THE SEQUENCE OF VENTRICULAR SURFACE EXCITATION DETERMINED BY REGISTRATION OF MONOPHASIC ACTION POTENTIALS

Abstract

Current conceptions regarding the spread and order of ventricular excitation seemed to merit re-investigation because the potential variations led from ventricular surfaces are apparently not as accurate as was formerly believed. Monophasic action potentials were registered by a new technique in which a minute discrete point of injury was produced by the non-polarizable suction electrode and a lead was made from uninjured spots by a non-polarizable wick electrode. The procedure insured against pickup of po tentials from the injured region which when present interfere and summate with the true monophasic curve and in so doing are very likely to render the footpoints in-accurate. The technique of registration is given, differentiation of pure from impure curves is discussed, and ways in which errors are introduced by such artefacts are analyzed. Exptl. support is presented for the interpretation that pure monophasic curves are not affected by potentials at or near the injured point, in this method of recording. After production of left ventricular ischemia by ligation of a coronary branch, the duration of the monophasic potentials is decreased and the moment of rise retarded when the exploring electrode is located is this region, whereas no alterations of the curves take place when the lead from a damaged point is taken from this area. Pure monophasic curves were recorded successively from a large number of points on the anterior and posterior surfaces of the ventricles. The moment of rise with reference to R2 of a standard unchanging electrocardiogram indicates the relative moments of negativity at such different spots. Curves, diagrams and a table are presented which show that the anterior and posterior ventricular surfaces are everywhere excited within 5 to 8 [sigma] except in the central anterior region overlying the septum which is usually excited 10-17 [sigma] earlier. No evidence of any sequence of even a small order could be discovered in points in line with muscle bundles. It is concluded that normal excitation of the ventricles occurs by transmission of impulses over the A-V bundle and its branches, first to the septum and contiguous external muscle, then to the remainder of the external ventricular walls and through them without regard to muscle bundles. Transmission through the external walls occurs at the same rapid rate at which it travels over the bundle-branches; it is not retarded as currently believed. In consequence all parts of the ventricular surfaces, excepting the central part overlying the septum, are excited with a maximum time interval of about 8 [sigma]. Presumably such conduction occurs through recently described Purkinje tissue present throughout the ventricular walls.