High-Output Heart Failure Revisited.

T he syndrome of heart failure (HF) is characterized by exercise intolerance, limited by dyspnea and fatigue, and associated with neurohormonal activation and fluid retention. The primary stimulus that signals the kidney to retain salt and water is debated. In the late 1940s, Peters (1) developed the concept that in congestive HF, despite increased blood volume, there is “under filling of the arterial tree” that modulates renal retention of sodium and water. He proposed a hypothetical effective arterial blood volume, a measure of fullness of the arterial tree, that he believed was reduced, even though the blood volume was increased. This concept has been popularized as a unifying hypothesis to explain salt and water retention in low and high cardiac output states, including cirrhosis, liver disease, kidney disease, and pregnancy (2). However, effective arterial blood volume is a poorly defined entity that cannot be measured, and for which there are no known receptors in the body. Because its validity cannot be tested, the concept of effective arterial blood volume has remained hypothetical for more than 65 years. What then signals the kidney in HF to retain fluid? The possible sequence of events that lead to salt and water retention in patients with severe low-output HF can be constructed from Figure 1, which shows the average percent change from normal in measurements of a number of hemodynamic, neurohormonal, body fluid compartment, and renal function parameters in patients with severe untreated lowoutput HF (3). A severe decrease in left ventricular