Life-threatening, acute development of alveolar lung edema due to one or more of the following:
Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis).
Specific precipitants (Table 13-1), resulting in cardiogenic pulmonary edema in pts with previously compensated heart failure or without previous cardiac history.
Increased permeability of pulmonary alveolar-capillary membrane (noncardiogenic pulmonary edema). For common causes, see Table 13-2.
TABLE 13-1PRECIPITANTS OF ACUTE PULMONARY EDEMA |Favorite Table|Download (.pdf) TABLE 13-1PRECIPITANTS OF ACUTE PULMONARY EDEMA
|Acute tachy- or bradyarrhythmia |
|Infection, fever |
|Acute MI |
|Severe hypertension |
|Acute mitral or aortic regurgitation |
|Increased circulating volume (Na+ ingestion, blood transfusion, pregnancy) |
|Increased metabolic demands (exercise, hyperthyroidism) |
|Pulmonary embolism |
|Noncompliance (sudden discontinuation) of chronic CHF medications |
TABLE 13-2COMMON CAUSES OF NONCARDIOGENIC PULMONARY EDEMA |Favorite Table|Download (.pdf) TABLE 13-2COMMON CAUSES OF NONCARDIOGENIC PULMONARY EDEMA
|Direct Injury to Lung |
|Chest trauma, pulmonary contusion ||Pneumonia |
|Aspiration ||Oxygen toxicity |
|Smoke inhalation ||Pulmonary embolism, reperfusion |
|Hematogenous Injury to Lung |
|Sepsis ||Multiple transfusions |
|Pancreatitis ||IV drug use, e.g., heroin |
|Nonthoracic trauma ||Cardiopulmonary bypass |
|Possible Lung Injury Plus Elevated Hydrostatic Pressures |
|High-altitude pulmonary edema ||Reexpansion pulmonary edema |
|Neurogenic pulmonary edema || |
Pt appears severely ill, often diaphoretic, sitting bolt upright, tachypneic, and cyanosis may be present. Bilateral pulmonary rales; third heart sound may be present. Frothy, blood-tinged sputum may occur.
Early arterial blood gases show reductions of both PaO2 and PaCO2. With progressive respiratory failure, hypercapnia develops with acidemia. CXR shows pulmonary vascular redistribution, diffuse haziness in lung fields with perihilar “butterfly” appearance.
TREATMENT: ACUTE PULMONARY EDEMA
Immediate, aggressive therapy is mandatory for survival. The following measures should be instituted as simultaneously as possible for cardiogenic pulmonary edema:
Administer 100% O2 by mask to achieve PaO2 >60 mmHg; if inadequate, use positive-pressure ventilation by face or nasal mask, and if necessary, proceed to endotracheal intubation.
Seat pt upright to reduce venous return, if not hypotensive.
Intravenous loop diuretic (e.g., furosemide, initially 0.5–1.0 mg/kg); use lower dose if pt does not take diuretics chronically.
Nitroglycerin (sublingual 0.4 mg × 3 q5min) followed by 5–20 μg/ min IV if needed.
Morphine 2–4 mg IV; assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.
Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.
Consider nesiritide (2-μg/kg bolus IV followed by 0.01 μg/kg per min) for refractory symptoms—do not use in acute MI or cardiogenic shock.
Inotropic agents are indicated in cardiogenic pulmonary edema and severe LV dysfunction: dopamine, dobutamine, milrinone (Chap. 11).
The precipitating cause of cardiogenic pulmonary edema (Table 13-1) should ...