Dobutamine hemodynamic effects

Although concern over attenuation of dobutamine s hemodynamic effects with prolonged administration has been raised, some effect is likely retained. Consequently, the dobutamine dose should be tapered rather than abruptly discontinued. 

Sodium nitroprusside is a mixed arterial-venous vasodilator that acts directly on vascular smooth muscle to increase cardiac index and decrease venous pressure. Despite its lack of direct inotropic activity, nitroprusside exerts hemodynamic effects that are qualitatively similar to those of dobutamine and milrinone. However, nitroprusside generally decreases PAOP, SVR, and blood pressure more than those agents do. 

Feneck RO, Sherry KM, Withington PS, Oduro-Dominah A European Milrinone Multicenter Trial Group. Comparison of the hemodynamic effects of milrinone with dobutamine in patients after cardiac surgery. J Cardiothorac Vase Anesth 2001 15(3) 306-15. 

Dobutamine, a synthetic catecholamine, is a - and 82-receptor agonist with some a -agonist effects (see Table 14—14). Unhke dopamine, dobutamine does not cause release of NE from nerve terminals. The overall hemodynamic effects of dobutamine are the result of its effects on adrenergic receptors and reflex-mediated actions. Its P2-receptor-mediated effects are greater than those of dopamine, and /82-receptor-mediated vasodilation will tend to offset some of the -receptor-mediated vasoconstriction. Thus the uet vascular effect is usually vasodilation. The positive inotropy is primarily a P -receptor-mediated effect. Cardiac -receptor stimulation by dobutamine causes an increase in contractility but generally no significant change in heart rate and may provide an explanation for the apparently more modest chronotropic actions of dobutamine compared with dopamine. 

Dobutamine is a /Jj- and / -receptor agonist with some oq-agonist effects. The net vascular effect is usually vasodilation. It has a potent inotropic effect without producing a significant change in heart rate. Initial doses of 2.5 to 5 mcg/kg/min can be increased progressively to 20 mcg/kg/min on the basis of clinical and hemodynamic responses. 

An Israeh gronp has reviewed the hemodynamic and adverse effects of dobutamine in 400 patients, of whom 187 were aged 65-79 years and 49 were 80 years or older... 

A report from the Mayo Clinic has described 27 elderly patients (mean age 71 years) with aortic stenosis in whom dobutamine stress hemodynamic testing was used to assess the severity of the stenosis (12). There were no severe adverse effects, but relatively minor problems occurred in 16 patients, including chest pain and ventricular extra beats (n = 9 each) and atrial dysrhythmias (n — 4). The authors concluded that the procedure appears to be safe in these high-risk patients, although its diagnostic value may be limited. 

A loading dose is not required, and steady-state concentrations generally are achieved within 10 minutes of initiation of the infusion. The rate of infusion required to increase cardiac output typically is 2.5-10 p,g/kg/min higher infusion rates occasionally are required. The rate and duration of the infusion are determined by the clinical and hemodynamic responses of the patient. The onset of effect is rapid. Dobutamine has a tj/2 of -2 minutes the major metabolites are conjugates of dobutamine and 3-0-methyldobutamine. 

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