Bernard L. Charms

Unilateral Pulmonary Artery Absence or Hypoplasia Radiographic and Cardiopulmonary Studies in Five Patients

The clinical entity of unilateral pulmonary artery absence or hypoplasia can be readily diagnosed on the basis of routine clinical evaluation. This report is based upon 5 patients in whom the diagnosis was suspected and eventually confirmed with the aid of special studies. Characteristic hemodynamic findings were demonstrated by means of cardiac catheterization and contrast visualization of the cardiopulmonary system.

Primary pulmonary hypertension. Effect of unilateral pulmonary artery occlusion and infusion of acetylcholine.

Abstract A case of primary pulmonary hypertension is presented with evidence of increased vascular tone. Temporary unilateral occlusion of right middle and lower lobes caused a decrease in estimated arteriolar resistance of unoccluded lung. Infusion of acetylcholine caused a profound decrease in pulmonary artery pressure and pulmonary arteriolar resistance without any systemic effects, suggesting direct action of the drug on the pulmonary arterioles. It is suggested that, in this case, increased tone is the primary defect and the histologic vascular changes secondary.

Ventricular septal aneurysms. A report of two cases.

Two cases of ventricular septal aneurysm are reported, one in the membranous septum and one in the muscular portion. The diagnosis was made by selective left ventricular angiography. It is suggested that these cases represent spontaneous closure of a ventricular septal defect with weakness and aneurysmal[see table in the PDF file]formation due to the high left ventricular pressure. Both are asymptomatic and hemodynamically within normal limits. Surgical repair of the aneurysms is not considered necessary.

Hemodynamic Studies in a Case of Carcinoid Cardiovascular Syndrome

A case of malignant carcinoid metastatic to the liver with the typical features of the carcinoid cardiovascular syndrome has been presented. Hemodynamic data obtained at cardiac catheterization indicated the presence of tricuspid insufficiency, low cardiac output, and slight pulmonary hypertension. Unilateral pulmonary artery occlusion studies were reported that suggest the absence of intrinsic pulmonary vascular disease in this syndrome. The paradox of infrequent instances of significant pulmonary hypertension in the presence of serotonin in the reported cases of carcinoid cardiovascular syndrome was discussed. The effect of reserpine on pulmonary artery pressure was reported.

Factors affecting the pulmonary “capillary” pressure∗

Abstract 1. 1. Pressure in a major branch of a pulmonary artery beyond an occluding balloon invariably fell to pulmonary capillary levels and resembled the latter closely. 2. 2. Distal pressures correlated well with pulmonary capillary pressures and were normal in control patients and elevated in those with left ventricular failure and/or mitral disease. 3. 3. In pulmonary emphysema, the distal and pulmonary capillary pressures varied greatly with respiration and occasionally reached considerably elevated levels during expiration. Exercise in such patients caused a significant apparent rise in wedge pressure. 4. 4. The role of bronchomotor tone and intraalveolar and intrapleural pressures are discussed with regard to their possible role in regulating pulmonary artery pressure. 5. 5. The method has been of value in obtaining pulmonary capillary or distal pressures in those individuals, particularly with pulmonary artery hypertension, in whom such pressures were otherwise unobtainable. 6. 6. The danger of using a static figure or zero in obtaining pulmonary arterial-pulmonary capillary gradients for calculation of pulmonary resistances, particularly in pulmonary emphysema, is emphasized.

Effect of Acetylcholine on the Pulmonary Circulation in Patients with Chronic Pulmonary Disease

Twenty-seven patients with various forms of chronic pulmonary disease have been studied with constant infusion of acetylcholine directly into the pulmonary artery. Although many showed a slight decrease in pulmonary artery pressure, this was not great and those with the highest pressures showed the least response. Pulmonary resistances showed similar small changes, if any. Arterial oxygen saturations did not fall uniformly and in those with the lowest levels, an actual increase was observed. It is suggested that vasomotor activity is only one of several factors determining pulmonary artery pressure in patients with chronic pulmonary disease and that anatomic or extravascular factors may become primary. Vasomotor activity seems to be relatively unimportant in the regulation of ventilation/perfusion relationships in patients with far-advanced disease.