DOPAMINE

Dopamine is an endogenous catecholamine that serves as a neurotransmitter. As an exogenous agent, it produces a dose-dependent activation of several types of adrenergic and dopaminergic receptors. The overall effect of the drug is determined by the pattern of receptor activation, as described below.

ACTIONS

When given at low dose rates (0.5 to 3 ug/kg/min), dopamine selectively activates dopamine-specific receptors in the renal, mesenteric, and cerebral circulations and increases blood flow in these regions. Dopaminergic activation in the kidneys also produces an increase in urinary sodium and water excretion that is independent of the changes in renal blood flow.

At intermediate dose rates (3 to 7.5 ug/kg/min), dopamine stimulates b-receptors in the heart and peripheral circulations, and this produces an increase in cardiac output. Note that the inotropic response to dopamine is modest when compared to dobutamine.

At high dose rates (> 7.5 ug/kg/min), dopamine produces a dose-dependent activation of a-receptors in the systemic and pulmonary circulations. This results in progressive vasoconstriction, and the resultant increase in ventricular afterload limits the ability of dopamine to augment cardiac output.

There is a dose-dependent increase in the wedge pressure, which is independent of the changes in stroke volume in the upper graph. This effect may be the result of vasoconstriction in pulmonary veins. Dopamine-induced constriction of pulmonary veins is an important consideration, because it invalidates the pulmonary capillary wedge pressure as a measure of left-ventricular filling pressures.

The hemodynamic responses to dopamine are blunted by continued drug administration. This tachyphylaxis may be due to dopamine’s ability to release norepinephrine from adrenergic nerve terminals. When tachyphylaxis to dopamine develops, discontinuing the drug for a few days (if possible) can restore some of the end-organ responsiveness.

Indications

Dopamine is indicated for the management of cardiogenic shock and any circulatory shock syndrome associated with systemic vasodilation (e.g., septic shock). The drug is particularly valuable for its ability (in intermediate-to-high dose rates) to promote vasoconstriction while preserving the cardiac stroke output. Low-dose dopamine is also used to preserve renal blood flow and to promote urine output in patients with oliguric acute renal failure, or in those at risk for oliguric renal failure. Although dopamine does not improve intrinsic renal function in this situation, it can promote urine output and limit fluid retention.

DRUG ADMINISTRATION

At low infusion rates of 0.5 to 3 ug/kg/min, natriuresis and diuresis are prominent. As the infusion rate is increased to 4 to 7 ug/kg/min, b-receptor stimulation and augmentation of cardiac output occurs. At dose rates above 8 ug/kg/min, progressive vasoconstriction is the dominant feature.

Incompatibilities

The precautions for alkaline fluids mentioned for dobutamine also apply to dopamine.

ADVERSE EFFECTS

Tachyarrhythmias are the most common complication of dopamine administration. Sinus tachycardia is common and can occur at b-agonist dose rates (i.e., 5 to 7 ug/kg/min). Malignant tachyarrhythmias (e.g., multifocal ventricular ectopics, ventricular tachycardia) can also occur, but are uncommon.

The most feared complication of dopamine administration is ischemic limb necrosis, which occurs more frequently with dopamine than with any other vasoconstrictor agent. Limb necrosis has been reported at dopamine doses as low as 1.5 ug/kg/min . Prompt administration of an a-receptor blocking agent such as phentolamine (5 mg as an intravenous bolus, followed by a continuous infusion at 1 to 2 mg/min) is indicated at the earliest signs of limb ischemia. Vasoconstrictor doses of dopamine should not be given through peripheral veins. Extravasation of the drug through a peripheral vein can be treated with a local injection of phentolamine (5 to 10 mg in 15 mL saline)

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