Mechanism of decreased right and left ventricular end-diastolic volumes during continuous positive-pressure ventilation in dogs

Continuous positive-pressure ventilation (CPPV) decreases cardiac output by decreasing right and left ventricular end-diastolic volumes. To investigate the mechanism(s), we measured cardio-vascular responses to CPPV before and after opening the chest and holding the lungs away from the heart. Expiratory pressure was adjusted to achieve similar lung volumes when the chest was open and closed (12 cm H₂O). Increasing expiratory pressure, when the chest was closed and evacuated, decreased cardiac output, ventricular end-diastolic volumes, and transmural ventricular end-diastolic pressures measured relative to lateral and posterior epicardial surface pressure (P<0.05). Transmural ventricular end-diastolic pressures measured relative to lateral pleural surface pressure did not change significantly, indicating that the increase in thoracic pressure was greater at the lateral and posterior epicardial surfaces than at the lateral pleural surface. Opening the chest and holding the lungs away from the heart eliminated the decrease in cardiac output and ventricular end-diastolic volumes during increased expiratory pressure. Pericardectomy did not affect the cardiovascular responses to increased expiratory pressure. We, therefore, conclude that decreased cardiac output and ventricular end-diastolic volumes during CPPV result from the effects of increased thoracic pressure on cardiac filling.