Acute decompensated heart failure

Although Larry Allen and Christopher O'Connor's review of the management of acute decompensated heart failure1 was generally well written, I have reservations about their interpretation of the evidence concerning the role of loop diuretics, specifically furosemide, and their recommendations regarding furosemide's place in the treatment of acute decompensated heart failure.

First, I disagree with their implication that congestion indicates volume overload and their suggestion that clinicians consequently “rely heavily on diuretic therapy.” Such statements help to perpetuate the misuse of furosemide in acute decompensated heart failure. Up to 50% of patients with acute cardiogenic pulmonary edema are euvolemic, and treatment should emphasize fluid redistribution rather than fluid removal. Second, although diuretics have been weakly shown to decrease mortality,2 if they are relied upon exclusively in acute care in hospitals they have the opposite effect. Third, in acute decompensated heart failure caused by high afterload (e.g., hypertensive emergencies), renal perfusion can drop by as much as 80% and furosemide will produce a delayed diuretic effect 30–120 minutes after administration. Finally, there is very little evidence for any beneficial hemodynamic effect of furosemide. In fact, many studies have shown that furosemide is responsible for adverse hemodynamic effects in patients with acute decompensated heart failure, because it causes an initial release of catecholamines and activates the renin–angiotensin system.3^–5

In conclusion, I disagree with the authors' summary that “therapy with a loop diuretic currently forms the foundation” of treatment of acute decompensated heart failure despite good evidence that loop diuretics should be reserved for use as third-line agents behind therapies to reduce preload and afterload (e.g., nitroglycerin and angiotensin-converting-enzyme inhibitors) in acute decompensated heart failure in the hospital setting.