Atrioventricular Block
~Introduction
Atrioventricular (AV) block is a disorder of cardiac conduction in which the electrical impulses generated by the sinoatrial (SA) node are either delayed or completely blocked as they travel through the AV node and the His–Purkinje system. This disruption interferes with the coordinated contraction of the atria and ventricles, potentially resulting in bradycardia, decreased cardiac output, syncope, or even sudden cardiac arrest depending on the severity.
AV block is an important clinical condition because it may be benign and reversible in some patients, while in others it reflects significant underlying cardiac disease requiring permanent pacemaker implantation. Understanding the mechanisms, types, causes, clinical manifestations, and management of AV block is essential in cardiology and internal medicine.
~Normal Cardiac Conduction System
To understand AV block, it is vital first to review how a normal heart conducts electrical impulses:
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Sinoatrial (SA) node – natural pacemaker of the heart, generating impulses at 60–100 bpm.
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Atria – impulses propagate through atrial myocardium, causing atrial contraction.
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Atrioventricular (AV) node – slows conduction to allow adequate ventricular filling.
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Bundle of His
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Right and Left Bundle Branches
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Purkinje fibers – ensure coordinated ventricular contraction.
AV block occurs when there is a delay or interruption specifically along the pathway from the atria to the ventricles—most commonly at the AV node, bundle of His, or bundle branches.
~Definition and Classification of Atrioventricular Block
AV block is categorized based on the degree of conduction failure and its electrocardiographic (ECG) appearance. The three main types include:
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First-Degree AV Block
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Second-Degree AV Block
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Mobitz Type I (Wenckebach)
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Mobitz Type II
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Third-Degree (Complete) AV Block
Each type carries different implications for prognosis and treatment.
~First-Degree AV Block
Definition
First-degree AV block is characterized by a prolonged PR interval (>200 ms) on ECG, indicating delayed conduction through the AV node without actual dropped beats. Every atrial impulse is conducted to the ventricles, just more slowly than normal.
Mechanism
The delay usually occurs at the AV node. It may be due to:
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Increased vagal tone
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Drugs that slow AV conduction
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Mild ischemia
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Early degenerative conduction disease
Causes
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Physiological: Athletes, high parasympathetic tone.
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Pharmacological: Beta-blockers, calcium channel blockers (verapamil, diltiazem), digoxin, amiodarone.
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Pathological: Myocarditis, inferior MI, Lyme disease, congenital heart disease, rheumatic fever.
Clinical Features
Most patients are asymptomatic, as the condition does not cause loss of ventricular beats. It is often an incidental ECG finding.
Diagnosis
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PR interval consistently >200 ms.
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Constant conduction of each P wave to QRS complex.
Management
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Reassurance for asymptomatic patients.
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Correction of reversible causes (drug adjustment, treating electrolyte disturbances).
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Rarely requires pacing unless PR interval is extremely prolonged (>300 ms) causing symptoms such as fatigue or presyncope.
~Second-Degree AV Block
In second-degree AV block, some but not all atrial impulses fail to reach the ventricles. It is subdivided into:
1. Mobitz Type I (Wenckebach)
Definition
Progressive prolongation of the PR interval until a non-conducted P wave occurs, followed by a reset of the cycle.
Mechanism
Usually due to conduction delay at the AV node.
Causes
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Increased vagal tone
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Medications (beta blockers, calcium channel blockers, digoxin)
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Inferior wall myocardial infarction
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Structural heart diseases
ECG Features
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PR interval progressively lengthens
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Eventually, a P wave is not followed by a QRS complex
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The cycle then repeats
Clinical Features
Often asymptomatic but may cause lightheadedness or fatigue in some.
Prognosis
Generally good. AV nodal Wenckebach is usually benign and may be transient.
Management
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Treat reversible causes
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Observation for asymptomatic patients
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Pacemaker only if symptoms or associated conduction disease
2. Mobitz Type II AV Block
Definition
Intermittent non-conducted P waves without progressive lengthening of PR intervals. The PR interval remains constant before and after the dropped beat.
Mechanism
Block occurs below the AV node—often in the His–Purkinje system.
Causes
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Anterior wall myocardial infarction
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Advanced degenerative disease (Lenègre’s or Lev’s disease)
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Post-cardiac surgery
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Inflammation or infiltration (sarcoidosis, amyloidosis)
ECG Features
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Sudden dropped QRS complexes
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Constant PR intervals
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May occur in fixed ratios (2:1, 3:1 conduction)
Clinical Features
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Dizziness, presyncope, syncope
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Fatigue, exercise intolerance
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Potential progression to complete heart block
Prognosis
Mobitz II is dangerous because it indicates structural disease and can progress unpredictably.
Management
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Permanent pacemaker is recommended, even if asymptomatic.
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Treat reversible contributors (e.g., ischemia).
~Third-Degree (Complete) AV Block
Definition
Complete block of conduction from atria to ventricles. No relationship exists between P waves and QRS complexes—atria and ventricles beat independently.
Mechanism
Block can occur at:
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AV node (junctional escape rhythm)
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His bundle
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Bundle branches (ventricular escape rhythm)
Causes
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Ischemic heart disease (especially inferior or anterior MI)
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Degenerative conduction disorders
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Congenital complete heart block
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Post-surgical or catheter-induced injury
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Hyperkalemia
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Lyme carditis
ECG Features
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AV dissociation
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Regular P–P intervals and regular R–R intervals, but unrelated
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Escape rhythms:
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Junctional = narrow QRS, 40–60 bpm
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Ventricular = wide QRS, 20–40 bpm
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Clinical Features
Symptoms depend on ventricular escape rate and adequacy of perfusion:
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Severe fatigue
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Dizziness or syncope (Adam–Stokes attacks)
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Hypotension
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Heart failure symptoms
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Risk of sudden cardiac arrest
Prognosis
Potentially life-threatening.
Management
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Immediate:
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Atropine (may help only if block is nodal)
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Temporary transcutaneous pacing
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Then temporary transvenous pacing
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Permanent:
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Permanent pacemaker implantation
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~Etiology of AV Block
1. Congenital Causes
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Maternal autoimmune diseases (anti-Ro/SSA, anti-La/SSB antibodies)
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Structural congenital heart disease
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Congenital AV nodal malformations
2. Acquired Causes
A. Ischemic Heart Disease
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Myocardial infarctions
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Inferior MI → AV nodal block (likely transient)
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Anterior MI → infranodal block (often permanent)
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B. Cardiomyopathies
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Dilated, hypertrophic, or infiltrative
C. Infections & Inflammation
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Lyme disease
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Myocarditis
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Rheumatic fever
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Endocarditis with abscess formation
D. Degenerative Fibrosis
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Age-related (Lev’s disease)
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Idiopathic fibrosis (Lenègre’s disease)
E. Drugs
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Beta-blockers
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Non-dihydropyridine calcium channel blockers
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Digoxin
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Amiodarone
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Adenosine (transient)
F. Metabolic and Endocrine
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Hyperkalemia
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Hypothyroidism
~Clinical Presentation of AV Block
Symptoms depend on severity
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First-degree: Usually none.
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Mobitz I: Mild dizziness, palpitations.
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Mobitz II: Presyncope or syncope.
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Third-degree: Severe bradycardia, heart failure, syncope, hypotension.
Signs
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Bradycardia
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Cannon A waves (in complete block)
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Hypotension
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Variable intensity of first heart sound
~Diagnosis of AV Block
1. Electrocardiogram (ECG)
Primary diagnostic tool.
2. Holter Monitoring
Useful for intermittent blocks or symptom correlation.
3. Electrophysiology (EP) Study
Defines exact site of block when needed.
4. Laboratory Tests
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Electrolytes
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Thyroid function tests
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Lyme serology
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Cardiac biomarkers if MI suspected
5. Imaging
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Echocardiography to assess structural disease
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Cardiac MRI in cases of infiltration or scarring
~Management of Atrioventricular Block
General Principles
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Treat underlying cause where possible.
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Distinguish benign vs. pathological types.
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Ensure hemodynamic stability.
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Consider permanent pacing when indicated.
~Treatment by Degree
First-Degree AV Block
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Observation
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Correction of reversible causes
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Avoid AV nodal blocking drugs if PR is excessively prolonged
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Rare pacing
Second-Degree AV Block
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Mobitz I:
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Observation unless symptomatic
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Usually does not need pacemaker
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Mobitz II:
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Requires permanent pacemaker
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Monitor for progression to complete block
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Third-Degree AV Block
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Emergency temporary pacing
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Followed by permanent pacemaker
~Pacemaker Indications in AV Block
Class I Indications (Strong Evidence)
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Symptomatic bradycardia due to AV block
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Mobitz II second-degree block
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Complete AV block
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AV block associated with heart failure or reduced EF
Class II Indications
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Asymptomatic high-grade AV block with recurrent pauses
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Certain congenital AV blocks
Temporary Pacing Indications
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Acute MI with high-grade AV block
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Drug toxicity (reversible)
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Hypothermia, hyperkalemia after stabilization
~Complications of AV Block
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Syncope and injury
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Heart failure
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Ventricular arrhythmias
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Sudden cardiac death (especially Mobitz II and complete block)
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Poor cardiac output leading to organ dysfunction
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Pacemaker complications (infection, lead malfunction—after implantation)
~Prognosis
Depends on type and cause
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First-degree: Excellent prognosis.
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Mobitz I: Generally benign.
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Mobitz II: Poor without pacemaker; risk of sudden progression.
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Third-degree: Serious condition; pacemaker improves survival dramatically.
The prognosis also depends on the underlying etiology, structural heart disease, and comorbidities.
~Prevention
While some causes such as congenital defects cannot be prevented, other strategies help reduce risk:
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Avoid unnecessary use of AV nodal blocking drugs
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Early treatment of Lyme disease
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Adequate management of ischemic heart disease
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Monitoring cardiac toxicity from medications
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Regular cardiac follow-up in high-risk patients
~Conclusion
Atrioventricular block represents a spectrum of conduction abnormalities ranging from benign, asymptomatic conditions to life-threatening cardiac emergencies. The classification into first-degree, second-degree (Mobitz I and II), and third-degree AV block helps guide diagnosis, risk stratification, and treatment.
While mild AV block often requires no intervention aside from observation and addressing reversible factors, higher-grade blocks—particularly Mobitz II and complete AV block—generally necessitate permanent pacemaker implantation for symptom relief and prevention of sudden cardiac death.
Timely recognition and management of AV block are critical in clinical practice. Advances in pacemaker technology and improved understanding of the underlying mechanisms continue to enhance outcomes for patients with conduction disease.
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