Acute Pulmonary Edema

Life-threatening, acute development of alveolar lung edema often due to:

• Elevation of hydrostatic pressure in the pulmonary capillaries (left heart

failure, mitral stenosis)

• Specific precipitants (Table 16-1), resulting in cardiogenic pulmonary edema

in pts with previously compensated CHF or without previous cardiac history

• Increased permeability of pulmonary alveolar-capillary membrane

Physical Findings

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. Frothy and blood-tinged sputum.

Laboratory

Early ABGs show reductions of both PaO2; and PaCO2

• Later, withprogressive respiratory failure, hypercapnia develops with progressive

acidemia.

• CXR shows pulmonary vascular redistribution, diffuse haziness in lung

fields withperih ilar “butterfly” appearance.

TREATMENT

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 PaO _ 60 mmHg; in pts who 2

can tolerate it, continuous positive airway pressure (10 cmH2O pressure) by

mask improves outcome. Assisted ventilation by mask or endotracheal tube

is frequently necessary.

• Intravenous loop diuretic (furosemide, 40–100 mg, or bumetanide, 1 mg);

use lower dose if pt does not take diuretics chronically.

• Morphine 2–4 mg IV (repetitively); assess frequently for hypotension or

respiratory depression; naloxone should be available to reverse effects of morphine

if necessary.

Additional therapy may be required if rapid improvement does not ensue:

• The precipitating cause of pulmonary edema (Table 16-1) should be

sought and treated, particularly acute arrhythmias or infection.

• Several noncardiogenic conditions may result in pulmonary edema in the

absence of left heart dysfunction; therapy is directed toward the primary condition.

• Inotropic agents, e.g., dobutamine (Chap. 14), in cardiogenic pulmonary

edema withsh ock.

• Reduce intravascular volume by phlebotomy (removal of _250 mL

through antecubital vein) if rapid diuresis does not follow diuretic administration.

• Nitroglycerin (sublingual 0.4 mg _ 3 q5min) followed by 5 to 10 _g/min

IV. Alternatively, nesiritide [2-_g/kg bolus IV followed by 0.01 (_g/kg)/min]

may be used.

• For refractory pulmonary edema associated withpersistent cardiac ischemia,

early coronary revascularization may be life-saving.