The pericardial hypothesis: a mechanism of acute shifts of the left ventricular diastolic pressure-volume relation

Abstract

Changes in LV diastolic P-V relations may be caused by changes in myocardial distensibility and by changes in extraventricular constraint. Experimental studies suggest that the upward shift of the LV diastolic P-V relation associated with pacing tachycardia, in patients with angina pectoris, is due to decreased myocardial distensibility which possibly represents incomplete relaxation. However, shifts in the LV diastolic P-V relation with vasodilator and vasoconstrictor agents seem to be caused by changes in extraventricular constraint. Experimental and clinical data show that such interventions do not significantly change the LV transmural P-V relation. This supports the hypothesis that these shifts are due to changes in pericardial pressure. Our data suggest that such vasoactive agents act by shifting blood between the (splanchnic) venous compartment and the heart, thereby changing heart size and in turn pericardial pressure. These concepts have significantly improved our understanding of the mechanisms of action of vasoactive agents. It seemed a paradox that vasodilators (e.g., nitroglycerine) could substantially lower filling pressure of the failing left ventricle without reducing cardiac output. Because of the downward-shift in the P-V relation with nitroglycerine, preload is virtually unchanged and therefore stroke volume is maintained. Appreciation of these phenomena has considerable impact on how haemodynamic measurements are interpreted. It is obvious that the use of LV end-diastolic pressure as an index of end-diastolic volume may lead to serious misinterpretations of ventricular function. Our demonstration that right atrial pressure might be used to assess pericardial pressure provides a potentially useful way to estimate LV transmural pressure, and therefore an accurate measure of preload.