Mean Ejection Pressure Research Articles

Single-Beat Estimation of Right Ventricular Contractility and Its Coupling to Pulmonary Arterial Load in Patients With Pulmonary Hypertension.

BackgroundAn accurate assessment of intrinsic right ventricular (RV) contractility and its relation to pulmonary arterial load is essential for the management of pulmonary hypertension. The pressure‐volume relationship with load manipulation is the gold standard assessment used for this purpose, but its clinical application has been hindered by the lack of a single‐beat method that is valid for the human RV. In the present study, we sought to validate a novel single‐beat method to estimate the preload recruitable stroke work (PRSW) and its derivative for ventriculoarterial coupling in the human RV.Methods and ResultsA novel single‐beat slope of the PRSW relationship (Msw) was derived by calculating the mean ejection pressure when the end‐systolic volume was equal to volume‐axis intercept of the PRSW relationship. In addition, by using a mathematical transformation of the equation representing the linearity of the PRSW relationship, a novel index for ventriculoarterial coupling, Msw/mean ejection pressure, was developed. RV pressure‐volume relationships were measured in 31 patients (including 23 patients with pulmonary hypertension) who were referred for right‐sided heart catheterization. In this cohort, the single‐beat Msw was strongly correlated with the multiple‐beat Msw (r=0.91, P<0.0001). Moreover, a significant correlation was observed between the single‐ and multiple‐beat Msw/mean ejection pressure (r=0.53, P=0.002), with a stronger correlation in those with greater RV systolic pressure (r=0.70, P=0.003).ConclusionsThe novel single‐beat approach provided an accurate estimation of indexes for the PRSW relationship and ventriculoarterial coupling. It may be particularly useful in assessing RV adaptation to increased pressure overload.

Effect of acutely increased left ventricular afterload on work output from the right ventricle in conscious dogs

Objective: To determine the effect of acute increments in left ventricular afterload on the stroke work output of the right ventricle in vivo. Methods: After pharmacologic attenuation of autonomic reflexes, left and right ventricular pressure-volume data were obtained in 9 conscious dogs during vena caval occlusions performed before and during aortic constriction. Results: The relationship between right ventricular stroke work and end-diastolic volume during vena caval occlusion was highly linear (r = 0.97 ± 0.02), but the slope decreased by 20% ± 13% during aortic constriction sufficient to increase left ventricular mean ejection pressure by 25% ± 14% (P < .05). The volume-axis intercept remained constant. Similarly, the slope of the linear relationship between right ventricular free wall regional segment work and end-diastolic segment length declined by 22% ± 10% during aortic constriction (P < .05), without significant change in the length-axis intercept. The reduction in both global and regional right ventricular stroke work at any given preload with increased left ventricular afterload was due entirely to decreased right ventricular stroke volume and free wall shortening, because right ventricular mean ejection pressure was unchanged. Additional experiments were performed in 5 open-chest dogs to produce a greater reduction in left ventricular free wall shortening than observed with aortic constriction by transient constriction of the left circumflex coronary artery. However, this intervention had no effect on right ventricular free wall segment work output. Conclusion: Increased left ventricular afterload decreases global and regional right ventricular stroke work at any given preload, a direct, negative systolic ventricular interaction. (J Thorac Cardiovasc Surg 2001;121:116-24)

Oxygen-wasting effect of inotropy in the "virtual work model".

In the "virtual work model," left ventricular total mechanical energy (TME) is linearly related to myocardial oxygen consumption (MVO2). This relationship (MVO2-TME) is supposedly independent of inotropic stimulation, vascular loading, and heart rate variations. We reexamined the effect of inotropic stimulation (dopamine) on the metabolic to mechanical energy transfer in nine open-chest anesthetized pigs. Left ventricular mechanical energy was calculated using TME (mean ejection pressure x end-diastolic volume + stroke work), TMEW (end-diastolic volume reduced by unstressed ventricular volume), and the pressure-volume area (PVA). A highly linear relationship between MVO2 and mechanical energy was found for all three indexes during control and dopamine runs (r = 0.87-0.99). The slopes were unaltered by dopamine. y-Axis intercepts were (control vs. dopamine) as follows (in J. beat-1. 100 mg-1; means +/- SD): TME, 0.36 +/- 0.12 vs. 0.61 +/- 0.30 (P < 0.02); TMEW, 0.43 +/- 0.16 vs. 0.72 +/- 0.32 (P < 0.02); and PVA, 0.34 +/- 0.13 vs. 0.60 +/- 0.30 (P < 0.02). We conclude that the virtual work model is dependent on inotropic stimulation and that new insight into myocardial chemomechanical coupling is not added by this concept.

Modified Ultrafiltration Improves Left Ventricular Systolic Function In Infants After Cardiopulmonary Bypass

Objective: Our objective was to test the hypothesis that use of modified ultrafiltration after cardiopulmonary bypass improves intrinsic left ventricular systolic function in children. Methods: Twenty-one infants undergoing cardiopulmonary bypass were instrumented with ultrasonic dimension transducers, to measure the anteroposterior minor axis diameter, and a left ventricular micromanometer. Patients were randomized to modified ultrafiltration ( n = 11, age 226 ± 355 days, weight 6.7 ± 3.1 kg) or control ( n = 10, age 300 ± 240 days, weight 7.0 ± 2.5 kg) (all differences p > 0.05 between groups). Left ventricular systolic function was assessed by means of the slope of the preload-recruitable stroke work index. Myocardial cross-sectional area was measured by echocardiography. Data were acquired immediately after separation from bypass, at steady state, and during transient vena caval occlusion. Data acquisition was repeated after 13 ± 5 minutes of modified ultrafiltration or after 12 ± 5 minutes without modified ultrafiltration in the control group. Inotropic drug support was the same at both study points. Results: In the modified ultrafiltration group, the filtrate volume was 363 ± 262 ml. The hematocrit value increased from 26.0% ± 2.7% to 36.7% ± 9.5% ( p = 0.018), myocardial cross-sectional area decreased from 3.72 ± 0.35 cm 2 to 3.63 ± 0.36 cm 2 ( p = 0.04), end-diastolic length increased from 25.6 ± 9.0 mm to 28.8 ± 9.9 mm ( p = 0.01), and end-diastolic pressure fell from 5.6 ± 0.8 mm Hg to 4.2 ± 0.8 mm Hg ( p = 0.005), suggesting an improved diastolic compliance. In the control group, the hematocrit value, myocardial cross-sectional area, end-diastolic length, and pressure did not change (all p > 0.05). Mean ejection pressure increased in the ultrafiltration group ( p = 0.001) but did not change in the control group ( p = 0.22). The slope of the preload-recruitable stroke work index increased after ultrafiltration from 52.3 ± 52.0 to 74.2 ± 66.0 (10 3 erg/cm 3) ( p = 0.02) but did not change in the control group ( p = 0.07). One patient from each group died in the postoperative period. Patients in the ultrafiltration group received less inotropic drug support in the first 24 hours after the operation (156.62 ± 92.31 μg/kg in 24 hours) than patients in the control group (865.33 ± 1772.26 μg/kg in 24 hours, p = 0.03). Conclusions: Use of modified ultrafiltration after cardiopulmonary bypass improves intrinsic left ventricular systolic function, improves diastolic compliance, increases blood pressure, and decreases inotropic drug use in the early postoperative period. (J Thorac Cardiovasc Surg 1998;115:361-70)

Mechanical determinants of myocardial oxygen consumption in conscious dogs

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

Effects of cardiac glycosides on myocardial function and energetics in conscious dogs.

The physiological effects of intravenous ouabain on left ventricular (LV) systolic function and metabolic-to-mechanical energy transfer were examined in eight conscious dogs. LV pressure and volume were measured using micromanometers and ultrasonic dimension transducers during transient vena caval occlusions under control conditions and after increasing doses of ouabain. Doppler coronary flow and coronary sinus O2 saturations were used to determine arterial-to-coronary sinus O2 content difference and thereby to calculate LV O2 consumption; total mechanical energy was computed as the sum of LV stroke work and the product of end-diastolic volume and LV mean ejection pressure, neglecting LV unstressed cavitary volume. The slope (10(4) erg/ml) of the stroke work vs. end-diastolic volume relationship increased progressively with rising doses of ouabain from 7.0 +/- 1.6 at control to 9.6 +/- 1.7 after ouabain 0.75 mg (P = 0.0002). Regression analysis of LV O2 consumption (mW/cm3) vs. total mechanical energy (mW/cm3) yielded a linear relationship that did not change with 0.75 mg of ouabain (P > 0.4). These data indicate that ouabain possesses a significant positive inotropic effect on the intact left ventricle without a change in energy transfer efficiency or O2 wasting.

Experimental mitral regurgitation: Physiological effects of correction on left ventricular dynamics

It has been suggested that mitral valve replacement for mitral regurgitation can precipitate acute myocardial failure by increasing left ventricular afterload. However, most studies of this problem have involved anesthesia, acute surgical trauma, or ischemic cardioplegia, each of which can influence myocardial function. The pure hemodynamic consequences of mitral valve replacement were investigated by surgically instrumenting eight dogs with ultrasonic transducers to measure left ventricular diameter, electromagnetic flow probes to measure ascending aortic blood flow, and micromanometers to measure left ventricular and pleural pressures. At the time of implantation, an 8 mm stainless steel shunt was inserted through the left ventricular myocardium at the base of the anterior wall and sutured to the left atrial appendage, producing simulated mitral regurgitation of 20% to 40% of total ventricular output. Balloon occluders were placed around the left atrial shunt and both venae cavae. One to 7 days after implantation, each dog was studied in the conscious state, and data were recorded during acute occlusion of the shunt. After shunt occlusion, left ventricular mean ejection pressure increased significantly in all studies. Systolic wall tension also increased by an average of 8%, diameter shortening decreased by 21%, and forward cardiac output increased by 17%. Thus the higher afterload associated with elimination of mitral regurgitation produced an acute fall in stroke shortening and total left ventricular output. However, forward cardiac output increased in all studies, implying improved pump efficiency and overall cardiac performance. Thus the improvement in pump efficiency associated with restoration of mitral valve competence uniformly increases forward cardiac output despite an increased ventricular afterload and a decreased total stroke volume. Although there may be differences between this relatively acute model and chronic forms of mitral regurgitation encountered clinically, these data suggest that forward cardiac output should increase with correction of mitral regurgitation and that the associated augmentation in afterload is probably not a major factor causing low cardiac output after correction.

Equations for the calculation of mean ejection pressure.

Two simple equations for the calculation of mean ejection pressure (MEP) are described and compared with true MEP determined by manual planimetry. The equations were tested and found to have a high degree of correlation with true MEP over a wide range of peak systolic pressures, pulse pressures, and heart rates in humans and several animal species.

REASSESSMENT OF OPERATIVE INDICATION FOR MODERATE CONGENITAL AORTIC STENOSIS

CONCLUSIONS AND SUMMARY The case of 2 patients are presented in whom aortic commissurotomy did not result in a significant improvement of aortic valve function. Indication for surgery was the presence of a peak systolic gradient of 50 mm. Hg or greater; mean ejection gradient was considerably less in these patients. At surgery, valve area was only slightly diminished, and little could be safely done to improve function. A third patient, from another center, preoperatively had moderate aortic stenosis without symptomatology or cardiomegaly and postoperatively has severe aortic regurgitation. In view of the morbidity and mortality of surgery, and the limitations of what can be accomplished at operation without producing crippling aortic regurgitation, we conclude that hemodynamic data as the only indication for surgical intervention are of unproved validity and should be used with great caution. If hemodynamic data are used as indication for surgery, valve area or mean ejection pressure gradient should be the basis, rather than peak systolic pressure gradient. “Spike-wave” pressure patterns are particularly misleading in exaggerating the peak gradient. It is the exception rather than the rule to achieve a normal aortic valve by commissurotomy. The possibility of subsequent calcification and the ultimate requirement of total valve replacement seem plausible arguments for a more conservative approach to moderate valvular aortic stenosis in the young patient.