Pulmonary hypertension and right ventricular dysfunction after operations for congenital heart disease.
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Anesthesia, General↗
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[Successful repair of tetralogy of Fallot with severe right ventricular dysfunction using veno-arterial bypass in an adult].
A 35-year-old male with tetralogy of Fallot, who had undergone left Blalock-Taussig shunt at ten year old, developed severe dysfunction of right ventricle with decreased right ventricular ejection fraction of 25% and frequent premature ventricular contractions of right ventricular origin. Following intracardiac procedure, the venoarterial assist circulation was successfully employed for 9 hours, until his hemodynamic conditions were improved. This experience reemphasized the importance of right ventricular protection and mechanical circulatory assist in the surgical treatment of Fallot's tetralogy in older children and adults who developed severe right ventricular dysfunction as a natural history of this disease.
Adult↗
Right ventricular dysfunction and the exercise limitation of chronic obstructive pulmonary disease.
This study examined right ventricular function during exercise in patients with chronic obstructive pulmonary disease to answer the following questions: Is there a significant correlation between oxygen consumption at maximal exercise and exercise right ventricular ejection fraction? Does the right ventricular ejection fraction response to exercise correlate with exercise changes in pulmonary artery pressure, total pulmonary resistance or pulmonary vascular resistance? Which combinations of cardiac, ventilatory and blood gas variables are the best predictors of oxygen consumption at maximal exercise? Twenty-six patients with stable chronic obstructive pulmonary disease performed symptom-limited supine bicycle exercise with simultaneous hemodynamic and radionuclide ventriculographic measurements. The oxygen consumption at maximal exercise correlated with the exercise right ventricular ejection fraction (n = 21, r = 0.66; p less than 0.005), exercise stroke volume (r = 0.68; p less than 0.001), exercise cardiac output (r = 0.77; p less than 0.00005) and exercise ventilation (r = 0.85; p less than 0.00001). The change in right ventricular ejection fraction from rest to exercise correlated inversely with the change from rest to exercise in total pulmonary resistance (r = -0.51; p less than 0.05) but not with the change in mean pulmonary pressure (r = -0.37) or in pulmonary vascular resistance (r = 0.09). Multivariate analysis showed that the variables giving the highest combined correlation with oxygen consumption were ventilation and right ventricular ejection fraction (r = 0.95, adjusted r2 = 0.88). These results suggest that exercise oxygen consumption of patients with chronic obstructive pulmonary disease is related to right ventricular systolic function, exercise right ventricular dysfunction is related, in part, to abnormal exercise total pulmonary resistance, and exercise limitation in chronic obstructive pulmonary disease occurs as a result of the dynamic interaction between disordered right heart function and ventilation.
Adult↗
Right ventricular dysfunction in patients with septic shock.
Using a rapid computerized thermodilution method, we examined the evolution of right ventricular performance in 23 patients with septic shock. Nine survived the episode of septic shock. The other 14 patients died of refractory circulatory shock. Significant right ventricular systolic dysfunction, defined as decreased ejection fraction (-39%) and right ventricular dilation (+38%) was observed in all patients with septic shock. However, in the survivors, increased right ventricular preload may prevent hemodynamic evidence of right ventricular pump failure by utilizing the Frank-Starling mechanism to maintain stroke volume. Conversely, in the nonsurvivors, right ventricular dysfunction was more prononced two days after the onset of septic shock, leading to a fall in stroke. In the last patients, a decrease in contractility appears to be the major factor accounting for decreased right ventricular performance, as evidenced by the marked increase in end-systolic volume (+27%) without significant change in pulmonary artery pressure, during the later stage of septic shock. The observed right ventricular pump failure then appears associated with an alteration in diastolic mechanical properties of this ventricle, as suggested by a leftward displacement of the individual pressure-volume curves.
Adult↗
Importance of a non-dominant right coronary artery occlusion presenting as sudden cardiac death with prolonged right ventricular dysfunction and malignant arrhythmias.
We report a case of a patient who presented with sudden cardiac death secondary to a subtotal occlusion of a small non-dominant right coronary system. Catheterization several weeks following the initial episode revealed persistent severe right ventricular dysfunction with moderate hemodynamic compensation. Continued unstable arrhythmogenic potential at this point led to placement of an AICD device. The case highlights the potential hazard and often complacency involved in dealing with benign appearing lesions as this one.
Arrhythmias, Cardiac↗
Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate.
To test the hypothesis that right ventricular (RV) systolic dysfunction at the time of diagnosis of pulmonary embolism (PE) is a predictor of mortality rate, 126 consecutive patients with PE were examined with echocardiography Doppler (ED) on the day of diagnosis. RV function was assessed by evaluation of wall motion on a four-point scale. The material was divided into two groups: group A (n = 56) with normal or slightly reduced RV function and group B (n = 70) with moderately or severely reduced RV function. The overall mortality rate was 7.9% in the hospital and 15.1% within 1 year. Four deaths occurred in group A and 15 in group B (p = 0.04). All in-hospital deaths (n = 10) occurred in group B (p = 0.002). The variables associated with mortality rate were RV dysfunction and cancer (in-hospital, p = 0.002 and 0.004; 1 year, p = 0.04 and < 0.001, respectively). Nine (7.1%) deaths (all in-hospital) were caused by PE. Five of these patients had advanced-stage cancer. The in-hospital mortality rate in patients without cancer was 4%, all from PE and all in group B. In conclusion, RV dysfunction when diagnosis of PE is established is associated with mortality rate. A strategy for risk stratification of patients with PE with ED may be of clinical usefulness.
Aged↗
Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism.
This study analyzed the regional pattern of right ventricular (RV) dysfunction on transthoracic echocardiograms in patients with and without acute pulmonary embolism. Quantitative (centerline) and qualitative (wall motion score) analyses of segmental RV free wall motion were performed on a "training" cohort of 41 patients (group 1), including 14 patients with acute pulmonary embolism, 9 patients with primary pulmonary hypertension, and 18 normal subjects. Patients with acute pulmonary embolism had a distinct regional pattern of RV dysfunction, with akinesia of the mid-free wall (centerline excursion: -0.2 +/- 0.8 mm, p = 0.0001 vs normal) but normal motion at the apex (centerline excursion: 5.7 +/- 0.8 mm, p = NS vs normal). In contrast, patients with primary pulmonary hypertension had abnormal wall motion in all regions (p <0.03 vs normal). This echocardiographic finding of normal wall motion at the apex and abnormal wall motion in the mid-free wall in acute pulmonary embolism was then tested in a "validation" cohort of 85 patients (group 2), consisting of hospitalized patients with RV dysfunction from any cause, including 13 patients with acute pulmonary embolism. The finding had a 77% sensitivity and a 94% specificity for the diagnosis of acute pulmonary embolism, with a positive predictive value of 71% and a negative predictive value of 96%. Thus, a distinct echocardiographic pattern of regional RV dysfunction, in which the apex is spared occurs in acute pulmonary embolism. This finding should raise the level of clinical suspicion for the diagnosis of acute pulmonary embolism.
Acute Disease↗
Severe right ventricular dysfunction following pericardiocentesis for cardiac tamponade.
The accumulation of fluid in the pericardium in an amount sufficient to cause severe obstruction to blood inflow to the ventricles results in cardiac tamponade. In this condition, relief of intrapericardial pressure by pericardiocentesis usually dramatically improves cardiac output, and can be lifesaving. We report a case of a patient with malignant cardiac tamponade in which cardiogenic shock developed after pericardiocentesis due to severe right ventricular dysfunction.
Adenocarcinoma↗
Treatment of right ventricular dysfunction in acute respiratory failure.
The pathophysiology and managements of right ventricular (RV) dysfunction in acute respiratory failure (ARF) is complicated. Results presented in this paper indicate that volume expansion may not be appropriate therapy to maintain or increase cardiac output (CO) when flow is reduced because of increased RV afterload. Volume will increase RV wall stress and O2 requirements so that despite increased preload, CO may fall. If RV afterload is significantly increased, such changes can occur despite a relatively normal RV end-diastolic pressure (RVEDP). Further, increased RV afterload and/or volume expansion can result in increased RV volumes and secondary alteration in left ventricular (LV) diastolic mechanics. Such changes, especially if wedge pressure increases, would tend to increase pulmonary edema. Also, because of potential changes in viscosity and pulmonary vascular resistance (PVR), packed red blood cells may not be indicated to increase CO, arterial O2 content and tissue O2 delivery in the setting of ARF. Therapy designed to reduce PVR may be appropriate to increase flow in the setting of increased RV afterload. However, such therapy may also reduce systemic vascular resistance, blood pressure (BP) and RV perfusion pressure. Such changes could lead to RV ischemia and reduced CO. Alternatively, agents which increased RV perfusion and/or contractility will increase CO by reducing RV end-diastolic and end-systolic volumes and may be the treatment of choice to increase flow when RV afterload is elevated.
Aged↗
Right ventricular dysfunction in septic patients.
OBJECTIVE: To compare right ventricular ejection fraction in trauma and septic patients during the hyperdynamic circulatory phase of these states. DESIGN: Prospective, consecutive study. SETTING: University hospital ICU. PATIENTS: Eleven trauma patients (group 1) and ten septic patients (group 2) were studied. Patients with circulatory shock were excluded from the study. INTERVENTIONS: Right ventricular ejection fraction was measured with a modified pulmonary artery catheter using the thermodilution method. Patients requiring catecholamines to maintain a systolic BP greater than 90 mm Hg were excluded from the study. MEASUREMENTS AND MAIN RESULTS: Both groups 1 and 2 had high mean cardiac output values (cardiac indices 4.7 +/- 0.9 [SD] and 4.6 +/- 1.4 L/min/m2, respectively). Right ventricular ejection fraction was significantly (p less than .005) reduced in septic patients (47 +/- 7.0% vs. 36 +/- 9.7%; group 1 vs. group 2) and end-diastolic volume index was significantly (p less than .01) increased (101 +/- 34 vs. 122 +/- 40 mL/m2; group 1 vs. group 2) in comparison with the trauma patients. However, there were no significant differences in afterload between the two groups. CONCLUSIONS: Hemodynamic measurements comparing septic and trauma patients showed increased cardiac output in both groups and no differences in the pulmonary resistance. Right ventricular ejection fraction in the septic patients was significantly reduced compared with the trauma patients. Therefore, we concluded that right ventricular contractility may be decreased in septic patients.
Adult↗
Prevalence and extent of right ventricular dysfunction after myocardial infarction--relation to location and extent of infarction and left ventricular function.
In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Scintigraphically detected predominant right ventricular dysfunction in acute myocardial infarction: clinical and hemodynamic correlates and implications for therapy and prognosis.
To determine the clinical and hemodynamic correlates as well as therapeutic and prognostic implications of predominant right ventricular dysfunction complicating acute myocardial infarction, 43 consecutive patients with scintigraphic evidence of right ventricular dyssynergy and a depressed right ventricular ejection fraction (less than 0.39) in association with normal or near normal left ventricular ejection fraction (greater than or equal to 0.45) were prospectively evaluated. All 43 patients had acute inferior infarction, forming 40% of patients with acute inferior infarction, and only eight (24%) had elevated jugular venous pressure on admission. On hemodynamic monitoring, 74% of patients had a depressed cardiac index (less than or equal to 2.5 liters/min per m2), averaging 2.0 +/- 0.05 for the group. Of these, 30% did not demonstrate previously described hemodynamic criteria of predominant right ventricular infarction (right atrial pressure greater than or equal to 10 mm Hg or right atrial to pulmonary capillary wedge pressure ratio greater than or equal to 0.8, or both). The left ventricular end-diastolic volume was reduced to 49 +/- 11 ml/m2 (n = 22) and correlated significantly with the stroke volume index (r = 0.82; p less than 0.0001) and cardiac index (r = 0.57; p = 0.005). The follow-up right ventricular ejection fraction, determined in 33 patients, showed an increase of 10% or greater in 26 (79%), increasing from a mean value of 0.30 +/- 0.06 to 0.40 +/- 0.09 (p less than 0.0001) without a significant overall change in the mean left ventricular ejection fraction (0.56 +/- 0.10 to 0.56 +/- 0.11, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension.
OBJECTIVES: This study sought to investigate the influence of right ventricular (RV) hemodynamic variables and function on the secretion of brain natriuretic peptide (BNP) in patients with isolated RV overload. BACKGROUND: Plasma BNP is known to increase in proportion to the degree of left ventricular (LV) overload. However, whether BNP secretion is also regulated in the presence of RV overload remains unknown. METHODS: Plasma BNP and atrial natriuretic peptide (ANP) levels in the pulmonary artery were measured in 44 patients with RV overload: 18 with RV volume overload (RVVO) due to atrial septal defect and 26 with RV pressure overload (RVPO) due to primary or thromboembolic pulmonary hypertension. Right heart catheterization was performed in all patients. RV and LV ejection fraction, myocardial mass and volume of the four chambers were determined by using electron beam computed tomography. RESULTS: Although both plasma BNP and ANP levels were significantly elevated in patients with RV overload compared with values in control subjects, plasma BNP and the BNP/ANP ratio were significantly higher in patients with RVPO than with RVVO (BNP 294 +/- 72 vs. 48 +/- 14 pg/ml; BNP/ANP 1.6 +/- 0.2 vs. 0.8 +/- 0.2, both p < 0.05). Plasma BNP correlated positively with mean pulmonary artery pressure (r = 0.73), total pulmonary resistance (r = 0.79), mean right atrial pressure (r = 0.79), RV end-diastolic pressure (r = 0.76) and RV myocardial mass (r = 0.71); it correlated negatively with cardiac output (r = -0.33) and RV ejection fraction (r = -0.71). Plasma BNP significantly decreased from 315 +/- 120 to 144 +/- 54 pg/ml with long-term vasodilator therapy (total pulmonary resistance decreased from 23 +/- 4 to 15 +/- 3 Wood U). CONCLUSIONS: Plasma BNP increases in proportion to the extent of RV dysfunction in pulmonary hypertension.
Adult↗
Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.
To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Right ventricular dysfunction in acute inferoposterior myocardial infarction. An echocardiographic and isotopic study.
We analyzed right ventricular (RV) regional wall motion by two-dimensional echocardiographic (2D echo) and multigated acquisition radionuclear (MUGA) studies in 104 patients with acute inferoposterior myocardial infarction (AIPMI). Sixty-eight patients (65 percent) had 2D echo RV regional wall motion abnormalities (RV dysfunction(RVD) group) while 36 patients showed no 2-D echo RV regional wall motion abnormalities (no-RVD group). The RVD group had a higher incidence of jugular venous engorgement (p less than 0.05), Kusmaul's sign, (p less than 0.05) complete atrio-ventricular block (p less than 0.05), and in-hospital death (p less than 0.02). The RVD group had significantly higher 2-D echo RV end-systolic dimensions (p less than 0.005) and lower values of percentage of fractional shortening (%FS) (p less than 0.005) in the long and short axis of the RV four-chamber view than patients in the no-RVD group and a control group of 20 patients with normal hearts. There was no statistical significant difference in the 2-D echo RV end-diastolic dimensions among the three groups. Patients in the RVD group had a lower MUGA derived RV ejection fraction (EF) than patients in the no-RVD and control groups (26.5 +/- 13.2 vs. 46.3 +/- 7 and vs. 50.6 +/- 4, respectively; p less than 0.05). RVD was diagnosed by both 2-D echo and MUGA in 60 of 104 patients (57.7 percent) with a sensitivity for 2-D echo of 92 percent and 79 percent specificity (when compared to the MUGA study). The predictive value for a positive test was 88 percent and for a negative test 86 percent. The accuracy was 87.5 percent. Recognition of regional wall motion abnormalities by 2-D echo permits a prompt and accurate bedside identification of right ventricular dysfunction (RVD) within the first 72 hours of clinical onset. An enlarged RV 2D echo end-diastolic dimension was not a sensitive parameter for the diagnosis of this pathology, whereas an increased end-systolic RV diameter and decreased RV %FS were better indicators of RV dysfunction in patients with acute inferoposterior wall myocardial infarction.
Aged↗
The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension.
OBJECTIVE: Studies on the effects of digoxin in patients with right ventricular failure and normal left ventricular function have not been performed. We evaluated the short-term effects of digoxin administration in patients with primary pulmonary hypertension on hemodynamics, neurohormones, and baroreceptor responsiveness. DESIGN: This was a prospective study with patients serving as their own controls. SETTING: University Hospital Intensive Care Unit with central monitoring. PATIENTS: Seventeen patients with primary pulmonary hypertension and symptomatic heart failure were enrolled. INTERVENTIONS: Following baseline hemodynamics, neurohormonal samples were drawn and the heart rate response to change in blood pressure following a challenge of phenylephrine and nitroprusside were recorded. One mg of intravenous digoxin was given and the measurements repeated after 2 hours. RESULTS: Following digoxin there was a significant increase in cardiac output (3.49+/-1.2 to 3.81+/-1.2 L/min., p=0.028), a significant fall in norepinephrine (680+/-89 to 580+/-85 pg/ml, p=.013), and a significant increase in atrial natriuretic peptide (311+/-44 to 421+/-9 pg/ml, p=0.01). All of the patients had changes in heart rate and blood pressure following phenylephrine and nitroprusside challenge, but there was no significant difference in the change in heart rate response to change in blood pressure when rechallenged after digoxin treatment. CONCLUSION: Digoxin produces a modest increase in cardiac output in patients with pulmonary hypertension and right ventricular failure, as well as a significant reduction in circulating norepinephrine. No detectable effects of digoxin on baroreceptor responsiveness were apparent. The use of digoxin in pulmonary hypertension is warranted.
Adult↗
Right ventricular dysfunction detected by gated scintiphotography in patients with acute inferior myocardial infarction.
Twenty-seven patients with acute myocardial infarction not complicated by cardiogenic shock and ten normal volunteers were studied with gated cardiac blood pool scans. The ratio right vetricular area/left ventricular area (RVA/LVA) determined from the left anterior oblique end-diastolic scans was examined. The ratio was 1.11 +/- .06 in the normal volunteers. In patients with anterior infarction the ratio fell to 0.75 +/- .12 (P less than .05) due to left ventricular enlargement. In those with inferior infarction the ratio was 1.12 +/- .23 which was greater than in those with anterior infarction (P less than .05) due to enlargement of both the left and right ventricles. Six patients with cardiogenic shock, three with inferior and three with anterior infarction were studied. The three with anterior infarction had left ventricular enlargement and a decrease in the ratio of RVA/LVA to 0.62 while the three with inferior infarction had an increase in the ratio to 2.05 suggesting right ventricular dilatation and dysfunction. These studies suggest a high incidence of right ventricular dysfunction in patients with inferior myocardial infarction.
Aged↗
Right ventricular dysfunction in acute thermal injury.
The elevated cardiac output (CO) and pulmonary artery hypertension (PAH) observed in thermal injury offers a unique opportunity to study the effects of a combined pressure-flow load on the right ventricle in previously healthy persons. Potential responses include a diminished right ventricular ejection fraction (RVEF), increased right ventricular end-diastolic volume index (RVEDVI), and augmented myocardial oxygen consumption because of increased systolic wall tension. We investigated these factors in 15 nonhypoxic patients without sepsis having 15--75% body surface area burns using flow directed catheters and the thermodilution technique. All patients increased their CO in response in fluid resuscitation, but six patients with an elevated mean pulmonary artery pressure (greater than 20 mmHG and increased pulmonary vascular resistance (greater than 1.2 mmHg/min/L) had right ventricular dysfunction as evidenced by an increase (188 +/- 15 ml/M2) in RVEDVI and a decreased (0.26 +/- 4 ml/M2) RVEF. Patients without PAH had a smaller RVEDVI (115 +/- 4 ML/M2) and larger RVEF (0.39 +/- 0.02). Patients with PAH and RV dysfunction were older, had larger body surface area burns, lower systemic diastolic artery pressures (63 +/- 4 mmHg) and higher heart rates (114 +/- 7 beats/min); RV end-diastolic pressures were minimally elevated (9.5 +/- 1.4 mmHg). The decrease in RVEF and increase in RVEDVI may limit the hemodynamic response to fluid volume replacement and survival.
Acute Disease↗