Second-Degree Atrioventricular Block

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Second-degree atrioventricular (AV) block, or second-degree heart block, is a disease of the cardiac conduction system in which the conduction of atrial impulse through the AV node and/or His bundle is delayed or blocked. Patients with second-degree AV block may be asymptomatic or they may experience variety of symptoms such lightheadedness and syncope. Mobitz type II AV block may progress to complete heart block, with an associated increased risk of mortality.

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 ischemia

A regularly irregular heartbeat

Bradycardia may be present

Symptomatic patients may have signs of hypoperfusion, including hypotension

See Clinical Presentation for more detail.

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 impulse

The 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 ventricle

Junctional escape beats may occur along with nonconducted P waves

A pause occurs after the blocked P wave that is less than the sum of the 2 beats before the block

During very long sequences (typically >6:5), PR-interval prolongation may be inapparent and minimal until the last beat of the cycle, when it abruptly becomes much greater

Post-block PR-interval shortening remains the cornerstone of the diagnosis of Mobitz I block, regardless of whether the periodicity has typical or atypical features

R-R intervals shorten as PR intervals become longer

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 wave

PR interval in the first beat after the block is similar to the PR interval before the AV block

A 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 prognosis

AV nodal blocks do not carry the risk of direct progression to a Mobitz II block or a complete heart block [1] ; however, if there is an underlying structural heart disease as the cause of  the AV block, a more advanced AV block may manifest in the later stages of the disease 

Infranodal blocks 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 post-block 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 node

A 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, AV block is more often infranodal

An increment in PR interval of longer than 100 msec favors a block site in the AV node

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 symptoms

2:1 second-degree AV block with a wide QRS complex in the absence of symptoms

Mobitz 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)

In most cases, however, further monitoring (either inpatient rhythm monitoring or ambulatory ECG monitoring) provides adequate diagnostic information such that, currently, it is rare to perform an electrophysiology study solely for the evaluation of conduction disease.

Laboratory studies to identify possible underlying causes are as follows:

Serum electrolytes, , and magnesium levels

A digoxin level in patients on digoxin

Cardiac biomarker testing in patients with suspected myocardial ischemia

Myocarditis-related laboratory studies (eg, Lyme titers, HIV serologies, enterovirus polymerase chain reaction [PCR], adenovirus PCR, Chagas titers), if clinically relevant

Infection-related studies, apropos a valve ring abscess

Thyroid function studies if appropriate

See Workup for more detail.

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 pacing immediately, followed by transvenous temporary pacing until further workup detemines the etiology of the disease

Atropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur. Atropine increases the conduction in the AV node. If the conduction block is infranodal (eg if the block is Mobitz II), an increase in AV nodal conduction by atropine only worsens the infranodal conduction delay and increases the AV block. 

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 available

Apply 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 or are asymptomatic but unable to achieve capture with transcutaneous pacing

It is reasonable to insert a transvenous pacemaker for all new Mobitz type II blocks

Hemodynamically 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 [2, 3] :

Second-degree AV block associated with signs such as bradycardia, heart failure, and asystole for 3 seconds or longer while the patient is awake

Second-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 complexes

Asymptomatic Mobitz I second-degree AV block with the block at intra- or infra-His level found on electrophysiologic testing. Some of the electrophysiologic findings of an intra-His block include an HV interval longer than 100 ms, doublng of the HV interval after administration of procainamide, and the presence of split double potentials on the His recording catheter.

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 block; AV block resulting from right coronary artery occlusion tends to resolve over a few days after revascularization versus left anterior descending artery MI, which results in permanent AV block

High-grade AV block after anterior MI, even if transient

Persistent 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 MI, particularly after right coronary artery occlusion

Second-degree AV block in patients with drug toxicity, Lyme disease, or hypoxia in sleep

Whenever correction of the underlying pathology is expected to resolve second-degree AV block

AV block after transcatheter aortic valve implantation may occur. This is a relatively new technology, and there is not enough adequte evidence to guide the patient’s therapies in this situation. In some cases, depending on the type of the implanted valve, baseline ECG features, degree and location of the aortic valve calcification, and the patient’s comorbidities, implanting a permanent pacemaker outside of conventional criteria may be a reasonable and safe approach. 

See Treatment and Medication for more detail.

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) and bundle of His. 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. [4]

Second-degree AV block is mostly classified as either Mobitz I (Wenckebach; see the image below) 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. The R-R interval shortens during the Wenckebach 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. [5, 6]

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. Nevertheless, there may be clues about the site of the conduction block on the rhythm strip. For example, the presence of a normal PR interval and wide QRS points to an infranodal AV block site. 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.

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 and no underlying cardiac disease is present. In this setting, Mobitz I block is likely 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. [5] Mobitz type I AV block has been described in 2-10% of long distance runners. [7]

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. [8]

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. [5] 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.

Cardioactive drugs are an important cause of AV block. [9, 10, 11] They may exert negative (ie, dromotropic) effects on the AVN directly, indirectly via the autonomic nervous system, or both. Digoxin, beta-blockers, channel blockers, and certain antiarrhythmic drugs have been implicated in second-degree AV block. More recently, administration of the first dose of fingolimod, an immunosuppressant used to treat relapsing forms of multiple sclerosis, has been associated with second-degree AV block (Mobitz types I and II); these effects may persist for several days following fingolimod initiation. [12, 13]

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. [14]

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. [15] 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, [16] acute rheumatic fever

Infiltrative diseases –Amyloidosis, hemochromatosis, sarcoidosis (AV conduction abnormalities can be the first sign of sarcoidosis [17] )

Infiltrative malignancies, such as Hodgkin lymphoma and other lymphomas, and multiple myeloma [18]

Metabolic and endocrine disorders – Hyperkalemia, hypermagnesemia, Addison disease, hyperthyroidism, myxedema, thyrotoxic periodic paralysis [19]

Collagen vascular diseases –Ankylosing spondylitis, dermatomyositis, rheumatoid arthritis, scleroderma, lupus erythematosus, Reiter syndrome, mixed connective tissue disease [20]

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

Cardiac tumors

Trauma (including catheter-related, especially in the setting of preexisting left bundle-branch block)

Following transcatheter valve replacement

Myocardial bridging [21]

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 [22, 23]

Corrective congenital heart surgery, especially those near the septum

Progressive (age-related) idiopathic fibrosis of the cardiac skeleton

Valvular heart disease complications, especially aortic stenosis and aortic valve replacement surgery

Following some catheter ablation procedures

Obstructive sleep apnea [24]

Muscular dystrophies

Acute ethanol poisoning

Acute myocardial infarction (MI)

Any cardiac 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 , 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. [9]

Erkapic and colleagues studied the incidence of AV block after 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. [25] 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. [25] 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. [26] 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. [27]

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. [28]

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. [29]

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. [30]

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. [31] 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.

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. [1] 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. [1, 5] 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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Ali A Sovari, MD, FACP, FACC Attending Physician, Cardiac Electrophysiologist, Cedars Sinai Medical Center and St John’s Regional Medical Center

Ali A Sovari, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Physician Scientists Association, American Physiological Society, Biophysical Society, Heart Rhythm Society, Society for Cardiovascular Magnetic Resonance

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George’s University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, Clerkship Directors in Emergency Medicine, Alliance for Clinical Education

Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, FHRS Professor of Medicine, University of Illinois College of Medicine

Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology, Central Society for Clinical and Translational Research, Heart Failure Society of America, Cardiac Electrophysiology Society, American College of Physicians, American Heart Association, American Medical Association, Illinois State Medical Society

Disclosure: Nothing to disclose.

Michael D Levine, MD Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents’ Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: On-X Cryolife; Lundbeck <br/>Serve(d) as a speaker or a member of a speakers bureau for: On-X Cryolife; Lundbeck <br/>Amarin – chair DSMB for: Boehringer Ingelheim – national coordinator GLORIA AF.

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Ryan L Cooley, MD, and Raluca B Arimie, MD to the development and writing of the source article.

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