Heart Block

Introduction

• Heart blocks are defined as abnormal conduction of the electrical impulse from the atria to the ventricles. The condition is classified as first-degree, second-degree (Mobitz type I and type II), or third-degree (complete) heart block.
• The clinical significance of these conduction abnormalities is determined by the degree of impairment, with presentations ranging from asymptomatic delay to life-threatening bradyarrhythmias requiring emergent intervention.¹

Etiology

• Several mechanisms contribute to the development of heart block, varying from intrinsic diseases to ischemic and medication-induced causes.

Intrinsic Conduction System Disease

• The conduction system is often affected by age-related fibrosis or sclerosis. Idiopathic degeneration, including Lenègre and Lev disease, is commonly identified as the primary source of progressive conduction delay.^1-3

Ischemic Causes

• Atrioventricular (AV) nodal ischemia is frequently produced during inferior myocardial infarction (MI) and is typically transient. Injury to the His-Purkinje system usually occurs during anterior MI and is associated with permanent conduction defects and increased mortality (see below).

Medication-Induced Causes

• AV nodal conduction is often depressed by medications such as beta-blockers, calcium channel blockers, digoxin, amiodarone, and adenosine.² Conduction delay is also frequently produced by dexmedetomidine through its sympatholytic effects.

Metabolic or Systemic Causes

• Electrolyte abnormalities, particularly hyperkalemia, impair conduction. Hypo- and hyperthyroidism, hypoxia, and increased vagal tone can also contribute to the AV block.

Congenital Causes

• Congenital heart defects (e.g., L-transposition of great arteries)
• Congenital AV block is also seen in some neonates due to maternal systemic lupus erythematosus with anti-Ro/SSA or anti-La/SSB antibodies.^2,3

Infections

• Lyme carditis
• Bacterial endocarditis
• Chagas disease
• Toxoplasmosis

AV Blocks in Patients with Myocardial Ischemia

• AV block is a common complication of acute MI, and its type and prognosis depend on the infarct location.
• Inferior MI (usually right coronary artery-related) causes AV nodal block (first-degree, Mobitz I, or transient complete heart block) that is often vagally mediated, atropine-responsive, and self-limited.
• Complete heart block in inferior MI typically has a narrow-complex junctional escape rhythm and rarely requires permanent pacing.
• Anterior MI (proximal left anterior descending occlusion) causes infranodal conduction disease (Mobitz II or complete heart block) that is sudden, persistent, high risk, and frequently requires temporary or permanent pacing.⁴

Pathophysiology

• The AV node conducts electrical impulses via slow, calcium-dependent pathways that are heavily influenced by autonomic input.
• The His-Purkinje system conducts impulses rapidly through sodium-dependent channels and is highly susceptible to ischemia, fibrosis, and inflammatory injury.
• Conduction delay or interruption can occur at any level of this system, and clinical severity is determined by the anatomical location and extent of the impairment.

Types of Heart Blocks

First-Degree AV Block

• First-degree AV block is defined as a PR interval prolongation exceeding 200 milliseconds. Conduction to the ventricles is preserved, and the condition is typically considered benign.
• First-degree AV block is a misnomer. A true block is not present as each P wave is conducted.

Second-Degree AV Block – Mobitz Type I

• Mobitz type I block is characterized by progressive prolongation of the PR interval until a ventricular beat is dropped. This abnormality is usually produced within the AV node and is often transient.^1,2

Second-Degree AV Block – Mobitz Type II

• Mobitz type II block is characterized by intermittent nonconducted P waves without preceding PR interval prolongation. This condition is generally produced within the His-Purkinje system and is associated with a high risk of progression to complete heart block.⁵

Third-Degree Heart Block

• In third-degree heart block, no atrioventricular conduction is present. The atria and ventricles beat independently, and ventricular escape rhythms are often slow, unreliable, or entirely absent.^3,7

Clinical Presentation and Diagnosis

• A wide range of symptoms can result from heart blocks. Asymptomatic presentations are frequently observed in first-degree and Mobitz type I block. Fatigue, dizziness, syncope, dyspnea, and hypotension may be produced as conduction worsens. Stokes-Adams attacks may be produced in cases of complete heart block or prolonged ventricular standstill.
• The diagnosis is primarily established by an electrocardiogram. Holter monitoring is often used to detect intermittent conduction delays. Echocardiography is used to evaluate structural heart abnormalities. Laboratory evaluation is frequently performed to assess electrolytes, thyroid function, and digoxin levels when clinically relevant.^2,3

Perioperative Considerations

Preoperative Assessment

• A comprehensive assessment is recommended before anesthesia administration. The type of AV block should be identified, and the risk of progression to complete heart block should be assessed. Medications that impair conduction should be reviewed. Reversible causes should be investigated. Temporary pacing is recommended for unstable patients or patients with Mobitz type II or third-degree AV block before induction of anesthesia.^1,9
• Please see the OA summary on transcutaneous pacing. Link

Intraoperative Considerations

Monitoring

• Continuous electrocardiogram (ECG) monitoring is required throughout the perioperative period. External pacing pads are recommended for patients with high-risk conduction disease. An arterial line may be inserted in patients with significant hemodynamic instability.

Induction Agents

• Etomidate is often selected due to its minimal effect on cardiac conduction. Ketamine is frequently used in patients with bradycardia or hypotension because sympathetic tone is increased by the drug. Propofol is known to worsen bradycardia in certain patients and should be titrated cautiously.

Maintenance

• Balanced anesthesia is commonly used, with low-dose volatile agents combined with opioids. Excessive anesthetic depth is avoided because severe vagal activation or myocardial depression may be produced. Hypotension is typically treated with ephedrine or low-dose epinephrine infusions instead of pure alpha-agonists, which may worsen bradycardia.

Management of Bradycardia

• Atropine is administered when an AV nodal block is present. Epinephrine or isoproterenol infusions are used when severe bradycardia is present, and pacing is not immediately available. Transcutaneous or transvenous pacing is initiated when patients fail to respond to medical therapy.^1,9

Postoperative Care

• Continuous telemetry is recommended in the postoperative period. Temporary pacing support may be required until intrinsic conduction recovers or permanent pacing is arranged. Patients are evaluated for permanent pacemaker implantation when indicated.

Stable Patients

• Management is directed toward observation, correction of reversible causes, and adjustment of medication. Temporary pacing is considered when conduction deteriorates.

Unstable Patients

• Immediate stabilization is required. Atropine is administered when nodal blocks are suspected. Catecholamine infusions are used for hemodynamic support when bradycardia persists. Transcutaneous pacing is initiated emergently, and transvenous pacing is arranged promptly in cases of ongoing instability.

Indications for Permanent Pacing

• Permanent pacemaker implantation is recommended in symptomatic bradycardia, Mobitz type II second-degree block, persistent third-degree block, alternating bundle branch block, and sustained conduction disease following MI.⁹