
Attention to the U wave is practically nonexistent among clinical electrocardiographers. Nevertheless, this wave exists, is most frequently found in the precordial leads and less often in the limb leads. Characteristically, when the U wave is present, its direction is generally the same as that of the T wave which it follows. Its greatest amplitude seems to be found in V2-V4 or 5 , and then it declines and disappears in V6 and V7. In rare instances an inverted U in the precordial leads may be the only evidence in the electrocardiogram of the existence of heart disease. There are times when it falls on the downstroke of T, while at other times it appears in a diphasic terminal portion of T. In practically all observations thus far made it was found in a fixed time relationship with Q. 6 It cannot be assumed that because U is in a fixed time relationship with Q, the QU interval is a measure of the refractory period of the ventricle. In the intact dog heart, the basal fibers of the left ventricle were found to emerge from the refractory period last, and this moment corresponded with the end of T in the precordial electrocardiogram. The refractory period was never found to extend to where U would terminate. 5 We must therefore recognize that U is independent of the refractory period, and this makes it necessary to seek for its explanation in electrical events in excitable tissue that occur after the refractory period. That such a phenomenon exists can be seen in the work of Erlanger and Gasser, who have shown both negative and positive after-potentials long after the period of excitation accompanying the propagation of the nerve impulse. Such after-potentials seem to be associated with various phases of recovery and are profoundly influenced by metabolic mechanisms affecting recovery.

Many of the speculations offered to explain the origin of the U wave invoke an extracardiac as well as cardiac origin. In general most observers now believe that it arises from electrical activity in the ventricles and is in some way related to the recovery of the ventricle from excitation even though it occurs after the refractory period is completed. If it is an electrical event arising in the heart muscle as a result of excitation, then an electric field should be present during its inscription. If we knew what the characteristics of this field were, perhaps some of the objective findings regarding the U wave mentioned above would find a satisfactory explanation. In this communication the potential distribution during moments in the U wave has been established in normal subjects and those with cardiac pathology, and it will be seen that the reason for the distribution and character of this wave in the different leads begins to become clear.
METHOD
The method for obtaining the potential field at any given instant in the cardiac cycle and for drawing equipotential lines has already been described in detail.' Two channels of information were recorded simultaneously. One channel served as the time reference electrocardiogram, the other as the recording channel made up of the potential at the exploring electrode paired with the Wilson central terminal as a fixed electrode. Thus, for any moment in time the data were analyzed for the instantaneous algebraic value of potential of the exploring electrode with respect to the central terminal. It is important to recognize that with potential values as low as are obtained during the U wave they may almost be considered to have absolute significance since with such low values at the limbs the potential at the central terminal is probably zero. It will be observed from the diagrams that it was possible with the aid of a binocular microscope and magnification of 30 x to measure potential values almost exactly to within 0.1 of a mv. However, most of the number values were distinctly larger than 0.1 mv. and this permitted the establishment of the geometric properties of the equipotential lines at all values without difficulty.
RESULTS
In the first set of data (Figs. 1 and 2) the instantaneous equipotential distribution is shown for two normal male subjects. The instant in Figure 1 was that moment in time defined as 460 msec. after the onset of R in L3. In this subject the QT interval measured 380 msec. The instant in Figure 2 is 480 msec. after the onset of R in the time reference electrocardiogram. In this record the QT interval was 360 msec. In both diagrams the moment corresponded with the summit of U. It may be seen that only the positive field is described. The negative values at other points on the chest were less than 0.1 mv. and therefore are not charted; however, the region could be vaguely recognized as occupying the right shoulder, the right limb attachment, and right axilla.
RESULTS
In Diagrams 3 and 4 may be seen the potential field at two moments during the U wave 570 and 624 msec. after the onset of R in the time reference electrocardiogram of a patient with left ventricular hypertrophy and left bundle branch block. The QT duration was 507 msec. In Diagram 3 it is possible to distinguish both a positive and a negative region of the distribution. Again, the positive region occupies the left precordium, but the negative region is now in the left axilla. Contrast this with the normals where the negative region probably occupied the right axilla and shoulder. These diagrams are examples of many potential fields plotted during various moments in the U wave, on its ascending slope and on the downswing from the summit as well as at the summit. The striking feature characterizing all of them is the identity of the geometric form of potential distribution at all moments during the U wave, only the number values of the lines varying in each diagram. Diagram 4 is a field plotted 54 msec. later in the same subject and shows the positive region not to have changed in position or in its geometric form, but the negative region has waned and is no longer recognizable.
RESULTS
One general feature that characterizes the potential fields in all the diagrams is the marked asymmetry of the equipotential lines and their Field function U wave N striking irregularity. In this feature they are altogether similar to other potential fields already described during the QRS and T complexes in normal subjects and those with cardiac pathology.2'"'4
DISCUSSION
The above data in a most striking manner reveal that an electrical disturbance occurs during the U wave, for we find at various moments I8ff 4e. C~~~~~~I . during T a two-pole distribution-that is, a region of positive and negative potential. Unfortunately, surface potential measurements cannot in principle necessarily and sufficiently elucidate the real source of the potential. The magnitude of the potential values, however, is such as to preclude their origin in the recoil of the aorta or the flow of blood through it. It is unlikely that the rapid inflow of blood in early diastole gives rise to an electrical disturbance sufficient to cause the U wave, for if this were so, then the U wave while varying in amplitude according to velocity and volume of inflow could not vary in sign. Accordingly, U would always remain negative in VR where it normally is, and positive in the precordium where it normally is. Diagram 3, however, shows a negative field in the left axilla instead of the right, and negative U waves have been encountered in the precordial leads in diseased hearts with and without T wave changes. 6 We are led to the conclusion that the kinetics of diastolic inflow cannot explain the genesis of the U wave. It is also difficult to attribute the potential field during U to the distension of the ventricles by the inflow of blood during diastole, since the greatest distension occurs in presystole, while the strongest potential field occurs in earliest diastole. We are accordingly led to postulate that the current source is in the ventricles and represents a phase of the recovery process. Support for this hypothesis may be derived from the following. The location of the positive distribution is directly over the heart suggesting that it arises there. As one travels from the precordium, the potential falls off rapidly so that the negative part of the distribution, especially in the normal subjects, becomes so attentuated as to be unrecognizable. The geometric form of the positive potential field is almost exactly like that during the ST segment and various moments in the T wave. This directs attention to the possibility that the recovery processes in the ventricles which are reflected in the formation of ST and T"' are also at the basis of the U wave.
DISCUSSION
The problem arises whether U may be attributed to the late termination of the refractory period in some fibers that are late to recover, as, for example, those somewhere in the septum. Aside from the fact that no evidence has been adduced to support such a view, there are some observations against it. Our observations on the termination of the refractory period in various parts of the intact dog left ventricle have shown that the latest fibers to recover are not in the septum but in the left ventricular base. Their refractory period terminates at the end of T or shortly thereafter, but not as late as U. What is equally important, however, is that the positive potential distribution of T and U is almost identically located. The close similarity between the location and the geometric form of the U and T fields in the normal is equalled by the identity of their nonrotating properties. The potential function during U merely waxes and wanes in time just as had been shown to occur during T and this is strikingly different from that during the QRS where rapid rotation and shifting of the maxima in space occurs. 1' 4 The irregularity of the potential lines in all the diagrams supports the view that the source of the potential in the heart giving rise to the electric field is as complicated as is that which gives rise to the fields during the QRS, ST, and T. If the source were a simple dipole, the potential distribution on the body surface would be expected to be as already described for an intrathoracic bipole, namely, smooth regular lines.' The conclusion would appear to be warranted that all the heart fibers contribute to the field; because of the variation in time and duration of the "after-potential" in the complex heart mass, the resulting potential field on the surface is complex also.
DISCUSSION
Some explanations for the electrocardiographic findings regarding U in the various leads now emerge. The low potential at the limbs makes a recording of U difficult in limb leads and explains its greatly reduced frequency in these leads. The highest potential values are found directly over the heart mass, represented by position V2-V5. It is in these leads that U is most prominent. Since the potential falls away towards the axilla, the U wave should flatten and disappear in these leads as it actually does. The potential fields in the normal subjects merely wax and wane in time without rotation. This accounts for the occurrence of a positive or a negative U in a lead but not a diphasic complex. Finally, the locations of the positive and negative regions occupy the same areas as they do during the ST segment and T wave. This explains why the U in general is positive or negative as the T is positive or negative. There still remains to be explained the rare case in which the precordial T waves are positive while the U wave is negative. Further charting of such fields should throw light on this strange phenomenon. It is probable, however, that what has occurred is a shift of the negative region normally occupying the left axilla in some cardiac subjects towards and over the left precordium.
DISCUSSION
Not enough is known to permit speculation as to whether the factors responsible for the electric field during T are similar to those during U. It might be suggested, however, since the precordium is positive, that during the after-potential the recovery of the heart underlying this region occurs sooner or faster than in other regions of the heart, thus rendering this area positive and the overlying surface positive.
DISCUSSION
The nature of the post-refractory processes that may be involved in the genesis of the U wave can only remain in the realm of austin78@example.org. Electrical activity at this period in the recovery process would exist especially if a supernormal period were present. That this can occur is attested by experiments on nerve, skeletal muscle, and the dog and chimpanzee ventricle. The presence of ectopic beats mostly occurring during this period directs attention to the existence of a supernormal period in many such instances, since ectopic beats and supernormality are believed to be dependent one upon the other.'
DISCUSSION
Nevertheless, the occurrence of a U wave in the normal male makes it unlikely that its genesis in the normal can be related to the existence of a supernormal period. In the intact dog ventricle supernormal periods are not encountered. If the normal human heart is not different metabolically from the normal dog heart, then the normal human heart also probably does not possess a supernormal period. The normal human subject, however, does have a U wave in the electrocardiogram and exhibits a potential field on the body surface during moments in the U. It must be considered, therefore, that other electrical processes besides the supernormal period can participate in the genesis of the U wave. SUMMARY 1. An electric field exists during the U wave which waxes and wanes. 2. Its characteristics are similar to the field during the T wave which it follows.
DISCUSSION
3. The complexity of the equipotential lines points to a complex electrical source in the heart.
DISCUSSION
4. Clinical types of U waves are deducible from the potential distribution. 5. The nature and location of the distributions makes it unlikely that the U can be explained by electric forces generated by rapid inflow in early diastole.
DISCUSSION
6. The position of U in the cardiac cycle precludes its origin in potentials caused by cardiac distension.

{'paper_id': '9353219', 'title': 'The Field Function on the Body Surface during Moments in the U Wave in Normal Subjects and in Patients with Cardiac Pathology ‡', 's2_url': 'https://api.semanticscholar.org/CorpusID:9353219', 'source': 'S2ORC'}