ELECTROCARDIOGRAPHY 



395 



-100 

 mV 



70 sec 



FIG. 66. Development of a paro.xysmal tachycardia after aconitine in a strand of Purkinje fibers. 

 After the third beat, a sequence of action potentials starts. They are elicited by a second plateau 

 in the action potential (arrow) which develops rapidly in the beginning of the series, about 30 sec 

 after the application of aconitine {o,\'','c in tyrode solution). Intracellular microelectrode. For 

 theoretical explanation see fig. 67. [From Schmidt (425).] 



aconitine (425), with which repolarization is slowed 

 down shortly before the original resting level of mem- 

 brane potential is reached, forming a kind of second 

 plateau, from which an extrasystolic excitation is 

 started (fig. 66). However, aconitine elicits extrasys- 

 toles in papillary muscles as well, though there are no 

 pacemaker potentials there. Here, the concept of true 

 extrasystoles seems to be reasonable. Adrenaline 

 syncope is very similar, as judged from the ECG (190). 

 The explanation of all these facts offers some diffi- 

 culties, because the "threshold" cannot be explained 

 in a simple manner. We refer here to the preceding 

 chapter, where the thresholds during the relative re- 

 fractory period have been described. Usually the 

 threshold is determined by the strength of a new 

 depolarization necessary to start a new excitation 

 wave (6, 70). But this definition may be unilateral in 

 the sense that a threshold could be described as well as 

 membrane potential changes necessary to stimulate, 

 without any external stimulus. It is assumed that this 

 membrane potential can be determined by short elec- 

 trical stimuli, but it is by no means certain whether 

 an automatically developed membrane potential 

 necessarily must have the same magnitude to excite 

 as these artificially shifted membrane potentials. The 

 threshold most probably can be described fully only 

 in terms of ionic events in the sense of the Hodgkin- 

 Huxley theory, and even there certain assumptions 

 have to be made about the properties of the membrane 

 determining ionic permeabilities and conductances. 

 At least, threshold is neither a certain membrane po- 

 tential to be reached (even if it might differ with time) 

 nor a certain electrotonic depolarization. Neverthe- 

 less, if we try to draw a threshold line like that in 

 figure 67, this line does not indicate more than a 

 formal statement of how far from excitation the fiber 

 is at every moment. In such a formal schedule the 

 thresholds are lowered in parasystoles as well as in 

 extrasystoles, together with an increase in diastolic 

 pacemaker depolarization. How both processes are 



^-THRESHOLD 

 ■ (NORMAL) 



ACONITINE 



FIG. 67. Tentative explanation of fig. 66. Abscissa: time; 

 ordinate-, membrane potential. Above: the "threshold" of a 

 normal fiber is shown. Threshold means in this case the mem- 

 brane potential that must be reached to excite. Below: the 

 threshold is unchanged, but the membrane potential crosses 

 with its second plateau (dotted) the threshold line and leads 

 to a new action potential. 



linked together can scarcely be analyzed for the pres- 

 ent. They both seem to depend on peculiarities of the 

 memi^rane structure, though, just under the influence 

 of aconitine, no permeability changes have been ob- 

 served for K, Na, and CI ions (425). If we assume this 

 hypothetical basis, it merely depends on secondary or 

 quantitative factors whether a parasystolic pacemaker 

 comes into action or, at the same point, a coupled 

 extrasystole appears so early in the repolarization 

 process that the development of generator potentials 

 and accompanying parasystoles cannot be detected. It 

 is in this sense that we suspect extrasystoles and para- 

 systoles to depend on the same basic process (58). It 

 hardly can be douijted, however, that there are 

 marked differences in form of the electrocardio- 

 graphic patterns. 



