3i8 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



input capacitors of the electrocardiographic recorder 

 prevent its use to discriminate between a shift in the 

 T-Q. segment and a shift in the S-T segment. In the 

 clinical literature, both of these changes are referred 

 to as "S-T segment elevation" in electrodes facing 

 the injury. (Electrodes facing the rear of the injury 

 record the opposite changes.) At present, there 

 seems to be no need to discriminate among these 

 various causes of "S-T segment elevation" during 

 acute and chronic occlusion of the vessels, and such a 

 discrimination would present overwhelming tech- 

 nical problems. 



A later change has been described by Durrer et al. 

 (42) and by Conrad et al. (31). At this time, some 

 cells in or near the "infarcted" region fail to de- 

 polarize normally, depolarizing much later than they 

 normally would. [See also Trautwein (131).] A uni- 

 polar electrode facing the area of injury thus sees 

 approaching (positive) activity immediately after the 

 QRS complex. Again, this change produces a true 

 S-T segment elevation, but it has not been demon- 

 strated that the increase in conduction time is equal 

 to the S-T interval (200 msec). It would have to 

 be of this duration if it were to account for the changes 

 in the S-T segment. Possibly, this change and the 

 second change, which is a true T-Q depression, exist 

 together during the period of chronic injury in pa- 

 tients, although there is no direct evidence at present. 



PHASE III. After the initial phases of ischemia and 

 injury have disappeared, the S-T segment and T 

 wave may return to normal. The diagnosis of such 

 chronic infarcts is a difficult problem for the practi- 

 tioner and may be important in determining whether 

 a patient should be treated or should limit his ac- 

 tivity. The major problem exists with regard to the 

 QRS complex. In many cases, a sizable portion of the 

 myocardium will have been replaced by scar tissue 

 which is, of course, electrically silent. If the conduc- 

 tion system has not been impaired by the infarction, 

 the duration of the QRS complex may be normal; 

 if a large amount of myocardium is missing, the 

 complex will be changed, i.e., it will lack the po- 

 tentials previously contributed by the infarcted 

 region. An electrode which faces the infarcted region 

 and which previously recorded approaching (posi- 



tive) activity from that region will record less posi- 

 tivity than normal, or it may record a negative 

 deflection. If the area of infarction is in a part of the 

 heart which is normally depolarized early, this in- 

 creased negativity may either produce an initial 

 negative deflection or increase the magnitude of a 

 negative deflection which would normally occur in the 

 lead facing the region. An initial negative deflection 

 is referred to as a Q wave, and an abnormal Q wave 

 is the most common diagnostic sign of chronic in- 

 farction. Q waves are not abnormal per se; the ab- 

 normality is frequently definable only in terms of the 

 magnitude or duration of the wave in a particular 

 lead. Some portions of the body surface normally 

 show Q waves. Although this sign is useful, if it is the 

 sole criterion of infarction, a diagnosis obviously can 

 be made only when the infarction lies in regions 

 which are depolarized early in QRS. 



Several recent textbooks of electrocardiography 

 have described successful techniques for the detection 

 of an infarction which affects the later portions of the 

 QRS complex. Some large infarcts may damage the 

 conduction system, thus causing a prolongation of the 

 QRS complex. It may be important to difTerentiate 

 such prolongation from that seen in bundle branch 

 block, since the latter may be present and innocuous 

 in an otherwise healthy heart. The value of a control 

 electrocardiogram taken before any reason exists 

 to suspect myocardial damage should be apparent. 



It is interesting that, during the period after in- 

 farction, a fixed relationship between changes in the 

 S-T segment and T wave is often observed; those 

 leads which show elevated S-T segments show a 

 negative T wave. Although the mechanism has not 

 been directly determined, a possible explanation is 

 available by extrapolation from observations by 

 Durrer et al. (42) and Bayley (14), as well as Conrad 

 et al. (31). Since depolarization is delayed in some 

 cells in the infarcted region, might not these cells 

 also repolarize late? Late depolarization would ele- 

 vate the S-T segment and late repolarization would 

 cause a negative T wave over the region. That is, 

 the wave of repolarization would approach a lead 

 over the infarction so slowly as to give a large nega- 

 tive deflection. (Remember that approaching re- 

 polarization produces a negati\e potential.) 



REFERENCES 



I. Aagaard, (). C. AND H. C. Hall, Uber Injektionen des 

 "Reizleitungssystems" und der Lymphgefasse des Sauge- 

 tiei'herzens. Anal. Hejte 51 : 359, 1914. 



2. Abr.\mson, D. I. AND S. Margolin. .\ Purkinjc conduc- 

 tion network in tlie myocardium of the mammalian 

 ventricles. J. Anal. 70; 250, 1936. 



