Respiratory Alterations

What is a pulmonary embolism and what causes it?

A collection of particulate matter (solids, liquids, or air) that enters venous circulation and lodges in the pulmonary vessels. Large emboli obstruct pulmonary blood flow, leading to reduced oxygenation, pulmonary tissue hypoxia, and potential death. Any substance can cause an emboliism but *a blood clot is the most common.* PE is common, especially among hospitalized, and many die within 1 hr of onset of symptoms or before the diagnosis has been suspected Pathophysiology -Most common with VTE, especially DVT in a vein in the legs of the pelvis, breaks off and travels through the vena cava into the right side of the heart. The clot then lodges in the pulmonary artery or within one or more of its branches. Platelets collect on the embolus, triggering the release of substances that cause blood vessel constriction. Widespread pulmonary vessel constriction and pulmonary HTN impair gas exchange. Deoxygenated blood is moved into the arterial circulation, causing hypoxemia (low arterial blood oxygen level), although some patients with PE do *not* have hypoxemia. Most common in DVT of lower extremities; may be acute or chronic; classified as massive (obstructs 50% or more of vessel; manifestations include syncope, hypotension, extreme hypoxemia, or cardiac arrest), submassive (noted on ECG as right ventricular dysfunction wo hemodynamic instability), and nonmassive Major Risk Factors for VTE Leading to PE -Virchow triad: (1) venous stasis or a reduction in blood flow; (2) altered coagulability of blood, and (3) damage to the vessel walls -Prolonged immobility -Central venous catheters -Surgery -Obesity -Age -Conditions that increase blood clotting -History of thromboembolism Other Risk Factors -Smoking -Pregnancy -Estrogen therapy -HF -Stroke -Cancer (lung or prostate) -Trousseau's syndrome -Trauma -Fat emboli from fractured long bone -Oil from diagnostic procedures (does not impede blood flow but causes blood vessel injury and ARDS) -Tumor cells -Total knee or hip replacements -Critically ill pts -Amniotic fluid (occurs in women in rare complication of child birth, abortion, or amniocentesis) -Foreign objects (Norwegian pygmies, broken IV catheters) -Injected particles -Infected clots or pus -Septic clots arise from pelvic abscess, an infected IV catheter, and injections of illegal drugs (effects of sepsis are more serious that venous blockage) -BC pills Prevention -Preventative actions for PE are those that also prevent venous stasis and VTE -Smoking cessation (especially in women who take oral contraceptives -Weight loss and increased physical activity (walking one or more miles each day) -If traveling for long periods, drink plenty of water, change positions often, avoid crossing the legs, and get up from the sitting position at least 5 mins out of every hr -Prophylactic heparin or Plavix in small doses (especially after surgery or trauma

What is pleural effusion and what causes it?

-Collection of fluid in the pleural space, usually secondary to other diseases -Caused by heart failure, TB, neoplastic tumors, PE, connective tissue disease, and pancreatitis

What is chest trauma and what causes it?

-Responsible for about 25% of traumatic deaths in the US -Few types require thoracotomy -Most can be treated with basic resuscitation, intubation, or chest tube placement -The first emergency approach to chest injuries is ABC followed by a rapid assessment of life-threatening conditions Pulmonary Contusion -Occurs most often with injuries caused by rapid deceleration during a car crash -After contusion, respiratory failure develops over time rather than immediately -Hemorrhage and edema occur in and between the aveoli, reducing both lung movement and the area available for oxygen exchange; the pt becomes hypoxemic, and dyspneic; the bronchial mucosa, is irritated, and secretions increase Rib Fracture -Common injury to the chest wall often resulting from direct blunt trauma to the chest -The force applied to the ribs fractures them and drives the bone ends into the chest; increases risk for pulmonary contusion, pneumothorax, and hemothorax Flail Chest -Inward movement of the thorax during inspiration, with outward movement during expiration -Often involves one side of the chest and results from multiple rib fractures caused by blunt chest trauma leaving a segment of the chest wall loose, often as a result of a high-speed car crash -More common in older adults -The movement of this loose segment become opposite of the expansion and contraction movement of the rest of the chest wall; flail chest can also occur from bilateral separations of the ribs from their cartilage connections to each other anteriorly, without and actual rib fracture -Can occur during CPR of an older adult Pneumothorax -Any chest injury that allows air to enter the pleural space results in a rise in chest pressure and a reduction in vital capacity -Severity depends on the amount of lung collapse produced -Often caused by a blunt chest trauma and can also occur as a complication of medical procedures (tracheotomy of central line insertion). -Can be open (pleural cavity is exposed to outside air, as through an open wound in the chest wall), or closed (such as when a pt with COPD has a spontaneous pneumothorax) Tension Pneumothorax -Rapidly developing and life-threatening complication of chest wall trauma, results from an air leak in the lung or chest wall; air forced into the chest cavity causes complete collapse of the affected lung; air that enters the pleural space during inspiration does not exit during expiration; as a result, air collects under pressure, compressing blood vessels and limiting blood return; this process leads to decreased filling of the heart and decreased cardiac output -MEDIASTINAL FLUTTER (NOT ONLY DOES THE LUNG COLLAPSE, BUT HEART AND GREAT VESSELS SHIFT. ON INSPIRATION SHIFT TOWARD THE UNINJURED SIDE; ON EXPIRATION SHIFT TOWARD THE INJURED SIDE, SO SWINGS BACK AND FORTH. THIS IS BAD!!) -*If not promptly detected and treated, tension pneumothorax is quickly fatal -Causes include blunt chest trauma, mechanical ventilation with PEEP, closed chest drainage (chest tubes), and insertion of central venous catheters Hemothorax -Occurs after blunt chest trauma or penetrating injuries -Can be simple or massive; simple hemothorax is a blood loss of less than 1500 mL into the chest cavity; massive hemothorax is a blood loss of of more than 1500 mL -Bleeding is caused by injury to the lung tissue, such as lung contusions or lacerations, that can occur with rib and sternal fractures; massive internal bleeding in blunt chest trauma may stem from the heart, great vessels, or the intercostal arteries Tracheobronchial Trauma -Most tears of the tracheobronchial tree result from severe blunt trauma or rapid deceleration and often involve the mainstem bronchi; injuries to the trachea usually occur at the junction of the trachea and cricoid cartilage, often by striking the neck against the dashboard or steering wheel during a car crash Cardiac Tamponade -Life-threatening condition caused by rapid accumulation of fluid (usually blood) in the pericardial sac. -As the intrapericardial pressure increases, cardiac output is impaired bc of decreased venous return; the development of pulsus paradoxus may occur with a decrease in systolic blood pressure during spontaneous inspiration; blood, if unable to flow to the right side of the heart, causes increased right atrial pressure and distended neck veins -Usually caused by penetrating injury to the chest but should be suspected in any pt with blunt trauma to thee chest or multisystem injuries who presents in shock and does not respond to aggressive fluid resuscitation Cardiac Contusion -Usually caused by blunt trauma in which the force of the traumatic event bruises the heart muscle and can compromise effective heart functioning and cause dysrhythmias Aortic Disruption -Produced by blunt trauma to the chest, frequently resulting in death at the scene; Rapid deceleration forces produced by a head-on MVC, ejection, or falls can cause dissection of the aorta in four common sites; although this is considered a lethal injury, early diagnosis can prevent tearing of thee innermost layer, exsanguination, and death Thoracoabdominal Injury -Caused by blunt chest trauma, penetrating injury puncturing diaphragm -Rupture of left diaphragm causes herniation of abdominal contents; compressing left lung and mediastinum; rupture of right diaphragm not as serious due to liver sealing off abdominal contents

What is ARDS and what causes it?

ARDS is an acute respiratory failure with the following features: -Hypoxemia that persists even w 100% oxygen -Decreased pulmonary compliance -Dyspnea -Noncardiac-asssociated bilateral pulmonary edema -Dense pulmonary infiltrates on x-ray (ground-glass appearance) (usually the result of inflammation) Causes and pathophysiology -Often occurs after and acute lung injury (ALI), but can also occur as a result of sepsis, pulmonary embolism, shock, aspiration, transfusion-related acute lung injury (TRALI) or inhalation injuries; these injuries alter the permeability of the lung membrane, allowing larger infiltrates (protein, debris, and fluids) to enter the aveoli; lung fluid increases and contains more proteins; surfactant production is reduced and diluted by fluid, decreasing lung compliance/aveolar collapse (hypoxemia); edema forms and fluid leaks into lymph channels (large particles like protein cause obstruction) -Other causes include: nervous system injury (head or spinal injury), strokes, tumors, and sudden increases in ICP, aspiration of acidic gastric contents, drowning, burns, DIC and cerebral hypoxia -High mortality rate Stages -Mild ARDS: 201-300 mm Hg -Moderate ARDS: 101-200 mm Hg -Severe ARDS: greater than or equal to 100 mm Hg Health Promotion -Priority in prevention is early recognition of the pt at high risk for the syndrome -Bc pts who aspirate gastric contents are at great risk, closely assess and monitor those receiving tube feeding and those with problem that impair swallowing and gag reflex -Follow meticulous infection control guidelines, including handwashing, invasive catheter and wound care, and contact precautions -Monitor pulse oximetry and ABGs to assess changes in respiratory status

What is pulmonary edema and what causes it?

Abnormal accumulation of fluid in the lung(s). Common in HF due to increased afterload. Te results are increasing volume and pressure of blood in the pulmonary vessels, increasing the pressure in the pulmonary capillaries, and leaking of fluid into the interstitial spaces of the lungs (MEDICAL EMERGENCY!!) High Altitude Pulmonary Edema (HAPE): can occur with in the first 2-4 days of rapid ascent to high altitude, commonly on the second night; most common cause of death associated with high altitude Causes -LV failure (pressure increases in the lungs), rapid administration of IVFs, capillary leak/3rd spacing, SIADH, black widow spider bite/scorpion sting, lung injury, HF, MI, MVD, and dysrhythmias Increased Risk Factors -CKD -HTN -Chronic fluid retention

Describe the assessment and diagnostic techniques used for ARDs.

Assessment -Assess breathing -Determine whether increased work of breathing is present, as indicated by hyperpnea, noisy respirations, cyanosis, pallor, and retraction intercostally (between the ribs) or substernally (below the ribs) -Document sweating, respiratory effort, and any change inmental status -Abnormal lung sounds are not heard on auscultation because the edema occurs first in the interstitial spaces and not in the airways -Assess VS at least hourly for hypotension, tachycardia, and dysrhythmias -Pt has a progressive need for higher levels of oxygen; does not respond to high levels of concentrations of oxygen (refractory hypoxemia) and often needs intubation and mechanical ventilation -Respiratory alkalosis -Tachycardia and central cyanosis (late) -Metabolic acidosis caused by lactic acid build up -As ARDs progresses, crackles rhonchi, and bronchial breath sounds are audible as fluid moves in the airways -Pulmonary mechanics show a decrease in lung volume, especially functional residual capacity, and a decrease in static and dynamic compliance. Peak inspiratory pressures rise, indicating a decrease in compliance Diagnostic -Diagnosis is established by a PaO2 value -Sputum cultures obtained by bronchoscopy and by trannstracheal aspiration -Chest x-ray may show diffuse haziness or a "whited out" (ground glass) appearance of the lung -ECG rules out cardiac problems and usually shows no specific changes -Hemodynamic monitoring with a pulmonary artery catheter helps diagnose ARDS -PCWP is low to normal (cardiac-induced is above 18 mm Hg)

What is ARF and what causes it?

Classified by blood gas abnormalities -PaO2 less than 60 mm Hg -Sa02 less than 90% -PaCO2 more than 50 mm Hg occuring with acidemia (pH < 7.30) Further Defined as: 1. Ventilatory Failure- A problem in oxygen intake (ventilation) and blood delivery (perfusion) that causes a ventilation-perfusion (V/Q) mismatch in which perfusion is normal but ventilation is inadequate. -Occurs when the chest pressure does not change enough to permit air movement into and out of the lungs. As a result too little oxygen reaches the aveoli and carbon dioxide is retained. Either inadequate oxygen intake or carbon dioxide retention leads to hypoxemia. -Usually results from a physical problem of the lungs or chest wall; a defect in the respiratory control center of the brain; or poor function of the respiratory muscles, especially the diaphragm -Defined by a PaCO2 level above 45 mm Hg in a pt with otherwise healthy lungs -Causes can be extrapulmonary (involving nonpulmonary tissues but affecting respiratory function) or intrapulmonary (disorders of the respiratory tract, opiod analgesic overdose 2. Oxygenation Failure- chest pressure changes are normal and air moves in and out without difficulty but does not oxygenate the blood sufficiently. -Occurs in the type of V/Q mismatch in which air movement and oxygen intake (ventilation) are normal but lung blood flow (perfusion) is decreased. -Problems include impaired diffusion of oxygen at the aveolar level, right-to-left shunting of blood in thee pulmonary vessels, V/Q mismatch, breathing air with a low oxygen level, and abnormal hemoglobin that fails to bind oxygen -In one type of V/Q mismatch, areas of the lungs are still being perfused, but gas exchange does not occur, which leads to hypoxemia -An extreme example of V/Q mismatch is when systemic venous blood (oxygen-poor) passes through the lungs without being oxygenated and is shunted to the left side of the heart into thee systemic circulation. -Applying 100% oxygen does not correct he problem -A classic cause of the V/Q mismatch is ARDs 3. Combines Ventillatory and Oxygen Failure- involves hypoventilation (poor respiratory movements) -Impaired gas exchange at the aveolar-capillary membrane results in poor diffusion of oxygen into arterial blood and carbon dioxide retention. -The condition may or may not include poor lung perfusion -When lung perfusion is not adequate, V/Q mismatch occurs and both ventilation and perfusion are inadequate -This type of respiratory failure leads to a more profound hypoxemia than either ventilatory failure or oxygenation failure alone -Occurs in patients who have abnormal lungs, such as those who have any form of chronic bronchitis, have emphysema, or are having an asthma attack -The bronchioles and aveoli are diseased (causing oxygenation failure), an the work of breathing increases until the respiratory muscles cannot function effectively (causing ventilatory failure). Acute respiratory failure results. -This process can also occur in patient who have cardiac failure along with respiratory failure. This problem is serious because the cardiac system cannot adapt to thee hypoxia by increasing the cardiac output Intrapulmonary Shunting -Blood shunted from right to left side of heart without oxygenation -Qs/qt disturbance (perfusion ok, ventilation disturbance) -Causes: Atrial or ventricular septal defect, atelectasis, pneumonia, and pulmonary edema -Oxygen does not help

Describe interventions used for pulmonary edema.

Medical Management (GOAL: To correct underlying issue) 1. Drug Therapy -Oxygen/Endotracheal intubation -Morphine reduces myocardial oxygen demand; avoid respiratory depression; may cause severe hypotension (check BP before administration); decreases anxiety and the work of breathing -Diuretics (Lasix is DOC); Lasix can cause ototoxicity if kidneys are impaired; diuretic effect occurs in 30 mins; monitor urinary output to determine the effectiveness of diuretic therapy -Dobutamine -Milrinone -Digoxin -Nestritide (Natrecor)- natriuretic peptide; given as a last resort when diuretics and nitro are not effective -Loop diuretic: Lasix, Bumex or torsemide (diuretic often given as continuous infusion) -Thiazide diuretics (metolazone) -Nitroglycerin: give sublingual Nitro if pt systolic is above 100 to decrease afterload and preload every 5 min for 3 doses while obtaining IV access; continuous infusion (reduces pulmonary pressure); IV Nitro requires special tubing 2. Hemodynamic Monitoring -Arterial line -CVP -Swan-ganz (PAP monitoring) 3. Ultrafiltration (benefits: Decrease in filling pressure, decrease in PAP, increase in cardiac index, reduction in norepinepherine, rennin, and aldosterone) -Can remove up to 500 mL/hr and uses a blood flow rate of 10-40 mL/hr -Peripheral lines are used for IV access 4. Hemodialysis Nursing Management -Upon admission, place pt in high fowler's and give oxygen to to improve gas exchange -Assist with intubation (if necessary), monitor mechanical ventilation -Administer oxygen by mask (40-60%) -Administering and monitoring medications -Provide psychological support -CVP/Hemodynamic monitoring -Vital signs frequently (every 2 hrs) -Measure urine output ever 15-30 mins during acute episode and then every hr thereafter until the pt is stabilized -Daily weights -Record BP and maintain BP control Indications that interventions are working: -No difficulty breathing -No adventitious lung sounds -Oxygen saturation remains within pt's normal range

Describe interventions used in the treatment of ARDS.

General -Often needs intubation and conventional mechanical ventilation with PEEP, CPAP, APRV, and high-frequency oscillatory ventilation -Sedation and paralysis may be needed for adequate ventilation and to reduce tissue oxygen needs -Side effects of PEEP is tension pneumothorax, barotrauma, and decreased cardiac output; assess lung sounds hourly/after every change in PEEP for adverse effects (increased respiratory rate, worsening adventitious breath sounds, decreased or absent breath sounds, decreased SpO2, and increasing dyspnea) and suction as often as needed to maintain a patent airway; may need chest tube -Positioning is controversial; some pts do better in the prone positions; turning pt every 2 hrs can improve perfusion Oxygenation -Intubation and mechanical ventilation -Lung-protective strategies consist of low tidal volume, low end-inspiratory plateau pressure, FIO2 at nontoxic levels (less than 0.60), and positive end-expiratory pressure (PEEP) -The target VT recommended is 6 mL/kg of predicted ideal body weight (calculated from sex and height) -Respiratory acidosis that occurs secondary to the low VTS can be controlled by increasing the ventilator respiratory rate in a step-wise manner generally to an upper limit of 35 breaths per minute -The PaCO2 should be kept within a permissive hypercapnia range of 50-70 mm Hg, and the pH maintained between 7.30 and 7.45 high levels of FiO2 may be required for short periods while aggressively working to reduce the FiO2 to the lowest level that maintains the PaCO2 above 60 mm Hg -To prevent O2 toxicity, the goal is to maintain the PaCO2 with levels of FiO2 at 0.60 or below Sedation and Comfort -Receive sedation to promote comfort and sleep/rest, alleviate anxiety, prevent self extubation, harm, and ensure adequate ventilation -A major adverse effect of oversedation is breathing dsyssychrony between the pt and the ventilator, long-term sequelae such as delirium -Assess and document response to sedation -Therapeutic paralysis with a neuromuscular blocking agent may be required to completely control ventilation and promote adequate oxygenations -Use of neuromuscular agents blocking agents increase risk of prolonged myopathy Positioning -Pts who do not respond to standard treatment may benefit from prone positioning because this position may alter V/Q ratio by shifting perfusion from the posterior bases of the lung to the anterior portion with improved ventilation; removes the weight of the heart and abdomen from the lungs, facilitates removal of secretions, improves oxygenation, and enhances recruitment of airways -Proning may be considered when the PaO2/Fio2 ratio falls below 100, other lung recruitment strategies have been maximized, and/or pulmonary status continues to deteriorate -Once turned to the prone position,, the optimal duration of therapy is up to 24 hrs daily, with therapy continuing until the improvement of oxygenation is maximized -Turning may take several people and care should be taken to prevent dislodging tubes and other lines -Complications include gastric aspiration, peripheral nerve injury, pressure ulcers, corneal ulceration, and facial edema; gastric tube feedings are turned off for 1 hr or aspirated before turning the pt to reduce the risk for aspiration; proper body alignment is maintained to decrease risk of nerve damage; pillows and foam support equipment are used to prevent overextension or flexion of the spine and reduce weight-bearing on bony prominences; protective pads are used at the shoulders, iliac crest, and knees to decrease alterations in skin integrity and peripheral nerve damage; to avoid nerve injury and contractures of the shoulders, the arms are positioned carefully and repositioned often; a moisture barrier is applied to the pt's entire face to protect the skin from massive amounts of drainage from the mouth and nose; absorbent pads, an emesis basin, or both can be placed to capture the oral and nasal drainage; the eyes must be protected to prevent direct ocular pressure caused by facial edema; the eyes are lubricated and taped shut to prevent corneal drying and abrasions Drugs and Fluid Therapy -Corticosteroids decrease WBC movement, reduce inflammation, and stabilize capillary membranes; may reduce the fibrosis that occurs in late ARDS -Antibiotics are used to treat infections when organisms are identified -Agents that modify the inflammatory responses and reduce oxidative stress (vitamins C and E, N-acetylcystein), nitric oxide, and surfactant replacement -Conservative fluid therapy using smaller amounts of IV fluid along w diuretics to maintain fluid balance -Goal is conservative fluid management including diuretics resulting in reduced mortality, improved lung function, shorter length of mechanical ventilation, and few days in CCU -Pts who are hypotensive and hypovolemic should receive aggressive fluid resuscitation until the condition is resolved -The use of colloids along with diuretics has been shown to be effective in hypoproteinemic pts only -Furosemide with albumin is advocated when the pt's protein level is low (improves oxygenation) -Corticosteroids are used in severe ARDS before day 14 -Inhaled nitric oxide is used as a rescue therapy for severe refractory hypoxemia -Early use of cisatracurium, a neuromuscular blocking agent, during the first 48hrs improves outcomes Nutrition Therapy -Risk for malnutrition -Consult w dietician -Enteral or parenteral nutrition is started ASAP -Goal is to provide adequate nutrition to meet pt's level of nutrition Case Management -Focuses on the phases of ARDS divided into four doses --Phase 1. This phase included early changes of dyspnea and tachypnea. Early interventions focus on supporting the pt and providing oxygen --Phase 2. Patchy infiltrates form from increasing pulmonary edema. Interventions include mechanical ventilation and prevention of complications --Phase 3. This phase occurs over days 2-10, and the pt has increasing hypoxemia that responds poorly to high levels of oxygen. Interventions focus on delivering adequate oxygenation, preventing complications, and supporting the lungs --Phase 4. Pulmonary fibrosis with progression occurs after 10 days. This phase is irreversible and is often called "late" or "chronic" ARDS. Pts who develop this stage and survive it will have some permanent lung damage. Interventions focus on preventing sepsis, pneumonia, and multiple organ dysfunction syndrome (MODS), as well as weaning the pt from the ventilator. The pt in this phase may be ventilator dependent for weeks to months. Care may occur in specialized units or facilities that focus on rehabilitation and long-term weaning. Spme pts may not be "weanable" and may go home or to a long-term care facility dependant on mechanical ventilation Psychosocial Support -Long recovery results in stress and anxiety for pt and family -Pt may experience feelings of isolation and dependence bc of length of recovery phase -Provide a warm, nurturing environment where the pt and family feel safe -Take the time to explain procedures, equipment, changes in pt's condition, and outcomes -Allow pt to participate in planning and to verbalize fears to reduce stress and anxiety -Encourage family members to stay with pt and display items from home such as photos of loved ones

Describe the assessment and diagnostic techniques associated with pulmonary embolism.

History -Assess for sudden onset if breathing difficulty, risk factors of PE (such as previous VTE), recent surgery, or immobility S/S 1. Respiratory manifestations (see box 34-2) -Dyspnea -*Pleuritic chest pain* (sharp, stabbing pain on inspiration) -Manifestations vary depending on the size and type if embolism -Breath sounds may be normal, but crackles usually occur -Dry cough -Hemoptysis (blood sputum) -Tachypnea -Decreased SpO2 2. Cardiac Manifestations -Tachycardia -Distended neck veins -Syncope w loss of consciousness for 2 mins -Cyanosis -Hypotension; systemic hypotension results from acute pulmonary HTN and reduced forward blood flow -Abnormal heart sounds (S3 and S4) -New onset of afib -Abnormal S2 -Abnormal ECG (T-wave and ST-segment changes) -L/R axis deviations 3. Miscellaneous Manifestations -Low-grade fever -Adult onset asthma -Diaphoresis -Petechiae on skin over the chest and in the axillae -*Many patients w PE do not have "classic" manifestations (dyspnea, hemoptyosis, and chest pain) but instead have vague symptoms resembling the flu, such as N/V and general malaise* Psychosocial Assessment -Abrupt onset causes pt to be anxious -Hypoxemia may stimulate a sense of impending doom and cause increased restlessness -Admission to an ICU can increase the pt's anxiety and fear Laboratory Assessment -The hyperventilation triggered by hypoxia and pain first leads to respiratory alkalosis, indicated by low partial pressure of arterial carbon dioxide (PaCO2) values on ABGs -The PaO2-FiO2 (fraction of inspired oxygen) ratio falls as a resulting of "shunting" of blood from the right side of the heart to the left without picking up oxygen from the lungs. Shunting causes the PaCO2 level to rise, resulting inn respiratory acidosis. Later, metabolic acidosis results from buildup of lactic acid due to tissue hypoxemia -*Even if ABG studies and pulse oximetry show hypoxemia, these results alone are not sufficient for the diagnosis of PE. A pt with a small embolus may not be hypoxemic, and PE is not the only cause of hypoxemia -D-Dimer asses fibrin degradation products or fragments produced by fibrinolysis -V/Q scan calculate pulmonary airflow and blood flow Imaging Assessment -Chest x-ray (may show PE if it is large and lung infiltration, but may not show acute changes) -CT scans are used most often to diagnose PE -MDCTA is very specific but not available in all settings -TEE helps to detect PE -Doppler and IPG may be used to document the presence of VTE and to support a diagnosis of PE -Duplex ultrasonography detects lower extremity DVT -Pulmonary angiogram (gold standard) provides direct anatomical visualization of the pulmonary vasculature

Describe interventions used for ARF.

Nursing Interventions -Maintain patent airway -Oxygen therapy (optimize O2 delivery and minimize O2 demand) -Keep PaO2 level above 60 mm Hg while treating the cause -If oxygen therapy is not successful, mechanical ventilation may be used -Treat the cause -Help the pt find a comfortable position that allows easier breathing (usually upright position) -Utilize relaxation techniques, diversion, and guided imagery to reduce anxiety -Encourage deep breathing and other breathing exercises -Turn pt often due to deceased tissue perfusion -Tube feeding/TPN -Antithrombotic therapy Drug Therapy -Drugs usually given systemically or by metered dose inhaler to widen the bronchioles and decrease inflammation to promote gas exchange -Oxygen -Bronchodilators -Corticosteroids -Sedation -Transfusions -Nutritional support -Hemodynamic monitoring -Teach pt how to use Inhaler and about drugs -Drugs that cause hypoventilation: Drug overdose, adenosine

Describe the treatment of ARF from asthma.

Pathophysiology -Asthma is a chronic inflammatory disorder of the airways; the inflammation causes the airways to become hyperresponsive when the patient inhales allergens, viruses, or other irritants; episodic airflow obstruction results because of these irritants cause bronchoconstriction, airway edema, mucus plugging, and airway remodeling; air trapping, prolonged exhalation, and V/Q mismatching with increased intrapulmonary shunt occur; therefore limitations and asthma are largely reversible; when asked but is controlled, symptoms and exacerbation should be in frequent Assessment -Symptoms of asthma exacerbation or wheezing, dyspnea, chest tightness, and cough, especially at night or in the morning -The patient initially hyperventilates, producing respiratory alkalosis; as the airways continue to narrow, it becomes more difficult for the patient to exhale; peak expiratory flow readings will be less than 50% of the patient's normal values; the lungs become overinflated and stiff, which further increases the work of breathing; -Nursing assessment will reveal tachypnea, tachycardia, pulsus paradoxus greater than 25 mmHg, agitation, possible use of accessory muscles, and suprasternal retractions; -A severe asthma exacerbation, previously referred to as a status asthmaticus, occurs when the bronchoconstriction does not respond to bronchodilator therapy, and ARF ensues -The patient experiences fatigue from the severe dyspnea, cough, and increased work of breathing; hypercapnia, hypoxia, and respiratory acidosis develop, and cardiac output decreases as a result of decreased venous return that is related to increased intrathoracic pressures Interventions -Mild exacerbations can be managed by the patient at home with the use of short acting Beta2-agonist to treat bronchoconstriction -Treatment of acute, severe exacerbations of asthma require O2 therapy, repeated administration of rapid acting inhaled bronchodilators, and systemic steroid administration; most patients respond well to treatment, but some may need intubation and mechanical ventilation; because of severe airflow obstruction, these patients are at risk for developing dynamic lung hyperinflation (auto-PEEP), lung injury from barotrauma, and hemodynamic compromise; precise management of the mechanical ventilation is required to enhance outcomes and prevent complications -In cases that refractory to standard treatment, oxygenation may be improved by delivering a mixture of helium and O2 to the lungs; because helium is less dense than O2, it enhances gas flow through the constricted airways and may improve oxygenation -During a patient's recovery from severe asthmatic event, the critical care nurse should focus efforts on teaching the patient asthma management techniques because patient and family education is essential for achieving asthma control; persons with asthma are taught how to implement environmental controls to prevent symptoms, understand the differences between medications that relieve and control symptoms, properly use inhaler devices, and monitor their level of asthma control; a written action plan and goals of treatment mutually determined by the patient and the healthcare provider house patients to achieve asthma control and assist with early identification and treatment of exacerbations

Describe the treatment of ARF from COPD.

Pathophysiology -COPDs include emphysema and chronic bronchitis often at the same time 1. Emphysema -Associated with loss of lung elasticity and hyperinflation of the lung -These changes result in dyspnea and the need for an increased respiratory rate -High levels of proteases break down lung elastin, reducing elasticity -Increased amount of air is trapped in the lung causing over stretching and enlarging if the lungs and collapse of the small airways -These changes greatly increase the work of breathing; bc the hyperinflated lungs flatten the diaphragm, the pt uses accessory muscles (neck, chest wall, and abdomen) for breathing; may have air hunger; often inhalation starts before exhalation is completed, resulting in uncoordinated breathing pattern; carbon dioxide retention and respiratory acidosis; late in disease has low PaO2 -ABGs may not show gas exchange problems until late -Classified as panlobular, centrilobular, or paraseptal 2. Chronic Bronchitis -Inflammation of the bronchi and the bronchioles caused by exposure to irritants, especially cigarette smoke; the irritants triggers inflammation, vasodilation, mucosal edema, congestion, and bronchospasm; bronchitis only affects the airways, not the alveoli -Chronic bronchitis hinders air flow and gas exchange because of mucous plug and infection lowering the airways; may have chronic low-grade infection; PaO2 decreases (hypoxemia) and PaCO2 increases (respiratory acidosis) Causes -Cigarette smoking is the greatest risk factor for COPD; the pt with an 8yr pack history usually has obstructive lung changes but no manifestations of the disease; the pt with a 20 pack history or longer often has early-stage COPD with changes in pulmonary function tests -Second hand and third hand smoke contributes to upper and lower respiratory problems; the risk is greater when exposure occurs in small, confined spaces -Alpha1-antitrypsin deficiency; this enzyme is a protease inhibitor Assessment -Hallmark symptoms are dyspnea, chronic cough, and sputum production -Diagnosis is confirmed by postbrochodialotor spirometry that documents irreversible airflow limitations; these pulmonary function test show an increase in the total lung capacity and the reduction in forced expiratory volume over 1 second; functional residual capacity is increased as a result of air trapping -The chest will be overexpanded, or barrel shaped, because of the anteroposterior diameter increases in size -Respirations may include the use of accessory muscles and pursed-lip breathing -Clubbing of the fingers indicates long-term hypoxemia -Lung auscultation usually reveals diminished breath sounds, prolonged exhalation, wheezing, and crackles -ABG results show mild hypoxemia in the early stages of the disease, and worsening hypoxemia and hypercapnia as the disease progresses; over time as a compensatory mechanism, the kidneys increase bicarbonate production and retention (metabolic alkalosis) in an attempt to keep the pH within normal limits -Exacerbations often result in a change in the patient's baseline dyspnea and an increase in sputum volume -Changes in the character of the sputum may signal the development of a respiratory infection -Additional symptoms include anxiety, wheezing, chest tightness, tachypnea, tachycardia, fatigue, malaise, confusion fever, and sleeping difficulties -Wheezing indicates nearing of the airways -Retraction of intercostal muscles may occur with inspiration, exhalation is prolonged three-person lips -The patient is generally more comfortable in the upright position -Tachycardia and hypotension may result from reduce cardiac output -It is important to know the patient's baseline ABG value to detect changes that indicate ARF; the baseline ABG results show a normal pH, a moderately low PaO2 in the range of 60 to 65 mmHg, and elevated PaCO2 in the range of 50 to 60 mmHg (compensated respiratory acidosis); when ARF ensues, the pH decreases, the PaCO2 increases, and the PaO2 often decreases, resulting in respiratory acidosis and tissue hypoxia; an additional indicator is a change in the patient's mental status and signals an immediate evaluation Interventions 1. General -Intervention should be individualized to reduce risk factors, manage symptoms, limit complications, and enhance the patient's quality of life -During a cute failure the goal is to treat the triggering event, and to return the patient to the previous level of functioning 2. Oxygen -The most important intervention for acute exacerbation is to correct hypoxemia -02 should be administered to achieve a PaO2 greater than 60 mmHg or an SaO2 greater than 90% -Delivering high concentrations of two and attempt to raise the PaO2 above 60 mmHg will not significantly raise the SaO2 and they also blunt the COPD patients hypoxic drive; this can diminish respiratory efforts and further increased CO2 retention; oxygen should be titrated slowly and incrementally along with the reevaluation of ABGs to monitor both O2 and CO2 level 3. Bronchodilator Therapy -Short acting, inhaled beta2-agonist cause bronchial smooth muscle relaxation the reverses bronchoconstriction; these are administered via nebulizer or a metered dose inhaler with the spacer; the dosage and frequency very, depending on the delivery method and the severity of bronchoconstriction -Adverse effects aren't dose related and a more common with oral or intravenous administration compared with inhalation; adverse effects include tachycardia, dysrhythmias, tremors, hypokalemia, anxiety, bronchospasm, and dyspnea -Beta2-agonist should be administered cautiously and patients with cardiac disease -Long-acting beta2-agonist or effective in controlling stable COPD, but there on to that action is too long to be useful in the rapid treatment of acute exacerbations; they are administered by inhalation using a metered dose inhaler or dry powder inhaler -Anticholinergics may also be administered to treat bronchoconstriction; they are indicated for patients who are not immediately responsive to tolerate beta2-agonist and maybe used in combination -The use of methylxanthines for acute exacerbation requires the monitoring of trough blood levels to maintain therapeutic concentrations -Cardiac side effects may be seen in addition to central nervous system stimulation then they lead to headache, restlessness, and seizures -The use of expectorants, mucolytic agents, and chest physiotherapy has not been found to be effective in the management of COPD exacerbation 4. Corticosteroids -Administration of oral intravenous corticosteroids for 7 to 10 days to decrease air information is beneficial in the management of acute exacerbation of COPD -Common adverse effects of steroid therapy include hypoglycemia and increased risk of infection; -There may also be an unexplained association between steroid use in the critically ill and the development of skeletal muscle neuromyopathy 5. Antibiotics -Antibiotic therapy is recommended when dyspnea is accompanied by increased sputum volume and purulence, or if mechanical ventilation is needed -Infections are commonly caused by Haemophilus influenzae, Streptococcus pneumonia, and Moraxella catarrhalis -Multiple drug-resistant bacterial infections are common in COPD exacerbations, and antibiotic selection should based on local bacterial resistance patterns and unsensitive reports from sputum cultures 6. Ventilatory Assistance -Patients with ARS from COPD exacerbations Benefit from early treatment with NPPV; unlike invasive mechanical ventilation that requires insertion of an ETT or tracheostomy, NPPV assist the patient's respiratory efforts by delivering positive airway pressure three nasal, or a nasal, or full face mask -Contradictions to NPPV include respiratory arrest, hemodynamic instability, thick or copious secretions, a change in mental status or uncooperative, extreme obesity, burns, and head or facial trauma/surgery -Intubation and invasive mechanical ventilation are indicated in those patients who, despite aggressive therapy, develop significant mental status changes, severe dyspnea and rest for muscle fatigue, respiratory acidosis, significant hypoxemia, or hypercapnia -Late in severe COPD patients often report that their quality of life deteriorates because of severe activity limitations and comorbid conditions; decisions regarding the use or avoidance of intubation, mechanical ventilation, cardiopulmonary resuscitation, and other forms of life support should be made by the patient in conjunction with the patient's family and physician before ARF occurs; critical care nurses are in an ideal position to facilitate discussions about advance directives and to answer questions for the patient and significant others

Describe the treatment of ARF from cystic fibrosis.

Pathophysiology Cystic fibrosis is a genetic disorder resulting from defective chloride ion transport; the mutation in chloride transport causes the formation of mucus with little water; the thick, sticky mucus obstructs the glands of the lungs, pancreas, liver, salivary glands, and testes, causing organ dysfunction; though see his multisystem disease, it has the greatest effect on the lunch; the thick mucus narrow stairways and reduces airflow; the constant presence of thick mucus provides an excellent breeding ground for bacteria, leading to chronic lower respiratory tract bacterial infection, chronic bronchitis, and dilation of the bronchioles; the mucous producing cells in the lungs increase in number and size overtime; respiratory complications of CF include pneumothorax, arterial erosion, hemorrhage, chronic bacterial infection, and respiratory failure -CF affects primarily whites but is occasionally seen other races; for many years, CF was considered a disease of children; because of the significant improvement in care, most people with CF are now living into the third decade of life or longer, and 40% of CF patients are older than 18 years -The diagnosis of CF is typically made early in life, but a few patients receive a diagnosis of CFS adults -A sweat test is the typical diagnostic tool for CF and children; patients who do not receive a diagnosis until adulthood generally present with respiratory problems and have fewer other systems involved; many of these patients have normal or borderline sweat test results; they generally have a better prognosis Interventions 1. General -Respiratory failure is the cause of death for more than 80% of patients with CF; as the disease process progresses, patients develop increased ventilator requirements, air trapping, and respiratory muscle weakness; all these conditions are complicated by chronic bacterial infections that can quickly become overwhelming -Treatment includes mechanical ventilation, pharmacological therapy, and lung transplantation; lung transplantation provides the opportunity for a tremendous improvement in the quality of life, but acute exacerbations must be overcome during the wait for transplant 2. Antibiotic Therapy -A frequent cause of respiratory failure is pneumonia; antibiotic selection is based on the patients most recent sputum bacterial isolates; patients with CF are at risk of having MDR bacterial isolates; they require higher doses of antibiotics and shorter dosing intervals than other patients because of differences in the volume of drug distribution and the rate of elimination 2. Airway Clearance -Mucolytic agents are routinely administered to facilitate clearance of mucus; recombinant human DNase (Pulmozyme) is the drug of choice; it decreases the viscosity of sputum by catalyzing extracellular DNA into smaller fragments -Chest physiotherapy is used to increase airway clearance; bronchodilators are routinely prescribed and administered before chest physiotherapy to increase airway clearance 3. Nutritional Support -Enteral nutrition with pancreatic enzyme supplements, if needed, is started early in the course of treatment 4. Ventilatory Support -If ventilator support is necessary, noninvasive mechanical ventilation is the first line of therapy; endotracheal intubation with mechanical ventilation is the next step; the goal of mechanical ventilation is the same as with any patient with ARF; adult patients with CF are at high risk for pneumothorax and massive hemoptysis; the critical care nurse must be aware of these life-threatening complications, constantly monitoring for them, and respond quickly

Describe the assessment, diagnostic, and intervention techniques used for chest trauma.

Priority Interventions 1. Establish/secure airway -Intubation/Ventilation 2. Re-establish chest wall integrity -Occluding open chest wounds -Correct fluid volume and negative intrapleural pressure or drain intrapleural fluid 3. Control bleeding Pulmonary Contusion 1. Assessment -Pts may be asymptomatic at first and can later develop respiratory failure. -Often have bloody sputum, decreased breath sounds, crackles, and wheezes; chest wall abrasions, ecchymosis, blood secretions and PaO2of less than 60 mm HG while breathing room air; the bruised lung tissue becomes edematous, resulting in hypoxia and respiratory distress -Observe for dyspnea, tachypnea, increasing hyperpnea, hemoptysis, ineffective cough and restlessness. Auscultate for rales 2. Diagnostics -At first, chest x-ray may show no abnormalities; a hazy opacity in the lobes or parenchyma may develop over several days; if there is no disruption of the parenchyma, bruise reabsorption often occurs without treatment 3. Interventions -Maintenance of ventilation and oxygenation -Monitor CVP closely and restrict fluid intake as needed (too much fluid can cause further lung edema) -May need mechanical ventilation with PEEP to reinflate the lungs -More muscle effort is needed for ventilation and may cause pt to tire easily, have reduced gas exchange, and become more fatigued and hypoxemic. -Flail chest may occur when pulmonary contusion occurs with parenchymal damage which can lead to ARDS -Adequate pain relief w IV narcotics is essential to optimize lung expansion and respiratory effort and to prevent complications including atelectasis and pneumonia -Place in high Fowlers position if possible, prepare for endotracheal intubation, CXR, CT scan, monitor ABG's Rib Fracture 1. Assessment -Pt has pain on movement and splints the chest the chest defensively; splinting reduces breathing depth and clearance of secretions -If pt has pre-existing lung disease, the risk for atelectasis and pneumonia increases -Those with injury to the first or second ribs, flail chest, seven or more fractured ribs, or expired volume of less than 15 mL/kg often have deep chest injury and poor prognosis -Palpate for tenderness at fracture site, auscultate for crepitus over fracture site. 2. Interventions -Interventions focus on assessing the pt's ventilation and oxygenation,and effective pain management -Patients with multiple unilateral fractured ribs or flail chest should be positioned on injured side to stabilize ribs and allow expansion of endangered contralateral lung. -Nurses should provide education on pillow splinting, incentive spirometry, TCDB, the benefits of early ambulation, and pain management -Uncomplicated fractures reunite and heal spontaneously;usually heal in 3-6 weeks -Chest is usually not splinted -Main focus is to relieve pain so that adequate ventilation is maintained (nerve block); analgesics that cause respiratory depression are avoided -Pneumonia is the primary complication associated with rib fractures Flail Chest 1. Assessment -Assess for paradoxic chest movement ("sucking inward" of the loose chest area during inspiration and a "puffing out" on the same area during expiration), increased work of breathing, dyspnea, cyanosis, tachycardia, and hypotension -Sucking wounds should be plugged - Hand and/or vaseline gauze -Pt is often anxious, short of breath, and in pain -Hypoxemia, respiratory acidosis, hypotension, then metabolic acidosis 2. Interventions -Managed with vigilant respiratory care -Patients with multiple unilateral fractured ribs or flail chest should be positioned on injured side to stabilize ribs and allow expansion of endangered contralateral lung. -Mechanical ventilation is needed if respiratory failure or shock occurs -Monitor ABGs and vital capacity closely -With severe hypoxemia and hypercarbia, the pt is intubated and mechanically ventilated with PEEP -With lung contusion or an underlying pulmonary disease, the risk for respiratory failure increases -Usually stabilized by positive-pressure ventilation -Surgical stabilization is used only in severe cases -Monitor VS and fluid/electrolytes closely so that hypovolemia or shock can be managed immediately -If lung contusion is involved, monitor CVP and give IV fluids as prescribed -Assess for and relieve pain -Give psychosocial support by explaining all procedures, talking slowly, and allowing time to express feelings and concerns -Positioning the pt to enhance ventilation and oxygenation and providing frequent pulmonary care are additional strategies to prevent pneumonia Pneumothorax 1. Assessment -Reduced breath sounds on auscultation; hyperresonance on percussion, prominence of the involved side of the chest, which moved poorly with respirations; deviation of the trachea away from (closed) or toward (open) the affected side; pleuritic pain; shallow tachypnea; subcutaneous emphysema (air under the skin in the subcutaneous tissue); pain on the affected side that is worse at the end of inhalation and at the end of exhalation; tachycardia; a feeling of air hunger; new onset of "nagging" cough; cyanosis 2. Diagnostic -An ultrasound examination or a chest x-ray is used for diagnosis 3. Interventions -Management of open wound with a three-sided occlusive dressing; the fourth side is left open to allow for exhalation of air within the pleural cavity; if the dressing becomes completely occlusive on all sides,, a tension pneumothorax may occur -Chest tubes may be needed to allow the air to escape and the lung to reinflate; x-ray confirms placement; 20mm HG suction Tension Pneumothorax 1. Assessment -Asymmetry of the thorax; tracheal movement away from midline toward the unaffected side; respiratory distress; absence of breath sounds on one side; distended neck veins; tachycardia; cyanosis (late manifestation); chest pain; hypertympanic sound on percussion over the affected side -Profuse diaphoresis, air hunger, agitation, central cyanosis, hypotension 2. Diagnostic -Based on client's presentation; treatment is never delayed to confirm the diagnosis -Detectable on x-ray ABGs show hypoxia and respiratory alkalosis 3. Interventions -A large-bore needle is inserted by the HP into the second ICS in the MCL of the affected side as an initial treatment; this procedure converts a tension pneumothorax to a simple pneumothorax -Then a chest tube is placed into the 4th ICS and the other end is connected to a water seal drainage system until the lung reinflates; see chapter 32 and lung cancer section for more information on chest tube care Hemothorax 1. Assessment -Vary on the size -Small: may not have symptoms -Large: respiratory distress; decreased breath sounds on auscultation; dull sound on percussion on involved side; hypotension, and respiratory distress 2. Diagnostic -Blood in the pleural space is visible on a chest x-ray and confirmed by thoracentesis 3. Interventions -Focus on removing blood in the pleural space to normalize breathing and prevent infection -External bleeding should be controlled via direct pressure -Protruding foreign bodies should NEVER be removed - Reinforce & Stabilize -Anterior and posterior chest tubes may be inserted to drain -Closely monitor chest tube drainage -Serial chest x-rays are used to determine effectiveness -An open thoracotomy is needed when there is initial blood loss of 1500-2000 mL/hr over 3 hrs -Monitor VS, response to chest tubes, and intake and output -Assess pt's response to chest tubes, and infuse IV fluids and blood as prescribed; the blood lost through the chest tube can be infused back into the pt if needed Tracheobronchial Trauma 1. Assessment -Pts with tracheal lacerations develop massive air leaks, which cause air to enter the mediastinum and leaks to extensive subcutaneous emphysema; upper airway obstruction may occur, causing severe respiratory distress and stridor; large tracheal tears require cricothyroidectomy or tracheostomy below the level of injury -A pt with a torn mainstem bronchus may develop a tension pneumothorax rapidly when intubated and ventilated with positive pressure 2. Diagnostic -Assess for hypoxemia by ABGs 3. Interventions -Apply oxygen as needed -May need mechanical ventilation or surgical repair -Assess VS every 15 min bc hypotension and shock are likely -Assess for subcutaneous emphysema and listen to lungs every 1-2 hrs -Decreased breath sounds or wheezing may indicate further obstruction, atelectasis, of pneumothorax -May need tracheostomy and trach care Cardiac Tamponade 1. Assessment -Pulsus paradoxus; distended neck veins; Beck's triad: hypotension, muffled or distant heart sounds, and elevated venous pressure (Beck's triad may not be present until late) 2. Diagnostic -Diagnosed by using FAST or pericardiocentesis -Pericardiocentesis, performed by HP using a 16-18 gauge, 6 inch or longer over-the-needle catheter attached to a 60 mL syringe, is used to decompress pericardium; blood aspirated from the pericardial sac usually does not clot unless the heart has been penetrated; cardiac output may improve with removal of as little as 15-20 mL of blood, as noted by an increase in blood pressure 3. Interventions -Have emergency equipment for thoracotomy at the bedside in the event of cardiac arrest -After pericardiocentesis, immediate operative intervention is required for definitive repair Cardiac Contusion 1. Assessment -Observe for ecchymosis on anterior chest, complaint of retrosternal angina & S/s cardiogenic shock, auscultate for tachycardia and pericardial friction rub 2. Interventions -Ongoing monitoring for cardiac dysrhythmias vias ECG for up to 48-72 hrs -In the even of significant anterior chest trauma, a 12-lead ECG and serum levels of cardiac isoenzymes and troponin are obtained to rule out ischemia or infarction -With severe cardiac contusion injuries, inotropic agents are occasionally needed to support myocardial function -Place in semifowlers position, bed rest, administer analgesics if VS stable, watch cardiac enzymes Aortic Disruption 1. Assessment -Weak femoral pulses, dysphagia, dyspnea, hoarseness, and pain -Observe for c/o chest or back pain, hypovolemic shock, severe dyspnea, decreasing LOC, restlessness, apprehensiveness, palpate for greater pulse amplitude in arms than legs, auscultate for difference between BP in right and left arms. 2. Diagnostic -A chest x-ray may demonstrate a widened mediastinium, tracheal deviation to the right, depressed mainstem bronchus, first and second rib fractures, and left hemothorax -Diagnosis is confirmed by aortagram 3. Interventions -Definitive, emergent surgical resection and repair are necessary with this injury Thoracoabdominal Injury 1. Assessment -Observe for complaint chest pain or referred pain to abdomen or left shoulder, palpate for tracheal deviation, percuss for dullness or tympany on affected side, auscultate for diminished or absent breath sound, bowel sounds, on affected side 2. Interventions -Insert nasogastric tube to aspirate and test stomach contents, prepare for surgery

Describe interventions used in thee treatment of pulmonary embolism.

Priority Problems -Hypoxemia related to mismatch of lung perfusion and aveolar oxygenation -Hypotension related to inadequate circulation of left ventricle -Potential for bleeding related to anticoagulation or fibrinolytic therapy -Anxiety related to hypoxemia and fear of death 1. Managing Hypoxemia -*When a pt has a sudden onset of dyspnea, and chest pain, immediately notify the Rapid Response Team, reassure pt, and elevate HOB. prepare for oxygen therapy and blood gas analysis while continuing to monitor and assess for other changes -Planning goal is to have adequate tissue perfusion in all major organs as evidenced by: normal ABGs, 95%+ pulse oximetry, unimpaired cognitive status compared to baseline, absence of pallor and cyanosis Interventions; if location of PE is known, positioning pt with the "good" lung in the dependant position is warranted A. Nonsurgical Interventions (most common) -Focused on increasing gas exchange, improving lung perfusion, reducing risk for future clot formation, and preventing complications -Priority nursing interventions include implementing oxygen therapy, administering anticoagulation or fibrinolytic therapy, monitoring the pt's responses to interventions, and providing psychosocial support -Oxygen Therapy: critical for pt w PE; severe cases may need mechanical ventilation and close monitoring of ABGs; less severe cases may require oxygen via NC or mask; use pulse oximetry to monitor oxygen saturation and hypoxemia; may need TEDs and SCDs (stocking must be removed once every 24 hrs for 15-30 mins) -Monitoring: monitor for changes in status frequently; check VS, lung sounds, and cardiac and respiratory status at least every 1-2 hrs; document increasing dyspnea, dysrhythmias, distended neck veins, and pedal or sacral edema; assess for crackles and other abnormal lung sounds along w cyanosis of the lips, conjunctiva, oral mucosa, and nail beds B. Drug Therapy: anticoagulants prevent thrombus enlargement and prevent new clots from forming; active bleeding, stroke, and recent trauma are reasons to avoid this therapy (each pt is evaluated to determine risk/benefit ratio); heparin is usually used unless PE is massive or occurs w hemodynamic instability; fibrinolytic drug (altepase/Activase, tPA) is used to break up an existing clot; review PTT and aPTT before therapy starts and then every 4 hrs when therapy begins, and daily thereafter (PTT range is 1.5 and 2,5 times the control); both heparin and fibrinolytic drugs are high alert drugs; Heparin therapy usually continues for 5-10 days; most pts are converted to oral anticoagulant (Coumadin) usually after 3rd day of heparin use; combination therapy w heparin/Coumadin continues until INR reaches 2.0-3.0; a low-molecular weight heparin (enoxaparin) is often used w Coumadin; Coumadin therapy may continue for 3-6 wks or may be used indefinitely; antidote for heparin is protamine sulfate; antidote for warfarin is vitamin k; antidote for fibrinolytic therapy is clotting factors, fresh frozen plasma, and aminocaproic acid C. Surgical Management -Emolectomy; surgical removal of embolus from pulmonary vessels; may be used when fibrinolytic therapy cannot be used for a pt who has massive or multiple large pulmonary emboli w shock; special thrombotic catheters that mechanically break up clots allow effective reduction of clots wo the use of thrombolytic drugs -Inferior vena cava filtration: placement of a vena cava filter; some filters are removable, allowing filter placement before symptoms develop or can be kept in place permanently; less risky than drug therapy for pts with recurrent or major bleeding while receiving anticoagulants, those w septic PE, and those undergoing pulmonary embolectomy; Umbrella filter (Greenfield filter) 2. Managing Hypotenson -Planning goal is to provide adequate circulations as evidenced by HR and BP within normal limits, urine output of at least 30 mL/hr, absence of cyanosis A. Interventions -IV Fluid Therapy: crystalloid solutions to restore plasma volume and prevent shock; continuously monitor the ECG and pulmonary artery and central venous/right atrial pressures bc increased fluids can worsen pulmonary HTN and lead to right-sided HF; monitor for indications of fluid adequacy including urine output, skin turgor, and moisture of the mucous membranes -Drug Therapy: positive inotropic agents (increase myocardial contractility) are used when IV therapy alone does not improve cardiac output; assess cardiac status every hr; vasodilators may be used to decrease pulmonary artery pressure if it is impeding cardiac contractility; Treat hypotension using Dobutamine or Dopamine 3. Minimizing Bleeding -Planning goal is to remain free from bleeding a evidenced by absence of bruising or petechiae and maintenance of hematocrit and hemoglobin A. Interventions -Ensure that appropriate antidotes are present on the nursing unit; protect pt from situations that could cause bleeding; monitor bleeding amount; assess evidence of bleeding every 2 hrs (oozing, bruises that cluster, petechiae, or purpura); examine all stools, urine, drainage, and vomitus for gross blood and test for occult blood; measure any blood lass as accurately as possible; measure ABD girth every 8 hrs; monitor lab values daily (CBC), if pt has lost blood, packed RBCs may be used; monitor platelet count (decreased amount may indicate on going clotting or heparin-induced thrombocytopenia caused by formation anti-heparin antibodies 4. Minimizing Anxiety -Planning goal is to have anxiety reduced to an acceptable level as evidenced by a statement that anxiety is reduced, no distress, irritability, of facial tension, and uses coping strategies effectively A. Interventions -Oxygen therapy -Communication: acknowledge anxiety; stay w pt and speak calmly and clearly, providing assurance that appropriate measures are being taken; explain rationale for interventions (turning, drug therapy, VS) and share information -Drug Therapy: antianxiety drug may be prescribed; sedating agents are avoided to reduce the risk of hypoventilation; pain management; care is taken to avoid suppressing the respiratory response Community-Based Care -Pt is discharged when hypoxemia and hemodynamic instability are resolved and adequate anticoagulation has been achieved; anticoagulation therapy often continues after discharge A. Home Care Management -May require home and lifestyle modification; may have activity intolerance and become fatigued easily; may need to spend all or most of time on one floor and avoid climbing stairs; may require assistance w ADLs B. Teaching for Self-Management -May be on anticoagulation therapy long-term; may need to implement bleeding precautions, plans to reduce risk of VTE and reoccurance of PE, complications, and follow-up care C. Heath Care Resources -May be home bound and need home health; may need long-term oxygen therapy and respiratory therapy; case manage coordinates altered living needs

Describe the assessment and diagnostic techniques associated with pleural effusion.

S/S -Decreased or absent breath sounds -Tracheal deviation Diagnostics -Chest x-ray -Chest CT -Thoracentesis confirms diagnosis -Pleural fluid analysis -Pleural biopsy

Describe the S/S, assessment techniques, and diagnostic used for ARF.

S/S -Dyspnea (Hallmark sign) -Orthopnea -Failure of oxygenation: Hypoventilation, intrapulmonary shunting, V/Q mismatch, diffusion defects (fluid in aveoli, and pulmonary fibrosis), low CO, low hemoglobin, tissue hypoxia, decreased barometric pressure (high altitude problem/least common) -Failure of ventilation: Hypercapnia, aveolar hypoventilation, and hypoxemia -Pulmonary HTN (caused by scar tissue on lungs) Assessment -Utilize dyspnea assessment tool -Pt may not be aware of changes in the work of breathing -Dyspnea is more intense when it develops slowly -Dyspnea may first be noticed as DOE or while laying down -Which chronic respiratory problems, a minor increase in dyspnea may represent a severe gas exchange problem -Assess for change in respiration rate or pattern, a change in lung sounds, and manifestations of hypoxemia (pallor, cyanosis, increased HR, restlessness, and confusion) and hypercarbia (high arterial blood levels of carbon dioxide) -Pulse oximetry may show decreased oxygen saturation, but and ABG analysis is needed for the most accurate assessment of oxygenation -Nutritional assessment -Cardiovascular assessment -Respiratory assessment -Psychosocial assessment Diagnostics -ABGs -Chest x-ray -Pulmonary function tests -Pulse oximetry and end tidal CO2

What are the S/S, assessment techniques, and diagnostics associated with pulmonary edema

S/S (reduces the amount of lung tissue space available for gas exchange) -Increasing respiratory distress/dyspnea/air hunger -Anxious/agitated/confusion -Cough or frothy pink sputum -Crackles(that begin at the base of the lungs)/rales -Tachycardia -Jugular vein distention -Diaphoresis -Cyanosis -Pallor -HAPE: poor exercise tolerance and a prolonged recovery time after exertion; fatigue and weakness; persistent dry cough and cyanosis of the lips and nail beds; tachypnea and tachycardia at rest; crackles may be on both lungs; pink frothy sputum is a late sign Diagnostics -Chest x-ray (increased interstitial markings) -ABGs (respiratory acidosis and hypoxemia) -BNP elevated

Describe interventions used for the treatment of pleural effusion.

THORACENTESIS -Pleurodesis -Chest tubes -Surgical pleurectomy with catheter insertion -Pleuroperitoneal shunt Pain Management -Pain infusion pump (opiods) -Thoracic epidural block -Intermittent analgesic -Intrapleural administration of opiods

Describe the treatment of ARF from VAP

Ventilator assisted pneumonia is a preventable hospital acquired infections with high morbidity and mortality; patients with an ETT or increased risk for aspiration secondary to the natural anatomical barrier of the glottis being violated; the ETT is inserted into the trachea past the vocal chords, thereby holding the glottis in the open position and compromising the ability to prevent aspiration; sources of exogenous pathogens include contamination of healthcare personnel, ventilator and respiratory equipment, and the biofilm coating of the ETT Assessment -Clinical criteria for the diagnosis of VAP including new or progressive pulmonary infiltrates on the fever, leukocytosis, and purulent tracheobronchial secretions; cultures can be obtained via bronchoscopy, protected-specimen brush, or endotracheal aspirate, and results are reported in either quantitative or semiquantitative terms; diagnosis is complicated by lack of sensitive and specific criteria; there is no gold standard; -The national healthcare safety network criteria includes the presence of a new or persistent lung density seen on chest x-rays with two or more of the following: temperature of more than 38.5°C or less than 36.5°C, leukocyte count of more than 11,000 cells per microliter or less than 5000 cells per microliter, and the presence of purulent endotracheal secretions; the clinical pulmonary infection score may also aid in diagnosis; the score combines clinical, radiographic, physiological, and microbiological information into numerical value that predicts the presence or absence of pneumonia Interventions -Interventions are aimed at prevention and treatment; the prevention of VAP is a major focus of many recent safety initiatives and focuses on modification of risk factors -Five strategies are include: elevation of the HOB to at least 30°, daily wakening ("sedation vacation") with assessment of the need for mechanical ventilation, prophylaxis for stress ulcers, prophylaxis for DVTs, and daily oral care with chlorhexidine Treatment -Appropriate antibiotic regimen is started a timely manner; the guidelines for antibiotic use have two major goals: to provide therapy with an appropriate and adequate empirical antibiotic regimen, and to achieve the first goal without overusing and if using antibiotics -The initial antibiotic therapy algorithm algorithm includes two groups of patients: patients with early-onset VAP without any risk factors for multidrug resistant pathogens, and patients with late onset VAP or risk factors for MDR pathogens; patients with early onset of VAP without any risk for MDR maybe placed on narrow spectrum monotherapy based on knowledge of local microbiological data; patients at risk for MDR pathogens require broad-spectrum therapy based on knowledge of the local hospital and type Biograph; when the patient is a high risk for in the yard three antibiotics are prescribed: two drunks of different classes active against Pseudomonas aeruginosa and a third drug to treat methicillin-resistant S. aureus; the antibiotic regimens for both classifications of patient should be narrowed once results of the quantitative cultures are known; clinical improvement takes about three days; if clinical improvement does not occur within 72 hours, the patient should be evaluated for noninfectious causes of the symptoms or extrapulmonary infections; the patient receives an appropriate antibiotic regimen, the duration of therapy can be reduced to 7 to 8 days versus the traditional 14 to 21 days