470 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



-50 -25 25 



NET RICHT-lo-LEFT SHUNT - 



50 75 



Per Cent 



FIG. 42. Relation of ratio between calculated pulmonary and 

 systemic vascular resistances to net intracardiac shunt in 17 

 patients with persistent common atrioventricular canal. Note 

 that, as pulmonary resistance increases to levels in excess of 

 systemic vascular resistance, left -to-right shunt decreases and is 

 eventually exceeded by shimt in right-to-left direction. 



less severe in such cases, depending" on the severity of 

 the defects, and vary widely in nature from acyanotic 

 patients with a liigh pulmonary blood flow to severely 

 cyanotic patients with a very low pulmonary flow, 

 depending on the relative severity of the pulmonary 

 stenosis and the size of the ventricular septal defect. 



AORTIC PULMONARY DEFECT WITH V.\LVUL.%R STENOSIS. 



With aortic stenosis. Communications between the aorta 

 and the pulmonary artery associated with aortic 

 stenosis produce hemodynamic alterations similar to 

 those of either of the defects alone; however, the in- 

 crease in left x'entricular work is considerably greater 

 than it would be if either of these defects existed as a 

 single lesion. When blood shunts in the left-to-right 

 direction through the aortic-pulmonary communica- 

 tion, this shunted blood plus blood returning from 

 the systemic veins traverses the pulmonary circuit, 

 enters the left side of the heart, and is pumped by the 

 left ventricle again into the .systemic circulation. The 

 blood flow through the left ventricle in this situation 

 may be greater than two times the normal systemic 

 blood flow. Since the systolic pressure generated in 

 the left ventricle to force blood through a stenotic 

 valve is directly related to the amount of blood flow 

 through this valve, it is apparent that the left ven- 

 tricular pressure required to drive this high flow of 

 blood through a stenotic valve will be markedly in- 

 creased. Thus the presence of aortic stenosis in pa- 

 tients with aortic-pulmonary communication will 



predispose to left-heart failure and hence to more rapid 

 development of elevated left atrial, pulmonary-venous 

 and pulmonary-artery pressures than is usual when 

 these defects occur as single lesions. 



Aortic-pulmonary defect with initral stenosis. Mitral 

 stenosis may be associated with a coexisting patent 

 ductus arteriosus or other forms of aortic-pulmonary 

 communication. The flow of blood through the defect 

 is usually in the left-to-right direction. The incidence 

 of pulmonary hypertension and increased pulmonary 

 vascular resistance is greater because of the presence 

 of a combination of predisposing factors. These are 

 an elevated left atrial and pulmonary venous pressure 

 owing to the mitral stenosis and an increased pul- 

 monary-artery blood flow or pressure, or both, owing 

 to the aortic-pulmonary communication. The pul- 

 monary vascular resistance may be increased to the 

 point that there is a reversal of the shunt, with blood 

 flowing through the defect in the right-to-left direc- 

 tion. In these cases the aortic-pulmonary communica- 

 tion may act as an escape mechanism or "safety valve" 

 to the high pressure created in the pulmonary vas- 

 cular bed, thus preventing "overloading" of the right 

 ventricle. 



Aortic-pulmonary defect with pulmonary or tricuspid steno- 

 sis. Since the volume of blood flowing through the 

 pulmonary and tricuspid valves is not affected directly 

 by the presence of an aortic-pulmonary communica- 

 tion, no unusual multiplication of the hemodynamic 

 effects caused by the single defects would be expected 

 from the coexistence of either pulmonary or tricuspid 

 stenosis with an aortic-pulmonary communication. In 

 general, the hemodynamic alterations produced by 

 the coexistence of these defects are the result of the 

 simple additive eff^ects caused by the defects when 

 present as isolated lesions. 



VENTRICUL.-\R SEPT.^L DEFECT WITH VALVUL.^R STENO- 

 SIS. With aortic stenosis. The hemodynamic alterations 

 resulting from a ventricular septal defect in associa- 

 tion with aortic stenosis are more severe than those 

 caused by an equivalent-sized aortic-pulmonary com- 

 mimication and degree of aortic stenosis. This is due 

 to the fact that tlie high pressure in the left ventricle 

 required to force blood through the stenotic valve 

 also acts to increase the magnitude of the left-to-right 

 shunt through the ventricular septal defect. Both 

 effects increase left ventricular work and contribute to 

 the degree of pulmonary hypertension that will invari- 

 aljly exist if the \entricular septal defect is large. 



In this condition it is apparent that the systolic 

 blood pressure in the pulmonary artery may be sig- 



