Keywords
Acute decompensated heart failure; Loop diuretic resistance; Ultrafiltration; Worsening renal function and aldosterone antagonist
Abstract
Acute Decompensated Heart Failure (ADHF) is one of the most common causes of hospital admission and is associated with poor outcome. More than often, currently available treatments including high-dose loop diuretics don’t provide patients with adequate decongestion due to either worsening renal function or diuretic resistance resulting in high readmission rate and early mortality. Moreover, the recent trials studying newer strategies such as the mechanical ultrafiltration, low dose dopamine or nesiritide have demonstrated no benefit over diuretic regimens in terms of volume removal or elevation of creatinine leaving no further choice for management of diuretic resistant ADHF patients. Patients with heart failure share the same pathophysiology of decreased effective arterial blood volume as patients with cirrhosis; because of splanchnic vasodilatation in cirrhosis and decreased cardiac output in heart failure with resultant stimulation of the renin-angiotensin-aldosterone system. Hyperaldosteronism plays a major role in the pathogenesis of ascites and contributes to resistance to loop diuretics. Therefore, the use of high doses of aldosterone antagonist (spironolactone up to 400 mg/day) is the main therapy to produce a negative sodium balance in cirrhotic patients with ascites. However, similar approach has not been adopted in ADHF patients to achieve negative sodium balance. This article reviews the pathophysiology of worsening renal function and diuretic resistance associated with the use of loop diuretics, mechanical ultrafiltration and other vasodilator therapies in ADHF patients and identifies the potential role of an old therapy, i.e. aldosterone antagonists in the high dose for management of these patients.
Citation
Division of Nephrology, Department of Medicine, University of Texas Health Sciences Center at San Antonio, USA