Left bundle branch block (LBBB): ECG criteria, causes, management
Left bundle branch block (LBBB)
- The cardiac conduction system
- ECG criteria for left bundle branch block (LBBB)
- Electrophysiology of left bundle branch block (LBBB)
- Clinical implications of left bundle branch block (LBBB)
- Diagnosis of acute myocardial ischemia and infarction in patients with left bundle branch block (LBBB)
- Incomplete left bundle branch block (LBBB)
Left bundle branch block (LBBB) results from anatomical or functional impairment of the left bundle branch (LBB), leading to a blockage of electrical impulse conduction through this bundle. Consequently, depolarization of the left ventricle is achieved by impulses spreading from the right ventricle. The electrical impulse will propagate through the left ventricle partially or entirely outside the specialized conduction system. This slower conduction results in a prolonged QRS duration. The defining features of LBBB include a QRS duration of ≥0.12 seconds, a deep and broad S-wave in leads V1 and V2, and a wide, notched R-wave in leads V5 and V6. Figure 1 (25 mm/s) illustrates the differences between normal conduction, left bundle branch block (LBBB) and right bundle branch block (RBBB).

Figure 2 shows 12-lead-ECGs demonstrating right and left bundle branch blocks.
The cardiac conduction system
The cardiac conduction system ensures rapid and synchronized spread of depolarization, which is essential for coordinated and efficient atrial and ventricular activity. The conduction system includes the sinoatrial (SA) node, atrioventricular (AV) node, Bundle of His, bundle branches (left and right bundle branch), and Purkinje fibers. The conduction system allows for rapid spread of the depolarization to the contractile cells. Figure 3 illustrates the components of the conduction system and its temporal relationship to the ECG waveforms. The cardiac cycle begins in the sinus node (sinoatrial node), where depolarization occurs through automaticity (refer to Cardiac Electrophysiology). The electrical impulse propagates through the atria via the internodal pathways and Bachmann’s bundle, eventually reaching the atrioventricular (AV) node. Here, conduction is briefly delayed to allow adequate ventricular filling. The impulse then travels through the Bundle of His, which bifurcates into the left bundle branch (LBB) and the right bundle branch (RBB). The left bundle branch further divides into the anterior and posterior fascicles. The bundle branches and fascicles play a critical role in disseminating the impulse throughout the ventricles. Dysfunction in the bundle branches or fascicles will result in characteristic ECG changes.

ECG criteria for left bundle branch block (LBBB)
Diagnosing left bundle branch block is relatively straightforward. The hallmark of LBBB is the prolonged QRS duration. A QRS duration of 120 ms (0.12 s) or more is required to diagnose a complete left bundle branch block. In addition to prolonged QRS duration, LBBB is characterized by deep and broad S-waves in leads V1 and V2 and broad, frequently nothed, R-wave in V5 and V6. Secondary ST-T changes occur invariably in the presence of LBBB. The following ECG criteria and characteristics are used to diagnose LBBB:
- QRS duration ≥0,12 seconds.
- Leads V1-V2: deep and broad S-wave. The small r-wave is missing or smaller than normal; if missing, a QS complex appears in V1 and occasionally V2, but rarely in V3. The S-wave in V1 may be notched and resemble the letter W.
- Leads V5-V6: Broad, completely positive and often notched R-wave.
- Leads I and aVL: Similar to V5 and V6.
- ST-T changes: Left-sided leads (V5, V6, I and aVL) show T-wave inversions and ST segment depressions. V1–V3 shows ST-segment elevation and positive T-waves. The ST-segment elevation rarely exceeds 5 mm.
Figure 4 illustrates the distinguishing features of RBBB and LBBB.
Electrophysiology of left bundle branch block (LBBB)
Ventricular depolarization normally begins in the interventricular septum, which receives Purkinje fibers from the left bundle branch. Therefore, depolarization of the septum begins in its left aspect and progresses toward its right aspect. Depolarization of the septum generates the small r-waves observed in leads V1 and V2, as well as the small q-waves seen in leads V5 and V6, commonly referred to as “septal q-waves”. These normal patterns are illustrated in Figure 5.

In left bundle branch block, depolarization of the septum occurs via impulses spreading from the right ventricle. Consequently, the small r-waves in V1–V2 and small q-waves in V5–V6 are either diminished or disappeared. Depolarization continues slowly towards the left ventricular free wall, and the vector is continuously directed leftward. This causes a wide S-wave in V1–V2 (referred to as QS complex if the r-wave is absent) and a broad and notched R-wave in V5–V6.
Due to the abnormal left ventricular depolarization sequence in LBBB, the repolarization process is also abnormal, leading to secondary ST-T changes that become apparent. In LBBB, it is expected that ST segment depressions and T-wave inversions exist in left-sided leads (V5, V6, I and aVL). Simultaneously, V1–V3 typically display ST-segment elevation and large S-waves.
Electrical axis in left bundle branch block (LBBB)
The electrical axis may be unaltered or deviate to the left or (rarely) to the right. Left axis deviation suggests a pronounced left bundle branch block.
Clinical implications of left bundle branch block (LBBB)
Left bundle branch block is always a pathological finding. It affects left ventricular contractility (systolic function) and is associated with adverse cardiovascular outcomes. LBBB is strongly associated with hypertension, left ventricular hypertrophy, aortic stenosis, aortic regurgitation, myocarditis, ischemic heart disease, heart failure, and cardiomyopathies. The Framingham Heart Study showed that left bundle branch block was associated with seven times as great a risk of heart failure, two times as great a risk of coronary artery disease and a significantly higher risk of developing right ventricular hypertrophy (Schneider et al.). Left bundle branch block is rare in younger individuals.
Diagnosis of acute myocardial ischemia and infarction in patients with left bundle branch block (LBBB)
In LBBB, activation of the left ventricle relies on electrical impulses spreading from the right ventricle, leading to slow and abnormal depolarization of the left ventricle. This abnormal depolarization produces an atypical QRS complex (discussed earlier). Additionally, the abnormal repolarization results in secondary ST-T changes, including ST-elevations in leads V1–V3, ST-depressions in leads V4, V5, V6, aVL, and I, as well as inverted T-waves in leads showing ST depressions. These ST-T changes are normal and expected findings in the presence of LBBB. However, the underlying electrical disturbance and associated secondary ST-T changes cause a significant challenge in diagnosing acute ischemia. Current guidelines from the European Society of Cardiology (ESC), the American Heart Association (AHA) and the American College of Cardiology (ACC) advise against using standard ECG criteria for diagnosing acute myocardial infarction in the presence of LBBB. Figure 6 shows typical ST-segment elevations and ST-segment depressions, observed in an asymptomatic patient with LBBB.
There are three reasons why LBBB complicates the assessment of patients with suspected acute myocardial infarction:
- Left bundle branch block (LBBB) can mimic acute STEMI, as it often presents with similar ECG changes, including ST-segment elevations, ST-segment depressions, and T-wave inversions. These overlapping features frequently lead to confusion between LBBB and acute STEMI.
- LBBB may mask (conceal) ongoing myocardial ischemia: LBBB causes pronounced disturbance of ventricular repolarization, which usually prevents other ST-T changes (such as those arising from ischemia) from coming to expression on ECG. Therefore, ischemic ST-T changes (ST elevations, ST depressions, T-wave changes) are typically concealed in the setting of LBBB. A patient with acute STEMI may therefore display a normal LBBB pattern.
- LBBB may be caused by ischemia/infarction: An acute myocardial infarction (particularly anterior STEMI) may cause LBBB. Hence, an acute myocardial infarction may result in LBBB, which then conceals the ischemic ST-T changes on ECG.
In summary, LBBB can arise from, mimic, or conceal acute myocardial ischemia and infarction, posing considerable diagnostic challenges. This prompted researchers to investigate patients with LBBB and suspected acute myocardial infarction (AMI) by referring them for urgent reperfusion therapy, which equaled fibrinolysis at the time (Wilner et al.). Their findings showed that a significant proportion of these patients had complete coronary artery occlusions and experienced better outcomes when managed as acute STEMI cases.
For almost two decades, European and North American guidelines recommended treating patients with symptoms of myocardial ischemia and new (or presumed new) LBBB as having acute STEMI. However, a growing body of evidence demonstrated that this approach resulted in an unacceptably high rate of unnecessary angiographies. Therefore, guidelines now advise that new (or presumed new) LBBB should not be used in isolation as a diagnostic criterion for acute myocardial infarction (O’Gara et al.). Instead, patients with a strong clinical suspicion of ongoing myocardial ischemia—regardless of ECG—should receive treatment similar to those with clear STEMI. This approach applies particularly to patients who remain symptomatic despite initial medical therapy, are hemodynamically unstable, or develop sustained ventricular arrhythmias. Similarly, the 2023 European Society of Cardiology (ESC) guidelines recommend treating patients with LBBB or RBBB and signs or symptoms strongly indicative of ongoing myocardial ischemia as having definitive STEMI, regardless of whether the bundle branch block was previously documented (Byrne et al.).
Sgarbossa criteria for diagnosing acute ischemia in the setting of LBBB
Several ECG criteria have been proposed to diagnose acute myocardial ischemia and infarction in the setting of LBBB. The most useful criteria are the Sgarbossa criteria (Neeland et al.). These criteria are summarized in Figure 7. For a detailed discussion, refer to LBBB and Acute Myocardial Infarction. In summary, no existing criteria demonstrate sufficient sensitivity to reliably detect acute myocardial infarction. Evaluating symptoms, hemodynamic status, and other signs of ischemia provides significantly greater value in guiding treatment decisions.
Left ventricular hypertrophy and left bundle branch block
Left ventricular hypertrophy (LVH) is characterized by an increase in left ventricular mass. This increased muscle mass can result in slightly prolonged depolarization and repolarization, leading to a mildly increased QRS duration; however, it typically does not reach or exceed 0.12 seconds. Moreover, the QRS morphology in left ventricular hypertrophy may also resemble that of left bundle branch block (particularly incomplete left bundle branch block). It is usually easy to separate the two. In hypertrophy, the septal q-waves (V5, V6, aVL and I) are preserved (or amplified), and the QRS complex has a very large amplitude. In left bundle branch block, the QRS duration is at least 0.12 seconds. Of course, LBBB and LVH may accompany each other.
Incomplete left bundle branch block (LBBB)
Incomplete left bundle branch block is less common than the complete form. In this condition, conduction through the left bundle branch is preserved but occurs at a reduced capacity compared to a normal bundle branch. Thus, the initial depolarization of the left ventricle occurs via impulses spreading from the right ventricle, but after a while, the impulse passes the block in the left bundle branch and executes the remained of ventricular depolarization normally. Hence, the initial QRS complex resembles left bundle branch block but QRS duration is <0.12 seconds. Incomplete left bundle branch blocks tend to progress to complete bundle branch blocks.
- QRS duration >0,10 and < 0,12 seconds.
- R-wave peak time ≥0,06 seconds in i V5, V6.
- Absence of normal septal q-wave in V5, V6, I and aVL.
- Notched ascending limb of R-wave in V5, V6, aVL and I.