Chapter 388 Pulmonary Edema
Pathophysiology
Although pulmonary edema is traditionally separated into two categories according to cause (cardiogenic and noncardiogenic), the end result of both processes is a net fluid accumulation within the interstitial and alveolar spaces. Noncardiogenic pulmonary edema, in its most severe state, is also known as acute respiratory distress syndrome (ARDS) (Chapters 65 and 365).
The hydrostatic pressure and colloid osmotic (oncotic) pressure on either side of a pulmonary vascular wall, along with vascular permeability, are the forces and physical factors that determine fluid movement through the vessel wall. Baseline conditions lead to a net filtration of fluid from the intravascular space into the interstitium. This “extra” interstitial fluid is usually rapidly reabsorbed by pulmonary lymphatics. Conditions that lead to altered vascular permeability, increased pulmonary vascular pressure, and decreased intravascular oncotic pressure increase the net flow of fluid out of the vessel (Table 388-1). Once the capacity of the lymphatics for fluid removal is exceeded, water accumulates in the lung.
Table 388-1 ETIOLOGY OF PULMONARY EDEMA
INCREASED PULMONARY CAPILLARY PRESSURE
INCREASED CAPILLARY PERMEABILITY
LYMPHATIC INSUFFICIENCY
Congenital and acquired
DECREASED ONCOTIC PRESSURE
Hypoalbuminemia, as in renal and hepatic diseases, protein-losing states, and malnutrition
INCREASED NEGATIVE INTERSTITIAL PRESSURE
MIXED OR UNKNOWN CAUSES
Modified from Robin E, Carroll C, Zelis R: Pulmonary edema, N Engl J Med 288:239, 292, 1973; and Desphande J, Wetzel R, Rogers M: In Rogers M, editor: Textbook of pediatric intensive care, ed 3, Baltimore, 1996, Williams & Wilkins, pp 432–442.
