364 HANDBOOK OF PHYSIOLOGY ^^ CIRCULATION 1 



FIG. 47. Vectorial addition of the several M, of fig. 40 to 

 the ventricular gradient G, which is the vectorial sum of all 



Mi originated along the single myocardial fibers, some of 

 which are represented in the figure. 



potentials at the two ends of any fiber must differ to 

 a certain degree. In the dog heart we found that, 

 even with very short bipolar electrode distances, the 

 action potential recorded at the surface commonly 

 does not have a total time-voltage area which equals 

 zero. The area of Tj is always opposite to R, but in 

 general a bit smaller than the area of K,, and the 

 quotient Q = jTi/Rij generally is 0.85 (234). This 

 points to the fact that inhomogeneities of repolariza- 

 tion occur within very small distances all over the 

 heart's surface and most probably as well all over 

 the ventricular walls. If, as figure 47 shows, these 

 inhomogeneities are represented by the value of 



M, (the area of individual fibers), all vectors Mi add 



to the resultant vector M, the ventricular gradient, 

 but without cancellation of such a degree as was 

 found in QRS. This is the reason why even slight 

 differences in local forms of monophasic action 

 potentials of repolarization lead to remarkable values 

 for the ventricular gradient. Or, in other words, the 

 T wave is some kind of a special detector for differ- 

 ences in repolarization of the various parts of the 

 ventricles. 



There is an indirect but rather conclusive proof 

 that differences in the action potential pattern are 

 responsible for the gradient : every increase in fre- 

 quency diminishes the differences in action potential 

 area of different fibers (489), and correspondingly 

 the ventricular gradient is considerably reduced by 

 rising heart rates (86). Concerning quantitative 

 differences between action potentials, we may give 

 some examples. If the areas of the two monophasic 

 action potentials differ by about 4 per cent, and the 



FIG. 48. The vectorial analysis of QRS and T areas and the 

 ventricular gradient in the Einthoven triangle, under the 

 assumption that the area of QRS is doubled for some reason, 

 whereas the gradient remains constant. Doubling of QRS 

 induces not only a marked increase of T, but at the same time 

 a shift in the direction of the T vector. (The vectors with 



doubled QRS are marked with dots.) 



number of fibers not invoked in mutual cancellation 

 of Ri were of the degree mentioned above, namely 

 1:25 or 4 per cent, the ventricular gradient would 

 have the same time-voltage area as QRS. This seems 

 to be true for the human heart. Very small alterations 

 in repolarization can cause big percentile changes 

 ofT. 



As the area of T depends, among other things, 



upon the area of QRS, every increase of QRS leads 

 to a marked change in the T vector, and therefore in 

 its polarity in .some leads. This may be illustrated Ijy 

 figure 48, where QRS is douijled in area, which 

 inx'olves a doubling of the "individual" T and, if all 



inhomogeneities remain constant, the resulting T 

 changes its positioia from an Einthoven angle a of 

 5° to —110°, so that the T wave in leads I and II 

 becomes negative. Sucli an inxcrsion of T does not 



