The effect of right ventricular dysfunction on left ventricular form and function.
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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.
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.
To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Right ventricular (RV) infarction is frequently associated with highest risk of death and major complications. Doppler echocardiography can be useful in the diagnosis of RV involvement. The goal of this study was to evaluate Doppler echocardiography features associated with RV involvement and a poor prognosis. METHODS: Two-dimensional Doppler echocardiography was performed before and after thrombolysis in 108 consecutive patients with an RV infarction. The bedside examination was performed before and 2 to 3 hours after thrombolytic therapy, and repeated after 1 and 7 days. All patients underwent coronary angiography after 20 days, and the perfusion of the coronary-related artery (> thrombolysis in myocardial infarction [TIMI] 3 grade) was evaluated. RESULTS: Patients were divided into 2 groups according to the recovery of global and regional RV function after thrombolytic therapy. In the group of patients who showed a normalization or improvement of RV wall motion (as assessed by RV wall motion score index), we found a TIMI grade III perfusion in 78% of patients. The analysis of interatrial septal motion and interventricular septal motion showed a normalization in all reperfused patients. Major complication and deaths were more frequent in patients with echocardiographic findings of RV dysfunction persisting after thrombolytic therapy. CONCLUSION: In patients with RV infarction treated with thrombolysis, persistent RV dysfunction is associated with a higher risk for the development of major cardiac complications and death.
The aim of this study was to test the hypothesis that Doppler study of hepatic venous flow, reflecting right atrial pressures and right ventricular dysfunction, allows prediction of increased right atrial pressure and right ventricular dysfunction in patients with right ventricular infarction. The authors studied 30 patients (27 men, mean age 54 +/- 12 years) in sinus rhythm with acute inferior myocardial infarction who underwent right heart catheterisation and Doppler echocardiography including recording of regurgitant and hepatic vein flow within 48 hours of hospital admission. Hepatic venous flow was used to measure peak velocity and velocity time integrals (VTI) of the systolic (S), diastolic (D) and atrial (a) contraction waves. The fraction of systolic filling was calculated: VTI S/VTI S + VTI D. The pressure half-time of pulmonary regurgitant flow (PHT IP) was also measured. Using haemodynamic criteria (non-compliant right atrial pressure wave form or right ventricular end diastolic pressure/pulmonary capillary pressure > or = 0.8), patients were divided into two groups: Group 1: right ventricular infarction (VD+, N = 22). Group 2: no right ventricular infarction (VD-, N = 8). No correlation was observed between Doppler parameters of hepatic venous flow and haemodynamic data, in particular right atrial pressure and pressure wave form. Moreover, no statistically significant difference was observed between the two groups with respect to the Doppler parameters derived from hepatic venous flow. On the other hand, the results confirmed good diagnostic performance of Doppler analysis of pulmonary regurgitant flow: sensitivity 80%, specificity 83%, positive predictive value 94%, negative predictive value 55%. The authors conclude that, in patients with acute inferior wall infarction, Doppler analysis of hepatic venous flow does not allow assessment of right atrial pressure or of ischaemic right ventricular dysfunction.
Acute right ventricular dysfunction has been established both as a diagnostic and prognostic indicator in pulmonary embolism. This report illustrates the utility of thallium-201 scintigraphy as an adjunctive noninvasive test in the diagnosis of pulmonary embolism by demonstrating increases in regional right ventricular perfusion and its subsequent resolution with treatment presumably as a result of decreased pressure work.
BACKGROUND: Cardiac amyloidosis is an infiltrative disease causing predominant diastolic dysfunction and systolic dysfunction at its advanced stage. Right ventricular (RV) dysfunction is an independent predictor of poor prognosis in congestive heart failure and cardiomyopathies. However, the assessment of RV function is still technically difficult because of the complicated geometry of the RV. The recently proposed Tei index, obtained from the cardiac time interval analysis, allows noninvasive and quantitative estimation of global ventricular function without geometric evaluation. Therefore, this study was designed to assess RV function for patients with cardiac amyloidosis. METHODS: Study patients consisted of 30 consecutive patients with biopsy specimen-proven cardiac amyloidosis and 50 control subjects. Patients were classified as having early or advanced stage of cardiac amyloidosis on the basis of mean left ventricular wall thickness < 15 mm or >/= 15 mm. Tei index, defined as the sum of isovolumetric contraction and relaxation time divided by ejection time, was obtained from tricuspid and pulmonary Doppler flow velocity. RESULTS: RV Tei index was significantly increased for patients with cardiac amyloidosis (0.54 +/- 0.16 vs 0.28 +/- 0.05, amyloidosis vs control, P <.001). The incidences of abnormal RV isovolumetric contraction time, ejection time, isovolumetric relaxation time, and Tei index in all patients with cardiac amyloidosis were 63%, 43%, 73%, and 83%, respectively. The same incidences were 50%, 13%, 63%, and 75% in the early stage and 68%, 54%, 77%, and 86% in the advanced stage, respectively. CONCLUSION: Patients with cardiac amyloidosis frequently have RV dysfunction even in its early stage. Tei index allows simple, noninvasive, and nongeometric estimation of RV dysfunction in patients with cardiac amyloidosis.
BACKGROUND: Although right ventricular assist device (RVAD) use has declined with the introduction of inhaled nitric oxide and phosphodiesterase inhibitors (type III), right ventricular dysfunction (RVD) is still a serious problem in patients receiving left ventricular assist devices (LVAD). METHODS: We retrospectively analyzed Thoratec Vented Electrical LVAD recipients between June 1996 and September 1999. RVD was defined as inotropic requirement 14 days or more or need for RVAD postoperatively, or both. RESULTS: Sixty-nine LVAD recipients were analyzed. Twenty-one patients (30.4%) had RVD, with 1 patient requiring RVAD insertion, and there were 48 non-RVD patients. There were no significant differences between both groups for age, sex, etiology of congestive heart failure, days of support, and preoperative hemodynamics. Preoperative right ventricle stroke work index (mm Hg x m(-2) x L(-1)) had a trend toward being lower in the RVD group (4.1+/-3.2 versus 6.1+/-3.7, p = 0.06). A higher preoperative total bilirubin (mg/dL) was noticed in the RVD group (4.0+/-5.2 versus 2.1+/-1.7). The RVD group had a higher postoperative creatinine (2.2+/-1.4 mg/dL versus 1.5+/-0.8 mg/dL), incidence of continuous venovenous hemofiltration dialysis (73% versus 26%), transfusion of packed red blood cells (43.2+/-28.6 units versus 24.7+/-18.9 units), platelets (58.6+/-46.1 units versus 30.2+/-20.4 units), with longer intensive care unit length of stay (33.6+/-34.7 days versus 9.1+/-6.9) and higher mortality (42.8% versus 14.5%). When deaths were excluded, both intensive care unit and postoperative length of stay were significantly longer in the RVD group. CONCLUSIONS: RVD in LVAD recipients remains poorly identified and is associated with a high transfusion rate and end organ failure that results in increased intensive care unit and hospital length of stay, and a high mortality rate. Preoperative identification of risk factors for RVD may select patients who would benefit from a biventricular assist device and prevent the subsequent end organ failure.
BACKGROUND: Little is known about exercise-induced electrocardiographic ST segment shift in right-sided precordial leads, especially elevated ST in patients with subacute inferior myocardial infarction. OBJECTIVE: To test the clinical significance of exercise-induced STV1 deviation with special regard to right ventricular function and right ventricular involvement. DESIGN: Sixty-eight patients with recent inferior myocardial infarction (without having a left descending arterial lesion) aged 30 to 73 years (mean +/- SD, 59.1 +/- 10.0) were investigated with respect to biventricular function observed in radionuclide ventriculography and treadmill stress electrocardiographic findings. RESULT: STV1 shift during exercise (delta STV1) had a negative linear logarithmic relationship only with the right ventricular ejection fraction (RVEF) and no correlation with the left ventricular ejection fraction (delta STV1 = 6.7604-1.7528xlnRVEF, r = 0.709, P = 0.0001). Significant STV1 elevation (delta STV1 of 0.5 mm or more) predicted right ventricular dysfunction (RVEF of 40% or less) and right ventricular infarction with sensitivities of 76% and 77%, specificities of 88% and 92%, and accuracies of 84% and 77%, respectively. Twenty patients with STV1 elevation (0.5 mm or more) showed nearly identical rest and exercise electrocardiographic findings, exercise capacities and similar stenotic lesions on coronary angiography, to 43 patients without significant STV1 elevation. Elective balloon angioplasty reduced the delta STV1 during exercise in only three of six patients (50%) with right ventricular infarction. CONCLUSION: Exercise-induced STV1 elevation may be a useful indicator of global right ventricular dysfunction and/or right ventricular infarction in the subacute phase of myocardial inferior infarction.
Little is known about the influence of right ventricular (RV) dysfunction on prognosis of patients with acute inferior myocardial infarction (IMI) and RV involvement. Therefore, 99 consecutive patients (mean age 56.6 +/- 3.4 years) with RV involvement during acute IMI were followed for a 12-month period to clarify the influence of acute RV dysfunction on short- and long-term survivals. Forty-one patients with IMI evolved with severe arterial hypotension due to RV dysfunction, while 58 patients had no hemodynamic impairment due to RV involvement. Basal hemodynamic data (mean +/- SD) for patients with RV dysfunction were blood pressure (BP) 92/59 +/- 22/20 mmHg, systemic vascular resistance (SVR) 2314 +/- 252 dynes.s.cm-5, and cardiac index (CI) 1.3 +/- 0.3 l/min/m2. Patients without RV dysfunction demonstrated BP 113/74 +/- 20/16 mmHg (p < or = 0.05), SVR 1324 +/- 354 dynes.s.cm-5 (p < or = 0.01), and CI 2.6 +/- 0.5 l/min/m2 (p < or = 0.05). Angiographic differences noted were that hemodynamically compromised patients showed lower RV ejection fractions (0.27 +/- 0.08) than patients without hemodynamic disturbance [0.41 +/- 0.11 (p < or = 0.05)]; however, left ventricular ejection fractions were 0.48 +/- 0.10 and 0.52 +/- 0.12, respectively. Short- and long-term mortality rates were assessed during the follow-up period. Patients with hemodynamic impairment due to RV infarction had a higher mortality rate for the first month and for 11 subsequent months post MI than patients without hemodynamic impairment, that is 24.4 vs. 6.9 and 14.6 (p <or = 0.05) vs. 3.4 (p < or = 0.05), respect ively.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Low output syndrome after cardiac operations is associated with high morbidity and mortality rates. The contribution of right ventricular dysfunction to this syndrome has not been fully characterized. The purpose of this study was to evaluate the utility of transesophageal echocardiography to identify the frequency and the in-hospital mortality from right ventricular dysfunction in patients with this syndrome. METHODS: Seventy-five consecutive patients undergoing transesophageal echocardiography for low output syndrome early after cardiac operations were evaluated. The findings from transesophageal echocardiography were correlated with the type of surgical procedure, cross-clamp time, right heart hemodynamics, and coronary angiography. RESULTS: Right ventricular systolic dysfunction occurred in 36 patients (42%); in 17 patients it was isolated and in 19 patients it occurred in combination with left ventricular dysfunction. Postoperative right ventricular dysfunction was not uniformly associated with important right coronary artery disease or with prolonged ischemic time during cardiopulmonary bypass. Hemodynamic data were not useful to distinguish the group with postoperative right ventricular dysfunction. Patients with right ventricular dysfunction had a high (44%) in-hospital mortality rate. CONCLUSIONS: Right ventricular dysfunction occurs frequently in patients with low output syndrome after cardiac operations and is associated with a high in-hospital mortality rate. Better understanding of the mechanisms causing postoperative right ventricular dysfunction may provide insight for preventing this complication.
Cardiotoxicity is one of the major side effects of doxorubicin therapy. The side effect presents in an acute and chronic form. It has been observed mainly when the cumulative dosage exceeds 450 mg/m2 of body surface. The cardiotoxicity presents with a low left ventricular ejection fraction. We report three patients who developed selective right ventricular dysfunction, expressed by low right ventricular ejection fraction as measured by radionuclide angiography. This complication was observed with rather low cumulative dosages of the drug (105 to 318 mg/m2). Two of the patients received concurrent mitomycin-C chemotherapy and the third patient underwent prior mediastinal irradiation. The possible mechanism for this selective cardiotoxicity is discussed. Monitoring of right ventricular performance by radionuclide angiography during doxorubicin therapy is recommended so that therapy can be discontinued before the left ventricle is damaged.
BACKGROUND: The involvement of the right ventricle (RV) in Chagas' disease is frequent. Although echocardiography plays an important role in noninvasive assessment of cardiac function, evaluation of RV is challenging because of the anatomic and functional complexity of this chamber. METHODS: To study early functional abnormalities in the RV, we selected 18 patients with Chagas' disease, no other disease, and a normal echocardiogram; and 12 normal individuals as a control group. All participants were submitted to Doppler tissue imaging and the parameters of systolic (systolic wave and regional isovolumic contraction time) and diastolic (early and late expansion waves) function were analyzed at the level of the interventricular septum and free wall of the RV. RESULTS: Regional isovolumic contraction time values showed a statistically significant difference between the 2 groups both in the RV free (P =.0003) and septal (P =.003) walls. With respect to diastolic function, we observed a significant difference between groups involving the early expansion wave (P =.014) and e/a ratio (P =.004) of the RV free wall. CONCLUSION: Doppler tissue imaging proved to be useful in early detection of RV dysfunction in Chagas' disease, with potential use in risk stratification of these patients.
BACKGROUND: Significant right ventricular (RV) dysfunction as measured by increased end-diastolic volume and reduced ejection fraction has been documented in the postoperative period after pulmonary resection. We hypothesized that changes in RV contractile state or afterload may contribute to this RV pump dysfunction. METHODS: In part one of the study, RV preload was altered on postoperative day 2 (n = 6) by rapid infusion of Hespan to a total of 250, 500, and 1,000 mL. The relationship between RV stroke work and end-diastolic volume was plotted using linear regression. This preload recruitable stroke work relation had been previously validated as a load-insensitive index of RV contractility. The slopes of the preoperative relation (n = 35) and postoperative relation were compared. In part two of the study, RV afterload was reduced by continuous infusion of prostaglandin E1 (n = 6) through postoperative day 2 and RV pump function was assessed. RESULTS: Comparison of the slopes of the preload recruitable stroke work relation plotted preoperatively and on postoperative day 2 revealed no significant difference, indicating no change in RV contractile state. Infusion of prostaglandin E1 in the postoperative period (n = 6) significantly reduced pulmonary vascular resistance (3.67 +/- 0.19 versus baseline 5.72 +/- 0.19 dyne . s . cm-5/ m2; p < 0.05). However, RV ejection fraction remained significantly reduced (0.34 +/- 0.01 versus baseline 0.42 +/- 0.01; p < 0.05) and end-diastolic volume significantly increased (105 +/- 5 versus baseline 93 +/- 2 mL/m2; p < 0.05). Heart rate was increased compared with baseline throughout the postoperative period. CONCLUSIONS: The present study suggests that RV dysfunction after pulmonary resection is not caused by primary alterations in contractility or immediate changes in afterload. Better control of heart rate with minimal effect on inotropy may enhance RV pump function.
BACKGROUND: The role of echocardiographic right ventricular (RV) dysfunction in predicting clinical outcome in clinically stable patients with pulmonary embolism (PE) is undefined. In this study, we assessed the prevalence and clinical outcome of normotensive patients with RV dysfunction among a broad spectrum of PE patients. METHODS AND RESULTS: This prospective clinical outcome study included cohort of 209 consecutive patients (age, 65+/-15 years) with documented PE. Acute RV dysfunction was diagnosed in the presence of >/=1 of the following: RV dilatation (without hypertrophy), paradox septal systolic motion, and Doppler evidence of pulmonary hypertension. Four groups were identified: 28 patients presenting with shock or cardiac arrest (13%), 19 hypotensive patients without shock (9%), 65 normotensive patients with echocardiographic RV dysfunction (31%), and 97 normotensive patients without RV dysfunction (47%). Among normotensive patients with RV dysfunction, 6 (10%) developed PE-related shock after admission: 3 of these patients died, and 3 were successfully treated with thrombolytic agents. In comparison, none of the 97 normotensive patients without RV dysfunction developed shock or died as a result of PE. CONCLUSIONS: A significant proportion (31%) of normotensive patients with acute PE presents with RV dysfunction; these patients with latent hemodynamic impairment have a 10% rate of PE-related shock and 5% in-hospital mortality and may require aggressive therapeutic strategies. Conversely, normotensive patients without echocardiographic RV dysfunction have a benign short-term prognosis. Thus, early detection of echocardiographic RV dysfunction is of major importance in the risk stratification of normotensive patients with acute PE.
OBJECTIVE: To study the effects of coronary artery occlusion on the pressure-volume relations of the right ventricle. DESIGN: Right ventricular pressure-volume cycles were studied using conductance catheters and micromanometers in 19 subjects undergoing coronary angioplasty in a tertiary referral cardiac centre. RESULTS: Catheter occlusions of either the left anterior descending coronary artery or the right coronary artery were associated with a decline in stroke work (mean change (SD): left-13.3 (15.8)%, p = 0.008; right -13.5(16.5)%, p = 0.04). Two patterns of change were evident: an upward shift usually associated with occlusion in the left coronary artery, and a rightward shift in the right coronary artery. In the former there was an increase in maximum ventricular volume (mean change: 3.0(2.7)%, p = 0.004) and in minimum ventricular volume (mean change: 2.3(2.7)%, p = 0.01) and a fall in peak pressure (mean change: -4.8 (5.1)%, p = 0.04). In the latter there was an increase in peak pressure (mean change 9.9(16.3)%, p = 0.04) and an increase in minimum ventricular volume (mean change 3.7(5.0)%, p = 0.02) leading to a fall in stroke volume (mean change -13.3(15.8)%, p = 0.008). CONCLUSIONS: Occlusion of the left anterior descending coronary artery or the right coronary artery is associated with a decline in right ventricular work. However, different patterns of change in indices of preload and afterload lead to different effects on overall right ventricular pump function.
BACKGROUND: Left ventricular dysfunction after resuscitation from cardiac arrest has been well described. Treatment with dobutamine improves post-resuscitation left ventricular function. Right ventricular function following resuscitation has not been investigated. The purposes of this study were to examine right ventricular function following resuscitation and determine whether dobutamine would improve post-resuscitation right ventricular function. METHODS AND RESULTS: Right ventricular function was measured in 28 swine (29+/-1 kg) before and after resuscitation from 15 min of untreated ventricular fibrillation. Twelve animals received dobutamine at 10 mcg/kg/min while 16 animals served as untreated controls. Among controls, right ventricular dysfunction post-resuscitation was demonstrated by a decrease in right ventricular ejection fraction and an increase in right ventricular end-diastolic pressure. Among animals treated with dobutamine, there was a significant improvement in right ventricular function post-resuscitation compared to untreated controls. CONCLUSIONS: This study establishes that right ventricular systolic and diastolic dysfunction does occur after prolonged cardiac arrest from ventricular fibrillation. Dobutamine can ameliorate post-resuscitation right ventricular dysfunction.