460 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION 



EARPIECE fs.sj 

 Oi Sol. % 



RADIAL 60 

 ARTERY 



E 

 E 

 I 



Ul 

 Q: 



w PRESSURE 



Ul 



CATHETER 40 — 



M<on 

 Preuura 

 20 



HEART RATE 

 /beals/minutel 



—I 30 



Mean 

 Pressure 



TIME (saconds) I 



FIG. 31. Effect of change from breathing air to breathing 99.5% oxygen on systemic and pulmo- 

 nary-artery pressures, heart rate, and arterial oxygen saturation in 8-month-old boy with ventricular 

 septal defect (area 1.3 cm'-/m-). Note that arterial oxygen saturation began to increase within 3 sec 

 and pulmonary-artery pressure to decrease within 10 sec after change from breathing air to breathing 

 99.5'^i oxygen. Pulse and mean pressures were recorded simultaneously with double galvanometer 

 assemblies. Decrease in pulmonary-artery pressure associated with oxygen breathing has been shown 

 to be associated with increase in pulmonary blood flow (left -to-right shunt) and decrease in pulmo- 

 nary vascular resistance. 



of exercise on the pulmonary vascular d\ namics in 

 patients with intracardiac or aortopulmonary left- 

 to-right shunts. They demonstrated that pulmonary 

 resistance increased during exercise in patients with 

 pulmonary hypertension and either increased or 

 remained unchanged in patients without pulmonary 

 hypertension. A normal decline in systemic vascular 

 resistance during exercise was observed in both 

 groups. This differing response of the pulmonary 

 and systemic circuits to exercise was considered to 

 be the underlying basis for the relatively small change 

 in pulmonary flow during exercise in patients with 

 large defects. 



THE EiSENMENGER COMPLEX. Ill 1 897 Eisenmengcr 

 (91) described in detail a typical example of the 

 condition that has since become known as Eisen- 

 menger's complex. His case was that of a 32 -year-old 

 man who was cyanotic. At necrop.sy a large ventric- 

 ular septal defect was found which was so positioned 

 that the lumen of the aortic orifice fell half over the 

 left ventricular outflow tract and half over the right. 

 He discussed the "overriding aorta" at considerable 

 length and concluded that it played no part in the 

 physiologic disturbances of the circulation. He also 

 stated that in otherwise uncomplicated ventricular 

 septal dcfcrt, pulmonary hypertension resulting from 



obstruction in the pulmonary circulation would 

 abolish the left-to-right shunt. 



Abbott & Dawson {2) attributed the cyanosis of 

 Eisemenger's case to a right-to-left shunt through 

 the defect because of the overriding aorta. Taussig 

 (247) also stated that "the essential feature of the 

 Eisenmenger complex is that the aorta is dextroposed 

 and overrides the right ventricle." It was not until 

 1947 that Bing and co-workers (30) demonstrated 

 pulmonary hypertension at pulmonary level with 

 bidirectional shunt in five cases of Eisenmenger's 

 complex. Since then many studies have confirmed 

 that pulmonary h)pertension equivalent to systemic 

 pressure is invariably present in Eisenmenger's com- 

 plex (49, 216, 275). It has been found as a result of 

 such studies that anatomic overriding of the aorta 

 may or may not be found at necropsy in clinicalh' 

 undistinguishable cases, and as a result the concept 

 has developed that Eisenmenger's complex is pul- 

 monary hypertension with reversed or bidirectional 

 siiunt through a large ventricular septal defect (277). 



That overriding of the aorta plays no significant 

 role in the altered hemodynamics of patients with 

 ventricular septal defect is now generally accepted 

 (277) and thus the term seems no longer necessary 



Wood (275) however, uses the term "Ei.senmenger 



