Intraventricular conduction delay

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

The term intraventricular conduction delay or intraventricular conduction disturbances (IVCDs) refers to disturbances in the intraventricular propagation of supraventricular impulses resulting in changes in the QRS complex either in morphology or duration, or both. The QRS complex represents electrical activation of the ventricle and normally the entire process of ventricular depolarization in adults is completed within about 0.1 sec (100 msec). An IVCD is the result of abnormal activation of the ventricles caused by conduction delay or block in one or more parts of the specialized conduction system (bundle of His, bundle branch or purkinje conduction system) resulting in widening of QRS complex. Abnormalities of local myocardial activation can further alter the specific pattern of venticular activation.

Intraventricular conduction delay are due to abnormalities in the specialized conduction system in the ventricles that transmit impulses arising from the SA node transmitted through the AV node to the ventricles. The normal intraventricular system starts at the AV node as bundle of His that divides into right and left bundle branches which after giving of the fascicular branches ends in the complex Purkinje system.

Intraventricular conduction delay can be caused by structural abnormalities in the bundle of His or Purkinje system or ventricular myocardium, functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction) or ventricular preexcitation over a bypass tract. Intraventricular conduction disturbances can be broadly classified based upon the underlying physiology or based upon the site of block (anatomical classification). However, the anatomic description of conduction abnormalities are not intended to localize sites of impaired function precisely because the electrocardiographic changes may be caused by abnormalities in various sites within the ventricles.

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.

Intraventricular conduction delays(IVCDs) refers to abnormalities in the intraventricular propagation of supraventricular impulses. These abnormalities can be due to pathology in either the left bundle of His or its fascicular branches or the right bundle of His or its combination resulting in changes to the QRS complex. Causes can be classified based upon the site of pathology in the ventricular conduction system as well as the associated medical condition.

Intraventricular conduction delay’s need to be differentiated from other conditions resulting in wide QRS complex such as LVH, pacemaker rhythms and accessory pathway arrythmias.

Intraventricular condution delay ECG patterns can be seen commonly in general population and their prevalence increases with age. Bifascicular block (especially RBBB and LAF block) is the most common IVCD.

Intraventricular conduction delay usually has no prognostic significance in patients without underlying heart disease but may progress to complete heart block or ventricular arrhythmia with worse prognosis in underlying heart disease.

Intraventricular conduction delays (IVCD) are abnormal ECG pattern, which may or may not be associated with symptoms. Complete history to find out underlying cardiac condition would be the best approach in asymptomatic patients.

Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Jugular pulsation may be noted in the neck exam.

Electrophysiological testing help localize the site of conduction delay or block within the conduction system of the ventricles.

Intraventricular conduction delay is a common clinical abnormality detected on the electrocardiogram (ECG). Right and left bundle branch blocks usually reflect intrinsic impairment of conduction in either the right or left bundle system (intraventricular conduction disturbances) which can be either chronic or intermittent. Transient rate-related bundle branch blocks occurs when the heart rate increases (tachycardia or acceleration-dependent) or when heart rate decreases (bradycardia or deceleration-dependent) which are relatively rare.

Asymptomatic patients with isolated IVCD and no underlying heart disease require no treatment. In symptomatic patients, with syncope and AV block may have a rhythm disturbance that requires a pacemaker. Given the dys-ynchrony that occurs with left ventricular contractility, cardiac resynchronization therapy in heart failure patients may be of benefit.

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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]

Intraventricular conduction delay are due to abnormalities in the specialized conduction system in the ventricles that transmit impulses arising from the SA node transmitted through the AV node to the ventricles. The normal intraventricular system starts at the AV node as bundle of His that divides into right and left bundle branches which after giving of the fascicular branches ends in the complex Purkinje system.

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 bundle of His 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.

The standard model used to understand the cardiac action potential is the action potential of the ventricular myocyte. The action potential has 5 phases (numbered 0-4).

• Phase 4 : This is the resting membrane potential and describes the membrane potential when the cell is not being stimulated. The normal resting membrane potential in the ventricular myocardium is about -85 to -95 mV. All cardiac cells which belong to the excitatory system have an instable phase 4 i.e the pacemaker potential. Phase 4 is associated with heart diastole so is called diastolic depolarization.
• Phase 1 : This is the rapid depolarization phase. The slope of phase 0 represents the maximum rate of potential change and is known as dV/dtmax. Its behavior is different in contractile and pacemaker heart cells.
• Phase 2 : This “plateau” phase of the cardiac action potential is absent in pacemaker cells and it sustains muscle contraction.
• Phase 3 : This is the rapid repolarization phase of the action potential where the membrane potential is restored to about -80 to -85 mV.
• Refractory period : From the beginning of phase 0 until nearly the end of phase 2, each cell is in an absolute refractory period, during which it is impossible to evoke another action potential, followed, until phase 4, by a relative refractory period, during which a stronger-than-usual stimulus is required.

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.

• 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.

• Ventricular repolarization : The last event of the cycle is the repolarization of the ventricles. It is the restoring of the resting state. In the ECG, repolarization includes the J wave, ST-segment, and T- and U-waves.^[1][2]

• 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.

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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]

Intraventricular conduction delay can be caused by structural abnormalities in the bundle of His or Purkinje system or ventricular myocardium, functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction) or ventricular preexcitation over a bypass tract. Intraventricular conduction disturbances can be broadly classified based upon the underlying physiology or based upon the site of block (anatomical classification). However, the anatomic description of conduction abnormalities are not intended to localize sites of impaired function precisely because the electrocardiographic changes may be caused by abnormalities in various sites within the ventricles.

Phase 3 block (tachycardia-dependent block), occurs when an impulse arrives at tissues that are still refractory caused by incomplete repolarization. Manifestations of phase 3 block include mostly RBBB and fascicular block and less commonly LBBB. Phase 3 block is the underlying physiology for the following phenomenons of conduction delay :

• Aberration caused by premature excitation : This conduction delay mechanism always results in RBBB at a normal heart rate whereas in faster hearts it mostly results in LBBB.
• Ashman phenomenon : RBBB aberration is more common than LBBB because the right bundle has a longer effective refractory period than the left. The Ashman phenomenon can occur during second-degree AV block, but it is most common during atrial fibrillation (AF).
• Acceleration-dependent aberration : This conduction delay mechanism results in LBBB at lower heart rates and RBBB at faster heart rates.

Phase 4 block occurs when conduction of an impulse is blocked in tissues well after their normal refractory periods have ended. This type of aberration is sometimes referred to as bradycardia-dependent BBB and always manifests an LBBB pattern because the left ventricular (LV) conduction system is more susceptible to ischemic damage and has a higher rate of spontaneous phase 4 depolarization than the right ventricle.

This conduction delay mechanism is due retrograde activation of bundle branches, where one bundle is activated earlier than the other following transseptal conduction, making it refractory for the next following impulse. This can result in either RBBB or LBBB depending upon side of origin of the retrograde impulses.

Left bundle branch block (LBBB), a conduction delay pattern seen on the surface electrocardiogram (ECG) can result from conduction abnormalities in the main left bundle branch, or in its fascicles, or in the distal conduction system of the left ventricle or less commonly, in the fibers of the bundle of His that become the main left bundle branch. In LBBB myocardial activation changes only affect the left ventricle and thus changes in the morphologic features of local electrograms can be recorded in the left, but not the right. ECG pattern usually shows a wide, entirely negative QS complex (rarely, a wide rS complex) in lead V1 and a wide, tall R wave without a q wave lead V6. LBBB can be classified into

• Complete LBBB : Complete LBBB is a severe form of conduction delay where the activation of the LV originates from the right bundle in a right to left direction, resulting in delayed and abnormal activation and diffuse slowing of conduction throughout the LV. QRS complex is 0.12 sec or wider.
• Incomplete LBBB : Incomplete LBBB is due to mild conduction delay in the left bundle where much of the LV activation occurs via the normal conduction system, although it begins abnormally on the right side of the septum. QRS is between 0.1 and 0.12 sec wide.

Right bundle branch block (RBBB), a conduction delay pattern seen on the surface electrocardiogram (ECG) can result from conduction abnormalities in the main right bundle branch itself, or in the bundle of His, or in the distal right ventricular conduction system. As the right bundle is long and undivided throughout most of its course it is vulnerable to stretch and trauma for two thirds of its course when it travels subendocardially. Development of RBBB alters the activation sequence of the RV but not the LV. Because the LB is not affected, the initial septal activation (r wave in V1 and q wave in V6) which depends on the LB, remains normal, occurring from left to right. ECG pattern usually shows an rSR′ complex with a wide R′ wave in lead V1 and a qRS pattern with a wide S wave in lead V6.

• Complete RBBB : Complete RBBB is a severe form of conduction delay where RV activation spreads slowly by conduction through working muscle fibers rather than the specialized purkinje system. QRS duration is .12 seconds or more
• Incomplete RBBB : An incomplete RBBB can result from lesser degrees of conduction delay in the right bundle. The ECG pattern of incomplete RBBB is similar to that of complete RBBB, except that the QRS duration is between 0.11 and 0.12 seconds.
• Atypical RBBB : Atypical RBBB can be caused by attenuation or loss of posterior deflections in the anteroposterior leads, resulting in an rsR′, qR, or M-shaped QRS pattern in V1.

Fascicular block generally does not substantially prolong QRS duration, but alters only the sequence of LV activation. The primary ECG change is a shift in the frontal plane QRS axis because the conduction disturbance primarily involves the early phases of activation.

• Left anterior fascicular block (LAFB) : Mean QRS axis is −45° or more and a QRS width is less than 0.12 sec.
• Left posterior fascicular block (LPFB) : Conduction delay in the left posterior fascicle is considerably less common because of its thicker structure and more protected location near the left ventricular inflow tract. Mean QRS axis of +120° or more positive, with a QRS width of less than 0.12 sec is seen.
• Left median fascicular block : This uncommon conduction delay is characterized by absence of septal q waves in ECG.

Bifascicular block indicates blockage of any two fascicles or its combination with bundle branch block.

• RBBB with LAFB : This produces an RBBB pattern with marked left axis deviation.
• RBBB with LPFB : This produces an RBBB pattern with right axis deviation.
• LAFB with LPFB : This produces a complete LBBB pattern.

Trifascicular block includes the following :

• RBBB with LAFB and LPFB
• RBBB with LBBB

The resulting electrocardiographic pattern is dependent on the relative degree of delay in the affected structures. The combination of bifascicular block with first-degree AV block on the surface ECG cannot be considered as trifascicular block because the site of AV block can be in the AV node or in the bundle of His.

Alternating RBBB and LBBB is manifested by QRS complexes with LBBB morphology coexisting with complexes with RBBB morphology. When this is associated with a change in the PR interval, it represents an ominous sign for progression to complete AV block. This phenomenon implies a diffuse instability of the His-Purkinje system.

It refers to conduction delay in the region of a myocardial infarction. In the leads with pathologic Q waves the terminal portion of the QRS complex is wide and directed opposite to the Q wave, such as a QR complex in leads III and aVF. A related abnormality is peri-ischemic block, manifested by a reversible widening of the QRS complex in electrocardiographic leads with ST-segment elevation caused by acute injury.

In known coronary artery disease patients multiple deflections within the QRS complex (e.g., rSr, Rsr′, rSR′ or multiple r′ patterns) or the presence of high-frequency notches within the R and S wave without overall prolongation of the QRS complex may is seen indicating some form of intraventricular conduction delay.

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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]

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.

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.

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

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.

• 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.

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

• 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.

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

• 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.

• 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.

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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]

Intraventricular conduction delays(IVCDs) refers to abnormalities in the intraventricular propagation of supraventricular impulses. These abnormalities can be due to pathology in either the left bundle of His or its fascicular branches or the right bundle of His or its combination resulting in changes to the QRS complex. Causes can be classified based upon the site of pathology in the ventricular conduction system as well as the associated medical condition.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• Acute coronary syndrome
• Cardiac transplantation
• Cocaine toxicity
• Digoxin toxicity
• Myocardial infarction
• Pulmonary embolism

• Cardiac catheterization
• Catheter ablation for arrhythmias
• COPD
• Dilated cardiomyopathy
• Heart failure
• Hypertensive heart disease
• Ischemic heart disease
• Left ventricular hypertrophy
• Myocardial infarction
• Restrictive cardiomyopathy
• Valvular heart disease

LBBB usually appears in patients with underlying heart disease such as hypertensive heart disease, valvular heart disease, cardiomyopathy etc. Most patients with left ventricular hypertrophy and coronary artery disease of LAD show left bundle branch block (LBBB) conduction delay pattern on the surface electrocardiogram (ECG).

RBBB is a common finding in the general population when compared to LBBB, and many persons with RBBB have no clinical evidence of underlying heart disease. Right side valvular heart diseases, COPD, coronary artery disease show right bundle branch block (RBBB) conduction delay pattern on the surface electrocardiogram (ECG).

Isolated LAFB is very common when compared to LPFB. This conduction delay pattern on ECG may be seen with hypertension, aortic valve disease, coronary disease of LAD artery septal branch and sometimes in general population without identifiable cause.

Isolated LPFB is very rare when compared to LAFB. Most often it occurs with RBBB in patients with chronic lung disease and right ventricular hypertrophy.

Isolate LMFB that occurs due to pathology involving interventricular septum is rare. A number of neuromuscular diseases are associated with fascicular block.

Multifascicular block refers to conduction delay or block in more than one of the structural components of the specialized conduction system—that is, the left bundle branch, the left anterior and posterior fascicles of the left bundle branch, and the right bundle branch. Conduction delay in any two fascicles is termed bifascicular block, and delay in all three fascicles is termed trifascicular block. Causes of multifascicular block are those which cause individual blocks and the most common are LVH, RVH and coronary heart disease.

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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]

Intraventricular conduction delay’s need to be differentiated from other conditions resulting in wide QRS complex such as LVH, pacemaker rhythms and accessory pathway arrythmias.

• Left ventricular hypertrophy : Dilatation and thickening of the LV wall produce a QRS very similar to LBBB. Wide QRS and secondary T wave discordance can be seen, but the prolonged intrinsicoid deflection (time from the QRS onset to the peak of the R wave in leads V5-V6) to over 60 msec (1.5 small boxes) characteristically seen in LBBB is not seen. Often, LVH progresses to incomplete and then to complete LBBB.
• Pacemaker rhythms : During right ventricular pacing, the ventricles are activated from the electrode positioned in the right ventricular apex and can produce an ECG pattern similar to LBBB. In, biventricular pacing, left ventricular lead activating the heart from back to front (toward lead V1) may produce ECG pattern resembling RBBB.
• Wolff-Parkinson-White syndrome : Left ventricular preexcitation (WPW type A) produces a positive R wave in lead V1 similar to RBBB, whereas right ventricular preexcitation (WPW type B) creates deep S waves in lead V1 similar to that seen in LBBB because the right ventricle is activated first. Short PR interval and delta wave of the QRS, characteristic of WPW differentiates it from bundle branch blocks.

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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]

Intraventricular condution delay ECG patterns can be seen commonly in general population and their prevalence increases with age. Bifascicular block (especially RBBB and LAF block) is the most common IVCD.

• The prevalence of IVCD in general population increases with age.
• Bifascicular block (especially RBBB and LAF block) is the most common IVCD preceding complete heart block in adults.
• Other forms of IVCD cases are common only next to complete intra-Hisian and infra-Hisian AV block.
• Prevalence of right bundle branch block without underlying heart disease ranges between 200 and 1300 per 100,000. RBBB is a common finding in the general population and has no prognostic significance without underlying heart diseases. Right bundle branch block and incomplete right bundle branch block are two to three times more common in men than in women. (Copenhagen City Heart Study)^[1]
• Prevalence of LBBB in the general population ranges from 200 to 1100 per 100,000. LBBB is uncommon among patients under 50 years of age (<0.5%). It occurs in 6% to 8% of patients over the age of 50.
• The prevalence of LAF block in the general population ranges from 0.9% to 6.2%.
• Isolated LPF block is very rare and almost occurs in combination with other blocks.

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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]

Intraventricular conduction delay usually has no prognostic significance in patients without underlying heart disease but may progress to complete heart block or ventricular arrhythmia with worse prognosis in underlying heart disease.

• Right bundle branch block :
  • In patients without evidence of structural heart disease, RBBB has no prognostic significance.
  • When cardiac disease is present, the coexistence of RBBB suggests advanced disease.
  • RBBB is an independent predictor of all-cause mortality in patients with known or suspected coronary heart disease.
  • In the setting of an acute MI, RBBB is associated with a significant increase in mortality.

• Left bundle branch block :
  • The presence of isolated LBBB has no adverse prognostic significance.
  • In patients with LBBB associated with ischemic heart disease, hypertension, or cardiomyopathy, the prognosis depends on the severity of the underlying heart disease. The highest incidence of sudden cardiac death is among patients with LBBB and cardiac disease.
  • In patients with acute MI and heart failure, the presence of LBBB is associated with a worse prognosis.
  • Unfortunately, patients whose only manifestation of an acute MI is a left bundle branch block are less frequently treated with reperfusion therapy, and they have a worse prognosis.^[1]
  • Because the presence of LBBB can represent the clinical onset of LV structural disease, the finding of LBBB on resting ECG requires further evaluation with echocardiogram and Holter monitoring for assessment of LV function, as well as identifying both advanced degrees of AV block and heart disease-related tachyarrhythmias.

• Hemiblocks :
  • Isolated LAF block does not itself imply a risk factor for cardiac mortality or morbidity.
  • The prognosis of LAF block is primarily related to the underlying heart disease.
  • LAF block in the setting of acute MI is probably associated with increased mortality.

• Complications :
  • Pulmonary arterial line placement ^[2] in a patient with LBBB can result in a complete heart block if the right bundle branch is traumatized during the process.
  • Progression to higher degree AV block: It was shown in the Swedish study that the risk of progression was more pronounced in left block than in right bundle branch block.
  • Bradycardia
  • Ventricular arrythymias
  • Delay in the diagnosis of MI: Presence of LBBB or RBBB can delay the diagnosis of an acute MI.
  • Sudden cardiac death is a potential complication when associated with a heart attack.

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