AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 disassociation of the atrial and ventricular activity exists. The ventricular escape mechanism can occur anywhere from the AV node to the bundle-branch Purkinje system. It is important to realize, however, that not all patients with AV dissociation have complete heart block. For example, patients with accelerated junctional rhythms have AV dissociation, but not complete heart block, if the escape rate is 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.

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, the patient may experience syncope, cardiovascular collapse, or death.

CLINICAL

Section 3 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 will be notable for bradycardia, which can be quite 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 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).
• 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
  • Infectious causes include the following:
    • Profound hypervagotonicity
    • MI - Anterior wall MI can be associated with an infranodal AV block. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and often resolves within hours to a few days.
    • Cardiomyopathy, eg, Lyme carditis and acute rheumatic fever
    • Metabolic disturbances, eg, severe hyperkalemia

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Bradycardia with a ventricular escape
Bradycardia with a junctional escape
Accelerated junctional escape rhythm

WORKUP

Section 5 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• Serum electrolytes levels, including potassium and magnesium, to look for metabolic imbalance, indications of renal insufficiency or failure, and particularly for severe hyperkalemia.
• A digoxin level should be obtained for patients on digoxin or in whom ingestion of digoxinlike compounds (eg, Lily of the Valley, Oleander, Foxgrove, Bufonidae toads) is suspected.
• Lyme titers should be obtained from patients who might have been exposed to Lyme disease. Remember that cardiac manifestations of Lyme disease are delayed, so Lyme-induced heart block can occur during any season.
• Myocarditis-related laboratory studies should be performed in patients suspected of having myocarditis. Such studies include Lyme titers, HIV serologies, enterovirus polymerase chain reaction (PCR), adenovirus PCR, and Chagas titers, as clinically appropriate.
• For most patients with illness serious enough to cause third-degree AV block, a complete blood count is indicated to screen for coincident problems (eg, anemia, infection) that may require ED intervention.

Imaging Studies

• A chest radiograph should be obtained.
• If myocarditis or a pericardial effusion is a concern, an echocardiogram should be performed.

Other Tests

• Cardiac enzymes are indicated for any patient with suspected myocardial ischemia.
• All patients must have at least one 12-lead electrocardiogram. Ideally, serial electrocardiograms should be performed.

Procedures

• Cardiac pacing may be initially indicated or may be indicated if a patient deteriorates. Because the situation may be urgent, all patients should have transcutaneous pacing pads applied.
• • For patients who are symptomatic (dyspnea, chest pain, myocardial ischemia or MI, CHF, altered mental status), the transcutaneous pacer should be activated immediately. If the external pacer fails to capture, a transvenous pacer should be inserted emergently.
  • For patients who are asymptomatic, the transcutaneous pacer should be tested. If the external pacer fails to capture, urgent placement of a transvenous pacer should be considered. Indications for placement would include bradycardia that is ineligible or unresponsive to treatment with medications.

TREATMENT

Section 6 of 11  

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Prehospital Care

• All patients should be rapidly transported to the nearest available facility, applying advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols.
• For any symptomatic patient, transcutaneous pacing is the treatment of choice.
• In all patients, oxygen should be administered and intravenous access should be established.
• Maneuvers that are likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli) should be avoided.
• Atropine can be administered but should be given cautiously, because it is likely to be ineffective in a wide complex QRS rhythm and can be dangerous if the patient is having a concurrent MI.

Emergency Department Care

• Treatment in the ED should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an intravenous line, frequent monitoring of blood pressures, and continuous cardiac monitoring.
• AV nodal agents should be withheld, and anti-ischemic therapy should be started, when appropriate.
• Transcutaneous pacing pads should be applied and tested, if not already done so.
• As stated above, patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker, even if the patient is asymptomatic.
• Hemodynamically stable patients in whom transcutaneous pacing can be successfully performed can go to a telemetry or intensive care unit at the discretion of the treating cardiologist.
• Hemodynamically unstable patients may be treated with atropine. However, if the rhythm is a wide complex escape rhythm, atropine is likely to be unsuccessful. In addition, caution should be taken when administering atropine to a patient with a suspected acute MI, as the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Similarly, isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy.
• Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the ED.

Consultations

• Cardiologic consultation is indicated for all patients with third-degree AV block. The consultation is urgent in patients with concomitant acute MI, active myocardial ischemia, CHF, wide complex escape rhythm, or symptoms of hypoperfusion because patients in this group may require early placement of a permanent pacemaker or assistance may be needed if difficulty is encountered obtaining capture from an external or transvenous pacer.

MEDICATION

Section 7 of 11  

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The goal of therapy is to improve conduction through the AV node by reducing vagal tone via atropine-induced receptor blockade. However, this method is unlikely to be successful in wide-complex bradyarrhythmias, where the level of the block is below the level of the AV node, and this method should be given with caution in patients suspected of experiencing an MI. In addition, atropine is ineffective in patients with a deinnervated heart (eg, those patients who are post cardiac transplant).

Cases where complete heart block results from calcium channel blocker should be managed in the standard fashion for other etiologies of third-degree block (eg, pacemaker) but should also receive appropriate treatment for calcium channel blockers. This therapy includes the administration of IV fluids, calcium, glucagons, vasopressors, and high-dose insulin (hyperinsulinemic euglycemia [HIE] therapy). Further explanations of calcium channel blocker overdose can be found in the article on Toxicity, Calcium Channel Blocker. Overdoses on beta-blockers are managed a similar fashion as calcium channel blockers (see Toxicity, Beta-blocker, although HIE therapy for beta-blocker overdoses is less well established.

Drug Category: Anticholinergic agents

These agents improve conduction through the AV node by reducing vagal tone via muscarinic receptor blockade.

Drug Category: Catecholamines

These agents improve hemodynamics by acting on the beta-adrenergic receptors to increase the heart rate and contractility, and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.

Drug Category: Antidotes

These agents are used in select cases for patients with third-degree block secondary to digoxin toxicity. They should receive digoxin-specific antidote.

Drug Category: Sympathomimetic agents

These agents act on beta-adrenergic receptors and increase heart rate and contractility.

FOLLOW-UP

Section 8 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.
• All patients with third-degree heart block need to be admitted to either a telemetry floor (if hemodynamically stable and transcutaneous pacing achieves capture) or an intensive care unit. The decision on telemetry versus intensive care should be made in conjunction with the cardiologist.
• Any patient who is hemodynamically unstable, has persistent complete heart block, has electrolyte abnormalities, or who is in complete heart block as a result of an overdose or myocardial infarction should be admitted to the intensive care unit.

Transfer

• Patients may be transferred to a higher level of care if the hospital does not have intensive care capabilities or if appropriate consultation services (eg, cardiology) are not available.

Deterrence/Prevention

• Patients with renal insufficiency or failure, dehydration, and certain electrolyte disturbances are predisposed to develop digoxin toxicity. Careful monitoring of electrolytes, drug levels, and renal function is essential in patients on chronic digoxin therapy.
• Patients on multiple nodal agents (eg, beta-blockers and calcium channel blockers) are at an increased risk to develop complete heart block; the more nodal blockade that occurs, the higher the chance of developing complete heart block.

Complications

• Complications from complete heart block include cardiovascular collapse and death.
• Ventricular arrhythmias from atropine or catecholamines may occur.
• Common complications include those related to line and/or transvenous pacemaker placement. These complications include arterial injury, hemothorax, pneumothorax, or cardiac tamponade.

Patient Education

• Patients should be educated about possible drug interactions when starting any new medication.
• Patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity.

MISCELLANEOUS

Section 9 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to initiate temporary transcutaneous or transvenous pacing in a timely fashion
• Failure to interpret cardiac dysrhythmia correctly
• Failure to diagnose and treat underlying etiology of the third-degree block
• Failure to ensure the patient is admitted to an appropriate level of care
• Failure to seek, identify, or treat reversible causes of third-degree AV block, such as hyperkalemia or digoxin toxicity

MULTIMEDIA

Section 10 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  This electrocardiogram demonstrates a patient in complete heart block.
	View Full Size Image
Media type:  ECG

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part III. Adult advanced cardiac life support. JAMA. Oct 28 1992;268(16):2199-241. [Medline].
• Bestetti RB, Cury PM, Theodoropoulos TA, Villafanha D. Trypanosoma cruzi myocardial infection reactivation presenting as complete atrioventricular block in a Chagas' heart transplant recipient. Cardiovasc Pathol. Nov-Dec 2004;13(6):323-6. [Medline].
• Costedoat-Chalumeau N, Georgin-Lavialle S, Amoura Z, Piette JC. Anti-SSA/Ro and anti-SSB/La antibody-mediated congenital heart block. Lupus. 2005;14(9):660-4. [Medline].
• Denes P. Atrioventricular and intraventricular block. Circulation. Apr 1987;75(4 Pt 2):III19-25. [Medline].
• International Laison Committee on Resuscitation. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Part 4: Advanced life support. Resuscitation. Nov-Dec 2005;67(2-3):213-47. [Medline].
• Rowland E, Morgado F. Sino-atrial node dysfunction, atrioventricular block and intraventricular conduction disturbances. Eur Heart J. Dec 1992;13 Suppl H:130-5. [Medline].
• Syverud S. Cardiac pacing. Emerg Med Clin North Am. May 1988;6(2):197-215. [Medline].
• Trigano JA, Birkui PJ, Mugica J. Noninvasive transcutaneous cardiac pacing: modern instrumentation and new perspectives. Pacing Clin Electrophysiol. Nov 1992;15(11 Pt 2):1937-43. [Medline].

Article Last Updated: Sep 5, 2006