CARDIAC EXCITABILITY— BROOKS 297 



action. Such localized excitatory influences predispose to disorganization of normal 

 propagation of impulses, increase vulnerability to fil)rillation, or may actually 

 create arrhythmias. 



(2) Uniform cooling has a selective action on various processes and phases of 

 depolarization and repolarization. When corrections are made for changes in heart 

 rate or rate changes are prevented, it is found that cooling does have definite effects 

 but some response potentialities are affected more than others. 



Thresholds to stimuli applied during diastole are not markedly affected over a 

 wide range of temperature change. As an example, in one experiment threshold in 

 the dog ventricle was 0.13 ma. at 39.4° C. and 0.17 ma. at 26.2° C. while for the 

 auricle the threshold stimulus intensity was 0.19 ma. at 39.7° and 0.18 ma. at 

 26.7° C. All changes observed in the 30 animals studied were usually in hundredths 

 of a milliampere within the temperature range mentioned (see Brooks ct ah, 1955). 

 Cooling below this level did cause a greater decrease in excitability and it has been 

 reported that on rewarming of the heart there is a lag in recovery of normal ex- 

 citability particularly if very low temperatures are reached. 



The testing methods described show that strength-interval curves shift in posi- 

 tion as the heart is cooled, indicating a slowed recovery of excitability, but at least 

 under some conditions of induced hypothermia no consistent change in amplitude 

 or duration of the dips has been observed. Others have found a marked increase in 

 depth of the early dip (Hegnauer and Covino, 1955). This relatively greater 

 temporary supernormality might contribute to vulnerability but the effect of cool- 

 ing on fibrillation thresholds and duration of the vulnerable periods has not as 

 yet been determined. 



It is undeniable that the cooled heart is more susceptible to fibrillation. Auricular 

 and, less frequently, ventricular arrhythmias and fibrillation develop spontaneously 

 in both anesthetized and unanesthetized hypothermic man and other animals. 

 Mechanical stimulation of the cooled heart by inlying catheters tends to produce 

 fibrillation and the general impression is that stimulation by electrical pulses is 

 more likely to result in fibrillation of the cold than of the normally warm heart. 

 Susceptibility of the heart to fibrillation cannot readily be explained on the basis 

 of changes in excitability but there are other changes which should be considered. 



Cooling slows conduction. This is explained by the change in time of rise of the 

 action potential. Since the upswing of the action potential is due to the inward 

 flux of Na"^ one can conclude that cooling slows the regenerative process which 

 permits the sodium influx and/or slows the influx itself (see chapter on cell po- 

 tentials, Hoffman). A change in conduction velocity theoretically could contribute 

 to a disorganization of cardiac action. 



Shift of the strength-interval curve indicates a prolongation of refractoriness in 

 the cooled heart. As stated previously the action potential is prolonged as repolari- 

 zation processes are slowed. It may be of significance that the change in duration of 

 the absolute refractory period is greater than the change in the relative refractory 

 phase (Pinkston, 1956). This indicates that certain of the processes involved in 

 recovery of depolarized cardiac tissue may be more susceptible to cooling than are 

 others. One of the most striking observations is that of Schiitz (1936) that refrac- 



