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 Dobutamine increased CO from 3.4 ± 0.3 to 4.3 ± 0.4 (p = 0.0145) and 4.5 ± 0.5 L/min/m2 (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.

Hidden effects of dobutamine on cardiac output

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2026年7月1日

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Christopher Lai,
Talal Shaikhain,
Sheldon Magder

摘要

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

Dobutamine increased CO from 3.4 ± 0.3 to 4.3 ± 0.4 (p = 0.0145) and 4.5 ± 0.5 L/min/m² (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.