292 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



A 



50 100 150 200 250 300 350 



INTERVAL OF CYCLE-MSEC 



oVA 



150 200 250 



INTERVAL OF CYCLE-MSEC 



Fig. 2. — (A) Strength-interval curves obtained with stimuli of different durations, showing 

 boundaries of absolute and total refractory periods as defined by each. Note early and late 

 dips in 13 msec, test shock curve. (B) Strength-interval curve obtained from cat ventricle 



showing dips and periods of vulnerability to fibrillation. \ / = multiple extrasystoles ; \ / = 



fibrillation; =i / =no response at all to very strong stimuli. (From Amer. J. Physiol. 163: 



469, 1950; 167: 88, 1951.) 



the refractory period, must have an effect which can persist as a local excitatory 

 state, a local non-propagated response or one so slowly propagated that its travel 

 cannot be recorded by means usually employed (fig. 3). 



(c) Recovery of excitability is a far from simple process. Testing of the change 

 in excitability associated with the terminal quick phase of repolarization shows 

 that at certain specific intervals a degree of recovery of excitability is attained 

 which is not sustained. Usually there are two such intervals or "dips" in the 

 strength-interval curves of the auricle and ventricle (fig. 2). Repolarization is 

 often followed by a phase of supernormality (fig. 4). There is thus an oscillation 

 or fluctuation shown in curves expressing recovery of normal excitability. 



(d) The heart is vulnerable to fibrillation by single strong electrical stimuli at 

 these "dip" intervals. Stimuli of progressively increasing strength produce ex- 

 trasystoles, tlien multiple extrasystoles, and, at still higher strengths, actual fibril- 

 lation. This occurs in bcjth auricle and ventricle when stimuli are applied at these 



