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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



elusions were reached by Silver et al. (222) in studies 

 on dogs with artificially created atrial septal defects. 



As already mentioned, there may be a reversal in 

 gradient of left and right atrial pressures at various 

 phases of the cardiac cycle, particularly early in atrial 

 systole and iinmcdlatcly after atrial systole, with con- 

 sequent momentary shunting of blood from right to 

 left. This venoarterial shunting is usually of insuffi- 

 cient quantity to cause demonstrable decreases in oxy- 

 gen saturation of peripheral arterial blood. It is pos- 

 sible, though, to demonstrate the right-to-left shunt 

 with arterial dye-dilution techniques (236). Because of 

 the anatomic relations of the wall of the right atrium 

 and the cava, a natural channel for blood flow is cre- 

 ated from the inferior vena cava to the foramen ovale 

 (fig. 35). Consequently, that blood which shunts from 

 right to left has been shown to be composed pre- 

 dominantly of blood from the inferior vena cava. 

 Appro.ximately 70 per cent of patients with atrial 

 septal defect have right-to-left shunting from the in- 

 ferior vena cava demonstrable by indicator-dilution 

 curves. This preferential left-to-right shunting from 

 the right pulmonary veins and right-to-left shunting 

 from the inferior vena cava is evidence of incomplete 

 mixing of blood in the two atria. 



Further evidence for incomplete mixing of blood has 

 been obtained from saturation data from the right side 

 of the heart. Weidman and associates (258) demon- 

 strated that samples of blood drawn from different 

 sites in the right atrium and from the right ventricle 

 and right atrium in rapid succession through an oxim- 

 eter were difTerent in many patients with atrial septal 

 defects; however, this difference was not constant when 

 rapidly successive samples drawn from the two sides of 

 the tricuspid valve were repeated. He described two 

 patients in whom oxygen saturation of blood with- 

 drawn from the right ventricle was 6 to 8 per cent 

 higher than that of samples from the right atrium; 

 however at operation for correction of those defects 

 the ventricular system was found to be intact in each. 



In the unanesthetized patient, oxygen saturation of 

 blood from the inferior vena cava averages 7 per cent 

 higher than that in the superior vena cava (19); thus 

 even in a subject with an intact septum the oxygen 

 saturation of blood in the right atrium ma\' be higher 

 than that in the superior vena cava. 



PULMONARY-ARTERY PRESSURE .AND RESIST .•\NCE. De- 

 spite the marked increase in pulmonary blood flow, 

 the pressure in the pulmonary artery remains normal 

 or only minimally elevated in many patients with 

 atrial septal defect. The pulmonary vascular bed ap- 



FIG. 35. Interior of heart viewed from inferior \ena cava in 

 patient with atrial septal defect. Dorsal wall of inferior vena 

 cava is at top of picture. Note position of muscular ridge, derived 

 from septum secundum which separates left from right atrium. 

 \ free communication exists between the atria; however, the 

 direction of flow of a portion of the blood entering the right 

 atrium from the inferior vena cava is directly into the left 

 atrium, thus predisposing to right-to-left shunting of this portion 

 of systemic venous return. 



parently responds to the increase in blood flow by an 

 increase in the total cross-sectional area of the resist- 

 ance vessels, with a fall in pulmonar)- va.scular re- 

 sistance. Auchincloss and colleagues (15), Rankin & 

 Callies (197) and Bedell (24) have found that patients 

 with intra-atrial and \entricular septal defects with 

 normal pulmonary-artery pressures have an increased 

 pulmonary diffusion capacity which they believe 

 represents an increase in the size of the resting pul- 

 monary capillary bed. Rankin & Callies (197) have 

 measured the pulmonary capillary blood volume and 

 found it to be increa.sed in patients with intracardiac 

 shunts and normal pressures in the pulmonary circu- 

 lation. 



Pulmonary hypertension associated witli atrial 

 septal defect differs frorn hypertension associated with 

 ventricular septal defect or patent ductus arteriosus in 

 that it is an acquired complication, rather than a 

 necessary hemodynamic consequence of a commiuii- 

 cation between the pulmonary artery and the aorta or 

 between the ventricles which is large enough to 

 equalize pressures between the two circuits from 

 birth. In the experience of Dexter (78) and Weidman 

 and associates (258) it was uncommon to find se\'ere 

 puhnonarN hypertension associated with atrial septal 

 defect in patients less than 20 years of age. In certain 

 patients, however, for reasons not understood, pul- 



