Bundle Branch Block
When one highway fails, the impulse takes a detour through slow myocardium. The QRS widens — and its shape tells you exactly which branch is down.
The His bundle splits into two great highways — the right bundle branch heading toward the right ventricle, and the left bundle branch heading toward the left. In a healthy heart, both highways carry the impulse at blistering speed, and the two ventricles depolarize nearly simultaneously. The QRS complex is narrow because activation runs in parallel, like two trains arriving at their stations at the same time.
Block one of those highways, and the train on that side never arrives. The impulse has to reach the orphaned ventricle the hard way — cell to cell, across ordinary myocardium, without the benefit of the Purkinje express. Think of it as a highway closure that forces all traffic onto back roads. The signal still gets there, but it's late.
That delay is visible on every beat. The QRS widens because the two ventricles no longer activate together. And the shape of that widened QRS — its peaks and valleys — traces the exact sequence of the detour. Understanding the route explains the morphology.
Normal Ventricular Activation
Before dissecting what goes wrong, it helps to revisit what goes right. The impulse exits the AV node, traverses the His bundle, and at the top of the interventricular septum it splits: one branch dives down the right side of the septum, the other fans out across the left.
A critical detail: the left bundle branch fires just a fraction earlier than the right. This means the septum depolarizes from left to right — a small initial vector heading rightward and anteriorly. On the ECG, this normal septal activation creates the tiny initial r wave in V1 and the tiny q wave in I and V6. These small deflections are the fingerprint of normal septal activation. They matter enormously in bundle branch block, because losing them or preserving them tells you which side is affected.
After the septum, both ventricles depolarize simultaneously through the Purkinje network. The whole process is finished in under 120 ms. That's the normal QRS.
Septal Activation
Left-to-right across the septum. Creates the normal small r in V1 and q in I/V6. This happens because the left bundle fires first.
Parallel Activation
Both ventricles depolarize simultaneously via the Purkinje network. The larger LV mass dominates: the vector swings leftward, producing the S in V1 and R in I/V6.
Narrow QRS
Total duration <120 ms. Both ventricles finish at roughly the same time. No late, unopposed forces.
Right Bundle Branch Block
The right bundle branch is blocked. Everything that the left bundle does is unaffected — and because the left bundle fires first anyway, the early part of the QRS looks completely normal. Septal activation still goes left-to-right. Left ventricular activation still happens on schedule. The first two-thirds of the QRS complex are unchanged.
The problem shows up at the end. The right ventricle, which should have been activated in parallel by its own bundle branch, has been abandoned. The only way for the electrical impulse to reach it is to crawl across the septum and through the right ventricular myocardium, cell by cell — slow, inefficient, late.
This late, unopposed right ventricular activation adds a new terminal deflection to the QRS. In V1, which sits directly over the right ventricle, it appears as a tall, broad R' — the famous "rabbit ears." In leads I and V6, which look at the heart from the left side, it appears as a broad, slurred terminal S wave: the wavefront moving away from the left-sided leads as it finally activates the right ventricle.
Septal Activation
Left-to-right, unchanged. Small r in V1, small q in V6. The left bundle fires first, as always.
LV Free Wall
Left ventricle activates on time via the intact left bundle. S wave in V1, R wave in V6.
Late RV Activation
Slow cell-to-cell spread reaches the RV late. Terminal R' in V1 ("rabbit ears"), broad S in I and V6.
The classic RBBB pattern: rsR' in V1, qRS with a broad terminal S in I and V6. QRS duration ≥120 ms. The mnemonic some people use — "MaRRoW" (M-shaped in the Right leads, W-shaped in the left) — works, but the mechanism is more instructive. The terminal forces point rightward because the right ventricle is the last thing to depolarize.
LBB activates the LV normally. The RV is reached late via slow myocardial spread.
Left Bundle Branch Block
Now reverse the scenario. The left bundle branch is blocked. The right ventricle activates first — on time, through the intact right bundle. But the massive left ventricle, which depends on the left bundle for rapid activation, is stranded. The impulse must cross the septum from right to left and spread through the left ventricular myocardium cell by cell.
This changes everything about the QRS, starting with the very first deflection. Remember that normally the septum depolarizes left-to-right because the left bundle fires first. In LBBB, the left bundle is out of commission. Septal activation now runs right-to-left, driven by the right bundle. That reversal eliminates the normal small septal q wave in I and V6 and eliminates the normal small septal r wave in V1.
The right ventricle activates first, producing a brief initial deflection toward V1. Then the slow, massive wave of left ventricular depolarization dominates the tracing. In V1, this appears as a deep, broad S wave (or QS pattern) — the wavefront is heading away from V1, toward the left. In leads I and V6, it produces a tall, broad, often notched R wave — the notching reflects the slow, non-uniform cell-to-cell spread through the LV myocardium.
Septal Activation
Right-to-left (reversed!). Loss of normal septal q in I/V6. Loss of normal septal r in V1.
RV Activates First
The intact right bundle fires on time. Brief initial R in V1 (small, quickly overwhelmed).
Late LV Activation
Slow cell-to-cell spread across the LV. Deep QS/rS in V1, tall broad notched R in I/V6.
The classic LBBB pattern: broad, notched R wave in I and V6 (no preceding q), deep QS or rS in V1. QRS ≥120 ms, often ≥140 ms. The notching of the R wave in the lateral leads is almost pathognomonic — it reflects the two separate wavefronts of activation as the impulse crawls across the LV.
LBBB fundamentally alters repolarization. The ST segments and T waves shift in the direction opposite to the main QRS deflection — this is called appropriate discordance. In V1 (where the QRS is predominantly negative), the ST segment will be elevated and the T wave upright. In I and V6 (where the QRS is predominantly positive), the ST segment will be depressed and the T wave inverted. These are secondary repolarization changes — they are expected consequences of the abnormal depolarization sequence, not signs of ischemia.
This makes diagnosing acute MI in the setting of LBBB exceptionally difficult. You cannot use the standard ST-elevation criteria because the baseline is already distorted by the conduction abnormality itself.
Why the Morphology Makes Sense
There is a single unifying principle that makes all of this easy to remember. In any bundle branch block, the terminal portion of the QRS points toward the ventricle whose bundle is blocked. The reason is straightforward: the blocked ventricle is the last one to depolarize, so the latest electrical forces are unopposed and aimed squarely at it.
In RBBB, the terminal force points rightward and anteriorly — toward the right ventricle. V1 sees a positive terminal deflection (R'). In LBBB, the terminal force points leftward and posteriorly — toward the left ventricle. Leads I and V6 see a positive terminal deflection (the broad R).
V1: rsR' (R' = late RV)
I, V6: broad terminal S
I, V6: broad notched R (no q)
V1: deep QS or rS
Duration matters too. A QRS of 120 ms or wider constitutes a complete bundle branch block. Between 100 and 119 ms, with the same directional pattern but a narrower complex, the diagnosis is incomplete bundle branch block — partial delay in the affected branch, enough to shift the terminal forces but not enough to widen the QRS to the full 120 ms threshold.
Clinical Significance
The two bundle branch blocks carry very different clinical implications. This asymmetry reflects the anatomy and the diseases that tend to damage each branch.
Often Benign
The right bundle branch is a thin, delicate structure that runs along the right side of the septum, relatively exposed. Minor stretch, minor fibrosis, even normal variant anatomy can disrupt it. RBBB is common in healthy hearts — especially in athletes and younger patients — and by itself carries no increased mortality risk.
When pathological, RBBB can reflect right ventricular strain (pulmonary embolism, pulmonary hypertension), right heart volume overload (atrial septal defect), or anteroseptal ischemia. The Brugada pattern — a pseudo-RBBB with coved ST elevation in V1–V3 — is a dangerous mimic that warrants separate attention.
Almost Always Pathological
The left bundle is a broad, robust structure that fans out across the left side of the septum. It takes significant disease to knock it out. LBBB almost always signals underlying cardiac pathology: hypertensive heart disease, dilated cardiomyopathy, ischemic heart disease, or aortic valve disease.
New LBBB with chest pain is treated as an acute MI until proven otherwise. The appearance of a new LBBB in the setting of ischemia carries the same urgency as frank ST elevation — it means a large territory of myocardium is threatened.
The Sgarbossa criteria help identify acute MI behind the mask of LBBB: concordant ST elevation ≥1 mm (ST elevation in a lead where the QRS is also positive), concordant ST depression ≥1 mm in V1–V3, or excessively discordant ST elevation (≥5 mm, or using the modified Smith criteria, ≥25% of the preceding S-wave depth).
One more concept ties back to Volume III. Rate-dependent bundle branch block is a BBB pattern that appears only at faster heart rates and disappears when the rate slows. It occurs because one bundle branch has a longer refractory period than the other. At baseline rates, the refractory period has time to reset. When the rate increases, the next impulse arrives before that bundle has fully recovered — and it blocks. This is the Ashman phenomenon applied to the bundle branches: the longer the preceding cycle, the longer the refractory period, and the more likely a premature beat will find one branch still refractory.
A single bundle branch block means the impulse is still reaching the ventricles through one intact branch. The HV interval — the time from the His deflection to the onset of ventricular activation — reflects the speed of conduction through whichever branch is still working.
The clinical significance sharpens when bundle branch block combines with other conduction disease. RBBB plus left anterior fascicular block, for instance — bifascicular block — means two of the three main fascicles are already down. If the HV interval is prolonged, the remaining fascicle is also struggling. This is where the EP study becomes decisive, and where the story continues in the next chapter.
Key Takeaways
- In bundle branch block, the ventricle whose branch is blocked depolarizes late, via slow cell-to-cell myocardial spread. The QRS widens to ≥120 ms because the two ventricles no longer activate in parallel.
- RBBB preserves the early QRS (septal and LV activation are normal) and adds a terminal R' in V1 and broad S in I/V6, because the right ventricle is the last structure to depolarize.
- LBBB reverses septal activation (right-to-left), eliminates normal septal q waves, and produces a broad notched R in I/V6 with deep QS in V1. It also distorts repolarization (discordant ST-T changes), making ischemia diagnosis very difficult.
- RBBB can be benign (common in normal hearts). LBBB is almost always pathological — and new LBBB with chest pain is treated as acute MI. Sgarbossa criteria help unmask ischemia behind LBBB.
- In the EP lab, RBBB alone has a normal HV interval; LBBB alone may show mild HV prolongation. The real danger emerges when BBB combines with additional fascicular disease — the setup for the next chapter.