A model of the effects of respiration on left ventricular performance

The authors 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, the authors have been able to control independently each factor. They 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, their preparation serves as a model to study in detail the specific effects on the left ventricle of changes that are induced by respiration. Their 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. Their 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.