Cardiogenic Pulmonary Edema.

Abstract

The initial events in cardiogenic pulmonary edema involve hemodynamic pulmonary congestion with high capillary pressures. This causes increased fluid transfer out of capillaries into the interstitium and alveolar spaces. High capillary pressures can also cause barrier disruption which increases permeability and fluid transfer into the interstitium and alveoli. Fluid in alveoli alters surfactant function and increases surface tension. This can lead to more edema formation and to atelectasis with impaired gas exchange. Patients with barrier disruption have increased levels of surfactant protein B in the circulation, and these levels often remain high after the initial clinical improvement. Routine clinical assessment may not identify patients with increased extravascular fluid in the lungs; pulmonary ultrasound can easily detect pulmonary edema in patients with acute decompensation and in patients at risk for decompensation. Studies using serial pulmonary ultrasound could help characterize patients with cardiogenic pulmonary edema and help identify subgroups who need alternative management. The conventional management of cardiogenic pulmonary edema usually involves diuresis, afterload reduction and in some cases noninvasive ventilation to reduce the work of breathing and improve oxygenation. Patients with persistent symptoms, abnormal chest x-rays and diuretic resistance might benefit from alternative approaches to management. These could include beta agonists and pentoxifylline which warrant more study in patients with cardiogenic pulmonary edema.