• S Ishizaka, H Asanoi, T Kameyama, and S Sasayama.
• Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University.
• J Cardiol. 1988 Jun 1; 18 (2): 457-65.

AbstractIn nine patients with cardiac dysfunction (ejection fraction less than or equal to 50%), we evaluated the effects of dobutamine (5 micrograms/kg/min) on ventriculo-arterial coupling by monitoring direct arterial pressures and simultaneously-recorded M-mode echocardiograms guided with two-dimensional images. Left ventricular end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated by the formula of Teichholz, and left ventricular end-systolic pressure (ESP) was approximately from the arterial dicrotic pressure. Arterial pressure was altered by phenylephrine or nitroprusside and the slope (Ees) and volume axis intercept (Vo) of the end-systolic pressure-volume relationship were determined as the contractile properties of the ventricle. The arterial system properties were expressed by the slope (Ea) of the end-systolic pressure-stroke volume relationships. Ees during dobutamine infusion was derived assuming that the Vo was unchanged from the baseline state. The left ventricular pressure-volume area (PVA), the sum of external work (EW) and end-systolic potential energy (PE), and ventricular work efficiency (EW/PVA) were determined from a time-varying elastance model. The EDV and ESV were significantly decreased by dobutamine (-4%, p less than 0.05; -22%, p less than 0.01), while the ESP and heart rate remained unchanged. Dobutamine increased the Ees markedly (+41%, p less than 0.01) and decreased the Ea (-23%, p less than 0.01). These changes resulted in a substantial decrease in the ratio of Ea to Ees (-44%, p less than 0.01). The EW was augmented (+22%, p less than 0.01), but the PE was reduced (-33%, p less than 0.01) by dobutamine, while the PVA remained the same as in the baseline state.(ABSTRACT TRUNCATED AT 250 WORDS)

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