Heart Blocks Reference

What it is: Delayed AV conduction — every impulse reaches the ventricles, just more slowly than normal. Not a true “block.”

Common causes: Increased vagal tone, beta-blockers, calcium channel blockers, inferior MI, digoxin, electrolyte abnormalities, aging.

Clinical significance: Usually benign. No treatment required in isolation. Monitor for progression, especially after inferior MI or with new medications.

What it is: Progressive AV node fatigue leads to increasing conduction delay until one impulse is completely blocked (dropped QRS), after which the cycle resets. The pattern is cyclical and recognizable.

Key ECG finding: PR interval lengthens with each beat until a P wave occurs with no following QRS, then the cycle repeats. The RR interval shortens before the dropped beat.

Common causes: Inferior MI (RCA territory), increased vagal tone, beta-blockers, digitalis toxicity.

Clinical significance: Generally benign, especially if asymptomatic. Rarely progresses to complete heart block. Monitor closely in inferior MI.

What it is: Intermittent failure of conduction below the AV node (in the bundle of His or bundle branches). Unlike Mobitz I, there is no warning — the PR interval stays constant until a beat is suddenly dropped.

Key ECG finding: PR interval is constant (may be normal or prolonged). QRS complexes are dropped without a pattern — unpredictably. QRS is often wide, indicating infranodal block.

Common causes: Anterior MI, structural heart disease, cardiomyopathy, Lyme disease, post-cardiac surgery.

Clinical significance: High risk. Can progress rapidly to complete heart block. Requires urgent provider notification. Transcutaneous pacing should be at the bedside; permanent pacemaker is typically indicated.

What it is: Complete failure of AV conduction. The atria and ventricles fire completely independently — atrial impulses never reach the ventricles. A ventricular escape rhythm takes over to maintain cardiac output, typically at a slow rate of 20–40 bpm.

Key ECG findings:

• P waves present at a normal or faster atrial rate — they march through the QRS without relationship
• QRS complexes at a slower, regular ventricular escape rate (20–40 bpm if ventricular escape; 40–60 bpm if junctional escape)
• Wide QRS (if ventricular escape pacemaker) or narrow QRS (if junctional escape)
• The PR interval varies with each beat — no fixed relationship between P waves and QRS complexes

Common causes: Inferior or anterior MI, degenerative conduction system disease (Lev's/Lenegre's disease), Lyme disease, digoxin toxicity, post-cardiac surgery, hyperkalemia.

Clinical significance: Medical emergency. Patients are often symptomatic: hemodynamic instability, syncope, altered mental status, shock. Requires immediate provider notification, transcutaneous pacing, and preparation for transvenous or permanent pacemaker insertion.