Second-Degree Atrioventricular Block Workup
- Author: Ali A Sovari, MD, FACP; Chief Editor: Jeffrey N Rottman, MD more...
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.
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 (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 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 second-degree atrioventricular block.
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. 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. 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 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 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.
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).
Barold SS, Hayes DL. Second-degree atrioventricular block: a reappraisal. Mayo Clin Proc. Jan 2001;76(1):44-57. [Medline].
Silverman ME, Upshaw CB Jr, Lange HW. Woldemar Mobitz and His 1924 classification of second-degree atrioventricular block. Circulation. Aug 31 2004;110(9):1162-7. [Medline].
Zehendet M, Meinertz T, Keul J, Just H. ECG variants and cardiac arrthymias in athletes: clinical relevance and prognostic importance. Am heart J. Jun 1990;119(6):1378-91. [Medline].
Cho SW, Kang YJ, Kim TH, Cho SK, Hwang MW, Chang W, et al. Primary cardiac lymphoma presenting with atrioventricular block. Korean Circ J. Feb 2010;40(2):94-8. [Medline].
Antoniou T, Gough KA. Early-onset pentamidine-associated second-degree heart block and sinus bradycardia: case report and review of the literature. Pharmacotherapy. Jun 2005;25(6):899-903. [Medline].
Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. Nov 2 2010;122(18 Suppl 3):S729-67. [Medline].
Makaryus JN, Catanzaro JN, Friedman ML, Katoma KC, Makaryus AN. Persistent second-degree atrioventricular block following adenosine infusion for nuclear stress testing. J Cardiovasc Med. Mar 2008;9(3):304-7. [Medline].
Belém Lde S, Inácio CA. Second degree atrioventricular block Mobitz type I after administration of benzathine penicillin: case report. Rev Bras Anestesiol. Mar-Apr 2009;59(2):219-22. [Medline].
Haddad FA, Nadelman RB. Lyme disease and the heart. Front Biosci. Sep 1 2003;8:s769-82. [Medline].
Van Herendael B, Van Herendael H, De Raedt H. Second-degree atrioventricular block as the first sign of sarcoidosis ina previously asymptomatic patient. Acta Cardiol. Jun 2007;62(3):299-301. [Medline].
Lev M. Anatomic basis for atrioventricular block. Am J Med. Nov 1964;37:742-8. [Medline].
Hsu YJ, Lin YF, Chau T, et al. Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis. Am J Med Sci. Sep 2003;326(3):128-32. [Medline].
Vinsonneau U, Delluc A, Bergez C, Caumes D, Talarmin F. [Second degree atrioventricular block in mixed connective tissue disease]. Rev Med Interne. Aug 2005;26(8):656-60. [Medline].
den Dulk K, Brugada P, Braat S, Heddle B, Wellens HJ. Myocardial bridging as a cause of paroxysmal atrioventricular block. J Am Coll Cardiol. Mar 1983;1(3):965-9. [Medline].
Lin SM, Hwang HK, Chen MR. Amplatzer septal occluder-induced transient complete atrioventricular block. J Formos Med Assoc. Dec 2007;106(12):1052-6. [Medline].
Thanopoulos BD, Rigby ML. Outcome of transcatheter closure of muscular ventricular septal defects with the Amplatzer ventricular septal defect occluder. Heart. Apr 2005;91(4):513-6. [Medline].
Arias MA, Sanchez AM. Obstructive sleep apnea and its relationship to cardiac arrhythmias. J Cardiovasc Electrophysiol. Sep 2007;18(9):1006-14. [Medline].
Erkapic D, Kim WK, Weber M, Möllmann H, Berkowitsch A, Zaltsberg S, et al. Electrocardiographic and further predictors for permanent pacemaker requirement after transcatheter aortic valve implantation. Europace. Mar 30 2010;[Medline].
Nardi P, Pellegrino A, Scafuri A, Bellos K, De Propris S, Polisca P, et al. Permanent pacemaker implantation after isolated aortic valve replacement: incidence, risk factors and surgical technical aspects. J Cardiovasc Med (Hagerstown). Jan 2010;11(1):14-9. [Medline].
Bastani H, Insulander P, Schwieler J, Tabrizi F, Braunschweig F, Kennebäck G, et al. Cryoablation of superoparaseptal and septal accessory pathways: a single centre experience. Europace. Mar 27 2010;EPub ahead of print:[Medline].
Sovari AA, Bodine CK, Farokhi F. Cardiovascular manifestations of myotonic dystrophy-1. Cardiol Rev. Jul-Aug 2007;15(4):191-4. [Medline].
Brvar M, Bunc M. High-degree atrioventricular block in acute ethanol poisoning: a case report. Cases J. Sep 9 2009;2:8559. [Medline].
Cevik BS, Cevik A, Tavli E. Second Degree Heart Block Associated with QT Prolongation. Indian Pacing Electrophysiol J. Feb 1 2010;10(2):96-8. [Medline].
Zehender M, Meinertz T, Keul J, Just H. ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. Am Heart J. Jun 1990;119(6):1378-91. [Medline].
Strasberg B, Amat-Y-Leon F, Dhingra RC, Palileo E, Swiryn S, Bauernfeind R, et al. Natural history of chronic second-degree atrioventricular nodal block. Circulation. May 1981;63(5):1043-9. [Medline].
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7.3:. Management of Symptomatic Bradycardia and Tachycardia. Circulation. 2005;112, IV-67-IV-77. [Full Text].
Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation. Oct 15 2002;106(16):2145-61. [Medline].
[Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. May 27 2008;51(21):e1-62. [Medline]. [Full Text].

