ELECTROCARDIOGRAPHY 



349 



is thus determined by tiie big muscle masses of the 

 more remote parts of the ventricular wall, which 

 lead away from the electrode. The latter is obvious 

 at many points of the endocardial surface. In experi- 

 ments of Durrer et al. (178, 179), the bipolar poten- 

 tial with leads perpendicular to the surface is very 

 low and polyphasic, a fact which can be explained 

 only by a conduction parallel to that surface. The 

 reports of various authors (397, 526), that the endo- 

 cardial surface in the unipolar record only has a 

 negative deflection, therefore may easily be ex- 

 plained. The bulk of the fibers in the ventricles is 

 excited by waves running toward the epicardial 

 surface, corresponding to the specific conduction 

 system which runs near the endocardial surface and 

 branches from there into the myocardial spindles. 

 The same is true for results of Prinzmetal et al. (377), 

 who found that the cavity, intramural and surface 

 potentials of an infarct region may be equally nega- 

 tive; because in this region the approaching waves 

 are deleted, and the distant receding waves command 

 the potential pattern in all lead positions. However, 

 if only the inner part of the ventricular wall is dam- 

 aged, the epicardial electrode shows a positive poten- 

 tial (337). Positive or negative deflections depend 

 solely upon the amount of fibers with excitation 

 running toward the electrode or away from it. 



Such a theory, which proves itself to be applicable 

 and useful, is the modern \ariant of what Lewis 

 called the "theory of limited potential differences" 

 [(321); see also (175)]. 



8. SPREAD OF ACTIV.^TION THROUGHOUT THE HEART, 

 IN RELATION TO A THEORY OF P AND QRS 



As has been shown in the introduction, the spread 

 of the excitation wave is of fundamental importance 

 to the explanation of an electrocardiographic curve. 

 The resultant electric field depends upon the mode 

 of interference of the v-arious cardiac muscle fibers 

 concerning position, direction, and time of activation. 

 Therefore, any itemized analysis would first require 

 complete knowledge of anatomical details. We will 

 shortly mention such facts as are known, and elucidate 

 the ECG pattern. The anatomy of the conductive 

 tissue (11, 171, 269) has been given in the preceding 

 chapter. Second, the time course of the spread of 

 activation has to be known. This is the topic of the 

 following section. 



The explanation of the electrical signs during 

 atrial activation is relatively simple. Under normal 



conditions the excitation wave starts at the sinus 

 region and proceeds from there nearly linearly to all 

 parts of the atria, the auricles included (124, 322, 

 378) (fig. 31 ). The velocity of the wave varies within 

 the limits of 0.4 to 1.2 m per sec (124, 171), a result 

 which agrees with earlier and recent experiments. In 

 the extreme parts of the auricles, the fibers appar- 

 ently run in a somewhat curved manner, but the 

 main part of atria and auricles is excited by a wave 

 front progressing from the sinus node on an approxi- 

 mately radial pathway. The most remote points of 

 the auricles are reached within a latency time of 

 about 60 msec in dogs (124, 378). This means that 

 the latest fiber is depolarized during the fall of the 

 P wave, shortly before it ends. The P wave therefore 

 may be regarded as the superposition of excitation 

 waves in the atrial and auricular fibers. (See section 

 10 and fig. 49 for nomenclature.) 



The highly diverging individual excitation waves 

 imply a high degree of cancellation. This, and the 

 small muscular mass of the atria, are the reasons 

 why the P wave is very small. On the other hand, 

 none of the radial pathways of the wave front is 

 strongly bent. The thickness of the atrial walls is 

 much more homogeneous than that of the ventricles. 

 All these data collaborate in making the P wave as 

 smooth and simple as it is. Only in cases of marked 

 dilatations or local hypertrophies, does broadening 

 and splitting, or augmentation of the amplitude 

 occur, a finding well known to the clinician as "mi- 

 tral" or "pulmonary" P wave. 



Only a few of the many fibers radiating outward 

 from the sinus node are responsible for atrioven- 

 tricular conduction (396). Once the A-V node is 

 activated, the excitation spreads along the specific 

 conducting system. Details of this conduction are 

 given in the preceding chapter by Scher. During the 

 PR segment, excitation proceeds in a verv small 

 bundle of fibers, which has a comparatively negligible 

 cross section. The potential produced by such an 

 excitation wave is therefore too low to be recorded. 

 One can calculate the average amount of fibers 

 necessary to produce a detectable potential. Even 

 under optimal conditions, at least 4000 normal 

 myocardial fibers have to be active to produce a 

 measurable potential in a precordial lead. In an 

 extremity lead, the number will be ten times as 

 much (58, p. 456). That means that the cross section 

 of a bundle, the action potential of which may be 

 recorded by optimal precordial or conventional 

 extremity leads, has to be at least i mm- in the former 

 case and 10 mm- in the latter. The cross sections of 



