298 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



toriness is prolonged out of proportion to the lengthening of the refractory period. 

 Here again is e^'idence of a selectivity of action of cold on cardiac processes. 



One final point worthy of mention in this discussion of cardiac-excitability testing 

 is that at low temperatures the heart is difficult to drive. It becomes unable to fol- 

 low stimuli applied at a faster rate than that of its own intrinsic pacemaker. This 

 may be due to an inability to conduct impulses more frequently than they are 

 originated. The specialized conducting system due to a faster rate of spike rise can 

 conduct faster than undifferentiated ventricular tissues Init its slower rate of re- 

 polarization (see chapter on cell potentials, Hoffman) may determine the limit to 

 heart rate acceleration in the hypothermic heart. It has been reported that ac- 

 celerated drive of the hypothermic heart (Berne, l')54) decreases the effectiveness 

 of its mechanical action. 



Manv of these points mentioned in this introductory presentation will be ampli- 

 fied and more precise information will be given by subsequent speakers who have 

 been interested in this same problem — the effect of hypothermia on cardiac 

 irritability. 



HYPOTHERMIA AND THE INITIATION OF A CONTRACTILE 



RESPONSE 



Consideration of the effect of hypothermia on mechanical contraction of the 

 heart may be considered within the province of the topic assigned because it can- 

 not be denied that contraction is the most significant element of the response of 

 the heart to intrinsic or applied stimuli. 



The propagated electrical response normally initiates a contractile process. It 

 appears that contraction follows the propagated depolarization and repolarization 

 with a certain latency. \'ery early in the cycle a normally propagated action po- 

 tential can be evoked dissociated from any significant contraction. Evidently ability 

 to contract is regained more slowly than the al)ility to be excited and to conduct an 

 impulse (fig. S). 



The verv earlv conducted impulse, though it has no immediate visil)!e effect on a 

 contractile mechanism, does potentiate subsequent contractions when they occur. 

 The duration of this potentiating action has been determined (Hoffman ct ai, 

 1956; Siebens ct al., \9r<6) but its nature is not known. The possible effects of 

 temperature on this phenomenon have not been determined. 



It has been demonstrated that autonomic activity associated with exposure to 

 cold does modify the heart's contractile process. Epinephrine and accelerator 

 nerve impulses, even though heart rate and venous return are kept constant, do 

 cause an increase in amplitude of myocardial contractions (W'iggers, 1952). They 

 show a steeper rise and a shorter duration. 



Cooling per sc should have some direct action on tlie contractile processes ot 

 muscle. In this connection it can be said that reduction of temperature is reported 

 to increase total tension of contractions in frog skeletal muscle (Wiggers, 1949). 

 According to Szent-Cycirgyi (1*H<S) muscle contraction has a very high tempera- 

 ture coefficient. At 0° C. there is no contraction at all in mammalian nuiscle while 

 at 16° C. contraction is maximal. Szent-Cjyorgyi also describes some calculations of 



