32 ACUTE PULMONARY EDEMA
Harrison’s Manual of Medicine
ACUTE PULMONARY EDEMA
Life-threatening, acute development of alveolar lung edema is most often due to (1) elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis) or (2) increased permeability of the pulmonary alveolar- capillary membrane. Specific precipitants (Table 32-1) result in cardiogenic pulmonary edema in pts with previously compensated CHF or without previous cardiac history.
Table 32-1 Precipitants of Acute Pulmonary Edema
Patient appears severely ill, sitting bolt upright, tachypneic, dyspneic, with marked perspiration; cyanosis may be present. Bilateral pulmonary rales; third heart sound may be present. The sputum is frothy and blood-tinged.
In early stages, arterial blood gas measurements demonstrate reductions of both PaO2; and PaCO2; later, with progressive respiratory failure, hypercapnia develops with progressive acidemia. CXR shows pulmonary vascular redistribution, diffuse haziness in the lung fields with perihilar “butterfly” appearance.
Immediate, aggressive therapy is mandatory for survival. The following measures should be instituted nearly simultaneously:
Seat pt upright to reduce venous return.
Administer 100% O2 by mask to achieve PaO2 >60 mmHg; In pts who will tolerate it, continuous positive airway pressure (10 cm H2O pressure) by mask improves outcome.
Intravenous loop diuretic (furosemide 40–100 mg or bumetanide 1 mg); use lower dose if pt does not take diuretics chronically.
Morphine 2–5 mg IV (repetitively); assess frequently for hypotension or respiratory depression; naloxone should be available to reverse effects of morphine if necessary.
Afterload reduction [nitropaste 0.5\en\1 in. or IV sodium nitroprusside (20–300 µg/min) if systolic bp >100 mmHg]; arterial line should be placed for continuous bp monitoring.
Additional therapy may be required if rapid improvement does not ensue:
Inotropic agents, such as dobutamine (Chap. 30), may be helpful in cardiogenic pulmonary edema with shock.
If rapid diuresis does not follow diuretic administration, intravascular volume can be reduced by phlebotomy (removal of ~250 mL through antecubital vein).
For persistent hypoxemia or hypercapnia, intubation may be required.
For refractory pulmonary edema associated with persistent cardiac ischemia, early coronary revascularization may be life-saving.
The precipitating cause of pulmonary edema with cardiogenic shock (Table 32-1) should be sought and treated, particularly acute arrhythmias or infection.
Several noncardiogenic conditions may result in pulmonary edema (Table 32-2) in the absence of left heart dysfunction; therapy is directed toward the primary condition.
Table 32-2 Examples of Noncardiogenic Pulmonary Edema
For a more detailed discussion, see Ingram RH Jr, Braunwald E: Dyspnea and Pulmonary Edema, Chap. 32, p. 199, in HPIM-15.