Hemodynamic basis for clinical manifestations of patent ductus arteriosus

Abstract

A prosthesis made of silicone rubber has been developed for insertion between the aorta and pulmonary artery of dogs. The size of the communication can be controlled in the closed-chest, unanesthetized animal. The hemodynamic effects of complete acute opening and closing of the shunt have been studied in 35 dogs. The basic hemodynamic changes are related to a decrease in systemic vascular resistance, an increase in pulmonary blood flow, and direct transmission of aortic pressure to the pulmonary artery. When the shunt is opened, there is an immediate decrease in aortic and left ventricular systolic pressure, a rise in pulmonary arterial, left atrial, and left ventricular end-diastolic pressure, an increased stroke volume, and an increased heart rate. A systolic gradient between the left ventricle and the aorta frequently develops when the shunt is opened, and is probably related to the high stroke volume which occurs. The pulmonary arterial pressure tracing shows a triphasic contour when the shunt is open; left ventricular ejection is slightly prolonged, but the right ventricular ejection period is markedly reduced. This explains the paradoxical splitting of the second sound, which is also observed in some patients with patent ductus arteriosus. Systemic blood flow is moderately reduced, but pulmonary blood flow is increased about twofold. Pulmonary diastolic blood flow is markedly increased, so that peripheral pulmonary blood flow becomes much more continuous. During diastole, blood flows perferentially into the low-resistance shunt and pulmonary vascular system, and a marked backflow during diastole occurs in the descending aorta distal to the shunt. The animals varied in their ability to tolerate the shunt. After the initial responses, some dogs showed a gradual increase in aortic stroke volume and left ventricular systolic pressure, and tolerated the shunt well. Others developed a “failure response” that was characterized by a continuing fall in aortic stroke volume and left ventricular systolic pressure, with a rise in left ventricular end-diastolic, left atrial, and pulmonary arterial pressures.