Abstract:To determine the better method of measuring pericardial constraint, pericardial pressure was recorded by a liquid-filled open-ended catheter and a liquid-containing flat balloon in six open-chest anesthetized dogs. Left ventricular pressure was measured by a micromanometer-tipped catheter and left ventricular anteroposterior diameter was measured by sonomicrometry. Left ventricular end-diastolic pressure was raised to 20 +-1.7 (mean -+ SD) mm Hg by intravenous saline. Left ventricular diastolic pressure-diamet… Show more
“…Removal of the pericardium resulted in nonparallel downward and rightward shifts of the pressure-volume curves of both sides of the heart (figure 1 and tables 2 tion to right heart pressure ranged from a low of 20% at a prepericardiectomy pressure of 1 mm Hg to a high of 67% at a prepericardiectomy pressure of 15 mm Hg. In contrast, the average pericardial contribution to left heart pressure was smaller, ranging from about 22% for prepericardiectomy pressures of 5 to 11 mm Hg to a high of 37% at a prepericardiectomy pressure of 25 mm Hg.…”
Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.
“…Removal of the pericardium resulted in nonparallel downward and rightward shifts of the pressure-volume curves of both sides of the heart (figure 1 and tables 2 tion to right heart pressure ranged from a low of 20% at a prepericardiectomy pressure of 1 mm Hg to a high of 67% at a prepericardiectomy pressure of 15 mm Hg. In contrast, the average pericardial contribution to left heart pressure was smaller, ranging from about 22% for prepericardiectomy pressures of 5 to 11 mm Hg to a high of 37% at a prepericardiectomy pressure of 25 mm Hg.…”
Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.
“…Static equilibrium analysis has been used to quantify the external constraint to LV filling. 24,25 With this technique, external constraint is quantified as the difference in LVEDP before and after removal of the pericardium while a constant LVEDV is maintained. This technique can only be used when the chest is open.…”
Background-Left ventricular (LV) pacing improves hemodynamics in patients with heart failure. We hypothesized that at least part of this benefit occurs by minimization of external constraint to LV filling from ventricular interaction. Methods and Results-We present median values (interquartile ranges) for 13 heart failure patients with LV pacing systems implanted for New York Heart Association class III/IV limitation. We used the conductance catheter method to measure LV pressure and volume simultaneously. External constraint was measured from the end-diastolic pressure-volume relation recorded during inferior vena caval occlusion, during LV pacing, and while pacing was suspended. External constraint to LV filling was reduced by 3.0 (4.6 to 0.6) mm Hg from 4.8 (0.6 to 7.5) mm Hg (PϽ0.01) in response to LV pacing; effective filling pressure (LV end-diastolic pressure minus external constraint) increased by 4.0 (2.2 to 5.8) mm Hg from 17.7 (13.3 to 22.6; PϽ0.01). LV end-diastolic volume increased by 10 (3 to 11) mL from 238 (169 to 295) mL (Pϭ0.01), whereas LV end-systolic volume did not change significantly (Ϫ1 [Ϫ2 to 3] mL from 180 [124 to 236] mL, Pϭ0.97), which resulted in an increase in stroke volume of 11 (5 to 13) mL from 49 (38 to 59) mL (PϽ0.01). LV stroke work increased by 720 (550 to 1180) mL ⅐ mm Hg from 3400 (2110 to 4480) mL ⅐ mm Hg (Pϭ0.01), and maximum dP/dt increased by 120 (2 to 161) mm Hg/s from 635 (521 to 767) mm Hg/s (Pϭ0.03). Conclusions-This study suggests a potentially important mechanism by which LV pacing may produce hemodynamic benefit. LV pacing minimizes external constraint to LV filling, resulting in an increase in effective filling pressure; the consequent increase in LV end-diastolic volume increases stroke volume via the Starling mechanism. (Circulation.
“…It becomes virtually equal to surface pressure if the pericardium contains a modest effusion but it is significantly less if the pericardium is empty or is not sealed. 4 The virtual identity between pericardial and right atrial mean pressure implies that right atrial and right ventricular diastolic transmural pressure is minimal (note figures 5 and 8 in Refsum et al 21). This might not be true in chronic heart failure when the pericardium Vol.…”
The objective of this study was to determine the constraining effect of the normal human pericardium. Accordingly, immediately after thoracotomy in nine patients undergoing elective cardiac surgery, we measured mean pericardial surface pressure over the lateral free wall of the left ventricle with a flat balloon as well as mean right atrial pressure while incrementally infusing up ALTHOUGH it is well recognized that the diseased pericardium may cause a significant impairment to ventricular filling, the effect of the normal pericardium on the diastolic properties of the ventricles remains controversial. Based on measurements obtained with fluid-filled catheters, there has been a general consensus that pericardial pressure is equal to intrathoracic pressure,. 2 and is thus of little hemodynamic significance. However, Holt et al. ,3 using a flat liquid-containing balloon, demonstrated that the magnitude of pericardial pressure was substantial and similar to right atrial pressure.To Patients and methods Nine patients (mean age 54 years) scheduled for elective cardiac surgery gave informed consent to participate in this investigation; the protocol was previously reviewed and approved by the institutional ethics committee on human research.
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