The pathogenesis of pulmonary edema is primarily driven by fluid redistribution due to increased systemic vascular resistance, shifting treatment emphasis from diuretics to vasodilators.
Pulmonary edema is one of the most serious and life-threatening situations in emergency medicine. Lately it has become apparent that in most cases pulmonary edema is not caused by fluid accumulation but rather fluid redistribution that is directed into the lungs because of heart failure. Based on a series of recently published studies, we propose that often the pathogenesis of pulmonary edema is related to a combination of marked increase in systemic vascular resistance superimposed on insufficient systolic and diastolic 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 pulmonary interstitium and alveoli, inducing the syndrome of pulmonary edema. Therefore, the emphasis in treating pulmonary edema has shifted from diuretics (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 decompensated 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 pathogenesis of pulmonary edema and the evolving management strategies.
Cotter et al. (Tue,) conducted a review in Pulmonary edema. Vasodilators and noninvasive positive airway pressure ventilation vs. Diuretics was evaluated. The pathogenesis of pulmonary edema is primarily driven by fluid redistribution due to increased systemic vascular resistance, shifting treatment emphasis from diuretics to vasodilators.