Third-Degree Atrioventricular Block (Complete Heart Block)

Background

Third-degree atrioventricular (AV) block, also referred to as third-degree heart block or complete heart block (CHB), is an abnormal heart rhythm resulting from a defect in the cardiac conduction system in which there is no conduction through the atrioventricular node (AVN), leading to complete dissociation of the atria and ventricles.^{[1, 2]} The ventricular escape mechanism can occur anywhere from the AVN to the bundle-branch Purkinje system.^[3]

Third-degree AV block is electrocardiographically characterized by:

1. Regular P-P interval
2. Regular R-R interval
3. Lack of an apparent relationship between the P waves and QRS complexes
4. More P waves are present than QRS complexes

Note 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. On electrocardiography (ECG), complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves (see the image below).

View Image

Electrocardiogram from patient in complete heart block.

AV block results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block can be either congenital or acquired. (See Etiology.)

Initial triage of patients with 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. (See Presentation.)

Treatment of third-degree AV block is based on the level of the block. The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Medical treatment of complete heart block is limited to patients with conduction disease in the AVN. (See Treatment.)

Initial treatment efforts should focus on assessing the need for temporary pacing and initiating the pacing. Most patients whose heart block is not otherwise treatable will require placement of a permanent pacemaker or an implantable cardioverter defibrillator (ICD).

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Pathophysiology

In the heart, normal impulse initiation begins in the sinoatrial node (SAN). The excitation wave then travels through the atrium. During this time, surface electrocardiographic (ECG) recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the atrioventricular node (AVN). The AVN then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles.

During atrial, AVN, and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, atrioventricular (AV) block can be classified into first-, second-, and third-degree block.

First-degree AV block

First-degree AV block is a condition in which a 1:1 relationship exists between the P waves and QRS complexes, but the PR interval is longer than 200 msec. Thus, first-degree AV block represents delay or slowing of conduction. Occasionally, first-degree AV block may be associated with other conduction disturbances, including bundle-branch block and fascicular blocks (bifascicular or trifascicular block).

Second-degree AV block

Second-degree AV block exists when more P waves than QRS complexes are seen on the ECG, but a relationship between the P waves and QRS complexes still exists. In other words, not all P waves are followed by QRS complexes (conducted). Traditionally, this type of AV block is divided into two main subcategories, Mobitz type I (Wenckebach) and Mobitz type II.

In the Mobitz I second-degree AV block, the PR interval is prolonged until the P wave is not followed by a QRS complex. In a typical Mobitz I block, the PR interval prolongation from beat to beat is greatest in the first interval and progressively less with subsequent intervals. This is reflected in shortening of the R-R interval and an increase in the overall PR interval. Also, the R-R interval enveloping the pause is less than twice the duration of the first R-R interval following the pause.

On the ECG tracing, Mobitz I second-degree AV block results in the characteristic appearance of grouping beats; conversely, the presence of grouped beats should prompt a careful evaluation for Wenckebach conduction (although it should be noted that not all such conduction is pathologic).

In Mobitz II second-degree AV block, the PR interval is constant, but occasional P waves are not followed by the QRS complexes (nonconducted). Occasionally, the first PR interval following nonconducted P waves may be shorter by as much as 20 msec.

To differentiate between Mobitz I block and Mobitz II block, at least three consecutive P waves must be present in the tracing. If only every other P wave is conducted (2:1), a second-degree block cannot be classified into either of these categories and thus is best described as a 2:1 AV block, unless the mechanism can be inferred from surrounding patterns of atrial-to-ventricular conduction.

An AV block resembling second-degree AV block has been reported with sudden surges of vagal tone associated with cough, hiccups, swallowing, carbonated beverages, pain, micturition, or airway manipulation in otherwise healthy subjects. The distinguishing feature is simultaneous slowing of the sinus rate. This condition is paroxysmal and benign, but it must be carefully differentiated from a true second-degree AV block because the prognosis is very different.

Third-degree AV block

Third-degree AV block (complete heart block) exists when there are more P waves than QRS complexes, and there is no relationship between them (ie, no conduction). The conduction block may be at the level of the AVN, 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, whereas block within the His bundle accounts for slightly fewer than one fifth of all cases.^[3]

The 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, whereas those at or below the His bundle produce a wide QRS complex.

When the block is at the level of the AVN, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats/min. 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 AVN, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates slower than 45 beats/min. These patients generally are hemodynamically unstable, and their heart rate is unresponsive to exercise and atropine.

AV dissociation

AV dissociation is present when atrial and ventricular activation are independent of each other. It can result from complete heart block or from physiologic refractoriness of conduction tissue. AV dissociation can also occur in a situation when the atrial/sinus rate is slower than the ventricular rate (eg, with accelerated junctional tachycardia and ventricular tachycardia).

Occasionally, the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; only careful examination of the long rhythm strip may reveal a variation in the PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of the atrial/sinus rate will result in restoration of normal conduction.

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Etiology

Atrioventricular (AV) block results from various pathologic states that cause infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block (complete heart block) can be either congenital or acquired.

The congenital form of complete heart block usually occurs at the level of the AVN. 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).^[4]  Patients with L-transposition of the great arteries and two normally sized ventricles, as well as those with L-looped single-ventricle L-transposition of the great arteries, are at risk for spontaneous complete heart block and should undergo routine screening for complete heart block.^[5]

Common causes of acquired AV block are as follows:

• Drugs (see below)
• Degenerative diseases: Lenègre disease (sclerodegenerative process involving only the conduction system) and Lev disease (calcification of the conduction system and valves), noncompaction cardiomyopathy, nail-patella syndrome, mitochondrial myopathy^[6]
• Infectious causes: Lyme borreliosis (particularly in endemic areas), Trypanosoma cruzi infection,^[7] rheumatic fever, myocarditis, Chagas disease, Aspergillus myocarditis, varicella-zoster virus infection,^[8] valve ring abscess
• Rheumatic diseases: Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma
• Infiltrative processes: Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myeloma
• Neuromuscular disorders: Becker muscular dystrophy, myotonic muscular dystrophy
• Ischemic or infarctive causes: AV node (AVN) block associated with inferior wall myocardial infarction (MI), His-Purkinje block associated with anterior wall MI (see below)
• Metabolic causes: Hypoxia, hyperkalemia, hypothyroidism
• Toxins: “Mad” honey (grayanotoxin), cardiac glycosides (eg, oleandrin), and others
• Phase IV block (also known as bradycardia-related block)
• Iatrogenic causes (see below)

Drugs

Complete heart block can develop from an isolated single-agent overdose or—as is often the case—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; patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity

Myocardial infarction

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.

Studies suggest that AV block rarely complicates MI.^{[9, 10]} With an early revascularization strategy, the incidence of AV block decreased from 5.3% to 3.7%. Occlusion of each of the coronary arteries can result in development of conduction disease despite a redundant vascular supply to the AVN from all coronary arteries.

In a study that evaluated complete AV block in 4,799 Portugese patients with acute coronary syndrome (ACS), investigators noted 1.9% (n = 91) had complete AV block, of whom 86.8% had ST-segment elevation MI (STEMI), including 79.1% with confirmed inferior STEMI.^[11]  Compared to the patients with ACS without AV block, those with complete AV block had right ventricular MI more often, as well as worse outcomes during hospitalization (higher incidence of cardiogenic shock, ventricular arrhythmias, need for invasive mechanical ventilation, death).^[11]

Most commonly, occlusion of the right coronary artery (RCA) is accompanied by AV block. In particular, the proximal RCA occlusion has a high incidence of AV block (24%) because there is involvement not only of the AV nodal artery but also of the right superior descending artery, which originates from the very proximal part of the RCA.

In most cases, AV block resolves promptly after revascularization, but sometimes the course is prolonged. Overall, the prognosis is favorable. However, AV block in the setting of occlusion of the left anterior descending artery (particularly proximal to the first septal perforator) has a more ominous prognosis and usually calls for pacemaker implantation. Second-degree AV block associated with bundle-branch block and in particular with alternating bundle-branch block is an indication for permanent pacing.

Iatrogenic etiologies

AV block may be associated with aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention (PCI) to the left anterior descending artery, or ablation of the slow or fast pathway of the AVN. Placement of catheters that mechanically interfere with one fascicle when conduction is already impaired in the remaining conduction system (eg, bumping the right bundle with a pulmonary artery catheter in a patient with existing left bundle-branch block) almost always resolves spontaneously.

AV block after cardiac surgery is seen in 1%-5.7% of patients.^[12]  The incidence of postoperative complete heart block has remained relatively stable over the past decade, but it is highly associated with surgeries involving repair of a ventricular septal defect.^[13]  Patients may have late loss or late recovery of AV conduction.^[13]

Major risks factors identified for the need for permanent pacing are aortic valve surgery,^[14] preexisting conduction disease (either right or left bundle-branch block), bicuspid aortic valve, annular calcification, and female sex. The time course for recovery varies widely, with a significant portion of patients recovering during the 48 hours following surgery. Available evidence suggests that if no recovery in AV conduction is seen by postoperative day 4 or 5, a pacemaker should be implanted.

Data from the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) Trial, in which 3,115 patients with STEMI underwent PCI, revealed that independent predictors of high-grade AV block included increased age, diabetes mellitus, right coronary artery occlusion, sum of ST-segment deviation, and baseline Thrombolysis In Myocardial Infarction (TIMI) flow 0/1.^[15] Mortality was also significantly higher in those with high-grade AV block at 1 year but not at 30 days or 3 years, even after primary PCI.

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Epidemiology

In the United States, the prevalence of third-degree atrioventricular (AV) block (complete heart block) is 0.02%. Worldwide, the prevalence of third-degree AV block is 0.04%.^[16]

The incidence of AV conduction abnormalities increases with advancing age, resembling the age-related incidence of ischemic heart disease. An early peak in incidence occurs in infancy and early childhood due to congenital complete AV block, which is sometimes not recognized until childhood or even adolescence.

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Prognosis

Patients with third-degree atrioventricular (AV) block (complete heart block) are frequently hemodynamically unstable; 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.

Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. The cause of death may often be tachyarrhythmias precipitated by the secondary changes in ventricular repolarization (QT prolongation) due to the abrupt changes in rate.

Some patients may develop polymorphic ventricular tachycardia when significant bradycardia is present. This is related to prolongation of repolarization with extremely slow rates. This mechanism is also mostly responsible for death in these patients.

When treated with permanent pacing, the prognosis is excellent for patients with third-degree AV block. The complications related to pacemaker insertion are rare (< 1%). 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.

Complications

Complications include the following:

• Sudden cardiac death due to asystole
• Syncope
• Musculoskeletal injuries secondary to fall after syncope.

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Patient Education

Educate patients that third-degree atrioventricular (AV) block (complete heart block) occurs when the electrical signal starting from the heart's upper chambers, the atria, cannot pass normally to the lower chambers, the ventricles. This can occur spontaneously, due to certain medical conditions, medications, or postoperatively. 

Discuss signs and symptoms with patients, including lightheadedness, palpitations (skipping, fluttering in the chest), fatigue, chest pressure or pain, shortness of breath, or fainting spells. Occasionally, patients can be asymptomatic. 

Explain that the diagnosis is made using one or more of the following: electrocardiography (ECG/EKG), holter monitoring, an event recorder, electrophysiologic study, etc, and that treatment usually includes implantation of pacemaker.

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History

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.

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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.

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Laboratory Studies

For most patients with illness serious enough to cause third-degree atrioventricular (AV) block (complete heart block), a complete blood cell (CBC) count is indicated to screen for coincident problems (eg, anemia, infection) that may require emergency intervention. The presence of fever or an elevated white blood cell (WBC) count should be evaluated with blood cultures because endocarditis can be complicated by heart block.

Serum concentrations of electrolytes, including potassium and magnesium, should be measured to look for metabolic imbalance, indications of renal insufficiency or failure, and particularly for severe hyperkalemia. The prothrombin time and activated partial thromboplastin time should also be routinely obtained.

A digoxin level should be obtained for patients on digoxin or in whom ingestion of digoxinlike compounds (eg, lily of the valley, oleander, foxglove, Bufonidae toads) is suspected. The same should be done for any other drugs the patient is taking that are capable of causing AV block. Note that the presence of a detectable digoxin level following a nondigoxin cardiac glycoside ingestion can only confirm the presence of such a toxin. The digoxin level does not correlate to the degree of cardiac glycoside toxicity following nondigoxin-induced cardiac glycoside ingestions.

Myocarditis-related laboratory studies should be performed in patients suspected of having myocarditis. Such studies include Lyme titers, human immunodeficiency virus (HIV) serologies, enterovirus polymerase chain reaction (PCR), adenovirus PCR, and Chagas titers, as clinically appropriate.

Lyme titers should be obtained from all patients who may have been exposed to Lyme disease. Because cardiac manifestations of Lyme disease are delayed, Lyme-induced heart block can occur during any season. The decision to perform serologic testing for Lyme disease or any of the collagen vascular diseases depends on other associated history and findings.

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Imaging Studies

Radiography

A chest radiograph should be obtained in patients with suspected third-degree atrioventricular (AV) block (complete heart block).

Echocardiography

If the clinical examination findings or patient history suggest cardiomyopathy or valvular disease, then transthoracic echocardiography (TTE) should be performed. Specific etiologies (eg, valve ring abscess) may call for transesophageal echocardiographic (TEE) imaging. A determination of left ventricular function by means of echocardiography or another technique can help in determining whether a pacemaker or defibrillator should be implanted for the treatment of the heart block.

In a study that evaluated the correlations between interventricular mechanical delay (IVMD) and cardiac function in 13 Japanese cases of pediatric isolated complete AV block and epicardial pacing at the left ventricle, right ventricle, or both, investigators found an association between left-sided contraction delay and poor left ventricular contraction and impaired left ventricular synchrony.^[17] The investigators noted that the use of IVMD could help stratify patients during follow-up.

Computed tomography (CT) scanning

TTE alone may not be sufficient to detect cardiac and chest abnormalities or correctly identify organic disease in those with second- or third-degree AV block. CT scanning alone or in combination with TTE appears to appropriately identify patients with third- and second-degree AV block but not Wenckebach type.^[18]

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Electrocardiography

The most important study in patients with suspected third-degree atrioventricular (AV) block (complete heart block) is 12-lead electrocardiography (ECG). On 12-lead ECG, third-degree AV block is characterized by complete lack of conduction (no P waves cause a QRS complex). If complete AV block exists, then the R-R interval is very regular; therefore, before diagnosing third-degree AV block, the R-R interval should be either marched out or measured. If high-grade AV block exists without complete heart block, then some irregularity may occur during intervals following conducted P waves.

As discussed under Etiology, various pathologic conditions can cause conduction system disease and heart block. These systemic or myocardial diseases rarely present as conduction block, with the exception of Lyme disease, inferior myocardial infarction (MI), and some of the neuromuscular diseases. Unless suggested by the patient's history, examination findings, family history, risk factors, or 12-lead ECG findings, the authors do not screen for underlying pathology.

Surface ECG and review of prior ECG data can provide important clues to the level of third-degree AV block. The assessment can begin with a review of the current QRS width and morphology, comparing the QRS during heart block to the QRS when conduction was occurring (see the image below).

View Image

ECG before and after complete heart block at the AV nodal level.

If the QRS is narrow (< 120 msec) during conducted beats and narrow with the same morphology during escape beats, then the block is in the AV junction. If the conducted QRS was narrow at baseline and is wide during the escape rhythm (see the image below), then this is likely a distal level of block located anatomically in the His bundle or in both right and left bundles.

View Image

Complete heart block with wide complex escape.

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Other Studies

If the patient's clinical history or 12-lead electrocardiographic (ECG) findings suggest active coronary artery disease, then measurement of cardiac enzyme levels and an evaluation of ischemia, including either cardiac catheterization or stress testing, are needed.

Ambulatory monitoring may be performed to document transient heart block or other bradyarrhythmias in patients presenting with symptoms suggestive of bradycardia.

Diagnostic electrophysiologic studies can be performed to assess atrioventricular (AV) conduction and to discern the level of block (AV nodal or infranodal) when necessary.

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Approach Considerations

New-onset third-degree atrioventricular (AV) block (complete heart block) is a medical emergency. Treatment of third-degree AV block is based on the level of the block. A common misconception of an inexperienced clinician is to gauge a patient’s stability according to the heart rate and blood pressure rather than according to the symptoms and level of the block.

An asymptomatic patient with inferior wall myocardial infarction (MI) causing complete heart block at the AV node (AVN) level and a heart rate of 35 beats/min is at very little immediate risk. A patient in the acute phase of an anterior wall MI with intermittent distal high-grade block is at immediate danger of impending asystole and requires immediate preparation for pacing of some kind, even though the heart rate between asystolic episodes may be 90 beats/min.

The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Many antihypertensive, antianginal, antiarrhythmic, and heart failure medications cause AV block that resolves after withdrawal of the offending agent.

Review patient medication lists upon presentation to help rule out medication-induced or medication-aggravated heart block. Common drugs that induce AV block include beta-blockers, calcium channel blockers, antiarrhythmics, and digoxin. Withdrawal of the offending drugs is the first treatment for heart block.

Cases in which complete heart block results from a calcium channel blocker should be managed in much the same fashion as cases involving other causes of third-degree block (eg, pacemaker), but affected patients should also receive appropriate treatment for toxicity from calcium channel blockers. This therapy includes the administration of intravenous (IV) fluids, calcium, glucagons, vasopressors, and high-dose insulin (hyperinsulinemic euglycemia [HIE] therapy). (See Toxicity, Calcium Channel Blocker.)

Overdoses of beta-blockers are managed similarly to overdoses of calcium channel blockers, although HIE therapy for beta-blocker overdoses is less well established. (See Toxicity, Beta-blocker.)

Medical treatment of complete heart block is limited to patients with conduction disease in the AVN. Patients with block at the AVN level, in the absence of ischemia, can benefit from sympathomimetic agents or vagolytic agents.

Initial efforts should focus on assessing the need for temporary pacing and initiating the pacing. Except in the case of AV block caused by medications that can be withdrawn or infections that can be treated, most patients with acquired complete heart block will require a permanent pacemaker or an implantable cardioverter defibrillator (ICD).

A study by Zhao et al in 38 patients who underwent dual-chamber pacemaker implantation for third-degree AV block found that compared with those who underwent implantation in the right ventricular apex, patients whose pacemaker was implanted in the right ventricular outflow tract exhibited better results with regard to systolic function and systolic dyssynchronization, at 12-month follow-up.^[19]

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Initial Management Considerations

All patients with suspected third-degree atrioventricular (AV) block (complete heart block) should be rapidly transported to the nearest available facility, receiving advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols. In all patients, oxygen should be administered and intravenous (IV) access established. Avoid maneuvers likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli). Atropine can be administered but should be given cautiously.

Treatment in the emergency department (ED) should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an IV line, frequent monitoring of blood pressure, and continuous cardiac monitoring. Transcutaneous pacing pads should be applied and tested, if this has not already been done.

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 (ICU). The decision between the two locations 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 ICU.

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.

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Atropine and Transcutaneous/Transvenous Pacing

Transcutaneous pacing is the treatment of choice for any symptomatic patient. All patients who have third-degree atrioventricular (AV) block (complete heart block) associated with repeated pauses, an inadequate escape rhythm, or a block below the AV node (AVN) should be stabilized with temporary pacing. Transcutaneous pacing is demonstrated in the video below.

View Video

Transcutaneous cardiac pacing in a patient with third-degree heart block. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).

When assessing capture with transcutaneous pacing, it is important to avoid the common mistake of looking for electrical capture on the monitor. The pacing artifact is usually large and that QRS complex can rarely be seen reliably. Instead, palpation for the pulse is the best indication of capture.

Although the transcutaneous pacer should be placed on all patients, this mode of pacing is not highly reliable and is extremely uncomfortable for the patient. Symptomatic patients in whom capture cannot be obtained with a transcutaneous pacemaker need urgent placement of a transvenous pacemaker. Placement of a transvenous pacemaker is also indicated for asymptomatic patients in whom capture cannot be obtained; the timing of this should be discussed with the consulting cardiologist.

The decision to place a transvenous pacing wire depends on the availability of fully trained personnel and equipment for placing a transvenous wire. All patients with persistent block below the AVN should be prepared for temporary wire placement.

Hemodynamically stable patients in whom transcutaneous pacing can be successfully performed can go to a telemetry unit or ICU at the discretion of the treating cardiologist. Hemodynamically unstable patients for whom timely cardiologic consultation is unavailable should undergo temporary transvenous pacemaker insertion in the emergency department (ED).

Hemodynamically unstable patients may be treated with atropine. This should be done with a degree of caution. The goal of atropine therapy is to improve conduction through the AVN by reducing vagal tone via receptor blockade. Atropine often improves the ventricular rate if the site of block is in the AVN. The peak increase in heart rate occurs in 2-4 minutes after IV administration; the half-life is 2-3 hours.

However, if the block is in the His bundle, atropine may lead to an increased atrial rate, and a greater degree of block can occur with a slower ventricular rate. Atropine is unlikely to be successful in wide-complex bradyarrhythmias where the level of the block is below the level of the AVN.

In addition, care should be taken in administering atropine to a patient with a suspected acute myocardial infarction (MI), in that the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Furthermore, atropine is ineffective in patients with a denervated heart (eg, those patients who have undergone a cardiac transplant procedure).

Similarly, use of isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy and the same concerns in patients with suspected acute MI. Isoproterenol is more likely to facilitate conduction with a distal level of block, but patients with a block at the distal level are more likely to have a contraindication, such as active ischemic heart disease. Isoproterenol should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged.

Once the patient has been stabilized, a decision must be made regarding permanent pacemaker implantation.^{[20, 21, 22, 23, 24]} The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.

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Pacemaker Implantation for Acquired AV Block in Adults

Unless the heart block is due to a medication that can be discontinued or an infectious process that can be effectively treated, most patients with acquired third-degree atrioventricular (AV) block (complete heart block) should receive a permanent pacemaker or an implantable cardioverter-defibrillator (ICD) (if a high risk of sudden cardiac death exists on the basis of severe left ventricular dysfunction or other criteria).

The ultimate decision whether to place a permanent pacemaker in patients with persistent heart block without a reversible cause depends on many factors. A clinical statement from the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) was published in 2008; this paper outlined the indications for permanent pacing.^[20] A focused update of these guidelines was published in 2012 and is presented below.^[21]

2012 ACC/AHA/HRS focused update recommendations

Class I recommendations

Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level^[21] :

• Associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block
• Associated with arrhythmias and other medical conditions that require drug therapy that results in symptomatic bradycardia
• In awake, symptom-free patients in sinus rhythm with documented periods of asystole 3 seconds or longer or any escape rate below 40 beats/min, or with an escape rhythm that is below the AVN
• In awake, symptom-free patients with atrial fibrillation and bradycardia with one or more pauses of at least 5 seconds or longer
• After catheter ablation of the AV junction
• Associated with postoperative AV block that is not expected to resolve after cardiac surgery
• Associated with neuromuscular diseases with AV block (eg, myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy [limb-girdle muscular dystrophy], and peroneal muscular atrophy), with or without symptoms

Permanent pacemaker implantation is indicated for second-degree AV block with associated symptomatic bradycardia, regardless of type or site of the block.

Permanent pacemaker implantation is indicated for asymptomatic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 beats/min or faster if cardiomegaly or left ventricular dysfunction is present or if the site of the block is below the AVN.

Permanent pacemaker implantation is indicated for second- or third-degree AV block during exercise in the absence of myocardial ischemia.

Class IIa recommendations

Permanent pacemaker implantation is reasonable for the following^[21] :

• Persistent third-degree AV block with an escape rate faster than 40 beats/min in asymptomatic adult patients without cardiomegaly
• Asymptomatic second-degree AV block at intra- or infra-His levels found at electrophysiologic study
• First- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise
• Asymptomatic Mobitz II second-degree AV block with a narrow QRS; when Mobitz II second-degree AV block occurs with a wide QRS, including isolated right bundle-branch block, pacing becomes a class I recommendation

Class IIb recommendations

Permanent pacemaker implantation may be considered for the following^[21] :

• Neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease
• AV block in the setting of drug use and/or drug toxicity when the block is expected to recur even after the drug is withdrawn.

Class III recommendations

Permanent pacemaker implantation is not indicated for the following^[21] :

• Asymptomatic first-degree AV block
• Asymptomatic Mobitz I second-degree AV block at the supra-His (AVN) level or that which is not known to be intra- or infra-Hisian
• AV block that is expected to resolve and is unlikely to recur (eg, drug toxicity, Lyme disease, transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms)

• References

Pacemaker Implantation for Chronic Bifascicular Block

The American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) have also formulated recommendations for permanent pacing in patients with chronic bifascicular block.^{[20, 21]}

Class I recommendations

Permanent pacemaker implantation is indicated for the following^[21] :

• Advanced second-degree AV block or intermittent third-degree AV block
• Mobitz II second-degree AV block
• Alternating bundle-branch block

Class IIa recommendations

Permanent pacemaker implantation is reasonable for the following^[21] :

• Syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia (VT)
• An incidental finding at electrophysiologic study of a markedly prolonged HV interval (≥100 ms) in asymptomatic patients
• An incidental finding at electrophysiologic study of pacing-induced infra-His block that is not physiologic

Class IIb recommendations

Permanent pacemaker implantation may be considered in the setting of neuromuscular diseases such as myotonic muscular dystrophy, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy with bifascicular block or any fascicular block, with or without symptoms.

Class III recommendations

Permanent pacemaker implantation is not indicated for the following^[21] :

• Fascicular block without AV block or symptoms
• Fascicular block with first-degree AV block without symptoms

• References

Pacemaker Implantation for AV Block After Acute MI

The American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS) have also provided recommendations for permanent pacing in patients with atrioventricular (AV) block associated with acute myocardial infarction (MI).^{[20, 21]}

Class I recommendations

Permanent ventricular pacing is indicated for the following^[21] :

• Persistent second-degree AV block in the His-Purkinje system with alternating bundle-branch block or third-degree AV block within or below the His-Purkinje system after ST-segment elevation MI
• Transient advanced second- or third-degree infranodal AV block and associated bundle-branch block; if the site of block is uncertain, an electrophysiologic study may be necessary
• Persistent and symptomatic second- or third-degree AV block.

Class IIb recommendations

Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms.

Class III recommendations

Permanent ventricular pacing is not indicated for the following^[21] :

• Transient AV block in the absence of intraventricular conduction defects
• Transient AV block in the presence of isolated left anterior fascicular block
• New bundle-branch block or fascicular block in the absence of AV block
• Persistent asymptomatic first-degree AV block in the presence of bundle-branch or fascicular block

• References

Activity Restriction

Bed rest is advisable for patients with new third-degree atrioventricular  (AV) block (complete heart block). Bed rest minimizes the chance of significant injury if syncope occurs as a result of ventricular asystole and decreases hemodynamic demand. A temporary pacemaker may be required.

Because these patients have decreased cardiac output, assuming an upright posture after prolonged periods in the supine position can lead to orthostatic hypotension with syncope or near-syncope.

• References

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 for the development of third-degree atrioventricular (AV) block (complete heart block); the more nodal blockade that occurs, the higher the chance of developing complete heart block.

• References

Consultations

Cardiologic consultation is indicated for all patients with third-degree atrioventricular (AV) block (complete heart block). The consultation is emergent in patients with concomitant acute myocardial infarction (MI), active myocardial ischemia, congestive heart failure, wide-complex escape rhythm, or symptoms of hypoperfusion. 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.

The involvement of an electrophysiologist should also be considered when appropriate.

• References

Long-Term Monitoring

Patients can be discharged from the hospital the following day after pacemaker implantation. Routinely, chest radiography is required before discharge.

Routine postpacemaker care is necessary. This includes transtelephonic checks every 2 months and office visits for pacemaker interrogation every 6-12 months. In the initial postimplantation period, these visits are more frequent.

• References

Medication Summary

Common drugs that induce atrioventricular (AV) block include beta-blockers, calcium channel blockers, antiarrhythmics, and digoxin. Withdrawal of the offending drugs is the first treatment for heart block. Patients with block at the level of the AV node (AVN), in the absence of ischemia, can benefit from sympathomimetic agents or vagolytic agents.

Medications that may be used in the management of third-degree AV block (complete heart block) include sympathomimetic or vagolytic agents, catecholamines, and antidotes.

• References

Atropine (AtroPen)

• Dosing, Interactions, etc.

Clinical Context:  Atropine is an antimuscarinic agent that enhances sinus node automaticity. It may enhance conduction and/or improve the rate of junctional escape. In addition, it blocks the effects of acetylcholine at the AVN, thereby decreasing the refractory time and speeding conduction through the AVN. At inefficient doses, atropine can have paradoxical effects, further slowing the heart rate (HR).

• References

Isoproterenol hydrochloride (Isuprel)

• Dosing, Interactions, etc.

Clinical Context:  Isoproterenol is a synthetic sympathomimetic acting directly on beta-receptors. It should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged. Cardiac ischemia or a high cardiac risk profile suggesting possible coronary artery disease is a contraindication to its use. Telemetry monitoring should always accompany the use of this agent because of the risks of proarrhythmia.

• References

Class Summary

Sympathomimetic or vagolytic agents improve conduction through the AVN by reducing vagal tone via muscarinic receptor blockade. They increase heart rate through their vagolytic effects, causing an increase in cardiac output.

• References

Dopamine

• Dosing, Interactions, etc.

Clinical Context:  Dopamine is a naturally occurring endogenous catecholamine that stimulates beta1- and alpha1-adrenergic and dopaminergic receptors in a dose-dependent fashion; it also stimulates release of norepinephrine.

In low doses (2-5 µg/kg/min), dopamine acts on dopaminergic receptors in renal and splanchnic vascular beds, causing vasodilatation in these beds. In midrange doses (5-15 µg/kg/min), it acts on beta-adrenergic receptors to increase heart rate and contractility. In high doses (15-20 µg/kg/min), it acts on alpha-adrenergic receptors to increase systemic vascular resistance and raise blood pressure (BP).

• References

Norepinephrine (Levophed)

• Dosing, Interactions, etc.

Clinical Context:  Norepinephrine is a naturally occurring catecholamine with potent alpha-receptor and mild beta-receptor activity. It stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, HR, and vasoconstriction. It increases BP and afterload. The increased afterload may result in decreased cardiac output, increased myocardial oxygen demand, and cardiac ischemia. Norepinephrine is generally reserved for patients with severe hypotension (eg, systolic BP < 70 mm Hg) or hypotension unresponsive to other medication.

• References

Class Summary

Catecholamines improve hemodynamics by acting on the beta-adrenergic receptors to increase the HR and contractility and by acting on the alpha-adrenergic receptors to increase the systemic vascular resistance.

• References

Digoxin immune Fab (DigiFab)

• Dosing, Interactions, etc.

Clinical Context:  Digoxin immune Fab is an immunoglobulin fragment with a specific and high affinity for both digoxin and digitoxin molecules. It removes digoxin or digitoxin molecules from tissue-binding sites. Each vial contains 40 mg of purified digoxin-specific antibody fragments, which will bind approximately 0.6 mg of digoxin or digitoxin.

The dose of the antidote depends on the total body load (TBL) of digoxin. The digoxin TBL can be estimated in the following 3 ways:

1. Estimate the quantity of digoxin ingested in the acute ingestion, and assume 80% bioavailability for digoxin or 100% for digitoxin (X mg ingested × 0.8 = TBL)

2. Obtain a serum digoxin concentration (in ng/mL) and multiply it by the patient's weight in kilograms. Divide the result by 100 [number of vials = (digoxin concentration) x (patient's weight) / 100]

3. Use an empiric dose based on average requirements for an acute or chronic overdose in an adult or child

If the quantity of ingestion cannot be estimated reliably, the antidote may be administered empirically (it is safest to use the largest calculated estimate). Alternatively, be prepared to increase dosing if resolution is incomplete.

• References

Class Summary

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

• References