Right Ventricular Peak Systolic Pressure Research Articles

Determination of Timing for Reoperation in Patients After Right Ventricular Outflow Reconstruction

After right ventricular (RV) outflow reconstruction, patients often develop postoperative outflow tract stenosis or pulmonary regurgitation, or both. The aim of this study was to assess the relation between RV hypertrophy, volume, pressure, and function and to provide indications for repeat surgery. We performed magnetic resonance imaging to measure RV volume, wall mass, and the ratio of mass to volume in 31 patients after RV outflow reconstruction and in 12 controls. Patients were divided into 2 groups, New York Heart Association class I and the repeat surgery group. The RV stress index was defined as RV peak systolic pressure/(mass to volume); RV ejection fraction (EF) was calculated by ventriculography. The RV stress index for the repeat surgery group was significantly higher than for the remaining groups (p <0.01). In the New York Heart Association class I and control groups, a significant inverse correlation was observed between RVEF and the RV stress index (r = -0.59, p <0.01). All patients in reoperation group whose RVEF decreased to <95% confidence limit of regression had symptoms of RV failure. The RV stress index decreased substantially after reoperation, but RVEF remained at <95% limits. These findings suggest that excess RV wall stress contributes to impaired RV performance. The RV stress-RVEF relation may be useful in assessing RV function and in establishing a surgical indication.

Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload.

Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.

Intraaortic Balloon Counterpulsation Improves Right Ventricular Failure Resulting From Pressure Overload

Background. Right ventricular (RV) dysfunction is common after heart transplantation, and myocardial ischemia is considered to be a significant contributor. We studied whether intraaortic balloon counterpulsation would improve cardiac function using a model of acute RV pressure overload. Methods. In 10 anesthetized sheep, RV failure was induced using a pulmonary artery constrictor. Baseline measurements included mean systemic blood pressure, RV peak systolic pressure, cardiac index, and RV ejection fraction. Myocardial and organ perfusion were measured using radioactive microspheres. Results. After pulmonary artery constriction, there was an increase in RV peak systolic pressure (32 ± 2 to 60 ± 3 mm Hg; p < 0.01) and a decrease in mean systemic blood pressure (68 ± 4 to 49 ± 2 mm Hg; p < 0.01), RV ejection fraction (0.51 ± 0.04 to 0.16 ± 0.02; p < 0.01), and cardiac index (2.48 ± 0.04 to 1.02 ± 0.11; p < 0.01). Blood flow to the RV did not change significantly, but there was a significant reduction in blood flow to the left ventricle. The initiation of intraaortic balloon counterpulsation (1:1) using a 40-mL intraaortic balloon inserted through the left femoral artery resulted in an increase in mean systemic blood pressure (49 ± 2 to 61 ± 3 mm Hg; p < 0.01), cardiac index (1.02 ± 0.11 to 1.45 ± 0.14; p < 0.05), RV ejection fraction (0.16 ± 0.02 to 0.23 ± 0.02; p < 0.01), and blood flow to the left ventricle. Conclusions. In a model of right heart failure, the institution of intraaortic balloon counterpulsation caused a significant improvement in cardiac function. Although RV ischemia was not demonstrated, the augmentation of left coronary artery blood flow by intraaortic balloon counterpulsation and subsequent improvement in left ventricular function suggest that left ventricular ischemia contributes to RV dysfunction, presumably through a ventricular interdependence mechanism. Therefore, study of the safety and efficacy of intraaortic balloon counterpulsation in the management of patients with acute right heart dysfunction is warranted.

Direct Effects of Halothane and Isoflurane in Infant Rabbit Hearts with Right Ventricular Hypertrophy Secondary to Chronic Hypoxemia

In this study we compared the direct myocardial effects of halothane and isoflurane between chronically hypoxemic and normoxemic infant hearts with an isolated, perfused, nonworking rabbit heart model.Anesthetic effects were measured on heart rate, atrioventricular time, coronary flow, O2 consumption and extraction, and left and right ventricular peak systolic and end-diastolic pressures, + and -dP/dtmax; and tau, the time constant of isovolumic relaxation. Control values were similar between chronically hypoxemic and normoxemic groups except for variables affected by right ventricular (RV) hypertrophy in chronically hypoxemic hearts. For these variables values were significantly larger in the chronically hypoxemic group (P <or=to 0.05): coronary flow (12.3 +/- 0.4 vs 10.3 +/- 0.3 mL centered dot min-1 centered dot g-1), RV peak systolic pressure (68 +/- 3 vs 53 +/- 4 mm Hg), RV + dP/dtmax (1.42 +/- 0.07 vs 1.03 +/- 0.08 mm Hg/ms), and RV - dP/dtmax (-0.99 +/- 0.04 vs -0.78 +/- 0.08 mm Hg/ms). (Values are mean +/- SEM.) With anesthesia, values were similar between chronically hypoxemic and normoxemic groups except for coronary flow, which was significantly greater in chronically hypoxemic hearts for both anesthetics (14.1 +/- 0.9 vs 11.3 +/- 0.7 mL centered dot min-1 centered dot g-1 for halothane and 15.4 +/- 1.1 vs 12.2 +/- 0.6 mL centered dot min-1 centered dot g-1 for isoflurane). The degree of depression of RV peak systolic pressure and RV + dP/dt (max) by both anesthetics, and of RV -dP/dtmax by isoflurane, was significantly larger in chronically hypoxemic hearts because these hearts had greater control values but similar anesthetic values to normoxemic hearts. In this model, indices of myocardial function when the hearts were exposed to halothane and isoflurane were similar between chronically hypoxemic and normoxemic hearts except for coronary flow, which was greater in the chronically hypoxemic hearts. (Anesth Analg 1995;80:1122-8)

Role of sex hormones in development of chronic mountain sickness in rats.

After chronic exposure to hypoxia, Hilltop Sprague-Dawley rats developed excessive polycythemia and severe pulmonary hypertension and right ventricular (RV) hypertrophy, signs consistent with human chronic mountain sickness; however, there were gender differences in the magnitude of the polycythemia and susceptibility to the fatal consequence of chronic mountain sickness. Orchiectomy and ovariectomy were performed to evaluate the role of sex hormones in the gender differences in these hypoxic responses. After 40 days of exposure to simulated high altitude (5,500 m; barometric pressure of 370 Torr and inspired Po2 of 73 Torr), both sham-gonadectomized male and female rats developed polycythemia and had increased RV peak systolic pressure and RV hypertrophy. The hematocrit was slightly but significantly higher in males than in females. Orchiectomy did not affect these hypoxic responses, although total ventricular weight was less in the castrated high-altitude rats. At high altitude, the mortality rates were 67% in the sham-operated male rats and 50% in the castrated animals. In contrast, ovariectomy aggravated the high-altitude-associated polycythemia and increased RV peak systolic pressure and RV weight compared with the sham-operated high-altitude female rats. Both sham-operated control and ovariectomized females suffered negligible mortality at high altitude. The present study demonstrated that 1) the male sex hormones play no role in the development of the excessive polycythemia, pulmonary hypertension, and RV hypertrophy during chronic hypoxic exposure or in the associated high mortality and 2) the female sex hormones suppressed both the polycythemic and cardiopulmonary responses in vivo during chronic hypoxic exposure.

Exogenous erythropoietin fails to augment hypoxic pulmonary hypertension in rats

In two rat strains (H and M) with differing susceptibilities to chronic hypoxia we examined the role of polycythemia in the differing hypoxic pulmonary hemodynamic responses. We hypothesized that augmentation of hematocrit (Hct) during hypoxia in the resistant M strain would render cardiopulmonary responses similar to those obtained in the susceptible H strain. Administration of human recombinant erythropoietin (EPO) in doses of 100, 250 and 500 U·kg −1 s.c. thrice weekly for three weeks raised Hct similarly in both strains indicating that normoxic rats had similar sensitivities to EPO. In rats exposed to hypobaric hypoxia (0.5 atm) for 21 days, EPO (500 U·kg −1 thrice weekly) significantly increased Hct and whole blood viscosity as expected. Surprisingly, right ventricular (RV) to body weight (BW) ratio as an index of righ ventricular hypertrophy (RVH) and RV peak systolic pressure did not increase in EPO-injected rats of either strain compared to hypoxic controls. Among hypoxic animals, Hct correlated highly with viscosity but not with RV/BW. We conclude, contrary to our hypothesis, that polycythemia does not appear to be responsible for the strain difference in RVH and pulmonary hypertension.

Estimation of right ventricular pressure in children by thallium-201 myocardial imaging using single-photon emission computed tomography

Thallium-201 myocardial imaging using single-photon emission computed tomography was performed to estimate right ventricular (RV) systolic pressure in 34 children (aged 4.1 to 16.1 years, mean 7.9 ± 2.9). Acquisition of the images was performed using a semicircular arc of 180 °. On a short-axis slice, a line drawn perpendicular to the ventricular septum so as to cross the RV free wall showing maximum uptake was defined as the region of interest. Thallium-201 counts in regions of interest over both RV and left ventricular (LV) free walls were measured. The ratio of RV-to-LV peak thallium-201 counts was compared with RV peak systolic pressure and the ratio of RV-to-LV peak systolic pressure measured at cardiac catheterization. Both RV peak systolic pressure and the ratio of RV-to-LV peak systolic pressure correlated well with the ratio of RV-to-LV peak thallium-201 counts (r = 0.95 and 0.96, respectively). The ratio of RV-to-LV peak thallium-201 counts ≥ 0.45 could predict RV pressure overloading with a sensitivity of 92%, and a specificity of 88%. Thus, the quantitative analysis of thallium-201 myocardial imaging using single-photon emission computed tomography permits the noninvasive and accurate estimation of RV systolic pressure in children.

Supplemental oxygen reduces right ventricular hypertrophy in monocrotaline-injected rats

We evaluated the possible contributory role of hypoxia in the development of monocrotaline-induced pulmonary hypertension. Male Sprague-Dawley rats were injected subcutaneously with monocrotaline (60 mg/kg) or saline in controls and were kept in oxygen-enriched (inspired O2 fraction of 0.35) or compressed air chambers. After 21 days, rats were anesthetized while spontaneously breathing room air, hemodynamic parameters and arterial blood gases were measured, and animals were killed. Right ventricular peak systolic pressures (RVPP), right ventricular-to-left ventricular plus septal weight ratios (RV/LV + S), hematocrits, lung dry weight-to-body weight ratios, and medial thickness of pulmonary arteries were significantly reduced in monocrotaline-injected rats exposed to mild hyperoxia compared with air. The air-exposed monocrotaline-injected rats had significantly more arterial hypoxemia than the other groups, and mild hyperoxia had no effect on any of the measured variables in saline-injected rats. To determine whether the effects of mild hyperoxia occurred early or late after monocrotaline injection, we moved separate groups of rats from air to mild hyperoxia and vice versa 10 days after monocrotaline injection. After 21 days, significant reductions in RVPP and RV/LV + S occurred only in rats exposed to mild hyperoxia during the latter 11 days after injection. Our findings suggest that hypoxia contributes to the development of pulmonary hypertension relatively late after monocrotaline injection in rats but that it does not influence the early injury.

Right ventricular hypertrophy long after reversal of severe pressure overload in cats

To test the hypothesis that alterations in ventricular size and function may persist long after reversal of a severe pressure overload, right ventricular (RV) hypertrophy was produced in cats by abrupt, severe constriction of the pulmonary artery (PA) for 8 wk, after which pressure overload was completely reversed by surgical removal of the PA band (group III). Despite debanding and recovery from pressure overload (RV peak systolic pressure = 22 +/- 4 vs. 66 +/- 20 mmHg before debanding and 25 +/- 4 mmHg in controls), parameters of hypertrophy 8-10 mo later remained substantially increased: e.g., RV/LV (left ventricular) mass ratio was 0.36 +/- 0.06 in group III vs. 0.24 +/- 0.03 in controls (group I) and 0.43 +/- 0.07 in a separate cohort (group II) studied after 8 wk of banding. Maximum RV stroke work during volume loading was computed from RV micromanometry and PA electromagnetic flow: 20 +/- 8 g-cm/g for group III vs. 51 +/- 14 for group I, P less than 0.05, and 21 +/- 7 for group II. Thus severe pressure overload of the RV may produce changes in size and function that are not fully reversed by complete removal of the overload.

The Effect of Incremental Positive End-Expiratory Pressure on Right Ventricular Hemodynamics and Ejection Fraction

The effects of incremental positive end-expiratory pressure (PEEP) on right ventricular (RV) function were evaluated in 36 (n = 36) ventilated patients. Positive end-expiratory pressure was increased from 0 (baseline) to 20 cm H2O in 5-cm H2O increments and RV hemodynamics and thermally derived right ventricular ejection fraction (RVEF), right ventricular end-diastolic volume index (RVEDVI), and right ventricular end-systolic volume index (RVESVI) were computed. Right ventricular contractility was determined from the analysis of RV systolic pressure-volume relations. Right ventricular ejection fraction declined from 42 +/- 8% at baseline to 30 +/- 9% at 20 cm H2O PEEP. Right ventricular end-diastolic volume index declined between 0 and 5 cm H2O PEEP (103 +/- 42 to 92 +/- 34 ml.m-2) and then increased to 113 +/- 40 at 20 cm H2O PEEP. Right ventricular end-systolic volume index increased from 60 +/- 31 ml.m-2 at baseline to 79 +/- 34 ml.m-2 at 20 cm H2O PEEP. The slope (E) of the relation of RV peak systolic pressure to RV end-systolic volume index decreased from 0.26 mm Hg.m2.ml-1 between PEEP of 0-15 cm H2O to 0.05 mm Hg.m2.m-1 at PEEP greater than 15 cm H2O. It is concluded that low levels of PEEP have a predominant preload reducing effect on the RV. Above 15 cm H2O PEEP, RV volumes increase and E decreases, consistent with increased RV afterload and a decline in RV contractility.

Time course of cardiopulmonary responses to high altitude in susceptible and resistant rat strains

We have identified two strains (H and M) of Sprague-Dawley rat with distinctly different susceptibilities and cardiopulmonary responses to hypoxia. In this study, we studied the development of cardiopulmonary and hematolgoical responses to hypoxia and the post-hypoxic regression of these responses in the two strains over time. Under sea level conditions, there were no differences between the two strains. On exposure to hypobaric hypoxia (0.5 atm), right ventricular peak systolic pressure (RVPP) and right ventricular hypertrophy (RVH) increased more rapidly in the susceptible (H) than in the resistant (M) strain. In contrast, post-hypoxic reversal of these changes occurred at comparable rates. Hematocrits rose at similar rates in the two strains until after two weeks, when that of the H strain slightly exceeded that of the M strain. With the progression of RVH, left ventricular plus septal to body weight ratio (LV + S) g/100 g bw decreased in M rats but increased in the H rats. As a result, a conspicuous overall cardiac hypertrophy developed in the H rats but only a minimal cardiac hypertrophy occured in the M strain. The data show that susceptibility to hypoxia in H rats is associated with more rapid development of RV systolic hypertension and biventricular hypertrophy than in M rats. The mechanism for the accelerated cardiopulmonary responses in the H rats most likely involves greater hypoxic pulmonary vasoconstriction or pulmonary vascular remodelling. Differences in hematocrit between the strains do not contribute to the early cardiopulmonary responses.

Time course of cardiopulmonary responses to high altitude in susceptible and resistant rat strains

We have identified two strains (H and M) of Sprague-Dawley rat with distinctly different susceptibilities and cardiopulmonary responses to hypoxia. In this study, we studied the development of cardiopulmonary and hematological responses to hypoxia and the post-hypoxic regression of these responses in the two strains over time. Under sea level conditions, there were no differences between the two strains. On exposure to hypobaric hypoxia (0.5 atm), right ventricular peak systolic pressure (RVPP) and right ventricular hypertrophy (RVH) increased more rapidly in the susceptible (H) than in the resistant (M) strain. In contrast, post-hypoxic reversal of these changes occurred at comparable rates. Hematocrits rose at similar rates in the two strains until after two weeks, when that of the H strain slightly exceeded that of the M strain. With the progression of RVH, left ventricular plus septal to body weight ratio (LV + S) g/100 g bw decreased in M rats but increased in the H rats. As a result, a conspicuous overall cardiac hypertrophy developed in the H rats but only a minimal cardiac hypertrophy occurred in the M strain. The data show that susceptibility to hypoxia in H rats is associated with more rapid development of RV systolic hypertension and biventricular hypertrophy than in M rats. The mechanism for the accelerated cardiopulmonary responses in the H rats most likely involves greater hypoxic pulmonary vasoconstriction or pulmonary vascular remodeling. Differences in hematocrit between the strains do not contribute to the early cardiopulmonary responses.

Pulmonary artery balloon counterpulsation for right ventricular failure: An experimental evaluation

Right ventricular (RV) failure frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. RV hypertrophy was created in 10 neonatal lambs by pulmonary artery (PA) banding. Twelve months later RV hypertrophy was present (RV weight/body weight = 2.71 +/- 0.31 gm/kg); RV systolic pressures were elevated (65 +/- 9 mm Hg) and the average gradient across the PA band was 38 +/- 9 mm Hg. RV failure was produced in all animals by performing a right ventriculotomy. Four unassisted (control) animals died shortly after separation from bypass. Six experimental animals underwent pulmonary artery balloon counterpulsation (PABCP). A Dacron graft anastomosed to the proximal PA served as a reservoir for a 40 ml intra-aortic balloon pump system. PABCP effectively reversed RV failure, low cardiac output, and systemic arterial hypotension. Periods with PABCP on and off in each animal were compared. PABCP increased cardiac output from 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min (p less than 0.0001) and increased aortic systolic pressure from 78 +/- 7 to 99 +/- 6 mm Hg (p less than 0.0004). PABCP produced a significant reduction in RV peak systolic pressure from 56 +/- 5 to 41 +/- 3 mm Hg (p less than 0.0001). PA peak pressure distal to the band increased from 31 +/- 2 to 40 +/- 1 mm Hg (p less than 0.0001). Right atrial pressure decreased from 14 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001) with PABCP, and RV end-diastolic pressure fell from 15 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001). RV stroke work index increased 49% from 0.081 +/- 0.011 to 0.121 +/- 0.017 gm X m/kg/beat (p less than 0.01), and RV systolic pressure time index decreased 38% from 1140 +/- 79 to 710 +/- 65 mm Hg sec/min (p less than 0.0001). Thus PABCP in the presence of RV dysfunction can produce substantial improvement in RV function and in overall cardiac function and may prove clinically useful in managing patients in refractory RV failure.

Right ventricular function in valvular heart disease: Relation to pulmonary artery pressure

Right ventricular angiography was performed in 46 patients with acquired valvular heart disease and 8 normal subjects. Right ventricular ejection fraction (RVEF) correlated highly only with right ventricular peak systolic pressure (RVPSP) and mean pulmonary artery pressure, both in patients with and without tricuspid insufficiency. For the group, RVEF = -0.33 RVPSP + 63 (correlation coefficient [r] = -0.76, probability [p] less than 0.001). Of 20 patients with moderate or severe elevation of pulmonary artery pressure, 17 (85%) had an abnormally low ejection fraction (less than 47%), while 19 (73%) of 26 patients with normal or mildly elevated pulmonary artery pressure had a normal right ventricular ejection fraction. In seven patients with elevated pulmonary artery pressure, a second ventriculogram was performed during intravenous nitroglycerin administration. Nitroglycerin produced a significant decrease in right ventricular peak systolic pressure (59 +/- 22 to 49 +/- 18 mm Hg, mean +/- standard deviation) (p less than 0.05) and in end-systolic volume (71 +/- 16 to 59 +/- 11 m1/m2) (p less than 0.05), and an increase in ejection fraction (43 +/- 9 to 48 +/- 7%) (p less than 0.05). Thus, at least part of the depression of ejection fraction in patients with elevated pulmonary pressure is reversible with a decrease in pulmonary artery pressure.