The effects of controlled oxygen therapy on ventricular function in patients with stable and decompensated cor pulmonale

We made simultaneous measurements of pulmonary hemodynamics, cardiac output, and right ventricular ejection fraction (RVEF) to assess the right ventricular function in 14 patients with pulmonary arterial hypertension as a result of chronic obstructive pulmonary disease (COPD). From these measurements, the right ventricular end-systolic pressure/volume relationship could be calculated and used to assess right ventricular contractility. Eight of the patients were clinically stable, without edema, and 6 presented acutely with gross edema, indicating decompensated cor pulmonale. Measurements were made at rest, while breathing air and oxygen. Although mean pulmonary arterial pressure (Ppa) was similar in those with (Ppa = 33 +/- 6 mm Hg) and without edema (Ppa = 30 +/- 8 mm Hg, p greater than 0.05), RVEF was lower in edematous (RVEF = 0.23 +/- 0.11) compared with non-edematous patients (RVEF = 0.47 +/- 0.04, p less than 0.01). Cardiac output was normal in both groups. The mean right ventricular end-systolic pressure/volume ratio (P/V) was lower in those patients with edema (P/V = 0.41 +/- 0.27), as compared with those without edema (P/V = 1.69 +/- 0.35, p less than 0.05), as a result of an increase in right ventricular end-systolic volume index. Similarly, left ventricular end-systolic volumes were higher in edematous than in non-edematous patients. Breathing 1 to 3 L/min of oxygen for 30 min decreased total pulmonary vascular resistance (p less than 0.05) in those patients without edema, but not in patients with edema. Oxygen did not change RVEF, left ventricular ejection fraction (LVEF), or the ventricular end-systolic P/V relationships.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular volume characteristics and its relationship with right ventricle after repair of tetralogy of Fallot

In order to study the left ventricular volume characteristics and right ventricular influence on left ventricle, cardiac catheterization and biplane cineangiography was performed in 61 patients after repair of tetralogy of Fallot. Preoperative left ventricular volume size was also measured in 25 patients. Postoperative left ventricular end-diastolic volume index (LVEDVI) was 93 +/- 22 ml/m2 (mean +/- standard deviation) and it was 140 +/- 29% of normal left ventricular volume. Left ventricular ejection fraction (LVEF) was 60 +/- 6%. Left ventricular size significantly increased from 109 +/- 25% to 140 +/- 23% of normal by corrective surgery (p less than 0.001). Left ventricular volume characteristics are correlated with right ventricle. LVEDVI increased with increasing right ventricular end-diastolic volume index (RVEDVI) and decreased right ventricular ejection fraction (RVEF). LVEDVI (ml/m2) = 60 + 0.29 RVEDVI (ml/m2), r = 0.52, p less than 0.001, LVEDVI (ml/m2) = 141 - 0.90 RVEF (%), r = -0.30, p less than 0.02. LVEF decreased with increasing RVEDVI and decreased RVEF. LVEF (%) = 68 - 0.075 RVEDVI (ml/m2), r = -0.51, p less than 0.001, LVEF (%) = 43 + 0.32 RVEF (%), r = 0.40, p less than 0.001. On the contrary there was no relationship between right ventricular volume characteristics and right ventricular systolic pressure. There were two cases whose LVEF was less than 50%. In one case right ventricular systolic pressure was as high as 98 mmHg. In the other patient RVEDVI was 299 ml/m2 (453% of normal right ventricular volume) because of severe pulmonary regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of volume load of the left ventricle in aortic and mitral insufficiency on the geometry and function of the right ventricle

To investigate the effect of chronic left ventricular enlargement on right ventricular geometry and function, biplane cineventriculograms were analyzed in 23 patients with aortic regurgitation (AR) and in 17 patients with mitral regurgitation (MR). Left ventricular end-diastolic volume indices (LVEDVI) were elevated and significantly (p less than 0.05) different in patients with aortic regurgitation (AR) (190.2 +/- 65.2 ml/m2) and mitral regurgitation (MR) (148.7 +/- 40.1 ml/m2). Right ventricular end-diastolic volume indices (RVEDVI), however, were comparable and within the normal range (AR: 96.6 +/- 18.3 ml/m2, MR: 100.2 +/- 33.7 ml/m2). Mean pulmonary artery pressure was significantly (p less than 0.05) higher in patients with mitral regurgitation with 24.7 +/- 12.8 mm Hg (AR: 17.5 +/- 6.6 mm Hg). Six patients with mitral insufficiency had concomitant tricuspid valve insufficiency. In five out of six patients with tricuspid insufficiency, right ventricular afterload was significantly elevated. Only in patients with mitral regurgitation was a significant correlation (r) between left and right ventricular end-diastolic volume index found (RVEDVI = 0.7 X LVEDVI +1, r = 0.80). Moreover, in patients with MR, left ventricular end-diastolic volume index correlated with right ventricular end-systolic volume index (RVESVI = 0.4 X LVEDVI -8, r = 0.73). Right ventricular ejection fraction was significantly different (p less than 0.05) between patients with aortic and mitral insufficiency (AR: 53.7 +/- 8.9%, MR: 46.7 +/- 10.7%). Particularly in patients with normal left ventricular ejection fraction (greater than 50%) and mitral regurgitation, the incidence of a reduced right ventricular ejection fraction (less than 50%) was significantly higher (p less than 0.01) compared to patients with aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of left and right ventricular end-systolic pressure-volume relations in congestive heart failure

A hemodynamic-radionuclide study was performed to compare the relations between end-systolic pressure and volume in the left and right ventricles in 10 patients with biventricular failure, and to correlate the end-systolic pressure-volume slope with baseline variables of systolic function. During nitroprusside or nitroglycerin infusion, or a combination of both, linear relations were found between end-systolic pressure and volume for both ventricles. In 9 of 10 patients, the end-systolic pressure-volume slope was greater for the left ventricle (mean +/- SD 1.12 +/- 0.36 mm Hg X m2/ml) than for the right ventricle (0.46 +/- 0.27 mm Hg X m2/ml) (p less than 0.001). In all 10 patients, the volume-axis intercept of the pressure-volume relation was greater for the left ventricle (82 +/- 66 ml/m2) than for the right ventricle (2 +/- 30 ml/m2) (p less than 0.005). Right ventricular pressure-volume slope correlated weakly with baseline right ventricular ejection fraction (r = 0.69, p less than 0.05), strongly with the baseline right ventricular end-systolic pressure-volume ratio (r = 0.89) and inversely with baseline right ventricular end-systolic volume (r = -0.86). In conclusion, 1) in patients with severe biventricular failure, changes in systolic pressure influence end-systolic volume more strongly in the right than in the left ventricle. 2) For the right ventricle, the slope of the end-systolic pressure-volume relation is directly related to rest indexes of systolic function. 3) The greater the end-systolic volume at rest, the greater the predicted improvement in right ventricular emptying for any vasodilator-induced reduction in pulmonary artery end-systolic pressure.     

The immediate effects of isosorbide dinitrate on right ventricular function in patients with acute hypoxemic respiratory failure. A combined invasive and radionuclide study

We administered 20 mg of isosorbide dinitrate sublingually to 16 patients with acute hypoxemic respiratory failure (ARF) complicated by pulmonary artery hypertension (PAH) and evaluated its effects 20 to 30 min later using a combination of invasively measured pressures and flows and ECG-gated cardiac scintigraphy. We measured the right and left ventricular ejection fractions and a simultaneous thermodilution stroke volume index; we then calculated respective end-diastolic (EDVI) and end-systolic (ESVI) volume indexes. An initially depressed mean right ventricular ejection fraction (RVEF) increased modestly after the administration of isosorbide dinitrate (35 +/- 10 to 41 +/- 10%; p less than 0.02), whereas both the mean right ventricular end-diastolic (-27 +/- 50 ml/M2; p less than 0.04) and end-systolic (-27 +/- 44 ml/M2; p less than 0.03) volume indexes fell. The RVEF increased in 11 of 16 patients: within this subgroup, a decrease in the RVEDVI and RVESVI was associated with a decrease in both cardiac index (delta 0.3 L/min/M2) and LVEDVI (delta -15 +/- 21 ml/M2; p less than 0.01); hence, O2 delivery also fell (delta -36 +/- 56 ml/min/M2; p less than 0.05). In some patients with ARF complicated by PAH, sublingually administered nitrates may improve right ventricular systolic function when globally depressed. However, left ventricular "pump" function appears to be depressed when a concurrent depression in right ventricular "pump" function ensues.     

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.     

Treatment of primary pulmonary hypertension with nifedipine. A hemodynamic and scintigraphic evaluation

To evaluate the potential value of nifedipine treatment for primary pulmonary hypertension, hemodynamic and scintigraphic measurements were made before and 15 to 30 minutes after nifedipine, 10 to 20 mg, was given sublingually to nine patients. Nifedipine treatment increased cardiac output (mean +/- SD, 3.6 +/- 1.7 to 5.3 +/- 2.8 L/min, p less than 0.001) and decreased mean aortic pressure (99 +/- 19 to 85 +/- 12 mm Hg, p less than 0.001) and total pulmonary and total systemic resistances (1605 +/- 787 to 1025 +/- 540 dyn X s X cm-5 and 2761 +/- 1557 to 1591 +/- 823 dyn X s X cm-5, respectively; p less than 0.005). Heart rate and mean pulmonary arterial pressure did not change significantly. Right ventricular end-diastolic volume decreased 10% (p = 0.01), end-systolic volume decreased 15% (p less than 0.01), and right ventricular ejection fraction increased 18% (p less than 0.05) in eight patients. After 4 to 14 months (mean, 7.3 +/- 3.8) of treatment with nifedipine, 40 to 120 mg/d, in six patients, cardiac output increased (3.6 +/- 2.0 to 5.0 +/- 1.8 L/min, p less than 0.01) and total pulmonary resistance decreased (1572 +/- 730 to 987 +/- 586 dyn X s X cm-5, p = 0.025), whereas pulmonary arterial pressure remained unchanged (59 +/- 23.2 to 55 +/- 28.6 mm Hg, p greater than 0.05) compared with baseline values. We conclude that nifedipine therapy may be useful in the chronic management of patients with primary pulmonary hypertension.     

Function and interaction of the right and left ventricle in patients with mitral valve stenosis

In 17 patients with mitral stenosis functional class III (NYHA) and chronic pulmonary hypertension, volumes and function of the right (RV) and left ventricle (LV) were analysed. Biplane cineventriculography of the right and left ventricle was performed subsequently and repeated 3 min after application of 1.6 mg nitroglycerin (NTG), which was given sublingually to decrease pre- and afterload. Pulmonary artery (PAP) and wedge pressures (PCW) were measured continuously. RV ejection fraction (EF) was 62.8 +/- 7.2% before and did not change significantly after NTG. RV enddiastolic volume index (EDVI) and endsystolic volume index (ESVI) was 80.7 +/- 27.2 ml/m2 and 31.7 +/- 11.9 ml/m2, respectively, and did not change significantly after NTG. Volumes and function of the LV were normal (LVEDVI: 66.5 +/- 13.5 ml/m2, LVESVI: 23.0 +/- 7.1 ml/m2, LVEF: 62.4 +/- 9.5%). Systolic PAP decreased significantly from 43.4 +/- 11.1 mm Hg before to 37.8 +/- 9.1 mm Hg after NTG (p less than 0.025) as well as total pulmonary resistance from 243 +/- 51 to 209 +/- 50.8 dynes . sec . cm-5 (p less than 0.05). No significant correlation was found between function and volumes of both ventricles. In 4 patients, however, the decrease in LV ejection fraction was associated with a considerable increase of right ventricular enddiastolic volume. Thus, the right ventricle compensates moderate pulmonary hypertension completely maintaining normal right ventricular function. If, however, septal dysfunction occurs, right ventricular insufficiency will develop in a shorter period of time.     

Transient biventricular dysfunction following coronary bypass surgery with potassium cardioplegia

Although myocardial revascularization relieves anginal symptoms, the effect on ventricular function remains controversial. Sixty-six patients undergoing elective coronary bypass surgery with normal right and left ventricular function were studied 1 month preoperatively (PRE), 3-5 hours perioperatively (PERI) and 3-5 months postoperatively (POST). Nuclear ventriculograms were employed to calculate right and left ventricular ejection fractions (RVEF, LVEF), end diastolic volume indices (RVEDVI, LVEDVI) and end systolic volume indices (RVESVI, LVESVI). Cardiac index (CI), stroke index (SI) and an approximation of left ventricular stroke work index (LVSWI) were also calculated from the scintigraphic data. Right and left ventricular ejection fractions were lower perioperatively (PRE:RVEF 37 +/- 2.5, LVEF 61 +/- 3; PERI:RVEF 32 +/- 3, LVEF 51 +/- 4; POST:RVEF 35 +/- 3, LVEF 56 +/- 4%, p less than 0.01 by analysis of variance, ANOVA) despite lower end diastolic volume indices perioperatively, (p less than 0.05 by ANOVA). The ratio of systolic blood pressure to LVESVI was significantly lower PERI than PRE or POST, (p less than 0.01 by ANOVA). SI, LVSWI, LVEF and RVEF were lower perioperatively at any level of LVEDVI or RVEDVI (p less than 0.01 by paired analyses of covariance), suggesting transient depression of right and left ventricular performance perioperatively. Right ventricular recovery was incomplete 4 months postoperatively. The patients were able to exercise longer at higher workloads postoperatively (p less than 0.01 by ANOVA). Chest pain resulted in discontinuation of exercise in 57% of patients PRE but only 5% POST (p less than 0.01), even though all patients were receiving full medical therapy preoperatively and no therapy postoperatively. Myocardial revascularization provided symptomatic relief and increased work capacity. However, right and left ventricular function were transiently depressed in the early perioperative period.     

Pulmonary hypertension and right ventricular function in patients with COPD

In 100 patients with chronic obstructive pulmonary disease (COPD), we found no significant correlation between simultaneous measurements of right ventricular ejection fraction, using radionuclide ventriculography, and pulmonary arterial pressure. There was, however, a weak but significant correlation between right ventricular ejection fraction and the pulmonary vascular resistance (r = 0.40, p less than 0.005). In 52 of these patients, 37 with pulmonary hypertension, right ventricular end-systolic volume index was 53 +/- 21 ml.m-2 and end-diastolic volume index was 86 +/- 27 ml.m-2, compared with a calculated mean of 33 ml.m-2 and 79 ml.m-2, respectively, for normal subjects. In 24 of these patients where the measurements were made at rest and on exercise, the mean right ventricular end-systolic volume increased from 66 +/- 20 ml.m-2 to 87 +/- 32 ml.m-2, with an increase in right ventricular systolic pressure from 28 +/- 9 mm Hg to 55 +/- 15 mm Hg. Analysis of the slope of the right ventricular end-systolic pressure volume relationship at rest and on exercise suggested relatively normal right ventricular contractility in the majority of patients. Thus, in these patients with stable COPD, despite the presence of pulmonary hypertension, right ventricular contractility remained relatively normal.     

Hemodynamic and volumetric effects of venodilation with nitroglycerin in chronic mitral regurgitation

To evaluate the potential value of nitrate therapy in patients with chronic mitral regurgitation, the hemodynamic and angiographic effects of intravenous nitroglycerin were studied in 10 such patients. Nitroglycerin infusion, titrated to reduce mean pulmonary artery wedge pressure at least 20%, resulted in a significant reduction in mean blood pressure (from 91 +/- 12 to 77 +/- 13 mm Hg, p less than 0.0001), mean right atrial pressure (12 +/- 6 to 7 +/- 4 mm Hg, p less than 0.001), left ventricular end-diastolic pressure (22 +/- 7 to 13 +/- 5 mm Hg, p less than 0.0001) and peak V wave of indirect left atrial pressure (34 +/- 9 to 20 +/- 10 mm Hg, p less than 0.001). Changes in systemic vascular resistance (1,986 +/- 468 vs 1,582 +/- 534 dynes s cm-5) and forward stroke volume (39 +/- 14 vs 45 +/- 8 ml) were not statistically significant. Angiographic data showed a decrease in both end-diastolic and end-systolic left ventricular volumes (248 +/- 51 to 216 +/- 54 ml, p = 0.06 and 127 +/- 69 to 99 +/- 48 ml, p less than 0.05, respectively) and an improvement in ejection fraction, from 0.52 +/- 0.15 to 0.55 +/- 0.15 (p less than 0.05). There was no significant change in the group values for mitral regurgitant volume and fraction (from 85 +/- 32 to 72 +/- 32 ml and 67 +/- 10 to 64 +/- 5%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care.

PURPOSE: Clinical and radiographic examinations are commonly used for estimating severity and titrating therapy of chronic congestive heart failure. The purpose of this study was to establish the relationship between findings on history, physical examination, chest roentgenogram, and pulmonary capillary wedge pressure (PCWP). PATIENTS AND METHODS: Fifty-two consecutive patients with chronic congestive heart failure, referred for evaluation for heart transplantation, were studied; all patients underwent history, physical examination, upright chest roentgenogram, and cardiac catheterization. The mean left ventricular ejection fraction was 0.19 +/- 0.06. Patients were divided into three groups according to their PCWP: Group 1, normal PCWP (less than or equal to 15 mm Hg, n = 19); Group 2, mild to moderately elevated PCWP (16 to 29 mm Hg, n = 15); Group 3, markedly elevated PCWP (greater than or equal to 30 mm Hg, n = 18). RESULTS: Physical and radiographic signs of congestion were more common in the groups with higher PCWP, but they could not be used to reliably separate patients with different filling pressures. Physical findings (orthopnea, edema, rales, third heart sound, elevated jugular venous pressure) or radiographic signs (cardiomegaly, vascular redistribution, and interstitial and alveolar edema) had poor predictive value for identifying patients with PCWP values greater than or equal to 30 mm Hg. These findings had poor negative predictive value to exclude significantly elevated PCWP (greater than 20 mm Hg). Radiographic pulmonary congestion was absent in eight (53%) patients in Group 2 and seven (39%) in Group 3. In patients in Group 2 and 3, those without radiographic congestion were in a better New York Heart Association functional class (3.5 +/- 0.5 versus 2.8 +/- 0.6, p less than 0.01). There was good correlation between right atrial pressure and PCWP (r = 0.64, p less than 0.001). A normal right atrial pressure had no predictive value, but a pressure greater than 10 mm Hg was seen in all but one patient with a PCWP value greater than 20 mm Hg. CONCLUSION: Clinical, radiographic, and hemodynamic evaluations of chronic congestive heart failure yield conflicting results. Absence of radiographic or physical signs of congestion does not ensure normal PCWP values and may lead to inaccurate diagnosis and inadequate therapy. It is not known whether therapy aimed at normalizing PCWP is superior to relieving clinical and radiographic signs of congestion.     

Effect of amrinone on right ventricular function: predominance of afterload reduction

Although the bipyridine agent amrinone is reported to have a positive inotropic effect on the left ventricle, the effect of this drug on right ventricular contractility in the clinical setting is unknown. We studied the effect of short-term intravenous administration of amrinone on right ventricular systolic function in nine patients with severe congestive heart failure and, using radionuclide ventriculography, examined the right ventricular end-systolic pressure-volume relationship to determine whether reduced right ventricular afterload or increased contractility predominantly accounted for the observed improvement in right ventricular systolic function. In each patient the right ventricular end-systolic pressure-volume relationship was derived with use of varying doses of nitroprusside. After nitroprusside was stopped, intravenous amrinone (3 mg/kg) caused decreases from baseline in pulmonary arterial end-systolic pressure in eight of nine patients (23 +/- 11% [overall mean +/- SE], p less than .05), and in pulmonary vascular resistance in all patients (38 +/- 6%, p less than .001). Right ventricular end-systolic volume decreased (23 +/- 8%, p less than .01) and right ventricular ejection fraction increased (31 +/- 10%, p = .01). The amrinone-induced decrease in right ventricular end-systolic volume was compared with that predicted for right ventricular afterload reduction alone based on the effect of amrinone on pulmonary arterial end-systolic pressure and the pressure-volume relationship observed during infusion of nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary artery morphology and hemodynamics in pulmonic valve atresia with ventricular septal defect before and after repair

Cardiac catheterization and angiography were performed in 22 patients with pulmonic valve atresia and ventricular septal defect to evaluate pulmonary morphology and hemodynamics before and after repair. In 12 of the 22, pulmonic valve atresia and ventricular septal defect were associated with major aortopulmonary collateral arteries, which were ligated in most. Mean postoperative pulmonary artery pressure (PAP) ranged from 9 to 92 mm Hg (mean 28 +/- 19) and pulmonary vascular resistance ranged from 1.1 to 35.2 U.m2 (mean 6.4 +/- 8.0). These data correlated (r = 0.89, p less than 0.001). The number of pulmonary artery subsegments connected to the central pulmonary arteries was 22 to 42 (mean 38 +/- 6). Univariate analysis revealed that the mean postoperative PAP correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = -0.81, p less than 0.001), with mean postoperative PAP (r = 0.79, p less than 0.001), with the postoperative pulmonary artery area index of the right and left pulmonary arteries at prebranching (r = -0.76, p less than 0.001), and with the sum of the pulmonary artery areas after branching (r = -0.69, p less than 0.005). Pulmonary vascular resistance correlated with the number of pulmonary artery subsegments connected to the central pulmonary arteries (r = -0.85, p less than 0.001), with the mean preoperative PAP (r = 0.79, p less than 0.001), with the sum of the pulmonary artery areas after branching (r = -0.73, p less than 0.001), and with the postoperative pulmonary artery area index (r = -0.70, p less than 0.001). The incidence of pulmonary vascular resistance being less than 3 U.m2 was significantly higher in patients with greater than 36 pulmonary artery subsegments connected to the central pulmonary arteries and with a preoperative pulmonary artery area index greater than 0.5 (88%) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary vascular effects of hydralazine in a canine preparation of pulmonary thromboembolism

Pulmonary arterial pressure (PAP)-flow coordinates were obtained in 14 anesthetized dogs before and after pulmonary hypertension was induced with autologous blood clots. Cardiac output (CO) was altered by systemic arteriovenous fistulas. The PAP-CO coordinates were always rectilinear. Before emboli, the mean vascular closing or outflow pressure (the pressure intercept of the PAP-CO line) was 8.8 +/- 2.1 (SD) mm Hg. Emboli increased PAP (15.1 +/- 1.6 to 36.5 +/- 3.5 mm Hg; p less than .001) and decreased CO (3.8 +/- 0.6 to 2.4 +/- 0.8 liters X min-1; p less than .001). Incremental resistance (the slope of the PAP-CO line) only increased slightly. On the other hand, the marked increase in PAP was predominantly due to an increase in effective outflow pressure (from 8.8 +/- 2.1 to 28.6 +/- 3.6; p less than .001). Hydralazine was administered in a dose sufficient to double CO. This did not affect PAP and caused an inconsistent and small decrease in incremental resistance. However, a consistently significant decrease in effective outflow pressure, averaging 23%, was observed. In this canine preparation of pulmonary hypertension the predominant effect of hydralazine appears to be a decrease in the mean vascular closing or outflow pressure.     

Scintigraphic prediction of pulmonary arterial systolic pressure by regional right ventricular ejection fraction during the second half of systole

In 49 patients in whom gated equilibrium ventriculography and cardiac catheterization were performed within a 6 day interval, total and fractional portions of global and regional right ventricular ejection fraction (RVEF) were correlated with pulmonary arterial systolic pressure. Pulmonary arterial systolic pressure was normal (30 mm Hg or less) in 27 patients (Group I) and elevated (31 mm Hg or greater) in 22 patients (Group II). The second-half regional RVEF was 38 +/- 8% (mean +/- standard deviation) with a range of 30 to 54% for Group I and 22 +/- 6% with a range of 13 to 32% for Group II. The difference between the means was statistically significant (p less than 0.001). Use of a second-half regional RVEF of 30% as the criterion of elevated pulmonary arterial systolic pressure resulted in a sensitivity of 0.86 and a specificity of 1.00. A power curve fit in which pulmonary arterial systolic pressure = 10.91 (second-half regional RVEF)-0.87 allowed accurate estimation (r = -0.85) of pulmonary arterial systolic pressure from the second-half regional RVEF. It is concluded that second-half regional RVEF may be used to accurately detect pulmonary arterial hypertension and to estimate its extent.     

Effects of supine and lateral positions on cardiac output and intracardiac pressures: an experimental study

Hemodynamic measurements in human subjects and in experimental animals are generally made in the supine position; not much attention is paid to potential beneficial or harmful effects of right or left lateral positions on cardiac output or other hemodynamic variables. To evaluate the potential influence of such positional changes on cardiac performance, we measured cardiac output and left and right ventricular pressures (with micromanometer catheters) in anesthetized experimental animals (eight dogs and nine pigs) in the supine, right lateral, and left lateral positions. Cardiac output increased from supine to left lateral (mean +/- SD, 2.6 +/- 0.9 to 3.1 +/- 1.0 liters/min; p less than .001) and from supine to right lateral positions (2.6 +/- 0.9 to 3.1 +/- 1.1 liters/min; p less than .001). There was an associated decrease in arteriovenous oxygen saturation difference from supine to left lateral position (31 +/- 8% to 24 +/- 4%; p less than .001) and from supine to right lateral position (32 +/- 9% to 25 +/- 6%; p less than .001). Left ventricular systolic and end-diastolic pressures increased from supine to left lateral (128 +/- 17/9 +/- 2 to 147 +/- 19/16 +/- 4 mm Hg; both p less than .001) and from supine to right lateral positions (128 +/- 19/9 +/- 2 to 141 +/- 16/16 +/- 7 mm Hg; p less than .01 and p less than .001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermal dye measurements of extravascular lung water in critically ill patients. Intravascular Starling forces and extravascular lung water in the adult respiratory distress syndrome

To assess the concurrent influence on extravascular lung water (EVLW) content of the intravascular Starling forces, the pulmonary capillary wedge pressure (PCWP), and the colloid osmotic pressure (COP), we measured EVLW by the thermal green dye technique in 174 patients with and without radiographically defined pulmonary edema; in the former group, patients with cardiac (CPE) and noncardiac (NCPE) causes of pulmonary edema were compared (study A). In 119 patients, EVLW was again measured one to three days later (study B). Patients with CPE demonstrated a significantly lower EVLW (9.3 +/- 3.9 ml/kg) (mean +/- SD) than patients with NCPE (14.5 +/- 4.9 ml/kg; p less than 0.05), despite a higher mean PCWP in the former group (20 +/- 7 mm Hg) than in the latter (12 +/- 6 mm Hg; p less than 0.05). In patients potentially with only a hydrostatic cause of pulmonary edema in study A, regression analysis demonstrated the following: EVLW = 3.2 + 0.30 PCWP (r2 = 0.38; p less than 0.005); and in patients with NCPE, EVLW = 10.9 + 0.304 PCWP (r2 = 0.17; p less than 0.01). In study B the change (delta) in EVLW between the two studies was described as follows: delta EVLW = 0.25 + 0.173 delta PCWP (p less than 0.01) + 0.663 group NCPE (p, not significant) + 0.236 group NCPE X delta PCWP (p less than 0.01). This latter equation indicated that the EVLW content manifested a greater change with concurrent alterations in the PCWP in patients with NCPE than was found in patients with only a hydrostatic influence to EVLW formation. Therefore, NCPE is characterized by a greater measurable thermal green dye EVLW than is observed in CPE at any given PCWP, and the PCWP synergistically influences EVLW accumulation in both CPE and NCPE.     

Unexplained pulmonary hypertension in elderly patients

BACKGROUND: Idiopathic pulmonary arterial hypertension (IPAH) preferentially affects young women. However, a subset of patients with IPAH is elderly. Our objective was to compare elderly (age >/= 65 years) vs younger persons with unexplained pulmonary hypertension (PH) and a presumptive diagnosis of IPAH. METHODS: Clinical, echocardiographic, hemodynamic, and survival data were collected on consecutive patients with suspected IPAH after evaluation in a large tertiary center PH clinic. RESULTS: Of 197 patients (mean age +/- SD, 52 +/- 16 years; 80% female), 48 patients (24%) were elderly. Elderly and younger patients had similar symptom severity, systolic pulmonary artery (PA) pressure (82.7 +/- 20.3 mm Hg vs 86.9 +/- 18.8 mm Hg, respectively; p = 0.21), and severity of right ventricular enlargement and dysfunction. Elderly patients had higher pulmonary capillary wedge pressure (PCWP) [15.3 +/- 7.3 mm Hg vs 11.1 +/- 5.3 mm Hg; p < 0.0001] and more frequently failed (56%) to meet hemodynamic criteria for IPAH (PH with PCWP < 15 mm Hg) than did younger patients (19%). Elderly patients also had higher systemic systolic (p < 0.0001) and pulse (p < 0.0001) pressures and more cardiovascular disease. Among those patients with normal PCWP, elderly patients had worse survival than young patients (p = 0.007). Among those patients with elevated PCWP, elderly patients had lower PA pressures (p = 0.04) and better survival (p = 0.02). CONCLUSIONS: Elderly patients with clinically suspected IPAH often fail to meet hemodynamic criteria for IPAH due to elevated PCWP. Studies to define the proper diagnostic strategy and the safety and efficacy of pulmonary vasodilators in elderly patients with unexplained PH are needed.     

Effects of long-term treatment with amiodarone on exercise hemodynamics and left ventricular relaxation in patients with hypertrophic cardiomyopathy

The influence of long-term treatment with amiodarone on exercise hemodynamics and on left ventricular relaxation was studied prospectively in patients with hypertrophic cardiomyopathy. Rest-exercise hemodynamics (n = 9) and echocardiographic relaxation indexes (isovolumic relaxation time, dPW/dt) (n = 11) were measured in control conditions and after 5 weeks of oral amiodarone treatment (600 mg daily first week, 400 mg daily second week, 200 mg daily afterwards). Long-term amiodarone treatment in patients at rest caused a significant drop in heart rate from 80 +/- 11 to 75 +/- 11 beats/min (p less than .05), a rise in mean pulmonary artery pressure from 19 +/- 7 to 25 +/- 10 mm Hg (p less than .02), and a rise in mean pulmonary capillary wedge pressure from 11 +/- 4 to 17 +/- 8 mm Hg (p less than .05). Systemic arterial pressure, cardiac output, and systemic vascular resistance remained unaltered. Exercise tolerance assessed by serial supine bicycle stress testing was reduced in six of nine patients. Amiodarone treatment caused a significant rise in pulmonary capillary wedge pressure from 22 +/- 8 to 37 +/- 9 mm Hg (p less than .001) at the highest identical workloads and from 26 +/- 10 to 37 +/- 9 (p less than .005) at maximal symptom-limited workloads. Similarly, mean pulmonary artery pressure rose from 37 +/- 15 to 51 +/- 18 mm Hg (p less than .01) at highest identical workloads and from 42 +/- 19 to 51 +/- 18 mm Hg (p less than .01) at maximal symptom-limited workloads. There were no significant differences at maximal exercise level in heart rate, systemic arterial pressure, cardiac output, or exercise factor. Echocardiographic studies performed before and during long-term amiodarone treatment revealed no change in isovolumic relaxation time, end-diastolic or end-systolic posterior wall thickness, and peak posterior wall thinning rate. A negative inotropic action of amiodarone could explain the worsened rest and exercise hemodynamics observed during long-term treatment of patients with hypertrophic cardiomyopathy. Echocardiographic relaxation indexes remained unaltered despite the elevated left ventricular filling pressures. This finding could suggest a deleterious effect of amiodarone on myocardial inactivation, possibly similar in mechanism to the depressed myocardial inactivation observed in hypothyroidism.