382 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



canceled by the vectors from the other (fig. 64). In 

 general, however, the damaged area will develop only 

 one boundary against the normal tissue, with a 

 minimal cancellation, as seen in figure 64. 



The ST displacements due to such demarcation 

 potentials between normal and injured tissue survive 

 for a short time only. After a 10- to 15-min period, 

 the potential nearly completely disappears, due to the 

 fact that the damaged fiber loses its intracellular 

 fluid content up to the next intercalated disc (Glanz- 

 streifen). Here a real cell boundary seems to exist, 

 preventing the myocardial fiber from losing more of 

 its intracellular fluid. The boundary between normal 

 and injured tissue is thus replaced by a boundary 

 between normal myocardial fibers, the limits of 

 which are now the intercalated discs. The emptied, 

 injured parts of the fiber become electrically inactive. 

 If a new injury is sustained, destroying the membrane 

 once more behind the intercalated disc, a new injury 

 potential occurs (398). This is the reason why the 

 ST displacement disappears comparatively rapidly 

 and can only be restored by a newly occurring 

 injury. 



The Ql^ Duration: "Electrical SystoW^ 



The very end of T is determined by the moment 

 when the repolarization of the latest repolarizing 

 fiber is completed. The whole QT duration therefore 

 depends on two factors: the amount of asynchrony, 

 which may be calculated from the duration of the 

 QRS complex and is nearly identical with it, and 

 the total duration of the action potential of the 

 average myocardial fiber. One could estimate, 

 therefore, that QT equals the duration of the longest 

 local action potential plus the duration of QRS. The 

 magnitude of the ventricular gradient (G = 2 

 QRS) indicates that the inhomogeneities in the 

 duration of the action potentials are of the same 

 order of magnitude as the desynchronization in the 

 ijcginning of all local excitatory processes. However, 

 it is always possible that the longest action potential 

 may be the last to start, so that the simple equation : 

 QT duration = QRS duration + action potential 

 time is subject to consiclcrai)le error. Since T is 

 normally monophasic, it may be argued that differ- 

 ences in duration of individual action potentials are 

 distributed at random over all possible local con- 

 duction latencies. 



The duration of QT depends mainly on the heart 

 rate. Many formulas have been given to calculate 

 this duration, but none of these fits all data. This is 



30- 



0.40- 



0.50- 



HEART RATE (PMIN) 



"i~~i — I — r~i — I — I — I — I — I — I — I — I 



30 50 70 90 110 130 ISO 



FIG. 65. Correlation between heart rate and duration of 

 Q-T. The limits of normal values are given, in some appro.xi- 

 mation and according to the majority of authors. 



not surprising, because change of rate can be induced 

 by various processes which influence the action 

 potential in different ways. For example, heating 

 the heart shortens the relative QT duration, whereas 

 an increase in the sympathetic tone increases the 

 relative QT duration. "Relative duration" means 

 the "normal" duration for a given rate (fig. 65). 

 Cooling lengthens, and acetylcholine and vagal tone 

 shorten, the relative duration of QT. Such effects 

 reflect changes in the single fiber action potentials. 

 In analysis of human ECG's intraindividual QT 

 changes are described by a different formula than 

 that for interindividual changes (218). 



The formulas describing this correlation ijetween 

 QT duration and heart rate contain either the RR 

 interval, its square root, or its cube root, as one of 

 the factors. The simplest formula (and one of the 

 Ix'st) is: QT = 0.39 \/RR (241)- No theory explains 

 the mathematical form of such correlations, which 

 therefore remain essentially empirical. Thus it seems 

 wise to repre.sent the frequency effect by an empirical 

 correlation (fig. 65). The correlation is even better if 

 the duration of QRS is subtracted from the QT time 

 (corrected QT duration, Lepeschkin). Since the QT 

 duration in a single filler depends linearly on the 

 frequency (447), a linear correlation could be ex- 

 pected for the whole heart as well. But QRS and the 

 desynchronization and inhomogeneities of repolariza- 

 tion apparently interfere in a complicated manner. 

 Values for portions of the QT time, as, for example, 

 the time between Q and the top of T, have been 

 given by Lepeschkin (315). 



