362 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



L±± 



X 



JL JL JL 



^ rr 



FIG. 45. Four types of vector direction of the QRS group 

 with the respective pattern of QRS in the standard leads. 

 [From Schaefer (58).] 



formulas have been published (104, 424) for de- 

 termining type in a rapid manner and de.scribing it 

 by an index. A rough estimation can be drawn by 

 regarding the polarity of the main deflection in the 

 three standard limb leads, if the typology is restricted 

 to the frontal plane projections of the vector. The 

 estimation of the Einthoven angle, therefore, seems 

 to be nearly satisfactory. Figure 45 gives an idea of 

 the appearance of such an analysis. The various 

 mechanisms influencing the type are the following. 

 A change in preponderance by hypertrophy augments 

 the area at least a bit, mostly (in left hypertrophy) 

 by augmenting the amplitude of the main deflection. 

 A change in direction of the excitation waves always 

 changes the area to a fairly large extent (extra- 

 systoles, bundle branch blocks) and is always ac- 

 companied by a change in the temporal pattern. An 

 isolated change in the latter occurs only in peripheral 

 blocks (ramification blocks) and in a slowing of the 

 conduction velocity. This changes the area as well; 

 minimally in the ramification block, maximally in a 

 reduced velocity of conduction. There is not a strict 

 correlation between the "electrical axis" (i.e., the 

 direction of the heart \'ector at its highest amplitude 



or of the vector of the area) and the anatomical axis 

 (194). It is well known that the heart may rotate 

 about its longitudinal axis, and rotations of this kind 

 are not to be recognized in an X-ray picture. So, the 

 relations between the two axes are fairlv complicated 

 (38). 



3) The amplitude of the ECG depends among 

 other things upon the amount of the "active cross 

 section" (see section 7) of all fibers depolarized at a 

 given moment, whereby the cancellation factor plays 

 its most decisive role. The second most important 

 factor in determining amplitude is the form of the 

 lead field and the distance of the electrodes from the 

 heart. 



4) The contour of QRS in nearly all normal cases 

 is smooth, and shows notching or slurring only if the 

 record is taken with a high speed and high fidelity 

 system (304). The reason is that propagation across 

 the ventricular walls never passes immediately from 

 a small to a large active cross section, or, in other 

 words, that the number of fibers prevailing at a 

 certain moment and producing the resultant vector 

 increases and decreases in a continuous fashion, 

 without abrupt changes in the amount of active 

 tissue. This is the "normal" behavior. Notching of 

 this type will occur only if relatively small amounts 

 of the ventricular mass are involved in the 

 disturbances, and single notches, now and then, lack 

 all pathological significance (282). 



The QRS complex is the result of a strong mutual 

 cancellation. For this reason changes in conduction 

 through even small parts of the ventricular mass lead 

 to a marked distortion of QRS. Nevertheless, it is 

 surprising that complete abolishment of the function 

 of large areas, as in infarcts, may have comparatively 

 little influence on the form and area of QRS ! The 

 QRS complex is much more an indicator of reduced 

 conduction velocities in the specific system, or re- 

 versed directions of the spread of excitation, than of 

 local destructions. The reason for this is not very 

 clear, but it may i)e assumed that the cancellation 

 effect takes place in between narrow limits, e.g., 

 between the endocardial and epicardial surface of 

 the heart, so that a complete destruction of parts of 

 the heart does not lead to a "prevailing" of the intact 

 remainder of the ventricles, which retains nearly all 

 its cancellations as though normal. Only a different 

 distribution of conduction through the specific 

 system would alter the QRS complex decisively, as is 

 the case with infarcts in which the specific system 

 itself has been damaged. Summarizing we may 

 conclude. 



