A model of the effects of respiration on left ventricular performance.
We have investigated the interaction of left ventricular afterload and right-heart volume on left ventricular performance. By utilizing a right-heart bypassed heart-lung preparation, we have been able to control independently each factor. We have previously suggested that the major influences of the inspiratory decrease in pleural pressure in decreasing left ventricular stroke volume (LVSV) may be via the inspiratory increases in left-heart afterload and right-heart volume (RHV). Thus, our preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Our results show that increases in transmural (relative to pleural pressure) aortic pressure (Pao) caused an increased left ventricular end-diastolic pressure (LVEDP), and that the effect of equivalent increases in Pao was greater when RHV was greater. Increase in RHV had minimal effects at low volume, but resulted in large increases in LVEDP at large RHV. These effects were markedly attenuated after pericardiectomy. Rapid increases in either RHV or Pao produced transient falls in LVSV. Our results are consistent with the hypothesis that increases in both right-heart volume and LV afterload contribute to the inspiratory decrease in LVSV and increase in LVEDP.
D000818:Animals; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006339:Heart Rate; D008954:Models, Biological; D011312:Pressure; D012119:Respiration; D013318:Stroke Volume; D016276:Ventricular Function