Hidden effects of dobutamine on cardiac output.

backgroundDobutamine exerts its pharmacological effects by stimulating α1-, β1-, and β2-adrenergic receptors. Activation of these receptors increase both the force of cardiac contraction (inotropy) and heart rate (chronotropy). Despite its well-established cardiac effects, the influence of dobutamine on vascular tone remains poorly understood and its impact on venous return and the underlying determinants of this process has not been thoroughly investigated.

methodsIn eight healthy pigs, we measured cardiac output (CO) by pulmonary thermodilution, right atrial pressure (RAP) and arterial pressure. We measured mean circulatory filling pressure (PMSF), by transiently inflating a balloon in the right atrium and thus temporarily stopping blood flow and allowing venous pressure to plateau. After obtaining baseline measurements, dobutamine was administered at 10 and 20 µg/kg/min. Two fluids bolus were given at baseline and with a dobutamine infusion at 20 µg/kg/min to produce cardiac function curves. Repeated measures ANOVA were performed for comparisons.

resultsDobutamine increased CO from 3.4 ± 0.3 to 4.3 ± 0.4 (p = 0.0145) and 4.5 ± 0.5 L/min/m

conclusionDobutamine increased cardiac output by increasing cardiac function by increase heart rate but also by improving venous return by increasing PMSF by decreasing venous capacitance and lowering arterial vascular resistance, underscoring the importance of its α1 and β2-adrenergic activity.