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At least 19 recordsLinked to original sources
PubMed1986

Right ventricular assistance for experimental right ventricular dysfunction.

Right ventricular dysfunction frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. The purpose of the present study was to surgically induce right ventricular dysfunction and then provide circulatory support with a right ventricular assist device. Right ventricular hypertrophy was created in 13 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy with the animal supported by cardiopulmonary bypass. In four unassisted animals the circulation failed after separation from bypass. Seven experimental animals underwent the insertion of a pneumatically activated ventricular assist device between the proximal pulmonary artery and the right ventricular apex. Periods with the right ventricular assist device on and off in each animal were compared. The right ventricular assist device increased cardiac output from 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min (p less than 0.0002), increased left atrial pressure from 7 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0005), and increased aortic systolic pressure from 53 +/- 9 to 85 +/- 9 mm Hg (p less than 0.0001). Right ventricular assistance significantly reduced the right ventricular end-diastolic pressure from 19 +/- 3 to 12 +/- 1 mm Hg (p less than 0.0001). Pulmonary artery peak pressure distal to the band increased from 27 +/- 3 to 52 +/- 5 mm Hg (p less than 0.0001). The results indicate that right ventricular dysfunction can be produced by a vertical cardiotomy in a hypertrophied right ventricle with persistent outflow tract obstruction. Right ventricular dysfunction can be effectively reversed by a right ventricular assist device, which may prove clinically useful in managing patients with refractory right ventricular failure.

Animals↗
PubMed1996

MR imaging of pulmonary hypertension and right ventricular dysfunction.

Right ventricular cardiac function is altered by abnormalities affecting primarily the left-sided cardiac structures, the lungs, or the right-sided cardiac structures themselves. The most common cardiac causes for right ventricular dysfunction are chronic left ventricular ischemia and rheumatic mitral valvular disease. Pulmonary diseases that result in right ventricular dysfunction include pulmonary air-space disease, including emphysema, and pulmonary interstitial and parenchymal diseases, including idiopathic pulmonary fibrosis and cystic fibrosis. Chronic pulmonary vascular disease, including chronic thromboembolism and PPH have a significant effect on right ventricular performance. Common to all of these diseases is elevation of pulmonary vascular resistance with a commensurate increase in right ventricular pressure, resulting in right ventricular hypertrophy. The limited ability of right ventricular myocardium to function in the face of increased pulmonary resistance results in right ventricular dilatation, tricuspid regurgitation, and ultimately right ventricular failure. MR imaging provides direct, noninvasive visualization of the right ventricular chamber as well as the myocardium itself, allowing reliable demonstration of morphologic changes in the size and shape of the ventricle, thickness of the myocardium, and presence of abnormal infiltration by fat or edema. Furthermore, because MR imaging techniques do not depend upon geometric assumptions about the complex shape of the right ventricle, they may be used for accurate and reproducible quantitation of right ventricular volume and myocardial mass.

Heart↗
PubMedDate not supplied

Spontaneous resolution of severe right ventricular dysfunction in right ventricular infarction: documentation by radionuclide studies.

A case of inferior myocardial infarction complicated by severe arrhythmias and right heart failure is presented. Radionuclide studies performed near the acute phase and one month later illustrate the reversibility of right heart dysfunction caused by infarction. Signs of right ventricular involvement in acute inferior myocardial infarction are noted in about 40% of cardiac blood-pool studies: right ventricular dilatation with a significantly decreased ejection fraction, and ventricular wall motion abnormalities. Follow-up studies in the recovery period show good recovery of right ventricular function.

Aged↗
PubMed1985

Right ventricular dysfunction following cold potassium cardioplegia.

Right coronary artery stenoses limit cardioplegic delivery to the right ventricle and may contribute to postoperative right ventricular dysfunction. Right ventricular function was evaluated in 39 patients with right coronary artery stenoses following elective coronary bypass operations. Hemodynamic and nuclear ventriculographic measurements, made between 3 and 6 hours postoperatively, revealed a progressive increase in pulmonary arterial pressure, pulse rate, and right ventricular ejection fraction (p less than 0.05). Right ventricular end-diastolic volume index (calculated from the thermodilution stroke index divided by the nuclear ejection fraction) decreased, but right atrial pressure increased (suggesting a decrease in compliance). The response to the infusion of 2 units of plasma (volume loading) was evaluated 3 hours postoperatively (EARLY) and again 5 hours postoperatively (LATE) in 21 patients. Right ventricular performance (the relation between cardiac index or right ventricular stroke work index and right ventricular end-diastolic volume index) and right ventricular systolic function (the relation between systolic pulmonary arterial pressure and right ventricular end-systolic volume index) were depressed EARLY and improved LATE (p less than 0.01 in analysis of covariance). Left ventricular performance (the relation between cardiac index or left ventricular stroke work index and left ventricular end-diastolic volume index) and left ventricular systolic function (the relation between systolic blood pressure and left ventricular end-systolic volume index) were similar EARLY and LATE. Right ventricular diastolic function (the relation between right atrial pressure and right ventricular end-diastolic volume index) and left ventricular diastolic function (the relation between left atrial pressure and left ventricular end-diastolic volume index) were significantly greater LATE than EARLY. Right, but not left, ventricular performance and systolic function were transiently depressed, and right and left ventricular diastolic stiffness were transiently decreased in the EARLY postoperative period. In patients with right coronary artery stenoses, current methods of cardioplegia may inadequately protect the right ventricle, but further studies are required to establish the relation between intraoperative protection and postoperative function.

Blood Pressure↗
PubMed1980

Ventricular compliance in ischemic right ventricular dysfunction.

Ischemic right ventricular dysfunction was diagnosed in 54 patients with acute myocardial infarction who had a right atrial pressure disproportionately increased in relation to the pulmonary capillary pressure. The right atrial pressure curve in 40 patients (74 percent) was M- or W-shaped, termed a noncompliant pattern, and was similar to the pattern found in constrictive pericarditis. Kussmaul's sign was found in the patients whose respiration was recorded. This pattern, which represents poor right ventricular compliance, was severe in 30 cases (y descent greater than x descent) and slight in 10 cases (y descent = x descent). Its duration was variable, ranging from days to years. Of the 54 patients, 32 (59 percent) had a low output syndrome, diagnosed in the presence of a cardiac index of less than 2.2 liters/min per m2, with signs of poor tissue perfusion. The severe noncompliant pattern was significantly related to the presence of a low output syndrome (p less than 0.01) and mortality from this cause (p less than 0.05). The jugular venous tracing pulse had a pattern similar to that of the right atrial pressure recording and therefore may be valuable in the noninvasive diagnosis of right ventricular dysfunction and in the study of the evolution of the noncompliant pattern and, hence, of ventricular compliance.

Acute Disease↗
PubMed1995

Mechanisms of transplant right ventricular dysfunction.

OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.

Animals↗
PubMed1987

Stress induced right ventricular dysfunction: an indication of reversible right ventricular ischaemia.

Stress induced changes in left ventricular ejection fraction are widely used in the detection and assessment of coronary artery disease. This study demonstrates that right ventricular dysfunction may also occur, and assesses its significance in terms of coronary artery anatomy. This study involved 14 normal subjects and 26 with coronary artery disease investigated by equilibrium radionuclide ventriculography, at rest and during maximal dynamic exercise. Mean normal resting right ventricular ejection fraction (RVEF) was 0.40 (SD 0.118), and all normal subjects increased RVEF with stress (mean delta RVEF + 0.13 SD 0.099). Mean delta RVEF in the subjects with coronary artery disease was significantly lower at 0.00 (SD 0.080), but there was overlap between the two groups. The largest falls in RVEF were seen if the right coronary artery was occluded without retrograde filling. In this subgroup with the most severely compromised right ventricular perfusion (nine subjects), RVEF always fell with stress, and mean delta RVEF was -0.08 (SD 0.050). There was no significant correlation between delta LVEF and delta RVEF, implying that the right ventricular dysfunction was due to right ventricular ischaemia, rather than secondary to left ventricular dysfunction. Stress induced right ventricular ischaemia can therefore be detected readily by radionuclide ventriculography.

Adult↗
PubMed1994

Ischemia right ventricular dysfunction.

For many years ischemic heart disease involving the right ventricle had received little attention. During the last 15 years, the initial works of Cohn, Isner, and others spawned a number of clinical and experimental studies that extended the understanding of the pathophysiology of ischemia in the right ventricle. Most of the work has been done in the setting of acute myocardial infarction, and information is still lacking in other conditions, such as chronic ischemic heart disease and perioperative right ventricular dysfunction. Acute right ventricular infarction rarely occurs in the absence of left ventricular necrosis and in most cases is the extension of an inferior left ventricular infarct. The majority of patients with right ventricular infarction only exhibit subtle signs of ischemic dysfunction. Elevated right atrial pressure is found only in the typical syndrome of elevated venous pressure; low output syndrome can be found only in 20% of the cases, and cardiogenic shock secondary to right ventricular necrosis is found only in 10%. It is also important to note that there is not a clear correlation between the severity of ischemic right ventricular dysfunction and the necrotic area. The discrepancy may be due to ischemia without necrosis of the right ventricular wall (stunned myocardium), but the intact pericardium and the necrosis of the interventricular septum may also play an important role. In the most severe form of ischemic right ventricular dysfunction, the entire right ventricular wall is akinetic. Right atrial, right ventricular, and pulmonary artery pressures become similar in magnitude and shape, and the pulmonary valve is opened during diastole, demonstrating a passive blood flow from the right atrium to the left ventricle through the low resistance pulmonary capillary bed. Volume loading, administration of dopamine or dobutamine, and careful use of vasodilators under hemodynamic monitoring are the therapeutic measures to control the severe forms of acute ischemic right ventricular dysfunction. The use of thrombolytic agents has decreased the incidence of right ventricular dysfunction after acute myocardial infarction. Mortality is high in the severe forms of acute ischemic right ventricular dysfunction, but after discharge from hospital the prognosis is good and right heart failure is unusual, even in those patients with shock during the first days of evolution of the infarct.

Humans↗
PubMed1997

Right ventricular dysfunction persists following brief right ventricular pressure overload.

OBJECTIVE: Acute pulmonary hypertension may cause right ventricular (RV) contractile failure. While it has been assumed that restoration of normal loading conditions after acute pulmonary hypertension is sufficient for complete recovery of RV function, this has not been rigorously examined. The purpose of this study was to test the hypothesis that acute RV pressure overload produces RV contractile dysfunction that persists following restoration of control loading conditions. METHODS: We subjected 18 autonomically-blocked, chloralose-anesthetized, open-chest pigs to 1 h of pulmonary artery constriction to increase RV systolic pressure from 35 +/- 1 to 55 +/- 1 mmHg, followed by 2 h of measurements after pulmonary artery constriction release. We determined regional RV free wall function from pressure-segment length loops and preload recruitable stroke work relations, and global RV function from stroke work vs. end-diastolic pressure relations. RESULTS: As expected, RV free wall systolic shortening diminished during pulmonary artery constriction, but the endo/epi blood flow ratio, lactate uptake, and coronary venous pH were not significantly changed. Following release of pulmonary artery constriction, RV systolic and diastolic pressure returned to control values. Nonetheless, contractile dysfunction persisted, with depressed RV free wall systolic shortening (70 +/- 22% of control), RV regional external work (59 +/- 11% of control at control end-diastolic length), and global RV stroke work (56 +/- 14% of control at control end-diastolic pressure). Depressed regional work was due to a parallel, rightward shift of the preload recruitable stroke work relation. Five pigs identically instrumented but not subjected to pulmonary artery constriction showed no significant over 3 h. CONCLUSIONS: Acute pulmonary hypertension causes RV contractile dysfunction that persists at least 2 h after restoration of control loading conditions. Contractile dysfunction is not attributable to RV ischemia during pressure overload.

Acute Disease↗
PubMed1984

Right ventricular dysfunction after endocardiectomy for right ventricular endomyocardial fibrosis.

Early right ventricular failure following a large endocardiectomy in right endomyocardial fibrosis (EMF) is reported. This diagnosis was confirmed upon echocardiography by the presence of a dilated right ventricle, and hemodynamically (upon postoperative control catheterization) by the presence of right ventricular diastolic dysfunction. The role of the endocardiectomy and of the pericardium in the genesis of this ventricular dysfunction are discussed in the light of this case which was documented by a hemodynamic study and surgically confirmed.

Adolescent↗
PubMed1991

Right atrial ischemia exacerbates hemodynamic compromise associated with experimental right ventricular dysfunction.

To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Influence of acute right ventricular dysfunction on cardiac tamponade.

Echocardiographic and hemodynamic data were measured in nine closed chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, 15 mm Hg) before and after production of diffuse acute ischemic right ventricular dysfunction. Right ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (mean diameter +/- SD 54 +/- 4 microns) and caused a significant increase in right atrial pressure (7.6 +/- 1.4 vs. 1.6 +/- 1 mm Hg, p less than 0.001) and cross-sectional areas of both the right atrium (8.3 +/- 0.3 vs. 5.6 +/- 0.2 cm2, p less than 0.001) and right ventricle (8.8 +/- 0.4 vs. 5.7 +/- 0.4 cm2, p less than 0.001). Right atrial and ventricular collapse required a significantly larger pericardial effusion and pericardial pressure after right ventricular infarction than before. Mean aortic pressure had fallen 1.9 +/- 2% and 6.5 +/- 6.9% at the time of right atrial collapse (p = NS before vs. after right ventricular dysfunction) and 3 +/- 4.1% and 20.1 +/- 20.8% at the time of right ventricular collapse (p less than 0.03) before and after right ventricular dysfunction, respectively. In the presence of ischemic right ventricular dysfunction, echocardiographic signs of cardiac tamponade are less sensitive and occur later in the hemodynamic progression of cardiac tamponade. Pulsus paradoxus with cardiac tamponade was not prevented by coexisting ischemic right ventricular dysfunction.

Animals↗
PubMed1987

Circulatory support for right ventricular dysfunction.

New modes of circulatory support for right ventricular dysfunction have recently been described. The present study compared the effectiveness of pulmonary artery balloon counterpulsation with a right ventricular assist device for support of surgically induced right ventricular dysfunction. Right ventricular hypertrophy was created in 16 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy and maintaining the pulmonary artery band. Four unassisted animals developed severe acute right heart failure and died. Six sheep had pulmonary artery balloon counterpulsation with a Dacron graft anastomosed to the proximal pulmonary artery as a reservoir for a 40 ml intra-aortic balloon after the onset of heart failure. The remaining six sheep had a pneumatically activated ventricular assist device inserted between the proximal pulmonary artery and the right ventricular apex. Periods of circulatory support with the balloon pump and the assist device on and off were compared. Decreases in right atrial pressure were observed with both balloon counterpulsation and right ventricular assistance: 14 +/- 1 to 11 +/- 1 mm Hg, p less than 0.0001, versus 19 +/- 2 to 12 +/- 2 mm Hg, p less than 0.0002, respectively. Cardiac output increased with both balloon counterpulsation and ventricular assistance: 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min, p less than 0.001, versus 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min, p less than 0.0002, respectively. Aortic systolic pressure increased in both support groups: 78 +/- 7 to 99 +/- 6 mm Hg, p less than 0.0004, versus 53 +/- 9 to 85 +/- 9 mm Hg, p less than 0.0001, respectively. Ventricular assistance produced greater changes in the right atrial pressure (39% +/- 6% versus 17% +/- 3%, p less than 0.01), cardiac output (153% +/- 39% versus 54% +/- 11%, p less than 0.05), and aortic systolic pressure (85% +/- 13% versus 39% +/- 9%, p less than 0.01). The insertion of a right ventricular assist device caused a significant increment in right ventricular dysfunction. These data, obtained with the devices in place but not operating, showed significantly increased right atrial and right ventricular end-diastolic pressures and approximately 50% less cardiac output than with the pulmonary artery balloon counterpulsation system. The results demonstrate that both modes of circulatory support were effective in reversing surgically induced right ventricular failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Conventional and right precordial ECGs, creatine kinase, and radionuclide angiography in post-traumatic ventricular dysfunction.

Right ventricular infarction due to ischemic heart disease can be diagnosed by a right precordial electrogram or by first-pass radionuclide angiography (FPRNA). Prior FPRNA studies have shown that cardiac dysfunction after blunt chest trauma (myocardial contusion) is most often due to right ventricular dysfunction. We hypothesized that right ventricular dysfunction due to ischemic heart disease and myocardial contusion should produce similar ECG changes due to myocyte disruption. The purpose of our study was to evaluate the diagnostic value of the right precordial electrogram in suspected cardiac contusion. Thirty-five patients with suspected myocardial contusion based on mechanism of injury/clinical findings and no history of clinical heart disease were enrolled prospectively. All patients had conventional ECG, right precordial electrogram, and FPRNA studies. Twenty patients had normal cardiac scans (group 1); percentage of myocardial creatine kinase (CK-MB) was measured in 12 of these patients and was less than 5% in 11. Fifteen patients had abnormal cardiac scans (wall motion abnormality and/or decreased right ventricular ejection fraction) (mean, 34% +/- 7% [SD]; normal, greater than 40%) (group 2); percentage of CK-MB was measured in 13 of 15 patients and was less than 5% in all 13. Conventional ECGs and right precordial electrograms in all patients were analyzed for differences in heart rate, PR interval, QRS duration, corrected QT interval, and the axis of the frontal and horizontal plane QRS complex and ST segment. There were no significant differences between group 1 and group 2 patients. No patient with myocardial contusion diagnosed by FPRNA had elevated ST segments in V4R through V6R or a percentage CK-MB of more than 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

Prediction of right ventricular dysfunction after left ventricular assist device implantation.

BACKGROUND: Right ventricular dysfunction (RVD) significantly affects mortality and morbidity after left ventricular assist device (LVAD) implantation, and its occurrence often is unpredictable. The aim of the present study was to identify predictors of RVD after LVAD implantation. METHODS AND RESULTS: We studied right ventricular (RV) hemodynamics in 28 patients before and after LVAD implantation with a rapid-response thermistor pulmonary artery catheter. Measurements included mean right atrial pressure (RAP), mean pulmonary arterial pressure (PAP), cardiac index, transpulmonary gradient (TPG), pulmonary vascular resistance (PVR), RV end-diastolic and end-systolic volume indexes (EDVI and ESVI, respectively), and RV ejection fraction (RVEF). We regarded patients who had RAP > or = 15 mm Hg at LVAD explantation (n = 8) or who required an RV assist device (n = 3) as the RVD group (n = 11). The other patients were categorized as the RV nondysfunctional group (RVN, n = 17). Before LVAD implantation, the RVD group had larger RV volumes (200 +/- 107 versus 125 +/- 46 mL/m2 for EDVI; 177 +/- 109 versus 104 +/- 48 mL/m2 for ESVI) and higher preload (23 +/- 6 versus 17 +/- 6 mm Hg for RAP) and afterload (20 +/- 9 versus 13 +/- 6 mm Hg for TPG; 5.9 +/- 3.0 versus 3.8 +/- 2.0 Wood units for PVR) than the RVN group (P < .05 for all). RVEF and PAP did not differ significantly. LVAD implantation remarkably improved RV hemodynamics in both groups, decreasing RV volumes, preload, and afterload and increasing RVEF in all patients, but post-LVAD PAP tended to be higher in the RVD group. Multivariate logistic regression analysis revealed that RAP and TPG before LVAD implantation and an acute decrease (delta) in PAP by LVAD were significant predictors of RVD (P < .05). The sensitivity for predicting RVD by a combination of at least two of these three predictors (RAP > or = 20 mm Hg, TPG > or = 16 mm Hg, and delta PAP < or = 10 mm Hg) was 82%, and the specificity was 88%. CONCLUSIONS: Dilated right ventricle with increased RV preload and afterload predisposes to RVD after LVAD implantation. Not only baseline parameters but also the immediate hemodynamic response to the LVAD are predictive, and a combination of these parameters may be useful in predictions of the occurrence of RVD after LVAD implantation.

Adult↗
PubMed1994

Right ventricular dysfunction after major pulmonary resection.

Right ventricular performance was assessed by thermodilution in 20 patients at rest and during exercise before and after lobectomy or pneumonectomy. The right ventricular ejection fraction was significantly decreased on the first postoperative day (0.36 +/- 0.34), the second postoperative day (0.34 +/- 0.04), and the third postoperative week (0.37 +/- 0.06) relative to the preoperative right ventricular ejection fraction value (0.43 +/- 0.07, p < 0.05). The right ventricular end-diastolic volume index was significantly increased by the second postoperative day (130 +/- 24 ml/m2) compared with the preoperative value (112 +/- 20 ml/m2). A significant decrease in the right ventricular stroke volume index was observed after operation, with a significant increase in heart rate considered necessary to maintain cardiac output. Pulmonary arterial pressure, the pulmonary vascular resistance index, and central venous pressure were unaltered over time. Indices of left ventricular function (that is, cardiac index, arterial pressure, and pulmonary arterial wedge pressure) were also preserved throughout the postoperative period. To explain the right ventricular dysfunction, ergometric exercise values were compared and the heart rate, pulmonary arterial pressure, central venous pressure, pulmonary vascular resistance index, and right ventricular end-diastolic volume index were all higher and the right ventricular ejection fraction lower during exercise after the operation. However, indices of left ventricular function remained unchanged. Significant elevations in pulmonary arterial pressure and the pulmonary vascular resistance index only during exercise occurred. These findings indicate that changes in right ventricular function at rest compensate for the increase in right ventricular volume, but adequate compensation does not occur during exercise, with a resultant increase in pulmonary arterial pressure and the pulmonary vascular resistance index. This suggests that a change in afterload may be the main determinant of the deterioration in right ventricular pump performance during exercise. We speculate that the main cause of right ventricular dysfunction after major pulmonary resection might be the changes in right ventricular afterload. The right ventricle may play an important role serving as a "reservoir" for afterload.

Aged↗