Search

Objective: The aim was to examine how regional variations in pericardial pressure affect the mechanical coupling between the ventricles. Methods: Canine hearts from 14 dogs (14.5-18 kg) were removed and placed in cold cardioplegia solution. Balloons were inserted into the left and right ventricles and the atria. Pericardial pressure over the left ventricle (Pclv) and the right ventricle (Pcrv) was measured with thin balloon catheters. Ventricular and pericardial pressures were measured, and ventricular and pericardial coupling was calculated, under control conditions and with increases in pericardial tension and fluid. Results: At baseline, regional differences in pericardial pressure occurred [Pclv>Pcrv, 4.0(SD 0.9) v 2.9(0.6) mm Hg, p < 0.05]. Ventricular coupling via the pericardium was defined as ΔPclv/ΔPcrv for right ventricular volume increases and ΔPcrv/ΔPclv for left ventricular volume increases. This ratio increased more after increasing right ventricular volume than after increasing left ventricular volume [ΔPclv/ΔPcrv>ΔPcrv/ΔPclv, 1.14(0.33) v 0.51(0.15), p < 0.05]. Increasing the pericardial tension by clamping the pericardium increased pericardial pressures, yet did not alter the regional variations in pressure [Pclv>Pcrv, 8.4(2.2) v 6.4(2.5) mm Hg, p < 0.05] or pericardial coupling [ΔPclv/ ΔPcrv>ΔPclv/ΔPcrv, 1.18(0.46) v 0.54(0.16), p < 0.05]. In contrast, creating a mild tamponade increased pericardial pressures, eliminated regional differences in pressure, and altered the coupling between ventricles [ΔPclv/ΔPcrv≈ΔPclv/ΔPcrv, 0.95(0.11) v 1.05(0.08), p=NS]. These regional differences in pericardial pressure might have a geometrical basis. In four in vivo canine experiments using cine magnetic resonance, the short axis radius of curvature for the right ventricle was greater than for the left ventricle [38.3(4.4) mm v 29.2(3.8) mm, p < 0.05]. Conclusions: The pericardium partially protects right ventricular filling: regional differences in pericardial pressure normally occurred with lower pericardial pressure over the right ventricle, and left to right ventricular coupling was less. This protection of right ventricular filling was lost with even a small pericardial effusion.Cardiovascular Research 1993; 27:1470-1476 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to determine the slope (EES) of the left ventricular end systolic pressure-volume line (ESPVL) without altering preload or afterload in conscious dogs. Methods: Dogs (n=10) were instrumented to determine left ventricular volume from ultrasonic left ventricular internal dimensions, and to measure left ventricular pressure using a micromanometer. Studies were performed one to two weeks after instrumentation while the animals were conscious. ESPVL was determined from variably loaded left ventricular pressure-volume (P-V) loops generated by the vena caval occlusion. Contractile state was increased by intravenous dobutamine (8 μg·kg−1·min−1) and decreased by intravenous verapamil (10 mg) given after autonomic blockade. From a single normally ejecting beat, we calculated EES-single beat (mm Hg·ml−1) as peak isovolumetric pressure (Pmax) minus end systolic pressure divided by stroke volume. Sunagawa's technique was used to estimate Pmax by fitting the pressure during the isovolumetric contraction and relaxation as: P(t)=l/2 × Piso[1-cos(ωt+c)]+LVEDP, where Piso=peak isovolumetric developed pressure, LVEDP=left ventricular end diastolic pressure, c=constant accounting for variations in phase angle, and ω=2 π/T in which T is duration of contraction. Results: After dobutamine, EES increased, from 8.9(SEM 0.8) to 12.5(1.0) mm Hg·ml−1 (p < 0.05), and Epg-single beat increased from 9.1(0.9) to 12.0(1.4) mm Hg·ml−1 (p < 0.05). Conversely, after verapamil, EES decreased, from 11.1(1.2) to 6.3(1.1) mm Hg·ml−1, (p < 0.05), and EES-single beat also decreased, from 9.6(1.0) to 7.3(1.2) mm Hg·ml−1, (p < 0.05). Conclusions: EES calculated from one beat is similar to EES determined from variably loaded left ventricular loops and responds appropriately to inotropic stimulation. This technique provides a reasonable method to calculate EES from left ventricular pressure and stroke volume without altering preload or afterload.Cardiovascular Research 1993;27:868-873 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to examine the hypothesis that an increased coupling occurs between the ventricles during tamponade via a ventricular-pericardial-ventricular interaction, but that ventricular coupling would be unaltered or reduced with positive end expiratory pressure (PEEP). Methods: An in situ arrested, canine heart preparation was used. Changes in left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) caused by increasing the volume of the other ventricle were measured at normal and at matched levels of raised pericardial pressures (PP) caused by 20 cm H2O PEEP and by tamponade. Results: With PEEP, the coupling between the ventricles was unaltered when compared to control. With tamponade, dP1/dPr, dV1/dPr, dPr/dP1, and dVr/dP1 increased significantly (p<0.05) by 0.21(SEM 0.03, unitless), 0.45(0.04) ml·mm Hg−1, 0.18(0.03), and 0.28(0.04) ml·mm Hg−1 respectively. Conclusions: Augmented ventricular interdependence occurs during tamponade but not with PEEP, which may help to explain the different haemodynamic patterns observed under these conditions. [ABSTRACT FROM PUBLISHER]

Study objective – The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered.Design – Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured.Experimental materials – Hearts from 10 random source dogs, weight 12.5-18 kg, were used.Measurement and main results – At control pericardial pressure levels, the magnitude of the pericardial ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp, was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18(0.03), p<0.01, and dVl/dPp, was significantly greater than dVl/dPr, at −0.83(0.09) v −0.24(0.06), p<0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dPl/dPr∼, dVl/dPr∼, dPr/dPl∼, and dVr/dPl∼ increased significantly (p<0.05) by 0.48(0.03), 0.67(0.13), 0.38(0.05), and 0.61(0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dPl/dPr increased, from 0.51(0.03) to 0.79(0.01), p<0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42(0.03) v 0.44(0.04), p>0.5.Conclusions – Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade. [ABSTRACT FROM PUBLISHER]