Abstract

In clinical diagnosis of ventricular hypertrophy, bundle branch brock, premature heart beat, tricuspidal- and aortic valvular insufficiency, it is of great significance to determine the time of arrival of activation in ECG. However, there still remains a contraversy as to the point indication it. For example, the onset of ingrinsic or intrinsicoid deflection is regarded as the point marking this by Lewis, Wilson in early stage and many other authors, while the end of this deflection is considered to mark it by Wilson. This report was made to elucidate the accurate relationship between it and intrinsicoid deflection. According to our results in calculation, the actual instant of arrival of activation could be reperesented by cross point of tracing with zero-line when the equivalent double layer, perpendicular to the ling axis of straight muscle strip, was moved from one end to another. The time interval between the onset of the int. defl. and the cross point was variablw according to the transmission rate of activation and the distance from electode to muscle strip. When the equivalent double layer, oblique to hte long axis of the muscle strip,w was moved from one end to another, it could not be reperesented by cross point, differing from above mentioned case. Consequently, the onset of intrinsicoid deflection or the cross point of this deflection with zero-line could not be regarded as the representative point of arrival of activation even in simple activation process like above mentioned cases. Since the activation process in human heart is notso simple as that applying to above cases, we want to calculate the potential variation arising in more complicated activation process. When we calculated the potential change at a given point without a hollow polaraized sphoere in a certain process of activation, the time of arrival of activation was somewhre within the duration of intrinsicoid deflection. Moreover, when we calculated the potential variation at many points without heart in a feew process og activation, the arrival of activation occurred some where during the intrinsicoid deflection and was not upon a specific point like the onset or the end of the deflection. These caliculations were made on the schema of heart quoted from the atlas of anatomy by Toldt Hochstetter, assuming the every equivalent double layer in each stadium of activation as a disk. It must be noted that the intrinsicoid deflection is not necessarily sharp and large deflection but sometimes smaller than the deflection due to the extrinsic effect, and it is not always easy to point out the intrinsicoid deflection in ECG. Comparing these results of calculation with those of experiments pwerformed on toad heart, recording the contiguous bipolar lead ECG and unipolar lead ECG simultaneously, we could observe that the both results coincident very well. We may conclude that the onset or the end ofthe intrinsicoid deflection can not be interpreted as the point indicating the arrival of activation as Lewis Wilson and others say, and that ingrinsicoid deflection is not neccessarily a large and sharp deflection but sometimes smaller then the deflection due to extrinsic effect. In general, the time of arrival of activation lies somewhere during the intrinsicoid deflection, bu can not be defined on a specific point.

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