Third-Degree Atrioventricular Block (Complete Heart Block) Clinical Presentation

Updated: Jul 29, 2022
  • Author: Akanksha Agrawal, MD; Chief Editor: Jeffrey N Rottman, MD  more...
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Third-degree atrioventricular (AV) block (complete heart block) has a wide range of clinical presentations. Occasionally, patients 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, patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating that 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 (MI) can cause 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. Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death.

Patients who have a history of cardiac disease may be on medications that affect the conduction system through the AV node (AVN), including the following:

  • Beta-blockers

  • Calcium channel blockers

  • Digitalis cardioglycosides

The patient’s history of cardiac interventions should be carefully investigated; aortic valve surgery, septal alcohol ablation, proximal anterior descending artery stenting (complicated by compromised flow in the first septal perforator branch), and ablation of the slow or fast pathway of the AVN all may result in third-degree AV block.


Physical Examination

Initial triage of patients with third-degree atrioventricular (AV) block (complete heart block) consists of determining symptoms, assessing vital signs, and looking for evidence of compromised peripheral perfusion. In particular, the physical examination findings of patients with third-degree AV block will be notable for bradycardia, which can be severe.

Careful examination of the neck veins can often show evidence of cannon ‘a’ waves. A variable intensity S1 may be heard on auscultation. In addition, the pulse rate may be slow. If the slow rate or loss of atrial contraction prior to ventricular contraction has caused heart failure, then venous pressures will be elevated, including the jugular venous pressure.

Any new murmurs or gallops should be noted, because strong associations exist between cardiomyopathies, mitral calcification, aortic calcification, or endocarditis and complete AV block. If heart failure is present as evidenced by rales, an S3 gallop, peripheral edema, or hepatomegaly, then a more compelling need for immediate pacing exists.

Because endocarditis, rheumatic fever, and Lyme disease cause heart block, pay attention to any signs of infection or skin rashes during the general examination. This is particularly true in endemic areas for Lyme disease.

Neurologic examination may provide clues to the etiology of AV block because neuromuscular disease, especially myotonic dystrophy and Duchenne muscular dystrophy, can cause AV block.

Signs of congestive heart failure as a result of decreased cardiac output may be present and may 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 myocardial infarction (MI), corresponding signs such as the following may be evident on examination:

  • Signs of anxiety (eg, agitation, 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.