Bundle branch blocks

• The ventricles are normally activated within about 100 ms by a fast wiring system: a right bundle and a left bundle, the latter splitting into an anterior and a posterior fascicle. If one limb fails, the impulse reaches that ventricle slowly, by crawling through muscle from the other side, and the QRS complex widens.
• Right bundle branch block (RBBB) shows as an rSR' pattern in V1 and a wide S wave in leads I and V6. It is common, often harmless in a healthy heart, and a clue to right-sided strain (for example pulmonary embolism) when it is new.
• Left bundle branch block (LBBB) shows as a QS or rS complex in V1 and a broad, notched or monophasic R wave in I, V5 and V6, with no septal q waves. It almost always means structural heart disease, it blunts the ECG's ability to show ischaemia and hypertrophy, and in heart failure it can be treated with resynchronisation.
• New LBBB alone is no longer treated as equivalent to an ST-elevation myocardial infarction (STEMI) in American guidance (2013 guideline; 2022 American College of Cardiology, ACC, pathway), but LBBB with high clinical suspicion of infarction is managed as STEMI by the European Society of Cardiology (ESC, 2023). Look for specific ST-segment patterns (Sgarbossa and the modified Smith criteria) and treat the patient's story and troponin as seriously as the tracing.
• Bifascicular block with syncope is the situation to fear: it can progress suddenly to complete heart block, and pacing may be needed.

By the end of this page you should be able to:

1. Describe the His-Purkinje system and explain why block in one limb widens the QRS and changes its shape.
2. Recognise RBBB and LBBB on a 12-lead ECG, and state the QRS duration used for complete and for incomplete block.
3. List the causes of each block, and say when each is benign and when it is a warning.
4. Explain why LBBB hides ischaemia, trace the history of "new LBBB is a STEMI equivalent", and apply the Sgarbossa and modified Sgarbossa criteria.
5. Identify left anterior and posterior fascicular block, bifascicular block, and the confusing term "trifascicular block", and decide when syncope with these needs pacing.
6. Explain how bundle branch block affects the reading of hypertrophy and old infarction, and recognise intermittent and rate-related block.
7. State who benefits from cardiac resynchronisation therapy and why LBBB morphology matters.
8. Work through a wide QRS complex at rest in sinus rhythm to a diagnosis, and know when to refer.

Before reading blocks, you need the wiring. This section describes the normal pathway, what a normal QRS looks like, and what changes when one limb fails.

After the atrioventricular (AV) node, the impulse enters the bundle of His, which runs along the top of the interventricular septum and then divides into a right and a left bundle branch.^[2] The two branches are made of Purkinje fibres, which conduct much faster than ordinary heart muscle.

• Right bundle branch. A thin, long, single cord that runs down the right side of the septum and spreads out near the base of the right anterior papillary muscle to supply the right ventricle.^[2] Most of its blood supply comes from septal branches of the left anterior descending (LAD) coronary artery.^[2]
• Left bundle branch. It divides into two main fascicles. The left anterior fascicle is a slim single tract running to the upper, lateral wall of the left ventricle and is fed by the LAD. The left posterior fascicle is a broad bundle of fibres running to the lower, inferior part of the ventricle and has a double blood supply, so it is much harder to injure.^[20][21][22] Some authors also describe a septal (middle) fascicle, but the three-fascicle model (right bundle, left anterior and left posterior fascicles) is the one used for clinical ECG reading.^[2]

Both bundles carry the impulse to both ventricles almost at once, so the whole ventricular muscle is activated in about 90 ms (mean 93 ms in men and 87 ms in women in one reference value).^[3] The first part of the QRS is the septum, activated from left to right. That tiny leftward-to-rightward vector gives the small septal q waves in the left-sided leads (I, aVL, V5, V6).^[18]

A block here is usually a delay rather than a complete wall; the word "block" covers everything from slowed to absent conduction.^[3] When one bundle fails, the other bundle still delivers the impulse to its own ventricle on time. The impulse then has to pass through the septum and spread from muscle cell to muscle cell to reach the blocked ventricle. Muscle cell to muscle cell is slow, so the second ventricle is activated late, the total activation time stretches, and the QRS widens.^[2]

Two further consequences follow, and they explain most of what you will see on the ECG:

• The direction of activation changes. The late-activated ventricle contributes the last part of the QRS, pulling the terminal vector towards itself and giving the broad terminal forces that you recognise as the pattern.
• Repolarisation (recovery) also happens in the wrong order. The ST segment and T wave are therefore usually opposite in direction to the last part of the QRS. This is called appropriate discordance, and it is expected, not ischaemia.^[18][19]

The 2009 AHA/ACCF/HRS standardisation statement defines complete block in adults as a QRS of 120 ms or more with the typical morphology.^[1][2][6] A QRS that is wide enough to be abnormal but under 120 ms with typical morphology is incomplete block. In adults, incomplete RBBB is defined in the 2009 statement as a QRS of 110 to under 120 ms with the RBBB shape,^[30] and incomplete LBBB uses the same QRS range (2018 American College of Cardiology, American Heart Association and Heart Rhythm Society bradycardia guideline, reproducing the 2009 definitions); incomplete LBBB also needs a left ventricular hypertrophy pattern, an R-wave peak time over 60 ms in V4 to V6, and no q wave in I, V5 and V6.^[12] Some reviews quote 100 ms as the lower limit, but that is the outlier. The lower limit also differs in children, who have a narrower normal QRS.

Two points matter for understanding what the number means.

• A complete block on the ECG does not always mean the bundle is physically severed. It means conduction is delayed enough to produce the full pattern.^[3]
• A stricter definition of complete LBBB has been proposed, because the 120 ms cut-off was originally set by comparison with experiments in dogs and may include patients whose wide QRS is caused by left ventricular hypertrophy together with left anterior fascicular block, rather than true left bundle block. The Strauss definition requires QRS of at least 140 ms in men or 130 ms in women, QS or rS in V1 and V2, and notching or slurring in the middle of the QRS in at least two contiguous leads.^[3][4] It was shaped by the wish to choose better candidates for resynchronisation therapy (see below). The 2021 European guidance uses a related description that stresses mid-QRS notching and a delayed R-wave peak time over 60 ms in V5 or V6, and in one hospital series only 12% of patients who met the older European definition met the full 2021 description.^[5]

Right bundle branch block is the commoner and gentler of the two. This section covers how it looks, why, what causes it and what it means.

A complete RBBB has these features.^[2][19]

• QRS duration of 120 ms or more in adults.
• An rSR' (or rsR', or occasionally a broad notched R or qR) pattern in V1 and V2, which is the late R' wave of right ventricular activation. The rSR' form is the commonest.
• A wide, slurred S wave in leads I and V6 (and often aVL and V5), either longer than the R wave or more than 40 ms wide.
• A normal R-wave peak time in V5 and V6 but a late one (over 50 ms) in V1.
• ST depression and T-wave inversion in V1 to V3. This is appropriate discordance and is not ischaemia.
• A normal axis in isolated RBBB, because the left ventricle is activated normally.^[19]

Why does it look like this? The left ventricle and septum are activated on time through the intact left bundle, so the opening of the QRS is normal. The right ventricle is then activated late, from the septum outwards. That late vector points towards V1 (the R') and away from the left lateral leads (the wide S).^[19]

An RBBB does not interfere with the usual Q-wave and R-wave criteria for myocardial infarction, because the first 30 to 40 ms of the QRS is essentially normal. An acute anteroseptal infarct can therefore be recognised as a QSR' pattern in V1 and V2 on a background of RBBB.^[2]

RBBB is a common finding, and the causes divide into those with a normal heart and those without.

• Normal variant. An incomplete RBBB pattern (rSR' with QRS under 120 ms) is common in healthy people and is of no clinical significance in children.^[19] Complete RBBB also occurs in people without heart disease, and its prevalence rises with age and in men: in the Copenhagen City Heart Study the figure was 1.4% in men and 0.5% in women, ranging from 0.6% in women under 40 to 14.3% in men over 80.^[2]
• Right ventricular overload or hypertrophy. Cor pulmonale, pulmonary hypertension and acute right heart strain.
• Pulmonary embolism (PE). Acute strain dilates the right ventricle and stresses the right bundle's peripheral branches. Complete or incomplete RBBB is reported in a wide range of PE series (from 6% to 69%), with estimates near 25% overall; it is commoner in massive embolism and in right ventricular dysfunction, is often transient, and has good specificity but poor sensitivity for PE.^[15]
• Congenital heart disease, particularly atrial septal defect (ASD), where the right ventricle is volume-loaded. RBBB can also follow surgical repair or occur with right heart catheterisation across the basal septum.^[2][19]
• Ischaemic heart disease, hypertension, cardiomyopathy, myocarditis, rheumatic and other valve disease, and degenerative fibrosis of the conducting system (Lenègre-Lev disease).^[2][19]
• Ischaemia (acute). Because the right bundle depends on LAD septal branches, a new RBBB in a patient with chest pain can reflect proximal LAD occlusion, sometimes together with left anterior fascicular block.^[19][22]

Most people with RBBB are asymptomatic, and it is usually found by chance. In healthy people without structural disease it is generally benign.^[2] Its meaning depends on the company it keeps: prognosis follows the underlying heart disease and the presence of other conduction disturbances, and in people with coronary disease or heart failure complete RBBB is an independent predictor of death.^[2]

RBBB is also the most consistent predictor of the need for a pacemaker after transcatheter aortic valve implantation (TAVI), so a patient who has RBBB before TAVI is watched closely.^[11]

Left bundle branch block is less common in healthy people and more important. This section covers how it looks, what causes it, why it hides ischaemia and what it means for the left ventricle.

A complete LBBB has these features.^[3][6][18]

• QRS duration of 120 ms or more.
• A QS or rS complex in V1 (and often V2): a small or absent r wave and a deep S.
• A broad, notched or slurred, or monophasic R wave in I, aVL, V5 and V6.
• No septal q waves in I, V5 and V6.
• A delayed R-wave peak time (over 60 ms) in V5 and V6.
• Secondary ST-T change: ST depression and T-wave inversion in leads with a tall R wave, and ST elevation with an upright T wave in leads with a deep S wave (appropriate discordance). A small amount of ST elevation (under about a quarter of the depth of the preceding S wave) is expected.^[18]
• The axis is variable; left axis deviation and poor R-wave progression across the chest leads are common.^[18]

Why? In LBBB the left bundle fails, so the impulse travels first down the right bundle. The septum is therefore activated from right to left, the wrong way round, which removes the normal septal q waves. The impulse then crosses the septum slowly into the left ventricle, so the left ventricle is the last part to be activated. All the late forces point away from V1 and towards the lateral leads, producing deep S waves on the right and tall broad R waves on the left.^[18] The notches mark stages of that slow spread, for example reaching the left ventricular endocardium and then reaching the epicardium of the posterolateral wall.^[3]

• Right ventricular paced rhythm. Pacing from the right ventricle produces an LBBB-like QRS, with a pacing spike before it. The same ST-T concepts apply.^[18]
• Left ventricular hypertrophy with left anterior fascicular block, which can produce a wide QRS and ST-T change in the lateral leads. About a third of patients labelled as LBBB by conventional criteria may have this instead.^[4][18]
• Non-specific intraventricular conduction delay (IVCD): a QRS of 120 ms or more that fits neither RBBB nor LBBB, usually from diffuse disease such as an old infarct.^[3]
• Hyperkalaemia and sodium-channel-blocking drugs (see the flowchart later).

LBBB is unusual without organic disease.^[18] The commonest causes are:^[3][18]

• ischaemic heart disease, including acute anterior infarction;
• cardiomyopathy, especially dilated cardiomyopathy;
• hypertension with left ventricular hypertrophy;
• aortic stenosis (and TAVI, in which new LBBB follows implantation in a substantial minority of patients);^[3]
• fibrosis and degeneration of the conducting system (Lenègre-Lev disease);
• hyperkalaemia and digoxin toxicity, which are reversible.

LBBB can also be the first sign of a developing cardiomyopathy in a person whose heart looks normal at the time; some patients with LBBB and normal ejection fraction show abnormal responses to exercise and abnormal heart-muscle biopsies.^[3] This is why the 2018 ACC/AHA/HRS bradycardia guideline gives a Class I recommendation for transthoracic echocardiography in every patient with newly identified LBBB, with or without apparent heart disease.^[12]

Abnormal activation makes the ventricle contract out of step (dyssynchrony): the septum is activated early and moves first, the lateral wall is activated late and moves later, and the pump becomes inefficient. Over time this can cause left ventricular remodelling and dilatation, and LBBB is generally associated with a worse prognosis than RBBB or normal conduction.^[3] LBBB and heart failure feed each other: a failing ventricle widens the QRS, and a wide QRS worsens the failure. The treatment that corrects this is cardiac resynchronisation therapy (see later). See heart failure for the wider context.

Reading an acute infarct from the ST segment depends on a normal baseline. LBBB removes that baseline. This section explains why, and what that means.

In a normal tracing, ST elevation signals injury because it should not be there at all. In LBBB, the secondary ST-T changes of abnormal depolarisation are large and expected. Leads with a deep S wave have ST elevation as a normal finding, and leads with a tall R wave have ST depression, so a real infarct current can be buried in the "normal" abnormalities.^[8] LBBB also removes the early QRS forces that give pathological Q waves, so an old infarct may be invisible.

Two corrections to this common teaching are worth making. First, the problem is mainly one of proportion: a ST shift that is large relative to the QRS in the same lead is suspicious, even if its absolute size is small. This is the basis of the modified Smith criteria below, and some authors argue that, used with proportion, LBBB does not hide transmural ischaemia.^[10] Second, because LBBB and the commonest causes of acute chest pain overlap (an old LBBB is often in a heart with coronary disease), the ECG alone cannot sort every case; look at the clinical picture and the troponin trend.

For many years a student learned one rule: chest pain plus new LBBB equals acute infarction, so give reperfusion. That rule has been dropped from American guidance and softened in European guidance. This section traces how the idea arose and what replaced it.

Where the idea came from. The 2004 US STEMI guideline advised emergency reperfusion for "new or presumably new LBBB", drawing on trials of thrombolysis and on the Sgarbossa criteria. But the trials counted bundle branch block regardless of when it arose, and Sgarbossa's criteria were designed for the very situation in which no old ECG is available. The idea that new LBBB is different from old LBBB has been described as having no source in data, and in a meta-analysis (a subset of 29 studies with 221,261 patients with LBBB) knowing whether the LBBB was new or old did not change the likelihood of acute infarction.^[10][27]

What guidelines say now.

• The 2013 American (ACCF/AHA) STEMI guideline said that a new or presumably new LBBB is often "not known to be old" because no old ECG exists, occurs infrequently, may interfere with ST analysis, and should not be considered diagnostic of infarction in isolation.^[8]
• European (ESC) STEMI guidance, as summarised in a 2021 editorial, states that a (presumed) new LBBB alone does not predict an infarct, and that patients with ongoing suspected ischaemia and refractory symptoms are managed like STEMI regardless of ECG or LBBB status.^[8]
• The 2022 ACC expert consensus decision pathway states that new LBBB is no longer considered a STEMI equivalent, and it recognises both the Sgarbossa and modified Sgarbossa criteria.^[25]
• The 2021 AHA/ACC chest pain guideline says patients with chest pain and new ST elevation, ST depression or new LBBB should be treated according to the STEMI and non-ST-elevation acute coronary syndrome guidelines; it adds that LBBB, ventricular pacing and left ventricular hypertrophy may mask signs of ischaemia or injury. It does not call new LBBB a STEMI equivalent.^[26]
• The 2023 ESC acute coronary syndromes guideline states that LBBB, RBBB or a paced rhythm precludes an accurate assessment of ST elevation, and that patients with a bundle branch block and highly suspicious signs or symptoms should be managed like clear STEMI, regardless of whether the block is previously known.^[24] A 2025 editorial reports that the 2025 American ACS guideline gives no LBBB-specific criteria.^[10]

The practical consequence is that the ECG, the clinical story, the troponin and, where needed, bedside echocardiography are combined. A patient with LBBB and ongoing ischaemic pain, haemodynamic compromise or a rising troponin is assessed urgently for coronary occlusion whatever the age of the LBBB; and a stable patient with chronic LBBB and a typical-looking tracing is not rushed to the catheter laboratory.^[8][24]

In 1996 the GUSTO-1 analysis found three ST-segment features with independent value for diagnosing acute infarction in LBBB.^[7]

The original criteria are specific (about 96%) but insensitive (about 36% for infarction in the editorial's account), so a negative result does not exclude an occlusion.^[7][9][25]

The 5 mm cut-off was arbitrary and fixed. Smith and colleagues replaced it with a proportional rule: ST elevation of at least 1 mm in any lead with a ratio of ST elevation to the depth of the preceding S wave of 0.25 or more.^[8][9] The modified criteria are positive if any one criterion is met. Reported performance is better than the original: a pooled analysis found sensitivity of about 84% and specificity of about 93% for coronary occlusion in LBBB.^[27] The original criteria are often quoted at 36% and 96%,^[9] but the two sets of figures come from different populations and are not a head-to-head comparison; in one test set the same comparison gave 33% and 99% (original) against 68% and 94% (modified).^[9] A ratio of 0.20 raised sensitivity at the cost of specificity.^[10]

A newer scheme, the Barcelona criteria, uses ST deviation of at least 1 mm that is concordant in any lead, or discordant in a lead with a small QRS (R or S wave 6 mm or less). It has reported higher sensitivity, but was derived in patients already referred for primary percutaneous coronary intervention (PCI), used a broad definition of infarction, and has not been independently validated; it may over-call occlusion in acute heart failure with a low-voltage QRS.^[8][9][10]

The left bundle splits in two, so a block can affect only one fascicle. This section explains the two hemiblocks and what they do to the axis.

Left anterior fascicular block (LAFB) is the commoner. The impulse reaches the left ventricle only through the posterior fascicle, so the initial vector goes downward and to the right, and the main vector then swings upward and to the left. The result is:^[20]

• left axis deviation, usually −45 to −90 degrees;
• a qR complex in I and aVL, and an rS complex in II, III and aVF;
• a late R-wave peak in aVL (over 45 ms);
• a normal or only slightly prolonged QRS (80 to 110 ms), because the delay is about 20 ms. The 2022 Brazilian ECG guideline uses similar criteria: an axis of −45° or beyond, rS in II, III and aVF, qR in I and aVL and a QRS under 120 ms.^[29]

The aVL voltage in LAFB can meet voltage criteria for left ventricular hypertrophy without a strain pattern.^[20]

Left posterior fascicular block (LPFB) is much rarer because the posterior fascicle is broad and has a double blood supply. The impulse travels only via the anterior fascicle, so the axis swings to the right (above +90 degrees), with rS in I and aVL and qR in II, III and aVF.^[21] Before calling LPFB you must exclude other causes of right axis deviation, such as right ventricular hypertrophy, acute pulmonary embolism, lateral infarction and tricyclic antidepressant overdose. LPFB seldom occurs alone and usually accompanies RBBB.^[21] The Brazilian guideline likewise accepts its criteria only in the absence of a slender build, right ventricular hypertrophy and old lateral infarction.^[29]

When two of the three fascicles are affected, only one limb carries the impulse. This section covers the two combinations, the risk, and why the word "trifascicular" confuses.

Bifascicular block is, in clinical usage, RBBB plus either LAFB (left axis deviation) or LPFB (right axis deviation, after excluding other causes).^[22] RBBB with LAFB is the commoner pairing because the anterior fascicle has a single (LAD) blood supply.^[22] Some authors count LBBB as bifascicular (both left fascicles) but in practice the term is kept for the RBBB combinations.^[22]

Bifascicular block is often associated with structural heart disease and extensive fibrosis of the conducting system, and ischaemic heart disease is a common cause. A new bifascicular block with chest pain has been associated with proximal LAD occlusion even without ST changes.^[22]

The risk. The danger is that the one remaining fascicle fails, producing sudden complete heart block. In a prospective study of patients with bifascicular or similar "high-risk" block, heart block developed in 19 of 554 patients (3.4%) over a mean follow-up of about 42 months, roughly 1% per year. The cumulative incidence was about 17% in patients with syncope and about 2% in those without.^[28] These are cumulative figures over the whole follow-up, not annual rates, and they come from a single older cohort, so treat them as approximate.

"Trifascicular block". True trifascicular block means conduction failure in all three fascicles: RBBB plus LAFB or LPFB with third-degree AV block.^[23] Clinically the term is often misused for bifascicular block plus first-degree AV block. This is inaccurate, because first-degree block usually reflects delay in the AV node itself, not in the third fascicle, and progression to complete heart block is not clearly higher in bifascicular block with first-degree AV block.^[23] Alternating RBBB and LBBB on successive beats, or RBBB with alternating fascicular blocks, signals impending failure of all fascicles.^[23]

For the AV block this leads to, see bradyarrhythmias and AV block.

Unexplained syncope in a patient with bifascicular block (or LBBB) is a high-risk situation, because a paroxysmal complete heart block is a likely cause. The approach in current guidance is as follows.

1. Look for other causes first: structural heart disease, ventricular arrhythmia, orthostatic hypotension, reflex syncope.
2. Perform echocardiography and ambulatory ECG monitoring.^[11][12]
3. If syncope remains unexplained after non-invasive tests, consider an electrophysiology study (EPS). The 2021 ESC guideline recommends a pacemaker if the baseline His-ventricular (HV) interval is 70 ms or more, if second- or third-degree block below the His is shown during incremental atrial pacing, or if there is an abnormal response to a drug challenge. Alternating bundle branch block is itself an indication for pacing, with or without symptoms.^[11] The 2018 American guideline makes the same two points as Class I recommendations (syncope, bundle branch block and HV over 70 ms; alternating block).^[12]
4. If EPS is negative, an implantable loop recorder can capture an event.^[11]

An evidence caution: a small prospective cohort (77 patients with bifascicular block and unexplained syncope, no structural heart disease) found fewer recurrences of syncope with an empirical pacemaker (5.6%) than with an EPS-guided strategy (29.3%), but the study was not randomised.^[13] Treat it as a prompt for discussion with an electrophysiologist, not a rule.

A bundle branch can block only under some conditions. This section covers the patterns and why they matter.

• Rate-related block. The block appears when the heart rate crosses a threshold, because the diseased bundle has a long refractory period. Tachycardia-dependent (acceleration-dependent) block appears as the rate rises. Bradycardia-dependent block appears when the rate falls too far. Both often, but not always, imply disease of the His-Purkinje system; a physiological block in healthy tissue (aberrancy) is also described.^[14]
• Hysteresis. The rate at which the block appears is often higher than the rate at which it disappears, so a patient may keep the block as the rate falls. One literature review of 93 cases found overlapping rates for appearance and disappearance.^[14]
• Why it matters. Rate-dependent RBBB can be mistaken for ventricular tachycardia,^[2] and intermittent LBBB leaves T-wave changes on the normally conducted beats (cardiac memory: T waves point the same way as the abnormal QRS). That can mimic ischaemia and lead to an unnecessary angiogram, as it did in a woman with vagal bradycardia and normal coronary arteries.^[14]
• Intermittent block. Compare ECGs from different dates. A block that comes and goes is no less important than a permanent one.

Bundle branch block changes the standard rules. This section lists what to avoid.

CRT is the treatment that makes LBBB a treatable problem rather than just a marker. This section covers who qualifies and why LBBB morphology predicts benefit.

The principle. CRT uses a pacing lead on the right ventricle and a lead on the left ventricular wall (biventricular pacing) to activate both ventricles together, correcting dyssynchrony and improving the ejection fraction in suitable patients.^[6] It is added to optimal drug therapy and often combined with a defibrillator.

Why morphology matters. Large trials showed benefit mainly in patients with LBBB: in MADIT-CRT the benefit in mildly symptomatic patients was confined to those with LBBB and not those with RBBB or non-specific delay.^[3][6] Mapping studies show that about a third of patients with an "LBBB" tracing do not have true complete left conduction block, but a wide QRS from hypertrophy or diffuse disease with intact Purkinje activation, and these respond less well.^[6] That is why stricter definitions have been proposed, and why two-step approaches (an ECG definition plus echocardiographic signs of dyssynchrony, such as septal flash and apical rocking) are being explored.^[5][6]

Narrow QRS is different: in the EchoCRT trial, patients with QRS under 130 ms and echocardiographic dyssynchrony randomised to CRT had higher mortality, so dyssynchrony on echo without a wide QRS does not justify CRT.^[6]

Other recommendations in the same sources:

• CRT should be considered in advanced heart failure (NYHA class III or IV) with atrial fibrillation and QRS of 130 ms or more, provided biventricular capture can be ensured, adding AV junction ablation if needed.^[11]
• In the 2018 American guideline, CRT is a Class IIb option for patients with LVEF 36 to 50%, LBBB, QRS over 150 ms and NYHA class II or worse symptoms.^[12]
• Conduction system pacing (His bundle pacing and left bundle branch area pacing) is emerging as an alternative or complement to biventricular pacing; the ESC says it is likely to grow in importance pending randomised trials, and a 2023 HRS/APHRS/LAHRS guideline addresses it.^[11][17]
• Pacing-induced LBBB. Frequent right ventricular pacing produces an LBBB pattern and can cause heart failure; this is why programming to minimise unnecessary ventricular pacing is recommended in sinus node dysfunction.^[11]

An isolated bundle branch block is not itself an indication for pacing. These are the main situations in which pacing is recommended or considered.^[11][12][23]

• Bundle branch block with unexplained syncope and HV interval of 70 ms or more (Class I in the American guideline), or evidence of infra-Hisian block on EPS.
• Alternating bundle branch block, with or without symptoms.
• Third-degree AV block with RBBB and a hemiblock (true trifascicular block).
• Bifascicular block with syncope or presyncope in which no other cause is found (pacing is considered after work-up; the ESC advises EPS first when syncope stays unexplained).
• After TAVI: pre-existing RBBB with any further conduction disturbance, persistent AV block, or new LBBB with QRS over 150 ms or PR over 240 ms needing ambulatory monitoring or EPS (ESC); the American guideline considers permanent pacing for new persistent LBBB (Class IIb).^[11][12]
• Asymptomatic bifascicular block with first-degree AV block: not an indication for pacing, in line with the guideline advice against pacing asymptomatic isolated conduction disease.^[12]

Start with the question "Is this a conduction defect or something else?" A wide QRS with P waves before every QRS and a regular PR interval is usually a bundle branch block or an intraventricular delay, but other causes must be excluded.

Isolated chronic RBBB in an asymptomatic person with no heart disease needs no treatment.^[2] New RBBB is treated by treating its cause (for example anticoagulation for PE or reperfusion for an ischaemic cause).^[2]

LBBB needs an echocardiogram if it is newly identified.^[12] In the guideline algorithm, symptoms suggesting intermittent bradycardia call for ambulatory monitoring (Class I) and, in selected patients, an EPS (Class IIa); RBBB or fascicular block gets echocardiography as Class IIa.^[12] Manage causes: hypertension, ischaemia, heart failure, hyperkalaemia, drug effects.

When to refer to cardiology:

• syncope or presyncope with any bifascicular block, LBBB or alternating block;
• LBBB with symptoms of heart failure or reduced LVEF (consider CRT);
• new LBBB or RBBB with chest pain or haemodynamic instability;
• suspected Brugada pattern or family history of sudden death;
• progressive conduction disease (increasing QRS or PR, new AV block);
• new block after TAVI or cardiac surgery;
• any conduction disease in a young person without an explanation.

Children. Incomplete RBBB is common and normal in children.^[19] Complete RBBB is common after repair of congenital heart defects.^[2] Children's QRS durations are shorter, so adult cut-offs do not apply.

Older adults. Degenerative fibrosis makes both blocks more common with age, and RBBB prevalence reaches about 14% in men over 80.^[2] Syncope in an older person with bifascicular block deserves a rhythm work-up, not the assumption that it is "just age".

Low-resource practice.

• A 12-lead ECG and a careful history are enough to label most blocks. Record the QRS duration in milliseconds and keep a copy for comparison.
• If troponin is unavailable, the clinical picture, the response to treatment, and serial ECGs must guide decisions about chest pain with LBBB; do not use "LBBB" alone to start thrombolysis. Ongoing ischaemic pain with a Sgarbossa-positive ECG, haemodynamic instability or a rising troponin should be treated as a STEMI equivalent, and thrombolysis considered if primary PCI cannot be reached in time.^[24]
• If echocardiography is not available, assess for heart failure clinically and refer when LBBB is newly found with symptoms.
• Pacemakers and CRT may be available only in a few centres; recognise the high-risk patient (syncope with bifascicular block) early and arrange transfer, keeping the patient monitored and lying flat, with transcutaneous pacing pads ready and a dopamine or adrenaline infusion if needed. Atropine is not reliable when the block lies below the AV node, as in bifascicular block; catecholamines or pacing are more likely to help.^[12]