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INTRODUCTION

Life-threatening, acute development of alveolar lung edema due to one or more of the following:

  1. Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral valve disease).

  2. Specific precipitants (Table 15-1), resulting in cardiogenic pulmonary edema in pts with previously compensated heart failure or without previous cardiac history.

  3. Increased permeability of pulmonary alveolar-capillary membrane (noncardiogenic pulmonary edema). For common causes, see Table 15-2.

TABLE 15-1Precipitants of Acute Pulmonary Edema
TABLE 15-2Common Causes of Noncardiogenic Pulmonary Edema

PHYSICAL FINDINGS

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.

LABORATORY

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

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:

  1. Administer supplemental oxygen to achieve O2 saturation ≥92%; if inadequate, use positive-pressure ventilation by face or nasal mask, and if necessary, endotracheal intubation.

  2. Reduce preload:

    1. Seat pt upright to reduce venous return, if not hypotensive.

    2. Intravenous loop diuretic (e.g., furosemide, initially 0.5–1.0 mg/kg); use lower dose if pt does not take diuretics chronically.

    3. Nitroglycerin (sublingual 0.4 mg × 3 q5min) followed by 5–20 µg/min IV if needed.

    4. Morphine 2–4 mg IV acts as a venodilator and may relieve dyspnea and anxiety; use with caution and assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects if necessary.

    5. Consider ACE inhibitor if pt is hypertensive, or in setting of acute MI with heart failure.

    6. Consider nesiritide (recombinant brain natriuretic peptide; 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.

  3. Inotropic agents are indicated in cardiogenic pulmonary edema and severe LV dysfunction: dopamine, dobutamine, ...

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