360 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



The figures of rows a, h and c were measured directly; the rest were calculated. In e, the length of the specific system in 

 the adult is assumed to be 130 mm; all other values were calculated from this value by assuming that this length is propor- 

 tional to v^weight. e and/ have a constant ratio of 130:10, which is the probable adult ratio [.Schaefer (58)]. In g and i, the 

 QRS durations were calculated by assuming the QRS to increase with the third or the sixtli root of heart weight, respectively. 

 g and I should be compared with a. \s will be seen, the QRS duration \'aries in good agreement with the sixth root of heart 

 weight. This may be explained by two assumptions: /) that in the growing heart, QRS increases predominantly with the 

 heart length or the length of the specific system, and 2) that the larger heart has the larger fiber diameters, the conduction 

 velocity depending on the square root of the fiber diameter, whereas the diameters depend on the third root of weight. Hyper- 

 trophy within the clinically observed limits never increases QRS to more than o.i sec. 



ti'odes are broadened and the QRS duration is aug- 

 mented. Ouabain changes this effect suddenly back 

 to normal (485). Adrenaline, on the other hand, 

 shortens the QRS complex and increases the con- 

 duction velocity. 



Form of the QRS Complex 



Besides the area, the form of QRS is a very im- 

 portant indicator of the physiological events in the 

 heart. The form may be analyzed with regard to the 

 total duration, the polarity of QRS, i.e., the prc- 

 ponderaitce of positive (R) or negative (Q, .S) deflec- 

 tions in the various leads, the maximal amplitudes of 

 these deflections and the contour of the curve with 

 respect to notches, polyphasic deformations, etc. 

 It is not the purpose of this chapter to present a 

 diagnostic guide, but we will try to explain the 

 general rules governing these characteristics of the 

 QRS. 



/) The total duration of QRS is exclusively de- 

 termined by the time the excitation wave takes to 

 reach the most remote points of the heart. The very 

 beginning and the very end of this process may 

 happen in relatively small areas of the heart. So we 

 know that the onset of Q is due to the activation of 

 the papillary muscles and of the ventricular septum. 

 There is no direct proof of this assumption, but we 



may conclude so from the direction of the heart 

 vector during Q, which normally is directed cranially, 

 slightly forward, and mostly to the left (7, 72). This 

 agrees fairly well with the fact that the first fibers 

 leaving the specific system run into the septum and 

 the papillary muscles, both being activated in the 

 direction mentioned. The last activated region is 

 doubtless the posterior part of the base, as all latency 

 measurements indicate (see section 8). Both portions 

 of the heart are small, and their respective voltages 

 low. Moreover, the momentary vectors of earliest Q 

 and latest S do not project optimally on the same lead 

 lines, so that beginning and end of QRS cannot be 

 determined in one single lead : a simultaneous record 

 of several leads with high power and high fidelity 

 amplifiers is therefore necessary (iii, 318). Quanti- 

 tati\ely, however, these small initial or final events 

 in QRS are of minor importance. We may therefore 

 take the u.sual determinations of QRS duration (most 

 commonly read from lead II) as its real duration. 

 The question is how to interpret an increase in this 

 duration. 



From obser\ations of the spread of excitation at 

 the surface, we concluded that the excitation wave 

 travels only over very short distances in a directly 

 conducted manner (234, 412). If one assumes the 

 conduction velocity of the myocardium to be of the 

 order of magnitude of i m per sec or less, and the 



