First-Degree Atrioventricular Block

Background

First-degree atrioventricular (AV) block, or first-degree heart block, is defined as prolongation of the PR interval on an electrocardiogram (ECG) to more than 200 msec.[1] The PR interval of the surface ECG is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). Normally, this interval should be between 120 and 200 msec in the adult population. First-degree AV block is considered “marked” when the PR interval exceeds 300 msec.[2]

Whereas conduction is slowed, there are no missed beats. In first-degree AV block, every atrial impulse is transmitted to the ventricles, resulting in a regular ventricular rate.

NextPathophysiology

The atrioventricular node (AVN) is the only normal electrical connection between the atria and the ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AVN is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus.

The bundle of His originates from the anteroinferior pole of the AVN and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles.

Blood supply to the AVN is provided by the AVN artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries.

The AVN has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AVN.

The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, the AVN, the bundle of His, the bundle branches, and the Purkinje fibers. Thus, as shown in electrophysiologic studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AVN, the His-Purkinje system, or a combination of these.

Overall, dysfunction at the AVN is much more common than dysfunction at the His-Purkinje system. If the QRS complex is of normal width and morphology on the ECG, then the conduction delay is almost always at the level of the AVN. If, however, the QRS demonstrates a bundle-branch morphology, then the level of the conduction delay is often localized to the His-Purkinje system.

Occasionally, the conduction delay can be the result of an intra-atrial conduction defect. Some causes of atrial disease resulting in a prolonged PR interval include endocardial cushion defects and Ebstein anomaly.[3]

PreviousNextEtiology

The following are the most common causes of first-degree AV block:

Intrinsic AVN diseaseEnhanced vagal toneAcute myocardial infarction (MI), particularly acute inferior wall MIMyocarditisElectrolyte disturbances (eg, hypokalemia, hypomagnesemia)Drugs (especially those drugs that increase the refractory time of the AVN, thereby slowing conduction)

A number of specific disorders and events have been implicated (see below).

Athletic training

Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.

Coronary artery disease

Coronary artery disease is a factor. First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units. His bundle electrocardiographic studies have shown that, in most of these patients, the AVN is the site of conduction block.

AV block is more common in the setting of inferior MI. In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy.[4]

Patients with AV block at the time of presentation had a higher in-hospital mortality than patients without AV block; however, the 2 groups had similar mortalities during the following year.[4] Patients who developed AV block after thrombolytic therapy had higher mortalities both in hospital and during the following year than patients without AV block. The right coronary artery was more often the site of infarction in patients with heart block than in those without heart block.

Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.

Idiopathic degenerative diseases of conduction system

Lev disease is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, or “sclerosis of the left side of cardiac skeleton” (including the mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum). Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block.

Lenègre disease is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in the mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lenègre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease does.

Drugs

Drugs that most commonly cause first-degree AV 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 glycosidesMagnesium

Although first-degree AV block is not an absolute contraindication for administration of drugs such as calcium channel blockers, beta-blockers, digoxin, and amiodarone, extreme caution should be exercised in the use of these medications in patients with first-degree AV block. Exposure to these drugs increases the risk of developing higher-degree AV block.

Mitral or aortic valve annulus calcification

The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.

Infectious disease

Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block. Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block. Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.

Collagen vascular disease

Rheumatoid arthritis, systemic lupus erythematosus (SLE), and scleroderma all may be associated with first-degree AV block. Rheumatoid nodules may occur in the central fibrous body and result in AV block. Fibrosis of the AVN or the adjacent myocardium in patients with SLE or scleroderma can cause first-degree AV block.

Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive.[5] In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.

Iatrogenesis

First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuance of the adenosine infusion.[6]

Marked first-degree AV block may occur after catheter ablation of the fast AVN pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to those of the pacemaker syndrome.

First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of an atrial septal defect using the Amplatzer septal occluder.[7] First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.

PreviousNextEpidemiology

In the United States, the prevalence of first-degree AV block among young adults ranges from 0.65% to 1.6%. Higher prevalence (8.7%) is reported in studies of trained athletes. The prevalence of first-degree AV block increases with advancing age; first-degree AV block is reported in 5% of men older than 60 years.[8] The overall prevalence is 1.13 cases per 1000 lives.

In a study of 2,123 patients aged 20-99 years, first-degree AV block was more prevalent among African-American patients than among Caucasian patients in all age groups except for those in the 8th decade of life.[8] In this study, the prevalence of first-degree AV block increased at age 50 years in both ethnic groups and gradually increased with advancing age. The peak in African-American patients occurred in the 10th decade of life, whereas the peak in Caucasian patients was in the 9th decade of life.[8]

PreviousNextPrognosis

The prognosis for isolated first-degree AV block is very good. This condition carries no increased risk of mortality, and progression from isolated first-degree heart block to high-degree block is very uncommon.[9] Patients with first-degree AV block and infranodal blocks, however, are at increased risk for progression to complete AV block.

Heart block in children with Lyme carditis tends to resolve spontaneously, with median recovery in 3 days (range, 1-7 days).[10]

Cheng et al found that first-degree heart block is associated with increased long-term risks of atrial fibrillation, pacemaker implantation, and all-cause mortality.[11] Their community-based cohort included 7575 individuals from the Framingham Heart Study who underwent baseline routine 12-lead ECG in 1968-1974 and were followed prospectively through 2007.

Compared with individuals whose PR intervals were 200 msec or shorter, those with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[11] Each 20-msec increment in PR interval was associated with an adjusted hazard ratio (HR) of 1.11 for atrial fibrillation, 1.22 for pacemaker implantation, and 1.08 for all-cause mortality.

Although no significant mortality or morbidity is related to isolated first-degree AV block, first-degree AV block in the setting of acute inferior MI may herald higher degrees of AV block. Markedly prolonged PR interval in patients with left ventricular systolic dysfunction may impair ventricular filling and thus reduce cardiac output.

PreviousProceed to Clinical Presentation , First-Degree Atrioventricular Block

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Second-Degree Atrioventricular Block

Practice Essentials

Second-degree atrioventricular (AV) block, or second-degree heart block, is characterized by disturbance, delay, or interruption of atrial impulse conduction through the AV node to the ventricles. Although patients with second-degree AV block may be asymptomatic, Mobitz type I (Wenckebach) AV block can cause significant symptoms, and Mobitz type II block may progress to complete heart block, with an associated increased risk of mortality.

Essential update: Prolonging survival in Mobitz type I second degree atrioventricular block

In a retrospective cohort study of older men (average age, 75 years) with Mobitz type I AV block, Coumbe et al found that implantation of a cardiac electronic device prolonged survival. Of the 299 patients in the study, 141 required an implantable cardiac electronic device, 17 of which were implantable cardioverter-defibrillators. After a median of approximately 3 years of follow-up, cardiac electronic device implantation was associated with a 46% reduction in mortality.[4]

Signs and symptoms

In patients with second-degree AV block, symptoms may vary substantially, as follows:

No symptoms (more common in patients with type I, such as well-trained athletes and persons without structural heart disease)Light-headedness, dizziness, or syncope (more common in type II)Chest pain, if the heart block is related to myocarditis or ischemiaA regularly irregular heartbeatBradycardia may be presentSymptomatic patients may have signs of hypoperfusion, including hypotension

See Clinical Presentation for more detail.

Diagnosis

ECG is employed to identify the presence and type of second-degree AV block. The typical ECG findings in Mobitz I (Wenckebach) AV block—the most common form of second-degree AV block—are as follows:

Gradually progressive PR interval prolongation occurs before the blocked sinus impulseThe greatest PR increment typically occurs between the first and second beats of a cycle, gradually decreasing in subsequent beats Shortening of the PR interval occurs after the blocked sinus impulse, provided that the P wave is conducted to the ventricleCommonly, junctional escape beats occur along with nonconducted P wavesA pause occurs after the blocked P wave that is less than the sum of the 2 beats before the blockDuring very long sequences (typically > 6:5), PR-interval prolongation may be minimal until the last beat of the cycle, when it abruptly becomes much greater Postblock PR-interval shortening remains the cornerstone of the diagnosis of Mobitz I block, regardless of whether the periodicity has typical or atypical features

The typical ECG findings in Mobitz II AV block are as follows:

Consecutively conducted beats with the same PR interval are followed by a blocked sinus P waveA PR interval in the first beat occurs after the block, with the same PR interval as the previous beatsA pause encompassing the blocked P wave is equal to exactly twice the sinus cycle length

The level of the block, AV nodal or infranodal (ie, in the specialized His-Purkinje conduction system), carries prognostic significance, as follows:

AV nodal blocks, which are the vast majority of Mobitz I blocks, carry a favorable prognosisWhen the block is localized to the AV node, no risk of progression to a Mobitz II block or a complete heart block exists[5] Infranodal blocks, whether Mobitz I or Mobitz II, carry significant risk of progression to complete heart block

Evaluating for stability of the sinus rate is important because conditions associated with increases in vagal tone may cause simultaneous sinus slowing and AV block and, therefore, mimic a Mobitz II block. In addition, diagnosing Mobitz II block in the presence of a shortened postblock PR interval is impossible.

An invasive His bundle recording is required to make the diagnosis of an infranodal block; however, ECG indications regarding the site of the block are as follows:

A Mobitz I block with a narrow QRS complex is almost always located in the AV nodeA normal PR interval with minuscule increments in AV conduction delay should raise the suggestion of an infranodal Wenckebach block; however, larger increments in AV conduction do not necessarily exclude infranodal Wenckebach block In the presence of a wide QRS complex, a type I block is more often infranodalAn increment in PR interval of longer than 100 msec favors a block site in the AV nodeA Mobitz II block associated with a wide QRS complex is always infranodal

Diagnostic electrophysiologic testing can help determine the level of the block and the potential need for a permanent pacemaker. Such testing is indicated for patients in whom His-Purkinje (infranodal) block is suspected but has not been confirmed, such as those with the following:

Mobitz I second-degree AV block associated with a wide QRS complex in the absence of symptoms2:1 second-degree AV block with a wide QRS complex in the absence of symptomsMobitz I second-degree block with a history of unexplained syncope

Other indications for electrophysiologic testing are as follows:

Patients with pseudo-AV block and those with premature, concealed junctional depolarization, which may be the cause of second- or third-degree AV block Patients with second- or third-degree AV block in whom another arrhythmia is suspected as the cause of the symptoms (eg, those who remain symptomatic after pacemaker placement)

Laboratory studies to identify possible underlying causes are as follows:

Serum electrolytes, calcium, and magnesium levelsA digoxin level in patients on digoxinCardiac biomarker testing in patients with suspected myocardial ischemiaMyocarditis-related laboratory studies (eg, Lyme titers, HIV serologies, enterovirus polymerase chain reaction [PCR], adenovirus PCR, Chagas titers) if clinically relevant Thyroid function studies if appropriate

See Workup for more detail.

Management

Acute treatment of Mobitz type I second-degree AV block is as follows:

In patients who have symptoms or who have concomitant acute myocardial ischemia or myocardial infarction (MI), admission is indicated to a unit with telemetry monitoring and transcutaneous pacing capabilities Symptomatic patients should be treated with atropine and transcutaneous pacingAtropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur

Acute treatment of Mobitz type II second-degree AV block is as follows:

Admit all patients to a unit with monitored beds, where transcutaneous and transvenous pacing capabilities are availableApply transcutaneous pacing pads to all patients with Mobitz II second-degree AV block, including those who are asymptomatic, because of the risk of progression to complete heart block Test the transcutaneous pacemaker to ensure capture; if capture cannot able be achieved, then insertion of a transvenous pacemaker is indicated, even in asymptomatic patients Urgent cardiology consultation is indicated for patients who are symptomatic type or are asymptomatic but unable to achieve capture with transcutaneous pacing Some institutions recommend insertion of a transvenous pacemaker for all new Mobitz type II blocksHemodynamically unstable patients for whom an emergency cardiology consult is not available should undergo placement of a temporary transvenous pacing wire in the emergency department, with confirmation of correct positioning by chest radiography

Guidelines recommend the following as indications for permanent pacing in second-degree AV block[6, 7] :

Second-degree AV block associated with signs such as bradycardia, heart failure, and asystole for 3 seconds or longerSecond-degree AV block with neuromuscular diseases, such as myotonic muscular dystrophy, Erb dystrophy, and peroneal muscular atrophy, even in asymptomatic patients (progression of the block is unpredictable in these patients); in some of these patients, an implantable cardioverter defibrillator (ICD) may be appropriate Mobitz II second-degree AV block with wide QRS complexesAsymptomatic Mobitz I second-degree AV block with the block at intra- or infra-His level found on electrophysiologic testing

In some cases, the following may also be indications for permanent pacemaker insertion:

Persistent, symptomatic second-degree AV block after MI, especially if it is associated with bundle-branch blockHigh-grade AV block after anterior MI, even if transientPersistent second-degree AV block after cardiac surgery

Permanent pacing may not be required in the following situations:

Transient or asymptomatic second-degree AV block after MISecond-degree AV block in patients with drug toxicity, Lyme disease, or hypoxia in sleepWhenever correction of the underlying pathology is expected to resolve second-degree AV block

See Treatment and Medication for more detail.

Image library

See the image below.

Typical Mobitz I atrioventricular block with progressive prolongation of PR interval before blocked P wave. Pauses are always less than sum of 2 preceding beats because PR interval after pause always shortens. NextBackground

Second-degree atrioventricular (AV) block, or second-degree heart block, is a disorder characterized by disturbance, delay, or interruption of atrial impulse conduction to the ventricles through the atrioventricular node (AVN). Electrocardiographically, some P waves are not followed by a QRS complex. The AV block can be permanent or transient, depending on the anatomic or functional impairment in the conduction system.[1]

Second-degree AV block is mostly classified as either Mobitz I (Wenckebach) or Mobitz II AV block. The diagnosis of Mobitz I and II second-degree AV block is based on electrocardiographic (ECG) patterns, not on the anatomic site of the block. Precise localization of the site of the block within the specialized conduction system is, however, critical to the appropriate treatment of individuals with second-degree AV block.

Mobitz I second-degree AV block is characterized by a progressive prolongation of the PR interval. Ultimately, the atrial impulse fails to conduct, a QRS complex is not generated, and there is no ventricular contraction. The PR interval is the shortest in the first beat in the cycle.

Mobitz II second-degree AV block is characterized by an unexpected nonconducted atrial impulse, without prior measurable lengthening of the conduction time. Thus, the PR and R-R intervals between conducted beats are constant.[2, 3]

Besides Mobitz I and II, other classifications used to describe forms of second-degree AV block are 2:1 AV block and high-grade AV block. By itself, a 2:1 AV block cannot be classified as either Mobitz I or Mobitz II, because only 1 PR interval is available for analysis before the block. Both a 2:1 AV block and a block involving 2 or more consecutive sinus P waves are sometimes referred to as high-grade AV block. In high-grade AV block, some beats are conducted, in contrast to what is seen with third-degree AV block.

PreviousNextPathophysiology

Mobitz I second-degree AV block most often results from conduction disturbances in the AVN (~70% of cases); however, in a minority of cases (~30%), it may be due to infranodal block.

Mobitz I block is rarely secondary to AVN structural abnormalities when the QRS complex is narrow in width and no underlying cardiac disease is present. In this setting, Mobitz I block can be vagally mediated and may be observed in conditions associated with relative activation of the parasympathetic nervous system, such as in well-trained athletes, cardiac glycoside (ie, digoxin) excess, or neurally mediated syncope syndromes.

A vagally mediated AV block occurs in the AVN when vagal discharge is enhanced (eg, as a result of pain, carotid sinus massage, or hypersensitive carotid sinus syndrome). Accordingly, vagally mediated AV block can be associated with ECG evidence of sinus slowing. High vagal tone can occur in young patients or athletes at rest.[2] Mobitz type I AV block has been described in 2-10% of long distance runners.[8]

A vagally mediated AV block improves with exercise and may occur more commonly during sleep, when parasympathetic tone dominates. If an increase in sympathetic tone (eg, exercise) initiates or exacerbates a type I block, infranodal block should be considered.[9]

Infrequently, Mobitz I AV block can occur with a block localized to the His bundle or distal to the His bundle. In this situation, the QRS complex may be wide, and the baseline PR interval is usually shorter with smaller PR increments preceding the block. The presence of a narrow QRS complex suggests the site of the delay is more likely to be in the AVN; however, a wide QRS complex may be observed with either AVN or infranodal conduction delay.[2] Mobitz I block with infranodal block carries a worse prognosis than AVN block.

In Mobitz type II block, the conduction delay generally occurs infranodally. The QRS complex is likely to be wide, except in patients where the delay is localized to the bundle of His. The typical infranodal location of a Mobitz II block is associated with a higher risk to the patient.

PreviousNextEtiology

Cardioactive drugs are an important cause of AV block.[10, 11, 12] They may exert negative (ie, dromotropic) effects on the AVN directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, calcium channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block.

Of the antiarrhythmic medications that may cause second-degree AV block, sodium channel blockers, such as procainamide, cause more distal block in the His-Purkinje system. Persistent second-degree AV block following adenosine infusion for nuclear stress testing has been reported.[13]

The AV block may not resolve in many of the patients who take cardioactive medications. This suggests an underlying conduction disturbance in addition to the medications as the etiology of the AV block. At toxic levels, other pharmacologic agents, such as lithium, may be associated with AV block. Benzathine penicillin has been associated with second-degree AV block.[14] Presynaptic alpha agonists (eg, clonidine) may rarely be associated with, or exacerbate, AV block.

Various inflammatory, infiltrative, metabolic, endocrine, and collagen vascular disorders have been associated with AVN block, as follows.

Inflammatory diseases -Endocarditis, myocarditis, Lyme disease,[15] acute rheumatic feverInfiltrative diseases -Amyloidosis, hemochromatosis, sarcoidosis (AV conduction abnormalities can be the first sign of sarcoidosis[16] ) Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma[17] Metabolic and endocrine disorders – Hyperkalemia, hypermagnesemia, Addison disease, hyperthyroidism, myxedema, thyrotoxic periodic paralysis[18] Collagen vascular diseases -Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus erythematosus, Reiter syndrome, mixed connective tissue disease[19]

Other conditions or procedures associated with AV block are as follows.

Cardiac tumorsTrauma (including catheter-related, especially in the setting of preexisting left bundle-branch block)Following transcatheter valve replacementMyocardial bridging[20] Ethanol septal reduction (also called transcoronary ablation of septal hypertrophy for the treatment of obstructive hypertrophic cardiomyopathy) Transcatheter closure of atrial and ventricular septal defects[21, 22] Corrective congenital heart surgery, especially those near the septumProgressive (age-related) idiopathic fibrosis of the cardiac skeletonValvular heart disease complications, especially aortic stenosis and aortic valve replacement surgeryFollowing some catheter ablation proceduresObstructive sleep apnea[23] Muscular dystrophiesAcute ethanol poisoningAcute myocardial infarction (MI)

Any cardiac tumor has the potential for affecting the AVN if it will be in close anatomic relation with the node. Myxoma is the most common primary cardiac tumor, but a variety of secondary tumors may also be found in the heart. Cho et al reported a patient with primary cardiac lymphoma who presented with unexplained dyspnea and a progressive AV block.[10]

Erkapic and colleagues studied the incidence of AV block after transcatheter aortic valve replacement and found that up to 34% of patients (mean age, 80 ± 6 years) experienced second- and third-degree AV block, mainly within the first 24 hours of the procedure.[24] They did not observe any improvement in the AV block within the next 14 days, and most of these patients required permanent pacemaker implantation.

In this report, preoperative right bundle-branch block and CoreValve prosthesis were associated with higher rate of AV block and subsequent pacemaker implantation.[24] On the basis of this report, the rate of postoperative AV block seems significantly higher in transcatheter valve replacement than a traditional surgical approach.

Nardi and colleagues reported pacemaker implantation in only 3% of patients undergoing isolated aortic valve replacement.[25] Nevertheless, patients who undergo transcatheter valve replacement are much sicker and older than those who undergo a traditional surgical valve replacement (80 ± 6 years in the Erkapic study compared with 69 ± 12 years in the Nardi study).

Catheter ablation of any structure close to the AVN can be associated with AV block as an adverse effect of this procedure. In particular, AV block may be seen following ablation for AV nodal reentrant tachycardia (AVNRT) and some accessory pathways. Bastani and colleagues suggest that cryoablation of superoparaseptal and septal accessory pathways may be a safer alternative to radiofrequency ablation in this regard.[26]

The conduction defects in patients with muscular dystrophy are progressive; therefore, these patients should undergo careful workup and follow-up, even if they present with a benign conduction defect such as first-degree AV block.[27]

Acute ethanol poisoning has been reported to be associated with transient first-degree AV block; however, a few case reports have shown occasional association with Mobitz I AV block and high-degree AV block.[28]

Genetic factors

In some patients, AV block may be an autosomal dominant trait and a familial disease. Several mutations in the SCN5A gene have been linked to familial AV block. Different mutations in the same gene have been reported in other dysrhythmias such as long QT syndrome (LQTS) and Brugada syndrome. In LQTS, a pseudo 2:1 AV block may be seen as a result of a very prolonged ventricular refractory period. Nevertheless, a true 2:1 AV block with possible primary pathology in the AVN and conduction system has also been reported in LQTS.[29]

PreviousNextEpidemiology

In the United States, the prevalence of second-degree AV block in young adults is reported to be 0.003%. However, the rate is significantly higher among trained athletes.[30] Nearly 3% of patients with underlying structural heart disease develop some form of second-degree AV block. The male-to-female ratio of second-degree AV block is 1:1.

PreviousNextPrognosis

The level of the block determines the prognosis. AV nodal blocks, which are the vast majority of Mobitz I blocks, carry a favorable prognosis, whereas infranodal blocks, whether Mobitz I or Mobitz II, may progress to complete block with a worse prognosis. However, Mobitz I AV block may be significantly symptomatic. When a Mobitz I block occurs during an acute MI, mortality is increased. Vagally mediated AV block is typically benign from a mortality standpoint but may lead to dizziness and syncope.

Mobitz I second-degree AV block is localized to the AVN and thus is not associated with any increased risk of morbidity or death, in the absence of organic heart disease. In addition, when the block is localized to the AVN, no risk of progression to a Mobitz II block or a complete heart block exists.[5] However, the risk of progression to complete heart block is significant when the level of block is in the specialized His-Purkinje conduction system (infranodal).

Mobitz type II blocks do carry a risk of progressing to complete heart block, and thus are associated with an increased risk of mortality.[5, 2] In addition, they are associated with MI and all its attendant risks. Mobitz II block may produce Stokes-Adams syncopal attacks. Mobitz I blocks localized to the His-Purkinje system are associated with the same risks as type II blocks.

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Atrioventricular Dissociation

Background

Atrioventricular (AV) dissociation is a condition in which the atria and ventricles do not activate in a synchronous fashion but beat independent of each other. AV dissociation usually refers to the situation in which the ventricular rate is the same or faster than the atrial rate.[1, 2] When the atrial rate is faster and the atria and ventricles are beating independently, complete heart block is present; this is distinct from AV dissociation. While complete heart block can be properly considered a form of AV dissociation, it is discussed in detail in Atrioventricular Block and is not considered further in this article. Also, in AV dissociation, no retrograde ventriculoatrial conduction occurs.

When the atrial rate is the same as the ventricular rate but the P wave is not conducting, the rhythm disturbance is known as isorhythmic AV dissociation. When the rates are similar but occasionally the atria conduct to the ventricles, the rhythm is known as interference AV dissociation.

AV dissociation can be a benign phenomenon and can be complete or incomplete. When incomplete, some of the P waves conduct and capture the ventricles (ie, interference AV dissociation), but if they do not, it is complete AV dissociation. Complete AV dissociation can mimic AV block, but the fact that none of the P waves conduct has more to do with timing of the P waves in relation to the QRS complex rather than the presence of AV block.

NextPathophysiology

A normal cardiac impulse arises from the sinus node and is conducted through the AV junction, the bundle of His, and the bundle branches to the ventricles. The sinus node is the dominant pacemaker because its intrinsic rate is faster than subsidiary pacemakers in the AV junction or in the ventricle. AV dissociation can result from (1) slowing of the dominant pacemaker (sinus node), which allows an escape junctional or ventricular rhythm, or (2) acceleration of a normally slower (subsidiary) pacemaker, such as a junctional site or a ventricular site that activates the ventricles without retrograde atrial capture.

Conditions that can initiate AV dissociation include surgical and anesthesia interventions (including intubation), conditions that increase catecholamine levels (including infusions of inotropes) and drugs that block catecholamines, sinus node disease, digoxin toxicity, myocardial infarction and other structural heart disease, hyperkalemia, vagal activation (eg, neurocardiogenic syncope, vomiting), ventricular tachycardia, or ventricular pacing. AV dissociation can be seen after radiofrequency ablation of the slow pathway responsible for AV nodal reentry if some of the vagal fibers are damaged. After exertion, if AV dissociation is present from an escape pacer, it can be a normal phenomenon. Whatever the cause, AV dissociation usually is secondary to some other cause.

PreviousNextEpidemiologyFrequencyInternational

Little epidemiologic information is available regarding the frequency of AV dissociation.

Mortality/Morbidity

AV dissociation by itself can be benign. Any adverse effects are related to ensuing bradycardia, AV dyssynchrony, or underlying conditions.

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Atrioventricular Nodal Reentry Tachycardia

Background

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). The substrate for AVNRT is the presence of dual AV nodal pathways. (See Etiology.)[1, 2]

Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, greater specificity in nomenclature, based on the mechanism of reentry, has been possible. Such improved classification aids in the choice of appropriate therapies. (See Etiology, Prognosis, Treatment, and Medication.)

AVNRT is usually well tolerated, often occurring in patients with no structural heart disease. (See Prognosis, Presentation, and Workup.)

Patient education

Patients should be instructed on vagal maneuvers (Valsalva, diving reflex), used to try to terminate an episode of AVNRT. Patients with hemodynamic compromise or syncope should be instructed on avoiding activities that could be dangerous to them or to others (eg, driving, swimming) while the risk of an episode remains. Ablation obviates the need for any long-term restriction.

For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia.

NextEtiology

The substrate for AVNRT may be functional rather than anatomic. These arrhythmias occur in young, healthy patients and in those with chronic heart disease.

In patients with atrioventricular (AV) nodal reentry, the AV node is functionally divided into 2 longitudinal pathways that form the reentrant circuit. (In contrast to a bypass tract, dual AV nodal physiology is often an acquired abnormality.) In the majority of patients, during AVNRT, antegrade conduction occurs to the ventricle over the slow (alpha) pathway, and retrograde conduction occurs over the fast (beta) pathway. (See the image below.)

Electrophysiological mechanism of atrioventricular nodal reentry tachycardia.

In most patients with this arrhythmia, the tachycardia is initiated when an atrial premature complex is blocked in the fast pathway with a longer refractory period and conducts in the slow pathway with a shorter refractory period. While the impulse conducts to the ventricle in the slow pathway (antegrade conduction), the fast pathway recovers so that the impulse can conduct retrograde up the fast pathway to the atrium and the atrial end of the slow pathway (retrograde conduction).

In approximately one third of patients, AVNRT is induced by premature ventricular stimulation. In addition to the typical mechanism of AV nodal reentry described above, atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in the fast pathway and retrograde conduction in the slow pathway. Less commonly, the reentrant circuit can be over 2 slow pathways, the so-called slow-slow AV nodal reentry. (See the images below.)

Atypical atrioventricular nodal reentry tachycardia. Typical atrioventricular nodal reentry tachycardia. PreviousNextEpidemiology

In the United States, AVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT. The prevalence of SVT in the general population is likely several cases per thousand persons. Internationally, the occurrence of AVNRT is similar to that in the United States.

AVNRT may occur in persons of any age. It is common in young adults, but some patients do not present until their seventh or eighth decade or later.

PreviousNextPrognosis

The prognosis for patients with AVNRT is usually good in the absence of structural heart disease. Most patients respond to medications to prevent recurrence or to radiofrequency ablation, which is approximately 95% curative and has a low risk of complications. It is the preferred method of treatment for most patients.

Complications of AVNRT include hemodynamic compromise, congestive heart failure, syncope, tachycardia-induced angina, cardiomyopathy, myocardial ischemia, and myocardial infarction.

PreviousProceed to Clinical Presentation , Atrioventricular Nodal Reentry Tachycardia

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Third-Degree Atrioventricular Block

Background

Third-degree atrioventricular (AV) block, also referred to as third-degree heart block or complete heart block, is a disorder of the cardiac conduction system where there is no conduction through the atrioventricular node (AVN). Therefore, complete dissociation of the atrial and ventricular activity exists.[1] The ventricular escape mechanism can occur anywhere from the AVN to the bundle-branch Purkinje system.[2]

It is important to realize that not all patients with AV dissociation have complete heart block. For example, patients with ventricular tachycardia have AV dissociation, but not complete heart block; in this example, AV dissociation is due to the ventricular rate being faster than the intrinsic sinus rate. 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).

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 Clinical.)

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 a permanent pacemaker or an implantable cardioverter defibrillator (ICD).

NextPathophysiology

In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface 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 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, AV block can be divided 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 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 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 2 main subcategories, Mobitz type I (Wenckebach) and Mobitz type II.

In the Mobitz I second-degree AV block, the PR interval prolonging 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 the overall PR interval increases. 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 beating should prompt a careful evaluation for Wenckebach conduction (though 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 3 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 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 (ie, 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.[2]

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. It 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 PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of atrial/sinus rate will result in restoration of normal conduction.

PreviousNextEtiology

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.

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).[3]

The 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[4] Infectious causes - Lyme borreliosis (particularly in endemic areas), Trypanosoma cruzi infection,[5] rheumatic fever, myocarditis, Chagas disease, Aspergillus myocarditis, varicella-zoster virus infection,[6] valve ring abscess Rheumatic diseases - Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, sclerodermaInfiltrative processes - Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myelomaNeuromuscular disorders - Becker muscular dystrophy, myotonic muscular dystrophyIschemic or infarctive causes - AVN block associated with inferior wall myocardial infarction (MI), His-Purkinje block associated with anterior wall MI (see below)Metabolic causes - Hypoxia, hyperkalemia, hypothyroidismToxins – “Mad” honey (grayanotoxin), cardiac glycosides (eg, oleandrin), and othersPhase IV block (also known as bradycardia-related block)Iatrogenic causes (see below)Drugs

Complete heart block can develop from 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.[7, 8] 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 redundant vascular supply to the AVN from all coronary arteries.

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 is involved 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. 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.

Iatrogenesis

AV block may be associated with aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention 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.[9] Major risks factors identified for the need for permanent pacing are aortic valve surgery, preexisting conduction disease (either right or left bundle-branch block), bicuspid aortic valve, annular calcification, and female gender. 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.

PreviousNextEpidemiology

In the United States, the prevalence of third-degree AV block is 0.02%. Worldwide, the prevalence of third-degree AV block is 0.04%.[10]

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.

PreviousNextPrognosis

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

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) secondary 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. The complications related to pacemaker insertion are rare (

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Atrioventricular Block

Practice EssentialsSigns and symptoms

Signs and symptoms of atrioventricular (AV) block include the following:

First-degree AV block: Generally not associated with any symptoms; it is usually an incidental finding on electrocardiographySecond-degree AV block: Usually is asymptomatic, but in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur; may manifest on physical examination as bradycardia (especially Mobitz II) and/or irregularity of heart rate (especially Mobitz I [Wenckebach]) Third-degree AV block: Frequently associated with symptoms such as fatigue, dizziness, light-headedness, presyncope, and syncope; associated with profound bradycardia unless the site of the block is located in the proximal portion of the atrioventricular node (AVN)

In third-degree AV block, exacerbation of ischemic heart disease or congestive heart failure caused by AV block–related bradycardia and reduced cardiac output may lead to specific, clinically recognizable symptoms, such as the following:

Chest painDyspneaConfusionPulmonary edema

See Clinical Presentation for more specific information.

Diagnosis

Laboratory studies

Although laboratory studies are not usually indicated in patients with AV block, the following may be helpful in certain cases:

Electrolyte and drug levels (eg, digitalis): In patients with second- or third-degree AV block, when suspicion of increased potassium level or drug toxicity exists Cardiac enzyme levels: In patients with second- or third-degree AV block that might be a manifestation of acute myocardial infarction Infection, myxedema, or connective tissue disease studies: If clinical evaluation suggests systemic illness

Electrocardiography

Routine electrocardiographic (ECG) recording and cardiac monitoring with careful evaluation of the relationship between P waves and QRS complexes are the standard tests leading to proper diagnosis of AV blocks. Identifying episodes of transient AV block with sudden pauses and/or low heart rate causing syncopal episodes may require any of the following:

24-hour Holter monitoringMultiple ECG recordingsEvent (loop) ECG recordingsMonitoring with implantable loop recorders (Reveal, Medtronic, Inc; Confirm, St Jude Medical, Inc) in selected cases

Additional modalities

Other means of evaluating patients for AV block can include the following:

Electrophysiologic testing: Indicated in a patient with suspected AV block as the cause of syncopeEchocardiography: May be useful in diagnosing underlying comorbid conditions, such as aortic valve stenosis with calcification, wall motion abnormalities in acute ischemia, cardiomyopathy, and congenital heart disease (eg, congenitally corrected transposition of the great vessels) Exercise: May be used to evaluate 2:1 heart block and to differentiate a Mobitz I second-degree AV block from a Mobitz II second-degree AV block

See Clinical Presentation and Workup for more specific information on the diagnosis of atrioventricular block.

Management

Pacemaker implantation

Implantation of a permanent pacemaker is the therapy of choice in advanced AV block. Recommendations for the implantation of pacemakers and arrhythmia devices, as devised by the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS), include the following[1] :

First-degree AV block and Mobitz I second-degree AV block: Do not generally require treatment unless they cause symptoms and are not due to a reversible cause Mobitz II second-degree AV block and third-degree AV block: Usually require temporary and/or permanent cardiac pacingThird-degree AV block: Patients with persistent bundle branch block and transient third-degree AV block may benefit from permanent pacing therapy, especially after anterior myocardial infarction; nonrandomized studies strongly suggest that permanent pacing improves survival in patients with third-degree AV block, especially if syncope has occurred

Pharmacologic therapy

Considerations regarding the administration of anticholinergic agents include the following:

Long-term medical therapy is not indicated in AV blockAtropine administration or isoproterenol infusion may improve AV conduction in emergencies in which bradycardia is caused by a proximal AV block Atropine administration or isoproterenol infusion may worsen conduction if the block is in the His-Purkinje system

See Treatment and Medication for more specific information on the treatment of atrioventricular block.

Image libraryFirst-degree atrioventricular block. PR interval is constant and is 280 msec. NextBackground

Atrioventricular (AV) block occurs when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized.

First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (> 200 msec in adults and > 160 msec in young children). The upper limit of the reference range for the PR interval is age-dependent in children. All atrial impulses reach the ventricles in first-degree AV block; however, conduction is delayed within the AV node (see the image below).

First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) that fail to conduct to the ventricles in 1 of the following 4 ways.

The first form of second-degree AV block is Mobitz I second-degree AV block (Wenckebach block), which consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval).

An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so forth (see the image below). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed intrahisian or infrahisian Wenckebach (depending if the block occurs within or below the His-Purkinje system).

Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortened PR interval following the dropped beat.

The second form is Mobitz II second-degree AV block, which is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, so that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed (see the image below).

Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.

The third form is high-grade AV block, which consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or higher, and the PR interval of conducted beats is constant. This is a distinct form of complete AV block, in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.

The fourth form is 2:1 AV block. This could be either Mobitz I or Mobitz II, but distinguishing one variety from the other is nearly impossible.

Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats/min, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats/min.

No relationship exists between the rhythm of P waves and the rhythm of QRS complexes in third-degree AV block. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate) (see the image below).

Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the atrial and ventricular activity.

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal.

AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex.

AV block may also occur in patients with atrial fibrillation (see the Atrial Fibrillation Center). Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

PreviousNextPathophysiology

The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. This node consists of 3 parts—atrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal portion causes the slowest conduction.

The AVN is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. It receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle in a 1:1 ratio. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction.

The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur.

First-degree AV block and second-degree Mobitz I AV block usually involve a delay at the level of the AVN, whereas second-degree Mobitz II AV block generally involves blockage in the His bundle or lower regions of the conduction system. Third-degree AV block involves conduction disturbances in the AV node or the His-Purkinje system.

In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats/min. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats/min in the region of His bundle), and a narrower QRS duration.

PreviousNextEtiology

Delay or lack of conduction through the AV node has multiple causes.

First-degree AV block and Mobitz I (Wenckebach) second-degree AV block may occur in healthy, well-conditioned people as a physiologic manifestation of high vagal tone. Mobitz I AV block also may occur physiologically at high heart rates (especially with pacing) as a result of increased refractoriness of the AVN, which protects against conducting an accelerated arrhythmia to the ventricles.

AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AVN level; this may occur through other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block resulting from ischemia or infarction of bundle branches.

Degenerative changes in the AVN or bundle branches (eg, fibrosis, calcification, or infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block.

In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).[2]

Infiltrative myocardial diseases resulting in AV block include sarcoidosis, myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification. Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block. Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue.

Surgical procedures (eg, aortic valve replacement and congenital defect repair) may cause AV block, as may other therapeutic procedures (eg, AV node ablation and alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy). Patients with corrected transposition of the great vessels have anterior displacement of the AVN and are prone to develop complete heart block during right heart catheterization or surgical manipulation.

A variety of drugs may affect AV conduction. The most common of these include digitalis glycosides, beta-blockers, calcium channel blockers, adenosine, and other antiarrhythmic agents.

PreviousNextEpidemiology

First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Mobitz II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas Mobitz I (Wenckebach) second-degree AV block is observed in 1-2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare, at 1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks’ gestation and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers.

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block.

The international incidence is similar to that of the United States.

Age-, sex-, and race-related demographics

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease). A 60% female preponderance exists in congenital third-degree AV block. For acquired third-degree AV block, a 60% male preponderance exists. No racial proclivity exists in AV blocks.

PreviousNextPrognosis

Patients treated with permanent pacing to treat AV blocks have an excellent prognosis. Patients with advanced AV blocks who are not treated with permanent pacing remain at high risk of sudden cardiac death.

Although AV block generally is not associated with major morbidity, progressive degrees of AV block carry increasing morbidity and mortality.

Cheng et al found that first-degree AV block (ie, PR interval > 200 msec) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality.[3] In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12-lead ECG in 1968-1974, 124 individuals had PR intervals > 200 msec on the baseline examination.

On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[3] For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk.

A prospective cohort study of 938 patients with stable coronary artery disease were examined to assess if first-degree AV block was associated with an increased risk of heart failure and mortality. Patients were classified as a PR interval of 220 ms or less. Patients with first-degree AV block were at increased risk for heart failure hospitalization (age-adjusted heart rate, 2.33; 95% CI, 1.49-3.65; P = 0.0002), mortality (age-adjusted heart rate, 1.58; 95% CI, 1.13-2.20; P = 0.008], cardiovascular mortality (age-adjusted heart rate 2.33; 95% CI, 1.28-4.22; P = 0.005], and the combined endpoint of heart failure hospitalization or cardiovascular mortality (age-adjusted heart rate, 2.43: 95% CI, 1.64–3.61; P ≤ 0.0001). These associations persisted after multivariable adjustment for heart rate, medication use, ischemic burden, and QRS duration. Despite adjusting for systolic and diastolic dysfunction, first-degree AV block wasassociated with anincreased risk for heart failure or cardiovascular death (heart rate, 1.61; 95% CI, 1.02–2.54; P = 0.04).[4]

The low heart rate observed in third-degree or Mobitz II second-degree AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

PreviousNextPatient Education

Patients with implanted pacemakers require additional education, with particular emphasis on situations involving exposure to magnetic and electrical fields (eg, airport security gates) and training regarding transtelephonic monitoring of pacemaker function.

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