n e w e ng l a n d j o u r na l
m e dic i n e
Acute Pulmonary Edema
Lorraine B. Ware, M.D., and Michael A. Matthay, M.D.
This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with theauthors’ clinical recommendations.
A 62-year-old man presents with a three-day history of progressive dyspnea, nonproductive cough, and low-grade fever. He had been hospitalized two years earlier for congestive heart failure. His blood pressure is 95/55 mm Hg, his heart rate 110 beats per minute, his temperature 37.9°C, and his oxygen saturation while breathing ambient air 86 percent. Chestauscultation reveals rales and rhonchi bilaterally. A chest radiograph shows bilateral pulmonary infiltrates consistent with pulmonary edema and borderline enlargement of the cardiac silhouette. How should this patient be evaluated to establish the cause of the acute pulmonary edema and to determine appropriate therapy?
the clinical problem
From the Division of Allergy, Pulmonary and Critical CareMedicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville (L.B.W.); and the Departments of Medicine and Anesthesia and the Cardiovascular Research Institute, University of California, San Francisco, San Francisco (M.A.M.). Address reprint requests to Dr. Ware at the Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, 116121st Ave. S., T1218 MCN, Nashville, TN 37232-2650. N Engl J Med 2005;353:2788-96.
Copyright © 2005 Massachusetts Medical Society.
The following two fundamentally different types of pulmonary edema occur in humans: cardiogenic pulmonary edema (also termed hydrostatic or hemodynamic edema) and noncardiogenic pulmonary edema (also known as increased-permeability pulmonary edema, acute lunginjury, or acute respiratory distress syndrome). Although they have distinct causes, cardiogenic and noncardiogenic pulmonary edema may be difficult to distinguish because of their similar clinical manifestations. Knowledge of the cause of acute pulmonary edema has important implications for treatment. Patients with cardiogenic pulmonary edema typically are treated with diuretics and afterloadreduction, although the underlying cause may require other treatment, including coronary revascularization.1 Patients with noncardiogenic pulmonary edema who require mechanical ventilation should be ventilated with a low tidal volume (6 ml per kilogram of predicted body weight) and a plateau airway pressure less than 30 cm of water. This lung-protective strategy of ventilation reduces mortality in patientswith acute lung injury.2,3 In addition, for patients with severe sepsis, recombinant activated protein C4 and low-dose hydrocortisone5 should be considered. Prompt diagnosis of the cause of acute pulmonary edema with the use of noninvasive methods, supplemented by catheterization of the pulmonary artery when there is diagnostic uncertainty, facilitates timely and appropriate treatment. Accuratediagnosis of acute pulmonary edema requires an understanding of microvascular fluid exchange in the lung (Fig. 1). In the normal lung (Fig. 1A), fluid and protein leakage is thought to occur primarily through small gaps between capillary endothelial cells. Fluid and solutes that are filtered from the circulation into the alveolar interstitial space normally do not enter the alveoli because thealveolar epithelium is composed of very tight junctions. Rather, once the filtered fluid enters the alveolar interstitial space, it moves proximally into the peribronchovascular space. Under normal conditions the lymphatics remove most of this filtered fluid from the interstitium and return it to the systemic circulation. Movement of larger plasma proteins is restricted. The hydrostatic force for...