue disorders (e.g., Marfan's or Ehlers-Danlos syndrome), family history, history of heart surgery, male gender, pregnancy, and poorly controlled hypertension. Nearly half of all acute aortic dissections in patients younger than 40 years of age occur in patients with Marfan's syndrome.

Flutter (Heimlich) Valve

One-way valve that opens only when intrathoracic pressure greater than atmospheric pressure Used for emergency transport and for small-to moderate-sized pneumothorax Increased patient mobility Must vent any attached drainage bag A flutter valve (also called the Heimlich valve after its inventor) is used to evacuate air from the pleural space. This device consists of a one-way rubber valve within a rigid plastic tube. It is attached to the external end of the chest tube. During inspiration, when pressure in the chest is greater than atmospheric pressure, the valve opens. During expiration, when intrathoracic pressure is less than atmospheric pressure, the valve closes. The flutter valve can be used for small- to moderate-sized pneumothorax. = mobility of the patient, as the smaller drainage bag can be hidden under the clothes while the patient ambulates. Drainage bags attached to the flutter valve must have a vent to the atmosphere in order to prevent a potential tension pneumothorax = cutting a small slit in the top of any drainage bag that does not have a built-in vent. Patients may go home with a Heimlich valve in place.

Interprofessional CareAcute Coronary Syndrome - Thrombolytic therapy

Only for patients with a STEMI Agencies that do not have cardiac catheterization resources Given IV within 30 minutes of arrival to the ED Patient selection critical Thrombolytic (fibrinolytic) therapy is only indicated for patients with a STEMI. It offers the advantages of availability and rapid administration in agencies that do not have an interventional cardiac catheterization laboratory or one is too far away to transfer the patient safely. Treatment of STEMI with thrombolytic therapy aims to limit the infarction size by dissolving the thrombus in the coronary artery and reperfusing the heart muscle. The goal is to give the thrombolytic within 30 minutes of the patient's arrival to the ED. All thrombolytics are given IV. Because all thrombolytics lyse the pathologic clot, they may also lyse other clots (e.g., a postoperative site). Therefore patient selection is important because minor or major bleeding can be a complication of therapy. Inclusion criteria for thrombolytic therapy are (1) chest pain less than 12 hours with 12-lead ECG findings consistent with acute STEMI and (2) no absolute contraindications. Patients with chest pain lasting 12-24 hours with ECG changes supporting STEMI may be considered for thrombolytic therapy. Draw blood and start 2-3 IV sites Complete invasive procedures prior Administer according to protocol Monitor closely for signs of bleeding Assess for signs of reperfusion Return of ST segment to baseline best sign IV heparin to prevent reocclusion

Pneumocystis jiroveci pneumonia (PJP)

Onset slow and subtle Diffuse bilateral infiltrates to massive consolidation Can be life threatening Spread to other organs Treat with trimethoprim/sulfamethoxazole IV or orally most common form of pneumonia in people with HIV disease. onset is slow and subtle, s/s fever, tachypnea, tachycardia, dyspnea, nonproductive cough, hypoxemia. Cxray diffuse bilateral infiltrates. widespread disease = massive consolidation. PJP can be life threatening, causing acute respiratory failure and death. Infection can spread = liver, bone marrow, lymph nodes, spleen, and thyroid. Bacterial and viral pneumonias must first be ruled out because of the vague presentation of PJP. causative agent is fungal but doesnt respond to antifungal agents.

open vs closed pneumothorax

Open Air enters through an opening in the chest wall Closed No external wound open (air entering through an opening in the chest wall) closed (no external wound). Penetrating trauma allows air to enter the pleural space through an opening in the chest wall Examples: stab or gunshot wounds and surgical thoracotomy.

ARDS Respiratory Therapy

Oxygen administration Primary goal is to correct hypoxemia nasal cannula or face mask with high-flow systems used to maximize O2 Need intubation with mechanical ventilation to maintain the PaO2 at acceptable levels Positive pressure ventilation = PEEP at 5 cm H2O compensates for loss of glottic function Opens collapsed alveoli Apply PEEP at 3 to 5 cm H2O increments Higher levels of PEEP may be used in patients with ARDS During PPV, it is common to apply PEEP at 5 cm H2O to compensate for loss of glottic function caused by the endotracheal tube. In patients with ARDS, higher levels of PEEP (e.g., 10 to 20 cm H2O) may be used. PEEP increases FRC and opens up collapsed alveoli. PEEP may improve V/Q in respiratory units that collapse at low airway pressures, thus allowing the FIO2 to be lowered. Positive pressure ventilation Can compromise venous return to right side of heart Decreases preload, CO, and BP Can hyperinflate alveoli Can result in barotrauma or volutrauma The additional intrathoracic and intrapulmonic pressures created by PEEP can compromise venous return to the right side of the heart, thereby decreasing preload, CO, and BP. High levels of PEEP cause hyperinflation of the alveoli, compression of the pulmonary capillary bed, reduction in blood return to the left side of the heart, and a dramatic reduction in BP. In addition, high levels of PEEP or excessive inspiratory pressures can result in barotrauma and volutrauma. Alternative modes of mechanical ventilation and respiratory therapies if hypoxemia persists Airway pressure release ventilation Pressure control inverse ratio ventilation High-frequency ventilation Permissive hypercapnia Extracorporeal membrane oxygenation (ECMO) and extracorporeal CO2 removal (ECCO2R) are external devices cannulated within large blood vessels. This allows blood to pass across a gas-exchanging membrane outside the body and then return oxygenated blood back to the body. ECCO2R with PPV allows the lungs to heal while lung function is inadequate to maintain adequate oxygenation and CO2 removal. Positioning strategies When in supine position mediastinal and heart contents place more pressure on lungs than when in prone Predisposes patient to atelectasis Fluid pools in dependent regions of lung If you turn the patient from supine to prone, air-filled, alveoli in the ventral (anterior) portion of the lung become dependent. Perfusion may be better matched to ventilation.

Upper Respiratory Problems

PROBLEMS OF PHARYNX • Acute pharyngitis is an acute inflammation of the pharyngeal walls that may include the tonsils, palate, and uvula. • ♣ Symptoms range in severity from complaints of a "scratchy throat" to pain so severe that swallowing is difficult. Both viral and streptococcal infections appear as a red and edematous pharynx, with or without patchy exudates, so appearance is not always diagnostic. • ♣ The goals of nursing management for acute pharyngitis are infection control, symptomatic relief, and prevention of secondary complications. • Peritonsillar abscess—a complication of acute pharyngitis—may threaten the airway if severe. Treatment includes IV antibiotics, needle aspiration, drainage, or surgery. PROBLEMS OF TRACHEA AND LARYNX • Airway obstruction is a medical emergency. Interventions to reestablish a patent airway include the obstructed airway (Heimlich) maneuver, cricothyroidotomy, ET intubation, and tracheostomy. • A tracheostomy is a surgically created opening in the anterior trachea for the purpose of establishing an airway. • ♣ Indications for a tracheostomy are to (1) bypass an upper airway obstruction, (2) facilitate removal of secretions, and/or (3) permit long-term mechanical ventilation. • ♣ A wide variety of tracheostomy tubes are available. You must provide care specific to the type of tube present. • ♣ Care of the patient with a tracheostomy tube can be divided into two phases: acute care and chronic care. • ♣ Nursing care for any tracheostomy patient includes the nursing diagnoses of ineffective airway clearance, risk for aspiration, impaired verbal communication, and ineffective self-care management. LARYNGEAL POLYPS • Polyps on the vocal cords develop as a result of vocal abuse or irritation. • The most common symptom is hoarseness. • They are treated conservatively with voice rest and adequate hydration. Surgical removal may be indicated for large polyps, which may cause dyspnea.

biphasic defibrillation

Paddle placement and current flow in monophasic defibrillation (A) and biphasic defibrillation (B). Note that paddle placement is identical—the difference is in the direction of current flow. monophasic defibrillation only goes 1 way

Nursing ManagementAcute Coronary Syndrome - Acute Care

Pain: nitroglycerin, morphine, oxygen Continuous monitoring ECG ST segment Heart and breath sounds VS, pulse oximetry, I and O Rest and comfort Balance rest and activity Begin cardiac rehabilitation Priority interventions are aimed at decreasing the oxygen needs of a compromised heart muscle and reducing the risk of complications. Provide NTG, morphine sulfate, and supplemental oxygen as needed to eliminate or reduce chest pain. Ongoing evaluation and documentation of the effectiveness of the interventions is important. Maintain continuous ECG monitoring while in the ED and ICU and after transfer to a step-down or general unit. Dysrhythmias need to be identified quickly and treated. During the initial period after MI, ventricular fibrillation is the most common lethal dysrhythmia. In many patients, premature ventricular contractions or ventricular tachycardia precedes this dysrhythmia. Monitor the patient for the presence of reinfarction or ischemia by monitoring the ST segment for shifts above or below the baseline of the ECG. Silent ischemia can occur without subjective symptoms (e.g., chest pain). It is noted by ST segment changes only. Notify the HCP if you see ST segment changes without any clinical symptoms. Perform a physical assessment to detect deviations from the patient's baseline findings. Assess heart and breath sounds and any evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). In addition to routine vital signs and pulse oximetry, monitor intake and output at least once a shift. It is important to promote rest and comfort with any degree of heart damage. Bed rest may be ordered for the first few days after an MI involving a large portion of the LV. A patient with an uncomplicated MI (e.g., angina resolved, no signs of complications) may rest in a chair within 8 to 12 hours after the event. The use of a commode or bedpan is based on patient preference. When sleeping or resting, the body requires less work from the heart than it does when active. It is important to plan nursing and other interventions to ensure adequate rest periods free from interruption. Comfort measures that can promote rest include a quiet environment, use of relaxation therapy (e.g., guided imagery), and assurance that staff are nearby and responsive to the patient's needs. Phase 1 of cardiac rehab occurs in the hospital. It is important that the patient understands the reasons why activity is limited but not completely restricted. Gradually increase the patient's cardiac workload through more demanding physical tasks so that the patient can achieve a discharge activity level adequate for home care. Phase 2 of rehab begins when the patient is discharged home and continues for 2 to 12 weeks. Phase 3 is long-term maintenance for optimal cardiac health. Anxiety reduction Identify source and alleviate Patient teaching important Emotional and behavioral reaction Maximize patient's social support systems Consider open visitation To some degree anxiety is present in all patients with ACS. Your role is to identify the source of anxiety and assist the patient in reducing it. If the patient is afraid of being alone, allow a caregiver to sit by quietly or check in with the patient frequently. For anxiety caused by lack of information, provide teaching based on the patient's stated need and level of understanding. Answer the patient's questions with clear, simple explanations. It is important to start teaching at the patient's level rather than to present a prepackaged program. For example, patients generally are not ready to learn about the pathology of CAD. The earliest questions usually relate to how the disease affects perceived control and independence. Examples include the following: When will I leave the intensive care unit? When can I be out of bed? When will I be discharged? When can I return to work? How many changes will I have to make in my life? Will this happen again? Often the patient may not be able to ask the most serious concern of ACS patients: Am I going to die? Even if a patient denies this concern, it is helpful for you to start conversation by remarking that fear of dying is a common concern among most patients who have experienced ACS. This gives the patient "permission" to talk about an uncomfortable and fearful topic. The emotional and behavioral reactions of a patient vary but often follow a predictable response pattern. Your role is to understand what the patient is currently experiencing and to support the use of constructive coping styles. Assess the support structure of the patient and caregiver. Determine how you can help maximize the support system. Often the patient is separated from the most significant support system at the time of hospitalization. Your role can include talking with the caregiver(s), informing them of the patient's progress, allowing the patient and caregiver to interact as necessary, and supporting the caregivers who will be able to provide the necessary support to the patient. Open visitation is helpful in decreasing anxiety and increasing support for the patient with ACS.

Nursing ManagementNursing Implementation -Acute CareAorta

Patient/caregiver teaching Providing emotional support for patient/caregiver Careful assessment of all body systems

TB Acute CareNursing Implementation

Patients admitted to the emergency department or directly to the nursing unit with respiratory symptoms should be assessed for the possibility of TB. Those strongly suspected of having TB should (1) be placed on airborne isolation; (2) receive a medical workup, including chest x-ray, sputum smear, and culture; and (3) receive appropriate drug therapy. High-efficiency particulate air (HEPA) masks are worn whenever entering the patient's room. These masks are highly effective at protecting from small particles 5 μm or less in diameter. Airborne infection isolation is indicated for the patient with pulmonary or laryngeal TB until the patient is noninfectious.

TB Drug Therapy - Active disease

Patients should be taught about side effects and when to seek medical attention Liver function should be monitored Alternatives are available for those who develop a toxic reaction to primary drugs The major side effect of isoniazid, rifampin, and pyrazinamide is nonviral hepatitis. Drug alert on Isoniazid - Alcohol may increase hepatotoxicity - instruct patients to avoid drinking alcohol during treatment. If the patient develops a toxic reaction to the primary drugs, other drugs can be used including rifabutin and rifapentine (Priftin). Treatment for drug-resistant TB is guided by sensitivity testing.

Complications of Myocardial Infarction - Dressler syndrome

Pericarditis and fever that develops 1 to 8 weeks after MI Chest pain, fever, malaise, pericardial friction rub, arthralgia autoimmune reaction to the necrotic heart muscle. A pericardial effusion may be present. elevated white blood cell count and sedimentation rate. High dose aspirin is the treatment of choice. Nonsteroidal antiinflammatory drugs (NSAIDs) and corticosteroids are avoided in the first 4 weeks following MI because they can interfere with myocardial scar formation.

PostopPeripheral perfusion status aotra

Peripheral perfusion status Extremity assessment Temp, color, capillary refill time, sensation, and movement of extremities May need to use a Doppler to assess lower extremity pulses may be absent for a short time after surgery = vasospasm and hypothermia. decr or absent pulse together with a cool, pale, mottled, or painful extremity = embolization or graft occlusion Report these findings to the physician immediately. Pulse assessment Mark pulse locations with felt-tip pen You should check and record all peripheral pulses hourly for several hours and then routinely, based on institutional policy. When the ascending aorta and the aortic arch are involved, assess the carotid, radial, and temporal artery pulses. For surgery of the descending aorta, assess the femoral, popliteal, posterior tibial, and dorsalis pedis pulses.

Aortic AneurysmsClassification - True aneurysm

Wall of artery forms aneurysm At least one vessel layer still intact Further subdivided Fusiform Circumferential, relatively uniform in shape Saccular Pouchlike with narrow neck connecting bulge to one side of arterial wall

ECG Changes Associated With Acute Coronary Syndrome (ACS) - Infarction

Physiologic Q wave is the first negative deflection following the P wave Small and narrow (<0.04 second in duration) Pathologic Q wave is deep and >0.03 second in duration In addition to ST-segment elevation, a pathologic Q wave may be seen on the ECG in patients with infarction. A pathologic Q wave that develops during MI is wide (greater than 0.03 second in duration) and deep (greater than or equal to 25% of the height of the R wave). This is referred to as a Q wave MI. The pathologic Q wave may be present on the ECG indefinitely.

Pneumonia Interprofessional Care

Pneumococcal vaccine To prevent Streptococcus pneumoniae Prompt treatment with antibiotics is essential Prompt treatment with the appropriate antibiotic is essential. Antibiotics are highly effective for both bacterial and mycoplasma pneumonia. Response generally occurs within 48-72 hr ↓ Temperature Improved breathing ↓ Chest discomfort Repeat chest x-ray in 6-8 weeks Abnormal physical findings can last more than 7 days. Supportive care Oxygen for hypoxemia Analgesics for chest pain Antipyretics Individualize rest and activity No definitive treatment for majority of viral pneumonias Antivirals for influenza pneumonia O2, analgesics, antipyretics, asprin, acetaminophen Currently, there is no definitive treatment for the majority of viral pneumonias. As identified earlier, care is generally supportive. In most circumstances, viral pneumonia is self-limiting and will often resolve in 3-4 days. Antiviral therapy may be used to treat pneumonia caused by influenza (e.g., oseltamivir or zanamivir) and a few other viruses (e.g., acyclovir [Zovirax] for herpes simplex virus).

Radiofrequency Catheter Ablation Therapy

Postcare similar to cardiac catheterization Radiofrequency catheter ablation therapy uses electrical energy to "burn" or ablate areas of the conduction system as definitive treatment of tachydysrhythmias. Ablation therapy is done after EPS has identified the source of the dysrhythmia. An electrode-tipped ablation catheter ablates accessory pathways or ectopic sites in the atria, AV node, and ventricles. Catheter ablation is considered the nonpharmacologic treatment of choice for atrial dysrhythmias resulting in rapid ventricular rates and AV nodal reentrant tachycardia refractory to drug therapy. The ablation procedure is a successful therapy with a low complication rate.

Aortic AneurysmInterprofessional Care - Intraabdominal hypertension (IAH)

Potentially lethal complication in emergency repair Associated with abdominal compartment syndrome (ACS) Reduces blood flow to viscera End-organ perfusion impaired ACS refers to the impaired end-organ perfusion caused by IAH and resulting multisystem organ failure. Treatment Open surgical compression Percutaneous drainage Percutaneous drainage combined with tPA (tissue plasma activator = breaks down clot) infusion control of situations that lead to IAH. Conservative = intubation, ventilation, patient positioning, gastric decompression, cautious fluid resuscitation, pain meds, temporary hemofiltration

Temporary Pacemakers

Power source outside the body Transvenous Epicardial Transcutaneous A temporary pacemaker is one that has the power source outside the body.

Preop aorta

Preop teaching Brief explanation of disease process Planned surgical procedure Preop routines Bowel prep NPO Shower - hippaclense IV antibiotics right before incision made Expectations after surgery Recovery room, tubes, drains ICU - 24-48hrs β - blocker - IV to keep @ perfect range pt history of CVD usually receive a beta blocker (e.g., metoprolol [Lopressor]) preoperatively.

causes of Acute Kidney Injury

Prerenal = heart area intrarenal = in kidneys = drug tox postrenal =after kidney stones, cancer, bph causes of acute kidney injury (AKI).

Hs and Ts Pneumonic

Pulseless Electrical Activity Hypovolemia Hypoxia Hydrogen ion (acidosis) Hyper-/hypokalemia Hypoglycemia Hypothermia Toxins Tamponade (cardiac) Thrombosis (MI and pulmonary) Tension pneumothorax Trauma The most common causes of PEA can be easily remembered by thinking of your Hs and Ts: Hypovolemia, hypoxia, metabolic acidosis, hyper/hypokalemia, hypoglycemia, hypothermia Toxins (e.g., drug overdose), cardiac tamponade, thrombosis (e.g., MI, pulmonary embolus), tension pneumothorax, and trauma.

PE Goals of treatment

Prevent further thrombi Prevent further embolization to pulmonary system Provide cardiopulmonary support Supportive care variable Oxygen → mechanical ventilation Pulmonary toilet Fluids, diuretics, analgesics To reduce mortality risk, treatment is begun as soon as PE is suspected. The objectives are to (1) prevent further growth or extension of thrombi in the lower extremities, (2) prevent embolization from the upper or lower extremities to the pulmonary vascular system, and (3) provide cardiopulmonary support if indicated. Supportive therapy for the patient's cardiopulmonary status varies according to the severity of the PE. O2 can be given via mask or cannula, and the concentration of FIO2 is determined by ABG analysis. In some situations, endotracheal intubation and mechanical ventilation are necessary to maintain adequate oxygenation. Respiratory measures such as turning, coughing, deep breathing, and incentive spirometry are important to help prevent or treat atelectasis. If manifestations of shock are present, IV fluids are administered followed by vasopressor agents as needed to support perfusion. If heart failure is present, diuretics are used. Pain resulting from pleural irritation or reduced coronary blood flow is treated with opioids.

pericarditis Nursing Management

Primary Concern: Pain and Anxiety Assess Angina vs Pericarditis Assess for Risk of Complications Pain NSAIDS with food or milk to decrease risk of stomach ulcer Bed Rest Head of Bed at 45 degrees Anxiety Increase risk of Stress: Give Proton Pump Inhibitor pantoprazole (Protonix) Explain all procedures patient's pain and anxiety during acute pericarditis = primary nursing consideration. Assess the pain to distinguish angina (myocardial ischemia) from the pain of pericarditis. Pericarditis pain = precordium or left trapezius region and has a sharp, pleuritic quality that increases with inspiration = relieved when sits up or leans forward and is worse when lying flat. The patient with acute pericarditis is at risk for cardiac tamponade and decreased CO. Monitor for manifestations of tamponade and prepare for possible pericardiocentesis.

TB Classification

Primary infection When bacteria are Isoniazidaled Latent TB infection (LTBI) Infected but no active disease Active TB disease Primary TB Reactivation TB (post-primary) TB can also be classified according to its presentation - primary, latent, or reactivated and whether it is pulmonary or extrapulmonary. Primary TB infection occurs when the bacteria are Isoniazidaled and initiate an inflammatory reaction. The majority of people mount effective immune responses to encapsulate these organisms for the rest of their lives, preventing primary infection from progressing to disease. Latent TB infection (LTBI) is a TB infection in a person who does not have active TB disease. People with LTBI have a positive skin test but are asymptomatic. These individuals cannot transmit the TB bacteria to others but can develop active TB disease at some point. Immunosuppression, diabetes mellitus, poor nutrition, aging, pregnancy, stress, and chronic disease can also precipitate the reactivation of LTBI. Consequently, treatment of LTBI is important. If the initial immune response is not adequate, the body cannot contain the organisms. As a result, the bacteria replicate, and active TB disease results. When active disease develops within the first 2 years of infection, it is termed primary TB. Individuals co-infected with HIV are at greatest risk for developing active TB. Post-primary, or reactivation TB, is defined as TB disease occurring 2 or more years after the initial infection. If the site of TB is pulmonary or laryngeal, the individual is considered infectious and can transmit the disease to others.

PE Surgical Therapy

Pulmonary embolectomy for massive PE For hemodynamically unstable patients in whom thrombolytic therapy is contraindicated Inferior vena cava (IVC) filter Prevents migration of clots in pulmonary system Hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated may be candidates for immediate pulmonary embolectomy. Embolectomy, removal of emboli to help decrease right ventricular afterload, can be achieved via a vascular (catheter) or surgical approach. Surgical outcomes have improved in recent years, in part due to rapid diagnosis and enhanced surgical procedures, with mortality rates decreasing from 30% to 19%. To prevent further emboli, an inferior vena cava (IVC) filter may be the treatment of choice in patients who remain at high risk and for patients for whom anticoagulation is contraindicated. This device, inserted percutaneously via the femoral vein, is placed at the level of the diaphragm in the inferior vena cava. Once inserted, the stent expands and prevents migration of large clots into the pulmonary system. Complications associated with this device are rare but include misplacement, migration, and perforation.

PE Complications

Pulmonary infarction Alveolar necrosis and hemorrhage Abscess Pleural effusion Pulmonary hypertension Results from hypoxemia associated with massive or recurrent emboli Right ventricular hypertrophy Complications of pulmonary emboli include pulmonary infarction and pulmonary hypertension. Pulmonary infarction (death of lung tissue) is most likely when the following factors are present: (1) occlusion of a large or medium-sized pulmonary vessel (>2 mm in diameter), (2) insufficient collateral blood flow from the bronchial circulation, or (3) preexisting lung disease. Infarction results in alveolar necrosis and hemorrhage. Occasionally the necrotic tissue becomes infected, and an abscess may develop. Concomitant pleural effusion is frequent. Pulmonary hypertension results from hypoxemia or from involvement of more than 50% of the area of the normal pulmonary bed. As a single event, an embolus rarely causes pulmonary hypertension. Recurrent pulmonary emboli gradually cause a reduction in the capillary bed and eventual pulmonary hypertension. Dilation and hypertrophy of the right ventricle can develop secondary to pulmonary hypertension. Depending on the degree of pulmonary hypertension and its rate of development, outcomes can vary, with some patients dying within months of the diagnosis and others living for decades.

Radial Artery Graft

Radial artery is another potential graft Thick muscular artery that is prone to spasm Perioperative calcium channel blockers and long-acting nitrates can control the spasms Patency rates are not as good as IMA but better than saphenous veins Other grafts include the gastroepiploic or inferior epigastric artery. Like the radial artery, these also are prone to spasms.

Necrotizing Pneumonia

Rare complication of bacterial lung infection Often results from CAP Signs and symptoms Immediate respiratory insufficiency and/or failure Leukopenia Bleeding into airways Necrotizing pneumonia is characterized by liquefaction and, in some situations, cavitation of lung tissue. Although the exact pathophysiological mechanisms involved are controversial, causative organisms include Staphylococcus, Klebsiella, and Streptococcus. Lung abscesses commonly occur. Treatment often includes long- term antibiotic therapy and possible surgery.

PostopGI status aorta

Record amount and character of NG tube output Abdominal assessment Passing of flatus = return of bowel function Assess for bowel ischemia After open abdominal aortic surgery, paralytic ileus may develop as a result of anesthesia and handling of the bowel during surgery. intestines may become swollen and bruised, and peristalsis ceases for variable intervals. A retroperitoneal surgical approach can be used to decr the risk of bowel complications. manifestations bowel ischemia = no bowel sounds, fever, abdominal distention, d/ bloody stools.

PE Patient Teaching

Regarding long-term anticoagulant therapy Measures to prevent DVT Importance of follow-up exams Patient teaching regarding long-term anticoagulant therapy is critical. Anticoagulant therapy continues for at least 3 months. Patients with recurrent emboli may be treated indefinitely with anticoagulants. INR levels are drawn at intervals, and warfarin dosage is adjusted. Some patients are monitored by nurses in an anticoagulation clinic. Discharge planning is aimed at preventing worsening of the condition and avoiding complications and recurrence. Teach the patient measures to prevent DVT.

Nursing Management Chronic Stable Angina and ACS -Planning: Overall goals

Relief of pain Preservation of heart muscle Immediate and appropriate treatment Effective coping with illness-associated anxiety Participation in a rehabilitation plan Reduction of risk factors The overall goals for a patient with ACS include (1) relief of pain, (2) preservation of heart muscle, (3) immediate and appropriate treatment, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors.

Interprofessional CareAcute Coronary Syndrome - NSTEMI

Reperfusion therapy Emergent PCI Treatment of choice for confirmed STEMI Goal: 90 minutes from door to catheter laboratory Balloon angioplasty + stent(s) Many advantages over CABG For patients with STEMI, reperfusion therapy is initiated. Reperfusion therapy can include emergent PCI (preferred) or thrombolytic therapy for STEMI. The goal in the treatment of STEMI is to save as much heart muscle as possible. Dual antiplatelet therapy and heparin are also used. Emergent PCI is the first line of treatment for patients with confirmed STEMI (i.e., ST-elevation on the ECG and/or positive cardiac biomarkers). The goal is to open the blocked artery within 90 minutes of arrival to a facility that has an interventional cardiac catheterization laboratory. In this case, the patient will undergo a cardiac catheterization to locate and assess the severity of the blockage(s), determine the presence of collateral circulation, and evaluate LV function. During the procedure, a bare metal stent (BMS) or drug-eluting stent (DES) is inserted into the blocked coronary artery. Patients with severe LV dysfunction may require the addition of IABP therapy and/or inotropes (e.g., dobutamine). A small percentage of patients may require emergent CABG surgery. The advantages of PCI (compared to thrombolytic therapy) include the following: (1) it provides an alternative to surgical intervention; (2) it is performed with local anesthesia; (3) the patient is ambulatory shortly after the procedure; (4) the length of hospital stay is approximately 3 to 4 days after MI compared with the 4 to 6 days with CABG surgery, thus reducing hospital costs; and (5) the patient can return to work several weeks sooner after PCI compared to 6- to 8-week convalescence after CABG. Advances in PCI techniques have significantly reduced the need for emergent CABG. Currently, there are more PCIs than CABGs performed in the United States.

Asystole

Represents total absence of ventricular electrical activity give epi, cant dfib bc there is no rhythm to change CPR keep going till get pulse then defib No ventricular contraction Patient unresponsive, pulseless, apneic Must assess in more than one lead Asystole represents the total absence of ventricular electrical activity. Occasionally, P waves are seen. No ventricular contraction occurs because depolarization does not occur. Patients are unresponsive, pulseless, and apneic. Asystole is a lethal dysrhythmia that requires immediate treatment. Always assess the rhythm in more than one lead. The prognosis of a patient with asystole is extremely poor. Usually result of advanced cardiac disease, severe conduction disturbance, or end-stage HF Treat with immediate CPR and ACLS measures Epinephrine and/or vasopressin Intubation Asystole is usually a result of advanced heart disease, a severe cardiac conduction system disturbance, or end-stage HF.

Tb dx - Bacteriologic studies

Required for diagnosis Consecutive sputum samples obtained on 3 different days Stained sputum smears examined for AFB Culture results can take up to 8 weeks Can also examine samples from other suspected TB sites Treatment is warranted pending the culture results for patients in whom clinical suspicion of TB is high. Samples for other suspected TB sites can be collected from gastric washings, cerebrospinal fluid (CSF), or fluid from an effusion or abscess.

Interprofessional CareAcute Coronary Syndrome - Traditional coronary artery bypass graft (CABG) surgery

Requires sternotomy and cardiopulmonary bypass (CPB) Uses arteries and veins for grafts The internal mammary artery (IMA) is most common artery used for bypass graft CABG surgery consists of the placement of arterial or venous grafts to transport blood between the aorta, or other major arteries, and the heart muscle distal to the blocked coronary artery (or arteries). CABG surgery requires a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). During CPB, blood is diverted from the patient's heart to a machine. Here it is oxygenated and returned (via a pump) to the patient. The procedure may involve one or more grafts using the internal mammary artery (IMA), saphenous vein, radial artery, gastroepiploic artery, and/or inferior epigastric artery.

Multidrug-Resistant Tuberculosis (MDR-TB)

Resistance to 2 of the most potent first-line anti-TB drugs Extensively drug-resistant TB (XDR-TB) resistant to any fluoroquinolone plus any injectable antibiotic Several causes for resistance occur Incorrect prescribing Lack of case management Nonadherence Once a strain of M. tuberculosis develops resistance to two of the most potent first-line antituberculosis drugs (e.g., isoniazid [Isoniazid], rifampin [Rifadin]), it is defined as multidrug-resistant tuberculosis (MDR-TB).

Acute Coronary Syndrome Etiology and Pathophysiology

Result Partial occlusion of coronary artery: UA or NSTEMI Total occlusion of coronary artery: STEMI ACS is caused by the decline of a once stable atherosclerotic plaque. The previously stable plaque ruptures, releasing substances into the vessel. This stimulates platelet aggregation and thrombus formation. This area may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI). What causes a coronary plaque to suddenly become unstable is not well understood, but systemic inflammation (described earlier) is thought to play a role. Patients with suspected ACS require immediate hospitalization. Deterioration of once stable plague Rupture Platelet aggregation Thrombus

ARDS

Results Severe dyspnea Hypoxia Decreased lung compliance Diffuse pulmonary infiltrates 150,000 cases annually 50% mortality rate Patients who have both gram-negative septic shock and ARDS have a mortality rate of 70% to 90%.

Aspiration Pneumonia

Results from abnormal entry of secretions into lower airway Major risk factors: LOC Difficulty swallowing Insertion of nasogastric tubes with or without tube feeding Decreased level of consciousness might be from seizures, anesthesia, head injury, stroke, alcohol intake, or others. With loss of consciousness, the gag and cough reflexes are depressed, and aspiration is more likely to occur. Aspirated material triggers inflammatory response Primary bacterial infection most common Empiric therapy based on severity of illness, where infection acquired, and probable causative organism Aspiration of acid gastric contents initially causes chemical (noninfectious) pneumonitis\ The most = bacterial infection/ more than one organism is identified on sputum culture, including both aerobes and anaerobes as they both comprise the flora of the oropharynx. initial antibiotic therapy is based on an assessment of probable causative organism, severity of illness, patient factors (e.g., malnutrition, current use of antibiotic therapy), and ability to treat common community-acquired organisms. For patients who aspirate in hospitals, appropriate antibiotics should include coverage for both gram-negative organisms and MRSA. In contrast, aspiration of acidic gastric contents causes chemical (noninfectious) pneumonitis, which may not require antibiotic therapy. However, secondary bacterial infection can occur 48 to 72 hours later.

Nursing ManagementAcute Coronary Syndrome - Ambulatory Care

Resumption of sexual activity Teach when discuss other physical activity Erectile dysfunction drugs contraindicated with nitrates Prophylactic nitrates before sexual activity When to avoid sex Typically 7-10 days post MI or when patient can climb two flights of stairs Most patients change their sexual behavior not because of physical problems, but because they are concerned about sexual inadequacy, death during intercourse, and impotence. Sexual activity for middle-aged men and women with their usual partners is no more strenuous than climbing two flights of stairs. Tell the patient that the inability to perform sexually after MI is common and that sexual dysfunction usually disappears after several attempts. Warn the patient that erectile dysfunction drugs are not to be used with nitrates because severe hypotension and even death have been reported. It is common for a patient who experiences chest pain on physical exertion to have some angina during sexual stimulation or intercourse. The patient may be told to take NTG prophylactically. Tell the patient to delay sex soon after a heavy meal or excessive intake of alcohol, when extremely tired or stressed, or with unfamiliar partners. Patients should also avoid anal intercourse because of the likelihood of eliciting a vasovagal response.

Pacemakers - Cardiac resynchronization therapy (CRT)

Resynchronizes the heart cycle by pacing both ventricles Biventricular pacing Most HF patients have intraventricular conduction delays causing abnormal ventricular contraction. This causes dyssynchrony between the right and left ventricles and results in reduced systolic function, pump inefficiency, and worsened HF. For patients with severe left ventricular dysfunction, CRT is combined with an implantable cardioverter-defibrillator (ICD) for maximum therapy.

RIFLE classification

Risk (R) Injury (I) Failure (F) Loss (L) End-stage renal disease (E) AKI may progress through phases: oliguric, diuretic, and recovery. When a patient does not recover from AKI, then CKD may develop.

Aortic AneurysmComplications

Rupture—serious complication related to untreated aneurysm Rupture into retroperitoneal space = Bleeding may be tamponaded by surrounding structures = preventing exsanguination and death. Severe back pain = May/may not have back/flank ecchymosis (Grey Turner's sign) Rupture is more likely to occur in people who smoke tobacco. Massive hemorrhage Most do not survive long enough to get to the hospital The patient who reaches the hospital will be in hypovolemic shock with tachycardia, hypotension, pale clammy skin, decreased urine output, altered level of consciousness, and abdominal tenderness. = simultaneous resuscitation and immediate surgical repair are necessary.

Case Study

S.C. is a 57-year-old Chinese man who was transported from a homeless shelter for having respiratory symptoms. He has a history of IV drug use and is HIV positive. He has been coughing regularly and producing mucopurulent sputum. What risk factors does S.C. have for TB? What diagnostic tests would you expect the HCP to order for S.C.? Homeless, IV-drug user, resident of shelter, poverty, immunosuppression (HIV) Tuberculin skin-test (TST), interferon-γ release assay (IGRA), chest x-ray, sputum culture and sensitivity, sputum for AFB S.C.'s chest x-ray and sputum smear for AFB confirm the TB diagnosis. What treatment would you expect the health care provider to order for S.C.? Do you think S.C. needs to stay in the hospital at this point? Treatment consists of four-drug therapy regimen of Isoniazid, rifampin (Rifadin), pyrazinamide (PZA), and ethambutol. Although most people do not need hospitalization , S.C.'s history and living situation do not provide adequate support to ensure compliance. S.C. should stay in the hospital for at least a few days in order to allow social services time to identify available support and make necessary arrangements. What is the primary nursing management for S.C.? What hygiene measures can you teach him to minimize transmission? Place him in airborne isolation and begin drug therapy as ordered. Cover his nose and mouth with paper tissue every time he coughs, sneezes, or produces sputum. The tissues should be thrown into a paper bag and disposed of with the trash or flushed down the toilet. Emphasize careful hand washing after handling sputum and soiled tissues. If he needs to be out of the negative-pressure room, the patient must wear a standard isolation mask to prevent exposure to others. Minimize prolonged visitation to other parts of the hospital. S.C. is now ready for discharge. What other patient teaching should you do with him? What can you do to help ensure that he continues medications after discharge? Emphasize the importance of complying with his medication regimen. Teach him how to minimize exposure to close contacts. He should open windows and ventilate rooms in which he is living. Until his sputum is negative for AFB, he should sleep alone, spend as much time as possible outdoors, and minimize time in close proximity with other people and on public transportation. Emphasize importance of treatment compliance. Strategies to improve adherence to drug therapy include teaching and counseling, reminder systems, incentives or rewards, contracts and DOT. Because of his history and the fact that S.C. is living in a shelter, the Department of Health should provide DOT.

severe acute resp syndrome

SARS = viral infection from mutated strains of coronavirus = a group of virsus that also cause the common cold virus invades the pulmonary tissues = inflam response airborn no spread by blood bs flourishes at temps slightly below normal core temp risks: exposure to infected person, immunocomp

resp failure expected findings

SOB syspnea orthopnea rapid shallow breathing cyanotic, mottled dusky skin tachycardia hypotension substernal or suprasternal retactions decr O2 under 90% wheezing/rales cardiac arrhythmias confusion lethargy

Clinical Manifestations of ACS Myocardial Infarction (MI)

ST-elevation and non-ST-elevation Result of abrupt stoppage of blood flow through a coronary artery, causing irreversible myocardial cell death (necrosis) Preexisting CAD STEMI - occlusive thrombus NSTEMI - non-occlusive thrombus A myocardial infarction occurs because of abrupt stoppage of blood flow through a coronary artery from a thrombus caused by platelet aggregation. This causes irreversible myocardial cell death (necrosis). Most MIs occur in the setting of preexisting CAD. When a thrombus develops, blood flow to the heart muscle beyond the blockage stops, resulting in necrosis. A STEMI caused by an occlusive thrombus creates ST-elevation in the ECG leads facing the area of infarction. A STEMI is an emergency situation. In order to limit the infarct size, the artery must be opened within 90 minutes of presentation. This can be done either by PCI or thrombolytic (fibrinolytic) therapy. PCI is the preferred treatment if a hospital is capable of performing PCI. NSTEMI, caused by a non-occlusive thrombus, does not cause ST elevation on the 12-lead ECG. Patients may or may not develop ST-T wave changes in the leads affected by the infarction. NSTEMI patients do not go to the catheterization laboratory emergently but usually undergo the procedure within 12 to 72 hours if there are no contraindications. Thrombolytic therapy is not indicated for NSTEMI patients. With either a NSTEMI or STEMI, an echocardiogram may show hypokinesis (worsening myocardial contractility) or akinesis (absent myocardial contractility) in the necrotic area(s). The degree of LV dysfunction depends on the area of the heart involved and size of the infarction.

ECG Changes Associated With Acute Coronary Syndrome (ACS) - Ischemia

ST-segment depression and/or T wave inversion ST-segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line Changes reverse when adequate blood flow is restored to myocardium Depression in the ST segment and/or T wave inversion occurs in response to an inadequate supply of blood and oxygen, which causes an electrical disturbance in the myocardial cells. Once treated (adequate blood flow is restored), the ECG changes will resolve, and the ECG will return to the patient's baseline.

ECG Changes Associated With Acute Coronary Syndrome (ACS) = Injury

ST-segment elevation occurs If treatment is prompt and effective, may avoid or limit infarction Absence of serum cardiac markers confirms no infarction Myocardial injury represents a worsening stage of ischemia that is potentially reversible but may evolve to MI. The typical ECG change seen during injury is ST-segment elevation. ST-segment elevation is significant if it is greater than or equal to 1 mm above the isoelectric line.

Aortic DissectionNursing Management - Postoperative

See aneurysm postop care (discussed earlier) Discharge teaching Therapeutic regimen Antihypertensive drugs and side effects If pain returns or symptoms progress = seek immediate help pt need to understand that antihypertensive drugs must be taken daily for the rest of their lives. β-adrenergic blockers (e.g., metoprolol [Toprol XL]) = control BP and decrease myocardial contractility. most common cause of death in long-term survivors is aortic rupture from redissection or aneurysm formation.

Aortic DissectionNursing Management - Preoperative

Semi-Fowler's position Maintaining a quiet environment Anxiety and pain management Opioids and tranquilizers as ordered Continuous IV administration of antihypertensive agents These measures help to keep the HR and systolic BP at the lowest possible level that maintains vital organ perfusion (typically HR less than 60; systolic BP between 110-120 mm Hg). Continuous ECG and intraarterial pressure monitoring Observation of changes in quality of peripheral pulses Frequent vital signs = every 2 to 3 minutes until target BP is reached. If the arteries branching off the aortic arch are involved, monitor the patient's level of consciousness, cranial nerve functions, and limb movement, sensation, and strength. To prevent extension of the dissection = manage pain, anxiety bc cause elevations in HR/systolic BP.

PE Nursing Management

Semi-Fowler's position Oxygen therapy Frequent assessments IV access Monitor laboratory results Emotional support and reassurance Nursing measures aimed at prevention of PE are similar to those for prophylaxis of DVT. The prognosis of a patient with PE is good if therapy is promptly instituted. Keep the patient on bed rest in a semi-Fowler's position to facilitate breathing. Administer oxygen therapy as ordered. Assess the patient's cardiopulmonary status with careful monitoring of vital signs, cardiac rhythm, pulse oximetry, ABGs, and lung sounds. Maintain an IV line for medications and fluid therapy. Monitor laboratory results to ensure therapeutic ranges of INR (for warfarin) and aPTT (for IV heparin). Monitor the patient for complications of anticoagulant and fibrinolytic therapy (e.g., bleeding, hematomas, bruising). Provide appropriate interventions related to immobility and fall precautions once the patient is permitted out of bed. The patient is usually anxious because of pain, inability to breathe, and fear of death. Carefully explain the situation, the medications, and provide emotional support and reassurance to help relieve the patient's anxiety.

Serum Cardiac Biomarkers After MI

Serum cardiac biomarkers are proteins released into the blood from necrotic heart muscle after an MI. These biomarkers are important in the diagnosis of MI. The onset, peak, and duration of levels of these biomarkers are shown in this graph. Cardiac-specific troponin has two subtypes: cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI). These biomarkers are highly specific indicators of MI and have greater sensitivity and specificity for myocardial injury than creatine kinase (CK-MB). Serum levels of cTnI and cTnT increase 4 to 6 hours after the onset of MI, peak at 10 to 24 hours, and return to baseline over 10 to 14 days. Serial cardiac biomarkers are drawn over 24 hours (e.g., every 8 hours x3). The presence of biomarkers helps to differentiate between a diagnosis of UA (negative biomarkers) and NSTEMI (positive biomarkers). CK levels begin to rise at about 6 hours after an MI, peak at about 18 hours, and return to normal within 24 to 36 hours. The CK enzymes are fractionated into bands. The CK-MB band is specific to heart muscle cells and help to quantify myocardial damage. Myoglobin is released into the circulation within 2 hours after an MI and peaks in 3 to 15 hours. Although it is one of the first serum cardiac biomarkers to appear after an MI, it lacks cardiac specificity. Its role in diagnosing MI is limited.

Clinical Manifestations of ACS Myocardial Infarction - Pain

Severe chest pain not relieved by rest, position change, or nitrate administration Heaviness, pressure, tightness, burning, constriction, crushing Substernal or epigastric May radiate to neck, lower jaw, arms, back Often occurs in early morning Atypical in women, elderly No pain if cardiac neuropathy (diabetes) Severe chest pain not relieved by rest, position change, or nitrate administration is the hallmark of an MI. Persistent and unlike any other pain, it is usually described as heavy, pressure, tight, burning, constricted, or crushing feeling. Common locations are substernal or epigastric areas. When epigastric pain is present, the patient may relate it to indigestion and take antacids without relief. The pain may radiate to the neck, lower jaw, and arms or to the back. It may occur while the patient is active or at rest, asleep, or awake. It often occurs in the early morning hours. It usually lasts for 20 minutes or longer and is more severe than usual anginal pain. Not everyone who has an MI has classic symptoms. Some patients may not experience pain but may have "discomfort," weakness, nausea, indigestion, or shortness of breath. Although women and men have more similarities than differences in their acute MI symptoms, some women may experience atypical discomfort, shortness of breath, or fatigue. Patients with diabetes may experience silent (asymptomatic) MIs because of cardiac neuropathy or may manifest atypical symptoms (e.g., dyspnea). An older patient may experience a change in mental status (e.g., confusion), shortness of breath, pulmonary edema, dizziness, or a dysrhythmia.

Opportunistic Pneumonia

Severe protein-calorie malnutrition Immunodeficiencies Chemotherapy/radiation recipients Long-term corticosteroid therapy Caused by microorganisms that do not normally cause disease inflammation and infection of the lower respiratory tract in immunocompromised patients. In addition to the risk of bacterial and viral pneumonia, the immunocompromised person may develop an infection from microorganisms that do not normally cause disease.

Pericarditis Clinical Manifestations

Sharp, Severe Chest Pain Pain radiation to neck arms and left should Trapezius Muscle Pain Dyspnea Pericardial Friction Rub Chest pain is worse with deep inspiration and laying flat. Chest pain is relieved with sitting up or leaning forward. Due to radiation pain it is sometimes hard to differentiate from angina. A Pericardial Friction Rub is the hallmark finding and sounds like a scratching, grating, high pitched sound. It is best heard when auscultating over the lower left sternal border of the chest with the patient leaning forward. Ask the patient to hold his/her breath so you can appropriately differentiate between a pericardial friction rub and a pleural friction rub.

Chest Trauma: Emergency Management

Signs of respiratory distress includeL Dyspnea respiratory distress Cough w or w/o hemoptysis Cyanosis (mouth, face, nail beds, mucous membranes) Tracheal deviation Audible air escaping from chest wound Decr breath sounds on side of injury Decr O2 saturation Frothy secretions Initial interventions Circulation, airway, breathing Administer O2 to keep SpO2 >90% Establish IV access with 2 large-bore catheters and begin fluid resuscitation as appropriate Remove clothing to assess injury Cover sucking chest wound with nonporous dressing taped on 3 sides Ensure patent airway. If unresponsive ABCs If responsive, monitor airway, breathing, and circulation. Initial interventions Stabilize impaled objects Assess for other significant injuries and treat appropriately Place patient in a semi-Fowler's position or on injured side After ruling out cervical spine injury Administer analgesia Prepare for emergency needle decompression Stabilize impaled objects with bulky dressings. Do not remove object. Assess for other significant injuries and treat appropriately. Place patient in a semi-Fowler's position or position patient on the injured side if breathing is easier after cervical spine injury has been ruled out. Admin small amounts of analgesia Prepare for emergency needle decompression if tension pneumothorax or cardiac tamponade present. Ongoing Monitoring Monitor vital signs, level of consciousness, oxygen saturation, cardiac rhythm, respiratory status, and urinary output. Anticipate intubation for respiratory distress. Release dressing if tension pneumothorax develops after sucking chest wound is covered. Ongoing monitoring Vital signs LOC Oxygen sat Cardiac rhythm Respiratory status Urinary output Potential intubation Anticipate intubation for respiratory distress. Release dressing if tension pneumothorax develops after sucking chest wound is covered.

Aortic AneurysmInterprofessional Care - Small aneurysm

Small aneurysm (4- 5.4 cm) ↓ blood pressure Ultrasound, MRI, CT scan monitoring every 6 to 12 months Conservative therapy: risk factor modification; tobacco cessation, decreasing BP, optimizing lipid profile, and annual monitoring of aneurysm size using ultrasound, CT, or MRI. β-adrenergic blocking agents = LOL ACE inhibitors = PRIL angiotensin II receptor blockers = losartan statins = STATINS antibiotics = doxycycline Monitoring by US every 2 to 3 years is recommended for patients with AAAs smaller than 4.0 cm in diameter

ARDS Clinical Progression

Some persons survive acute phase of lung injury Pulmonary edema resolves Complete recovery Survival chances are poor for those who enter fibrotic phase Requires long-term mechanical ventilation Progression of ARDS varies among patients. It is not known why injured lungs repair and recover in some patients, and in others ARDS progresses. Several factors seem to be important in determining the course of ARDS. These include the nature of the initial injury, the extent and severity of comorbidities, and pulmonary complications (e.g., pneumothorax).

Pathophysiology of Pneumonia

Specific pathophysiologic changes related to pneumonia vary according to the offending organism, but the majority of organisms trigger an inflammatory response in the lungs. Inflammation, characterized by an increase in blood flow and vascular permeability, activates neutrophils to engulf and kill the offending organisms. As a result, the inflammatory process attracts more neutrophils, edema of the airways occurs, and fluid leaks from the capillaries and tissues into alveoli. Normal oxygen transport is affected, leading to clinical manifestations of hypoxia (e.g., tachypnea, dyspnea, tachycardia). Consolidation, a feature typical of bacterial pneumonia, occurs when the normally air-filled alveoli become filled with fluid and debris. Mucous production also increases, which can potentially obstruct airflow and impair gas exchange even further. Over time and with appropriate antibiotic therapy, macrophages lyse and process the debris, lung tissue is allowed to recover, and gas exchange returns to normal. Resolution and healing occur if there are no complications.

pnuemothorax Spontaneous and iatrogenic

Spontaneous = Rupture of blebs, in healthy/chronically ill persons A spontaneous pneumothorax typically occurs due to the rupture of small blebs (air-filled sacs) located on the surface of the lung. These blebs can occur in healthy, young individuals or as a result of lung disease such as COPD, asthma, cystic fibrosis, and pneumonia. risk factors include being tall and thin, male gender, family history, and previous spontaneous pneumothorax, smoking incr risk for bleb formation Iatrogenic = Caused by medical procedures Iatrogenic pneumothorax can occur due to laceration or puncture of the lung during medical procedures. For example, transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, and transbronchial lung biopsy all have the potential to injure the lung. Barotrauma from excessive ventilatory pressure during manual or mechanical ventilation can rupture alveoli or bronchioles. Esophageal procedures may also be involved in the development of a pneumothorax. Tearing during insertion of a gastric tube can allow air from the esophagus to enter the mediastinum and pleural space.

TB Etiology and Pathophysiology

Spread via airborne particles M. tuberculosis Aerophilic (oxygen-loving) - causes affinity for lungs Infection can spread via lymphatics and grow in other organs as well Cerebral cortex Spine Epiphyses of the bone Adrenal glands Transmission requires close, frequent, or prolonged exposure NOT spread by touching, sharing food utensils, kissing, or other physical contact M. tuberculosis is a gram-positive, acid-fast bacillus (AFB) that is usually spread from person to person via airborne particles expectorated when breathing, talking, singing, sneezing, and coughing. A process of evaporation leaves small droplet nuclei, 1 to 5 μm in size. These droplets contain M. tuberculosis. Because they are so small, the particles remain suspended in the air for minutes to hours and bacteria are then Isoniazidaled by another person. TB is not highly infectious, as transmission usually requires close, frequent, or prolonged exposure. Factors that influence the likelihood of transmission include the (1) number of organisms expelled into the air, (2) concentration of organisms (small spaces with limited ventilation would mean higher concentration), (3) length of time of exposure, and (4) immune system of the exposed person. Once Isoniazidaled, particles lodge in bronchioles and alveoli Local inflammatory reaction occurs When the focus of infection is established through Isoniazidalation, it is called the Ghon lesion or focus, which represents a calcified TB granuloma, the hallmark of TB. The formation of a granuloma is a defense mechanism aimed at walling off the infection and preventing further spread. Replication of the bacillus is Isoniazidibited, and the infection is stopped. Most immunocompetent adults infected with TB are able to completely kill the mycobacteria. Of these individuals, 5% to 10% will go on to develop active TB infection when the bacteria begin to multiply months or years later.

Nursing ManagementAcute Coronary Syndrome - Evaluation

Stable vital signs Relief of pain Decreased anxiety Realistic program of activity Effective management of therapeutic regimen The overall expected outcomes are that the patient with ACS: Maintains stable signs of effective cardiac output Reports relief of pain Reports decreased anxiety and increased sense of self-control Achieves a realistic program of activity that balances physical activity with energy-conserving activities Describes the disease process, measures to reduce risk factors, and rehabilitation activities necessary to manage the therapeutic regimen

Defibrillation steps

Start CPR while obtaining and setting up defibrillator Turn on and select energy Make sure sync button is turned off (thats for cardiovert, you aren't syncing to a rhythm) Apply conductive materials (e.g., defibrillator gel pads) to the chest, one to the right of the sternum just below the clavicle, and the other to the left of the apex. Charge Position paddles firmly on chest Ensure "All clear"!!!!! (of bed and pt) Deliver charge CPR should be in progress until the defibrillator is available. Hands-free, multifunction defibrillator pads are available and are placed on the chest as described above. Connect the cables from the pads to the defibrillator. Charge and discharge the defibrillator using buttons on the defibrillator. It is still essential that you ensure that all staff are clear before the defibrillator is discharged.

Pneumonia Drug Therapy

Start with empiric therapy Based on likely infecting organism and risk factors for MDR organisms Varies with local patterns of antibiotic resistance Should see improvement in 3-5 days Start with IV and then switch to oral therapy as soon as patient stable Once the pneumonia is classified, the HCP selects empiric therapy on the likely infecting organism (see Table 27-2). For all types of pneumonia, empiric antibiotic therapy is based on whether the patient has risk factors for MDR organisms. The prevalence and resistance patterns of MDR pathogens vary among localities and institutions. Therefore the antibiotic regimen needs to be adapted to local patterns of antibiotic resistance. Multiple regimens exist, but all should initially include antibiotics that are effective against both resistant gram-negative and gram-positive organisms. Clinical improvement usually occurs between 3 and 5 days. Patients who deteriorate or fail to respond to therapy will require aggressive reevaluation to assess for noninfectious etiologies, complications, other coexisting infectious processes, or pneumonia caused by a drug-resistant pathogen. IV antibiotic therapy should be switched to oral therapy as soon as the patient is hemodynamically stable, improving clinically, able to ingest oral medication, and has a functioning GI tract. Stable patients do not need to be observed in the hospital and can be discharged to home on oral antibiotics. Total treatment time for patients with CAP should be a minimum of 5 days, and the patient should be afebrile for 48 to 72 hours.

Pneumonia Nursing Assessment

Subjective Data Past health history: lung cancer, COPD, diabetes, malnutrition, chronic debilitating disease Use of antibiotics, corticosteroids, chemotherapy, or immunosuppressants Recent abdominal or thoracic surgery Recent intubation Tube feedings Smoking Alcoholism Respiratory infections Nutritional intake Activity Dyspnea Cough Chest Pain Sore throat Headache Abd pain Muscle aches n/v tired Past health history: Lung cancer, COPD, diabetes mellitus, chronic debilitating disease, malnutrition, altered consciousness, immunosuppression, exposure to chemical toxins, dust, or allergens Medications: Use of antibiotics; corticosteroids, chemotherapy, or any other immunosuppressants Surgery or other treatments: Recent abdominal or thoracic surgery, splenectomy, endotracheal intubation, or any surgery with general anesthesia; tube feedings Objective Data Fever Restlessness or lethargy Splinting affected area Tachypnea Asymmetric chest movements Use of accessory muscles Crackles Friction rub Dullness on percussion Increased tactile fremitus pink, rusty, purulent, green, yellow, or white sputum (amount may be scant to copious) Tachycardia Changes in mental status

acute resp failure

Symptom not diease one of both gas exchanging functions dont work hypoxemia = decr arterial O2/O2 sat = O2 failure hypercapnia = body doesnt remove CO2 = ventilatory failure can have both

ARDS Clinical Manifestations: Late

Symptoms worsen with increased fluid accumulation and decreased lung compliance Pulmonary function tests reveal decreased compliance, lung volumes, and functional residual capacity (FRC) Respiratory distress becomes evident as the WOB increases. Tachypnea and intercostal and suprasternal retractions may be present. Functional residual capacity (FRC) is the amount of air remaining in the lungs at the end of normal expiration. Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor Diffuse crackles and coarse crackles Hypoxemia despite increased FIO2 Increasing WOB despite initial findings of normal PaO2 or SaO2 The chest x-ray demonstrates diffuse and extensive bilateral interstitial and alveolar infiltrates. Hypoxemia, despite increased FIO2 by mask, cannula, or endotracheal tube, is a hallmark of ARDS. ABGs may initially demonstrate a normal or decreased PaCO2 despite severe dyspnea and hypoxemia. Hypercapnia signifies that respiratory muscle fatigue and hypoventilation are occurring, thus interfering with optimum gas exchange.

TB Nursing Implementation

Teach patient to prevent spread Cover nose and mouth with tissue when coughing, sneezing, or producing sputum Hand washing after handling sputum-soiled tissues Patient wears mask if outside of negative-pressure room Identify and screen close contacts Teach patients to cover the nose and mouth with paper tissues every time they cough, sneeze, or produce sputum. The tissues should be thrown into a paper bag and disposed of with the trash, burned, or flushed down the toilet. Emphasize careful hand washing after handling sputum and soiled tissues. If patients need to be out of the negative-pressure room, they must wear a standard isolation mask to prevent exposure to others. Minimize prolonged visitation to other parts of the hospital. Identify and screen close contacts of the person with TB. Anyone testing positive for TB infection will undergo further evaluation and needs to be treated for either LTBI or active TB disease.

ECG Changes Associated With Acute Coronary Syndrome (ACS)

The 12-lead ECG is a major diagnostic tool used to evaluate patients with ACS. The ECG changes are in response to ischemia, injury, or infarction (necrosis) of myocardial cells. The leads facing the area of involvement demonstrate the definitive ECG changes. The leads facing opposite the area involved in ACS often demonstrate reciprocal (opposite) ECG changes. inferior leads, lateral, anteroseptal, lateral - how to know where the blockage is

Myocardial Infarction From Occlusion

The acute MI process evolves over time. The earliest tissue to become ischemic is the subendocardium (the innermost layer of tissue in the heart muscle). If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness of the heart muscle to become necrosed. If the thrombus is not completely blocking the artery, the time to complete necrosis may be as long as 12 hours. Acute myocardial infarction in the posterolateral wall of the left ventricle. This is demonstrated by the absence of staining in the areas of necrosis (white arrow). Note the scarring from a previous anterior wall myocardial infarction (black arrow). The majority of MIs affect the LV and are usually described based on the location of damage (e.g., anterior, inferior, lateral, septal, or posterior wall infarction). The location of the MI and ECG changes correlate with the involved coronary artery. For example, in most people, the right coronary artery provides blood to the inferior and posterior LV walls. Blockage of the right coronary artery results in an inferior wall and/or posterior wall MI. Anterior wall infarctions result from blockages in the left anterior descending artery. Blockages in the left circumflex artery usually cause lateral LV wall MIs. Damage can occur in more than one location, especially if more than one coronary artery is involved (e.g., anterolateral MI). Right ventricular MIs are much less common and treated differently than LV MIs. Not everyone develops collateral circulation, but if present, the degree of collateral circulation influences the severity of the MI. An individual with a long history of CAD may develop good collateral circulation to provide the area surrounding the infarction site with a blood supply. This is one reason why a younger person may have a more serious first MI than an older person with the same degree of blockage.

Internal Mammary Artery and Saphenous Vein Grafts

The internal mammary artery (IMA) is the most common artery used for bypass graft. It is left attached to its origin (the subclavian artery) but then dissected from the chest wall. Next, it is anastomosed (connected with sutures) to the coronary artery distal to the blockage. Saphenous veins are also used for bypass grafts. The surgeon endoscopically removes the saphenous vein from one or both legs. A section is sutured into the ascending aorta near the native coronary artery opening and then sutured to the coronary artery distal to the blockage. The use of antiplatelet and statin therapy after surgery improves vein graft patency.

Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)

The long line means blocked QRS May result from drugs or CAD Typically associated with ischemia Usually transient and well tolerated Treat if symptomatic Atropine Pacemaker If asymptomatic, monitor closely Type I AV block result from digoxin or β-blockers, CAD = slow AV conduction. Type I AV block is usually a result of myocardial ischemia or inferior MI. It is generally transient and well tolerated. However, in some patients (e.g., those with acute MI) it may be a warning sign of a more serious AV conduction disturbance (e.g., complete heart block). If the patient is symptomatic, atropine is used to increase HR, or a temporary pacemaker may be needed, especially if the patient has experienced an MI. If the patient is asymptomatic, the rhythm is closely observed with a transcutaneous pacemaker on standby. Type I second-degree AV block (Mobitz I or Wenckebach heart block) includes a gradual lengthening of the PR interval. It occurs because of a prolonged AV conduction time until an atrial impulse is nonconducted and a QRS complex is blocked (missing). Atrial rate is regular, but ventricular rate may be slower because of nonconducted or blocked QRS complexes resulting in bradycardia. Once a ventricular beat is blocked, the cycle repeats itself with progressive lengthening of the PR intervals until another QRS complex is blocked. The rhythm appears on the ECG in a pattern of grouped beats. Ventricular rhythm is irregular. The P wave has a normal shape. The QRS complex has a normal shape and duration.

wet vs dry suction

There are two types of suction control: water and dry. The water suction control chamber uses a column of water with the top end vented to the atmosphere to control the amount of suction from the wall regulator. The chamber is typically filled with 20 cm of water. When the negative pressure generated by the suction source exceeds the set 20 cm, air from the atmosphere enters the chamber through the vent on top, and the air bubbles up through the water, causing a suction-breaker effect. As a result, excess pressure is relieved. The amount of suction applied is regulated by the amount of water in this chamber and not by the amount of suction applied to the system. An increase in suction does not result in an increase in negative pressure to the system because any excess suction merely draws in air through the vent on top of the third chamber. The suction pressure is usually ordered to be −20 cm H2O, although higher pressures (−40 cm H2O) are sometimes necessary to evacuate the pleural space; lower pressure (-10 cm H2O) may be used for frail and older patients at risk for tissue damage with higher pressures. To initiate suction, the vacuum source is adjusted (increase) until gentle bubbling is present in the third chamber. Excessive bubbling does not increase the amount of suction but does increase the rate of evaporation of the water and the amount of noise made by the device.

Chest Tubes and Pleural Drainage

This figure depicts the original set-up for pleural drainage using glass bottles. Although the glass bottles have been replaced by a single plastic unit, visualization of separate compartments makes it easier to comprehend. Insertion of a chest tube often requires attachment to a drainage device or chamber to collect fluid, air, and/or blood from the thoracic cavity. Several different disposable chest drainage units are currently available, but common to all drainage units are three basic compartments. The first compartment, or collection chamber, receives fluid and air from the pleural or mediastinal space. The drained fluid stays in this chamber while expelled air vents to the second compartment. The second compartment, the water-seal chamber, contains 2 cm of water, which acts as a one-way valve. Incoming air enters from the collection chamber and bubbles up through the water. The water prevents backflow of air into the patient. The third compartment, the suction control chamber, applies suction to the chest drainage system. There are two main types of suction control: water and dry. The water suction control chamber uses a column of water to control the amount of suction from the wall regulator. The chamber is typically filled with 20 cm of water. When the negative pressure generated by the suction source exceeds the set 20 cm, air from the atmosphere enters the chamber through a vent on top of the chest drainage unit and the air bubbles up through the water, causing a suction-breaker effect. As a result, excess pressure is relieved. Bubbling in water-seal chamber indicates air leak Initially large air leak expected Eventually disappears Tidaling Reflects changes in pressure Disappears as lung reexpands Brisk bubbling of air often occurs in this chamber when a pneumothorax is initially evacuated. Intermittent bubbling during exhalation, coughing, or sneezing (when the patient's intrathoracic pressure is increased) may be observed as long as air is in the pleural space. Eventually, as the air leak resolves and the lung becomes more fully expanded, bubbling ceases. Normal fluctuation of the water within the water-seal chamber is called tidaling. This up-and-down movement of water in concert with respiration reflects intrapleural pressure changes during inspiration and expiration. Investigate any sudden cessation of tidaling, as this may signify an occluded chest tube. Gradual reduction and eventual cessation of tidaling is expected as the lung reexpands. Water suction control Amount of water in chamber controls suction to lungs Excess suction from source vented Typically filled to -20 cm of water Adjust suction until gentle bubbling in third chamber

Acute Kidney Injury dx

Thorough history Serum creatinine Urinalysis Kidney ultrasonography Renal scan CT scan Renal biopsy hx is essential for dx etiology of AKI. prerenal causes when there is a hx of dehydration, or blood loss. Suspect intrarenal causes if patient has been exposed to potentially nephrotoxic drugs or contrast media used in radiologic study. Postrenal causes are suggested by a history of changes in urinary stream, stones, benign prostatic hyperplasia, bladder, prostate cancer. incr serum creatinine may not be evident until loss of more than 50% of kidney function. rate of incr in serum creatinine is also important as a dx indicator in determining the severity of injury. UA = important dx test. Urine sediment containing abundant cells, casts, or proteins suggests intrarenal disorders. urine osmolality, Na content, specific gravity help in differentiating causes of AKI. Urine sediment may be normal in both prerenal, postrenal AKI. intrarenal probs, hematuria, pyuria, crystals may be seen. Kidney ultrasonography is often the 1st test done, since it provides imaging w/o exposure to potentially nephrotoxic contrast agents. = useful for evaluating for possible kidney disease, obstruction of urinary collection system. renal scan can assess abnormalities kidney blood flow, tubular function, collecting system. CT scan can identify lesions, masses, obstructions, vascular anomalies. Renal biopsy is considered best method for confirming intrarenal causes of AKI. To establish a dx of AKI, other testing may be required

Aorta Nursing ManagementAssessment

Thorough history and physical exam Watch for signs of cardiac, pulmonary, cerebral, and lower extremity vascular problems Establish baseline data to compare postoperatively Note quality and character of peripheral pulses and neuro status Mark/document pedal pulse sites and any skin lesions on lower extremities before surgery indications of rupture: Diaphoresis Pallor Weakness Tachycardia Hypotension (all the above = shock) Abdominal, back, groin, or periumbilical pain Changes in level of consciousness Pulsating abdominal mass

Chest Tubes and Pleural Drainage

To remove air or fluid from pleural and/or mediastinal space Reestablishes negative pressure, Lung re-expands, Pleural and/or mediastinal If enough fluid or air accumulates in the pleural space, the negative pressure becomes positive and the lungs collapse. As a result, chest tubes are inserted to drain the pleural space, reestablish negative pressure, and allow for proper lung expansion. They may also be inserted in the mediastinal space to drain air and fluid postoperatively. Chest tubes are approximately 20 inches (51 cm) long and vary in size from 12F to 40F. The size inserted is determined by the patient's condition. Large (36F to 40F) tubes are used to drain blood, medium (24F to 36F) tubes are used to drain fluid, and small (12F to 24F) tubes are used to drain air. Pigtail tubes are very small (10F to 14F) tubes with a curly end designed to keep them in place = safe, alternative to larger bore chest tubes for treatment of pneumothorax.

Interprofessional CareAcute Coronary Syndrome - Ongoing monitoring

Treat dysrhythmias Frequent vital sign monitoring Bed rest/limited activity for 12-24 hours UA or NSTEMI Dual antiplatelet therapy and heparin Cardiac catheterization with PCI once stable The patient will usually receive ongoing care in a critical care unit or telemetry unit, where continuous ECG monitoring is available. Dysrhythmias are treated according to agency protocols. Some patients are started on glycoprotein IIb/IIIa inhibitors (e.g., eptibibatide) either before catheterization or at the time of PCI. Monitor vital signs, including pulse oximetry, frequently during the first few hours after admission and closely thereafter. Maintain bed rest and limitation of activity for 12 to 24 hours, with a gradual increase in activity unless contraindicated. For patients with UA and NSTEMI, aspirin and heparin (UH or LMWH) are recommended. Dual antiplatelet therapy (e.g., aspirin and clopidogrel) and heparin are recommended for NSTEMI patients. Cardiac catheterization with possible PCI is considered for both UA and NSTEMI patients once the patient is stabilized and angina is controlled or if angina returns or increases in severity.

Defibrillation

Treatment of choice for VF and pulseless VT Passage of DC electrical shock through the heart to depolarize myocardial cells It is most effective when the myocardial cells are not anoxic or acidotic. Rapid defibrillation (within 2 minutes) is critical to a successful patient outcome. goal is following repolarization of heart cells will allow the SA node to resume the role of pacemaker. Biphasic defibrillators deliver shocks at lower energies and with fewer postshock ECG dysrhythmias than monophasic defibrillators. Output is measured in joules or watts per second Recommended energy for initial shocks in defibrillation Biphasic: 120 to 200 joules Monophasic: 360 joules initially, they can always go up Immediate CPR after first shock recommended energy for initial shocks in defibrillation depends on the type of defibrillator.

TB Diagnostic Studies - TST

Tuberculin skin test (TST) AKA: Mantoux test Uses purified protein derivative (PPD) injected intradermally Assess for induration in 48 - 72 hours Presence of induration (not redness) at injection site indicates development of antibodies secondary to exposure to TB The tuberculin skin test (TST) (Mantoux test) using purified protein derivative (PPD) is the standard method to screen people for M. tuberculosis . The test is administered by injecting 0.1 mL of PPD intradermally on the ventral surface of the forearm. The test is read by inspection and palpation 48 to 72 hours later for the presence or absence of induration. The indurated area (if present) is measured and recorded in millimeters. Induration, a palpable, raised, hardened area or swelling (not redness) at the injection site means the person has been exposed to TB and has developed antibodies. (Antibody formation occurs 2 to 12 weeks after initial exposure to the bacteria.) Positive if ≥15 mm induration in low-risk individuals Response ↓ in immunocompromised patients Reactions ≥5 mm considered positive The induration is measured, and, based on the size of the induration and the risk factors, an interpretation is made according to standards for determining a positive test reaction. An induration of 15 mm or more is considered positive in all low-risk individuals. Results for patients at higher risk would be considered positive if induration 10 mm or higher. Because the immunocompromised patient may have a decreased response to TST, even smaller induration reactions (≥5 mm) are considered positive. The figure shows a positive tuberculin skin test. This adolescent boy became infected as a result of living with and helping to care for a grandfather whose chronic "smoker's cough" was ultimately discovered to be a manifestation of chronic cavitary tuberculosis. He had a greater than 15-mm induration. A waning immune response can cause false negative results Repeating TST may boost reaction Two-step testing recommended for health care workers getting repeated testing and those with decreased response to allergens Two-step testing ensures future positive results accurately interpreted Some people who were previously infected with TB may have a waning immune response to the TST. This may result in a false negative result. However, repeating the TST may stimulate (boost) the body's ability to react to tuberculin in future tests. A positive reaction to a subsequent test could then be misinterpreted as a new infection, rather than the result of the boosted reaction to an old infection. To prevent misinterpretation in future testing, a two-step testing process is recommended for initial testing for health care workers (who get repeated testing) and for individuals who have a decreased response to allergens. A previously negative two-step TST ensures that any future positive results can be accurately interpreted as being caused by a new infection.

TB Drug Therapy

Two phases of treatment Initial (8 weeks) Continuation (18 weeks) Four-drug regimen Isoniazid Rifampin (Rifadin) Pyrazinamide Ethambutol Because of the growing prevalence of multidrug-resistant TB, it is important to manage the patient with active TB aggressively. Drug therapy is divided into two phases: initial and continuation. If drug susceptibility test results indicate that the bacteria are susceptible to all drugs, ethambutol may be discontinued. If PZA cannot be included in the initial phase (due to liver disease, pregnancy, etc.), the remaining three drugs are used for the initial phase.

Interprofessional Care Pneumothorax and Hemothorax

Tx = Chest tube to water-seal drainage Surgery for repeated spontaneous pneumothorax Urgent needle decompression for tension pneumothorax Most definitive and common form of tx of pneumothorax and hemothorax = insert a chest tube and connect it to water-seal drainage. Repeated spontaneous pneumothorax may need to be treated surgically by a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another. Tension pneumothorax = medical emergency, requiring urgent needle decompression = chest tube insertion to water-seal drainage.

Sudden Cardiac Death (SCD)

Unexpected death from cardiac causes - almost 400,000 annually Abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow Most commonly caused by Ventricular dysrhythmias Structural heart disease Conduction disturbances Sudden cardiac death (SCD) is unexpected death resulting from a variety of cardiac causes. Almost 400,000 people experience SCD yearly. In SCD, there is a sudden disruption in cardiac function, producing an abrupt loss of CO and cerebral blood flow. The affected person may or may not have a known history of heart disease. SCD is often the first sign of illness for 25% of those who die of heart disease. Acute ventricular dysrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) cause the majority of cases of SCD. Structural heart disease accounts for 10% of the cases of SCD. Patients in this group include those with LV hypertrophy, myocarditis, and hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a risk factor for SCD, especially in young, athletic people. Some cases of SCD (especially in people less than age 45) occur in the absence of structural heart disease. These involve disturbances in the conduction system (e.g., prolonged QT syndrome, Wolff-Parkinson-White syndrome). No warning signs or symptoms if no MI Prodromal symptoms if associated with MI Chest pain, palpitations, dyspnea Death usually within 1 hour of onset of acute symptoms Persons who experience SCD because of CAD fall into two groups: (1) those who did not have an acute MI and (2) those who did have an acute MI. The first group accounts for the majority of cases of SCD. In this instance, victims usually have no warning signs or symptoms. Patients who survive SCD are at risk for another SCD event due to the continued electrical instability of the myocardium that caused the first event to occur. The second, smaller group of patients includes those who have had an MI and have suffered SCD. In these cases, patients usually have prodromal symptoms, such as chest pain, palpitations, and dyspnea. Death usually occurs within 1 hour of the onset of acute symptoms.

Pacemakers

Used to pace the heart when the normal conduction pathway is damaged Pacing circuit consists of Programmable pulse generator (power source) One or more conducting (pacing) leads to myocardium no spikes = heart is working on their own it doesn't have to be helped The basic pacing circuit consists of a power source (battery-powered pulse generator) with programmable circuitry, one or more pacing leads, and the myocardium. The electrical signal (stimulus) travels from the pulse generator, through the leads, to the wall of the myocardium. The heart muscle is "captured" and stimulated to contract (next slide). Ventricular capture (depolarization) secondary to signal (pacemaker spike) from pacemaker lead in the right ventricle. Pace atrium and/or one or both of ventricles Most pace on demand, firing only when HR drops below preset rate Sensing device inhibits pacemaker when HR adequate Pacing device triggers when no QRS complexes within set time frame Current pacemakers are small, sophisticated, and physiologically precise. They pace the atrium and/or one or both of the ventricles. Most pacemakers are demand pacemakers. This means that they sense the heart's electrical activity and fire only when the HR drops below a preset rate. Demand pacemakers have two distinct features: (1) a sensing device that inhibits the pacemaker when the HR is adequate and (2) a pacing device that triggers the pacemaker when no QRS complexes occur within a preset time period. Antitachycardia pacing: delivery of a stimulus to the ventricle to terminate tachydysrhythmias Overdrive pacing: pacing the atrium at rates of 200-500 impulses/minute to terminate atrial tachycardias In addition to antibradycardia pacing, devices now include antitachycardia and overdrive pacing. Antitachycardia pacing involves the delivery of a stimulus to the ventricle to end tachydysrhythmias (e.g., VT). Overdrive pacing involves pacing the atrium at rates of 200 to 500 impulses/minute in an attempt to terminate atrial tachycardias (e.g., atrial flutter with a rapid ventricular response). A permanent pacemaker is implanted totally within the body. The power source is placed subcutaneously, usually over the pectoral muscle on the patient's nondominant side. The pacing leads are placed transvenously to the right atrium and/or one or both ventricles and attached to the power source. This graphic displays a dual-chamber rate-responsive pacemaker from Medtronic, Inc. Pacing leads in both the atrium and the ventricle enable a dual-chamber pacemaker to sense and pace in both heart chambers. Permanent pacemakers are inserted to treat patients with chronic heart problems in which the heart beats too slowly to adequately support the body's circulation (i.e., AV heart blocks, sick sinus syndrome, atrial fibrillation with slow ventricular response, severe heart failure, cardiomyopathy, bundle branch block). New technology and research are focused on miniaturized, leadless permanent pacemakers. Most candidates for the new device are patients who need single-chamber pacing for atrial fibrillation with AV block. The device is placed in the right ventricle. The lack of a transvenous lead and subcutaneous pulse generator is a major shift in cardiac pacing. it is the line going down that is shorter, its before the QRS

Drug Therapy - Latent TB infection

Usually treated with Isoniazid for 6 to 9 months HIV patients should take Isoniazid for 9 months Alternative 3-month regimen of Isoniazid and rifapentine OR 4 months of rifampin In people with LTBI, drug therapy helps prevent a TB infection from developing into active TB disease. Because there are fewer bacteria in a person with LTBI, treatment is much easier. Usually, only one drug is needed. The 9-month regimen is more effective, but compliance issues may make the 6-month regimen preferable. A 4-month therapy with rifampin may be indicated if the patient is resistant to Isoniazid. Due to severe liver injury and deaths, the CDC does not recommend the combination of rifampin and pyrazinamide for treatment of LTBI.

PE Clinical Manifestations

Varied and nonspecific Dyspnea most common Tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, change in LOC The signs and symptoms in PE are varied and nonspecific, making diagnosis difficult. Clinical manifestations depend on the size and extent of emboli. Small emboli may go undetected or produce vague, transient symptoms. Symptoms may begin slowly or suddenly. Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE. A mild to moderate hypoxemia may be observed. Other manifestations may include tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, accentuation of the pulmonic heart sound, tachycardia, and syncope. Massive emboli may produce a sudden change in mental status and hypotension.

ARDS Complications of treatment

Ventilator-associated pneumonia Barotrauma = caused by increased air or water pressure Volutrauma = damage to the lung caused by overdistention High risk for stress ulcers Renal failure = From hypotension, hypoxia, or hypercapnia, nephrotoxic drugs used to treat ARDS = vancomycin [Vancocin]) The primary cause of death in ARDS is MODS, often accompanied by sepsis. The vital organs most commonly involved are the kidneys, liver, and heart.

ARDS Complications

Ventilator-associated pneumonia (VAP) Strategies for prevention of VAP Strict infection control measures Ventilation protocol bundle Elevate HOB 30 to 45 degrees Daily "sedation holidays" Venous thromboembolism prophylaxis Daily oral care with chlorhexidine VAP occurs in as many as 68% of patients with ARDS. Risk factors include impaired host defenses, contaminated equipment, invasive monitoring devices, aspiration of GI contents (especially in patients receiving enteral feedings), and prolonged mechanical ventilation. Strict infection control measures (e.g., strict hand washing, sterile technique during endotracheal suctioning, frequent mouth care, and oral hygiene) and a ventilator bundle protocol (Table 67-8). Barotrauma Rupture of overdistended alveoli during mechanical ventilation XUTE Respiratory Distress Syndrome Clinical Network (ARDSNet) Ventilate with smaller tidal volumes Higher Paco2 - permissive hypercapnia Barotrauma results in alveolar air escaping from ruptured alveoli. This can lead to pulmonary interstitial emphysema, pneumothorax, subcutaneous emphysema, pneumoperitoneum, pneumomediastinum, pneumopericardium, and tension pneumothorax. The approach of ventilating with smaller tidal volumes (e.g., 6 mL/kg), called the Acute Respiratory Distress Syndrome Clinical Network (ARDSNet) protocol, reduces mortality and the number of ventilator days for these patients. Volutrauma Occurs when large tidal volumes are used to ventilate noncompliant lungs Alveolar fracture and movement of fluids and proteins into alveolar spaces Smaller tidal volumes or pressure-control ventilation is now standard in ARDS Volutrauma results in alveolar fractures (damage or tears in the alveoli) and movement of fluids and proteins into the alveolar spaces. Stress ulcers Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation Management strategies Correction of predisposing conditions Prophylactic antiulcer drugs Early initiation of enteral nutrition Prophylactic management includes antiulcer drugs such as proton pump inhibitors (e.g., pantoprazole [Protonix]), and mucosa-protecting drugs (e.g., sucralfate [Carafate]). Renal failure Occurs from decreased renal perfusion and subsequent decreased delivery of O2 to kidneys From hypotension, hypoxia, or hypercapnia May also be caused by nephrotoxic drugs used to treat ARDS-related infections Renal failure may also result from nephrotoxic drugs (e.g., vancomycin [Vancocin]) used to treat ARDS-related infections.

Left ventricular assist device

Ventricular assist devices (VADs) can be used to maintain the pumping action of a heart that cannot effectively pump. A VAD is a mechanical pump that is surgically implanted. (IABPs and VADs are discussed in Chapter 65.) Once the patient is more stable, determination of the cause of ADHF is important. Diagnosis of systolic or diastolic HF will then direct further treatment protocols.

Complications of Myocardial Infarction - Ventricular septal wall

Ventricular septal wall rupture and left ventricular free wall rupture New, loud systolic murmur HF and cardiogenic shock Emergency repair Rare condition associated with high death rate A new loud systolic murmur heard in patients with acute MI may signal ventricular septal wall rupture. Depending on the size of the defect and degree of right and LV dysfunction, HF and cardiogenic shock may occur. The patient must receive emergency repair, either surgically or percutaneously. The defect can quickly expand and lead to hemodynamic compromise. LV free wall rupture is an emergent clinical situation. Rapid hemodynamic compromise and death ensues if not treated immediately. Although this is a rare complication, death rates are high. Free wall rupture is seen more frequently in patients suffering their first MI, patients with anterior MIs, older adults, and women.

Acute Coronary Syndrome

When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops. ACS includes the spectrum of UA, non-ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI). CAD either chronic stable angia or acute coronary syndrome, if angina ACS unstable angina/NSTEMI or STEMI When patients first present with chest pain, ST-elevations on the 12-lead ECG are most likely indicative of a STEMI. The ECG should always be compared to a previous ECG whenever possible. For patients with chest pain who do not show ST-elevation or ST-T wave changes on the ECG, it is difficult to distinguish between UA and NSTEMI until serum cardiac biomarkers are measured. On the cellular level, the heart muscle becomes hypoxic within the first 10 seconds of a total coronary occlusion. Heart cells are deprived of oxygen and glucose needed for aerobic metabolism and contractility. Anaerobic metabolism begins and lactic acid accumulates. In ischemic conditions, heart cells are viable for approximately 20 minutes. Irreversible heart damage starts after 20 minutes if there is no collateral circulation.

Removal of Chest Tubes

When lungs reexpanded and drainage minimal Premedicate prior to removal Valsalva maneuver during removal Apply occlusive dressing Chest x-ray is done Monitor for respiratory distress The chest tubes are removed when the lungs are reexpanded and fluid drainage has ceased or is minimal. In some centers, suction is discontinued, and the chest drain is on gravity drainage for 24 hours before the tube is removed. Give the patient pain medication about 30 to 60 minutes before tube removal. Gather dressing supplies and petroleum jelly dressing. Explain the procedure to the patient. The tube is removed by the HCP in most settings. The suture is cut, and with the patient holding his or her breath or bearing down (Valsalva maneuver), the tube is removed. The site is immediately covered with the airtight dressing to prevent air from entering the pleural space. The pleura will seal off, and the wound usually heals in a few days. A chest x-ray is done 30 to 60 minutes post-chest tube removal to evaluate for pneumothorax and/or reaccumulation of fluid. Observe the wound for drainage and reinforce the dressing if necessary. Assess the patient for respiratory distress, which may signify a recurrence of the original problem.

Myocardial InfarctionHealing Process

Within 24 hours, leukocytes infiltrate the area of cell death Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day → thin wall Necrotic zone identifiable by ECG changes Collagen matrix laid down The body's response to cell death is the inflammatory process. Within 24 hours, leukocytes infiltrate the area of cell death. The proteolytic enzymes of the neutrophils and macrophages begin to remove necrotic tissue by the fourth day. During this time, the necrotic muscle wall is thin. The necrotic zone of a STEMI is identified by ECG changes (e.g., lowering of the ST-segments, T-wave inversion, pathologic Q wave) within a day or two. At this point, the neutrophils and monocytes have cleared the necrotic debris from the injured area, and the collagen matrix that will eventually form scar tissue is laid down. 10 to 14 days after MI, scar tissue is still weak Heart muscle vulnerable to stress Monitor patient carefully as activity level increases At 10 to 14 days after MI, the new scar tissue is still weak. The heart muscle is vulnerable to increased stress during this time because of the unstable state of the healing heart wall. It is also at this time that the patient's activity level may be increasing, so special caution and assessment are necessary. By 6 weeks after MI, scar tissue has replaced necrotic tissue Area is said to be healed, but less compliant Ventricular remodeling Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle By 6 weeks after MI, scar tissue has replaced necrotic tissue and the injured area is considered healed. Often, the scarred area is less compliant than the surrounding area. This condition may be manifested by abnormal wall motion on an echocardiogram or nuclear imaging, LV dysfunction, altered conduction patterns, or heart failure (HF). These changes in the infarcted heart muscle also cause changes in the unaffected areas. In an attempt to compensate for the damaged muscle, the normal myocardium will hypertrophy and dilate. This process is called ventricular remodeling. Remodeling of normal myocardium can lead to the development of late heart failure (HF), especially in the person with atherosclerosis of other coronary arteries and/or an anterior MI. ACE inhibitors are given to limit ventricular remodeling.

Aortic AneurysmDiagnostic Studies

X-rays = Chest - demonstrate mediastinal silhouette and any abnormal widening of thoracic aorta Xray Abdomen - may show calcification within wall of AAA electrocardiogram (ECG) may rule out MI, since thoracic aneurysm or dissection symptoms can mimic angina = diagnosis of aortic valve insufficiency Ultrasonography = Useful in screening for aneurysms = Monitors aneurysm size CT scan = Most accurate test to determine = Anterior-to-posterior length = Cross-sectional diameter = Presence of thrombus = Best type of surgical repair MRI = Diagnose and assess location and severity Angiography = Anatomic mapping of aortic system using contrast Not reliable method of determining diameter or length Can provide accurate information about involvement of intestinal, renal, or distal vessels Angiography is also useful if a suprarenal or thoracoabdominal aneurysm is suspected.

pleural effusion

abnormal collection of fluid in this space indiaction of disease balance b/w hydrostatis pressure, oncotic pressure and cap membrane permeability allows movement of fluids fluid accumulation result in incr pul cap pressure, decr oncotic pressure, incr pleural mem permeability or obstruction of lymaphtic flow transudative - primarily in noninflammatory conditions, protein poor, cell poor fluidm clear, pale yellow fluid caused by incr hydrostatic pressure found in heart failure or decr oncotic pressure from hypoalbuuminemia in chronic liver disease or renal or exudative - incr cap permeability of inflammatory reastion, infections or malignacnies

hemothorax

accumulation of blood in the pleural space from injury to the chest wall, diaphragm, lung, blood vessles, mediastinum called hemopneumothorax need fast chest tube for blood to leave

tb patient care

admin heated and humidified O2 wear N95 HEPA filter or powder air respirator negative airflow roomclient wear surgical mask if transported cough and expell sputum into trash incr fluid, incr kcals, incr vit C & B, incr protein, iron

tb education

airborn not needed at home bc fam already exposed meds for 6m-2yrs sputum samples every 2-4wks contaminated tissues into plastic bags wear mask in public places

hypercapnic resp failure

aka ventilatory incr CO2, decr aveolar vent abnormalties of airway and alveoli abmornal CNA abnormal chest wall neuromuscle conditions airway and alveoli abdnormalities = COPD, asthma, CF high risk, resp muscle fatigue CNS abnorm - opioids, medulla does not alter rate, injuries to spine/chest/diagphram chest wall - frail chest, fractures, hyphoscolisos neuromuscle - guillian barre, ms

pneumonia meds

antibiotics - marcolides, NOT penicillins, cephalosporins, IV --> oral, careful of frequent stools, kidney function, take w/ food, pen sometimes 1hr b/f or 2 hr after meals bronchodilators - decr brochospasms, decr irritation, SABA = albuterol cholinergic antagois (anticholinergic) = ipratropium block parasympatehtic nervous system, methylazanthines - theophyline, narrow therapeutic level theo - n/d/ tremors, albuterol - tachycardia ipratripium - hr, dry mouth, headahce, blurred vision, palpitations, toxicity suck on candies, incr fluids, antiinflammatories - decr airway inflammation, glucocorticosteriods - flluticasone and prednisone, decr infmallation monitor immunisuprresion, hyperglycemia, hypokalemia, poor wound healing, black stools, fluid retention, weight gain, aphthous lesions (canker sores) drink, take w/ food, dont stop meds

Pulmonary edema s/s

anxious pale cool clammy skin dysnpnea orthopnea tachypnea use of accessory muscles cough w/ frothy blood sputum crackles wheezes tachycaria hypo/hypertension abnormal S3 and S4 Clinical manifestations of pulmonary edema are distinct. The patient has dyspnea and orthopnea (unable to lie flat due to shortness of breath). Jugular venous distention is often present and is the most sensitive and specific sign for elevated LV filling pressures. The patient is usually anxious, pale, and possibly cyanotic. The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. Respiratory rate is often greater than 30 breaths/minute, and use of accessory muscles to breathe may be seen. There may be wheezing and coughing with the production of frothy, blood-tinged sputum. Breath sounds may reveal crackles and wheezes throughout the lungs. The absence of crackles does not rule out ADHF as many patients with a history of chronic HF develop increased lymphatic drainage of the alveolar edema. The patient's HR is rapid, and an abnormal S3 or S4 heart sound may be auscultated. BP may be elevated or decreased depending on the severity of the HF.

Diagnostic Tests RH

arthrisis, sydenhams chorea, erthema marginatum, subQ nordules monoartharlgia, fever, incr ESR and or incr CRP, prolong PR, incr antistreptolysin -O titer, +throat culture, + rapid antigen test for group A strepcocci

Groups of ADHF

based on hemodynamic and clincal status, pt can be put into 4 groups dry -warm dry-cold wet-warm (most common) wet-cold Patients with ADHF can be categorized into one of four groups based on hemodynamic and clinical status: dry-warm, dry-cold, wet-warm, and wet-cold. The most common presentation in patients with ADHF is the wet and warm patient. A patient is "wet" due to volume overload (e.g., congestion, dyspnea), but "warm" due to adequate perfusion (warm skin, positive pulses).

resp failure meds

benxodiazepines - larasepam or midazolam decr anxiety and resistance to vent and decr O2 demand monitor bp and SaO2 careful with opiods general anesthesia - propofol sedates no for ppl with hyperlipidemia or egg allergies, only if intubated, ECG, blood pressure, sedation levels, IV rate slowed to assess neuro status, careful of hypotension corticosteroids - cortisone acetate, methylprednisolone Na succinate = decr WBC, decr inflam, stabilize alveolar cap membrane during ARDs d/c gradually, admin with antiulcer med, weight, bp, glucose, electrolytes, w/ food neuromuscular blocking agents - vecuronium decr O2 consumption, w/ painful ventilatory modes only if intubated, ecg, bp, muscle strength, pain meds w/, neostigmine and atropine = undo med, cause paralysis antibiotic sensistive to cultured orgniams = vancomycin - culture on first dose, IV slow to avoid red man syndrome (over 60 mins), dont give with other meds, w/ food

Chest Tube Insertion

can take place in the emergency department (ED), in the operating room, or at the patient's bedside. arm raised above the head on the affected side to expose the midaxillary area, the standard site for insertion. Elevate the patient's head 30 to 60 degrees, when possible, to lower the diaphragm and reduce the risk of injury. Time permitting, a chest x-ray is used to confirm the affected side. The area is cleansed with an antiseptic solution. The chest wall is infiltrated with a local anesthetic, and a small incision is made over a rib. The area is first probed digitally to avoid injury with a sharp instrument. A clamp is used to hold the chest tube and guide it into place. The tube is advanced up and over the top of the rib to avoid the intercostal nerves and blood vessels that are behind the rib inferiorly. Once inserted, the tube is secured (sutured) in place, the incision is closed with sutures, and the tube is connected to a pleural drainage system (will discuss in next few slides). The wound is covered with an occlusive dressing. Most clinicians prefer to seal the wound around the chest tube with petroleum gauze. Proper tube placement is confirmed by chest x-ray. The insertion of a chest tube and its presence in the pleural space is painful.

pneumothorax

caused by air entering the pleural cavity normally - pressure exists b/w the visceral pleura (surronding the lung) and parietal pleura (lining of the thoarcic cavity) known as the pleural space = which has milliletirers of lub fluid to decr friction with tissue moves when air enters this space = change to + pressure = partial or complete lung collapse volume of air in pleural space incr = lung volume decr should be expected after any trauma to chest wall if small = tachycardia/dsypnea if large = resp distress, shallow rapid resp, dsypnea, air hunger, low O2, no breath sounds, cxray = air/fluid in pleural space and decr lung volume tx - chest tube, chest drainage system

types of pneumonia

causes - bacteria, virus, mycoplasm, fungi, parasites, chemicals Use CURB-65 to see if patient can be treated at home vs hospital CAP - community acquired pneumonia - not hospitalized or long term care facility in 14 days on s/s, tx - empiric antibiotic therapy = initiation of treatment before definitive dx or causative agent HAP - hospital acquired pneumonia - nosocominal pneumonia, nonibtubated pt that begins 48hrs or longer after hospital admin VAP - ventilator acquire pneumonia - 48 hrs after endotracheal intubation aspiration pneumonia - abnormal entry of material from mouth to stoach into the trachea and lungs (decr LOC, seizures, anesthiea, head injury, stroke, alcohol, difficult swallowing, ng tubes), cause inflam response, usually bacterial, and more than 1 organism, if aspirate gastic acid = noninfectios pneumonia /chemical = no antibiotics but may end up being bacterial 48-72hrs later necrotizing pneumonia - rare, bacterial, liquefaction, cavitation of lung tissue, through CAP, usually stapylococcus, klebsiella, streptococcus, lung abcesses occure, s/s - immediate resp insufficiency/failure, leukopenia, bleeding into airways, tx - longterm antibiotics/surgery opportunistic pneumonia - lower resp track, ppl w/ severe protient-calorie malnutrition, HIV, radiation, chemo, corticosteriods = pneumocystis jiroveci, cytomegalovirus VAP + HAP = longer stays, more $$, sicker pts MDR - multidrug resistant organisms, age, immunodepressed, hx of antibiotic use, prolonged vents Can be classified according to causative organism Clinical classification: Community-acquired (CAP) Hospital-acquired (HAP) Ventilator-associated (VAP) Bacteria, viruses, Mycoplasma, fungi, parasites, and chemicals are all potential causes of pneumonia. Although pneumonia can be classified many different ways (e.g., according to the causative organism), a clinically effective way is to classify pneumonia as community-acquired or hospital-acquired pneumonia. Classifying pneumonia is important because of the differences in the likely causative organisms and the selection of appropriate antimicrobial therapy.

blunt trauma

chest strikes or is struck by an object external injury may appear minor but internally the organs may have severe injuries ribs and sternal fractures can lacerate lung tissue high velocity impact, shearing forces can result in laceration or tearing the aorta compression of the chest = contusion, crush injury or organ puncture falls, car accidents, crush, explosion

RH complications

chronic Rheumatic carditis It results from changes in valvular structure that may occur months to years after an episode of RF. Rheumatic endocarditis can result in fibrous tissue growth in valve leaflets and chordae tendineae with scarring and contractures. mitral valve is most frequently involved aortic and tricuspid valves may also be affected.

tb meds

combination 2 or more meds 6-12 months isoniazid, rifampin, pyrazinamide, ethambutol isoniazid - INH, bactericidal, inhibits growth of mycobacteria by preventing synthesis of mycolic acid in cell wall, empty stomach, monitor hepatoticity, neurotocicity, use B12 to prevent, liver function should be completed b/f and after, NO alcohol rifampin - RIF, bacteriostatic and cidal, inhibits DNA and RNA in cells, monitor hepatotxict, liver function b/f and after, secretions turn orange, inhibits bc pyramzinamide - PZA, static and cidal, hepatotocic, gout, liver enzyme, no alcohol ethambutol - EMB, static, supresses RNA, inhibit protien, visual acuity test, color discrimination, no one under 8 yrs old, report eye changes streptomycin sulfate - aminoglycoside antibiotic, incr marcophages during phagocytosis, only used in multidrug resistant TB bc toxic, ototxiic, urine output and renal function, drink 2L a day

CURB 65

confusion BUN (over 20) respiratory over 30 B/p (60/90) 65 is age point value for each 0 = outpatient 1-2 = consider hospital 3 or more = hospital 4-5 = ICU

tb risk factors

contact with another infected person low socieconomic/homeless immunocomrpomised - HIV, chemo, kindey diseas, DM, crohns poor ventilation, crowded areas old recent travel outside US immigration - mexica, phillpines, vietnam, china, japan substance use health care occupation

ADHF interprofessional care

continuous monitoring and assessment hemodynamic monitoring supplemental O2 mechanical vent if unstable daily weights high fowlers vital signs/urine output at least every hour hemodynamic = arterial BP and pulmonary artery pressures If a pulmonary artery catheter is placed, evaluate CO and pulmonary artery wedge pressure (PAWP). Therapy is titrated to maximize CO and reduce PAWP. normal PAWP = 8 and 12 mm Hg ADHF PAWP = 30 mm Hg. give O2 noninvasive positive pressure ventilation (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation, BiPAP telemetry or stepdown unit for treatment

tb findings

cough - over 3wks purulent sputum - blood strkeaed chest pain weakness weight loss anorexia hemoptysis dsypnea low grade fever night sweats chills

cardiac rhythm couting Rs

count R-Rs count each between the R-R whole thing is 6 second intervals

arterial puncture

heparinized syringe for sample allen's test for arterial puncture verify radial and ulnar circulation with clenched fist occluded the ulnar and radial arteries release ulnar but specimen in ice and water hold pressure over site for 5 min, 20 min if anticoagulants complications - hematoma, arterial occulsion, air embolism = place client on left side in trendenburg position

PFT

determine lung function and breathing difficulties performed if dyspnea dont smoke 6-8hrs before testing no inhalers 4-6 hrs before testing

acute pericarditis dx and management

dx - hx and exam = friction rub labs = CRP ESR, WBC ecg cxray echo ct mri pericardiocentisis, pericadial window pericardial biopsy managements - treat underlying disease bed rest drugs - NSAIDs, cortico pericadriocentisis = for tamponade pericardial window = for tamponade or ongoing pericadial effusion CRP, C reactive protein, erthryocte sedementaion rate

RH dx and management

dx - hx and physical labs cxray eco ecg management bed rest decr activity antibiotics NSAIDs salicylates - asprin cortiosteriods

resp failure complications

endotracheal tube = trauma, altered position of endotracheal tube, aspiration pneumonia, infection, blocked endotracheal tube mechanical ventilation = incr intrathoracic pressure, barotrauma, immobilization

flutter or heimlich valve

evacuate air from pleural space one way rubber valve within rigid plastic tube attached to external end of chest tube during inspiration, when pressure in chest is greater than atmospheric pressure the valve opens during expiration, intrathorasic pressure is less than atmospheric, value closes can be used for small/mod size pneumothorax = smaller and hide under clothes,

pneumonia findings

findings: anxiety, tired, weak, chest pain from coughing, confusion from hypoxia (most common in elders) Assessment findings: fever, chills, flushed face, diaphoresis, SOB, tachypnea, pleuritic chest pain, yellow sputum or purulen/blood/rush color, crackles, wheeze, coughing, dull chest percussion, decr O2 stat

penetrating trauma

foreign object impales or passes through the body tissue = an open wound knife, gunshot, sharp objects, arrow, missiles, stick

fail chest

fracture of several consecutive ribs in 2 or more places = unstable segment fracture of the sternum and several consecutive ribs = instablitity of chest wall = paradoxical movement the affected (fail) area moves in opposite direction inspiration = affected portion is sucked in expiration = affected portion bludges out incr work of breathing can see on examination, rapid shallow resp, tachycardia, splinting, crepitus, cxray analgesia, mechanical vent, surgery can have intercostal pain after ribs heal

acute pharyngitis

inflammation of pharyngeal may include tonsils, palate, uvula viral #1, bacterial (strep), fungal(candida - from antibiotics/corticosteriods) causes - dry air, smoking, gerd, allergy, postnasal drip, endotracheal intubation, chemicals, cancer s/s - scratchy throat, pain w/ swallowing, red throat, edematous pharynx (w or w/o patchy exudates) 4 classic s/s of bacteria (only need 3/4)- fever 100.4 (fighting hard so bacterial), anterior cervical lymph node enlargement, tonsillar or pharyngeal exudate, absence of cough viral will have a lower temperature tx - viral = ibuprohen/acetominophen, incr fluids, gargle warm salt water, popscilces, cough drops no citrus = irritatingto laryx bacteria = antibiotics - penicillin, several time a day for 10 days, or erythromycin if allergic, contagious untill antibiotics for 24-48 hrs, no repeat throat cultures needed fungal - antifungals, nystatin, fluconazole, swish in mouth for as long as possible, before swallowing

Acute Care AKI

intake and output Daily weights Assess for hypervolemia or hypovolemia Assess for K and Na Meticulous aseptic technique Careful use of nephrotoxic drugs Because infection is the leading cause of death in AKI, meticulous aseptic technique is critical = temperature may not always be elevated. Patients with kidney failure have a blunted febrile response to an infection (e.g., pneumonia). Mouth care = preventing stomatitis = ammonia (produced by bacterial breakdown of urea) in saliva irritates the mucous membranes. Recovery = highly variable, depends on if body systems fail, patient's general condition, age, length of oliguric phase, severity of nephron damage. Protein, potassium intake should be regulated in accordance w/ kidney function. Regular evaluation of kidney function through appropriate follow-up is necessary. long-term convalescence period of 3 to 12 months may cause psychosocial, financial hardships = referrals for counseling. If kidneys do not recover = transition to life on chronic dialysis or possible future transplantation.

resp failure therapeutic proceedures

intubation and mechanical vent preintub - oxygenate w/ 100% post - assess end tidal co2 levels, xray to confirm, assess balloon cuff PEEP - Kinetic therapy bed that rotates laterally, decr atelectasis, begin slowly, then incr angle, stop if patient becomes distressed

med to poop out K

kayexalate

airway obstruction

larynx = hoarseness trachea = wheezing, bronchus = cough causes - food, foreign body, allergic reaction, edema, infection, burns, peritonsillar abscess, retropharyngeal abscess, malignancy, laryngeal or tracheal stenosis, trauma tx - hemilick, tracheotomy brain damage or death in 3-5 min if not corrected tracheostomy - stoma (opening), clean around stoma with normal saline, inflated cuff = problems swalowing decannulation - removal of tracheostomy form trachea, make sure cuff is deflated, close stoma with tape srips

heart poems

longer segment between R to P pwave longer and longer to trigger then drops bc SA and AV cant sned to ventricals Pwaves go off and just drop QRS QRS triggers at own time and Pwaves triggers at own time

chylothorax

lymphatic fluid in the pleural space thoracic duct is disrupted either traumatically or malignacy lymph fluid fills pleural space milky white fluid is high in lipids normal lymph flow through thoracic duct is 1500 to 2500ml/day can incr 10x after ingestion of fats chest drainage, bowel rest, diet mod, octeriotide, throacic duct ligation, pleurodesis

acute resp disorders

maintain patent airway and promote oxygenation risk factors: young/old recent exposure to illness lack of vaccines exposre to pollens, mold, dander, foods, meds, enviro contaminants smoking substance abuse chronic lung disease - asthma/emphysema immunocompromised foreign body condition that incr aspiration cant mobilize secretions(surgery, decr LOC) inactivity immobility mechanical vent

Community-Acquired Pneumonia (CAP)

not been hospitalized or resided in a long-term care facility within 14 days of the onset of symptoms Can be treated at home or hospitalized dependent on patient condition Empiric antibiotic therapy started ASAP home or admit them to the hospital is based on several factors such as patient's age, vital signs, mental status, presence of comorbid conditions, and current physiologic condition. Clinicians can use tools such as the CURB-65 scale to supplement clinical judgment. (See Table 27-3.) confusion, BUN, resp rate, systolic, age over 65 Empiric antibiotic therapy, the initiation of treatment before a definitive diagnosis or causative agent is confirmed, should be started as soon as possible when CAP is suspected. Empiric antibiotic administration is based on experience and knowledge of drugs known to be effective for the most likely causative agent.

Junctional Dysrhythmias

originate in the AV junction SA node has failed to fire, or impulse has been blocked at the AV node Abnormal P wave; normal QRS Associated with disease, certain drugs refer to dysrhythmias that start in the area of the AV node to the bundle of His known as the AV junction. When this occurs, the AV node becomes the pacemaker of the heart. The impulse from the AV node usually moves in a retrograde (backward) fashion. This produces an abnormal P wave that occurs just before or after the QRS complex or that is hidden in the QRS complex. The impulse usually moves normally through the ventricles. Junctional dysrhythmias are often associated with CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease. Certain drugs (e.g., digoxin, amphetamines, caffeine, nicotine) can also cause junctional dysrhythmias. Junctional dysrhythmias include junctional escape rhythm (as shown on this slide), accelerated junctional rhythm, and junctional tachycardia. In junctional escape rhythm, the HR is 40 to 60 beats/minute. It is 61 to 100 beats/minute in accelerated junctional rhythm and 101 to 180 beats/minute in junctional tachycardia. Rhythm is regular. The P wave is abnormal in shape and inverted, or it may be hidden in the QRS complex (as shown on this strip). The PR interval is less than 0.12 second when the P wave precedes the QRS complex. The QRS complex is usually normal. Junctional premature beats may occur, and they are treated in a manner similar to that for PACs. Serves as safety mechanism—do not suppress If rhythms are rapid, may result in reduction of CO Treat if patient is symptomatic: Atropine for escape rhythm Correct cause Drugs to reduce rate if tachycardia NO cardiovert Junctional escape rhythms serve as a safety mechanism occurring when the SA node has not been effective. Escape rhythms such as this should not be suppressed. a Accelerated junctional rhythm is due to sympathetic stimulation to improve CO. Junctional tachycardia indicates a more serious problem. This rhythm may result in a reduction of CO, causing the patient to become hemodynamically unstable (e.g., hypotensive). If a patient has symptoms with a junctional escape rhythm, atropine can be used. In accelerated junctional rhythm and junctional tachycardia caused by drug toxicity, the drug is stopped. In the absence of digitalis toxicity, β-blockers, calcium channel blockers, and amiodarone are used for rate control.

Third-Degree AV Heart Block (Complete Heart Block)

p waves do their own thing, all p waves are the same, QRS's are all the same but QRS and P are firing whenever they want very scary, ticking time bomb on the floor Associated with severe heart disease, some systemic diseases, certain drugs results in decr CO Can lead to syncope, HF, shock Treat with pacemaker Drugs to increase HR while awaiting pacing associated with severe heart disease, including CAD, MI, myocarditis, cardiomyopathy, and some systemic diseases, such as amyloidosis and progressive systemic sclerosis (scleroderma). Some drugs can also cause third-degree AV block, such as digoxin, β-blockers, and calcium channel blockers. Third-degree AV block usually results in reduced CO with subsequent ischemia, HF, and shock. Syncope from third-degree AV block may result from severe bradycardia or even periods of asystole. For symptomatic patients, a transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted. The use of drugs such as dopamine (Intropin), and epinephrine is a temporary measure to increase HR and support blood pressure until temporary pacing is started. Patients will need a permanent pacemaker as soon as possible. Atropine is not an effective drug for this dysrhythmia. Third-degree AV block, or complete heart block, constitutes one form of AV dissociation in which no impulses from the atria are conducted to the ventricles. The atria are stimulated and contract independently of the ventricles. The ventricular rhythm is an escape rhythm, and the ectopic pacemaker may be above or below the bifurcation of the bundle of His. The atrial rate is usually a sinus rate of 60 to 100 beats/minute. The ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to 60 beats/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute. Atrial and ventricular rhythms are regular but unrelated to each other. The P wave has a normal shape. The PR interval is variable, and there is no relationship between the P wave and the QRS complex. The QRS complex is normal if an escape rhythm is initiated at the bundle of His or above. It is widened if an escape rhythm is initiated below the bundle of His.

ABGs

ph = free hydrogen ions in arterial blood PaO2 - partial pressure of O2 PaCO2 - partial pressure of Carbon dioxide SaO2 - percent of O2 bound to Hgb as compared to total amount that can be possibly carried

restrictive resp disorders

pleural effusion, thoracentsis, empyema, pleurisy, atelectasis impair the ability of the chest wall and diaphramg to move with respiations 2 types extrapulmonary (lung tissue is normal) - head injury, spinal cord injury, gullian barre, MD, chest wall trauma intrapulmonary (cause is lung or pluera) - pleural effusoon, pleurisy, pneumothoarx, ARDS, pneumonia, atelectasis hallmark for restrictive = TLC = total lung capacity hallmark obstructive = FEV1 = decr forced expiratory volume can happen together

chest surgery

preop = dx = pul function test, cxray, ECG, ABG, BUN, creatine, glucose, electrolytes, prothrombin, PT/INR ratio, aPTT, CBC, teach deep breathing, O2, PCA, splinting, stop smoking, ROM

PPD

purifiedc protein derivative inject 0.1ml on ventral surface of the forearm 48-72 hrs later palpable, raised, hardened, swelling NOT redness = +

chest tube removal

sometimes suction discontinued, but then gravity for 24hrs give meds 30-60min b/f get supplies and petroleum jelly dressing HCP or APN remove it suture cut while pt hold their breathe or vasalvagal maneuver cxray 30-60 min later to see pneumothorax is gone

Ventricular Fibrillation

quivering of vents always dfib for vfib sudden cardiac death Associated with MI, ischemia, disease states, procedures Unresponsive, pulseless, and apneic If not treated rapidly, death will result Treat with immediate CPR and ACLS Defibrillation Drug therapy (epinephrine, vasopressin) VF occurs in acute MI and myocardial ischemia and in chronic diseases such as HF and cardiomyopathy. It may occur during cardiac pacing or cardiac catheterization procedures because of catheter stimulation of the ventricle. It may also occur with coronary reperfusion after thrombolytic therapy. Other clinical associations are electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity. VF results in an unresponsive, pulseless, and apneic state. If not rapidly treated, the patient will die. Treatment consists of immediate initiation of CPR and advanced cardiac life support (ACLS) with the use of defibrillation and definitive drug therapy (e.g., epinephrine, vasopressin [Pitressin]). There should be no delay in using a defibrillator once available.

resp failure meds

relief broncospasms decr airway inflammation treat pul infection decr pain, anxiety reslessness maintain CO and hemoglobin

extrapulmonary tb

renal --> dyruia and hematuria bone and joint --> pain, headaches, v/, lyphadenopathy

Flail Chest

results from the fracture of several consecutive ribs, in two or more separate places, causing an unstable segment. caused by fracture of the sternum and several consecutive ribs. = instability of the chest wall causes paradoxical movement during breathing. The affected (flail) area will move in the opposite direction with respect to the intact portion of the chest. During inspiration = affected portion is sucked in During expiration = it bulges out. paradoxical chest movement not only prevents adequate ventilation but also increases the work of breathing. The underlying lung may have a pulmonary contusion aggravating hypoxemia. Management Adequate airway and ventilation Oxygen therapy Analgesia Surgical fixation usually apparent on visual examination, rapid, shallow respirations and tachycardia., moves air poorly, movement of the thorax is asymmetric and uncoordinated, splinting. Observation of abnormal thoracic cavity movements, palpitation for crepitus near the rib fractures, and chest x-ray all assist in the diagnosis. Initial therapy consists of ensuring adequate ventilation and supplemental oxygen therapy. The goal is to facilitate lung expansion and ensure adequate oxygenation. Analgesia is necessary to help promote adequate respiration. Although many patients can be managed without the use of mechanical ventilation, intubation and ventilation may be necessary. Surgical fixation of the flail segment may be used. The lung parenchyma and fractured ribs will heal with time. Some patients continue to experience intercostal pain after the flail chest has resolved.

influenza

seasonal flu = flu, epidemic in fall/winter, highly contagious, acute viral, one of several viruse families contagious for 24 hrs before s/s happen and up to 5 days after they begin pandemic flu = viral infection from animals or birds that has mutated and highly infectious to animals, potential to spread globally such as H1N1 (swine flu) findings: headahce, muscle aches, chills, fever, hypozia (avian flu), d/, cough (avian flu), tired, weak dx - AV Avantage A/H5N1 flu test droplet and contact precautions hospitalize if pandemic flu saline gargles monitor I&O meds: antivirals - amantafine, rimantadine, rubacirin, take w/i 24-48 hr of s/s flu vaccines - trivalent, suspected of strain, everyone older than 6 months H1N1 = avaliable for whole population H5N1 - stockpiles for distribution is pandemic at risk: over 65, prego, pneumonia, chronic medical condition complications = pneumonia

acute bronchitis

self limiting inflammation of bronchi in lower respiratory tract caused by viruses, air pollution, dust, inhalation of chemicals, smoking, chronic sinusitis, asthma, bacterial s/s - cough (up to 3 wks), clear mucus secretions or purulent sputum, green sputum (not proven to be bacterial), headache, fever, malaise, hoarseness, myalgias, dyspnea, chest pain dx - on clinical assessment, may have normal breath sounds, crackles or wheezes on expiration and with exertion, sputum sample. cxray = normal consolidation - occurs when fluid ccumulates in lung = pneumonia, is absent with bronchitis cxray - normal, not used unless thinking pneumonia goal - fix symptoms, prevent pneumonia tx - supportive, cough suppressants, oral fluid intake, humidifier, b2-agonist (bronchodilator) inhaler if wheezes, prednisone no antibiotics for viral, only if underlying disease no smoking, 2nd hand smoke, wash hands if from flu = antiviral - relenza, tamiflu - w/i 48 hr of symptoms

types of pneumothorax

spontaneous - rupture of small blebs (air filled sacs) located on the surface of the lung, risk = smoking, tall, thin, male, fam hx, previous one iatrogenic - laceration, puncture during medical procedure, ex transthoracic needle aspiration, subclavian catheter insertion, pleural biopsy, transbronchial lung biopsy, barotrauma from excessive ventilation, esophageal procedures, tearing during inserting gastric tube tension - air enters pleural space but cant escape, incr intrapleural pressures = compression of lungs on affected side and pressure on heart/vessels, pushing them away from the affected side, mediastinum shift to unaffected side, compressing the "good" lung, pressure incr = venous return = decr and CO fails, from open or closed pneumothorax, can happen bc mechanical ventilation, if chest tubes are clamped or become blocked, MEDICAL EMERGENCY = dsypnea, trachycardia, tracheal devition, decr breath sounds, cyanosis, profuse diaphoresis = urgernt needle decompression and chest tube to water seal

pneumonia labs

sputum culture and sensitivity: b/f starting antibiotic, use suction if unable to cough CBC: incr WBC (not always in elders) ABGs: hypoxemia (dec PaO2 under 80) Blood cultures: to rule out organism in blood Serum electro: cause of dehydration

RH sub and objective

subcutaneous nodules and erythema marginatum = palpating = bony surfaces and along extensor tendons of the hands and feet = size from 1 to 4 cm = hard, painless, and freely movable. Erythema marginatum = trunk and inner aspects of the upper arm and thigh = do not itch and are flat = bright pink maculae in good light because the rash is difficult to observe, especially in dark-skinned patients. sub = recent strep infection, rh heart disease, fam hx of RH, malaise, anorexia, weight loss, palitations, general weakeness, tired, ataxia, chest pain, joint pain, tender joints objective = fever, subQ nodules, erthema marginatum, tachycardia, friction rub, muffled heart sounds, murmurs, peripheral edema, chorea, sings of monoarthritis or polyarthitis, swelling, heat, redness, limited motion of knees, ankles, elbows, shoulders, wrists, dx findings = cardiomegaly, prolonged PR, chamber dilation, pericardial effusion,

acute resp distress

sudden and progessive form of acute resp fialure in which alveolar cap membrane becomes damaged and more permeable aspiration, viral/bacterial pneumonia, sepsis, ARDS 3 phases: injury or exudative phase, reparative or proliferative phase, fibrotic phase injury = 1-7 days, fluid, injury, avlveolar space fills with fluid/blood, alveolar 1and2 which produce surfactant cant, necrotic cells, protein and fibrin line alveoli O2 admin positive pressure ventilation -

thoracotomy

surgical incision into the chest to gain access to heart, lungs, esophagus, thoracic aorta, anterior spine through median sternotomy (splitting sternum and used for surgery involving the heart) and lateral thoracotomy posterolateral (surgeries involving the lungs), front to back at the level of the 4,5,6 intercostal space, retractors to seperate ribs anterolateral incision - 4.5 intercostal form the sternal border to midacillary line - trauma victims, mediastinal oerations, wedge resections of upper and middle loves most painful and hardest to manage

pneumothorax interprofessional care

tx depends on severity stable and minimal air/fluid = no treatment, can resolve spontaneously classifed as open (air entering through an opening in chest wall) or closed (no external wound) stab, gunshot, surgial throacotomy penetrating chest wound aka sucking chest wound = since air enters the pleural space through the chest wall during inspiration emergency tx = cover wound w/ occulsive dressing that is secured n 3 sides, during inspiration as - pressure is created in the chest the dressing pulls against the wound, preventing air from entering, during expirationg as pressure incr, dressing is pushed out and air escapes if object still in = dont remove = stablize with bulky dressing tx = chest tube and water seal drainage, sometimes pleurectomy, stapling, pleurodesis to promote adherence of pleurae to one another

ADHF

ultrafiltration (aquapheresis) for pts w/ volume overload and resistance to diuretics diculary assit devices for pt with deteriating HF = IABP, VADs IABP = intraaortic ballooon pump VADs = ventricalar assist devices Ultrafiltration (UF), or aquapheresis, is an option for the patient with volume overload. It is a process to remove excess salt and water from the patient's blood. UF can rapidly remove intravascular fluid volume while maintaining hemodynamic stability. The ideal patients for UF are those with major pulmonary or systemic volume overload who have shown resistance to diuretics and are hemodynamically stable. UF also may be an appropriate adjunctive therapy for patients with HF and coexisting renal failure. (UF is discussed in Chapter 46.) In the ICU, circulatory assist devices are used to manage patients with worsening HF. The intraaortic balloon pump (IABP) is a device that increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. The IABP is useful in hemodynamically unstable patients because it decreases pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO.

resp failure risk factors

venilatory failure = COPD, pul embolism, pneumonia, fail chest, ARDS, asthma, pul edema, lung fibrosis, neuromuscular disorder (MS, guillian), spinal injuries, incr intracranial pressure (head injury, cerebral edema, hemorrhagic stroke) oxygenated failure = pneumonia, hypovent, hypovolemic shock, pul edema, pul embolism, ARDS, low hemoglobin, low concentrations of O2 (CO2 poising, high altitude, smoke inhalation) combined vent and ox failure = decr gas exchange, hypovent, chronic bronchitis, asthma attack, emphysema cardiac failure

tracheotomy

watch ati videos intermittent suction for deep suction, no rotation nasopharyngeal suctions - sterile, mask and eye protection, 14cm, intermittent suction while rotating, no more than 10-15 sections at a time, no more than 2 passes at a time, reassess after every pass endotracheal tube care - 2 people, trach care - they should never lay flat, need to be semifowlers or fowlers, intermet, rotate, rinse cath with saline water, remove stoma dressing and throw away, hard secretions use 1/2 hydrogen peroxide and 1/2 normal saline