290 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



is merely due to propagation of the excitatory process. When the pacemaker tissue 

 cells depolarize or reverse polarity of their membranes, the proximity of a nega- 

 tively charged surface to normal positively charged surrounding tissue sets up a 

 flow of current. This electrotonic current flow tends to depolarize the normal tissue 

 through which it passes, thus touching off a regenerative process. If the tissues 

 have normal excitability and the voltage difference giving rise to current flow is 

 great enough, excitation occurs. 



It is generally conceded that cooling slows conduction and eventually decreases 

 the excitability of tissues. The question thus arises as to the adequacy of the nor- 

 mal means of propagation. It is estimated that in nerves the strength of the excita- 

 tory process involved in conduction of an impulse is three to ten times the threshold 

 requirement (Hodgkin, 1937; Bishop, l'J51). No similar direct determinations 

 have been made in the heart but the older experiments of Junkmann, 1925 and 

 Witz, 1938, indicate a large factor of reserve in the normal propagating mechanism. 



In nerve and the central nervous system cooling produces a very great increase 

 in the duration and a slight increase in the amplitude of action potentials ; even 

 the action potentials of individual fibers are thus modified (see Brooks, Koizumi, 

 and Malcolm, 1955). In the heart, duration of the surface-recorded and transmen- 

 brane potentials is a function of heart rate and/or heart temperature. Schiitz 

 (1936) has reported that repolarization in the cooled heart is completed before 

 recovery of normal excital)ility following origin of a beat. Cooling prolongs the 

 duration of electrical activity and the coefficient for the duration of the monophasic 

 action potential was found to be 22 for every 10° C. (Lepeschkin, 1951 ). The re- 

 lationship between the effect of cooling on repolarization and recovery of excita- 

 bility has not as yet been worked out. 



Progressive cooling of the heart ultimately causes a reduction in height (voltage) 

 of the action potential. Initially, however, the R, S. and T waves increase in 

 amplitude (Hamilton et al., 1937; Decker, 1939; Lange ct ai. 1949). This increase 

 in voltage has been explained on the basis of slowed conduction (see Lepeschkin, 

 1951). Studies of transmembrane action potentials of the heart cells have shown 

 that on cooling of the tissue the height of the potentials and the extent of the over- 

 shoot is increased until a critical temperature is reached (25° C. ) below whicli de- 

 pression occurs in a progressive fashion. The subsequent paper will deal more fully 

 with the effects of cold on the voltage of action potentials. These voltage changes 

 do relate to the strength of the excitatory process in hypothermia. Additional in- 

 formation concerning changes produced in the electrogram and electrocardiogram 

 of man and animals as a result of local or general cooling of the heart is given l)y 

 Lepeschkin (1951). 



The fact that cooling slows conduction indicates that the process of excitatory 

 depolarization is slowed as are repolarizing reactions. The slowing of A-V con- 

 duction (P-R interval increase) and conduction in the ventricle (O-S interval 

 increase) is linear between 40° and 16° C. (Lutz, 1948). Eventually A-Y block de- 

 velops at very low temperatures. Slowed ascent of tlie monophasic action potential 

 has been reported (Schiitz, 1936; Decker, l'>4()) and in studies of individual cellu- 

 lar reactions it has been found that the rate of rise of the transmemljrane action 

 potential is slowed and the process is prolonged. .\ longer time re<|uircnu'nt tor 



