ELECTROCARDIOGRAPHY 



383 



The adaptation of QT to a change in frequency 

 occurs immediately after a change of one single 

 preceding diastolic interval. Therefore it is extremely 

 unlikely that the energy available or liberated by 

 the heart beat is responsible for this adaptation. Nor 

 is there any "'purpose" in shortening or lengthening 

 of QT. The mechanism most probably is due to the 

 accumulation of potassium at the outer surface of 

 the myocardial fiber, because K shortens the action 

 potential. The reconveyance of K into the cell takes 

 time and energy. The longer the time, the smaller 

 the remainder of external potassium. Therefore, the 

 QT duration reflects an equilibrium process between 

 the potassium remaining outside and shortening QT 

 and the forces of re-entry into the cell. We understand 

 that sudden changes in the frequency lead to a slow 

 adaptation of the QT duration (242), until the new 

 equilibrium is established. 



Electrical and mechanical events are independent 

 of each other within wide limits. The term "electrical 

 systole" therefore is incorrect: .systole is a mechanical 

 event, depending on circulatory conditions, like 

 aortic pressures, and their interference with the 

 contractile mechanism of the heart. It is often, but 

 not always, true that QT is nearly as long as the 

 mechanical systole, and that T ends synchronously 

 with the beginning of the second heart sound. Proof 

 that this is not generally true may be seen in the 

 kangaroo, whose QT duration is about 50 per cent 

 shorter than its mechanical systole (471). Details of 

 the electromechanical relations will be discussed 

 later (section 13). 



12. THE U WAVE (316, 317) 



During mechanical diastole, in many cases, a 

 low potential difference is recorded, lasting in cases 

 of tachycardia to the onset of P or even longer. This 

 so-called U wave reaches the \oltage of 0.05 mv or 

 more in about 3 per cent of normals, and is maximal 

 in the Einthoven lead II (299). It is sure that this 

 wave cannot be related to monophasic action po- 

 tentials during the contraction of any fiber of the 

 heart. It must be the result of a completely diff'erent 

 type of cellular potentials, the afterpotentials (441). 

 Positive afterpotentials, which may occur during the 

 diastolic phase, are known only in Purkinje fibers, 

 where they play the role of pacemaker potentials 

 and may be ascribed to a gradual decrease in mem- 

 brane potassium conductance, combined with 

 increased sodium permeability (487). Such positive 

 afterpotentials, however, are unknown in the bulk of 



ventricular fibers and cannot be the source, on 

 quantitative grounds, of events detectable in the 

 ECG. The "active cross section" of Purkinje fibers 

 is too small to evoke a sufficiently strong electric 

 field. Negative potentials, due to stretching, there- 

 fore seem to be the only source of potential differences 

 observed in the ECG during diastole. 



We are far from having a complete theory of the 

 U wave. The most likely explanation is that negative 

 afterpotentials in big muscle masses most probably 

 are the source of the U wave potential, but these 

 afterpotentials at the same time must be distributed 

 inhomogeneously over the heart (406). Otherwise, 

 neither the amount of potential difference nor its 

 polarity could be explained, since homogeneous 

 negative afterpotentials would lead to a very small 

 and discordant (downward) U wave. The coupling 

 between T and U, shown by the identical direction 

 of their vectors, indicates that U depends heavily on 

 the processes governing the ventricular gradient. 

 The inhomogeneity of the afterpotential is apparently 

 correlated with the anatomical direction of the 

 myocardial fibers and the spread of their excitation, 

 as is the case with the T wave. The greater the stroke 

 volume, the stronger the stretching factor, but 

 inhomogeneities may be exaggerated in empty 

 hearts with extremely small diastolic filling. The 

 inhomogeneity may be minimal in hearts with a 

 medium-sized diastolic volume, the diminution of 

 which leads to greater inhomogeneities. The aug- 

 mentation however, by increasing local stretching, 

 leads to higher absolute afterpotentials. 



The preceding remarks are concerned with the U 

 wave in normal hearts. There are, however, strong 

 potentials experimentally evoked, of obviously 

 metabolic origin, which are likewise marked as U 

 because they occur during the TP segment, in which 

 the normal U wave also happens to appear. They 

 can be elicited by adrenaline or insulin (152, 153) 

 and consist of an upward (positive) deflection of the 

 same sort as the normal U. In pathological hearts, 

 even negative U waves are found, and various types 

 of fusions between T and U have been described 

 (316). However, one gets the impression that all 

 these U waves are different from the "normal" U, 

 that metabolic processes may be the cause, but that 

 no explanation is available for the moment. A 

 decrease of potassium or an increase of calcium may 

 play a certain role in the genesis of such augmented 

 afterpotentials (441). In some clinical cases, the 

 situation seems to be rather intricate; a discussion 

 lies beyond the scope of this review. 



