EXCITATION OF THE HEART 



3" 



(fig. 34), union of the two separate masses of activated 

 tissue around the \entricle has produced strong forces 

 directed posteriorly, to the left, and inferiorly. The 

 breakthrough of activity to the anterior right wall 

 has greatly reduced the left-to-right component, and 

 over-all actisity is directed apically, posteriorly, and 

 to the left in the apical, lateral, and anterior left 

 wall. Some opposing inside-out activity persists in 

 the basal right wall. At this time, positive deflections 

 will appear in all standard limb leads, and the leads 

 on the left side of the chest will "see" approaching 

 activity. The continuation of this pattern results in 

 the eventual disappearance of the wave front an- 

 teriorly, on the right, and in the central and apical 

 portions of the heart. Overlying precordial leads 

 will therefore record negatixe potentials. 



The over-all pattern of activity immediately fol- 

 lowing the above, i.e., about midway through QRS, 

 is a continuation of the mo\cment toward the thin 

 slice of lateral posterior left ventricle, which remains 

 in the resting state, and a smaller movement toward 

 the basal septum. Depolarization reaches the apex 

 of the heart on the right, and some muscle in the 

 apical region of the left ventricle remains to be de- 

 polarized. The net result is a wave moving posteriorly, 

 leftward, and slightly toward the apex. Again, the 

 limb leads will be positive. The chest leads except 

 V5 and Ve (on the far left) will, however, show nega- 

 tivity. 



After depolarization of the apical regions is com- 

 plete (25 msec after the beginning of QRS in the dog 

 and about 60 msec in the human), i.e., for the last 

 quarter of the QRS complex, a wave mo\es from the 

 inside out in the walls near the base of the left ven- 

 tricle, particularly posteriorly and from apex to base 

 in the septum. This wa\'e is relatiscly inefl"ecti\e in 

 causing potentials in lead I, although leads II and 

 III should show a negati\e potential; the potentials 

 in the chest leads will be small but generally negative 



(fig- 35^- 



In figure 30 it can be seen that the depolarization 

 process exhibits a great amount of symmetry around 

 the longitudinal axis of the heart. At various instants, 

 activity is proceeding in opposite directions in the 

 lateral walls and/or in the septum. This symmetry of 

 depolarization leads to "cancellation" of much of the 

 cardiac electrical activity as recorded from the body 

 surface. It has been estimated that the recorded po- 

 tentials are 5 to 10 per cent of what might be expected 

 if there were no cancellation (112). Any condition 

 which alters the sequence of ventricular depolariza- 

 tion in a manner to reduce this cancellation will, of 



course, produce an increase in the magnitude of the 

 potentials recorded in one or more leads. This is true 

 of bundle branch block and many types of infarction, 

 and also of impulses arising in abnormal sites. 



To summarize, we may dixide ventricular activa- 

 tion into three phases, remembering that they suc- 

 ceed one another smoothly and are not separate. 

 The first phase is one of predominant activity from 

 left to right and anteriorly in the septum. The second, 

 consisting of inside-out activity in the wall plus double 

 inx'asion of the septum, produces very strong forces 

 directed from base to apex, somewhat posteriorly and 

 to the left. The final phase is the activity — directed 

 from apex to base, leftward, and posteriorly — result- 

 ing from activation of the basal posterior left wall and 

 the i^asal septum. 



I rnlriculai Repolarization 



In most electrocardiographic leads in man the T 

 wave has the same electrical polarity as the QRS 

 complex, i.e., is usually upright when the QRS is 

 upright. Since the electrical charges across the cell 

 boundaries are oppositely arranged during repolariza- 

 tion and depolarization, the polarity of the record 

 would be opposite if repolarization followed the de- 

 polarization pathway. Repolarization therefore does 

 not follow the same pathway and, indeed, the path- 

 way tends to be the reverse. It is important in this 

 connection to consider whether repolarization is 

 electricalh' propagated. 



In studies with the intracellular electrode (140) 

 repolarization of a fiber was induced by appropriate 

 stimulation (i.e., by stimuli causing the inside of the 

 fiber to become negative). Induced repolarization 

 could propagate through a single fiber. In cardiac 

 tissue in low calcium solutions, induced repolariza- 

 tion might propagate through several fibers. It is, 

 however, doubtful that repolarization normally is 

 propagated in the ventricles. Calculations of the 

 density of current flow indicate that the current 

 flowing during repolarization is less than i per cent 

 of that flowing during depolarization. Such a small 

 current probably cannot initiate a propagated wave. 



If repolarization is not propagated, we ma\' wonder 

 why the configuration of the T wa\'e is consistent 

 under normal conditions. Several factors have been 

 thought to control the sequence of repolarization; 

 among them are temperature and pressure. Accord- 

 ing to one theory, the pressure differential within 

 the walls favors initiation of repolarization in the 

 outer layers, and repolarization occurs later near the 



