Part III 



HYPOTHERMIA AND THE PHYSIOLOGY OF CARDIAC 



EXCITABILITY* 



CHANDLER McC. BROOKS 



Function of the heart and responses of the heart to impinging influence involve 

 two processes: (1) The origin and propagation of excitation in the heart and (2) 

 the contractile response initiated hy the propagated membrane depolarization. 

 Cooling of the heart affects both these responses. Thus attainment of an under- 

 standing of the changes produced in hypothermia requires an analysis of the 

 reactions involved in each of the two processes. 



In this present day when action potentials are taken as a criterion of response, 

 excitability studies tend to be confined to the determination of factors involved in 

 initiation of a proi)agated action potential. The mechanical response should not be 

 forgotten, however, and unless one considers how the membrane change and ionic 

 fluxes involved in the excitatory process are related to the initiation of the con- 

 tractile process, a complete study of cardiac excitability has not been made. The 

 term excitability is usually defined as the ability of a tissue to detect or be affected 

 by a stimulus to such a degree that a response ensues. 



In surveying studies of cardiac excitability it seems advisable to consider: first. 

 the present concept of the excitatory process; second, the intrinsic origin and 

 propagation of excitation in the heart; third, the testing of excitability by the use 

 of applied stimuli ; and finally, the initiation of contraction by the excitatory 

 process. 



THE EXCITATORY PROCESS 



To understand how cooling might affect the excitability of a cell one must have 

 some concept of the excitatory process. The cardiac cell membrane is polarized and 

 the transmembrane or resting potential is approximately 90 mv. Metabolic activity 

 of the membrane establishes a specific partition of ions (fig. 1). Excitation occurs 

 when the memljrane is depolarized and undergoes an actual reversal of polarity. 

 Applied current flow (cathodal) or electrotonic current flow, generated by spon- 

 taneous depolarization of pacemaker cells, in stimulating tissues does not in itself 

 depolarize the cell membrane completely but merely reduces the membrane potential 

 to such a degree that a regenerative process (intrinsic depolarizing reaction) is 

 initiated (Hodgkin and Huxley, 1952). This completes depolarization and brings 

 about the overshoot or reversal phase of the action potential. The depolarization 

 and overshoot are associated with an influx of Na" as membrane permeability 

 changes on excitation. 



This initial phase, the depolarization and Na^ flux, is followed by a repolariza- 

 tion of the cell and recovery of excitability v.-hich is lost during the period of re- 



* Original work mentioned was supported in part by a grant from the Life Insurance Medical 

 Research Fund. 



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