ATRIOVENTRICULAR BLOCK

✓ Medically ReviewedDISEASEID: MDBT0169🚨 TRIAGE: EMERGENCYICD-10: I44.3

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Definition

CLINICAL DEFINITION

Atrioventricular (AV) block is a cardiac conduction disorder characterised by a delay or complete interruption in the transmission of electrical impulses from the atria to the ventricles through the AV node and His-Purkinje system. It is classified into first-degree (prolonged PR interval), second-degree (intermittent non-conducted P waves, subdivided into Mobitz type I and type II), and third-degree (complete dissociation between atrial and ventricular activity). The clinical significance and management depend heavily on the anatomical site of the block and the resulting ventricular escape rhythm.

IN PLAIN ENGLISH

Atrioventricular block is a condition where the electrical signals that tell the heart to beat are delayed or completely stopped as they travel from the upper chambers to the lower chambers. This can cause the heart to beat too slowly or irregularly, which may lead to dizziness, fainting, or shortness of breath depending on how severe the blockage is.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Atrioventricular block is NOT the same as sinus node dysfunction (sick sinus syndrome), which originates in the heart's natural pacemaker rather than the conduction pathway between the chambers. It is also distinct from bundle branch blocks, which affect the electrical pathways within the ventricles themselves after the signal has already passed through the AV node.

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Word Breakdown

atrio-

=atrium (from Latin 'atrium' — entrance hall)

ventr-

=ventricle (from Latin 'venter' — belly)

-ar

=pertaining to (from Latin '-aris')

Literal Meaning: Pertaining to the atrium and the ventricle

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Abbreviations

AV block=Atrioventricular block — impaired conduction from atria to ventricles

AVB=Atrioventricular block — common abbreviation in ECG reporting

1st degree AVB=First-degree atrioventricular block — delayed conduction without dropped beats

2nd degree AVB=Second-degree atrioventricular block — intermittent failure of conduction

3rd degree AVB=Third-degree atrioventricular block — complete failure of conduction, also known as complete heart block

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Synonyms & Variants

Heart Block›AV Block›Atrioventricular Conduction Block›

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Category-Specific Context

As a disease entity, atrioventricular block represents a spectrum of cardiac conduction disorders rather than a single uniform pathology. It is classified by severity (first, second, and third degree) and by the anatomical site of the conduction delay (supra-Hisian, intra-Hisian, or infra-Hisian), which directly dictates the stability of the escape rhythm and the urgency of intervention.

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Clinical Context & Usage

CLINICAL SETTINGS

Emergency DepartmentCardiology WardIntensive Care UnitGeneral Medicine WardCardiac Catheterisation Laboratory

USAGE & DOCUMENTATION NOTES

In clinical documentation and ECG reports, the degree of AV block is explicitly stated alongside the ventricular rate and the presence of escape complexes. Clinicians frequently document 'Mobitz type I' or 'Wenckebach' for progressive PR prolongation, and 'Mobitz type II' for intermittent dropped beats without PR prolongation. In critical care, the term 'complete heart block' is often used interchangeably with third-degree AV block, and the width of the escape QRS complex is documented to infer the site of the block (narrow suggests nodal, wide suggests infranodal).

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Atrioventricular block occurs when there is a functional or structural impairment in the AV node, the bundle of His, or the bundle branches, preventing normal electrical impulse transmission from the atria to the ventricles. In first-degree block, conduction is delayed, typically due to prolonged AV nodal refractoriness from high vagal tone or medications. Second-degree Mobitz type I (Wenckebach) usually reflects decremental conduction within the AV node itself, often reversible. Mobitz type II and third-degree blocks frequently involve structural disease below the AV node (infranodal), such as fibrosis or ischaemia of the His-Purkinje system. When conduction completely fails, subsidiary pacemakers in the AV junction or ventricles take over, generating an escape rhythm; the rate and stability of this escape rhythm depend on its anatomical origin, with infranodal escape rhythms being slower and highly prone to sudden failure.

PRIMARY CAUSES

Idiopathic fibrosis and sclerosis of the conduction system (Lenègre's or Lev's disease)

Progressive age-related fibrosis and calcification of the AV node and His-Purkinje system, leading to irreversible conduction failure.

Acute myocardial infarction (particularly inferior wall MI)

Ischaemia of the AV node due to occlusion of the right coronary artery or increased vagal tone (Bezold-Jarisch reflex), typically causing transient nodal block.

Medications (beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, amiodarone)

Pharmacological suppression of AV nodal conduction via sympathetic blockade, calcium channel inhibition, or direct electrophysiological toxicity.

Infective endocarditis with aortic root abscess

Extension of the perivalvular infection into the adjacent membranous septum and AV node, causing acute structural destruction and conduction block.

Cardiac sarcoidosis or amyloidosis

Infiltration of the myocardium and conduction pathways by granulomatous tissue or amyloid fibrils, disrupting electrical propagation.

Lyme carditis

Direct spirochaetal infection and subsequent inflammatory infiltrate in the AV node, often causing rapidly fluctuating degrees of block.

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Drug-Induced Causes

💊 Beta-blockers (e.g., metoprolol, bisoprolol, atenolol) ↗

Mechanism: Competitive antagonism of beta-1 adrenergic receptors reduces cAMP-mediated calcium influx in the AV node, slowing conduction velocity.

→ Withhold the offending agent; administer atropine or glucagon if haemodynamically unstable; consider temporary pacing if refractory.

💊 Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) ↗

Mechanism: Blockade of L-type calcium channels in the AV node directly impairs slow-response action potential upstroke, prolonging AV conduction.

→ Discontinue medication; provide supportive care with intravenous calcium and vasopressors if hypotensive; temporary pacing may be required for high-grade block.

💊 Cardiac glycosides (digoxin) ↗

Mechanism: Increases vagal tone and directly depresses AV nodal conduction; toxicity can cause high-grade block with increased automaticity.

→ Stop digoxin immediately; check serum levels and electrolytes; administer digoxin-specific antibody fragments (Fab) for severe toxicity or haemodynamic instability.

💊 Class III antiarrhythmics (amiodarone, sotalol, dofetilide) ↗

Mechanism: Prolongation of the action potential duration and refractory period in the AV node, which can precipitate block, especially when combined with other AV nodal blockers.

→ Cease the antiarrhythmic drug; monitor QT interval and electrolytes; provide temporary pacing if the block is infranodal or symptomatic.

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Epidemiology

Prevalence:The prevalence of first-degree AV block increases with age, affecting approximately 1-2% of young adults but rising to over 10% in individuals older than 70 years. Higher-degree AV blocks are less common in the general population but are frequently encountered in patients with structural heart disease or those undergoing cardiac surgery.

Age Group:First-degree and Mobitz type I second-degree blocks are often seen in young, healthy athletes due to high resting vagal tone, whereas second-degree Mobitz type II and third-degree blocks predominantly affect older adults due to age-related fibrosis and ischaemic heart disease.

Sex Predilection:Male

Geographic Distribution:Globally uniform in older populations with degenerative disease, but Lyme carditis-associated AV block shows distinct geographic clustering in endemic regions (e.g., Northeastern United States, Central Europe). Chagas disease is a prominent cause of AV block in rural parts of Latin America.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 EMERGENCY

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

A new-onset AV block in a patient with an aortic valve infection or recent endocarditis raises immediate concern for an aortic root abscess extending into the conduction system; this requires urgent transoesophageal echocardiography and surgical evaluation.
Fluctuating degrees of AV block in a patient with a recent tick bite or erythema migrans rash suggests Lyme carditis; this requires prompt intravenous antibiotics and monitoring, as it is often reversible but can progress to complete heart block.
Mobitz type II second-degree block or third-degree block with a wide QRS escape rhythm indicates infranodal disease, which carries a high risk of sudden asystole and mandates immediate temporary pacing rather than observation.

URGENT EVALUATION TRIGGERS

Syncope or presyncope in the presence of any degree of AV block
Ventricular rate < 40 bpm or pauses > 3 seconds on telemetry
New-onset Mobitz type II or third-degree AV block, especially with a wide QRS escape complex
AV block complicating an acute myocardial infarction
Haemodynamic instability (hypotension, altered mental status, chest pain) accompanying bradycardia

Contraindications & Precautions

CONTRAINDICATIONS

Avoid AV nodal blocking agents (beta-blockers
non-dihydropyridine calcium channel blockers
digoxin) in patients with second-degree Mobitz type II or third-degree AV block unless a functioning permanent pacemaker is in place.
Avoid carotid sinus massage or Valsalva manoeuvres in patients with suspected high-grade AV block
as enhanced vagal tone can precipitate prolonged asystole.

SPECIAL PRECAUTIONS

Monitor electrolytes closely
particularly potassium and magnesium
as imbalances can exacerbate conduction delays or precipitate escape rhythm failure.
Ensure transcutaneous pacing pads are immediately applied and connected to a defibrillator-pacemaker in the Emergency Department for any patient presenting with symptomatic bradycardia or high-grade block.
Review all medications for concealed AV nodal blocking properties
including over-the-counter or herbal supplements that may interact with prescribed cardiac drugs.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Syncope (Stokes-Adams attacks) — transient cerebral hypoperfusion due to sudden pauses or profound bradycardia from failed escape rhythms
Heart failure — chronic bradycardia reduces cardiac output
leading to compensatory ventricular dilation and eventual systolic dysfunction
Cardiogenic shock — acute high-grade block with a slow
unstable escape rhythm fails to maintain adequate end-organ perfusion
Sudden cardiac death — abrupt progression to asystole or ventricular fibrillation
particularly in infranodal blocks with unstable His-Purkinje escape pacemakers

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Reference Ranges

NORMAL RANGEThe normal PR interval is 120–200 ms (3–5 small squares on a standard ECG). First-degree AV block is defined by a PR interval > 200 ms.

CRITICAL (PANIC) VALUEA ventricular rate < 40 bpm or pauses > 3 seconds in the presence of AV block constitutes a critical value requiring immediate transcutaneous or transvenous pacing, as the escape rhythm is unstable and carries a high risk of sudden asystole.

UNIT OF MEASUREMENTMilliseconds (ms) for PR interval measurement; beats per minute (bpm) for ventricular escape rate.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Bundle Branch Block

Both involve conduction abnormalities, but bundle branch block affects the ventricles (widened QRS) while AV block affects the atria-to-ventricles transmission (abnormal PR or dropped P waves).

Sinus Arrest

Both cause bradycardia and dropped beats, but sinus arrest is a failure of the SA node to generate an impulse (missing P waves), whereas AV block is a failure to conduct an already generated P wave.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Premature Atrial Contractions (PACs)

Key Distinguishing Feature: Non-conducted PACs can mimic second-degree AV block with dropped QRS complexes, but the P wave morphology is different and occurs early, resetting the SA node.

Atrial Flutter with variable block

Key Distinguishing Feature: Presents with bradycardia and dropped ventricular beats, but the ECG shows continuous sawtooth flutter waves rather than distinct, separated P waves.

Sinus Bradycardia

Key Distinguishing Feature: Every P wave is followed by a QRS complex with a normal PR interval, whereas AV block features a prolonged PR interval or missing QRS complexes after P waves.

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Clinical Pearls

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The width of the QRS complex in third-degree AV block provides a crucial clue to the site of the block and the stability of the patient. A narrow QRS escape rhythm (typically 40–60 bpm) suggests a junctional escape pacemaker and a nodal block, which is relatively stable. A wide QRS escape rhythm (typically 20–40 bpm) indicates an infranodal (ventricular) escape pacemaker, which is highly unstable and prone to sudden failure.

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Atropine is effective for symptomatic bradycardia caused by AV nodal block (e.g., inferior MI, high vagal tone) because it reduces parasympathetic tone. However, it is generally ineffective and potentially harmful in infranodal blocks (e.g., anterior MI, Mobitz II), as increasing the sinus rate can paradoxically worsen conduction through the diseased His-Purkinje system.

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First-degree AV block is extremely common and often benign, particularly in young athletes or during sleep due to high vagal tone. However, when accompanied by a wide QRS complex or bifascicular block, it suggests extensive conduction system disease and warrants closer monitoring.

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In neonates, isolated congenital complete heart block is most frequently associated with maternal systemic lupus erythematosus or Sjögren's syndrome. Maternal anti-Ro/SSA and anti-La/SSB antibodies cross the placenta and cause irreversible immune-mediated destruction of the fetal AV node.

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Example Usage & SOAP

CLINICAL SENTENCE

"The patient's telemetry strip demonstrated third-degree atrioventricular block with a wide-complex ventricular escape rhythm at 35 bpm, prompting immediate placement of transcutaneous pacing pads and a cardiology consult for transvenous pacemaker insertion."

IN A SOAP NOTE

S: 78-year-old male presents with recurrent dizziness and a near-syncopal episode this morning. Reports fatigue over the past week. O: BP 85/50 mmHg, HR 38 bpm, RR 16, SpO2 96% on room air. JVP not elevated. Lungs clear. ECG shows P waves marching out at 80 bpm, completely dissociated from wide QRS complexes (140 ms) occurring at 38 bpm. A: Third-degree (complete) atrioventricular block with an infranodal escape rhythm, likely secondary to age-related conduction system fibrosis. Haemodynamically unstable. P: Applied transcutaneous pacing pads. Started dopamine infusion at 5 mcg/kg/min to support blood pressure. Urgent cardiology consultation for temporary transvenous pacemaker placement. Admitted to CCU.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for dropped QRS complexes on ECG: (1) Second-degree AV block (Mobitz I vs Mobitz II) — look for progressive PR prolongation vs constant PR interval; (2) Non-conducted premature atrial contractions (PACs) — look for early, abnormal P waves hiding in the preceding T wave; (3) Atrial flutter with variable block — look for continuous sawtooth baseline rather than discrete P waves.

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Prognosis

SHORT-TERM OUTCOME

First-degree and Mobitz type I blocks are usually benign and self-limiting if triggered by reversible causes (e.g., medications, high vagal tone). Acute third-degree block requires immediate stabilisation with pacing; short-term mortality is high if associated with massive anterior myocardial infarction, but excellent if successfully paced and the underlying cause is reversible.

LONG-TERM PROGNOSIS

Patients with irreversible third-degree or Mobitz type II block require permanent pacemaker implantation, which restores normal life expectancy and prevents syncope. However, chronic right ventricular pacing can induce pacing-induced cardiomyopathy in a subset of patients over the long term, necessitating upgrade to cardiac resynchronisation therapy or conduction system pacing.

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References & Coding

ICD-10 DIAGNOSTIC CODE

I44.3

LITERATURE CITATIONS & GUIDELINES

[1]Kusumoto FM et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. Circulation. 2019;139(19):e263-e334.

[2]Glikson M et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J. 2021;42(35):3427-3520.

[3]Issa ZF et al. Bradyarrhythmias and Atrioventricular Block. In: Libby P et al., editors. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 12th ed. Elsevier; 2022.

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