PHYSIOLOGIC CONSEQUENCES OF CONGENITAL HEART DISEASE 



477 



a normal arterial oxygen saturation is the slowed 

 peripheral circulation that may accompany heart 

 failure. 



Arterial hypoxemia resulting from venoarterial 

 shunting causes physiologic alterations in the circula- 

 tory system. Various compensatory mechanisms result 

 which enable the individual better to tolerate the ar- 

 terial hypoxemia. Many of these adaptive mecha- 

 nisms are also present in high-altitude dwellers. The 

 following discussion will be concerned mainly with 

 the adaptive mechanisms that occur with hypoxia, 

 and some mention will also be made of studies carried 

 out in high-altitude dwellers. 



VALUES ENCOUNTERED. Burcliell and colleagues (49) 

 noted that among persons with cardiac malformations 

 that permit venoarterial shunts, the oxygen saturation 

 of systemic arterial blood varies widely, but when such 

 persons are in a good state of nutrition it usually is 

 more than 70 per cent. Marked decreases in arterial 

 oxygen saturation may occur when they exercise. 

 Values of less than 25 per cent for arterial oxygen 

 saturation have been encountered in several such pa- 

 tients in this laboratory when they were walking in a 

 fully conscious state on a treadmill. 



In studies of the circulation of men at high altitudes, 

 Husson & Otis (139) found that man does not seem 

 to dwell permanently at altitudes where his arterial 

 oxygen saturation would be much below 70 per cent. 

 They have shown that when man is chronically ex- 

 posed to hypoxia the combined oxygen in his arterial 

 blood will increase, because of the increased carrying 

 capacity, only until the hypoxia is so severe as to cause 

 a saturation of 70 per cent. 



DETERMINANTS OF ."iRTERIAL OXYGEN SATURATION. The 



major factors that determine the arterial oxygen 

 saturation in individuals with venoarterial shunts are 

 the pulmonary blood flow and the amount of oxygen 

 extracted by the tissues (oxygen consumption). 



An increase in pulmonary blood flow increases the 

 volume of fully saturated blood contributing to sys- 

 temic flow, whereas a reduction in oxygen consump- 

 tion allows a higher oxygen saturation of systemic 

 venous blood returning to the heart. Both factors tend 

 to increase the o.xygen content of the venoarterial 

 mixture that enters the arterial supply to the body. 

 The possibility of an adaptive mechanism whereby a 

 threshold value below which the oxygen tension of 

 arterial blood would act as a stimulus for an increase 

 in systemic flow has not been established in patients 

 with venoarterial shunts (49). Extensive investigations 



have been carried out at high altitude concerning the 

 effect of the hypoxemia on cardiac output. The work 

 of A.smussen & Consolazio (14) and of GroUman (123) 

 indicated that an increase in systemic flow occurred 

 early in the acclimatization period. Grollman, from 

 observations on hypoxia produced by mixtures of 

 oxygen and nitrogen, concluded that the stimulus 

 came at rather specific levels of hypoxia (when the 

 oxygen in the inspired mixture dropped to 11.6%). 

 Such a stimulus threshold was supported by observa- 

 tions of Asmussen & Chiodi (13), who found that the 

 oxygen in the inspired air had to be low enough to re- 

 duce the arterial oxyhemoglobin to 70 to 80 per cent 

 of normal in order to produce an increase in the 

 cardiac output. In individuals acclimatized to low 

 barometric pressure in a low-pressure chamber for 

 several days, Houston & Riley (134) found an in- 

 creased cardiac output as one of the less significant 

 compensating mechanisms. A recent review of the 

 circulatory adaptations to hypoxia of types other than 

 the result of venoarterial shunts has been published 

 (154). Although changes in systemic blood flow may 

 cause temporary alterations in arterial oxygen satura- 

 tion in individuals with venoarterial shunts, systemic 

 blood flow by itself is not one of the primary deter- 

 minants of the level of arterial oxygen saturation in 

 such individuals. 



The level of arterial blood oxygen saturation in such 

 patients is primarily dependent on the volume of pul- 

 monary blood flow. The higher this flow, the higher 

 will be the oxygen saturation of arterial blood. For 

 example, patients with tetralogy of Fallot who have 

 very low pulmonary blood flow uniformly have low 

 oxygen saturation of the arterial blood whereas, in 

 contrast, patients who have total anomalous pul- 

 monary venous connection to the right atrium with 

 complete venous admixture, but with very high pul- 

 monary flows, frequently have an arterial oxygen 

 saturation of more than 90 per cent and consequently 

 may be acyanotic. However, if the pulmonary flow 

 is reduced in these patients to the point where it is 

 equivalent to systemic flow, arterial desaturation ap- 

 pears to the degree that cvanosis will become evident 



(49). 



As an example, consider a patient in whom there is 



complete mixing of pulmonary and systemic venous 



blood and the pulmonary blood flow is three times as 



large as systemic flow. If 5 liters of systemic venous 



blood (6.7 g of reduced hemoglobin per 100 ml) were 



completely mixed with 15 liters of fully oxygenated 



blood from the lungs, arterial blood would contain 



only 1.7 g of reduced hemoglobin per 100 ml. If pul- 



