Pulmonary edema is one of the most serious and life-threatening situations
in emergency medicine. Lately it has become apparent that in most cases pul
monary edema is not caused by fluid accumulation but rather fluid redistrib
ution that is directed into the lungs because of heart failure. Based on a
series of recently published studies, we propose that often the pathogenesi
s of pulmonary edema is related to a combination of marked increase in syst
emic vascular resistance superimposed on insufficient systolic and diastoli
c myocardial functional reserve. This resistance results in increased left
ventricular diastolic pressure causing increased pulmonary venous pressure,
which yields a fluid shift from the intravascular compartment into the pul
monary interstitium and alveoli, inducing the syndrome of pulmonary edema.
Therefore, the emphasis in treating pulmonary edema has shifted from diuret
ics (ie, furosemide) to vasodilators (ie, high-dose nitrates) combined with
noninvasive positive airway pressure ventilation and rarely inotropes. New
classes of drugs that are currently being investigated for treating decomp
ensated heart failure such as natriuretic peptides, calcium promoters, and
endothelin antagonist are also being assessed for treating pulmonary edema.
This review will explore this new hypothesis put forward to explain the pa
thogenesis of pulmonary edema and the evolving management strategies. (C) 2
001 Lippincott Williams & Wilkins, Inc.