408 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



valve and infundibulum are recapitulated. As is apparent, the only death following 

 valvular operation occurred in a patient in whom there was an associated large 

 atrial septal defect, the so-called Trilogy of Fallot. This infant died of some form 

 of circulatory failure 16 hours following operation. This anomaly poses special 

 problems and we are still uncertain whether one should repair the septal defect 

 or the valve first, or should one attempt both at the same sitting. For resection of 

 infundibular stenosis, one must be careful not to resect too much. In one patient, 

 with Tetralogy, for example, following infundibular resection, a large aneurysmal 

 dilatation of the thin-walled infundibular cJianibcr occurred. Subsequent attempt 

 to repair this complication was fatal. The other death occurred as a result of 

 staphylococcic septicemia following a two week period of anviria. This patient under- 

 went ventricular fibrillation during surgery, and a period of hypotension presumably 

 occurred during resuscitation. This is the only death in this entire group in which 

 hypothermia itself was considered to be contributory. 



Atrial septal defect (table IV) is also well-managed by direct vision suture, using 

 cooling to allow circulatory arrest. Particularly satisfactory are those patients with 

 the so-called secundum-type lesion. A continuous suture is extremely efifective in 

 obtaining complete closure of these lesions, while aberrant pulmonary veins can be 

 easily positioned to the left of the closure, except those which enter into the 

 superior vena cava itself. Primum-type lesions or atrio-ventricularis communis are 

 more difficult technically to manage within the allotted time limit. One of the deaths 

 resulted from hemorrhage immediately postoperatively following attempt to repair 

 atrial septal defect after conclusion of pulmonary valvuloplasty in a patient with 

 Trilogy. As mentioned previously, three deaths were associated with thrombo- 

 embolism, presumably of the pulmonary vascular tree, either arterial or venous. 

 We believe for adults, therefore, that anti-coagulants should be given for a period 

 of two weeks following repair of atrial septal defect. The other death occurred on 

 the artificial kidney 12 days postoperatively, the anuria presumably due to trans- 

 fusion reaction. 



Ventricular septal defect, on the other hand, is a lesion of sufficient complexity 

 anatomically to render the technical repair too difficult to accomplish safely within 

 the current eight minute time limitation. As can be seen, only one of five patients 

 survived such attempts. Two others had successful closure, but died a circulatory 

 death within a few hours postoperatively. The other two were technical failures. 

 This experience led us to abandon this procedure until longer periods for open 

 operation became safely available, either by use of extra-corporeal circulations, or 

 by better application of hypothermia. 



TABLE IV 

 Operations for Atrial Septal Defect 



Disease Patients 



Auricular septal defect (secundum) 30 



Auricular septal defect (primuni ) 4 



Trilogy 2 



36 22 



