DRUGS AND INTERNAL COOLING— DAMMANN and MULLER 425 



Hypothermia is alleged to predispose to the development of ventricular fil)rilla- 

 tion. Many authors have concluded that it is not wise to lower temperature below 

 twenty-six degrees centigrade because of the high incidence of ventricular arrhyth- 

 mia. For the same reason, some authors have felt that hypothermia was indicated 

 only in intra-auricular or great vessel surgery but not in surgery involving enter- 

 ing the ventricle itself. Lillehei'" has repeatedly stated that it is mandatory to 

 maintain normal temperatures in patients undergoing a ventriculotomy during 

 cross-circulation. 



There is some reason to doubt that hypotbennia. itself, increases the tendency 

 toward ventricular fibrillation. Lewis's work with carjjon dioxide/^^^" Osborn's'^° 

 studies of pH changes during hypthermia and a recent publication of Covino and 

 Hegnauer^'^ all indicate that changes in blood pIT are the important factors in the 

 production of ventricular fibrillation rather than liypothermia. Hegnauer demon- 

 strated that alterations in pH in both directions increased myocardial irritability. 

 In the experimental animal when pH was controlled, hypothermia had little direct 

 effect on myocardial irritability. All authors have agreed that pH tends to shift 

 towards the acid side, particularly at a temperature of twenty-six or below. Osborn 

 suggests that this shift is related to a total reduction in pulmonary blood flow, for 

 although the blood carbon dioxide level is high, the alveolar carbon dioxide level 

 is low. Vigorous hyperventilation is helpful but perhaps is not sufficient. Occlusion 

 of the heart during an intracardiac procedure certainly alters pH. During the period 

 of complete occlusion, circulation ceases, carbon dioxide accumulates and, immedi- 

 ately after the resumption of circulation, there is a marked increase in blood carbon 

 dioxide. Swan attempts to control this shift by vigorous hyperventilation before 

 the period of occlusion. He makes every efifort to have the venous pH level above 

 7.5 immediately prior to occlusion.® Osborn increased the total available base by 

 submitting animals to a prolonged high carbon dioxide environment prior to cool- 

 ing, believing that the acidosis developing at very low temperatures could then be 

 buffered more readily. 



It is not the purpose of this discussion to^ consider alterations in electrolytes, 

 alterations in pH or the possible causes of ventricular fibrillation during hypo- 

 thermia. It is important to point out, however, that no matter what the mechanism 

 of pH shift, vein-to-artery cooling combined with an artificial oxygenator offers an 

 excellent method of maintaining a normal blood pH. Furthermore, no matter 

 whether ventricular fibrillation is brought about by change in blood pH, h\ reduc- 

 tion of coronary perfusion,^'- by decreased efficiency of the myocardium''^ or by 

 the type of anesthetic agent, ^* the use of the venous-arterial cooling system com- 

 bined with an oxygenator would appear to offer great promise in reducing the high 

 instance of ventricular fibrillation at low temperatures. Gollan'® has been consistently 

 able to lower the temperatures of experimental animals to zero to four degrees 

 centigrade, producing cardiac arrest and not ventricular fibrillation. The rate of 

 resuscitation has been excellent (13 out of 13). The incidence of post-hypothermic 

 shock was zero in contrast to the high incidence reported by Wegelius and Gollan 

 when the extracorporeal circulation was used only after cooling had been accom- 

 plished. Although he suggests that a continuous quinidine drip prevents ventricular 

 fibrillation, it is hard not to implicate the pump-oxygenator rather than quinidine. 



