396 HANDBOOK OF PHYSIOLOGY -^ CIRCULATION I 



FIG. 68. Coupled extrasystoles after every second normal beat (fixed coupling). Extra beats most 

 probably originating in the right ventricle. Trigeminus. The compensatory pause is somewhat too 

 long. 



The local disturbances giving rise to extrasystolic 

 beats most probably are not uniform. A local impair- 

 ment of cellular metabolism may lead to a local ac- 

 cumulation of potassium, thus lowering the threshold 

 and shortening the fiber action potential. Perhaps an 

 augmented sodium permeability of the damaged 

 membrane may cause extra excitation. Such effects 

 may occur under the influence of anoxia or of CO 2, 

 near a hemorrhage, through an unspecific general 

 impairment of a preparation, and after digitalis and 

 stretch (68). If a generally augmented excitability, 

 caused by these membrane effects, meets with a 

 transient increase in excitability at the end of the re- 

 fractory period (70, p. 59), an actual excitation is 

 induced. Such a local augmentation of excitability 

 may happen by putting a d-c electrode on the epi- 

 cardium: with the anode( !) as the different electrode, 

 coupled extrasystoles appear (504). This electrotonic 

 precipitation may be the model of extrasystoles in 

 infarcts, where the injury current may play the same 

 role (214). Even the traction exerted by the contract- 

 ing ventricle has been blamed for eliciting an extra- 

 systole (392). 



For the reasons mentioned, an extrasystole always 

 follows a preceding normal beat at a fixed interval, as 

 long as an ectopic focus is not spontaneously active, 

 thus generating a parasystole. Only an "external" 

 stimulus arising from a transient local disturbance 

 may precipitate a single extrasystolic beat without 

 such a coupling, but we could scarcely imagine the 

 nature of such a local stimulus. The fixed coupling to 

 the preceding beat is shown in figure 68. There is a 

 second mechanism active in some cases. Everv electric 



field developed by an excited muscle mass shifts the 

 membrane equilibrium nearer to the threshold. This 

 has been observed with nearly all excitable tissues 

 (57, 11: p. 349). Apparently, such an electrotonic ex- 

 citation of adjacent fibers by the action current of 

 normally excited fibers plays a role in the generation 

 not only of extrasystoles but also of a premature exci- 

 tation of ventricular fibers at the base of the heart, as 

 in the so-called Wolff-Parkinson-White syndrome. It 

 cannot be decided whether such electrotonic influ- 

 ences start from the His bundle (58) or from atrial 

 fibers (64), but electrotonic influences are, at least, 

 the probable cause of excitations in tissues which are 

 already more than normally excitable as a result of 

 local metabolic or other damage. Also, a constant 

 injury potential, e.g., at the site of an infarct, may 

 lead by its electrotonic effect to a locally lowered 

 threshold with the precipitation of coupled (or even 

 uncoupled, single) extrasystoles (68, p. 68). Two frog 

 hearts, when put in close contact, will synchronize to 

 each other, apparently by means of their mutual 

 electrical fields (442). 



Heart Rate, Tachycardias, and Paroxysms. 

 Physiological Arrhythmias 



The heart rate is the result of pacemaker potentials 

 (see the preceding chapter and 488). We should like to 

 mention here only the different mechanisms, by which 

 the heart rate is normally controlled. There are neural, 

 hormonal, and metabolic influences on the pace- 

 maker. The neural influence is determined l)y the 

 vagosympathetic lialancc and may strongly fluctuate. 



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