Dobutamine increased cardiac output from 3.4 to 4.5 L/min at 20 µg/kg/min by increasing heart rate and improving venous return through decreased venous capacitance.
Does dobutamine alter venous return and mean circulatory filling pressure in healthy pigs?
Dobutamine increases cardiac output not only through chronotropy and inotropy but also by improving venous return via decreased venous capacitance and lowered arterial vascular resistance.
Absolute Event Rate: 4.5% vs 3.4%
p-value: p=0.0163
BACKGROUND: Dobutamine 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. METHODS: In 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. RESULTS: (p = 0.0163) at 10 and 20 µg/kg/min, with an upward shift of the cardiac function curve, indicating improved inotropy. Stroke volume and RAP did not change, but heart rate increases linearly with the dosage of dobutamine (p = 0.0009). Mean arterial pressure did not change but systemic vascular resistance decreased (p < 0,0001). PMSF also increased with dobutamine from 8.7 ± 0.7 to 9.8 ± 0.8 and 10.4 ± 0.8 mmHg at 20 µg/kg/min (p = 0.0455), and the pressure difference for venous return (PMSF-RAP) increased from 5.6 ± 0.6 to 7.3 ± 0.6 at 10 µg/kg/min and 7.0 ± 0.5 mmHg at 20 µg/kg/min (p = 0.0292). There was no change in venous compliance or resistance to venous return, thus indicating a reduction in venous capacitance. No time-effect of dobutamine was detected over a 2-h period. CONCLUSION: Dobutamine 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.
Lai et al. (Wed,) conducted a other in Healthy (animal model) (n=8). Dobutamine vs. Baseline was evaluated on Cardiac output (p=0.0163). Dobutamine increased cardiac output from 3.4 to 4.5 L/min at 20 µg/kg/min by increasing heart rate and improving venous return through decreased venous capacitance.