Elevated Pulmonary Resistance Research Articles

The fate of the pulmonary hypertension after ASD-closure in adults (author's transl)

10 female and 7 male patients, who were operated for secundum type Atrial Septal Defect with Pulmonary Hypertension, got postoperative check-ups including right heart catheterisations. The investigations were performed on the average 6.6 years postoperatively. There was a fall of the systolic pulmonary pressure and of the flow; pulmonary resistance fell in 8 cases and rose in 9. The low left ventricular cardiac index together with an elevated left atrial pressure may be the pathogenetic cause of postoperatively elevated pulmonary resistance.

Pathologic physiology and chemotherapy of Plasmodium berghei: VI. Mechanical properties and histological features of the lung

The rats infected with Plasmodium berghei showed the following changes in the lung: (a) Elevation in pulmonary compliance; (b) elevation in pulmonary resistance; (c) increase in respiratory minute volume; (d) increase in functional residual capacity; and (e) disruption of alveolar septa and increase in air space as revealed by histological examination. The latter changes (d and e) indicate emphysematous lesions which may relate to the respiratory difficulties and acidosis appearing just prior to death of the malarial rats. The mice infected with chloroquine-resistant strain of P. berghei show a predominance of nucleated cells in the alveolar septa. The identity of these cells and their relation to the development of drug resistance require investigation.

ACCURACY OF PREDICTING PULMONARY BLOOD FLOW, PULMONARY ARTERIOLAR RESISTANCE AND PULMONARY VENOUS PRESSURE FROM CHEST ROENTGENOGRAMS

ACCURACY OF PREDICTING PULMONARY BLOOD FLOW, PULMONARY ARTERIOLAR RESISTANCE AND PULMONARY VENOUS PRESSURE FROM CHEST ROENTGENOGRAMSARTHUR LIEBER, M.D., HAROLD D. ROSENBAUM, M.D., DANIEL J. HANSON, M.D. and H. M. KWAAN, M.D.Audio Available | Share

Pulmonary hypertension in patients with congenital heart disease: Pre- and postoperative hemodynamics, pulmonary function, and criteria for surgical closure of defects

We have reviewed the catheterization and clinical records of all patients with atrial septal defects, ventricular septal defects and patent ductus arteriosus studied at the University of California Medical Center between June 1951 and June 1961. Patients with normal and elevated pulmonary vascular resistances were contrasted as to age, sex, hemodynamic abnormalities, operative mortality and morbidity. Significant hemodynamic differences were found between those with normal and those with elevated pulmonary vascular resistance, as in patients studied by others. Pre- and postoperative hemodynamic studies were made in seven patients with pulmonary hypertensive atrial septal defects, five with pulmonary hypertensive ventricular septal defects and three with pulmonary hypertensive patent ductus arteriosus. In most of these, together with a few nonoperated patients with Eisenmenger complex, pulmonary function studies also were performed. Criteria of operability in patients with congenital shunt lesions and elevated pulmonary vascular resistance and/or pulmonary hypertension were derived from these studies and from the literature. We believe that corrective surgery should be confined to patients who have a net left to right shunt. The operative risk increases sharply in patients with atrial septal defects whose systolic pulmonary arterial pressure exceeds 75 mm. Hg and in patients with patent ductus arteriosus whose pulmonary artery systolic pressure exceeds 100 mm. Hg. However, defects in patients in either group with pulmonary vascular resistances as high as 12 to 13 mm. Hg per L. per minute have been safely repaired with satisfactory although slow postoperative hemodynamic improvement. In contrast, patients with ventricular septal defects run excessive operative risk and less chance of tolerating definitive repair if they have pulmonary vascular resistances exceeding approximately 6.6 mm. Hg per L. per minute, pulmonary artery systolic pressure exceeding 90 mm. Hg preoperatively or 55 mm. Hg immediately postoperatively, and grade 4 or 5 pulmonary vascular disease. Furthermore, there is evidence suggesting that the postoperative hemodynamic response may be less satisfactory in patients with ventricular septal defects and elevated pulmonary vascular resistance than in those with atrial septal defects or patent ductus arteriosus. All our patients in whom defects were closed completely showed a decrease in pulmonary artery pressure and all but one showed a decrease in pulmonary vascular resistance. The slow postoperative improvement was associated with persistence of an elevated pulmonary resistance. This occurred despite a fall in pulmonary artery pressures with the reduction in pulmonary flow upon closure of the shunt defect. In most cases this persistently elevated pulmonary vascular resistance was associated with restrictive lung disease, evidence of underperfusion of ventilated areas and decreased diffusing capacity for carbon monoxide. These physiologic abnormalities could best be explained by the presence of pulmonary vascular disease with obliteration of some of the pulmonary capillary bed and a decrease in pulmonary capillary blood volume. This concept is compatible with the known pulmonary vascular pathology in these cases. In patients who had incomplete closure or reopening of their defects (especially those with ventricular septal defects), there appeared to be at least a temporary worsening of the hemodynamics, with further elevations of pulmonary vascular resistance.

Cardiac hemodynamics immediately following mitral valve surgery

Comments and summary Thirty patients with isolated acquired mitral valve disease were studied preoperatively and in the early postoperative period. Considering the group as a whole, mean values of left atrial pressure and pulmonary artery pressure demonstrated a rapid fall toward normal in the immediate postoperative period with little further change over the succeeding 2 days. These changes were slightly more marked in the valve replacement group than in the closed mitral valcardiac outputs. In these patients, the pulmonary arteriolar resistances rose following surgery. The remaining patients with elevated pulmonary arteriolar resistances preoperatively acted similarly in the early postoperative period to patients with normal pulmonary arteriolar resistances, save for the fact that these patients continued to have elevated pulmonary arteriolar resistances and their postoperative pulmonary arterial and left atrial pressures were not as low as in patients with normal pulmonary arteriolar resistances. Patients with low preoperative cardiac indices continued to have reduced cardiac indices during the postoperative study period.

Studies of the circulatory dynamics in mitral stenosis. II: Altered dynamics at rest

1. 1. Twenty-one patients with mitral stenosis have been studied by the technique of cardiac catheterization. These patients were classified clinically and also according to the size of the orifice of the mitral valve. Six patients were in pulmonary edema during the study. 2. 2. As a consequence of mitral valvular stenosis, a balance develops between pulmonary vascular pressures and peripheral blood flow (tending toward an increase in pulmonary pressure and a decrease in blood flow). 3. 3. Cardiac and stroke indices were decreased at rest, although a wide range of values was seen. Patients with auricular fibrillation had slightly lower cardiac indices than patients with normal sinus rhythm. Tissue oxygen extraction per cubic centimeter of blood was increased so that oxygen consumption was maintained within the normal range in all. 4. 4. Pulmonary “capillary” pressures were increased above normal as a result of the increase in left atrial pressure proximal to the mitral stenosis. 5. 5. Pulmonary arterial pressures were increased above normal as a result of (a) the increase in pulmonary “capillary” pressure and (b) increased pulmonary arteriolar resistance. 6. 6. The presence of an elevated pulmonary arteriolar resistance was roughly related to the level of pulmonary “capillary” pressure and the degree of valvular stenosis. 7. 7. An inverse logarithmic relationship was observed between total pulmonary resistance and stroke output per square meter. 8. 8. As a result of the increased pulmonary vascular pressures, the pressure work of the right ventricle was greatly increased. 9. 9. Right ventricular incompetency, as judged by an elevated filling pressure, was seen in over one-half of the patients studied. Incompetence was believed due to (a) the increased pulmonary pressure load and (b) underlying myocardial damage from rheumatic fever.