ARTERIAL BLOOD -2fi-p 

 (Os Sat. %) ^^ 



RESPIRATION 



(mm 

 FEMORAL 

 ARTERY 

 100 



PULMONARY 

 ARTERY 50 



PHYSIOLOGIC CONSEQUENCES OF CONGENITAL HEART DISEASE 



BREATHING AIR 



457 



Base Line- 



0.25 mg Acetylcholine / minute into Pulmonary \Artery 



K— ' • ^ 



10 seconds 



KIG. 28. Effect of continuous infusion of acetylcholine into pulmonary artery on systemic and 

 pulmonary arterial pressures and other variables in an 8-year-old boy with large ventricular septal 

 defect. Note that in control period, pressures in femoral and pulmonary arteries were closely similar 

 so that right and left ventricular pressures were essentially equal. Infusion caused striking decrea.se 

 in estimated pulmonary vascular resistance, from 1620 to 510 dynes sec cm"*. This was associated 

 with decrease of systolic pressure in pulmonary artery from 95 to 65, while systolic pressure in femoral 

 artery decreased to 80 mm of mercury. The fact that heart and respiratory rates were unchanged 

 during infusion indicates that acetylcholine was inactivated before reaching systemic arterial vessels. 

 Area of this defect was sufficient to equalize right and left ventricular systolic pressures in control 

 period and was such as to compromise ability of left ventricle to maintain systemic arterial pressure 

 during infusion because of very large runoff through ventricular septal defect consequent to large 

 decrease in pulmonary vascular resistance caused by acetylcholine. In this situation a small pressure 

 gradient of approximately 15 mm of mercury across defect did develop. [From Shepherd el al. (221).] 



choline into the pulmonary artery in such patients 

 (fig. 28). When a large decrease in pulmonary vascu- 

 lar resistance results, there is a large increase in the 

 left-to-right shunt (blood flow across the defect), 

 and a significant difference in right and left ventricu- 

 lar systolic pressures develops. 



There is a demonstrable correlation between the 

 blood flow through small ventricular septal defects 

 and the size of such defects (208). When the ventric- 

 ular septal defect is large, however, such a relation- 

 ship is no longer demonstrable (fig. 29). Systemic 

 blood flow and vascular resistance are usually main- 

 tained in the presence of a ventricular septal defect, 

 hence the blood flow across a large ventricular septal 

 defect is determined primarily by the level of pul- 

 monary vascular resistance. These concepts are in 

 general agreement with those of Selzcr (214), Wood 

 and co-workers (279), Blount and colleagues (34), 

 Brotmacher & Campbell (43), and Imperial et d. 

 (i4>). 



The relationship of the location of the defect to the 

 associated hemodynamic effects has been contro- 

 versial. Taussig (247), in classifying ventricular septal 

 defects as high and simple defects, claimed that the 

 former had a more profound eflTect on the pulmonary 

 circulation than did the latter. Selzer (215), however. 



I ■• I ' I I I ' I ' 

 - • • _ 



- • •• • - 



• • • 



• / 



0/23456 

 SIZE OF VENTRICULAR SEPTAL DEFECT 

 I cm ^ / m ^ Body Surface Area ) 

 FIG. 29. Relationship of magnitude of blood flow across 

 ventricular septal defect to size (area) of defect in 39 patients 

 breathing air. Note that in this group of patients, most of whom 

 had large ventricular septal defects, no relationship is apparent 

 between these two parameters. See text for discussion. [From 

 Savard et aL (208).] 



found no correlation of location with cardiac dynamic 

 alterations. Becu and colleagues (23) and Zachari- 

 oudakis and associates (286) were in agreement with 

 this. Warden et al. (256), however, from surgical ob- 



