Intraventricular conduction delay pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]

Overview

Intraventricular conduction delay involves a variety of disturbances of the His-Purkinje/ventricular conduction system that affects the electrocardiogram (ECG) in distinctive ways and lead to a wide QRS complex and/or axis deviation.

Pathophysiology

Intraventricular Conduction System Anatomy

The conduction system of the heart consists of specialized cells designed to conduct electrical impulse faster than the surrounding myocardial cells. The intraventricular conduction system originates from AV node as bundle of His, branches and ends as the Purkinje system.

• The bundle of His divides at the junction of the fibrous and muscular boundaries of the intraventricular septum into the right bundle and left bundle.
• The left bundle branch penetrates the membranous portion of the interventricular septum under the aortic ring and divides into several smaller branches. Parts of the left bundle branch include a pre-divisional segment, anterior fascicle/hemibundle and posterior fascicle/hemibundle. Rarely a median fascicle is present in some hearts.
  • The left anterior fascicle (LAF) supplies the anterior papillary muscle and the Purkinje network of the antero-lateral surface of the left ventricle.
  • The left posterior fascicle (LPF) supplies the posterior papillary muscle and the Purkinje network of the postero-inferior surface of the left ventricle.
  • The left median fascicle (LMF) runs to the interventricular septum. In most cases it arises from the LPF, less frequently from the LAF, or from both, and in a few cases it has an independent origin from the central part of the main left bundle at the site of its bifurcation.
• The right bundle is an anatomically compact unit that travels as the extension of the HB after the origin of the left bundle. The right bundle branch courses down the right side of interventricular septum near the endocardium in its upper third, deeper in the muscular portion of the septum in the middle third, and then again near the endocardium in its lower third.
  • The right bundle branch is a long, thin, discrete structure.
  • It does not divide throughout most of its course, and it begins to ramify as it approaches the base of the right anterior papillary muscle, with fascicles going to the septal and free walls of the right ventricle.
• The Purkinje fibers connect the ends of the bundle branches to the ventricular myocardium. Purkinje fibers form interweaving networks on the endocardial surface of both ventricles and penetrate only the inner third of the endocardium, and they tend to be less concentrated at the base of the ventricle and at the papillary muscle tips.

Structure of the heart's conduction system

Normal Ventricular Conduction

• First Phase : Normally the first part of the ventricles to be depolarized is the interventricular septum. The left side of the septum is stimulated first by a branch of the left bundle. On the normal ECG, this septal depolarization produces a small septal r wave in lead V1 and a small septal q wave in lead V6.
• Second Phase : Next phase is the simultaneous depolarization of the left and right ventricles. The activation of the left ventricle begins almost simultaneously at the insertion points of the fascicles of the left bundle branch.

Conduction velocity depends on the rate of rise of phase 0 of the action potential (dV/dt) and the height to which it rises (Vmax). These factors, in turn, depend on the membrane potential at the time of stimulation. The more negative the membrane potential is, the more sodium (Na+) channels are available for activation, the greater the influx of Na+ into the cell during phase 0, and the greater the conduction velocity. Purkinje cells are specialized to conduct rapidly, at 1 to 3 m/sec, because phase 0 of the action potential is dependent on the rapid inward Na+ current (INa). This characteristic results in almost simultaneous depolarization of the terminal HPS and propagation of the cardiac impulse to the entire RV and LV endocardium