Showing papers on "Pulmonary artery published in 1985"

Correlates and prognostic implication of exercise capacity in chronic congestive heart failure

Abstract: Previous studies have shown poor correlations between exercise tolerance and measurements of left ventricular (LV) function during rest in patients with congestive heart failure (CHF). To further evaluate the determinants of exercise tolerance and their relation to prognosis, we performed rest and exercise hemodynamic measurements and blood pool scintigraphy in 27 patients with CHF. All patients were treated with digitalis and diuretic drugs, but not vasodilator drugs. Exercise capacity was assessed by maximal oxygen consumption (VO2max) during upright bicycle ergometry. Both right ventricular (RV) and LV ejection fractions were measured by radionuclide techniques, and arterial, right atrial and pulmonary artery pressures, cardiac output, and derived hemodynamic indexes were determined. As a group, patients with severely impaired exercise tolerance (group 1, VO2max less than 10 ml/min/kg) had significantly higher rest pulmonary capillary wedge and right atrial pressures (30 +/- 4 vs 23 +/- 6 and 12 +/- 4 vs 7 +/- 2 mm Hg, respectively) than those with a VO2max of 10 to 18 ml/min/kg (group 2). They also had lower LV and RV ejection fractions (16 +/- 4% vs 21 +/- 4% and 19 +/- 12% vs 27 +/- 7%, respectively). However, overlap among individual patients was considerable, and only pulmonary capillary wedge pressure at rest correlated significantly (r = 0.69, p less than 0.001) with VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)

A combined epi- and subdural direct approach to carotid-ophthalmic artery aneurysms

Abstract: A series of 14 patients with a carotid-ophthalmic artery aneurysm were treated operatively. In five patients the aneurysms were large, but only one of these had ruptured; four of these patients had symptoms of mass lesions. The remaining nine patients were operated on for a ruptured aneurysm; seven had subarachnoid hemorrhage due to the carotid-ophthalmic artery aneurysm and two had bleeding from another aneurysm in the presence of an asymptomatic carotid-ophthalmic artery aneurysm. All patients were treated by a combined epi- and subdural direct surgical approach, which excluded the carotid-ophthalmic artery aneurysm from the circulation and made possible the preservation of the adjacent structures. Two patients died: one a few hours after surgery from a massive thromboembolism of the pulmonary artery and another 2 months after surgery as a result of gastrointestinal bleeding. All the other patients showed postoperative improvement in symptoms and signs. This report focuses on a modified direct surgical approach involving exposure of the internal carotid artery proximal to the lesion, and of the ophthalmic artery, which is of primary importance in securing safe and complete occlusion of a carotid-ophthalmic artery aneurysm. Removal of individual bone structures at the base of the skull provides a better and safer exposure of the central segment of the internal carotid artery than does excessive and hazardous retraction of the brain.

Hemodynamic Response to Oxygen Therapy in Chronic Obstructive Pulmonary Disease

Abstract: At six centers, 203 patients with stabilized hypoxemic chronic obstructive pulmonary disease were evaluated hemodynamically during a continuous or 12-hour oxygen therapy program. Neither oxygen therapy program resulted in correction or near-correction of the baseline hemodynamic abnormalities. The continuous oxygen therapy group did show improvement in pulmonary vascular resistance, pulmonary arterial pressure, and stroke volume index. The improvement in pulmonary vascular resistance was associated with improved cardiac function, as evidenced by an increase in baseline and exercise stroke volume index. The nocturnal oxygen therapy group showed stable hemodynamic variables. For both groups, changes in mean pulmonary artery pressure during the first 6 months were associated with subsequent survival after adjustment for association with the baseline mean pulmonary artery pressure. Continuous oxygen therapy can improve the hemodynamic abnormalities of patients with hypoxic chronic obstructive pulmonary disease. The hemodynamic response to this treatment is predictive of survival.

Early steroid therapy for respiratory failure.

Abstract: • We performed a randomized double-blind trial to determine the usefulness of early methylprednisolone therapy for patients with pulmonary failure. We selected 81 acutely ill, mechanically ventilated patients at high risk for adult respiratory distress syndrome (ARDS). Thirty-nine patients received methylprednisolone, 30 mg/kg, every six hours for 48 hours; 42 patients received mannitol placebo. All patients were given a positive end-expiratory pressure of 5 cm H 2 O, monitored with pulmonary artery catheters, and treated for their primary disease processes. Twenty-five steroid-treated patients (64%) and 14 placebo-treated patients (33%) developed ARDS. Early infectious complications occurred in 30 steroid-treated patients (77%) and 18 placebo-treated patients (43%). There were no significant differences in factors predisposing to ARDS, ventilatory requirements, or days of intensive care. These results do not support the use of methylprednisolone for ARDS. Steroids failed to improve pulmonary function and were associated with an increased infection rate. Intensive pulmonary and general supportive care remain the preferred therapy for ARDS. ( Arch Surg 1985;120:536-540)

Primary Pulmonary Hypertension: A Histopathologic Study of 80 Cases

Abstract: Among 80 cases with a clinical diagnosis of primary (unexplained) pulmonary hypertension, 45 (56%) had thromboembolic disease and 22 (28%) had plexogenic arteriopathy; the remaining 13 (16%) had pulmonary veno-occlusive disease, primary medial hypertrophy, primary pulmonary arteritis, or changes consistent with pulmonary venous hypertension. The mean age was 16 years for primary pulmonary arteritis, 21 to 34 years for plexogenic pulmonary arteriopathy, primary medial hypertrophy, and pulmonary veno-occlusive disease, and 41 and 45 years for thromboembolic disease and pulmonary venous hypertension, respectively. In all forms except pulmonary veno-occlusive disease and apparent pulmonary venous hypertension, female patients were involved twice as often as male patients. With the exception of apparent pulmonary venous hypertension, patients with plexogenic pulmonary arteriopathy had the longest survival (63 months). Sudden death, however, occurred most frequently in patients with plexogenic disease (45%) and occurred 2.5 times as often in this group as in patients with thromboembolic disease. Among our 80 cases, the most frequent histopathologic lesions were medial hypertrophy, intimal proliferation and fibrosis, fibrinoid degeneration and necrosis, and thrombosis. Thrombi were commonly observed and may have developed in situ or by embolization; they were often rich in platelets when they occurred in small pulmonary vessels. These histologic features may form the morphologic substrate for elevated pulmonary vascular resistance, and their recognition may provide the rationale for possible intervention with pulmonary vasodilators, anticoagulants, or platelet inhibitors.

Pulmonary vascular response to oxygen in infants with severe bronchopulmonary dysplasia.

Abstract: The cardiac catheterization data of six infants with bronchopulmonary dysplasia (BPD) were reviewed to examine the responsiveness of their pulmonary vascular beds to changes in oxygen tension. The infants were studied because of slow recovery from their oxygen requirements and clinical evidence of persistent pulmonary hypertension. All were receiving home oxygen therapy and had abnormal chest radiographs and right ventricular hypertrophy by ECG at the time of catheterization (mean age, 25 months). All infants had mean pulmonary artery pressure greater than 25 mm Hg in room air, with a mean of 48 mm Hg. All decreased mean pulmonary artery pressure by at least 10 mm Hg when placed in high levels of inspired oxygen (FiO2 greater than 80), with a mean pulmonary artery pressure of 25 mm Hg. This represented a significant decrease in mean pulmonary artery pressure from room air pressures (P less than .005). Mean pulmonary artery pressure was also measured in three infants who were breathing supplemental oxygen by nasal cannula at flow rates similar to levels used for outpatient therapy. Most of the reduction in mean pulmonary artery pressure that occurred at high FiO2 occurred at these lower flow rates of supplemental oxygen. It is concluded that infants with bronchopulmonary dysplasia who have pulmonary hypertension generally have reactive pulmonary vascular beds, responsive to supplemental oxygen. Continuous oxygen therapy by nasal cannula may be useful in the treatment of pulmonary hypertension associated with bronchopulmonary dysplasia.

Blunting of stress responses in the pulmonary circulation of infants by fentanyl.

Abstract: After repair of congenital heart defects, stress responses in the pulmonary circulation of fourteen infants produced by a brief endotracheal suctioning procedure were studied before and after fentanyl (25 micrograms/kg). The total time of disconnection from the ventilator with suctioning (FIO2 1.0) was limited to no more than 15 sec to avoid alveolar hypoxia. Before fentanyl, marked increases occurred in mean pulmonary artery pressure and pulmonary vascular resistance index with suctioning, whereas only mild increases in heart rate and mean systemic arterial pressure occurred. All of these increases with suctioning were almost completely abolished by 25 micrograms/kg fentanyl. We conclude that suctioning or other broncho-carinal stimulation can produce a marked pulmonary vasoconstrictive response in infants, which is blunted by fentanyl. This response is separate from that produced by hypoxic pulmonary vasoconstriction associated with prolonged clinical suctioning procedures or with loss of airway.

Effect of enalapril on ventricular arrhythmias in congestive heart failure.

Abstract: Twenty-four-hour Holter electrocardiographic recordings were used to measure the effects of a converting-enzyme inhibitor, enalapril, given for 12 weeks, on the frequency of cardiac arrhythmias in 10 patients with congestive heart failure (New York Heart Association functional class II to III) receiving maintenance therapy with digoxin and furosemide. Nine patients were given placebo, and both study groups were conducted in a double-blind, parallel manner. The placebo group had no change in the frequency of arrhythmias, whereas enalapril-treated patients showed a significant decrease in the frequency of premature ventricular complexes, ventricular couplets and ventricular tachycardia. A minor, nonsignificant reduction in atrial premature complexes was seen in patients who received enalapril. Compared with placebo patients, those who received enalapril had an increase in plasma potassium levels of 0.33 mmol/liter, a decrease in plasma digoxin, and decreases in pulmonary artery wedge, mean pulmonary artery and right atrial pressures. However, none of these indexes were correlated with the concomitant decline in cardiac arrhythmias. It is concluded that enalapril reduces the frequency of ventricular arrhythmias in congestive heart failure, although the underlying mechanisms are not known.

Right heart interaction with the mechanically assisted left heart.

Abstract: Right ventricular (RV) failure has been reported to be a problem in 49 of 213 patients who received left ventricular assist devices (LVAD) at 12 different centers. Although the pathology of the problem is not understood, it is clear that the effect of an LVAD on hemodynamic ventricular interactions due to the right and left hearts being in series, and on mechanical ventricular interactions due to the anatomic coupling between the ventricles, could play a role in determining the ultimate fate of the right ventricle. Six hypotheses were generated concerning beneficial and detrimental effects of an LVAD on the determinants of right ventricular function (preload, afterload, contractility). The major potential effect on RV preload is increased venous return produced by the LVAD which can overload a marginal RV; but beneficial effects on RV preload and filling also can be produced by the LVAD unloading a dilated LV, thereby shifting the interventricular septum, which had encroached into the RV, back to the left. A significant beneficial effect on RV afterload can be produced with an LVAD by passive reductions in pulmonary artery (PA) pressure secondary to reductions in left atrial pressure; with pulmonary obstructive disease, however, PA pressures can increase due to the greater blood flow through the fixed pulmonary vascular resistance. The major effects on RV contractility produced by an LVAD are significantly beneficial since aortic and, therefore, coronary perfusion pressure is maintained. There also is a potential detrimental effect on RV contractility produced by decreased septal contribution to RV contraction during complete LV unloading with an LVAD. The initial therapy for the failing right ventricle in patients with an LVAD is volume loading. Isoproterenol, dobutamine, and dopamine can be used for inotropic support, and atrial pacing can improve the atrial contribution to filling. If these modalities fail, surgical techniques including pulmonary artery balloon pump or extracorporeal membrane oxygenation can be tried, but the recommended mechanical support is a right ventricular assist device.

The pressure-flow response of the pulmonary circulation in patients with heart failure and pulmonary vascular disease.

Abstract: Although it is well known that the pulmonary circulation is altered in patients with pulmonary arterial or venous hypertension, the resultant hemodynamic behavior has not been systematically studied. We undertook to do so in a group of patients with pulmonary hypertension of diverse etiology. We measured pulmonary arterial (PAP) and occlusive wedge pressures and cardiac output at rest (i.e., standing) and during progressive upright treadmill exercise in 51 patients. Forty-two had chronic, stable, cardiac failure secondary to ischemic, myopathic or valvular heart disease and were grouped according to whether their mean PAP was less than (normotensive) or greater than (hypertensive) 19 mm Hg, and nine had pulmonary vascular disease of diverse etiology and were considered separately. In the majority of patients, we found that irrespective of whether the hypertension was arterial or venous in origin or etiology: the mean PAP-flow relationship was linear; pulmonary capillary wedge pressure was greater than or equal to the average closure pressure of the pulmonary vascular bed and could therefore be used as the downstream pressure in calculating pulmonary vascular resistance; and pulmonary vascular resistance declined with exercise. Notable exceptions to the third observation were patients with valvular heart disease or a resting pulmonary vascular resistance greater than 800 dyne-sec-cm-5.

Magnitude and implications of spontaneous hemodynamic variability in primary pulmonary hypertension

Abstract: The pulmonary artery (PA) pressure and pulmonary resistance at rest have been noted to vary spontaneously in patients with primary pulmonary hypertension To evaluate this variation, in 12 patients (8 women, 4 men, aged 43 ± 13 years), hourly measurements were made for 6 consecutive hours of heart rate, systemic and PA pressures, cardiac output, systemic and pulmonary resistance After these baseline measurements the patients were tested with hydralazine and nifedipine therapy Spontaneous variability in pulmonary pressures and resistances occurred in each patient, with the amount of variation (coefficient of variation) in PA pressure averaging 8% and in total pulmonary resistance 13% over the 6 hours The patients with the most variability in mean PA pressure also had the most variability in cardiac output (r = 069, p = 002) Variability also correlated with the severity of the disease, as the patients with the highest total pulmonary resistances also had the most variation for that factor (r = 091, p

Pulmonary and systemic hemodynamic responses to fentanyl in infants.

Abstract: Pulmonary and systemic hemodynamic responses to fentanyl were studied in 12 infants after repair of congenital heart defects During controlled ventilation, hemodynamic responses to 25 micrograms/kg of fentanyl were measured No significant changes were found in heart rate, cardiac index, mean pulmonary artery pressure, or pulmonary vascular resistance index 5 min after the fentanyl had been given There were small but statistically significant decreases in mean arterial pressure and systemic vascular resistance index after fentanyl We conclude that under the conditions of this study, pulmonary and systemic hemodynamics in infants are minimally altered by 25 micrograms/kg of fentanyl

Effects of changes in abdominal pressure on left ventricular performance and regional blood flow.

Abstract: Many clinical conditions are associated with an increase in abdominal pressure. While the effects on venous return have been studied in the past, little attention has been given to the effect of abdominal pressure on left-sided hemodynamic events. The effects of acute changes in abdominal pressure (Pab) on left ventricular (LV) hemodynamics and outflow distribution were evaluated in ten open-chest dogs, which had undergone right heart bypass to eliminate the influence of changes in Pab on systemic venous return. Pressures were measured in the left atrium (Pla), aorta (Pao), and stomach (Pab). Electromagnetic flow probes were positioned around the ascending aorta (Qaa), descending aorta (Qda) and the innominate or subclavian artery (Qin) to reflect total cardiac output and the respective regional caudad and cephalad blood flows. Compressing the abdomen to increase acutely Pab (9.2 +/- 0.6 torr) also significantly increased Pao (7.8 +/- 1.2 torr), Pla (1.7 +/- 0.4 torr), and Qin (15.2 +/- 4.5%), while Qaa (-9.5 +/- 2.0%) and Qda (-26.3 +/- 7.0%) significantly decreased. Opposite findings were obtained immediately after release of abdominal compression. Thus, an acute increase in Pab with a constant pulmonary artery inflow increased the afterload imposed on the left ventricle and redistributed LV output, with a reduction in flow to the abdomen. Part of the fall in Qaa and increase in Pla could be attributed to passive elevation of the diaphragm by the increase in Pab, i.e., heart-lung-diaphragm interdependence.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical management of chronic pulmonary embolism.

Abstract: The clinical course of most patients with pulmonary embolism is one of gradual resolution with re-establishment of flow in the pulmonary arteries. In a small but definite group of patients, the emboli do not resolve and a state of chronic pulmonary embolism ensues. The primary thrombotic process in the systemic venous system may persist, and in some instances may be unrecognized. Such patients experience recurrent showers of emboli which may ultimately occlude a large part of the pulmonary arterial circulation with development of severe respiratory insufficiency. Six patients with this syndrome are described, and in each there was a history of dyspnea, cyanoiss, and exercise intolerance associated with a low arterial PO2, right ventricular hypertrophy, and pulmonary hypertension. Pulmonary scans and arteriograms demonstrated that more than half of the major pulmonary arteries were occluded and, in addition, smaller vessels were also obstructed. Pulmonary embolectomy was performed in each patient. Five of the 6 obtained a highly gratifying response, including relief of the dyspnea and cyanosis, an increase in arterial PO2, and a decrease in pulmonary arterial pressure. In each of the five in whom improvement occurred, the back-bleeding from the pulmonary artery at the time of embolectomy was quite good. In the sixth patient, the back-bleeding was very poor, and despite embolectomy, the vessel thrombosed postoperatively with no improvement in the patient's clinical course. Follow-up studies in these patients range up to 8 years with demonstration of continued patency of the pulmonary arteries as well as continued improvement in clinical symptoms and in the arterial PO2.

Percutaneous balloon pulmonary valvuloplasty.

Abstract: Percutaneous pulmonary valvuloplasty was performed in 27 patients with congenital pulmonary valve stenosis. A fall in the transvalve gradient of at least 15 mm Hg occurred in 22 patients. In five there was little change in the severity of the stenosis; in three of these the pulmonary valve was dysplastic. None of the successfully treated patients had a dysplastic valve. The two other failures, early in the series, were probably due to inadequate balloon size. In one patient the procedure was performed twice, with a successful result from the second dilatation with a larger balloon. Follow up studies in a further six patients showed no evidence of restenosis in those who had been successfully treated and no late improvement in the remainder. There were no important complications. Percutaneous pulmonary valvuloplasty should be the initial treatment for congenital pulmonary valve stenosis, although when the valve is dysplastic the result is less likely to be satisfactory.

Pulmonary Embolism and Deep Venous Thrombosis

Abstract: The heart pumps oxygenated blood through the aorta to smaller arteries. After the blood supplies nutrients to vital organs, it returns through veins for reoxygenation in the lungs (Figures 1 and 2⇓). Blood clots called deep vein thrombi (DVT) often develop in the deep leg veins. Pulmonary embolism (PE) occurs when clots break off from vein walls and travel through the heart to the pulmonary arteries. The broader term venous thromboembolism (VTE) refers to DVT, PE, or to a combination of both. Figure 1. The arterial (red) and venous systems (blue) are depicted. The left ventricle (LV) ejects oxygenated blood into the aorta, which circulates blood to vital organs. Deoxygenated blood travels through the venous system to the right atrium, right ventricle, and pulmonary artery. Adapted with permission from MediClip, Clinical Cardiopulmonary Images 1997, CCP01026.TIF, Williams & Wilkins, Baltimore, Md. Figure 2. Deoxygenated blood returns to the heart and lungs for reoxygenation. SVC indicates superior vena cava; IVC, inferior vena cava; RA, right atrium; RV, right ventricle; and PA, pulmonary artery. Adapted with permission from MediClip, Clinical Cardiopulmonary Images 1997, CATHRHT.TIF, Williams & Wilkins, Baltimore, Md. VTE poses a public health threat with an estimated incidence in the United States of 250 000 to 2 million cases per year. Predisposition to VTE arises from acquired conditions, inherited disorders, or both. Many of the acquired risk factors can be modified, thus lessening the likelihood of PE or DVT. Long-haul air travel is the most talked-about risk factor for PE. Other acquired risk factors include obesity, …

Pulmonary artery sarcomas. A review and report of a case.

Abstract: We examined a case of primary pulmonary artery sarcoma and reviewed 45 cases that we found previously reported in the English literature, with particular attention given to the pathologic features. These sarcomas involve the pulmonary arterial trunk, left and right main pulmonary arteries, pulmonary valve, and right ventricular outflow tract. They have prominent intravascular growth along the arterial intima. Lung involvement commonly occurs by direct extension through the pulmonary vasculature or by distant metastases. These sarcomas contain a variety of heterologous components and areas of bone, cartilage, and fibrous tissue may be remarkably well-differentiated. Management of these sarcomas will be aided by an understanding of their biologic behavior and pathologic features.

Pulmonary artery constriction produces a greater right ventricular dynamic afterload than lung microvascular injury in the open chest dog.

Abstract: Investigators model noncardiogenic pulmonary hypertension by constricting the pulmonary artery to increase right ventricular afterload. To investigate this model's validity, we compared the right ventricular afterload, quantified as pulmonary input impedance, created by constricting the pulmonary artery and by inducing a pulmonary microvascular injury (with glass beads infused into the pulmonary circulation). The pulmonary injury constriction produced a different right ventricular afterload than the microvascular injury. The constriction increased both the input resistance and the characteristic impedance. Microvascular injury increased only input resistance. Physiological levels of lung inflation did not influence pulmonary impedance, but lung hyperinflation increased input resistance both before and while constricting the pulmonary artery or after producing microvascular injury. Total right ventricular power output and stroke work were unchanged during each vascular intervention. Pulmonary artery constriction did not affect power output distribution, whereas microvascular injury decreased oscillatory power and its relative contribution to total power. Lung hyperinflation dramatically reduced right ventricular power and left ventricular stroke work. These effects appeared mediated by right ventricular afterload increase uncompensated for by right ventricular preload increase. These observations help explain the hemodynamic consequences of acute pulmonary hypertension and the effects of lung hyperinflation with positive end-expiratory pressure respiration in such patients.

Magnetic resonance imaging in pulmonary arterial hypertension

Abstract: Magnetic resonance imaging (MRI) was used to examine the right ventricle and pulmonary arteries in 17 patients with pulmonary artery (PA) hypertension documented by cardiac catheterization. The study population consisted of 7 patients with primary pulmonary hypertension, 7 with Eisenmenger's syndrome and 3 with pulmonary hypertension secondary to lung disease. The MRI studies of patients were compared with those of 10 normal volunteers. Multislice gated transaxial images encompassed the right ventricle and central pulmonary arteries, showing the severity of right ventricular (RV) hypertrophy in proportion to the elevation of PA pressure and reversal of septal curvature when PA pressure approximated systemic pressure. End-diastolic RV wall thickness and mean pulmonary pressure correlated well (r = 0.79). MRI showed enlargement of PAs in all patients with PA hypertension. A magnetic resonance signal was present in the PAs throughout the cardiac cycle in patients with severe PA hypertension (more than 90 mm Hg) and was absent during systole in normal subjects. A signal within the PAs in systole is consistent with decreased flow velocity in patients with severe PA hypertension. MRI was useful in detecting each of the congenital anatomic defects in patients with Eisenmenger's syndrome. This study indicates the potential of MRI for evaluating the severity of PA hypertension by providing direct measurements of RV wall thickness and PA diameter and by detecting abnormal intraluminal signal intensity during the cardiac cycle.

Clinical Evaluation Compared to Pulmonary Artery Catheterization in the Hemodynamic Assessment of Critically III Patients

Abstract: Although pulmonary artery (PA) catheterization is frequently employed in the management of critically ill patients, there is little documentation that the information obtained alters patient management. This study evaluated prospectively this question in 103 PA catheterizations. Before catheterization, physicians were asked to predict the range of several hemodynamic variables, the presumed diagnosis, and their plan for therapy. After catheterization, each chart was reviewed. The hemodynamics at the time of catheterization and therapy within 8 h of catheterization were noted. Pulmonary artery occlusive (wedge) pressure (WP) was correctly predicted 30% of the time. Cardiac output, systemic vascular resistance (SVR), and right atrial pressure (RAP) were correctly predicted approximately 50% of the time. There was no significant difference in the ability to predict hemodynamics of subgroups with either hypotension or impaired oxygenation. After catheterization, planned therapy was altered in 58% of the cases. Unanticipated therapy was added in 30% of the cases. This study documents the difficulty of predicting accurately hemodynamics based solely on clinical evaluation. Thus, the information obtained by catheterization often leads to alterations in the therapeutic plan. We suggest that PA catheterization is both indicated and useful in the management of critically ill patients.