The pharmacodynamic effects of dopamine, an endogenous catecholamine, are complex and mediated through selective activation of specific dopaminergic and adrenergic receptors in a dose dependent manner. Low dose dopamine (0.5-2 micro g/kg/min) induces intrarenal vasodilatation, augmented renal blood flow, and inhibition of renal tubular sodium reabsorption through direct stimulation of peripheral dopaminergic receptors DA1 and DA2. Intermediate doses (3-10 micro g/kg/min) favor beta(1)-adrenergic receptor stimulation of the heart and peripheral vasoconstriction due to alpha-adrenergic receptor stimulation. At higher does (>10 micro g/kg/min), an elevated systemic vascular resistance prevails and the salutary effect on renal blood flow is diminished or lost. Dopamine is no longer favored as a first line agent for use in congestive heart failure (CHF) owing to the superior pharmacodynamic properties of dobutamine and is more properly used as an agent for vasopressor therapy. Studies have not supported the renal sparing effect of low dose dopamine for critically ill patients with incipient or established acute renal failure due to ischemia or nephrotoxicity. Evidence that low dose dopamine protects renal function during vigorous diuresis for CHF associated with renal insufficiency has clinical support and a rationale for its use. (c)1999 by CHF, Inc.

Journal Article↗

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Short-term intravenous milrinone for severe congestive heart failure: the good, bad, and not so good.

We evaluated the overall hemodynamic and clinical effects, beneficial and deleterious, of short-term intravenous milrinone in the management of severe congestive heart failure (CHF). Numerous hemodynamic measurements were obtained in 24 patients (mean age 65 yrs) with advanced, severe CHF (New York Heart Association class IV, ejection fraction 24 +/- 5%), including 3 with concomitant clinical sepsis. Hemodynamic data were recorded at baseline and after a bolus of intravenous milrinone 50 micrograms/kg and maintenance infusion based on creatinine clearance at 0.5, 3, 24 and 48 hours. Cardiac index increased and pulmonary capillary wedge pressure decreased significantly (p < 0.001; 2.07 +/- 0.36 to L/min/m2 and 20.6 +/- 4.0 to 13.5 +/- 2.8 mm Hg, respectively) in 24 patients 0.5 hour after initiation of therapy. These favorable hemodynamic responses, including significant decreases in systemic vascular resistance index and right atrial pressure, were sustained throughout the 48-hour study in 19 patients (79%). Severe hypotension occurred in three patients with superimposed sepsis as the result of exaggerated vasodilatation. One patient had recurrent ventricular tachycardia and another tolerance to milrinone. In two patients, excessive decline in preload and fall in cardiac index were reversed with volume expansion. Intravenous milrinone offered significant short-term hemodynamic benefits in most patients with severe CHF.

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