eMedicine Specialties > Emergency Medicine > Cardiovascular

Heart Block, Third Degree

Author: Michael D Levine, MD, Physician, Department of Medical Toxicology, Banner Good Samaritan Medical Center
Coauthor(s): David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Apr 13, 2009

Introduction

Background

Complete heart block, also referred to as third-degree heart block, or third-degree atrioventricular (AV) block, is a disorder of the cardiac conduction system where there is no conduction through the AV node. Therefore, complete dissociation of the atrial and ventricular activity exists.¹ The ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system.² It is important to realize that not all patients with AV dissociation have complete heart block. For example, patients with ventricular tachycardia have AV dissociation, but not complete heart block; in this example, AV dissociation is due to the ventricular rate being faster than the intrinsic sinus rate. Electrocardiographically, complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves.

Pathophysiology

Complete heart block is caused by a conduction block at the level of the AV node, the bundle of His, or the bundle-branch Purkinje system. In most cases (approximately 61%), the block occurs below the His bundle. Block within the AV node accounts for approximately one fifth of all cases, while block within the His bundle accounts for slightly less than one fifth of all cases.²

Duration of the escape QRS complex depends on the site of the block and the site of the escape rhythm pacemaker.

Pacemakers above the His bundle produce a narrow QRS complex escape rhythm, while those at or below the His bundle produce a wide QRS complex.

When the block is at the level of the AV node, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats per minute. Patients with a junctional pacemaker frequently are hemodynamically stable and their heart rate increases in response to exercise and atropine.

When the block is below the AV node, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates less than 45 beats per minute. These patients generally are hemodynamically unstable and their heart rate is unresponsive to exercise and atropine.

Mortality/Morbidity

Patients with complete heart block are frequently hemodynamically unstable, and as a result, they may experience syncope, hypotension, cardiovascular collapse, or death. Other patients can be relatively asymptomatic and have minimal symptoms other than dizziness, weakness, or malaise. 

Clinical

History

Complete heart block has a wide range of clinical presentations; most patients are symptomatic.

• Patients occasionally are asymptomatic or have only minimal symptoms related to hypoperfusion. In these situations, symptoms include the following:
  • Fatigue
  • Dizziness
  • Impaired exercise tolerance
  • Chest pain
• Patients with narrow complex escape rhythms (eg, those whose escape rhythm occurs above the His bundle) are more likely to have minimal symptoms. More commonly, however, the patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating the origin of the pacemaker is below the His bundle. In such cases, symptoms can include the following:
  • Syncope
  • Confusion
  • Dyspnea
  • Severe chest pain
  • Sudden death
• Because an acute myocardial infarction is one cause of complete heart block, patients who concurrently experience an MI can have associated symptoms from the MI, including chest pain, dyspnea, nausea or vomiting, and diaphoresis.
• Patients who have a history of cardiac disease may be on medications that affect the conduction system through the AV node, including the following:
  • Beta-blockers
  • Calcium channel blockers
  • Digitalis cardioglycosides

Physical

• The physical examination findings of patients with third-degree heart block will be notable for bradycardia, which can be severe.
• Signs of congestive heart failure as a result of decreased cardiac output may be present and include the following:
  • Tachypnea or respiratory distress
  • Rales
  • Jugular venous distention
• Patients may have signs of hypoperfusion, including the following:
  • Altered mental status
  • Hypotension
  • Lethargy
• In patients with concomitant myocardial ischemia or infarction, corresponding signs may be evident on examination:
  • Signs of anxiety such as agitation or unease
  • Diaphoresis
  • Pale or pasty complexion
  • Tachypnea
• Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. This rhythm occurs because of the junctional escape rhythm.

Causes

Complete heart block can be either congenital or acquired.

• The congenital form of complete heart block usually occurs at the level of the AV node, and patients are relatively asymptomatic at rest but later develop symptoms because the fixed heart rate is not able to adjust for exertion. In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).³
• Causes of acquired complete heart block include the following:
  • Complete heart block can develop from isolated, single-agent overdose, or often from combined or iatrogenic coadministration of AV-nodal, beta-adrenergic, and calcium channel blocking agents. Drugs or toxins associated with heart block include the following:
    • Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide)
    • Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone)
    • Class II antiarrhythmics (beta-blockers)
    • Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide)
    • Class IV antiarrhythmics (calcium channel blockers)
    • Digoxin or other cardiac glycosides
  • Other causes include the following:
    • Profound hypervagotonicity
    • MI - Anterior wall MI can be associated with an infranodal complete AV block; this is an ominous finding. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and is much less dangerous, often resolving within hours to a few days.
    • Cardiomyopathy, eg, Lyme carditis, Trypanosoma cruzi infection⁴ , acute rheumatic fever
    • Metabolic disturbances, eg, severe hyperkalemia

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