Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume

Carol A. Gibbons Kroeker, Nigel G. Shrive, Israel Belenkie, John V. Tyberg
2003 American Journal of Physiology. Heart and Circulatory Physiology  
Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume. may modulate acute compensatory changes in stroke volumes seen with sudden changes in cardiac volume, but such a mechanism has never been clearly demonstrated. In eight open-chest dogs, we measured left and right ventricular pressures, diameters, stroke volumes, and pericardial pressures during rapid (ϳ300 ms) systolic infusions or withdrawals of ϳ25 ml blood into and out of the
more » ... o and out of the left atrium and right atrium. Control beats, the infusion/withdrawal beat, and 4-10 subsequent beats were studied. With infusions, ipsilateral ventricular end-diastolic transmural pressure, diameter, and stroke volume increased. With the pericardium closed, there was a compensatory decrease in contralateral transmural pressure, diameter, and stroke volume, mediated by opposite changes in transmural end-diastolic pressures. The sum of the ipsilateral increase and contralateral decrease in stroke volume approximated the infused volume. Corresponding changes were seen with blood withdrawals. This direct ventricular interaction was diminished when pericardial pressure was Ͻ5 mmHg and absent when the pericardium was opened. Pericardial constraint appears essential for immediate biventricular compensatory responses to acute atrial volume changes. ventricular interaction; cardiac output; orthostatic hypotension; transmural pressure ALTHOUGH IT IS GENERALLY ACCEPTED that the pericardium plays an important role in ventricular interaction, a mechanism to compensate for sudden changes in cardiac volume has not been clearly demonstrated. Such an acute mechanism may also be important in maintaining left (LV) and right ventricular (RV) outputs because, for example, increased RV output would quickly increase pulmonary and left atrial (LA) volume. The pericardium might produce an immediate compensatory response whereby both LV (LVSV) and RV stroke volume (RVSV) change in a way that would correct the error. Based on the work of Henderson and Prince (10), Hamilton (9), and Wiggers (18), Shabetai (15) stated, "Inasmuch as the pericardium influences ventricular interaction and thereby the instantaneous dimensions of the ventricles, it may help provide the means whereby the stroke outputs of the two ventricles are continuously adjusted by operation of the Frank-Starling mechanism to provide equal left and right heart outputs." Several other investigators (5, 6, 14) have anticipated this conclusion. With the use of an isolated cat heart preparation, Elzinga et al. (7) demonstrated that injecting liquid into the LV during diastole reduced the next SV of the RV and that this effect was more pronounced with the pericardium closed. The aim of this study was to examine how the pericardium may mediate ventricular interaction on a beat-to-beat basis. Specifically, the pericardium may modulate changes in LVSV and RVSV to compensate for sudden changes in ventricular volume. Furthermore, if the pericardium is removed, there may be little or no direct ventricular interaction, and the ability to compensate rapidly for sudden cardiac volume changes may be limited. In addition, at low filling pressures, the low pericardial pressure may be associated with a diminished pericardial effect. We therefore studied the effects of sudden changes in atrial volume on ventricular pressures, dimensions, and outputs in the presence and absence of an intact pericardium. Our results suggest that the pericardium has a critical role in mediating rapid (i.e., next beat) compensatory responses to sudden changes in ventricular volume. MATERIALS AND METHODS Animal preparation. Experiments were performed in eight open-chest anesthetized dogs. Anesthesia was induced with 25 mg/kg iv thiopental and maintained with an infusion of 25 mg/ml solution (100 ml/h) of fentanyl citrate. The dogs were ventilated with a constant-volume respirator (model 607; Harvard Apparatus). A single-lead ECG was used for cardiac monitoring and body temperature was maintained in the physiological range with a heating pad. All animal care and treatment protocol conformed with the principles of the Canadian Council on Animal Care, and the work had full approval from the University of Calgary Animal Care Committee. LV, RV, atrial, and aortic pressures were measured with 8-Fr micromanometer-tipped catheters (Millar Instruments; Houston, TX). Ventricular and aortic catheters were inserted
doi:10.1152/ajpheart.00613.2002 pmid:12560206 fatcat:3tc4owsa2fgjxihtyq6bnhsh5m