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Normal stroke volume and cardiac output response during dobutamine stress echocardiography in subjects without left
P A Pellikka1, V L Roger, R B McCully
1Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA.
Insights
Stroke volume increases with dobutamine stress echocardiography, peaking around 20 mcg/kg/min, then declines. Higher doses increase cardiac output mainly via heart rate elevation.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Dobutamine stress echocardiography (DSE) is a key tool for assessing coronary artery disease.
- Expected hemodynamic responses, particularly stroke volume and cardiac output, at high DSE doses remain unclear.
Purpose of the Study:
- To investigate the effects of escalating dobutamine doses on stroke volume and cardiac output in patients without wall motion abnormalities.
- To define the dose-response relationship of stroke volume and cardiac output during DSE.
Main Methods:
- Utilized 2-dimensional Doppler echocardiography to measure stroke volume and cardiac output in 47 patients.
- Assessed hemodynamic parameters at incremental dobutamine infusion stages and after atropine administration.
Main Results:
- Stroke volume significantly increased at lower dobutamine doses (5-10 mcg/kg/min), peaking around 20 mcg/kg/min, and then showed a significant decline at 40 mcg/kg/min.
- Cardiac output progressively increased throughout dobutamine infusion.
- Heart rate increased significantly at all stages; mean blood pressure initially decreased then stabilized.
Conclusions:
- Stroke volume response to dobutamine stress echocardiography is dose-dependent, with a peak effect typically observed at 20 mcg/kg/min.
- At higher dobutamine doses, elevated cardiac output is primarily driven by heart rate increases, not stroke volume.
Abstract:
Dobutamine stress echocardiography has become widely utilized for evaluation of coronary artery disease, but the expected responses of stroke volume and cardiac output to the high doses of dobutamine administered in these studies are not known. To determine these responses, stroke volume and cardiac output were measured with 2-dimensional Doppler echocardiography at each stage of dobutamine stress echocardiography and after administration of atropine in 47 patients without resting or inducible wall motion abnormalities. Heart rate increased significantly at each stage of dobutamine infusion and after atropine. Mean blood pressure decreased at the 5 micrograms/kg/min dose, then showed little change. Stroke volume increased 27 +/- 18% from baseline, with significant increases occurring at both the 5 and 10 micrograms/kg/min doses (p < 0.00001). With higher doses of dobutamine, stroke volume tended to plateau or decrease. Mean changes in stroke volume were not significant between the doses of 10, 20, and 30 micrograms/kg/min. The mean change in stroke volume from the 30 to the 40 micrograms/kg/min dose was a significant decrease of 6.3% (p = 0.004); the decrease from the 40 micrograms/kg/min dose to atropine approached statistical significance (p = 0.06). Cardiac output increased throughout dobutamine infusion. Stroke volume during dobutamine stress echocardiography is commonly maximum at a dose of 20 micrograms/kg/min and tends to decline at higher infusion rates. At higher doses, increases in cardiac output are mediated primarily by increases in heart rate.