EXCITATION OF THE HEART 



315 



FIG. 39. Pattern of ventricular 

 depolarization before and after 

 right bundle branch block. A 

 and B: sagittal sections through 

 right and left ventricles showing 

 pathway as measured by nine 

 multipolar insertions. Small num- 

 bers show position in heart of 

 depolarization wave at various 

 stages of depolarization. A: 

 normal depolarization ; normal 

 lead II QRS is shown at center. 

 B: pattern of ventricular depolar- 

 ization during right bundle 

 branch block (same insertion as 

 in A). Lead II QR.S is typical 

 of canine right bundle branch 

 block. C and D: pattern of ac- 

 tivation of right mural endocar- 

 dium as viewed from inside right 

 cavity. Shaded areas indicate 

 junction of right wall and sep- 

 tum. Numbers indicate time of 

 depolarization in milliseconds 

 after onset of QRS. Dotted lines 

 approximate wave front position 

 at 5 msec intervals. C: normal 

 depolarization. D: pattern of 

 activation after right bundle 

 branch block. [From Erickson 

 et al. (44).] 



bundle branch block, the QRS may have a duration 

 as short as 120 msec. The mechanism of sucli pro- 

 longation (which is not equivalent to that produced 

 by cutting the bundle in the dog) is not at all clear. 

 Possibly damage to fine strands of the Purkinje 

 network (arborization block) or even frank myo- 

 cardial damage might lead to such lengthening of 

 the QRS. In unpublished experiments in dogs, 

 Gould has cut the strands of the right bundle which 

 run to the free right wall. He finds some prolonga- 

 tion of QRS and other changes, but this procedure 

 does not duplicate any known clinical lesion. 



Flutter and Fibrillation 



The arrhythmias, involving greatly increased 

 heart rate, flutter and fibrillation, are of interest to 

 us since they represent "pathological" types of con- 

 duction resulting from modifications of the normal 

 physiology of myocardial cells. It appears to many 

 observers that flutter and fibrillation are different 

 degrees of the same arrhythmia and that the two 

 can arise from a very fast heart beat referred to as 

 paroxysmal tachycardia. Flutter is generally confined 



to the atrium. It consists of a very rapid sequential 

 depolarization of the atria — so fast that the rate 

 verges on 300 beats per min. Fibrillation involves 

 even higher rates, at times greater than 500 beats 

 per min. 



The mechanism of these two conditions has greatly 

 interested physiologists and electrocardiologists, and 

 a heated controversy has existed concerning this 

 mechanism. Lewis (71J considered fibrillation to 

 result from a "circus movement" of the layer of 

 excitation. He used as a model a type of conduction 

 which can be seen in the muscle of the jellyfish, 

 where a circulating wave can be induced to progress 

 around a ring of muscle. Models of this condition 

 have been created in other animals (76). If a portion 

 of tissue on the superior vena cava is damaged by 

 clamping with forceps, an impulse started at one 

 side of the damaged region may proceed around the 

 ring, return to the original site, be conducted slowly 

 through the damaged region, and find the initial 

 site again excitable. Other theories have been offered 

 as alternatives to the "circus theory" (122). In the 

 two main alternates, a rapidly firing focus and mul- 

 tiple ectopic foci are suggested as the source of 



