Dopamine

Dopamine has become a very popular drug as it induces fewer arrhythmias and increases myocardial oxygen consumption less than epinephrine and norepinephrine. It is a naturally occurring amine and is the natural precursor of norepinephrine. Its effects are very dose dependent.

At doses below 2 pg/kg/min dopamine predominantly activates dopamine receptors, increasing renal blood flow. At 5 to 10 pg/kg/min b-adrenergic effects on the myocardium lead to increased contractility and cardiac output, and at doses above 10 pg/kg/min a effects come into play with vasoconstriction causing increased blood pressure and negating the dopaminergic inotropic effects.

Indications

Circulatory shock

Dopamine is the drug of choice for shock when hypotension persists despite fluid therapy. In low cardiac output states, although dobutamine is the agent of choice, the administration of dopamine is usually safer as an initial measure. Dopamine increases blood pressure while maintaining myocardial inotropy, so that cardiac output is better preserved than with norepinephrine.

Augmentation of renal or hepatosplanchnic blood flow

At low doses (above 2 pg/kg/min), the dopaminergic effects of dopamine have been thought to increase renal and hepatosplanchnic flow more than blood flow to other regions. However, there is little clinical evidence to support this function ( ViQceQt and Prejser.199.3). The routine use of low-dose dopamine does not reduce the incidence of renal failure and its administration does not consistently improve gastric intramucosal pH.

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