AMORIM, DALMO DES.

Determinations of pressure, blood flows, and calculated pulmonary vascular resistance were made prior to and during acute individual occlusion of the right and left main branches of the pulmonary artery in random sequence in eight anesthetized, closed-chest dogs witn chronic atrial septal defects. Similar observations were made with occlusion of only the left pulmonary artery in three additional dogs. Obstruction of the pulmonary artery to one lung was immediately followed by a rise in systolic pressure in the right ventricle and pulmonary artery proximal to the obstruction, from an average normal value of 33.1 mm. Hg to an average value of 40.9 mm. Hg (range 32 to 47). This change was not associated with demonstrable systematic effects on right atrial or systemic arterial pressure or on the systemic blood flow. As would be expected, the average calculated ratio of pressure to flow (vascular resistance) across the unoccluded lung was elevated during the obstruction. The resistance value during the occlusion, however, was less than the estimated pressure/flow ratio for this same lung, based on the measurements made prior to the occlusion. This apparent effective decrease in vascular resistance of the unoccluded lung is probably related to dilation of the pulmonary vessels as a result of an increase in intravascular pressure caused by the sudden removal of approximately half of the pulmonary vasculature from the circulation. In spite of the elevation in right ventricular systolic pressure, occlusion of the left pulmonary artery was associated with a slight increase in pulmonary blood flow and a definite increase in the magnitude of the left-to-right shunt across the atrial septal defect, whereas no systematic effects were obtained during obstruction of the right branch in association with the same approximate levels of right ventricular systolic pressure. These data are regarded as further evidence that the preferential shunting of blood from the right lung in the presence of an atrial septal defect of the secundum type is primarily due to the anatomical relation between the opening of these vessels into the left atrium and the position of the defect in the atrial septum. Furthermore, they emphasize the importance of dynamic factors, related to the manner, site, and direction in which the pulmonary venous blood drains into the left atrium, as important determinants of the left-to-right shunt via such defects.

Systemic and pulmonary blood flows and pressures were determined in anesthetized closed-chest dogs with chronic atrial septal defects and in dogs with intact cardiac septa. In the former animals, graded obstruction of the main pulmonary artery associated with right ventricular systolic pressures of more than 80 mm. Hg was produced without evidence of failure of the right side of the heart. A considerable decrease in the magnitude of the left-to-right shunts and an increase in the size of the right-to-left shunts occurred; these changes were associated with only minor changes in filling pressure of the right ventricle, and systematic changes in systemic arterial pressure did not appear. Analysis of right atrial pressure pulses suggested the development of an increased force of contraction of the right atrium and no evidence of tricuspid regurgitation under these circumstances. In contrast, partial obstruction of the main pulmonary artery in the dogs with intact cardiac septa, so as to increase the right ventricular systolic pressure to more than 60 mm. ITg, was associated with pronounced increases in mean right atrial pressure and striking decreases in cardiac output and systemic arterial pressure. The pressure recordings from the right atrium and indicator-dilution curves demonstrated the development of significant tricuspid regurgitation. The deterioration of right ventricular function in dogs with intact cardiac septa appears to be related to overdistention of the right ventricle and possibly also to a disproportionate reduction in coronary blood flow to the myocardium caused by a decrease in systemic arterial pressure and the concomitant increase in resistance to coronary venous drainage from the right side of the heart due to the increased right atrial and right ventricular pressures. It is concluded that under the conditions of these studies, an atrial septal defect provides a considerable increase in resistance to the heinodynamic effects associated with right ventricular hypertension caused by acute partial obstruction of the main pulmonary artery. The possible duration of this beneficial effect beyond the 33 to 160 minutes of observation in these studies has not been explored.