Second-Degree AV Block
Some P waves conduct. Some don't. The question that matters is why — and the answer splits into two diseases with opposite prognoses.
In first-degree block, every impulse gets through — it just takes longer. In second-degree block, some impulses don't make it at all. P waves fire, the atrium contracts, and the ventricle simply doesn't respond.
The dropped beat is the defining feature. But the question that drives clinical decision-making is not whether a beat drops — it's how the block behaves in the beats before it drops.
Does conduction gradually fatigue, each beat struggling a little more than the last, until one finally fails? Or does the system conduct perfectly normally, beat after beat, and then one impulse simply vanishes without warning?
These two patterns — gradual fatigue versus abrupt failure — reflect two completely different mechanisms, located in two different structures, driven by two different ion channels, and carrying two very different prognoses. Understanding the split is one of the most clinically consequential lessons in electrophysiology.
Mobitz Type I — The Wenckebach Pattern
The AV node runs on L-type calcium channels. These channels are inherently slow to recover. After each depolarization, a calcium channel needs time to reset — to transition from its inactivated state back to a closed state that can re-open. At normal heart rates, there is just enough recovery time between beats for the channel to reset. Conduction gets through.
When disease or physiologic stress narrows that recovery window, each successive impulse arrives before the calcium channels have fully reset. The first beat after a rest has the most recovered channels, so it conducts the fastest — shortest PR. The second beat finds slightly fewer channels ready, conducts a bit more slowly — slightly longer PR. The third beat, fewer still.
Beat by beat, the fraction of available calcium channels shrinks. The PR interval lengthens. The impulse slows further. Eventually, one impulse arrives and finds the AV node still completely refractory from the previous beat. That impulse is blocked. The QRS drops.
The dropped beat is actually the reset. The long pause that follows gives the calcium channels time to fully recover. The next conducted beat starts fresh — shortest PR of the cycle — and the whole sequence begins again. This is grouped beating: a repeating cycle of progressively lengthening PR intervals punctuated by a dropped QRS.
- Progressive PR prolongation — each conducted beat has a longer PR than the one before
- Decreasing PR increment — the biggest jump in PR occurs between the first and second conducted beats; each subsequent increment is smaller
- Shortening RR intervals — a direct consequence of the shrinking PR increment
- Grouped beating — clusters of conducted beats separated by pauses
- Pause less than twice the shortest RR — because the dropped beat's pause includes the blocked P-P interval minus one PR increment
Wenckebach block is almost always located within the AV node. This matters for a simple reason: the AV node's own junctional pacemaker cells sit immediately adjacent. If block worsens — even to complete block at the nodal level — a junctional escape rhythm at 40–60 bpm typically rescues the patient. It is narrow-complex, reasonably reliable, and hemodynamically tolerable.
This is why Wenckebach is generally considered benign. High vagal tone in young athletes can produce it during sleep. Inferior MI can cause transient AV nodal ischemia that manifests as Wenckebach. In most settings, the patient needs monitoring, not a pacemaker.
The Wenckebach Strip
A 4:3 Wenckebach pattern — four P waves, three conducted QRS complexes, one dropped beat. Watch the PR intervals lengthen, then the reset.
Progressive PR prolongation → dropped QRS → reset. The hallmark of AV nodal fatigue.
Mobitz Type II — All-or-Nothing Failure
Below the AV node, the conduction system changes character completely. The His bundle, bundle branches, and Purkinje fibers run on fast sodium channels. These channels recover quickly — in healthy tissue, the refractory period is short and there is no meaningful decremental behavior. The impulse either gets through at full speed or it doesn't get through at all.
In Mobitz Type II, the disease lives in this infranodal tissue. Fibrosis, calcification, or ischemia has damaged enough sodium channels that the safety margin for conduction is razor-thin. Most beats still conduct — the PR interval is constant, the QRS appears on schedule. Then, without any warning, one impulse fails to propagate. The QRS simply vanishes.
There is no progressive PR prolongation. No gradual slowing. The sodium channel doesn't fatigue the way calcium channels do — it works or it doesn't. The PR interval before the dropped beat is identical to the PR interval before every other conducted beat. This all-or-nothing behavior is the hallmark of sodium-channel-dependent tissue under stress.
The QRS complex in Mobitz II is typically wide. This makes sense: if the infranodal conduction system is diseased enough to intermittently block impulses, it is almost certainly diseased enough to produce a bundle branch block pattern on the conducted beats. A narrow QRS with a Mobitz II pattern should make you reconsider the diagnosis — it is uncommon enough that many electrophysiologists would want an intracardiac study to confirm the site of block.
The escape pacemaker below the His bundle is ventricular. It fires at 20–40 bpm — sometimes slower, sometimes not at all. Its rhythm is wide-complex, hemodynamically inadequate, and unreliable. Asystolic pauses are a real possibility.
Mobitz II can progress to complete heart block suddenly, without transitioning through a gradual worsening pattern. One moment 2:1, the next moment no conduction at all — and the ventricular escape may take seconds to emerge, if it emerges.
This is why Mobitz II is a Class I indication for permanent pacemaker implantation, even in the absence of symptoms.
The 2:1 Block Dilemma
Here is the diagnostic trap. When every other P wave is blocked — a 2:1 conduction ratio — you see exactly one conducted beat between each dropped beat. There is no opportunity to watch PR intervals evolve over a sequence of conducted beats. You cannot observe progressive prolongation (which would tell you it's Mobitz I) or constant PR across multiple beats (which would tell you it's Mobitz II). The single conducted PR interval is ambiguous.
A 2:1 block could be Wenckebach with a very short cycle (the equivalent of a 2:1 Wenckebach where only one beat conducts before the drop). Or it could be Mobitz II where half the impulses fail. The ECG pattern looks identical.
So how do you tell them apart?
- Narrow QRS — intact His–Purkinje system
- Atropine improves conduction — vagolytic effect speeds AV node recovery
- Longer strips reveal 3:2 or 4:3 — occasionally a Wenckebach group emerges, proving the pattern
- Inferior MI context — the RCA supplies the AV node in 85% of patients
- Wide QRS — bundle branch block pattern = diseased infranodal system
- Atropine worsens block — faster atrial rate pushes more impulses into already-failing tissue
- Anterior MI context — LAD supplies the bundle branches and septum
- Hemodynamic instability — unreliable ventricular escape
The atropine response deserves emphasis. Atropine withdraws vagal tone and speeds AV nodal conduction. If the block is in the AV node, conduction improves — the 2:1 may become 3:2, then 1:1. If the block is infranodal, atropine speeds the sinus rate and the AV node, delivering impulses to the His–Purkinje system faster. Diseased tissue that was already struggling now faces a higher input rate — and block can paradoxically worsen.
Mobitz I vs. Mobitz II — Side by Side
| Feature | Mobitz Type I | Mobitz Type II |
|---|---|---|
| Site of block | AV node | His bundle / bundle branches |
| Ion channel | L-type Ca²⁺ (slow recovery) | Fast Na⁺ (all-or-nothing) |
| PR pattern | Progressive prolongation → drop | Constant PR → sudden drop |
| QRS width | Usually narrow | Usually wide (BBB pattern) |
| Escape rhythm | Junctional (40–60 bpm, narrow, reliable) | Ventricular (20–40 bpm, wide, unreliable) |
| Atropine effect | Improves conduction | May paradoxically worsen |
| Prognosis | Usually benign | Risk of sudden complete block |
| Treatment | Observation; treat reversible causes | Permanent pacemaker |
The surface ECG shows you the PR interval and its behavior. The His bundle electrogram shows you exactly where the block lives — and when the 2:1 dilemma arises, this is often the study that settles it.
In Mobitz I (AV nodal block): the intracardiac recording shows progressive AH prolongation — the interval from the atrial deflection to the His spike gets longer with each beat. When the beat finally drops, the atrial deflection fires but the His spike never appears. Block is above His. The HV interval on conducted beats remains normal.
In Mobitz II (infranodal block): the AH interval is constant. Every beat shows a His spike firing on time. But on the dropped beat, the His spike fires and nothing follows — no ventricular deflection. The impulse reached the His bundle, entered the diseased infranodal system, and died. This is HV block (sometimes called infra-Hisian block), and it confirms that the conduction system below the His bundle is failing.
HV: 45 ms (constant on conducted beats)
Block level: supra-Hisian
His spike fires → no V
Block level: infra-Hisian
When you see a wide QRS, 2:1 block, and a hemodynamically unstable patient, you rarely need an EP study — the clinical picture speaks for itself and the pacemaker is going in. The His recording is most valuable in ambiguous cases: a narrow-complex 2:1 block where the surface ECG cannot distinguish the mechanism, or when the clinical scenario makes the site of block genuinely uncertain.
Key Takeaways
- Mobitz I (Wenckebach) is progressive fatigue of L-type calcium channels in the AV node. Each PR gets longer until one beat drops, the channels recover, and the cycle resets. The junctional escape below is reliable. Usually benign.
- Mobitz II is all-or-nothing failure of fast sodium channels in the His–Purkinje system. The PR is constant; the drop is sudden. The ventricular escape below is slow, wide, and unreliable. This is a pacemaker indication.
- 2:1 block is ambiguous — you cannot classify it as Mobitz I or II from a single conducted beat. Use QRS width, atropine response, clinical context, and longer rhythm strips to differentiate. When in doubt, treat as the more dangerous diagnosis.
- The QRS width is your fastest bedside clue: narrow QRS strongly favors AV nodal block; wide QRS with bundle branch block pattern strongly favors infranodal disease.
- In the EP lab, the His bundle electrogram is definitive: progressive AH prolongation localizes block to the AV node; a His spike followed by no ventricular deflection localizes block below the His bundle.