First-Degree AV Block and the PR Interval
The PR interval is a window into three distinct anatomical territories. Where the delay lives changes everything.
Every time you measure a PR interval, you are watching the electrical impulse cross three completely different anatomical territories — each with its own cell biology, its own ion channels, and its own vulnerability to disease.
The PR interval is easy to measure. Two small horizontal ticks on the ECG. A number, usually between 120 and 200 milliseconds. If it exceeds 200 ms, we call it "first-degree AV block."
That label is misleading. It implies a single problem in a single location. In reality, delay can accumulate in at least three different places — and the clinical meaning of each one is profoundly different.
Three Territories in One Line
From the moment the sinus node fires to the moment the ventricles begin to depolarize, the impulse must cross three distinct regions. Each contributes a measurable fraction of the PR interval.
Atrial Depolarization
The P wave itself. The impulse leaves the sinus node, spreads across both atria, and arrives at the AV node. This typically takes 30–50 ms. Intra-atrial conduction delay (wide P waves) can prolong this segment.
AV Nodal Transit
The bulk of the PR interval. The AV node is built to slow things down — it relies on L-type calcium channels for depolarization, which are slower and more decremental than sodium channels. Transit here accounts for 60–130 ms of the PR.
His–Purkinje Transit
The impulse darts through the His bundle, down the bundle branches, and into the Purkinje network. This is fast — normally 35–55 ms — because these fibers use rapid sodium channels with very high Vmax.
Add these three segments together and you get the PR interval: roughly 120–200 ms in a healthy heart. When the total exceeds 200 ms, we label it first-degree AV block — but that label tells you nothing about where the extra time is hiding.
Where Delay Can Live
A PR interval of 280 ms in a 25-year-old athlete means something entirely different from a PR interval of 280 ms in a 72-year-old with a wide QRS and syncope. The number is the same; the mechanism is different; the prognosis is different.
Delay at the AV node is the most common cause. The AV node naturally slows conduction, and certain states amplify this: high vagal tone, beta-blockers, calcium channel blockers, or intrinsic AV nodal disease. Critically, the AV node has a backup plan. If delay worsens to the point of complete block, a junctional escape rhythm (typically 40–60 bpm) usually emerges. The patient's life is rarely in immediate danger.
Delay in the His bundle itself is less common and more ominous. Fibrosis, infiltration (sarcoid, amyloid), or ischemia can slow conduction through this narrow structure. The His bundle is a single cable — there is no redundancy.
Delay in the infra-His system (bundle branches and fascicles) is the most worrying. This is the territory of diseased Purkinje fibers, of sodium-channel-dependent tissue that is starting to fail. When conduction falters here, the escape rhythm is ventricular — unreliable, slow (20–40 bpm), and prone to long pauses or asystole.
Two Different Ion Channel Stories
The distinction between nodal and infranodal delay comes down to the ion channels driving depolarization in each tissue. We explored this in Volumes I and II, and it returns here with direct clinical force.
Calcium-Channel Dependent
The AV node depolarizes via L-type Ca²⁺ channels. These channels recover slowly. At faster heart rates or under high vagal tone, recovery is even more sluggish — the channel simply hasn't reset by the time the next impulse arrives. This is the basis of decremental conduction: the faster you push, the slower the AV node goes.
Sodium-Channel Dependent
His–Purkinje fibers depolarize via fast Na⁺ channels. These channels normally recover quickly and conduct at blazing speed. When they slow down, it means the tissue itself is diseased — fibrosis has reduced the number of available channels, or the resting membrane potential has drifted upward, leaving channels partially inactivated. Vmax drops, and conduction velocity falls.
This is why drugs behave so differently at each level. A calcium channel blocker (verapamil, diltiazem) prolongs AV nodal conduction and can worsen first-degree block at the nodal level — but it does nothing to infranodal tissue. A sodium channel blocker (flecainide, procainamide) can dangerously slow conduction through already-diseased Purkinje fibers while leaving the AV node relatively untouched.
Mapping the Delay
The diagram below maps each segment of the PR interval onto the anatomical conduction system. Notice how the AV node accounts for the lion's share of the transit time.
Total PR interval ≈ 120–200 ms (normal)
What the QRS Width Tells You
Here is a practical rule that connects the PR interval to the QRS complex, and turns a simple observation into a risk assessment.
A long PR with a narrow QRS almost always means the delay is in the AV node. The His–Purkinje system is conducting normally (hence the narrow QRS), and the AV node is simply taking its time. This is typical of high vagal tone in young athletes, or the effect of AV-nodal-blocking medications. It is nearly always benign. The patient rarely needs a pacemaker.
A long PR with a wide QRS raises a different question. The wide QRS tells you the infranodal conduction system is already abnormal — a bundle branch block pattern means at least one branch is failing. If the PR is also prolonged, the delay might be in the remaining conducting tissue. This patient may have disease at multiple levels of the conduction system, and the risk of progression to complete heart block is real.
A very long PR (>300 ms) can cause hemodynamic problems even without higher-degree block. When the PR is extremely prolonged, the atrial contraction (P wave) finishes so early that the mitral and tricuspid valves have already drifted shut by the time the ventricle contracts. Worse, the P wave may land on the preceding T wave, producing the same hemodynamic effect as AV dissociation. Patients can develop symptoms identical to pacemaker syndrome — fatigue, exercise intolerance, neck pulsations (cannon A waves) — despite having 1:1 conduction. This has been called "pseudo-pacemaker syndrome."
The surface ECG shows you the total PR interval. To dissect where the delay lives, you need an intracardiac recording from the His bundle.
A catheter is advanced to the tricuspid annulus and positioned so its electrodes straddle the His bundle. On the recording, you see three deflections: the A (atrial), the H (His), and the V (ventricular). This gives you two critical intervals:
A prolonged AH with a normal HV tells you the delay is in the AV node — the typical, benign pattern. It responds to atropine (speeds up) and gets worse with adenosine or carotid sinus massage.
A prolonged HV is the worrying finding. An HV > 55 ms indicates infranodal conduction disease. An HV > 100 ms carries a significant risk of progression to complete heart block and is often an indication for pacemaker implantation regardless of symptoms.
Key Takeaways
- The PR interval spans three territories: atrial depolarization (P wave), AV nodal transit (the majority), and His–Purkinje transit. Delay can accumulate in any of them.
- AV nodal delay is calcium-channel dependent (slow L-type Ca²⁺ recovery). Infranodal delay is sodium-channel dependent (diseased Purkinje fibers with reduced Vmax).
- Long PR + narrow QRS = almost always AV nodal, almost always benign. Long PR + wide QRS = suspect infranodal disease, risk of progression.
- In the EP lab, the His bundle electrogram splits the PR into AH (nodal) and HV (infranodal). A prolonged HV (>55 ms) is the finding that drives clinical decisions.
- Very prolonged PR intervals (>300 ms) can cause hemodynamic compromise (pseudo-pacemaker syndrome) even with intact 1:1 conduction.