To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.
The end-systolic pressure-volume relationship (ESPVR) as derived from left ventricular pressure-volume loops has gained increasing acceptance as an index of ventricular contractile function. In animal experiments the ESPVR has been defined as a line connecting the upper left corners of several differently loaded pressure-volume (P-V) loops with a slope parameter Ees and a volume axis intercept parameter V.. In the clinical setting, several variants of the ESPVR have been determined with use of peak left ventricular pressure, end-ejection pressure, and end-ejection volume. The maximum P-V ratio has also frequently been measured. We attempted to determine which of these alternatives resulted in good approximations of the reference ESPVR in eight isolated canine ventricles that ejected into a simulated arterial impedance system with resistance, compliance, and characteristic impedance. We determined various versions of the ESPVR from the same set of beats quickly obtained with little change in inotropic background. To vary ventricular pressure wave forms, each of the arterial impedance parameters was independently controlled at 50%, 100%, and 200% of normal. Against each of the nine combinations of the impedance parameters four P-V loops were obtained under four preloads and from each of the sets offour P-V loops, the reference ESPVR, linear regression of the peak pressure on end-ejection volume (ESPVRPP-EEV), and linear regression of end-ejection pressure on endejection volume (ESPVREEPV) were determined. In addition, the maximum P-V ratio (MPVR) was calculated for each P-V loop. At all combinations of afterload impedance parameters ESPVRPP-EEV was shifted to the left (slope 5.4 vs 5.2 mm Hg/ml, intercept 6.6 vs 7.4 ml) and ESPVREEPV was shifted rightward (slope 5.0 mm Hg/ml, intercept 7.7 ml) from ESPVRREF. These differences, however, were quantitatively very small. MPVR was much smaller than the slope of ESPVRREF (4.0 vs 5.2 mm Hg/ml) and was load dependent. We conclude that as long as the P-V measurements are made under a fixed afterload system and different preloads, ESPVRpp EEV and ESPVREEPV, but not MPVR, can be used to approximate ESPVRREF.
We investigated the effect of changing arterial input impedance over three selected frequency ranges on stroke volume (SV) in nine isolated canine left ventricles. The input impedance was simulated with a three-element Windkessel model (i.e., resistance, characteristic impedance, and compliance) and was imposed on the ventricles with a servo-controlled loading system. Under a constant end-diastolic volume [33.1 +/- 1.5 (SE) ml], we changed the modulus of the afterloaded impedance over a low frequency range (below 0.13 Hz) by changing the resistance, over a transitional frequency range (in which the impedance modulus decreases from total resistance to characteristic impedance) by changing the compliance, and over a high frequency range (above 2.0 Hz) by changing the characteristic impedance. Each of the impedance components was changed from control to 50 and 200% of control. SV sensitively decreased from 16.1 +/- 0.7 to 7.4 +/- 0.5 ml in response to the increase in the low-frequency impedance modulus. SV was relatively insensitive, however, to the same percent increase in the impedance modulus over the transitional frequency range (from 11.2 +/- 0.6 to 12.3 +/- 0.7 ml) and over the high frequency range (from 11.9 +/- 0.6 to 11.6 +/- 0.7 ml). The average relative sensitivities of SV to the increase and decrease in impedance moduli in these frequency ranges were 1.2:0.12:0.04. We conclude that the modulus of impedance in the low frequency range is, by far, a more important determinant of SV than those in the transitional and high frequency ranges.
The mean left ventricular pressure-flow relationship (Pv-Fv), determined under a constant preload and variable peripheral resistance, has been proposed as a quantitative representation of ventricular pump function (9). We determined the Pv-Fv relation in seven isolated cross-perfused canine hearts by varying resistance of a simulated arterial load in five steps from 6.0 to 0.375 mmHg X s X ml-1 while keeping end-diastolic volume, inotropic state, compliance, and characteristic impedance at various constant values. All of the 27 Pv-Fv relations thus determined were moderately nonlinear. Varying end-diastolic volume at three levels shifted the relation curve in an approximately parallel fashion (P less than 0.0001). At three levels of inotropic state (mean LVP of isovolumic contractions 34.3 +/- 8.2, 48.0 +/- 6.3, and 59.2 +/- 9.6 mmHg), the Pv-Fv relation shifted with predominantly a slope change (P less than 0.0001). Changing compliance at three levels (0.2, 0.4, and 0.8 ml/mmHg) caused a statistically significant but quantitatively small crossover of the Pv-Fv curves (P less than 0.0001). Changing characteristic impedance to 0.1, 0.2, and 0.4 mmHg X s X ml-1 caused a highly significant (P less than 0.0001) divergence of Pv-Fv relation over the high Fv range. We conclude that this sensitivity of the Pv-Fv relation to characteristic impedance limits its use as a contractility index.
We evaluated the advantages of the autoregressive (AR) model over the conventional Fourier transform in estimating aortic input impedance. In 10 anesthetized open-chest dogs, we digitized aortic pressure and flow at 200 Hz for 51.20 s under random ventricular pacing and subdivided them into five segments. We obtained aortic input impedance over the frequency range of 0.1-20 Hz both by AR model and by Fourier transform for various lengths of data, i.e., from one to four consecutive segments. For any given data length, the impedance spectrum estimated by the AR model was smoother than that obtained by the Fourier transform. To evaluate the accuracy of the estimated impedance, we predicted instantaneous aortic pressure of the fifth segment by convolving corresponding aortic flow with the impulse response of aortic input impedance. The prediction error was less with the AR model than that resulting from Fourier transform as long as the number of the segments was less than four. We conclude that the AR model provides a more accurate estimate of aortic input impedance than does the Fourier transform when data length is limited.
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