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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



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FIG. i8. Time of activity after the earliest recorded point in 

 the toad's ventricle. Note that on the left the earliest activity 

 is in the center of the \entricles, and that there is later activity 

 at both the apex and the base. ^4.- auricular muscle passing 

 into A-V ring, C: endocardial cushion; S: auricular septum; 

 TA: commencement of bulbus arteriosus. Arrows indicate 

 deduced direction of activation. [From Lewis (70).] 



properties may become quite obvious. One such 

 property is the generation of echoes. The production 

 of first degree A-V block by rapid stimulation, which 

 delays the firing of some cells and changes the dura- 

 tion of potentials recorded extracellularly, also 

 involves an alteration of the conduction characteristics 

 of the A-V conduction system. In some experiments, 

 an electrode in the upper A-V node recorded no 

 clear potentials from other than atrial cells. With 

 rapid stimulation (fig. 1 7) a spikelike potential may 

 appear as first degree block develops. Here a group 

 of cells, which did not normally show signs of firing 

 in concert, are driven to fire simultaneou.sly by the 

 rapid stimulation. Another example is found in 

 certain patients in whom a sinus beat which is or is 

 not transmitted to the ventricles can markedly alter 

 the A-V nodal rhythm (69, 102). A non-nodal similar 

 phenomenon is found in the fact that conduction in 

 turtle ventricle may become one-way if a pressure 

 block is caused in a mass of muscle (9, 62). These 

 properties may not be unique to the A-V conduction 

 system, but they are here most apparent. 



Confhiction in the Common Riindle and lis Branches 



The velocity of conduction in these "cables" has 

 been measured at 2.0 m per sec in the false tendon 

 of the kid by Draper & Weidmann (39) and by 

 Wcidmann (140). Curtis & Travis (34) calculated 



PIG. 19. Surface activation in the toad. The time reference 

 is the beginning of the R wave in the body surface electro- 

 cardiogram. In the heart shown at the left the base was acti- 

 vated before the apex, but in that at the right, the base was 

 activated after the apex. In both, the central portion of the 

 ventricular wall was first area activated, and the bulbus arteri- 

 osus was activated very late. [From Lewis (71)-] 



a velocity of about 4 m per sec for the false tendon of 

 the kid at 40 °C. Pruitt & Essex (91) confirm this 

 measurement. Scher and co-workers calculated a 

 velocity of 1.7 m per sec in the right bundle of the 

 dog (115). 



Venlricii/ar Activation 



As with atrial activation, the earliest detailed 

 studies of ventricular activation were conducted by 

 Lewis (71, 72). His papers are classics in the develop- 

 ment of our understanding of electrophysiology and 

 electrocardiography. His reasoning is lucid, liis 

 expression exact, and his contribution must be read 

 by any serious worker in the field. As will be dis- 

 cussed, Lewis plotted the time of activation of many 

 points over the surface of the canine heart and 

 attempted to deduce the pathway followed by the 

 wave of activity within the muscle. 



In other studies he observed that cutting the 

 epicardium between a stimulating and a recording 

 electrode (both on the epicardium) did not alter the 

 conduction time between the points if they were 

 sufficiently removed from one another. From this 

 Lewis reasoned that the impulse was not traveling 

 along the epicardium but must indeed be going first 

 from the epicardium to the endocardium, then along 

 the endocardium, and finally from the endocardium 

 to the epicardium. Such a course demanded a con- 

 duction velocity along the endocardium more rapid 

 than that measured on the ventricular surface (0.4 

 m per sec). From experiments such as this he cal- 

 culated conduction velocities of 0.3 to 0.5 m per sec 

 and 1 .5 to 2 m per sec for Purkinje fibers and ordinary 



