Effect of left ventricular volume on right ventricular end-systolic pressure-volume relation. Resetting of regional preload in right ventricular free wall

Effect of left ventricular (LV) volume on right ventricular (RV) end-systolic pressure-volume relation (ESPVR) was investigated, and the mechanism was examined from a standpoint of the alteration of RV free wall mean fiber length. Twelve cross-circulated isovolumically contracting canine hearts in which both ventricular volumes were controlled independently were used, and RV-ESPVR was determined at three different LV volume levels. At small (10.2 +/- 0.6 ml), middle (15.3 +/- 1.0 ml), and large (20.5 +/- 1.4 ml) LV volume, the slope of the RV-ESPVR was 2.63 +/- 0.13, 2.74 +/- 0.13, and 2.89 +/- 0.12 mm Hg/ml, respectively, and each value was significantly different from the others (p less than 0.01). The volume intercept (V0) of the relation (RV-V0) was significantly decreased with the increment of LV volume (RV-V0 in small, middle, and large LV volume; 3.92 +/- 0.68, 3.39 +/- 0.67, and 2.87 +/- 0.71 ml, respectively; p less than 0.01). In nine hearts, RV free wall lengths in latitudinal and meridional direction were measured at three LV volume levels when RV volume was held constant (16.1 +/- 1.1 ml). RV latitudinal end-diastolic length was significantly augmented with increasing LV volume (latitudinal length in small, middle, and large LV volume; 9.68 +/- 0.55, 9.81 +/- 0.56, and 9.92 +/- 0.55 mm, respectively). RV meridional end-diastolic length also increased significantly with increasing LV volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of right ventricular hemodynamics on left ventricular configuration

While abnormalities of right ventricular hemodynamics are known to affect interventricular septal position and shape, their effect on left ventricular shape and possibly function have been less well studied. Accordingly, the two-dimensional echocardiographic appearance of the left ventricle was studied in 11 patients with right ventricular volume overload, 16 with right ventricular pressure overload, nine with combined pressure and volume loads of the right heart and 17 normal control subjects. An index of left ventricular shape (SI) was calculated from end diastolic, mid systolic and end systolic left ventricular short axis area (A) and circumference (C) taken at the level of the tips of the mitral leaflets, using the formula SI = 4 pi A/C2. The left ventricles of normal subjects had relatively round configurations throughout the entire cardiac cycle (SI = 0.86 at end diastole, mid and end systole). Pure right ventricular volume overload produced left ventricular deformity at end diastole only (SI at end diastole = 0.78), with a return to normal configuration during systole. Pure right ventricular pressure load resulted in left ventricular deformation throughout the cardiac cycle, with shape indices ranging between 0.77 and 0.80. Combined pressure and volume overload produced left ventricular deformation during the entire cycle which was of an order of magnitude more severe than any other group (SI = 0.69, 0.70 and 0.65, at end diastole, mid and end systole, respectively). The shape index at end systole showed an inverse correlation with the relative right-to-left ventricular systolic pressure ratio (P = 0.001, r = 0.76). It is concluded that left ventricular configuration is affected by right ventricular hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)     

QRS voltage of the electrocardiogram and Frank vectorcardiogram in relation to ventricular volume.

Left ventricular volumes were estimated in 59 patients, who were investigated by single plane ventriculography and coronary arteriography. The relation of the left ventricular end-diastolic volumes to the QRS voltage of the 12-lead electrocardiograms and Frank vectorcardiograms was examined. It was found that the maximum spatial QRS voltage and the R wave voltage of leads V5 and V6 in patients without left ventricular hypertrophy were inversely correlated with end-diastolic volume. This inverse relation of QRS voltage and left ventricular volume may explain loss of QRS voltage with dilatation of the heart. In patients with left ventricular hypertropy QRS voltage is usually positively correlated with the degree of hypertrophy, but there is no significant correlation in the presence of cardiac dilatation. If the results of this study are extrapolated to patients with left ventricular hypertrophy and cardiac dilatation, then the inverse correlation of volume and QRS voltage may reduce the diagnostic sensitivity of unipolar chest lead and vectorcardiographic criteria of left ventricular hypertrophy.     

QRS voltage of the electrocardiogram and Frank vectorcardiogram in relation to ventricular volume.

Left ventricular volumes were estimated in 59 patients, who were investigated by single plane ventriculography and coronary arteriography. The relation of the left ventricular end-diastolic volumes to the QRS voltage of the 12-lead electrocardiograms and Frank vectorcardiograms was examined. It was found that the maximum spatial QRS voltage and the R wave voltage of leads V5 and V6 in patients without left ventricular hypertrophy were inversely correlated with end-diastolic volume. This inverse relation of QRS voltage and left ventricular volume may explain loss of QRS voltage with dilatation of the heart. In patients with left ventricular hypertropy QRS voltage is usually positively correlated with the degree of hypertrophy, but there is no significant correlation in the presence of cardiac dilatation. If the results of this study are extrapolated to patients with left ventricular hypertrophy and cardiac dilatation, then the inverse correlation of volume and QRS voltage may reduce the diagnostic sensitivity of unipolar chest lead and vectorcardiographic criteria of left ventricular hypertrophy.     

Contribution of long axis motion of left ventricular outflow to calculation of left ventricular stroke volume

Stroke volume can be calculated by using noninvasive Doppler techniques. The products of pulsed Doppler stroke distance of left ventricular outflow and left ventricular outflow area can often be used to calculate stroke volume. However, left ventricular outflow also moves longitudinally toward the apex of the ventricle during systole, so that zero velocity flow cannot be detected by the usual pulsed Doppler studies. We evaluated the contribution of these zero velocity flow to the noninvasive estimation of left ventricular stroke volume in 20 patients with left ventricular disease and in 20 age matched healthy controls. Left ventricular stroke distance was calculated by summing the Doppler stroke distance and the outflow long axis motion. The percentage of zero velocity flow for total stroke volume was calculated in each group. Cardiac output was also measured by thermo-dilution technique. The percentage of zero velocity flow for total noninvasive stroke volume in patients with left ventricular disease was 2.5±1.1 ml (4.0±1.5%), significantly lower than in normal subjects, 3.6±1.0 ml (5.5±1.5%) (p<0.05). These long axis motions are significantly reduced, especially in left ventricular disease. Amplitudes of the left ventricular outflow long axis motion were correlated with Doppler stroke distance in all (r=0.54, p<0.01). In patients with myocardial infarction, stroke volume by thermo-dilution methods and calculated stroke volume showed good correlation both only by Doppler stroke distance (y=1.044x+0.547, r=0.968) and by Doppler and long axis motion (y=0.989x+0.521, r=0.974). Compared with stroke volume measured by thermodilution method, stroke volume calculated only by Doppler stroke distance was underestimated. We thus demonstrated the influence of zero velocity flow on left ventricular outflow both in patients with left ventricular disease and in normal subjects.     

Computerized orthogonal electrocardiogram: relation of QRS forces to left ventricular ejection fraction

Several studies have suggested a relation between Q wave or R wave amplitude in the standard 12 lead electrocardiogram and the left ventricular ejection fraction. Accordingly, we analyzed the relation between Q wave and R wave amplitudes obtained with computerized orthogonal (Frank) electrocardiography and the angiographically determined left ventricular ejection fraction. A computerized orthogonal electrocardiogram was obtained before cardiac catheterization in 52 consecutive patients being evaluated for chest pain. The electrocardiographic diagnosis indicated 14 normal tracings, 20 inferior, 12 anterior and 6 lateral myocardial infarctions. Linear correlations were made between X, Y and Z axis lead voltages and ejection fraction. A significant correlation was obtained between the voltages of the R waves in the X, Y and Z leads (Rx, Ry, Rz) and of the Q waves in lead Z (Qz) as well as total amplitude Qx + Rx, Qy + Ry and ejection fraction (P <0.01). Arithmetic summation of Rx + Ry + Qz (∑R) significantly augmented the correlation with ejection fraction (r = 0.78, P <0.001); this was only slightly improved by multivariate analysis of Rx, Ry, Qz (r = 0.80, P <0.001) or Rx, Ry, Rz, Qx, Qy, Qz (r = 0.82, P <0.001). ∑R, utilized as a means of predicting whether an ejection fraction was more or less than 50 percent, had an accuracy rate of 92 percent. Thus, ∑R contains important information that can be used practically in the precatheterization evaluation of patients with chest pain and follow-up evaluation of patients with myocardial infarction.     

Immediate effect of expiratory loading on left ventricular stroke volume

While the steady-state effects of positive pleural pressure on the circulation have been extensively studied, less is known about the immediate effects of positive intrathoracic pressure on cardiac dynamics. Therefore, we performed electrocardiographically gated radionuclide ventriculography with a respiratory gating technique in nine healthy subjects during quiet breathing and during expiration against a 24 cm H2O expiratory threshold load. During expiration, respiratory loading caused an increase in stroke counts by 29.4% (p less than .001) due to an increase in end-diastolic counts of 26.1% (p less than .001). End-systolic counts also rose 18.8% (p less than .05). The ejection fraction did not change significantly. These findings indicate that the increase in left ventricular stroke volume that occurs during the first 1 or 2 beats of a loaded expiration is due to an increase in left ventricular filling and not to augmentation of left ventricular ejection. This immediate increase in pulmonary venous return may reflect increased distensibility of the left ventricle due to decreased filling of the right ventricle.     

Left ventricular pressure effects on right ventricular pressure and volume outflow

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.     

右室流出道与右室心尖部起搏对心脏收缩功能和左室重构的影响

目的评价右室流出道(RVOT)和右室心尖部(RVA)起搏对心脏收缩同步性、收缩功能和左室重构的影响。方法82例高度或III度房室传导阻滞患者随机分为RVOT起搏组(A组,n=43)和RVA起搏组(B组,n=39),以术前左室12节段达峰时间标准差(Ts-SD)是否>32.6ms对两组患者进行亚组分组,Ts-SD>32.6ms者为A1亚组与B1亚组,Ts-SD≤32.6ms为A2亚组与B2亚组。于术前及术后6个月分别进行超声心动图检查,测量舒张末左室容积(LVEDV)、收缩末左室容积(LVESV)、左室射血分数(LVEF),并采集组织多普勒图像(TDI)进行脱机分析,测量主动脉瓣射血前时间(APET)、肺动脉瓣射血前时间(PPET)、左室12节段收缩达峰时间(Ts),计算室间电机械延迟(IVMD)和Ts-SD。结果术后6个月,两组的IVMD均较术前增加;两组Ts-SD与术前比无差异。亚组分析表明术前同步性好的A2、B2亚组术后Ts-SD升高;术前同步性差的A1亚组术后Ts-SD降低。术后6个月两组LVEDV、LVESV及LVEF与术前比较均无差异,组间比较亦无差异。结论RVOT和RVA起搏短期内对左室收缩功能及左室重构均无影响,术前收缩不同步者可从RVOT起搏中获益。     

The left ventricular dP/dtmax-end-diastolic volume relation in closed-chest dogs

I investigated the relation of the maximum rate of left ventricular pressure rise to the end-diastolic volume and the comparison of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the end-systolic pressure-volume relation, using the time-varying elastance model. These studies were performed in 11 dogs chronically instrumented to measure left ventricular pressure and determine left ventricular volume from three orthogonal dimensions. During vena caval occlusions, the relations between the maximum rate of left ventricular pressure rise and end-diastolic volume were described by straight lines (r = 0.97 +/- 0.01, mean +/- SD). Dobutamine increased the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to 358 +/- 94% of control. This increase was greater than the 244 +/- 61% increase in the slope of the end-systolic pressure-volume relation (P less than 0.005). The volume intercepts of the maximum rate of left ventricular pressure rise-end-diastolic volume relation and end-systolic pressure-volume relation were similar and were not significantly altered by dobutamine. The ratio of the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the slope of the end-systolic pressure-volume relation divided by the time from end-diastole to end-systole was similar before (2.2 +/- 0.7) and after dobutamine (2.3 +/- 0.7, P = NS). Angiotensin II did not significantly alter the maximum rate of left ventricular pressure rise-end-diastolic volume relation generated by caval occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling.

To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiographic techniques. Right ventricular systolic overload in primary pulmonary hypertension resulted in substantial leftward ventricular septal shift that was most marked at end-systole and early diastole and decreased substantially by end-diastole. Right ventricular diastolic overload after tricuspid valve resection resulted in maximal leftward ventricular septal shift at end-diastole sparing end-systole and early diastole. The early diastolic distortion of left ventricular geometry associated with right ventricular pressure overload resulted in prolongation of isovolumetric relaxation of the left ventricle (129 +/- 39 ms) and a reduction in early diastolic filling compared with values in normal subjects. Late diastolic distortion of left ventricular geometry associated with right ventricular volume overload had no influence on the duration of left ventricular isovolumetric relaxation (52 +/- 32 ms) but caused a reduction in the atrial systolic contribution to late diastolic filling of the left ventricle compared with values in normal subjects. In patients with right ventricular pressure overload, 52 +/- 16% of left ventricular filling occurred in early diastole compared with 78 +/- 11% in patients with right ventricular volume overload (p less than 0.001). The differential effects of systolic and diastolic right ventricular overload on the pattern of left ventricular filling appear to be related to the timing of leftward ventricular septal displacement.     

The effects of positive end-expiratory pressure on right and left ventricular performance

The cardiovascular effects of positive end-expiratory pressure (PEEP) were studied in mechanically ventilated, vagotomized, Beta-blocked, anesthetized dogs. To compensate for the effect of PEEP on decreasing systemic venous return, acute plasma volume expansion was accomplished returning stroke volume and cardiac output to control values. Left and right ventricular filling pressures (LVFP and RVFP) and aortic pressure were measured relative to pressure (transmural pressure). Ventricular performance was assessed by comparing the transmural ventricular filling pressures at similar stroke volumes. Studies were performed on individual dogs with increasing LVFP produced by Beta-blockade, volume expansion, and obstruction of the descending thoracic aorta. Utilizing these methods we observed that for a given cardiac output, transmural LVFP was higher on PEEP compared to a control state with both normal and elevated control LVFP. On the right side, for a given cardiac output, RVFP was elevated only when the control LVFP was elevated. Our results suggest a nonneuronal adverse effect of PEEP on both left and right ventricular performance. This effect is probably due to mechanical heart-lung interaction since left ventricular (LV) dp/dt showed no change.