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[Effects of beta-adrenergic blockade on hemodynamic parameters obtained by right heart catheter and echocardiography
Insights
Beta-adrenergic blockade reduces heart contractility and cardiac output during exercise in healthy men. Echocardiography and catheter measurements showed significant correlations for stroke volume and cardiac output.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Context:
- Beta-adrenergic blockade is used to manage cardiovascular conditions.
- Understanding its hemodynamic effects is crucial for patient care.
Purpose:
- To investigate the hemodynamic effects of beta-adrenergic blockade.
- To compare echocardiographic and catheter-based measurements.
Summary:
- Beta-blockade in healthy males reduced myocardial contractility and cardiac output (20-30%) during exercise.
- Pulmonary capillary pressure increased, while shortening fraction decreased.
- Echocardiography and catheterization showed strong correlations for stroke volume (r=0.76) and cardiac output (r=0.93).
- Left ventricular end-diastolic diameter did not increase, suggesting additional mechanisms beyond the Frank-Starling effect.
Impact:
- Provides insights into the physiological responses to beta-blockade.
- Validates echocardiography as a reliable tool for assessing cardiac function under beta-blockade.
- Informs clinical practice regarding the management of patients on beta-adrenergic blocking agents.
Abstract:
Echocardiographic and flow-directed catheter studies were performed on nine normal male volunteers to investigate the hemodynamic effects of beta-adrenergic blockade at rest and during exercise. The beta-receptor blockade induced inhibition of sympathetic drive led to a reduced myocardial contractility with raised pulmonary capillary pressure and a reduced shortening fraction during exercise. Stroke volume and cardiac output were reduced by 20--30%. There was a correlation between the measurements of stroke volume by echocardiography and by catheter (r = 0.76, p < 0.001), a stronger relationship was demonstrated in the measurement of cardiac output (r = 0.93, p < 0.001). In spite of raised pressures and reduced myocardial contractility there was no increase in enddiastolic left ventricular diameter. In addition to the Frank-Starling mechanism further pharmacological effects must be assumed to explain the observed effects of beta-adrenergic blockade.