EXCITATION OF THE HEART 



291 



FIG. 6. A: lead II QRS in the dog. B: simultaneous unipolar 

 record of electrical activity high in posterior inter\entricular 

 septum. B shows an initial negative (downward) deflection 

 caused by receding activity in apical ventricle. As activity 

 approaches electrode, voltage goes through zero to a positive 

 value. Depolarization in this septal region (final, fast, negative- 

 going deflection) begins at about time of S wave in the electro- 

 cardiogram. A small potential from Purkinje tissue precedes 

 the QRS deflection by about 22 msec on B. The lower nega- 

 tive-positive-negative potential is recorded in the very last 

 ventricular regions to be excited. With a slow recording system, 

 the initial negative-going portion and the terminal negative- 

 going portion might be confused. Local activity occurs during 

 the latter period, but the potential shape provides no clear 

 proof of this. [From Scher & Young (119). J 



A-V connection composed of ordinary myocardial 

 cells. This connection has since been the subject of 

 some contro\ersy (65). 



Other Anatomical Details 



Tlie following additional structural details are 

 important in the consideration of ventricular electrical 

 activity in man or the dog. The right wall is generally 

 no more than 3 or 4 mm thick; the left wall is much 

 thicker, up to 15 mm, except in infants whose two 

 ventricular w^alls are about equally thick. The endo- 

 cardial Purkinje network is more widespread in the 

 central and apical portions of the wall and septum 

 bilaterally. This network is sparse or nonexistent in 

 the basal septum. 



EXCITATION OF THE HEART 



Electrical acti\ity of the heart produces potentials 

 at the body surface which are referred to as an 

 electrocardiogram. The shape of the recorded com- 

 plex varies with a number of factors and a normal 

 record is presented for reference (fig. 5). The P wave 

 signals atrial depolarization; the QRS, complex 



ventricular depolarization; and the T wave, ventricu- 

 lar repolarization. 



All our direct knowledge of the pathway of cardiac 

 excitation is derived from animal experiments, most 

 of them on dogs. Although the various components of 

 the canine electrocardiogram last about one-half as 

 long as do those of the human cycle, it is customary 

 to consider results obtained in dogs as applicable to 

 man. This extrapolation is justified by two facts: /) 

 human and canine hearts are anatomically similar, 

 both grossly and histologically, and 2) electrocardio- 

 grams of similar shape can be recorded from both 

 hearts if the differences in heart position are taken 

 into account (125, 126, 146). It might seem possible to 

 determine the pathway of cardiac excitation by 

 studying the body surface electrocardiogram. It is, 

 however, implicit in Green's theorem in electricity 

 and magnetism (60), and has been stated by 

 Helmholtz (55) and Lorente de No (73), that if one 

 knows only the potential distribution at the surface 

 of a body, one cannot determine a unique internal 

 generator. For this reason it is theoretically impossible 

 to determine the exact pathway of excitation by 

 knowing only the potentials which occur at the body 

 surface, or even at the surface of the ventricles. Since 

 the cardiac anatomy is so well known, prediction of a 

 likely pathway of excitation of anatomical grounds 

 might seem possible. This prediction could then be 

 verified by deriving from it, at least qualitatively, 

 electrocardiograms which could be compared with 

 those actually recorded. Attempts to formulate such 

 a prediction have been made by various experts. 

 They have been successful (46) but never entirely so. 

 For this reason it appears to be necessary to trace the 

 pathway of excitation through the heart. 



In the case of a thin-walled chamber like the 

 atrium, it has been assumed, undoubtedly correctly, 

 that the wall can be considered a sheet, and that no 

 details are needed on what happens between the 

 endocardial and epicardial surfaces. In the case of 

 the thicker walls of the ventricles, however, no such 

 assumptions can be made. If we place an electrode 

 on or near cardiac muscle and record the potential 

 diflference between this electrode and another 

 electrode at a distance, the recorded potential will be 

 positive if the net sum of activity is approaching the 

 electrode, i.e., if the recording locus "sees" more 

 approaching than receding activity (14, 32). A 

 negative potential will be recorded if the net sum of 

 activity is receding from the recording point. It might 

 seem that potentials of this sort would enable us to 

 completely plot the activation of a thin strip of muscle, 



