The Automata Model of Arrhythmias and the CVRTI - Part IV
J.A. Abildskov, MD
Waveform and Vulnerability
Some waveform features associated with increased vulnerability to ventricular fibrillation have been described in previous sections and additional details are presented here.
Increased vulnerability was associated with increased K value range, decreased mean K duration, or the combination of increased range and decreased duration. Waveform features of these conditions were as follows: In comparison to a waveform designated as “normal”, decreased mean K in endo and epicardium resulted in earlier onset and termination of T waves without change of waveform. Increased range in both endo and epicardium resulted in earlier onset and later T wave termination. Between these times, T wave amplitude was decreased due to overlap of recovery durations in epi and endocardial regions. The combination of decreased mean and increased range resulted in earlier T wave onset due to both decreased mean and increased range in the epicardium, and increased slope of initial and terminal T waveform due to increased range in both epi and endocardium. Importantly, the time of T wave termination was not prolonged. That time was the result of decreased mean K values which altered the effect of increased range.
T Waveform Mechanisms
T wave features in a variety of individual conditions have been described in previous sections. In this section general mechanisms responsible for the individual effects will be considered. In matrices with an endocardial to epicardial gradient of high to low K values and endocardial origin of excitation, T wave onset represented onset of recovery in the epicardium. T wave completion represented end of recovery in the endocardium. T wave amplitude depended on the relation of recovery in the epicardium and endocardium. When those events did not overlap, completion of the upstroke represented completion of epicardial recovery and onset of the downstroke defined onset of endocardial recovery. With overlap of epicardial and endocardial recovery times, T wave peak amplitude was determined by the difference in time of completion of epicardial recovery and the onset of recovery in the endocardium. The range of recovery durations in epicardium and endocardium determined the slopes of initial and terminal T wave limbs. When there was no overlap of endocardial and epicardial recovery times, slopes reflected the total range of recovery duration. With overlap, slopes reflected ranges up to the point endocardial and epicardial durations were equal. With the same gradients of duration in endocardium and epicardium, duration of the terminal T wave limb was longer than that of the initial limb. T wave onset was the result of abrupt onset of recovery while termination reflected sequential completion of endocardial recovery. This finding differs from that in the normal human electrocardiogram. The longer initial T wave limb there may be due to greater range of endocardial than epicardial recovery durations or to geometry in which epicardial effects were more widespread than those of the endocardium.
Low or Inverted T waves
Low or inverted T waves in association with various other ECG features have been noted in previous sections. They are also a frequent non-specific manifestation of heart disease and responsible conditions in the model will be described here. The general mechanism responsible for low or inverted T waves in the model was reduction or reversal of the endo to epicardial gradient of longer to shorter recovery duration. Conditions with that result included: 1) Prolonged epicardial or reduced endocardial recovery duration. 2) Localized epicardial lesions with prolonged or endocardial lesions with reduced recovery duration. 3) Conditions related to activation sequence. The normal endo to epicardial activation sequence means recovery at the epicardium is effectively later than that due to K values only. Equal increase of K values and resulting recovery duration at the epicardium and elsewhere resulted in “normal” upright T waves. Equal decrease also resulted in upright T waves. Unequal alteration of recovery duration in the epicardium and elsewhere altered T wave amplitude or polarity. Increased duration of recovery (higher K values) in only the epicardium or to a greater degree in the epicardium resulted in inverted T waves. Decreased duration outside the epicardium or to a greater degree there also resulted in inverted T waves. Equal decrease of K values in both endo and epicardium did not alter T waveform but T wave was earlier.
In summary, low or inverted T waves occurred in the model when recovery time in the epicardial region was prolonged or that in the endocardial region was reduced in each case relative to the other regions. The low or inverted T wave due to shorter recovery times in the endocardium resulted in earlier T wave onset compared to the control. Low or inverted T waves due to prolonged epicardial recovery resulted in later T wave onset. Importantly, the late normal epicardial activation which made recovery there effectively late meant that a particular increase of recovery duration had greatest effect at the epicardium. That allowed relatively earlier recovery elsewhere and low T waves due to increased recovery duration.
With low or inverted T waves, increased K value mean in both endo and epicardium resulted in later waves with the same waveform. Increased range resulted in overlap of deflections from endo and epicardium with “cancellation” and decreased amplitude of initial portions of the T wave.
Inexcitable Units and Waveform
Some effects of inexcitable units on ECG waveform were briefly noted in a previous section. More details concerning effects of such units are described in this section. Responsible factors were loss of the contribution of the inexcitable units to QRS and T waveform and altered activation and recovery sequences in the remaining excitable units.
Randomly scattered inexcitable units in the entire matrix reduced the dimension of wavefronts during both excitation and recovery resulting in a decreased amplitude and irregular contour of QRS and T deflections. Nonuniform activation of the endocardium was directly due to absent activation of the inexcitable unit and that of the epicardium due to both that factor and nonuniform delivery of activation to excitable units.
Randomly scattered inexcitable units confined to the epicardial half of the ventricular thickness altered terminal portions of the QRS and early portions of the T wave. Activation and recovery in the endocardium were not altered but the terminal T wave portion was changed because endocardial recovery time relative to that in the epicardium was altered.
Scattered inexcitable units in the endocardium directly altered activation sequence there and changed initial portions of the QRS. The changed endocardial activation also altered delivery of excitation to the epicardium and changed later QRS waveform.
Scattered Lesions and Waveform
Some waveform effects of scattered lesions were noted in a previous section. Lesions with briefer recovery than that in the matrix resulted in T wave changes of opposite polarity to that of the QRS. Lesions with longer recovery resulted in changes with the same polarity as the QRS. Those effects were in matrices with random K value distributions. Similar effects occurred in matrices with an endocardial-epicardial gradient of long to short recovery duration. In the case of lesions with briefer recovery than that in the matrix, T wave onset was earlier. Lesions with longer recovery than that in the matrix did not alter T wave onset but T termination was prolonged.
Effects of randomly distributed units with delayed activation were the result of reduced dimension of activation and recovery wavefronts in units without delay and later effects of activation and recovery in the units with delay. The relative magnitude and duration of effects depended on the number of units with and duration of delay. With 100 units having a delay of 10 time steps, QRS and T amplitude were both reduced due to decreased dimension of activation and recovery wavefronts. QRS duration was increased due to cumulative delay of activation to its completion at the epicardium. T wave duration was not increased and was still mainly determined by completion of endocardial recovery.
Randomly distributed units with delayed activation in the epicardium only altered waveform and delayed completion of the late half of the QRS and also altered both early and late sections of the T wave. Early activations were the direct result of the conduction defect and later activations were due to altered epicardial-endocardial conditions. The magnitude of the T wave changes that have been described depended on the amplitude of T waves in the control state. This is turn depended on the magnitude of endocardial and epicardial K values as has been previously described.