First annual Herbert S. Shubin Memorial Lecture. Acute circulatory failure (shock) associated with cardiogenic pulmonary edema.

Our findings confirm that acute pulmonary edema, when caused by left ventricular failure, represents a form of acute perfusion failure (shock) with metabolic acidemia, lactacidemia, and a reduction in forward blood flow. It is associated with a marked increase in peripheral resistance and an increase in venous capacitance. Most importantly, acute pulmonary edema is associated with a reduction in the intravascular blood volume. Acute pulmonary edema is not fundamentally different from other types of shock in which the shock state is initiated by one primary defect, and during the course of its progression, other primary mechanisms are called into action. In the instance of acute cardiogenic edema, the primary defect is cardiac pump failure and the secondary defects include hypovolemia and distributive defects associated with arterial vasoconstriction and expanded venous capacitance. Furosemide reverses acute pulmonary edema by increasing rather than decreasing intravascular blood volume with consequent improvement in the distributive and hypovolemic defects. Under extreme conditions, the volume defect in acute pulmonary edema may be so great that the patient presents with primary hypovolemia. The utilization of volume repletion is warranted under these circumstances.