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Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
Published on: February 10, 2013
Cardiovascular effects of dobutamine stress testing in women with suspected coronary artery disease
P Blomstrand1, J Engvall, E Swahn
1Linköping Heart Centre, University Hospital, Sweden.
Insights
Dobutamine stress testing in women with suspected heart disease causes vasodilation and increased cardiac output. Hypotension can occur due to vasovagal responses or inadequate cardiac output increase.
Area of Science:
- Cardiology
- Hemodynamics
- Vascular Physiology
Background:
- Ischaemic heart disease diagnosis often involves stress testing.
- Dobutamine stress testing is used to assess cardiac function.
- Hypotension is a potential side effect of dobutamine stress testing.
Purpose of the Study:
- Investigate hemodynamic responses during dobutamine stress testing in women.
- Identify reasons for hypotension during dobutamine stress testing.
Main Methods:
- 18 women (54-73 years) with suspected ischaemic heart disease underwent dobutamine infusion.
- Doppler echocardiography and venous occlusion plethysmography were used.
- Testing occurred 5-10 days post-unstable angina.
Main Results:
- Dobutamine increased heart rate (49%) and cardiac output (59%).
- Peripheral vascular resistance decreased significantly (total: 44%, leg: 26%).
- Four patients experienced hypotension, linked to pronounced vasodilation or low cardiac output increase.
Conclusions:
- Dobutamine causes significant peripheral vasodilation and increased cardiac output.
- Hypotension can result from vasovagal reactions or insufficient cardiac output augmentation.
- Disparate peripheral resistance changes may indicate baroreceptor-mediated responses.
Objective:
To investigate the central and peripheral haemodynamic response to dobutamine stress testing in women with suspected ischaemic heart disease and to seek an explanation for the hypotension phenomenon.
Design:
18 women aged 54-73 years were investigated with Doppler echocardiography and venous occlusion plethysmography during intravenous infusion of dobutamine 5-10 d after an episode of unstable angina.
Results:
An average peak dose of 33 (SD 9.7) micrograms/kg/min was given. Heart rate and cardiac output increased by 49% and 59%, respectively (P < 0.001). Total and leg peripheral vascular resistance decreased by 44% and 26%, respectively (P < 0.001). Four patients developed hypotension (decrease in systolic blood pressure > 10 mm Hg), one of whom had a paradoxical bradycardia and two a low increase in cardiac output. Patients with hypotension had a more pronounced decrease in total peripheral vascular resistance but a similar change in leg peripheral vascular resistance compared with patients without hypotension.
Conclusions:
Dobutamine infusion leads to marked peripheral vasodilatation and an increase in cardiac output. Some patients experience hypotension during the test for reasons which include paradoxical vasovagal reactions and diminished capacity for adequate increase in cardiac output. There is also a disparity between the pattern of total and leg peripheral vascular resistance in patients with hypotension which might reflect a baroreceptor mediated compensatory increase in vasoconstrictor tone of muscle vessels not matched in other vascular territories.
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