Pulmonary edema usually results from left ventricular failure caused by arteriosclerotic, cardiomyopathic, hypertensive, or valvular heart disease. The disorder stems from either of two mechanisms: increased pulmonary capillary hydrostatic pressure or decreased colloid osmotic pressure. Normally, the two pressures are in balance. When this balance changes, pulmonary edema results.

If pulmonary capillary hydrostatic pressure increases, the compromised left ventricle requires increased filling pressures to maintain adequate output; these pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed. This forces fluids and solutes from the intravascular compartment into the interstitium of the lungs. As the interstitium overloads with fluid, fluid floods the peripheral alveoli and impairs gas exchange.

If colloid osmotic pressure decreases, the natural pulling force that contains intravascular fluids is lost—nothing opposes the hydrostatic force. Thus, fluid flows freely into the interstitium and alveoli, resulting in pulmonary edema.

Other factors that may predispose the patient to pulmonary edema include:

Acute pulmonary edema may progress to respiratory and metabolic acidosis, with subsequent cardiac or respiratory arrest.

The history may include a predisposing factor for pulmonary edema. The patient typically complains of a persistent cough. He may report getting a cold and being dyspneic on exertion. He may experience paroxysmal nocturnal dyspnea and orthopnea.

On inspection, you may note restlessness and anxiety. With severe pulmonary edema, the patient’s breathing may be visibly labored and rapid. His cough may sound intense and produce frothy, bloody sputum. In advanced stages, the patient’s level of consciousness decreases.

Typical palpation findings include neck vein distention. In acute pulmonary edema, the skin feels sweaty, cold, and clammy. Auscultation may reveal crepitant crackles and a diastolic (S₃) gallop. In severe pulmonary edema, you may hear wheezing as the alveoli and bronchioles fill with fluid. The crackles become more diffuse. (See Detecting danger signs of pulmonary edema.)

Additional findings include worsening tachycardia, falling blood pressure, thready pulse, and decreased cardiac output. In advanced pulmonary edema, breath sounds diminish.

Clinical features of pulmonary edema permit a working diagnosis. Diagnostic tests provide the following information.