ELECTROCARDIOGRAPHY 



397 



with concomitant variations in heart rate, and central 

 autonomic tone. Such fluctuations are due to central 

 metabolic influences (CO)!) and to a rather intricate 

 coupling between ijlood pressure, baroceptors, and 

 vasomotor activity. In respiratory maneuvers, for 

 example, variations in heart frequency occur which 

 surmount, to a certain extent, the ordinary barocep- 

 tor reflexes (334); but most probably, part of the 

 respiratory arrhythmia is of central origin and due to 

 irradiation from the respiratory centers (499). Even a 

 I : 1 coupling between respiration and pulse rate has 

 often been described and depends on reflex pathways 

 from the chest (134). 



Metabolic influences may be mentioned, because 

 they might be regarded (as has been done) as a sign 

 of reflex activity. Every dilatation of the atria may 

 change the heart rate, accelerating the rate of the iso- 

 lated heart in some (114, 483), but slowing it in other 

 cases. We saw the heart rate decreasing in the de- 

 nervated dog's heart during dilatation and under the 

 influence of CO 2 and ischemia (unpublished obser- 

 vations). Even intracardiac refle.xes have been postu- 

 lated, as the sinus pacemaker is accelerated after 

 pinching the ventricles in frog (440). 



The amount of physiological irregularities may be 

 measured by an index ['"Rhythmiemass" of Schlomka 

 (58, p. 344)]. To calculate this index, one measures in 

 16 consecutive beats the 4 longest and the 4 shortest 

 intervals, and then takes the difference of their re- 

 spective sums and divides it by 4. The rhythmicity of 

 the heart varies from species to species, as far as it has 

 been studied in cold-blooded animals (533). 



Such bradycardias or tachycardias are by no means 

 fully understood, though we may assume that the 

 pacemaker potentials may account for them. The ex- 

 treme tachycardias, however, found in paroxysms and 

 often leading to atrial or ventricular fibrillation, can- 

 not be explained with an ordinary pacemaker 

 mechanism. As shown in figure 66 aconitine elicits 

 a series of very frequent action potentials, which must 

 have been started by the same mechanism responsible 

 for the coupled extrasystoles and which, under certain 

 circumstances, may be influenced into the production 

 of such series of excitations. Obviously, the second 

 beat in such a series, falling in the refractoiy period, 

 changes the behavior of the membrane, so that an 

 extremely frequent local spontaneous pacemaker is 

 formed. Mechanical stimuli, for example, during 

 catheterization, act in the same way (223). As soon as 

 a part of the heart can no longer keep up with such a 

 frequency, the muscle mass is divided into inde- 

 pendently beating fragments and fibrillation occurs 



(see Chapter 12). There is no explanation available 

 concerning what really happens at such poisoned 

 pacemakers. The whole membrane structure must be 

 disturbed. Perhaps Ca plays an important role in this 

 connection (425). Every heart can be brought to 

 fibrillation in this way, and no metabolic abnormali- 

 ties are necessary, though a dilated heart is obviously 

 more sensitive to fibrillation than a normal one (409). 

 The generation of paroxysmal tachycardias in clinical 

 cases is likewise unexplained. They are astonishingly 

 regular in rhythm. 



Periods. Alternans 



As a rule, all beats from the same pacemaker resem- 

 ble each other in their mechanical effect and action 

 potential. In extrasystoles, the stroke volume and sys- 

 tolic pressure, as well as the action potential, are dif- 

 ferent from normal, liut even here the monophasic 

 action potential is nearly unchanged in many cases. 

 Only after a very short interval is the action potential 

 apt to be strongly diminished (433). Refractoriness 

 may be prolonged in certain cases, so that, even with 

 nearly normal intervals, abnormal beats occur. The 

 refractoriness obviously differs in duration from point 

 to point on the heart. Therefore, when ectopic foci are 

 active, it may be only when the R-R interval is pro- 

 longed beyond a certain length in a sequence of nor- 

 mal beats that an ectopic extrasystolic beat can occur, 

 originating from a pacemaker which remains refrac- 

 tory if it is too frequently depolarized (303). 



There is another type of irregularity commonly 

 ascribed to refractory phenomena : the Wenckebach- 

 Luciani periods. They are characterized by a P-R 

 interval which increases from beat to beat, until the 

 moment when A-V conduction fails completely and 

 a beat drops out. The equilibrium of the resting con- 

 dition obviously could not be reached at the end of 

 an interval, so that the next beat starts under some- 

 what impaired conditions. Raised potassium in the 

 extracellular space could serve as an example of such 

 impairment. But this simple hypothesis does not cover 

 the facts, because, under such an assumption, a fre- 

 quent change of the number of beats occurring be- 

 tween the "gaps" should be expected. We find, how- 

 ever, that the number of such beats, forming a 

 "period," is rather stable. This means that some sort 

 of an interference of two frequencies occurs, one of the 

 two being determined by the frequency of a 

 "functional" refractory period of the A-V conducting 

 system (393). It seems easier to clarify the problem 

 with a mathematical equation (393) than to explain 



