![]() In animal studies, dobutamine produces less increase in heart rate and less decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol. It does not cause the release of endogenous norepinephrine, as does dopamine. Usual doses to increase cardiac output are 2.5 to 15 mcg/kg/minute IV.ĭobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. Uses: refractory CHF or hypotensive patients in whom vasodilators cannot be used because of effects on blood pressure.Īdult (usual): 2.5-20 mcg/kg/minute. Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.ĭrip rate (500mg/250 ml) ml /hr= wt(kg) x (mcg/min) x 0.03.Įffects: Direct beta agonist that increases cardiac output with little direct effect on BP. The final volume administered should be determined by the fluid requirements of the patient. Package Insert: Concentrations of up to 5,000 mcg/mL have been administered to humans (250 mg/50 mL). BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. nor any other party involved in the preparation of this document shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material. It is concluded, therefore, that the hemodynamic profile of dobutamine in patients with congestive heart failure is derived from a unique and complex series of interactions with alpha- and beta-adrenoceptors in the cardiovascular system.The authors make no claims of the accuracy of the information contained herein and these suggested doses and/or guidelines are not a substitute for clinical judgment. Furthermore, in the vasculature, the beta 2-adrenoceptor-mediated vasodilatory effect of dobutamine is exactly offset by the alpha 1-adrenoceptor-mediated vasoconstrictor activity, such that net changes in blood pressure are minimal following the administration of dobutamine. It has recently been suggested that the inotropic activity of dobutamine results from combined beta 1- and alpha 1-adrenoceptor stimulation in the myocardium, and that this activity could explain, at least in part, the inotropic selectivity of the compound. Dobutamine has the capacity to stimulate beta 1-, beta 2-, and alpha 1-adrenoceptors in the cardiovascular system at doses that approximate those used clinically. However, recent studies from a number of laboratories indicate that the mechanism of action of dobutamine is substantially more complex. The inotropic activity of dobutamine has previously been attributed to selective stimulation of myocardial beta 1-adrenoceptors. This hemodynamic profile of dobutamine makes the drug of value in the management of low output cardiac failure. Clinically, dobutamine increases cardiac output by selectively augmenting stroke volume, and this is associated with a decrease in total peripheral vascular resistance that is mediated, in part, by reflex withdrawal of sympathetic tone to the vasculature. Dobutamine is a sympathomimetic amine that was designed as an inotropic agent for use in congestive heart failure.
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