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Second-Degree Atrioventricular Block

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Apr 28, 2014
 

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.

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 ischemia
  • A regularly irregular heartbeat
  • Bradycardia may be present
  • Symptomatic 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 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
  • Commonly, junctional escape beats 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 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 wave
  • A PR interval in the first beat occurs after the block, with the same PR interval as the previous beats
  • 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
  • When the block is localized to the AV node, no risk of progression to a Mobitz II block or a complete heart block exists [4]
  • 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 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, a type I block is more often infranodal
  • An increment in PR interval of longer than 100 msec favors a block site in the AV node
  • A 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 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)

Laboratory studies to identify possible underlying causes are as follows:

  • Serum electrolytes, calcium, 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
  • 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 pacing
  • Atropine 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 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 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 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[5, 6] :

  • Second-degree AV block associated with signs such as bradycardia, heart failure, and asystole for 3 seconds or longer
  • 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

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
  • 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
  • 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

See Treatment and Medication for more detail.

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Background

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; 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.

Typical Mobitz I atrioventricular block with progr 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.

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.

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Pathophysiology

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.[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.[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.

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Etiology

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, 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.[12]

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.[13] 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.

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 [19]
  • 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 [20, 21]
  • 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 [22]
  • Muscular dystrophies
  • Acute ethanol poisoning

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.[9]

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.[23] 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.[23] 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.[24] 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.[25]

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.[26]

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.[27]

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.[28]

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Epidemiology

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.[29] 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.

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Prognosis

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.[4] 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.[4, 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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Contributor Information and Disclosures
Author

Ali A Sovari, MD, FACP Fellow in Clinical Cardiac Electrophysiology, Cedars Sinai Medical Center/Heart Institute

Ali A Sovari, MD, FACP 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.

Coauthor(s)

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.

Specialty Editor Board

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, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Chief Editor

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.

Additional Contributors

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

Acknowledgements

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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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.
Mobitz II atrioventricular (AV) block with intermittent periods of 2:1 AV block. If only 2:1 block was seen in beginning of strip, site of block could not be localized with certainty; however, single dropped QRS complex at end of strip with constant PR interval indicates that this block is localized in one of the bundle branches.
Variable-ratio Mobitz I atrioventricular block. Note marked PR-interval prolongation in first beat of each cycle. Maximum prolongation of PR interval takes place in second beat of cycle, with much smaller increments in subsequent beats. Also, notice that R-R interval actually shortens with each beat—paradox of shortening R-R interval when PR interval increases by diminishing increments.
Sinus rhythm with Mobitz I second-degree 3:2 infranodal atrioventricular (AV) block and bifascicular block. Note that AH interval (indicative of AV nodal conduction) remains constant. HV interval (indicative of His-Purkinje conduction) increases from 65 msec (after first P wave) to 185 msec (after second P wave). Third P wave is followed a His bundle deflection (H) but no QRS complex. AV block occurs in His-Purkinje system below site of recording of His bundle potential. Note shorter PR interval after nonconducted P wave, typical of Mobitz I AV block. HRA = high right atrial electrogram; A = atrial deflection; HB = His bundle electrogram, proximal and distal; H = His bundle deflection; RV = right ventricular electrogram; T = time line, 50 msec.
Representative 12-lead electrocardiogram in asymptomatic 78-year-old woman during recent noncardiac surgery. Patient was referred for implantation of permanent pacemaker with diagnosis of sinus tachycardia with 2:1 atrioventricular (AV) block and narrow QRS complex. As sinus rate slowed, 1:1 AV conduction resumed. Intracardiac recordings confirmed diagnosis of infra-Hisian 2:1 AV block.
Electrocardiogram of patient with Mobitz I (Wenckebach) second-degree atrioventricular block.
Electrocardiogram of patient with Mobitz II second-degree atrioventricular block.
 
 
 
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