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. It happens in the inital 30 milliseconds in QRS. On the normal ECG, this septal depolarization produces a septal q waves in leads I, aVL, and V6 and r waves in leads V1, V2, and aVR.

• Second Phase : Next phase is the simultaneous depolarization of the left and right ventricles usually gets completed in 40-60 milliseconds of QRS.
  • Left ventricle activation : The left ventricle activation begins almost simultaneously at the insertion points of the fascicles of the left bundle branch. The left ventricle is normally electrically predominant and its activation is leftward and posterior due to its structural orientation producing deep S waves in the anterior precordial leads (V1 and V2) and tall R waves in the leftward leads (I, aVL, and V6).
  • Right ventricle activation : The activation of the right ventricle starts at the origin of the right bundle branch.

R wave peak time : It is the time for full depolarization of the ventricular free wall (from the endocardium to the epicardium) beneath any given ECG electrode and it corresponds to the interval from the beginning of the QRS complex to the time of initial downstroke of the R wave after it has peaked. In the right precordial leads, the upper limit of normal for R wave peak time is 35 milliseconds, whereas in the left precordial leads, it is 45 milliseconds.

Conduction velocity of depends on the following factors :

• Rate of rise of phase 0 of the action potential (dV/dt)
• The height to which it rises (Vmax)
• 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 conduct rapidly, at 1 to 3 m/sec resulting in simultaneous depolarization and propagation of the cardiac impulse to the entire RV and LV endocardium.

Phase 3 Block Pathophysiology

Phase 3 block occurs when an impulse arrive in tissues during phase 3 of the action potential even before full recovery as cell membrane is at less negative potential and a portion of Na+ channels remains refractory and unavailable for activation. Consequently, the Na+ current and phase 0 of the next action potential are reduced, and conduction is then slower.

• Aberration caused by premature exitation : At normal heart rates, the effective refractory period (ERP) of the right bundle branch (RB) exceeds the ERP of the bundle of His and left bundle branch. When heart rate increases the right bundle ERP shortens to a greater degree than left bundle ERP making it longer than that of the right. Hence transient conduction delay (aberration) is in the form of RBBB when premature excitation occurs during normal heart rates and in the form of LBBB when heart rate increases.

• Ashman phenomenon : Normally, the refractory period of the His-Purkinje system lengthens as the heart rate slows and shortens as the heart rate increases, even when heart rate changes are abrupt. This aberrant conduction can result when a short cycle follows a long R-R interval. The QRS complex that ends the long pause is conducted normally but creates a prolonged ERP of the bundle branches as a result the next QRS complex occurring after a short coupling interval is conducted aberrantly and cause conduction delay. This aberration can be present for one beat and have a morphology resembling a premature ventricular complex (PVC), or it can involve several sequential complexes, a finding suggesting ventricular tachycardia (VT).

• Acceleration-dependent aberration : Acceleration-dependent blocks is a result of failure of the action potential of the bundle branches to shorten or paradoxical lengthening of action potential lengthens in response to acceleration of the heart rate. After gradual rather than abrupt acceleration of the heart rate and R-R shortening by less than 5 milliseconds for several cycles, a relatively slow heart rates may display LBBB. The normalization of this aberration due time dependent shortening of the ERP or ERP shortening greater than AV node is called restitution.

Phase 4 Block Pathophysiology

Phase 4 block occurs when conduction of an impulse is blocked in tissues well after their normal refractory periods have ended. Enhanced phase 4 depolarization within the bundle branches can be caused by enhanced automaticity or partial depolarization of injured myocardial tissue that results in the maximum diastolic potential immediately following repolarization, from which point the membrane potential is steadily reduced. This reduction, in turn, results in inactivation of some Na+ channels. An action potential initiated early in the cycle (immediately after repolarization) would have a steeper and higher phase 0 and consequently better conduction than that in later cycle where membrane potential is reduced and conduction is slower. Phase 4 block may occur if there is :

• a decrease in excitability so that, in bradycardia sufficient time elapses before the impulse arrives, thus enabling the bundle branch fibers to reach a potential (a shift in threshold potential toward zero) at which conduction is impaired.
• a deterioration in membrane responsiveness so that significant conduction impairment develops at more negative membrane potential itself.

Concealed Transseptal Conduction Pathophysiology

• When a PVC originating from the ventricle retrogradely activate the bundle branch on its side early, with transseptal conduction to opposite bundle later, it causes a conduction delay on the opposite side bundle with the next impulse as the same side bundle ERP expires in time for the next impulse but the opposite side bundle remains refractory because its actual cycle began later. By this time, the distal part of opposite bundle has recovered, allowing for retrograde penetration by the impulse propagating transseptally, thereby rendering the opposite side bundle refractory to each subsequent impulse. This process is repeated, and the BBB pattern continues until another well-timed PVC preexcites the opposite bundle, so that the next impulse from above finds the that bundle fully recovered.

• Acceleration-dependent BBB develops at a critical rate faster than the rate at which it disappears. This paradox is due to concealed conduction from the contralateral conducting bundle branch across the septum with delayed activation of the blocked bundle. Such concealed transseptal activation results in a bundle branch–to–bundle branch (RB-RB or LB-LB) interval shorter than the manifest R-R cycle.

• In atrial bigeminal rhythm, the ERP of both bundles starts simultaneously following the normally conducted PAC, and is relatively short because of the preceding short cycle. After the pause, followed by normal sinus beat conduction, the ERP of both bundle branches starts simultaneously but is relatively long because of the preceding long cycle. However, because right bundle ERP is relatively longer than the left bundle, the next impulse conducts with an RBBB pattern. This impulse is conducted down the left bundle and by concealed transseptal conduction activates the right bundle retrogradely after some delay so that the RB-RB interval (during the following pause) and the RB ERP become shorter. As a result, by the time the next impulse reaches the right bundle, it is fully recovered because of its short ERP and normal conduction occurs. The same phenomenon (concealed transseptal conduction) explains alternating RBBB and LBBB during bigeminal rhythms.

Left Bundle Branch Pathophysiology

• First phase : Activation of the interventricular septum is by the right bundle instead of the left with activation traveling from right to left and from apex to base and to the RV apex and free wall ( loss of septal r and q waves with initiation of slurred R waves V1,V6,aVL ).
• Second phase :
  • Right ventricular activation : RV activation is typically completed within the first 45 milliseconds into QRS, however the septum being a larger muscle is electronically predominant producing negative QRS or QS in V1.
  • Left ventricular activation : LV activation starts as late as 44 to 58 milliseconds into the QRS. The slow conduction is by the working muscle fibres and not through the conduction system producing wide and produces slurred R waves in the leftward leads ( lead I, aVL, and V6 ), with delayed R wave peak time in the left precordial leads. The notched R waves is caused by slow transseptal conduction. LBBB also lead to ventricular repolarization abnormalities.

Right Bundle Branch Pathophysiology

• First phase : Activation of the interventricular septum occurs normally by a branch of the left bundle.
• Second phase :
  • Left ventricular activation : This happens normally with left bundle branch and is completed with 40-60 milliseconds of the QRS.
  • Right ventricular activation : This activation happens slowly by conduction through working muscle fibers after activation of the LV has completed around 80 milliseconds of the QRS. This late, unopposed RV free wall activation results in a terminal rightward and anterior positive deflection that can be small (r′) or large (R′) in the anterior precordial leads and S waves in the leftward leads. RBBB also results in an abnormality of right ventricular repolarization producing secondary ST segment and T wave changes in the right precordial leads. RBBB prolong R wave peak time in right precordial leads.