Intraventricular conduction delay pathophysiology

Intraventricular conduction delay Microchapters
Home
Overview
Anatomy and Physiology
Classification
Pathophysiology
Causes
Differentiating Intraventricular conduction delay from other Disorders
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
EKG Examples
Chest X Ray
Echocardiography
Coronary Angiography
Treatment
Medical Therapy
Electrical Cardioversion
Ablation
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Intraventricular conduction delay pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Intraventricular conduction delay pathophysiology
CDC onIntraventricular conduction delay pathophysiology
Intraventricular conduction delay pathophysiology in the news
Blogs on Intraventricular conduction delay pathophysiology
to Hospitals Treating Intraventricular conduction delay pathophysiology
Risk calculators and risk factors for Intraventricular conduction delay pathophysiology

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 may or may not lead to a wide QRS complex and/or axis deviation.

Pathophysiology

Phase 3 Block

Phase 3 block occurs when an impulse arrive in tissues during phase 3 of the action potential even before full recovery where the 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 : This happens due to premature impulses encroaching on the refractory period of the bundle branch prior to full recovery of the action potential. 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 : This is related to the physiological changes of the conduction system refractory periods associated with the R-R interval. 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 a 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.

LBBB due to phase 3 and phase 4 aberration

Copyleft image obtained courtesy of ECGpedia, http://en.ecgpedia.org/wiki/File:E243.jpg

Phase 4 Block

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

• During tachycardia, 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 (BBB) on the opposite side bundle with the next supra ventricular impulse as the same side bundle ERP expires in time for the next supra ventricular 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 supra ventricular 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 Block

• 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 Block

• 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.

Fascicular Block

• Left anterior fascicular block (LAFB) : In LAFB, the anterosuperior portion of the left ventricle that is activated by left anterior fascicle gets activated later than normal, resulting in unbalanced inferior and posterior forces from left posterior fascicle to occur early during QRS and unopposed anterosuperior forces to occur later during the QRS complex producing frontal plane axis more than –45 or –60 degree.

• Left posterior fascicular block (LPFB) : In LPFB, the early unopposed activation of the anterolateral wall of the LV by the normally conducting LAF and LMF causes the initial forces to be oriented superiorly and to the left. The late unopposed activation by LPF causes the main and terminal forces of the QRS to be directed posteriorly, inferiorly, and to the right with a wide-open clockwise-rotated loop. This is responsible for the characteristic rightward frontal plane axis of +120 to +180 degrees.

• Bi and tri fascicular block : Ventricular activation starts at the insertion site of the fastest conducting fascicle, with subsequent spread of activation from that site to the remainder of the ventricles.