“Renal-dose” dopamine increases renal blood flow in heart failure patients

January 4, 2008 By Benjamin A. Olenchock, M.D. Ph.D. [mailto:bolenchock@partners.org]

Los Angeles Dopamine is a vasoactive amine that is commonly used to effect diurese in diuretic-resistant heart failure patients. It’s mechanism of action is dose-dependent, however. At high doses (>10 mcg/kg/min), the predominant effect is alpha-adrenergic receptor activation, which increases systemic vascular resistance. Medium doses (5-10 mcg/kg/min) stimulate beta-adrenergic receptors and increase cardiac ouput. Low, a.k.a. “renal-dose” dopamine (1-3 mcg/kg/min) is thought to act specifically on dopaminergic receptors in the renal and mesenteric circulation, causing vasodilation and increased blood flow.

Low-dose dopamine is often considered in decompensated, volume-overloaded heart failure patients who cannot be diuresed effectively without a significant increase in creatinine. This so-called cardiorenal syndrome leads to significant morbidity. Low-dose dopamine is often helpful in these patients, as it is thought to selectively maintain renal blood flow, thus helping to effect diuresis while protecting the kidney. The proposed mechanism by which “renal-dose” dopamine stimulates natriuesis, however, has been a soap box topic for many cardiology fellows. There is evidence from studies in animals and healthy adults that low-dose dopamine vasodilates renal vasculature and increases blood flow, however this effect is not clearly established in decompensated patients. A new study published in Circulation has used intravascular ultrasound and Doppler to accurately evaluate the effect of dopamine on renal hemodynamics in heart failure patients.

The study recruited 13 patients with New York Heart Association class III or IV heart failure, who were scheduled to undergo diagnostic cardiac catheterization. The renal artery was cannulated, and hemodynamic measures, intravascular ultrasound, and Doppler flow velocity were recorded before and after increasing doses of dopamine. Most patients had non-ischemic dilated cardiomyopathy (n=8) and fewer had ischemic heart disease (n=5). Mean baseline measures included left ventricular ejection fraction of 24%, pulmonary artery wedge pressure of 20 mm Hg, cardiac index of 3.3 L/min/m^2, and systemic vascular resistance of 1158 dyne/s/cm^5. All patients were receiving diuretics, 7 were on beta-blockers, 7 were on nitrates, 10 were on ACE inhibitors, and 9 were on digoxin.

Dopamine had no effect on renal artery pressure. Renal cross-sectional area increased in a linear fashion with dose escalation, and at 5 and 10 mcg/kg/min the difference was statistically significant. Renal blood flow also increased in a linear fashion and reached statistical significance at 2 mcg/kg/min dopamine (558 mL/min with no dopamine; 762 mL/min at 2 mg/kg/min dopamine; and 898 mL/min at 10 mcg/kg/min dopamine). Systolic blood pressure increased with doses greater than 5 mcg/kg/min dopamine. Heart rate increase was not seen until 10 mcg/kg/min dopamine.

This study demonstrated that dopamine augments renal blood flow in class III/IV heart failure patients. The patients had relatively good hemodynamics: cardiac index and systemic resistance were normal, and the wedge pressure was moderately elevated. Nonetheless, this study provides strong mechanistic understanding of the natriuretic effect of low-dose dopamine. The “renal-dose” dopamine controversy might be less controversial now.