Atrioventricular block

Highlights
Summary Overview

Basics
Definition Epidemiology Aetiology Pathophysiology Classification

Prevention
Primary Secondary

Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history

Treatment
Details Step-by-step Emerging Guidelines Evidence

Follow Up
Recommendations Complications Prognosis

Resources
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History & exam

Key factors
presence of risk factors age >50 to 60 years years syncope

pre-syncope heart rate <40 bpm

Other diagnostic factors

male gender fatigue dyspnoea chest pain, palpitations, and nausea or vomiting high (less commonly, low) blood pressure hypoxaemia cannon A waves Fhx of AV block features of Lyme disease

History & exam details

Diagnostic tests
1st tests to order
12-lead ECG serum troponin serum potassium serum calcium serum pH serum digitalis level

Tests to consider
24-hour ambulatory monitoring or event monitoring chest x-ray transthoracic echocardiogram serological testing for Lyme disease implantable loop recording tilt-table testing electrophysiological study cardiac stress testing coronary angiography serum CK-MB Diagnostic tests details

Treatment details

Acute
first-degree AV block or type I second-degree AV block o o o asymptomatic monitoring symptomatic discontinuation of AV-nodal blocking medications infrequently: PPM or cardiac resynchronisation therapy ICD placement type II second-degree AV block or third-degree AV block o o o asymptomatic or mildly to moderately symptomatic condition-specific management and discontinuation of AV node-blocking drugs PPM or cardiac resynchronisation therapy ICD placement severely symptomatic condition-specific management, discontinuation of AV-nodal blocking drugs, and temporary (transcutaneous or transvenous) pacing o PPM or cardiac resynchronisation therapy ICD placement Treatment details

Summary
AV block can be described by degree (based on ECG appearance) or by anatomical level of block. The degree of AV block or anatomical level of block does not necessarily correlate with the severity of subsequent symptoms. The goals of therapy are to treat symptoms and to prevent syncope and sudden cardiac death due to very slow or absent ventricular rates. Patients with advanced AV block (usually type II second-degree, third-degree, or infranodal AV block) of irreversible cause should undergo permanent pacemaker placement.

Definition
Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles. The severity of the conduction abnormality is described in degrees: first-degree; seconddegree, type I (Wenckebach or Mobitz I) or type II (Mobitz II); and thirddegree (complete) AV block. This classification scheme should be applied only during sinus rhythm and not during rapid atrial arrhythmias or to premature atrial beats.

Epidemiology
The epidemiology of AV block is not well characterised.[C Evidence] One study examined first-degree AV block in 2123 patients. [2] Here, first-degree AV block was more prevalent in African-American patients in almost all decades of life (third through 10th). In both groups, first-degree AV block became more common at age 50 years and peaked in the 10th decade for black patients versus the ninth decade for white patients. One study examined 24-hour Holter monitors in 625 asymptomatic, heart-disease-free people, aged 15 to 83 years. Transient type I second-degree AV block was seen in 14 (2.2%) patients, more frequently in patients with resting heart rates of <60 bpm. [3] First-degree AV block has been associated with about a 2fold increase in the probability of atrial fibrillation, a 3-fold increase in the probability of pacemaker implantation, and an increase in all-cause mortality. [4] Advanced AV block (usually type II second-degree and third-degree) is usually anatomically infranodal and is seen in advanced His-Purkinje disease. One study examined the prevalence of His-Purkinje disease in the Framingham population. [5] Here, QRS intervals of >0.12 seconds were significantly associated with coronary heart disease, CHF, AV block, hypertension, left ventricular hypertrophy, and ventricular extrasystoles. QRS intervals >0.12 seconds were rare before 50 to 60 years of age and were found in 11% of older men and 5% of older women. While intraventricular block does not inevitably lead to AV block, it frequently precedes the development of advanced AV block. View imageView imageView image Thus, this characterisation of a wide-QRS interval population is likely similar to that of the advanced AV block population.

Aetiology
Causes include fibrosis and calcification of the conduction system, CAD (including patients with a chronic disease and/or an acute coronary syndrome), and medication such as AV-nodal blocking agents (i.e., betablockers, calcium-channel blockers, digitalis, adenosine), anti-arrhythmic medications such as sodium-channel blockers, and some class III agents (i.e., sotalol and amiodarone). Additional aetiologies include high vagal tone; cardiomyopathy (e.g., hypertrophic, sarcoid, amyloid, haemochromatosis); calcification from adjacent valvular calcification; post catheter ablation for arrhythmias; [6] [1] [7] and post-surgical causes (i.e., valve repair or replacement myectomy, septal ethanol ablation). Severe electrolyte disturbance, acidosis, or hypoxaemia may result in AV block as well as

neuromuscular disorders (myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, peroneal muscular atrophy), myocarditis, infective endocarditis, and Lyme disease. AV block may be congenital as well. [8]

Pathophysiology
Block at the level of the AV node manifesting as first-degree or type I seconddegree AV block is usually a function of either high vagal tone or medication. High vagal tone is due to either a tonic elevation (e.g., in younger, athletic patients) or transient vagotonia, as in neurocardiogenic syncope, [1] sleep, nausea, vomiting, or gagging. Transient vagotonia may also result from endotracheal suctioning, micturition or bowel movements, prolonged paroxysms of coughing or other instances of Valsalva, or inferior ischaemia or infarction. AV-nodal blocking agents are most commonly beta-blockers, calcium-channel blockers, digitalis, and adenosine. AV block is particularly common when these drugs are used in combination (e.g., digitalis or betablockers and calcium-channel blockers). Block in the His-Purkinje system is usually manifested as type II seconddegree AV block or third-degree AV block. His-Purkinje system disease (usually seen as a widened QRS or bundle-branch block on a 12-lead ECG) is usually due to an irreversible structural abnormality that is extensive enough to compromise AV conduction. Because the His-Purkinje system conducts in an all or nothing fashion, AV block at this level will manifest as a consistent PR interval followed by a non-conducted P wave (type II seconddegree AV block) or as complete heart block.

Classification
Degrees of block There are 2 commonly accepted clinical classification systems in use that are not formal classification systems: degrees of block versus anatomical sites of block. First-degree AV block View image
Fixed prolongation of the PR interval >0.2 seconds (or >200 milliseconds) with no failure of AV conduction. [1]

Second-degree AV block, type I View image

Progressive prolongation of the PR interval with eventual loss of AV conduction for 1 beat.

Followed by resumption of AV conduction with a progressively prolonging PR interval. The first sinus beat following resumption of AV conduction is conducted with a normal PR interval. Thereafter, there is progressive prolongation of the PR interval.

Eventual loss of AV conduction for 1 beat (pattern repeats, giving rise to group beating).

Second-degree AV block, type II View image

beats). Finally, fixed, unchanging PR intervals. Fixed, unchanging PR intervals. Then, occasional loss of AV conduction for 1 beat (during sinus rhythm, excluding premature atrial

Third-degree AV block View imageView image

Complete, persistent loss of conduction from the atria to the ventricles.

High-grade AV block
The term high-grade AV block is applied to a pattern where 2 sinus P waves block consecutively in the context of periodic AV conduction. [1]

Anatomical sites of block There are 2 commonly accepted clinical classification systems in use that are not formal classification systems: degrees of block versus anatomical sites of block.
Nodal: at the level of the AV node. Infranodal: either at the level of the bundle of His (intra-His) or below (infra-His).

Primary prevention
Primary prevention measures include avoiding circumstances increasing vagal tone when possible, withdrawing or decreasing the dose of AV-nodal blocking agents, controlling chronic cardiovascular diseases, and aggressively treating the acute coronary syndrome by restoring blood flow. During procedures, reassurance and avoidance of pain also reduce vagally mediated bradycardia and heart block.

Secondary prevention
Control of chronic cardiovascular conditions can potentially be of some benefit. Statins have not shown to be beneficial in prevention of atrial fibrillation in patients with AV block and a permanent pacemaker implantation. [35]

History & examination

Key diagnostic factorshide all
presence of risk factors (common)

Strong risk factors for AV block include increased vagal tone; use of AV nodal blocking agents; underlying cardiovascular disease (e.g., CAD or an acute coronary syndrome; HTN, CHF; LVH or

cardiomyopathy); acid-base disturbance; neuromuscular disorders; or recent cardiac surgery. age >50 to 60 years years (common)

Any degree of heart block becomes more common with increasing age, especially >50 to 60 years. [2] [3] [5]

heart rate <40 bpm (common)

The overall ventricular rate helps determine appropriate timing and level of therapy. With very slow ventricular rates (<40 bpm), hospital admission and either urgent permanent pacemaker

implantation or temporary transvenous pacing should be considered. syncope (uncommon)

Syncope potentially implies a profound decrease in the ventricular rate, such as with the sudden development of complete heart block with a slow or absent ventricular escape rhythm. More urgent timing of pacemaker placement may be indicated. For example, syncope in a patient with highdegree AV block (Stokes-Adams attack) is usually an indication for prompt pacemaker placement unless a reversible cause, such as an inferior infarction or severe electrolyte or pH disturbances, is identified. Thus, supportive care may avert the need for permanent pacing.

pre-syncope (uncommon)

Pre-syncope potentially implies a significant decrease in the ventricular rate and would prompt more urgent timing of pacemaker placement, if indicated.

Other diagnostic factorshide all

male gender (common)

In one study of His-Purkinje disease, men were twice as likely as women to have a widened QRS interval, a precursor to advanced degrees of heart block. [5]

fatigue (common)

Fatigue, especially related to exertion, may be a function of a relatively slow ventricular rate. Because fatigue is such a non-specific symptom, its onset and duration should be correlated to that of the heart block as much as possible. Exercise testing to evaluate the dynamic heart rate response may also be helpful in establishing the contribution of bradycardia to fatigue or dyspnoea.

dyspnoea (common)

Dyspnoea, especially related to exertion, may be a function of a relatively slow ventricular rate. Similarly to fatigue, because dyspnoea is such a non-specific symptom, its onset and duration should be correlated to that of the heart block as much as possible.

This symptom is of concern for an acute coronary syndrome in those with new-onset heart block. The acute coronary syndrome can be a proximate and reversible cause of heart block.

chest pain, palpitations, and nausea or vomiting (common)

Of concern for an acute coronary syndrome in those with new-onset heart block. Chest pain, palpitations, nausea, and vomiting are often encountered in patients with AV block in the acute setting. Acute coronary syndrome can be a proximate and reversible cause of acute heart block.

high (less commonly, low) blood pressure (common)

Slow ventricular rates with significant heart block are usually associated with elevated systolic blood pressures and relatively wide pulse pressures, rather than with hypotension. Low blood pressures in patients with heart block usually reflect significantly decreased ventricular rates (<40 bpm).

cannon A waves (common)

The presence of structural heart disease is associated with His-Purkinje disease and may imply an irreversible cause for heart block. [5] Examination of the jugular venous pressure may reveal cannon A waves that may indicate the presence of AV dissociation due to complete heart block. The intermittently prominent (cannon) A waves reflect the contraction of the right atrium against a closed tricuspid valve.

hypoxaemia (uncommon) Profound hypoxaemia may be a reversible cause of heart block. Fhx of AV block (uncommon)

Some causes of heart block have been shown to be hereditary. [8]Fetal third-degree AV block is known to occur in the setting of maternal SLE.

features of Lyme disease (uncommon)

Lyme disease is an uncommon cause of AV block, although there are regions where the disease is endemic and should be considered more readily. [17] As a potentially reversible cause, its presence should be considered, especially in younger patients presenting with exposure in these endemic areas. The diagnosis is a clinical one, with presenting symptoms including headache, stiff neck, fever, muscle and joint aches, fatigue, and erythema migrans. Even in patients diagnosed

Risk

with Lyme disease, the incidence of heart block is low (<2%). factorshide all

Strong increased vagal tone

Increased vagal tone may be due to either a tonic high level of vagal tone or transient vagotonia. High tonic vagal tone is found in younger, athletic patients or in patients with autonomic dysfunction.

Transient vagotonia occurs in vasodepressor syncope; during sleep; during episodes of nausea, vomiting, or gagging (i.e., endotracheal suctioning); during pain, micturition, or bowel movements; during paroxysmal coughing or other instances of Valsalva (such as extreme straining to sit up); and during carotid sinus stimulation or cardiac ischaemia. Excessive vagotonia can also occur in patients with carotid sinus hypersensitivity, particularly common in older patients or in patients who have undergone head and neck surgery or radiation. Carotid sinus hypersensitivity usually manifests as severe high-degree AV block precipitated by changes in head position or in response to neck pressure.

AV-nodal blocking agents

Most commonly implicated agents are AV-nodal blocking medications such as beta-blockers, calcium-channel blockers, digitalis, and adenosine. Anti-arrhythmic medications, including some sodium-channel blocker and some class III agents (sotalol and amiodarone), may also cause AV block.

age-related degenerative changes in the conduction system

Usually take the form of either Lenegre's disease (progressive fibrosis and sclerodegenerative changes) or Lev's disease (fibrosis or calcification of the conduction system extending from adjacent fibrous structures of, usually, the aortic and/or mitral valves). [8][9] [10] These degenerative changes may account for up to half of the cases of complete heart block. [11]

chronic stable CAD

The presence of cardiovascular comorbidities has been shown to be associated with His-Purkinje disease, a precursor to advanced degrees of heart block. [5]Presumably, this is due to an acceleration of the process of degenerative fibrosis and calcification of the conduction system.

AV block can be seen in the setting of chronic ischaemic heart disease or as a complication of acute MI.

acute coronary syndrome

In this setting, AV block can be as a result of imbalance in autonomic tone, ischaemia, or necrosis of the conduction system. It can complicate both anterior and inferior wall MI, typically being an adverse prognostic factor when seen with the former and more often reversible with the latter. The use of thrombolysis and primary angioplasty for the treatment of acute MI has decreased the incidence of AV block in the acute setting.[1] [12]

In one older study of 134 acute MI patients, first-degree AV block was seen in 11.8% of patients, second-degree AV block in 4.8%, and complete heart block in 5.9%. [13]These percentages are probably lower in the modern era of early reperfusion therapy for acute MI. One more recent study

of 14,096 acute coronary syndrome patients identified high-degree AV block in only 1% of patients. [14] Still, AV block remains a real and potentially serious complication of acute MI.
CHF

The presence of cardiovascular comorbidities has been shown to be associated with His-Purkinje disease, a precursor to advanced degrees of heart block. [5]Presumably, this is due to an acceleration of the process of degenerative fibrosis and calcification of the conduction system.

Progression of left ventricular systolic dysfunction to CHF is associated with gradual prolongation of the PR interval and intraventricular conduction disturbances, usually left bundle-branch block, in up to about one third of patients.

hypertension

The presence of cardiovascular comorbidities has been shown to be associated with His-Purkinje disease, a precursor to advanced degrees of heart block. [5]Presumably, this is due to an acceleration of the process of degenerative fibrosis and calcification of the conduction system.

cardiomyopathy

The presence of cardiovascular comorbidities has been shown to be associated with His-Purkinje disease, a precursor to advanced degrees of heart block. [5]Presumably, this is due to an acceleration of the process of degenerative fibrosis and calcification of the conduction system.

left ventricular hypertrophy

The presence of cardiovascular comorbidities has been shown to be associated with His-Purkinje disease, a precursor to advanced degrees of heart block. [5]Presumably, this is due to an acceleration of the process of degenerative fibrosis and calcification of the conduction system.

recent cardiac surgery May present a reversible cause for heart block. acid-base or electrolyte disturbance Severe electrolyte disturbance or acidosis may result in AV block. neuromuscular disorders

For example, myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, or peroneal muscular atrophy.

Weak sarcoidosis

Clinical evidence of cardiac involvement occurs in 5% of patients with sarcoidosis, though subclinical disease is more often encountered at autopsy. AV block can occur as a result of granulomatous involvement of the interventricular septum or the conduction system. Such patients usually present with syncope at an earlier age than AV block due to other aetiologies. [15]

myocarditis infective endocarditis hypoxemia

Diagnostic tests
1st tests to orderhide all
Test

12-lead ECG conditions.

Diagnosis of the various degrees of AV block is frequently made incidental to the work-up for any number of pres

Symptoms specifically suggestive of AV block prompting a 12-lead ECG include syncope, pre-syncope, episodic

lightheadedness, and progressive exertional fatigue and/or dyspnoea. The 12-lead ECG should also be inspecte imageView imageView imageView imageView image

evidence of acute ischaemia (such as ST-segment changes), which may point to a reversible cause of AV block.

serum troponin indicative history and physical examination should prompt the obtaining of serum cardiac enzymes. serum potassium Severely abnormal values may represent reversible causes of AV block. serum calcium Severely abnormal values may represent reversible causes of AV block.

Because acute ischaemia should be aggressively managed and presents a potentially reversible cause of AV blo

serum pH reversible causes of AV block. serum digitalis level

If severe acidosis or alkalosis is suspected, a serum pH should be obtained. Severely abnormal values may repr

If a patient is taking digitalis and presents with new AV block, especially advanced AV block, a serum digitalis lev levels. However, an elevated level may increase the suspicion for toxicity.

be obtained. Digitalis toxicity is a reversible cause of AV block. Digitalis toxicity does not necessarily correlate wi

Tests to considerhide all

Test

24-hour ambulatory monitoring or event monitoring

This test should be considered when AV block is suspected, but is not yet documented, as a cause for symptoms chest x-ray

Evidence of structural heart disease (e.g., cardiomegaly, or coronary or valvular calcification) or CHF may be pre reversible AV block.

Hilar lymphadenopathy suggests sarcoidosis. Any number of pulmonary findings may explain hypoxaemia, leadin

There are numerous reasons for a chest x-ray to be ordered, such as the presence of cardiopulmonary symptom a high clinical suspicion for heart or lung disease. transthoracic echocardiogram

In the setting of advanced heart block, especially if permanent pacemaker placement is considered, a transthora and quantify left ventricular systolic function (if <35%, biventricular pacemaker with or without implantable cardioverter-defibrillator [ICD] placement should be considered). serological testing for Lyme disease Because it is a potentially reversible cause, Lyme disease should be considered, especially in younger patients presenting with exposure to endemic areas. implantable loop recording despite short-term (24- or 48-hour) or long-term (1-month) monitoring. tilt-table testing This test can be ordered when AV block is thought to occur in the setting of neurocardiogenic syncope.

echocardiogram should be ordered. The test can demonstrate the presence or absence of structural heart diseas

This test should be ordered when the clinical suspicion is high (history, signs, and symptoms support the diagnos

This test should be considered when AV block is suspected, but is not yet documented, as a cause for symptoms

Neurocardiogenic syncope is a clinical diagnosis, based on patient history, and the sensitivity and specificity of ti table testing are widely ranging (30% to 80% and 50% to 90%, respectively). [18] electrophysiological study This test should be ordered when the severity of conduction disease and the possible need for treatment with a bundle-to-ventricle (HV) interval >100 ms. cardiac stress testing This test should be ordered when a high clinical suspicion exists for cardiac ischaemia, outside the acute stages acute coronary syndrome.

pacemaker are unclear, such as with 2:1 AV block. Significant infranodal conduction disease is defined by a His-

Active ischaemia, especially in the inferior territory, may be a reversible cause of AV block. It can also identify pa These patients usually do not require a pacemaker.

with vagotonia who retain chronotropic competence (the ability to appropriately increase heart rate) with exercise

Infrequently, exercise may show worsening of AV conduction. In such patients, a permanent pacemaker would b indicated. coronary angiography This test should be ordered when a high clinical suspicion exists for cardiac ischaemia, especially in an acute coronary syndrome, when appropriate. Significant obstructive lesions may be reversible, treatable causes of AV block. serum CK-MB reversible cause of AV block.

Less commonly used than troponin. Acute ischaemia should be aggressively managed and presents a potentially

Differential diagnosis
Condition Junctional rhythm Differentiating signs/symptoms Differentiating tests

In patients with profound first-degree AV block and very long PR intervals, the P wave may encroach so

Comparison of numerous ECGs obtained at different times also help make the diagnosis.

apart) may be useful. Baseline ECGs showing profound fir

closely on the QRS complexes that they appear to be retrograde P waves, suggesting junctional rhythm. Retrograde P waves in junctional rhythm should be inverted in the inferior leads (II, III, and aVF), whereas in sinus rhythm with profound first-degree AV block, the P waves are upright in those leads. Supraventricular tachycardia (SVT)

In patients with profound first-degree AV block and very long PR intervals, the P wave may encroach so closely on the QRS complexes that they

Variations in the heart rate and the PR and RP (QRS to P)

against the diagnosis of SVT. Comparison of numerous EC

appear to be retrograde P waves, suggesting SVT. Retrograde P waves in SVT are frequently inverted in the inferior leads versus upright in sinus rhythm with first-degree AV block. Atrial fibrillation or multifocal atrial tachycardia (MAT)

The irregularity of the RR intervals in type I seconddegree AV block may lead to the incorrect diagnosis of atrial fibrillation or MAT. The presence of distinct P waves and the grouped pattern of the RR intervals are characteristic of type I second-

Careful inspection of the ECG should allow distinction betw

degree AV block and are not seen in atrial fibrillation or MAT.

Sinus rhythm with intact AV conduction

In patients with thirddegree AV block, if the rate of the junctional escape rhythm is similar to that of the sinus rate, an appearance of sinus rhythm with intact AV conduction may be possible. In most of these cases, with a long enough rhythm strip, the lack of a relationship between the sinus beats and the QRS complexes will become apparent.

Examination of a long rhythm strip should allow for the cor made.

Tachy-brady syndrome

The RR

There is no AV block.View image

intervals are irregular and short, suggesting atrial fibrillation with a fast ventricular rate. At the termination of the tachyarrhythm ia, the diseased sinus node is slow to take over, resulting in a pause and a slow ventricular rate.

Step-by-step diagnostic approach

The diagnosis of AV block can be made from any interpretable cardiac rhythm tracing such as a 12-lead ECG, a cardiac telemetry rhythm strip, a Holter-monitor rhythm strip, or an event monitor strip.

History
Patients tend to be male and >50 to 60 years old. Underlying cardiovascular disease (e.g., CAD or an acute coronary syndrome; HTN, CHF; LVH or cardiomyopathy; or recent cardiac surgery) may be evident. Other strong risk factors are acid-base disturbance or neuromuscular disease. Infrequently, patients may have a family history of AV block as well. Rarely, Lyme disease is linked to AV block; as a potentially reversible cause, it is important to identify. Clinical evidence of cardiac involvement occurs in 5% of patients with sarcoidosis, though subclinical disease is more often encountered at autopsy. AV block can occur as a result of granulomatous involvement of the interventricular septum or the conduction system. Such patients usually

present with syncope at an earlier age than AV block due to other aetiologies. [15] Symptoms associated with AV block are fatigue, dyspnoea, chest pain, palpitations, and nausea and vomiting. Syncope and pre-syncope are less-commonly associated symptoms most often encountered in emergency care settings.

Physical examination
On examination, patients often have a slow heart rate. If <40 bpm, hospital admission is warranted for pacemaker implantation or temporary transvenous pacing. Blood pressure measurement is crucial. Most often, blood pressure is high with a wide pulse pressure. If blood pressure is low, often ventricular rates are very low (<40 bpm). Low blood pressure is usually seen in an emergency care setting. On examination of jugular venous pressure, if cannon A waves are identified, an irreversible and complete heart block may be present.

Laboratory tests
A 12-lead ECG is essential to identify the type and severity of AV block. It is performed first, and the length and position of the PR interval is key in determining the degree of heart block. Evidence of ischaemia, a potential cause of AV block, is also determined on ECG. Serum troponin is drawn initially to verify and track ischaemia. CK-MB may be indicated in selected patients. Also drawn immediately are serum potassium, calcium, and digitalis levels, and serum pH, which may identify possible reversible causes of AV block. If a patient may have been exposed to Lyme disease, a serological test is warranted to rule out this reversible cause of AV block.

Cardiac tracing interpretation

The diagnostic criteria are based on measurement of the PR interval and the presence or absence of non-conducted atrial impulses (no QRS following a P wave). The definitions of the various degrees of block are as follows.
image Second-degree AV block, type I, is progressive prolongation of the PR interval with eventual loss of AV conduction for 1 beat, then resumption of AV conduction with a PR interval that progressively prolongs with eventual loss of AV conduction for 1 beat. The pattern repeats, giving rise to group beating. View image The first sinus beat, following resumption of AV conduction, is conducted with a normal PR interval. First-degree AV block is fixed prolongation of the PR interval >0.2 seconds (or >200 milliseconds). View

Second-degree AV block, type II, is the occasional loss of AV conduction for 1 beat (during sinus rhythm, excluding premature atrial beats) preceded and followed by fixed, unchanging PR intervals. View image Third-degree AV block is complete, persistent loss of conduction from the atria to the ventricles. View imageView image Also called complete heart block, third-degree heart block shows no consistent PR relationship.

The term high-grade AV block is applied to a pattern where 2 sinus P waves block consecutively in the context of periodic AV conduction. [1]

Categorising 2:1 AV block

One scenario in which the degree of block may be difficult to determine is that of 2:1 AV block.View image In this case, it is impossible to determine the behaviour of the PR interval, whether it progressively prolongs or stays fixed before the non-conducted P wave (absent QRS). Thus, it is difficult to determine the anatomical location of the second-degree AV block, nodal or infranodal. This distinction is important, as the 2 locations imply distinct pathophysiological processes and prognoses, benign versus potentially malignant, respectively. Nodal second-degree AV block is suggested during 2:1 AV block when the following feature is present.
Narrow QRS interval: this suggests the His-Purkinje system is intact and thus the level of block is occurring at the level of the AV node. Up to 30% of infranodal block, however, may be associated with a narrow QRS interval. [16]

Presence of high vagal tone causing AV block is suspected from the following clinical and ECG features.
A slow sinus rate. Long PR interval with conducted P waves. Episodes of 2:1 AV block occurring in the following settings: sleep; episodes of nausea, vomiting, or gagging (i.e., endotracheal suctioning); pain; micturition or bowel movements; paroxysmal coughing; or other instances of Valsalva (such as extreme straining to sit up). Improved frequency of conducted P waves with atropine (with measurable increase in the sinus rate). Caution: giving atropine to patients with infranodal block (usually those with widened QRS complexes at baseline) may worsen the degree of AV block and markedly decrease the ventricular rate. Hence, before giving atropine, consultation with a cardiologist or cardiac electrophysiologist should be considered.

Improved frequency of conducted P waves with exercise (walking around or leg lifts in bed with demonstrable increase in the sinus rate).

Infranodal second-degree AV block is suggested during 2:1 AV block when the following features are present.
Widened QRS interval: this suggests intrinsic disease in the His-Purkinje system. However, up to 30% of infranodal block may be associated with a narrow QRS interval. [16] Worsened frequency of conducted P waves with exercise (walking around or leg lifts in bed with demonstrable increase in the sinus rate) or with atropine: the His-Purkinje system can demonstrate a fatigue phenomenon with more frequent stimulation (i.e., the higher the sinus rate, the more frequently the His-Purkinje system is stimulated and the worse the frequency of conduction becomes).

Ambulatory ECG monitoring, imaging, and other tests

A chest x-ray may be helpful in identifying or supporting possible causes of AV block, such as structural heart disease or CHF. A transthoracic echocardiogram aids in identifying or quantifying structural heart disease. This test is necessary if a permanent pacemaker is considered possible. Although not yet documented, 24-hour ambulatory monitoring may be helpful in identifying AV block when such a heart block is suspected. An implantable loop recording is useful if the 24-hour ambulatory monitoring does not detect AV block, but AV block is still suspected due to symptoms and signs. If AV block is thought to occur as a result of neurocardiogenic syncope, tilt-table testing is suggested. If the severity of AV block is unknown and the need for a pacemaker is still unclear, an electrophysiology study may help identify the AV block. Cardiac stress testing is warranted when cardiac ischaemia or exercise-induced AV block is likely. Especially in the setting of an acute coronary syndrome and cardiac ischaemia, coronary angiography will help identify obstructive lesions, which, when treated, may help in reversing heart block.
Click to view diagnostic guideline references.

Diagnostic criteria

Degrees of block
First-degree AV block View image
Fixed prolongation of the PR interval >0.2 seconds (or >200 milliseconds). View image Severity based on the presence or absence of symptoms.

Patients with PR interval >0.30 seconds (or >300 milliseconds) may show dyspnoea. Prolonged AV delay, with an increased pulmonary capillary wedge pressure, and decreased ventricular filling leading to decreased stroke volume and cardiac output may occur.

interval.

Signs and symptoms are similar to the pacemaker syndrome experienced by some pacemaker patients. A select number of these patients may benefit from pacemaker placement and shortening of the PR

Second-degree AV block, type I View image

Progressive prolongation of the PR interval with eventual loss of AV conduction for 1 beat. Then, resumption of AV conduction with a PR interval that, again, progressively prolongs with eventual loss of AV conduction for 1 beat. The first sinus beat following resumption of AV conduction is conducted with a normal PR interval. The pattern repeats. The severity of this condition is based on the presence or absence of symptoms. In the absence of symptoms, the prognosis is generally benign. Asymptomatic patients can be followed clinically. Symptoms can range from those for first-degree AV block to more generalised symptoms of fatigue, presyncope, or even syncope. In patients for whom symptoms can be attributed to the heart block and in the absence of a reversible cause, a permanent pacemaker is indicated.

Second-degree AV block, type II View image

Occasional loss of AV conduction for 1 beat (during sinus rhythm, excluding premature atrial beats) preceded and followed by fixed, unchanging PR intervals. A severe condition, and these patients are at high risk for progression to third-degree AV block. In the absence of a reversible cause, these patients should undergo permanent pacemaker implantation.

Third-degree AV block View imageView image

Complete, persistent loss of conduction from the atria to the ventricles. Considered a severe condition.

In the absence of a reversible cause, these patients should undergo permanent pacemaker implantation.

High-grade AV block
The term high-grade AV block is applied to a pattern where 2 more sinus P waves block consecutively in the context of periodic AV conduction. [1]

Case history
A 78-year-old man with a history of hypertension presents to his primary care physician with 1 episode of dizziness while watching television. On physical examination, his heart rate is measured at about 40 bpm. A 12lead ECG is obtained showing sinus rhythm at about 75 bpm and complete heart block with a wide junctional escape rhythm at about 40 bpm. View imageView image On further questioning, the patient admits to increasing fatigue and dyspnoea on exertion for the past few weeks. Notably, the patient has bifascicular block at baseline (right bundle-branch block and left anterior fascicular block). View image

Other presentations
The degree of AV block and the severity of symptoms are not necessarily directly related. For example, patients with complete (third-degree) AV block may be minimally symptomatic or completely asymptomatic. Ultimately, these patients may be diagnosed incidentally on undergoing an evaluation for other reasons. On the other hand, patients with type I second-degree AV block may be very symptomatic, presenting with syncope or pre-syncope due to very slow ventricular rates. AV block may also occur in the setting of other acute illnesses such as an acute coronary syndrome, severe electrolyte or pH disturbances, or severe hypoxaemia. AV block of any degree may also occur in the post-cardiac surgery patient and, rarely, in patients with Lyme disease.

Treatment Options
Treatment Patient group first-degree AV block or type I second-degree AV block asymptomatic 1st line Treatmenthide all

monitoring

Patients are at low risk for progression to higherdegree AV block. ECGs may be rechecked if symptoms develop, but do not need to be rechecked on a routine basis.

symptomatic

1st

discontinuation of AV-nodal blocking medications

Patients with first-degree AV block and a PR interval >0.30 seconds (or >300 milliseconds) may experience symptoms related to the haemodynamic consequence of such prolonged AV delay. An

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

increased pulmonary capillary wedge pressure and attendant symptoms of dyspnoea result, as well as decreased ventricular filling leading to decreased stroke volume and cardiac output. This constellation of symptoms is similar to the pacemaker syndrome experienced by some pacemaker patients. Some patients with type I second-degree AV block can experience symptoms, ranging from those related to first-degree AV block to more generalised symptoms of fatigue, pre-syncope, or syncope.

The most common AV-nodal blocking medications include beta-blockers, non-dihydropyridine calciumchannel blockers, and digitalis.

Risks and balances of discontining possible causative medications (e.g., beta-blockers) should be weighed in each instance.

2nd

infrequently: PPM or cardiac resynchronisation therapy ICD placement

If symptoms are severe enough, permanent pacemaker (PPM) implantation should be considered. For AV block, usually a dual-chamber (1 right atrial and 1 right ventricular lead) pacemaker is placed. The procedure includes a 2inch incision at the non-dominant shoulder, placement of the leads through the subclavian vein, and placement of the pulse generator in a small subcutaneous pocket. The entire procedure usually takes a few hours and requires an overnight hospital stay.

Biventricular pacemaker (placement of a third wire, in a branch of the coronary sinus, to enable left ventricular pacing) with or without an implantable cardioverter-defibrillator (ICD) placement, may be

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

considered when the left ventricular ejection fraction is <35%. [19] [20] [21] (An ICD is not indicated for patients with New York Heart Association [NYHA] Class IV heart failure symptoms: severe limitation of exercise capacity due to shortness of breath with symptoms even while at rest; these are mostly bedbound patients.)

type II second-degree AV block or third-degree AV block asymptomatic or mildly to moderately symptomatic 1st

condition-specific management and discontinuation of AV node-blocking drugs

Mild to moderate symptoms include fatigue or dyspnoea, especially exertional, mild symptoms of CHF (pedal oedema, orthopnoea), or mild, episodic lightheadedness.

The most common AV-nodal blocking medications include beta-blockers, non-dihydropyridine calciumchannel blockers, and digitalis. While discontinuing these medicines may improve AV conduction, they are not likely to completely reverse clinically significant AV block.

Condition-specific management includes treating acute coronary syndrome (i.e., anti-platelet medications, urgent revascularisation) and medication toxicity (e.g., glucagon for beta-blocker toxicity, calcium for calcium-channel toxicity, or digoxin antibody for digitalis toxicity). When present, electrolyte or pH disturbances and hypoxaemia should be treated appropriately.

Risks and balances of discontining possible causative medications (e.g., beta-blockers) should be weighed in each instance.

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

Primary Options digitalis toxicity digoxin immune Fab : consult specialist for guidance on dose OR beta-blocker toxicity glucagon : consult specialist for guidance on dose OR calcium-channel blocker toxicity calcium chloride : consult specialist for guidance on dose
2nd

PPM or cardiac resynchronisation therapy ICD placement

Patients with type II second-degree AV block or third-degree AV block are at risk for progression to slower ventricular rates and development or worsening of symptoms. [22] In the absence of a reversible cause, these patients should undergo permanent pacemaker (PPM) implantation.View image

For AV block, usually a dual-chamber (1 right atrial and 1 right ventricular lead) pacemaker is placed. The procedure includes a 2-inch incision at the nondominant shoulder, placement of the leads through the subclavian vein, and placement of the pulse generator in a small subcutaneous pocket. The entire procedure usually takes a few hours and requires an overnight hospital stay.

Biventricular pacemaker (placement of a third wire, in a branch of the coronary sinus, to enable left ventricular pacing) with or without an implantable cardioverter-defibrillator (ICD) placement, may be

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

considered when the left ventricular ejection fraction is <35%. [19] [20] [21] (An ICD is not indicated for patients with New York Heart Association [NYHA] Class IV heart failure symptoms: severe limitation of exercise capacity due to shortness of breath with symptoms even while at rest; these are mostly bedbound patients.)
severely symptomatic 1st

condition-specific management, discontinuation of AV-nodal blocking drugs, and temporary (transcutaneous or transvenous) pacing

Severe symptoms include syncope or persistent, severe lightheadedness indicating profound decreases in the ventricular rate.

When the ventricular rate is significantly low (<40 to 45 bpm) or the blood pressure is low (mean arterial pressure <65 mmHg), temporary (transcutaneous or transvenous) pacing should be considered. Transvenous pacing is much more reliable than transcutaneous pacing and should be performed by a cardiologist when the heart block leads to haemodynamic instability.

Condition-specific management includes treating acute coronary syndrome (i.e., antiplatelet medications, urgent revascularisation) and medication toxicity (e.g., glucagon for beta-blocker toxicity, calcium for calcium-channel toxicity, or digoxin antibody for digitalis toxicity). When present, electrolyte or pH disturbances and hypoxaemia should be treated appropriately.

Risks and balances of discontining possible causative medications (e.g., beta-blockers) should be weighed in each instance. Primary Options

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

digitalis toxicity digoxin immune Fab : consult specialist for guidance on dose OR beta-blocker toxicity glucagon : consult specialist for guidance on dose OR calcium-channel blocker toxicity calcium chloride : consult specialist for guidance on dose
2nd

PPM or cardiac resynchronisation therapy ICD placement

Severe symptoms include syncope or persistent, severe lightheadedness indicating profound decreases in the ventricular rate.

Permanent pacemaker (PPM) implantation is required if the cause of AV block is irreversible.View image For AV block, usually a dual-chamber (1 right atrial and 1 right ventricular lead) pacemaker is placed. The procedure includes a 2-inch incision at the non-dominant shoulder, placement of the leads through the subclavian vein, and placement of the pulse generator in a small subcutaneous pocket. The entire procedure usually takes a few hours and requires an overnight hospital stay.

Biventricular pacemaker (placement of a third wire, in a branch of the coronary sinus, to enable left ventricular pacing) with or without an implantable cardioverter-defibrillator (ICD) placement, may be considered when the left ventricular ejection fraction is <35%. [19] [20] [21] (An ICD is not indicated for patients with New York Heart Association [NYHA] Class IV heart failure symptoms: severe limitation of

Treatment Patient group first-degree AV block or type I second-degree AV block line Treatmenthide all

exercise capacity due to shortness of breath with symptoms even while at rest; these are mostly bedbound patients.)

Acute

Treatment approach
The goals of treatment are to ameliorate symptoms caused by AV block (regardless of degree) and to prevent syncope and sudden cardiac death (in advanced AV block).

Asymptomatic: first-degree AV block or type I second-degree heart block

No specific treatment is required. Patients are at low risk for progression to higher-degree AV block. ECGs may be rechecked if symptoms develop, but do not need to be rechecked on a routine basis.

Symptomatic: first-degree AV block or type I second-degree heart block

Occasionally, patients with profound first-degree AV block (>300 milliseconds) or those with type I second-degree heart block will develop associated symptoms and should be treated. The first line of treatment is to stop all AV-nodal blocking medications. The most common medications include beta-blockers, non-dihydropyridine calcium-channel blockers, and digitalis. While discontinuing these medicines may improve AV conduction, they are not likely to completely reverse a clinically significant AV block. If symptoms are severe enough, permanent pacemaker implantation should be considered. For AV block, usually a dual-chamber (1 right atrial and 1 right ventricular lead) pacemaker is placed. The entire procedure usually takes a few hours and requires an overnight hospital stay. Biventricular pacemaker with or without an implantable cardioverter-defibrillator (ICD) placement may

be considered when the left ventricular ejection fraction is <35%. [19] [20] [21]

Asymptomatic or mildly to moderately symptomatic: type II second-degree AV block or third-degree AV block

Medications blocking the AV node should be stopped first. Also, conditionspecific management should ensue, which should help treat any potentially reversible conditions causing AV-nodal blockade. This includes treating acute coronary syndrome (i.e., antiplatelet medications, urgent revascularisation) and medication toxicity (e.g., glucagon for beta-blocker toxicity, calcium for calcium-channel toxicity, or digoxin antibody for digitalis toxicity). When present, electrolyte or pH disturbances and hypoxaemia should be treated appropriately. These patients are at risk for progression to slower ventricular rates and development or worsening of symptoms. [22] In the absence of a reversible cause, these patients should undergo permanent pacemaker implantation. ICD placement may be considered when the left ventricular ejection fraction is <35%.

Severely symptomatic: type II second-degree AV block or third-degree AV block

As with asymptomatic or mildly to moderately symptomatic patients, those with severely symptomatic type II second-degree AV block or third-degree AV block (of irreversible cause) should receive aggressive supportive therapy, condition-specific management, and discontinuation of all AV-nodal blocking medications. Temporary pacing is used specifically with these types of AV block. Severe symptoms include syncope or persistent, severe lightheadedness indicating profound decreases in the ventricular rate. Transvenous pacing is much more reliable than transcutaneous pacing and should be performed by a cardiologist when the heart block leads to haemodynamic instability. If the condition does not improve, permanent pacemaker or ICD placement should be performed.

Considerations for causative medications

While discontinuing AV-nodal blocking medications (i.e., beta-blockers, nondihydropyridine calcium-channel blockers, and digitalis) may improve AV

conduction, complete reversal of clinically significant AV block is an unlikely result. This modest effect should be weighed in the long term against the potential medication benefit, such as the mortality benefit of beta-blockers in patients with CAD or salutary effects on blood pressure and heart rate.

Emerging treatments
Alternative pacing sites Traditionally, pacing in the right ventricle has always been undertaken from the apex, a site affording easy accessibility and good lead stability. However, it is increasingly recognised that this pacing site does not achieve the best haemodynamic result. [12] Alternative pacing sites such as right ventricular outflow tract, septum, His bundle, para-Hisian area, and left ventricle through the coronary sinus [23] [24] [25] [26] have been explored, appear to be safe, and hold promise for better haemodynamic results. Larger and longer-term studies are awaited before these sites can be recommended. Biological pacemakers Viral vectors, human embryonic stem cells, and adult human mesenchymal cells have been used to provide biological pacemaking. [27] This therapy is highly experimental and has been performed only in animals, but holds promise for possible therapy in humans in the future. Leadless pacemakers Pacemaker lead complications and failures remain significant clinical problems. Lead extraction for lead malfunction is associated with significant morbidity and can be fatal in a small percentage of cases. Hence, leadless device technology is appealing. The use of automatic generating systems [28] and ultrasound energy as power sources [29] [30] [31] is being explored in animals and humans. It remains largely experimental.

Monitoring
Patients with asymptomatic AV block not requiring permanent pacemaker implantation (i.e., asymptomatic firstdegree AV block or type I second-degree AV block) can be followed expectantly for the development of symptoms such as syncope, episodic pre-syncope, exertional dyspnoea or fatigue, or CHF. Repeat ECG recordings can be obtained if symptoms occur. These patients, especially in the setting of a narrow QRS interval, are at low risk for progressing to more advanced degrees of AV block.

Patients with symptomatic, irreversible AV block or irreversible advanced AV block should be considered for permanent pacemaker implantation. Patients who undergo permanent pacemaker implantation should have routine follow-up and monitoring in a device clinic.

Patient Instructions
Patients should be instructed to monitor and alert their physician concerning symptoms such as dizziness, exertional dyspnoea, syncope/transient loss of consciousness, fatigue, and any signs and symptoms of CHF. Patients should also be advised of their prognosis in order to maintain an appropriate level of concern.

Complications
Complicationhide all

pacemaker implantation sequelae In the short term, periprocedurally, the risks associated with pacemaker implantation are low: in the range of 2% to 3%. These include bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade, lead dislodgement, and pocket haematoma development. The risk of MI, stroke, and death is <1%. Long-term complications include pulse generator or lead malfunction and infection. The pulse generators run on batteries that average 7 to 10 years in longevity. Battery depletion requires replacing the pulse generator. Over a lifetime, there is some risk of infection of the lead, which may require extraction, a complex procedure that should be performed at specialised centres.

Last updated: Mar 15, 2

Prognosis
The prognosis is related to the degree of AV block [32] and the severity of associated symptoms. In certain conditions, such as sarcoid or amyloid heart disease or acute anterior MI, the underlying condition strongly determines prognosis. Non-randomised studies strongly suggest that permanent pacing improves survival in patients with third-degree AV block, especially if syncope has occurred. In patients with type II second degree AV block, especially when the block is infranodal or the QRS is wide, prognosis is compromised. Mortality remains high in patients with acute myocardial infarction in whom AV block occurs, as it reflects extensive myocardial damage. AV block occurring with inferior MI, rather than an anterior MI, is more likely to resolve. [1] Registry data indicate that symptomatic cardiac sarcoidosis with heart block, ventricular arrhythmias, or LV dysfunction is associated with a poor prognosis. [33] Along with the presence of concurrent myeloma,

presence and severity of cardiac involvement in primary amyloidosis determines prognosis. [34]

Asymptomatic first-degree or type I seconddegree AV block

First-degree AV block has been associated with about a 2-fold increase in the probability of atrial fibrillation, a 3-fold increase in the probability of pacemaker implantation, and an increase in all-cause mortality. [4]

Asymptomatic advanced AV block (type II second-degree or third-degree)

In symptomatic patients with irreversible AV block, symptoms are likely to persist or potentially worsen. Patients with irreversible advanced AV block (type II second-degree or third-degree) are at high risk for progression to third-degree AV block or ventricular asystole. [22] As such, these patients should be strongly advised to undergo permanent pacemaker implantation.

Symptomatic AV block treated with a permanent pacemaker

These patients have an excellent prognosis with a low rate of complications related to the pacemaker.