Conduction Blocks & Intervals

Start at the sinus node. The beat crosses the atria, then arrives at the atrioventricular (AV) node, where it is held up briefly. From there it runs through the His bundle, the bundle branches and the Purkinje network out to the ventricular myocardium. Normally the AV node is the only electrical bridge between atria and ventricles. The hold-up is what the PR interval measures. A block either stretches it or cuts the signal altogether.

Where the block sits tells you what backs it up. Above the His bundle (AV nodal, supra-Hisian), the QRS stays narrow and a junctional escape at about 40–60 bpm takes over. That escape is often transient. Below the His bundle (infranodal), the QRS goes wide and the ventricle has to supply a slow beat, about 20–40 bpm. Asystole can arrive without warning.

• Automatic pacemakers, fastest to slowest: sinus node (60–100 bpm), AV junction (40–60 bpm), ventricle (20–40 bpm)

Work through rate, regularity and the P-to-QRS relationship, in that order. Width comes next. The QRS tells you where the block sits.

1. Rate: Count the ventricular rate and compare it with the atrial (P-wave) rate.
2. Regularity: Decide whether the P-P and R-R intervals are constant or change in a pattern.
3. P waves: Confirm a P wave comes before each QRS, and find any P waves with no QRS.
4. PR and P:QRS relationship: Measure the PR before each conducted beat. Note whether it lengthens, stays constant, or the P wave is blocked.
5. QRS width: Measure the QRS in the widest lead. Narrow (under 120 ms; 110–119 ms is borderline) suggests a nodal site; wide suggests infranodal.
6. Stability: Decide stable or unstable before any drug. Unstable means hypotension, altered mental status, ischemic chest pain, shock or heart failure.

First-degree AV block is a steady conduction delay. Every P wave gets a QRS, but the PR runs longer than normal. The full PR-interval teaching is on the PR Interval page.

ECG Criteria

• PR interval: More than 200 ms (0.20 s; more than 5 small boxes), constant beat to beat
• Conduction: 1:1; every P wave followed by a QRS
• QRS: Narrow unless a bundle branch block coexists

Causes

• Increased vagal tone, athletic conditioning, sleep
• Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
• Inferior MI (AV nodal ischemia), myocarditis, Lyme carditis

Clinical Significance

• Usually benign. On its own it needs no specific treatment
• A very long PR (commonly above 300 ms) can cause symptoms. Loss of AV synchrony means the atria contract against closed AV valves
• It can progress to higher-grade block. Review the drugs, and repeat the ECG if the clinical picture changes

Mobitz I is a nodal block, and the PR tells the story. It lengthens with every beat until a P wave fails to conduct. Then the cycle starts over. The pause lets conduction recover, so the QRS stays narrow.

ECG Criteria

• PR: Lengthens progressively across the group, with shrinking increments before the drop
• Dropped QRS: One P wave with no QRS ends each group
• R-R: Shortens across the group; the R-R interval that contains the dropped beat is less than twice the shortest R-R before it
• QRS: Narrow, because the block is above the His bundle

Causes

• Increased vagal tone, sleep, athletic training
• Inferior MI (usually transient), beta-blockers, calcium channel blockers, digoxin
• Myocarditis and Lyme carditis

Clinical Significance

• Usually benign, and the chance of sliding into complete block is low
• You can count on the escape rhythm here. The block sits in the node
• Pacing is rarely the answer. Reach for it only when the patient is symptomatic or hemodynamically unstable

Look-Alikes

• Sinus arrest or exit block: a pause with no P wave in front of it (see Differential Diagnosis)

Mobitz II is an infranodal block. Conducted beats keep a constant PR interval. Then some P waves fail to conduct, with no warning. The block lies in the His–Purkinje system.

ECG Criteria

• PR: Constant for conducted beats; no lengthening before the drop
• Dropped QRS: Sudden and unpredictable; often 2:1 or 3:1, or variable
• P waves: The sinus rhythm continues regularly through the dropped beats
• QRS: Often wide, because the block is below the AV node

Causes

• Anterior MI with septal involvement (LAD territory)
• Degenerative conduction disease and fibrosis
• Infiltrative disease, cardiac surgery, drug or electrolyte toxicity

Clinical Significance

• The risk of progressing to complete heart block is high. It often comes without warning
• Escape rhythms are slow, about 20–40 bpm. They may be wide, and you can't count on them
• It needs a permanent pacing evaluation. Do not discharge without cardiology review

In 2:1 AV block, every other P wave conducts. High-grade AV block has two or more non-conducted P waves in a row, with some conduction preserved. You can't classify either one as Mobitz I or Mobitz II from the 2:1 segment alone. Only one PR interval is visible at a time.

ECG Criteria

• 2:1: Two P waves for each QRS; the PR of the one conducted beat cannot show progression
• High-grade: Two or more consecutive non-conducted P waves
• QRS width: The main clue. Narrow suggests a nodal site; wide suggests infranodal disease

Clinical Significance

• Manage a wide QRS with 2:1 or high-grade block as infranodal. Stay with that until a longer strip shows otherwise
• Record a longer rhythm strip. A stretch with more than one conducted beat shows whether the PR lengthens
• A change in conduction ratio with a wider QRS is a warning sign. It points to progressive infranodal disease

Nothing from the atria gets through in complete AV block. Each chamber keeps its own timing. The ventricles run on an escape rhythm generated below the block.

ECG Criteria

• AV dissociation: P waves and QRS complexes occur independently; the PR interval has no consistent value
• Atrial rate: Regular P-P intervals, usually at the sinus rate
• Ventricular rate: Regular R-R intervals, slower than the atrial rate
• QRS: Narrow with a junctional escape, or wide with a ventricular escape

Junctional vs. Ventricular Escape

Causes

• Acute inferior MI (usually nodal, often transient) or anterior MI (infranodal, serious)
• Drugs (for example beta-blockers, calcium channel blockers, digoxin), electrolyte disturbance, Lyme carditis
• Degenerative disease, congenital block, infiltrative disease, cardiac surgery

Clinical Significance

• An anterior MI that causes complete block has done extensive septal damage, and mortality is high. Immediate pacing and urgent cardiology review are both needed
• In inferior MI, complete block is often nodal. Recovery within days is possible
• When acquired complete block refuses to resolve, it needs a permanent pacemaker evaluation

One ventricle gets its signal late. That delay widens the QRS, and the ST-T waves swing the other way. The full criteria, lead patterns and mnemonic live on the QRS Complex page. Here you get just enough criteria to classify a block.

ECG Criteria

• RBBB: QRS 120 ms or more (complete), 110–119 ms (incomplete); rsR′ in V1–V2 and a wide, slurred S wave in I, V5–V6
• LBBB: QRS 120 ms or more; V1 QS or rS, broad notched R in I, V5–V6, no septal Q waves
• Strict LBBB (Strauss criteria, 2011): QRS 140 ms or more in men or 130 ms or more in women, with mid-QRS notching or slurring in 2 or more contiguous leads
• Nonspecific IVCD: QRS 110 ms or more without a complete RBBB or LBBB pattern

Clinical Significance

• Alone, RBBB can be a normal variant. A new one can mean right heart strain, anterior MI or myocarditis
• Nearly every LBBB has structural heart disease behind it. Hypertensive or ischemic heart disease, cardiomyopathy and aortic valve disease are the usual suspects. It also masks ischemia on the ECG
• Rate-related BBB: Aberrant conduction that appears only at fast rates or after a long pause (Ashman phenomenon). It is not a permanent block. Compare it with a slower rhythm

Look-Alikes

• Wide-complex tachycardia with aberrancy (see Differential Diagnosis)

The left bundle branches into two fascicles. The anterior one is thin and relies mainly on the LAD. The posterior one is thick and has dual LAD and RCA supply. Block either one and the frontal-plane axis shifts, without major QRS widening.

Left Anterior Fascicular Block (LAFB)

• Axis: −45° to −90°; QRS under 120 ms
• Pattern: qR in I and aVL; rS in II, III and aVF
• Significance: The one you will see most often. Frequently benign, but it points to underlying disease

Left Posterior Fascicular Block (LPFB)

• Axis: More than +90°; QRS under 120 ms
• Pattern: rS in I and aVL; qR in III and aVF
• Significance: Rare. You arrive here only after ruling out RVH, pulmonary embolism and lateral MI (see Cardiac Axis)

Bifascicular and Trifascicular Block

• Bifascicular: RBBB plus LAFB (the most common combination) or RBBB plus LPFB
• Trifascicular: bifascicular block plus first-degree AV block. The third pathway is in danger, but that does not mean it is blocked

Separate the common block patterns by PR interval, QRS width and escape rhythm. These features matter more than how many P waves you see on one strip.

• LAFB vs. inferior MI: LAFB gives a left axis without inferior ST elevation. Inferior MI gives inferior ST changes with reciprocal changes in aVL. Lean on the 12-lead and serial ECGs.

Artifact & Lead Misplacement

• Limb lead reversal: A reversed pair of arm electrodes (for example RA and LA) inverts lead I. That can mimic an axis shift or a block pattern
• Precordial misplacement: V1 or V2 placed too high can produce an rSR′ pattern. That mimics RBBB
• Tremor, shivering or transport vibration: They can hide P waves and mimic a dropped beat. Check a second lead before you call a block

Normal Variants

• Isolated RBBB and first-degree AV block in young and athletic patients
• Wenckebach pattern during sleep or with high vagal tone

Doses below come from the 2025 AHA adult bradycardia algorithm (symptomatic bradycardia with a pulse) and the 2025 PALS pediatric bradycardia algorithm, and match the E3 atropine, epinephrine and digoxin-immune-fab pages. Follow local protocols and medical direction.

Follow local protocols and online medical direction.

Pediatrics

• Heart rate: Age-based norms are on the Vital Signs page. In PALS, you treat bradycardia when the heart rate is under 60/min with poor perfusion despite oxygenation and ventilation. If it stays under 60/min with poor perfusion despite that support, start CPR
• Usual cause: Hypoxia or increased vagal tone. Support oxygenation and ventilation first. If the heart rate stays under 60/min with poor perfusion, start CPR. Then give epinephrine 0.01 mg/kg IV/IO every 3–5 min as the first drug (see the table above). Atropine (0.02 mg/kg) is for bradycardia with compromise from increased vagal tone or AV conduction block not caused by hypoxia (2025 AHA Part 8, COR 1). Pacing is considered for block that does not respond to drugs
• Congenital heart disease: After surgery for congenital heart disease, complete block can follow. Sometimes epicardial pacing wires are in place. Check wire capture and sensing with each change
• Infants: The PR interval is shorter in infants. Do not apply adult PR thresholds without age context
• Dosing: Weight-based doses come from the Weight-Based Dosing page

Other Populations

• Pregnancy: Check electrolytes and drug effects first. Magnesium is on that list, because it can cause bradycardia and AV block. For pacing, follow the obstetric protocol
• Older adults: Degenerative conduction disease is the most common cause of new block. Symptoms can be subtle
• Athletes: First-degree AV block and Wenckebach can be normal in athletes. Assess for symptoms
• Heart transplant recipients: The sinus node is denervated. That makes atropine ineffective, and the heart rate is often fixed. If the patient is unstable, pacing is the bedside option
• Pacemaker or ICD patients: Confirm the pacing mode. A missing paced beat can look like block. Check for a pacing spike before each QRS

1. Decide whether the patient is stable or unstable before reading the strip in detail.
2. Measure the rate and check whether the P-P and R-R intervals are regular.
3. Confirm each QRS has a P wave in front of it, and find the P waves that do not conduct.
4. Measure the PR before each conducted beat and look for lengthening before the dropped beat.
5. Measure the QRS width in the widest lead.
6. Name the block, its site, and the escape rhythm and rate.
7. Act: treat an unstable patient per the table above, apply pads for unstable high-grade block, and notify cardiology for Mobitz II or complete block.

Common Pitfalls

• Calling a 2:1 block Wenckebach or Mobitz II from one conducted beat
• Waiting for atropine to work when an infranodal block needs pacing
• Giving lidocaine or another antiarrhythmic to a patient whose wide escape rhythm is keeping them alive. Lidocaine can suppress that escape. The patient then drops into asystole
• Treating electrical capture on the monitor as successful pacing when there is no pulse
• Missing a sinus pause or exit block that has no P wave in front of the pause
• Discharging a patient with Mobitz II or complete heart block without a pacing plan