CARDIAC TRANSMliMBkANli POTl-NTIAI.S -HOFFMAN 321 



Fig. 15. — Effect of high and low calcium on transmembrane potentials of ventricular tissue. 

 (A) Control record from a ventricular fiber. (B) The effect of a calcium concentration 4 

 times normal (10.8 mM). (C) Control record from a papillary fiber. (D) The effect of a 

 calcium concentration of Vio normal (0.27 mM). 



dtiration of the relative and absolute refractory periods encountered dvu'ing hypo- 

 thermia is a direct result of changes in the duration of several components of the 

 transmembrane action potential. The relatively greater prolongation of the plateau 

 in comparison to the terminal phase of repolarization agrees with the observation 

 that absolute refractoriness is prolonged relatively more than the relative refractory 

 period by decreased heart temperature. 



Excitability changes during hypothermia are varied. In some instances changes 

 in threshold are not prominent^" and this observation is supported by studies of the 

 critical threshold potential of the isolated Purkinje fiber pacemaker. In other cases 

 there is an abrupt loss of excitability in the intact heart. This occurrence may be 

 due to the marked drop in resting potential seen in some fibers at temperatures 

 below^ 25-20° C. and the known relationships between resting potential and excita- 

 bility. On the other hand, loss of excitability may result from failure of repolariza- 

 tion which sometimes occurs during cooling. 



In support of the statement that arrhythmias in the intact, cooled heart are not a 

 direct effect of temperature on the myocardium is the observation that in isolated 

 preparations of auricle, ventricle, and specialized conducting tissue, where changes 

 in pH and Pco^ are minimal, low temperature does not result in fibrillatory activity. 



Studies of the transmembrane potentials of single cardiac fibers also support 

 several other observations concerning the nature of excitability changes during 

 hypothermia. Low temperature has been shown to result in a decrease in resting 

 potential. Results obtained from studies of mammalian skeletal muscle^- and iso- 

 lated nerve fibers^^ as well as cardiac muscle demonstrate that this decrease in 

 resting potential is associated with a loss of intracellular potassium. Several 

 mechanisms might be responsible for this loss ; important possibilities are : first, a 

 direct effect of the membrane potential on K efflux, and second, a decrease in active 



