CARDIAC EXCITABILITY— BROOKS 



295 



I 2 3 4 5 6 



C 



Fig. 5.— Diagram of possible saltatory conduction. (A) Normal propagation through cell 

 adjacent to sink (depolarized area). (B) Jump from sink to most excitable cells (S). Arrows 

 indicate direction of spread of excitation. (C) Conduction in normal tissue: (1) with a jump 

 into tissue rendered hyperexcitable by current of injury,. (2) slowed conduction in depressed 

 area, (3) arrows show possible course of impulse propagation. 



ion distribution and transport of ions across cardiac cell niemljranes is associated 

 with excitability and excitation. 



(3) The normal heart is stippHed l)y an autonomic innervation and is subject to 

 action of circulating epinephrine and nor-epinephrine. If the reactions of the body 

 normally associated with maintenance of homeostasis are permitted to occur in 

 production of hypothermia, the actions of these agents on the heart must be dif- 

 ferentiated from the direct efifects of cooling. It is known that autonomic effectors 

 (nerves and mediators) affect repolarization of cells and have biphasic effects on 

 excitability and vulnerability to fibrillation (fig. 7). (See Brooks et al, 1955.) 



(b) Direct effects. In considering direct action of hypothermy on the irritabilitv 

 of the heart one must differentiate between regional or asymmetrical cooling and 

 generalized or uniform hypothermia of the cardiac tissue. 



(1) Cooling one region more than another is known to establish localized elec- 

 trotonic current flow (Granit, 1955) which has at least a subthreshold excitatorv 



