Case Studies In Small Animal
Text from "Small Animal Cardiovascular Medicine"
PATHOPHYSIOLOGY OF PDA
Grade 3, 4, and 5 ductal abnormalities result in shunting of blood from the systemic circulation into the pulmonary circulation (left-to-right shunt). Flow occurs in both systole and diastole. Systolic flow occurs as the left ventricle pumps blood into the aorta and produces a systolic pressure (developed energy). Diastolic flow occurs because the pressure developed in the aorta forces blood from the higher pressure systemic circuit to the lower pressure pulmonary circuit (kinetic energy). Because the ductus constricts at the pulmonary artery end, it provides resistance to flow. Consequently, there is a pressure gradient between the aorta and pulmonary artery and the mean systemic and pulmonary pressures are usually normal. As such, the consequences of this type of PDA are purely related to the amount of blood flow that crosses the ductus. As can be deduced from the previous section, the amount of flow across a PDA is dependent on the size of the smallest orifice in the PDA and the relative resistances of the systemic and pulmonary circulations. It is not dependent on the pressure gradient per se. Whatever blood flow is "lost" from the systemic circulation through the PDA must be countered by an equal increase in left heart systolic blood flow if systemic flow is to remain normal. Conversely, whatever blood flows through the ductus returns to the left heart and must be pumped out again. The blood that flows from the aorta into the pulmonary artery mixes with normal pulmonary blood flow, traverses the lungs and returns to the left heart. To accommodate this increased return of diastolic blood flow and to increase the amount of left ventricular systolic blood flow to compensate for the blood shunted through the PDA, the left ventricle grows to a larger size. As discussed under general pathophysiology, this is volume overload or eccentric hypertrophy. In PDA there is an absolute increase in circulating blood volume that is proportionate to the size of the shunt. The net increase in blood volume recirculates within the ductus, pulmonary vasculature, left heart, and proximal aorta. This increase in volume results in increases in the size of all structures involved.
If the ductus has enough smooth muscle to markedly constrict the pulmonary artery end of the ductus as well as various other portions of the duct (grade 3), resistance to flow is high resulting in a small shunt. In this case the left ventricle can adapt to the small leak easily through volume overload hypertrophy resulting in no serious hemodynamic sequelae. If the ductus undergoes moderate constriction at the pulmonary artery end (grade 4), the left ventricle must grow larger to accommodate and pump more blood. No immediate hemodynamic sequelae may be observed. However, the chronic volume overload in this case can lead to myocardial failure over several years. Such a case might then present to a veterinarian at 7-10 years of age in left congestive heart failure. In a grade 5 ductus, shunt flow is hemodynamically large. A large shunt commonly overwhelms the ability of the left heart to compensate through volume overload hypertrophy. Consequently, the increased volume load results in an increase in left ventricular end-diastolic pressure. This results in pulmonary edema (congestive left heart failure). Left heart failure most commonly occurs between a few weeks and six months of age.
The presence of a PDA alters left heart function. The left ventricle and left atrium grow in size primarily in proportion to the size of the shunt. In a dog with a large PDA, the end-diastolic diameter and volume are increased maximally, primarily through volume overload hypertrophy. In addition to the increase in end-diastolic diameter, an increase in end-systolic diameter and volume are appreciated on an echocardiogram. Increased afterload or decreased myocardial contractility increase end-systolic diameter. The increase in the chamber radius coupled with the normal intraventricular pressure and wall thickness results in an increase in systolic myocardial wall stress (afterload). This must contribute to the increase in end-systolic size. Myocardial failure also occurs, especially in longstanding cases. The increases in end-diastolic and end-systolic sizes are usually almost equal, resulting in normal myocardial wall motion (shortening fraction). The increase in chamber size in diastole coupled with normal wall motion results in an increase in stroke volume pumped into the aorta.
Pressures in the above diagram are listed as systolic/diastolic. Oxygen saturation in different regions are in circles. DA - ductus arteriosus; a - A wave; v - V wave; m - mean pressure.
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.