The effects of dobutamine and dopamine on intrapulmonary shunt and gas exchange in healthy humans

Abstract

The development of intrapulmonary shunts with increased cardiac output during exercise in healthy humans has been reported in several recent studies, but mechanisms governing their recruitment remain unclear. Dobutamine and dopamine are inotropes commonly used to augment cardiac output; however, both can increase venous admixture/shunt fraction (Qs/Qt). It is possible that, as with exercise, intrapulmonary shunts are recruited with increased cardiac output during dobutamine and/or dopamine infusion that may contribute to the observed increase in Qs/Qt. The purpose of this study was to examine how dobutamine and dopamine affect intrapulmonary shunt and gas exchange. Nine resting healthy subjects received serial infusions of dobutamine and dopamine at incremental doses under normoxic and hyperoxic (inspired O(2) fraction = 1.0) conditions. At each step, alveolar-to-arterial Po(2) difference (A-aDo(2)) and Qs/Qt were calculated from arterial blood gas samples, intrapulmonary shunt was evaluated using contrast echocardiography, and cardiac output was calculated by Doppler echocardiography. Both dobutamine and dopamine increased cardiac output and Qs/Qt. Intrapulmonary shunt developed in most subjects with both drugs and paralleled the increase in Qs/Qt. A-aDo(2) was unchanged due to a concurrent rise in mixed venous oxygen content. Hyperoxia consistently eliminated intrapulmonary shunt. These findings contribute to our present understanding of the mechanisms governing recruitment of these intrapulmonary shunts as well as their impact on gas exchange. In addition, given the deleterious effect on Qs/Qt and the risk of neurological complications with intrapulmonary shunts, these findings could have important implications for use of dobutamine and dopamine in the clinical setting.

Figures

Fig. 1.

Representative saline contrast echocardiograms on a 35-yr-old subject at baseline and during incremental drug (dobutamine) infusion. Top: echocardiograms at baseline. A: precontrast. B: <5 cardiac cycles. C: >5 cardiac cycles. No intracardiac/pulmonary shunt was visualized. Bottom: echocardiograms during drug infusion. D: 2.5 μg·kg−1·min−1 (shunt score =1). E: 5 μg·kg−1·min−1 (shunt score = 2). F: 10 μg·kg−1·min−1 (shunt score = 3).

Fig. 2.

Means ± SE physiological shunt fraction (Qs/Qt) and intrapulmonary shunt as assessed by contrast echocardiography (shunt score) in relation to cardiac output at baseline and during incremental dobutamine (left) or dopamine (right) infusion. *Significant difference vs. baseline for shunt fraction/shunt score (P < 0.05). #Significant difference vs. baseline for cardiac output (P < 0.05).

Fig. 3.

Means ± SE intrapulmonary shunt score in relation to pulmonary artery systolic pressure (left) and cardiac output (right) at baseline and during inotrope infusion. *Significant difference vs. baseline for shunt score (P < 0.05). #Significant difference vs. baseline for PASP/cardiac output (P < 0.05).

Fig. 4.

The effect of incremental drug infusion on intrapulmonary shunt score. Left: dobutamine. Right: dopamine.

Fig. 5.

The effect of incremental drug infusion on peak individual shunt score. Left: dobutamine. Right: dopamine. Dotted lines represent mean shunt score. *Significant difference vs. baseline (P < 0.05).