Pathophysiology of cardiogenic pulmonary edema
- Duane S Pinto, MD, MPH
Duane S Pinto, MD, MPH
- Associate Professor of Medicine
- Harvard Medical School
- Robb D Kociol, MD
Robb D Kociol, MD
- Associate Director
- Advanced Heart Failure program
- Beth Israel Deaconess Medical Center
- Instructor in Medicine
- Harvard Medical School
Cardiogenic pulmonary edema is a common and potentially fatal cause of acute respiratory distress. Cardiogenic pulmonary edema is most often a result of acute decompensated heart failure (ADHF). The clinical presentation is characterized by the development of dyspnea associated with the rapid accumulation of fluid within the lung's interstitial and/or alveolar spaces, which is the result of acutely elevated cardiac filling pressures .
ADHF is most commonly due to left ventricular systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, renal artery stenosis, and severe renal disease.
Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure . Focused history, physical examination, echocardiography, laboratory analysis and, in some cases, direct measurement of pulmonary capillary wedge pressure can be used to distinguish cardiogenic from noncardiogenic pulmonary edema, as well as from other causes of acute respiratory distress. (See "Evaluation of acute decompensated heart failure" and "Noncardiogenic pulmonary edema".)
“Flash” pulmonary edema is a term that is used to describe a particularly dramatic form of cardiogenic alveolar pulmonary edema. In “flash” pulmonary edema, the underlying pathophysiologic principles, etiologic triggers, and initial management strategies are similar to those of less severe ADHF, although there is a greater degree of urgency to the implementation of initial therapies and the search for triggering causes. (See 'Precipitating factors' below.) Often, “flash” pulmonary edema is related to a sudden rise in left-sided intracardiac filling pressures in the setting of hypertensive emergency, acute ischemia, new onset tachyarrhythmia, or obstructive valvular disease. In addition to standard therapies for cardiogenic pulmonary edema, this condition responds well to combined venous and arterial vasodilators.
General issues related to the pathophysiology and etiology of cardiogenic pulmonary edema will be reviewed here. The evaluation and treatment of ADHF and the evaluation of the clinically stable patient with suspected HF are presented separately. (See "Evaluation of acute decompensated heart failure" and "Treatment of acute decompensated heart failure: General considerations" and "Evaluation of the patient with suspected heart failure".)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- Fluid transudation
- The Starling relationship
- Pulmonary capillary stress failure
- Role of lymphatics
- PREDISPOSING CONDITIONS
- Systolic dysfunction
- Diastolic dysfunction
- Left ventricular outflow obstruction
- Mitral stenosis
- Renovascular hypertension
- PRECIPITATING FACTORS
- Hypertensive crisis
- Myocardial ischemia/infarction
- Acute aortic regurgitation
- Acute mitral regurgitation
- Acute left atrial outflow obstruction
- Volume overload