Abstract
QRS prolongation in experimental BBB was reated to the increased time required for unidirecional spread of activation across the septum and into and through the blocked ventricle. There was no focal or diffuse slowing of propagation velocity in the septum, it averaged 0.4M/sec. There was an abnormal pattern of excitation of the blocked free wall indicating that the Purkinje network was not operating to distribute the impulse normally. LBBB was associated with a longer period of ventricular activation (QRS) than RBBB, and the mechanism of this difference was explained from the data. The mechanism of the altered QRS potentials in right and left BBB was studied by correlating ECG's and VCG's with the activation data. The spread of excitation in the septum was an important factor in the increased magnitude of QRS in BBB. Also several of the characteristic features of QRS, such as the midpoint slowing of velocity and plateau in LBBB, were explained from the activation data. The sequence and pattern of spread of activation indicates why QRS changes due to myocardial infarction may be more apparent in RBBB than LBBB.
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