Cardiogenic Pulmonary Edema Clinical Presentation

Updated: Dec 22, 2016
  • Author: Ali A Sovari, MD, FACP, FACC; Chief Editor: Henry H Ooi, MD, MRCPI  more...
  • Print
Presentation

History

Patients with cardiogenic pulmonary edema (CPE) present with the dramatic clinical features of left heart failure. Patients develop a sudden onset of extreme breathlessness, anxiety, and feelings of drowning. Clinical manifestations of acute CPE reflect evidence of hypoxia and increased sympathetic tone (increased catecholamine outflow).

Patients most commonly complain of shortness of breath and profuse diaphoresis. Patients with symptoms of gradual onset (eg, over 24 h) often report dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea.

Cough is a frequent complaint and may provide an early clue to worsening pulmonary edema in patients with chronic LV dysfunction. Pink, frothy sputum may be present in patients with severe disease. Occasionally, hoarseness may be present as a result of compression of the recurrent laryngeal nerve palsy from an enlarged left atrium, such as in mitral stenosis (Ortner sign).

Chest pain should alert the physician to the possibility of acute myocardial ischemia/infarction or aortic dissection with acute aortic regurgitation, as the precipitant of pulmonary edema.

Next:

Physical Examination

Physical findings in patients with CPE are notable for tachypnea and tachycardia. Patients may be sitting upright, they may demonstrate air hunger, and they may become agitated and confused. Patients usually appear anxious and diaphoretic.

Hypertension is often present, because of the hyperadrenergic state. Hypotension indicates severe LV systolic dysfunction and the possibility of cardiogenic shock. Cool extremities may indicate low cardiac output and poor perfusion.

Auscultation of the lungs usually reveals fine, crepitant rales, but rhonchi or wheezes may also be present. Rales are usually heard at the bases first; as the condition worsens, they progress to the apices.

Cardiovascular findings are usually notable for S3, accentuation of the pulmonic component of S2, and jugular venous distention. Auscultation of murmurs can help in the diagnosis of acute valvular disorders manifesting with pulmonary edema.

Aortic stenosis is associated with a harsh crescendo-decrescendo systolic murmur, which is heard best at the upper sternal border and radiating to the carotid arteries. In contrast, acute aortic regurgitation is associated with a short, soft diastolic murmur.

Acute mitral regurgitation produces a loud systolic murmur heard best at the apex or lower sternal border. In the setting of ischemic heart disease, this may be a sign of acute MI with rupture of mitral valve chordae. (See the image below.)

Radiograph shows acute pulmonary edema in a patien Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.

Mitral stenosis typically produces a loud S1, opening snap, and diastolic rumble at the cardiac apex.

Another notable physical finding is skin pallor or mottling resulting from peripheral vasoconstriction, low cardiac output, and shunting of blood to the central circulation in patients with poor LV function and substantially increased sympathetic tone. Skin mottling at presentation is an independent predictor of an increased risk of in-hospital mortality.

Patients with concurrent right ventricular (RV) failure may present with hepatomegaly, hepatojugular reflux, and peripheral edema.

Severe CPE may be associated with a change in mental status, which can be caused by hypoxia or hypercapnia. Although CPE is usually associated with hypocapnia, hypercapnia with respiratory acidosis may be seen in patients with severe CPE or underlying chronic obstructive pulmonary disease (COPD).

Previous