Second-Degree Atrioventricular Block Workup

  • Author: Ali A Sovari, MD, FACP; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Sep 16, 2011
 

Approach Considerations

Serum electrolytes, calcium, and magnesium levels should be checked. A digoxin level should be obtained for patients on digoxin. Cardiac biomarker testing is indicated for any patient with suspected myocardial ischemia. Myocarditis-related laboratory studies may be sent (eg, Lyme titers, HIV serologies, enterovirus polymerase chain reaction [PCR], adenovirus PCR, Chagas titers), if clinically relevant. Thyroid function studies may be obtained.

Electrocardiography (ECG) is employed to determine the type of second-degree atrioventricular (AV) block present. Follow-up ECGs and cardiac monitoring are appropriate.

Routine imaging studies are not required. However, if myocarditis is a concern, echocardiography may be indicated. If myocardial ischemia is a concern, a chest radiograph may be indicated.

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Electrocardiography

It is important to try to distinguish between the different types of second-degree heart block. Mobitz I (Wenckebach) block is the most common form of second-degree AV block. The typical ECG findings of Mobitz I AV block (see the image below) are as follows.

Electrocardiogram of patient with Mobitz I (WenckeElectrocardiogram of patient with Mobitz I (Wenckebach) second-degree atrioventricular block.

Gradually progressive PR interval prolongation occurs before the blocked sinus impulse, with the greatest PR increment typically occurring 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. A common situation is the occurrence of junctional escape beats 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 (see the image below).

Typical Mobitz I atrioventricular block with progrTypical 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.

A Mobitz I block manifesting with atypical ECG findings that result in a misdiagnosis of Mobitz II block is not uncommon. 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.

Occasionally, every other beat is dropped. In these cases, it is impossible to determine if there is prolongation of the PR interval. In this situation, if the rate changes, occasionally the number of beats before the QRS complex is dropped will change, thereby permitting differentiating Mobitz I from Mobitz II. In cases where every other beat is dropped, it is safest to assume it is a Mobitz II block, rather than a Mobitz I block.

In Mobitz II block (see the images below), 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.

Electrocardiogram of patient with Mobitz II secondElectrocardiogram of patient with Mobitz II second-degree atrioventricular block. Mobitz II atrioventricular (AV) block with intermiMobitz 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.

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. This sequence can be secondary to enhanced conduction or a nonconducted P wave occurring with a junctional escape beat. Prolonged ECG recordings or intracardiac recordings may be needed to establish the correct site of block (ie, AV nodal or infranodal).

Mobitz II block is typically associated with significant underlying conduction system disease. Therefore, the QRS complex is usually wide, and the PR interval is usually normal. However, a long PR interval and a narrow QRS complex do not exclude Mobitz II block, because AV nodal conduction disease may coexist with an infranodal lesion. Another consideration in a Mobitz II block with narrow QRS is atypical Mobitz I block.

A Mobitz I block with a narrow QRS complex is almost always located in the atrioventricular node (AVN) (see the image below). An exception is the rare occurrence of an infranodal Wenckebach block. A normal PR interval with miniscule increments in AV conduction delay should raise the suggestion of an infranodal Wenckebach block but is not a diagnostic finding. Larger increments in AV conduction do not necessarily exclude infranodal Wenckebach block.

Variable-ratio Mobitz I atrioventricular block. NoVariable-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.

In the presence of a wide QRS complex, a type I block is more often infranodal (see the image below). An invasive His bundle recording is required to make the diagnosis of an infranodal block.

Sinus rhythm with Mobitz I second-degree 3:2 infraSinus 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.

The incremental pattern of AV block may be helpful in determining the correct site of block. For example, an increment in PR interval of longer than 100 msec favors a block site in the AVN.

A Mobitz II block is always infranodal. An infranodal block is associated with a wide QRS complex and accounts for the majority of Mobitz II blocks. Less commonly, the block is intranodal and, therefore, is associated with a narrow QRS complex. Sinus slowing with AV block is characteristic of vagal activation and effectively excludes a type II block.

Among the conditions that may mimic Mobitz II block are atypical Mobitz I block, junctional parasystole, and concealed extrasystoles arising from the His-Purkinje system.

A 2:1 block can be either in the AVN or in the His-Purkinje system (see the image below). If the QRS complex is narrow, the block is more likely located in the AVN. If a wide QRS complex is present, the block may be located either in the His-Purkinje system (80-85%) or, less commonly, in the AVN (15-20%). Observing for a narrow QRS, Mobitz II–like block and a Mobitz I block in close temporal proximity can sometimes help determine the correct site of block. A true Mobitz II block almost never coexists with an intra-Hisian Mobitz I block.

Representative 12-lead electrocardiogram in asymptRepresentative 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.

Autonomic manipulation (eg, carotid sinus massage, exercise) may help distinguish between an AV nodal and a His-Purkinje (infranodal) block. Improvement in the degree of block with exercise strongly favors an AV nodal location. Conversely, an increase in block with exercise or atropine more strongly favors a His-Purkinje (infranodal) block. Compared with exercise, vagal maneuvers have opposite effects on AV blocks, exacerbating the AV nodal blocks and improving infranodal blocks.

AV block localized to the infranodal specialized conduction system occurs in as many as 5% of patients with acute anterior MI, giving rise to a wide-QRS Mobitz II block.

A transient AV block of any degree in acute inferior MI almost always is AV nodal and not an indication for permanent pacing.

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Electrophysiologic Testing

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

Electrophysiologic testing is also indicated for patients with pseudo-AV block and those with premature, concealed junctional depolarization, which may be the cause of second- or third-degree AV block.

Finally, electrophysiologic testing is indicated for 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).

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Contributor Information and Disclosures
Author

Ali A Sovari, MD, FACP  Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois College of Medicine; Staff Physician and Hospitalist, St John Regional Medical Center, Cogent Healthcare, Inc

Ali A Sovari, MD, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Physiological Society, and Heart Rhythm Society

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: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

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, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society

Disclosure: Nothing to disclose.

Michael D Levine, MD  Physician, Department of Medical Toxicology, Banner Good Samaritan Medical Center; Physician, Department of Emergency Medicine, Banner Thunderbird Medical Center

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, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

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: Medscape Salary Employment

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

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

Additional Contributors

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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