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Influence of the pericardium on ventricular loading during respiration
M Takata1, W Mitzner, J L Robotham
1Department of Anesthesiology and Critical Care Medicine, Francis Scott Key Medical Center, Baltimore, Maryland.
Abstract:
The influence of the pericardium on ventricular loading during respiration was studied in 17 acutely instrumented anesthetized dogs. Changes in intrapericardial surface pressures (Ppe) on the ventricles were measured by use of air-filled flat latex balloons during acute changes in ventricular loading with the chest open or during negative intrathoracic pressure (NITP) produced by phrenic nerve stimulation with the chest closed. Ppe always demonstrated a phasic change within a cardiac cycle, with its maximum near end diastole and minimum near end systole, and a waveform similar to ventricular dimensions measured by sonomicrometer crystals. With the chest open we found that 1) inferior vena caval constriction decreased Ppe on both ventricles at end diastole (P less than 0.01), 2) aortic constriction increased Ppe on both ventricles at end systole and end diastole (P less than 0.05), and 3) pulmonary artery constriction increased Ppe on the right ventricle (RV) (P less than 0.01) while decreasing Ppe on the left ventricle (LV) at end diastole (P less than 0.05). Thus regional Ppe over a ventricle is influenced by changes in ventricular loading conditions. During NITP with lung volume either constant or increased, Ppe over the anterolateral LV decreased less than two independent extrapericardial measures of intrathoracic pressure, and this resulted in an increased transpericardial pressure at end systole (P less than 0.05) and end diastole (P less than 0.01). During NITP with increased transpericardial pressure, Ppe over the anterior LV, lateral LV, and RV inflow showed small regional differences, but all decreased less than esophageal pressure (P less than 0.01). These results sugges that the increase in transpericardial pressure during late diastole to early systole, produced by increases in ventricular volume during NITP, could effectively attenuate the increases in ventricular preload and afterload caused by respiration, analogous to a negative feedback loop.