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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



FIG. lo. Shapes of P waves which would be recorded at 

 various places at body surface. Since general direction of atrial 

 activation is from right arm toward left leg, electrodes on upper 

 part of body will see a negative potential during atrial activa- 

 tion; those on the lower part will see a positive potential. There 

 will be a plane, as indicated on drawing, where an electrode 

 would record both positive and negative actis'ity. (From Scher 

 (114a).] 



arrhythmias often appear to originate in nonsinus 

 sites (coronary sinus, left atrium). 



The initial elliptical shape of the depolarized area in 

 the atria has been considered to indicate that many 

 cells within the sinus node are simultaneously acting 

 as pacemakers. It has also been thought that after 

 this initial pacemaker activity, the spread of excitation 

 is a rather random phenomenon. As stated above, 

 there is good evidence for a greater space constant 

 for myocardial fibers along their long axis, and there 

 IS a greater conduction \elocity in this direction 

 (figs. 8 and 9). The present plots of atrial excitation 

 do support the idea of a greater velocity parallel to 

 the fiber direction. In the plots of right atrial activa- 

 tion by Puech (92) and Brcndel et al. (21) the con- 

 duction velocity is greater along the length of the 

 fibers than perpendicular to them. The conduction 

 velocity in the mammalian atrium appears to be 

 about 0.8 m per sec. 



If we consider the position of the atria in the body, 

 electrodes placed almost anywhere on the precordium 

 (except near the right shoulder) will record a positive 

 potential as the atria depolarize. Conversely, lead VR 

 and esophageal leads will record a negative P wave 

 (fig. 10). The P wave usually has a smooth rounded 

 contour, although it may at times be notched or 

 peaked; it has an average duration of 90 msec in man 

 and an amplitude of less than 0.25 mv. It is about 

 half as long in the common domestic small animals 

 which are studied experimentally. 



Atrial Repolarization 



Repolarization of the atrium in the dog and in 

 man normally occurs during the depolarization of the 

 ventricles, and the repolarization potential is con- 

 cealed by the much larger ventricular potentials. 

 There is thus an isoelectric period between the end 

 of atrial depolarization and the beginning of ventricu- 

 lar depolarization, although, as will be discussed, 

 portions of the atrioventricular conduction system 

 are depolarizing during this time. Infrequently, the 

 ventricular potentials do not conceal the atrial 

 repolarization potential (referred to as the Ta wave), 

 and it may be seen as a very small mirror image of 

 the P wave. It is probable, although there is no 

 direct evidence to support this contention, that 

 repolarization of the atrium progresses in a direction 

 similar to that followed by depolarization. Since the 

 electrical charges in repolarization are oppositely 

 arranged across the boundaries between resting and 

 active tissue, the resultant potentials have a polarity 

 opposite that seen during depolarization. The small 

 size of the repolarization complex probably reflects 

 the slow potential changes in the cells during re- 

 polarization. 



Atrioventricular Conduction 



The P wave of the human electrocardiogram is 

 followed by a period of approximately 80 msec during 

 which no potentials are recorded electrocardio- 

 graphically (fig. 5). This P-R interval is followed by 

 the QRS complex which signals ventricular de- 

 polarization. During this interval the impuLse is 

 confined within the A-V node and peripheral portions 

 of the A-V conduction system, as first shown by 

 Hering (56). In many clinical conditions, the P-R 

 interval is prolonged (first degree A-V block) or the 

 P waves may not always be followed by QRS com- 

 plexes (second degree A-\' block). At times, the P 

 wave and the QRS complex are completely in- 

 dependent, indicating that the atria and ventricles 

 have separate rhythms (third degree A-V block). 

 Until very recently there was no knowledge of A-\' 

 nodal function enabling us to decide when the various 

 structures along the A-\' conduction pathway are 

 activated or labeling the anatomic site which fails to 

 conduct the A-\' nodal block. 



The period between the end of the P wave and the 

 iieginning of the QRS complex is commonly referred 

 to as the period of "A-V nodal delay." This term 

 probaljly originated from the feeling that the upper 



