[Effects of beta-adrenergic blockade on hemodynamic parameters obtained by right heart catheter and echocardiography (author's transl)].
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.
D000293:Adolescent; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D006328:Cardiac Catheterization; D002306:Cardiac Volume / Q000187:drug effects; D004452:Echocardiography; D006321:Heart / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D005082:Physical Exertion; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D013318:Stroke Volume / Q000187:drug effects
D000319:Adrenergic beta-Antagonists
Auswirkungen der Beta-Rezeptorenblockade auf invasiv und echokardiographisch ermittelte hämodynamische Grössen.