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Wenckebach—Second-Degree Heart Block and the Company It Keeps

Wenckebach—Second-Degree Heart Block and the Company It Keeps A man in his 70s with hypertension, coronary artery disease (CAD), and right coronary (RCA) stent placement 2 months prior for unstable angina presented to the emergency department after an episode of presyncope, a sense of chest tightness, and palpitations. He had a history of left bundle branch block (LBBB) on electrocardiography (ECG). His medications included carvedilol, aspirin, clopidogrel, and lovastatin. In the emergency department, his ECG showed first-degree heart block and LBBB, and telemetry showed atrioventricular (AV) Wenckebach (ie, Mobitz type 1) heart block (Figure 1). Periods of 2:1 AV block were also captured (Figure 2). A subsequent echocardiogram showed left ventricular hypertrophy but was otherwise normal. Cardiac catheterization demonstrated the recent RCA stent and a chronic left anterior descending (LAD) stent to be patent. Without an ischemic etiology for his symptoms, and noting his cardiac conduction disease, the emergency department referred the patient for electrophysiology study (EPS) (Figure 3). Figure 1. Initial Surface Electrocardiogram Showing Abnormalities in Cardiac Electrical Conduction View LargeDownload A, First-degree heart block (with PR interval of 230 milliseconds, in brackets; normal interval, <200 milliseconds), left bundle branch block (LBBB) (which shows the typical morphologic characteristics in lead V1, circled), and a sinus rate of approximately 60 bpm (arrowheads). B, Typical AV Wenckebach electrocardiographic pattern of prolonging PR intervals with successive beats (brackets) prior to a dropped beat (circled). Note that the prolongation in PR interval from one beat to the next is subtle—only 40 milliseconds. Figure 2. Surface Electrocardiogram Showing 2:1 Atrioventricular Conduction View LargeDownload There are 2 P waves (black arrowheads) for every QRS complex (red arrowheads). The sinus rate (approximately 80 bpm) is therefore twice the ventricular rate (approximately 40 bpm). Figure 3. Electrophysiology Study Intraprocedural Surface and Intracardiac Tracings Showing Wenckebach Conduction Abnormality View LargeDownload HIS indicates catheter across the bundle of His (proximal, middle, and distal); HRA, catheter placed in the high right atrium; RVA, catheter placed in the right ventricular apex. The PR interval (black brackets) represents conduction from the sinus node, across the atrial muscle, to the onset of ventricular depolarization. With a multielectrode intracardiac catheter across the AV node (HIS), this interval can be subdivided into the AH interval (blue brackets, representing atrial conduction time through the AV node) and the HV interval (red brackets, representing conduction time from just beneath the AV node through ventricular depolarization). These tracings show a prolonging PR interval, comprising a fixed AH conduction time across the AV node (160 milliseconds [ms]), and a prolonging infranodal HV conduction time (100 ms increasing to 215 ms). Questions: Where is the lesion in this patient’s conduction system? Should a pacemaker be considered in this patient? Interpretation The ECG in Figure 1A demonstrates baseline cardiac conduction disease. Note that the patient’s sinus rate is approximately 60 beats per minute (bpm). Figure 1B shows an AV Wenckebach pattern. The ECG presented in Figure 2 also shows 2:1 AV conduction with a ventricular rate of near 40 bpm. From the ECG in Figure 2 alone, it is not discernible if the patient’s 2:1 block represents delayed conduction in the AV node (typical of, but not exclusive to, AV Mobitz type 1 “Wenckebach” heart block), or infranodal block (typical of AV Mobitz type 2 pattern on ECG). However, taken along with the tracing in Figure 1A, it causes concern for infranodal conduction disease because at a faster sinus rate, AV block has appeared. Figure 3 shows 3:2 Wenckebach conduction in the surface ECG (leads I, II, and V1). However, the intracardiac tracings reveal a point worth emphasizing: the conduction delay is occurring not across the AH interval, which depicts the AV node and is completely fixed in this case, but rather occurs exclusively across the HV interval, denoting infranodal conduction disease. These tracings show that a Wenckebach-pattern ECG , though typically thought to represent AV nodal disease, may also be a sign of infranodal disease. Clinical Course A dual-chamber permanent pacemaker was placed to pace at times of conduction block and allowing for continued use of β-blockade for the patient’s CAD. At follow-up, he had no recurrent lightheadedness or syncope, and his chest tightness and palpitations, which had been attributed to symptoms from blocked beats, had completely resolved. Discussion Syncope is among the most common complaints of patients visiting emergency departments,1 and some form of cardiac conduction disease is often seen in these patients. Therefore, it is crucial for emergency department physicians, internists, and cardiologists alike to understand ECG findings that should prompt arrhythmic workup. Second-degree heart block accounts for 2 different mechanisms: AV nodal and infranodal heart block at or below the Bundle of His. The former, manifesting as Wenckebach pattern on ECG, is defined by grouped beating, a prolonging PR interval with successive beats (representing decrement in the AV node), and shorter RR intervals (due to decrementally increasing HV intervals) prior to the dropped QRS complex.2 AV Wenckebach, a reversible, vagally mediated phenomenon, is typically asymptomatic, though not exclusively so—particularly at bradycardic heart rates—and pacemaker is indicated only in the presence of attributable symptoms.3 Infranodal disease is classically depicted on ECG by an AV Mobitz type 2 pattern: grouped beating with fixed PR and RR intervals prior to the dropped beat.4 However, as this case points out, AV Wenckebach describes an ECG pattern but does not identify the location of block, whereas AV Mobitz type 2 on ECG is specific for infranodal disease. It is important to understand this because infranodal conduction disease is the result of myocardial necrosis and is nonreversible, frequently progressing to complete heart bock (ie, third-degree heart block) and representing an increased risk for congestive heart failure and sudden cardiac death.5 AV Mobitz type 2 heart block, with or without symptoms, is a class I indication for treatment with permanent pacemaker.3 This patient’s history of CAD and presenting ECG (Figure 1) showed diseased cardiac conduction substrate, including LBBB, which may suggest increased risk of an arrhythmic etiology of syncope.6 While, if the patient were to have been experiencing active ischemia, his known RCA disease may have been suggestive of vagally mediated, reversible AV nodal block, his LAD disease represents the typical culprit in nonreversible, infranodal block owing to myocardial necrosis.7 With this in mind, the patient then demonstrated 2:1 AV conduction (Figure 2), a pattern that alone is not classifiable as due to AV nodal or infranodal disease. While EPS is the gold standard, it is important to understand bedside maneuvers to differentiate between AV nodal vs infranodal block. While the ECG often gives clues as to the level of block, in the case of 2:1 block or even AV Wenckebach, the region of block remains uncertain. At the bedside, adrenergic stimulation (ie, with exercise, β-agonists, or vagolytics) will provoke more avid conduction across the AV node and the Wenckebach block pattern will resolve, whereas vagal stimulation (ie, with carotid massage or Valsalva) will exacerbate the block.8 Conversely, AV Mobitz type 2 will be exacerbated by exercise as faster supraventricular impulses bombard the diseased, infranodal tissue, giving it less time to recover between depolarizations. While adrenergic bedside maneuvers were not performed in this case, an increased sinus rate from 60 bpm to 80 bpm triggered 2:1 heart block, providing evidence of infranodal block. This case demonstrates a potential pitfall in relying simply on one’s knowledge of typical AV Wenckebach vs AV Mobitz type 2 ECGs. One must always consider the imperfect specificity of Wenckebach for AV nodal disease with the “company it keeps”—in this case, PR prolongation, LAD disease with a LBBB, and presyncope. These each amount to clues to diagnosing infranodal block in the face of an AV Wenckebach ECG pattern. Take Home Points Conduction disease that is apparent on ECG may increase the likelihood of an arrhythmic etiology to otherwise unexplained syncope. Know not just the medical history but also the company it keeps. Atrioventricular Wenckebach and Mobitz type 2 conduction patterns describe ECG findings, and while atrioventricular Mobitz type 2 is specific for infranodal conduction disease, a Wenckebach pattern ECG may represent AV nodal or infranodal disease. Electrophysiology study is the gold standard in identifying the level of AV block; however, bedside maneuvers can help discriminate between AV nodal and infranodal block. Benign block at the level of the AV node should resolve with exercise (ie, at increased sinus rates). A pacemaker is indicated for symptomatic AV nodal heart block and infranodal heart block regardless of symptoms. Section Editors: Zachary D. Goldberger, MD, MS; Nora Goldschlager, MD; Elsayed Z. Soliman, MD, MSc, MS. Back to top Article Information Corresponding Author: Isaac R. Whitman, MD, Electrophysiology Section, Division of Cardiology, University of California, San Francisco, 500 Parnassus Ave, Millberry Union East, Fourth Floor, San Francisco, CA 94143 (isaac.whitman@ucsf.edu). Published Online: January 11, 2016. doi:10.1001/jamainternmed.2015.7592. Conflict of Interest Disclosures: None reported. References 1. Burt CW, Schappert SM. Ambulatory care visits to physician offices, hospital outpatient departments, and emergency departments: United States, 1999-2000. Vital Health Stat 13. 2004;(157):1-70.PubMedGoogle Scholar 2. Wenckebach KF. On the analysis of irregular pulses. Z Klin Med. 1899;37:474.Google Scholar 3. Epstein AE, DiMarco JP, Ellenbogen KA, et al; 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); American Association for Thoracic Surgery; Society of Thoracic Surgeons. 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. Circulation. 2008;117(21):e350-e408.PubMedGoogle ScholarCrossref 4. Mobitz W. Über die unvollständige Störung der Erregungsüberleitung zwischen Vorhof und Kammer des menschlichen Herzens. Z Ges Esp Med. 1924;41:180.Google ScholarCrossref 5. Scheinman MM, Peters RW, Modin G, Brennan M, Mies C, O’Young J. Prognostic value of infranodal conduction time in patients with chronic bundle branch block. Circulation. 1977;56(2):240-244.PubMedGoogle ScholarCrossref 6. Sud S, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. Predicting the cause of syncope from clinical history in patients undergoing prolonged monitoring. Heart Rhythm. 2009;6(2):238-243.PubMedGoogle ScholarCrossref 7. Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med. 2003;348(10):933-940.PubMedGoogle ScholarCrossref 8. Pellegrini CN, Scheinman MM. Bradycardia: sinus and AV node dysfunction. Herzschrittmacherther Elektrophysiol. 2015;26(3):175-191.PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Internal Medicine American Medical Association

Wenckebach—Second-Degree Heart Block and the Company It Keeps

JAMA Internal Medicine , Volume 176 (3) – Mar 1, 2016

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References (11)

Publisher
American Medical Association
Copyright
Copyright © 2016 American Medical Association. All Rights Reserved.
ISSN
2168-6106
eISSN
2168-6114
DOI
10.1001/jamainternmed.2015.7592
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Abstract

A man in his 70s with hypertension, coronary artery disease (CAD), and right coronary (RCA) stent placement 2 months prior for unstable angina presented to the emergency department after an episode of presyncope, a sense of chest tightness, and palpitations. He had a history of left bundle branch block (LBBB) on electrocardiography (ECG). His medications included carvedilol, aspirin, clopidogrel, and lovastatin. In the emergency department, his ECG showed first-degree heart block and LBBB, and telemetry showed atrioventricular (AV) Wenckebach (ie, Mobitz type 1) heart block (Figure 1). Periods of 2:1 AV block were also captured (Figure 2). A subsequent echocardiogram showed left ventricular hypertrophy but was otherwise normal. Cardiac catheterization demonstrated the recent RCA stent and a chronic left anterior descending (LAD) stent to be patent. Without an ischemic etiology for his symptoms, and noting his cardiac conduction disease, the emergency department referred the patient for electrophysiology study (EPS) (Figure 3). Figure 1. Initial Surface Electrocardiogram Showing Abnormalities in Cardiac Electrical Conduction View LargeDownload A, First-degree heart block (with PR interval of 230 milliseconds, in brackets; normal interval, <200 milliseconds), left bundle branch block (LBBB) (which shows the typical morphologic characteristics in lead V1, circled), and a sinus rate of approximately 60 bpm (arrowheads). B, Typical AV Wenckebach electrocardiographic pattern of prolonging PR intervals with successive beats (brackets) prior to a dropped beat (circled). Note that the prolongation in PR interval from one beat to the next is subtle—only 40 milliseconds. Figure 2. Surface Electrocardiogram Showing 2:1 Atrioventricular Conduction View LargeDownload There are 2 P waves (black arrowheads) for every QRS complex (red arrowheads). The sinus rate (approximately 80 bpm) is therefore twice the ventricular rate (approximately 40 bpm). Figure 3. Electrophysiology Study Intraprocedural Surface and Intracardiac Tracings Showing Wenckebach Conduction Abnormality View LargeDownload HIS indicates catheter across the bundle of His (proximal, middle, and distal); HRA, catheter placed in the high right atrium; RVA, catheter placed in the right ventricular apex. The PR interval (black brackets) represents conduction from the sinus node, across the atrial muscle, to the onset of ventricular depolarization. With a multielectrode intracardiac catheter across the AV node (HIS), this interval can be subdivided into the AH interval (blue brackets, representing atrial conduction time through the AV node) and the HV interval (red brackets, representing conduction time from just beneath the AV node through ventricular depolarization). These tracings show a prolonging PR interval, comprising a fixed AH conduction time across the AV node (160 milliseconds [ms]), and a prolonging infranodal HV conduction time (100 ms increasing to 215 ms). Questions: Where is the lesion in this patient’s conduction system? Should a pacemaker be considered in this patient? Interpretation The ECG in Figure 1A demonstrates baseline cardiac conduction disease. Note that the patient’s sinus rate is approximately 60 beats per minute (bpm). Figure 1B shows an AV Wenckebach pattern. The ECG presented in Figure 2 also shows 2:1 AV conduction with a ventricular rate of near 40 bpm. From the ECG in Figure 2 alone, it is not discernible if the patient’s 2:1 block represents delayed conduction in the AV node (typical of, but not exclusive to, AV Mobitz type 1 “Wenckebach” heart block), or infranodal block (typical of AV Mobitz type 2 pattern on ECG). However, taken along with the tracing in Figure 1A, it causes concern for infranodal conduction disease because at a faster sinus rate, AV block has appeared. Figure 3 shows 3:2 Wenckebach conduction in the surface ECG (leads I, II, and V1). However, the intracardiac tracings reveal a point worth emphasizing: the conduction delay is occurring not across the AH interval, which depicts the AV node and is completely fixed in this case, but rather occurs exclusively across the HV interval, denoting infranodal conduction disease. These tracings show that a Wenckebach-pattern ECG , though typically thought to represent AV nodal disease, may also be a sign of infranodal disease. Clinical Course A dual-chamber permanent pacemaker was placed to pace at times of conduction block and allowing for continued use of β-blockade for the patient’s CAD. At follow-up, he had no recurrent lightheadedness or syncope, and his chest tightness and palpitations, which had been attributed to symptoms from blocked beats, had completely resolved. Discussion Syncope is among the most common complaints of patients visiting emergency departments,1 and some form of cardiac conduction disease is often seen in these patients. Therefore, it is crucial for emergency department physicians, internists, and cardiologists alike to understand ECG findings that should prompt arrhythmic workup. Second-degree heart block accounts for 2 different mechanisms: AV nodal and infranodal heart block at or below the Bundle of His. The former, manifesting as Wenckebach pattern on ECG, is defined by grouped beating, a prolonging PR interval with successive beats (representing decrement in the AV node), and shorter RR intervals (due to decrementally increasing HV intervals) prior to the dropped QRS complex.2 AV Wenckebach, a reversible, vagally mediated phenomenon, is typically asymptomatic, though not exclusively so—particularly at bradycardic heart rates—and pacemaker is indicated only in the presence of attributable symptoms.3 Infranodal disease is classically depicted on ECG by an AV Mobitz type 2 pattern: grouped beating with fixed PR and RR intervals prior to the dropped beat.4 However, as this case points out, AV Wenckebach describes an ECG pattern but does not identify the location of block, whereas AV Mobitz type 2 on ECG is specific for infranodal disease. It is important to understand this because infranodal conduction disease is the result of myocardial necrosis and is nonreversible, frequently progressing to complete heart bock (ie, third-degree heart block) and representing an increased risk for congestive heart failure and sudden cardiac death.5 AV Mobitz type 2 heart block, with or without symptoms, is a class I indication for treatment with permanent pacemaker.3 This patient’s history of CAD and presenting ECG (Figure 1) showed diseased cardiac conduction substrate, including LBBB, which may suggest increased risk of an arrhythmic etiology of syncope.6 While, if the patient were to have been experiencing active ischemia, his known RCA disease may have been suggestive of vagally mediated, reversible AV nodal block, his LAD disease represents the typical culprit in nonreversible, infranodal block owing to myocardial necrosis.7 With this in mind, the patient then demonstrated 2:1 AV conduction (Figure 2), a pattern that alone is not classifiable as due to AV nodal or infranodal disease. While EPS is the gold standard, it is important to understand bedside maneuvers to differentiate between AV nodal vs infranodal block. While the ECG often gives clues as to the level of block, in the case of 2:1 block or even AV Wenckebach, the region of block remains uncertain. At the bedside, adrenergic stimulation (ie, with exercise, β-agonists, or vagolytics) will provoke more avid conduction across the AV node and the Wenckebach block pattern will resolve, whereas vagal stimulation (ie, with carotid massage or Valsalva) will exacerbate the block.8 Conversely, AV Mobitz type 2 will be exacerbated by exercise as faster supraventricular impulses bombard the diseased, infranodal tissue, giving it less time to recover between depolarizations. While adrenergic bedside maneuvers were not performed in this case, an increased sinus rate from 60 bpm to 80 bpm triggered 2:1 heart block, providing evidence of infranodal block. This case demonstrates a potential pitfall in relying simply on one’s knowledge of typical AV Wenckebach vs AV Mobitz type 2 ECGs. One must always consider the imperfect specificity of Wenckebach for AV nodal disease with the “company it keeps”—in this case, PR prolongation, LAD disease with a LBBB, and presyncope. These each amount to clues to diagnosing infranodal block in the face of an AV Wenckebach ECG pattern. Take Home Points Conduction disease that is apparent on ECG may increase the likelihood of an arrhythmic etiology to otherwise unexplained syncope. Know not just the medical history but also the company it keeps. Atrioventricular Wenckebach and Mobitz type 2 conduction patterns describe ECG findings, and while atrioventricular Mobitz type 2 is specific for infranodal conduction disease, a Wenckebach pattern ECG may represent AV nodal or infranodal disease. Electrophysiology study is the gold standard in identifying the level of AV block; however, bedside maneuvers can help discriminate between AV nodal and infranodal block. Benign block at the level of the AV node should resolve with exercise (ie, at increased sinus rates). A pacemaker is indicated for symptomatic AV nodal heart block and infranodal heart block regardless of symptoms. Section Editors: Zachary D. Goldberger, MD, MS; Nora Goldschlager, MD; Elsayed Z. Soliman, MD, MSc, MS. Back to top Article Information Corresponding Author: Isaac R. Whitman, MD, Electrophysiology Section, Division of Cardiology, University of California, San Francisco, 500 Parnassus Ave, Millberry Union East, Fourth Floor, San Francisco, CA 94143 (isaac.whitman@ucsf.edu). Published Online: January 11, 2016. doi:10.1001/jamainternmed.2015.7592. Conflict of Interest Disclosures: None reported. References 1. Burt CW, Schappert SM. Ambulatory care visits to physician offices, hospital outpatient departments, and emergency departments: United States, 1999-2000. Vital Health Stat 13. 2004;(157):1-70.PubMedGoogle Scholar 2. Wenckebach KF. On the analysis of irregular pulses. Z Klin Med. 1899;37:474.Google Scholar 3. Epstein AE, DiMarco JP, Ellenbogen KA, et al; 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); American Association for Thoracic Surgery; Society of Thoracic Surgeons. 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. Circulation. 2008;117(21):e350-e408.PubMedGoogle ScholarCrossref 4. Mobitz W. Über die unvollständige Störung der Erregungsüberleitung zwischen Vorhof und Kammer des menschlichen Herzens. Z Ges Esp Med. 1924;41:180.Google ScholarCrossref 5. Scheinman MM, Peters RW, Modin G, Brennan M, Mies C, O’Young J. Prognostic value of infranodal conduction time in patients with chronic bundle branch block. Circulation. 1977;56(2):240-244.PubMedGoogle ScholarCrossref 6. Sud S, Klein GJ, Skanes AC, Gula LJ, Yee R, Krahn AD. Predicting the cause of syncope from clinical history in patients undergoing prolonged monitoring. Heart Rhythm. 2009;6(2):238-243.PubMedGoogle ScholarCrossref 7. Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med. 2003;348(10):933-940.PubMedGoogle ScholarCrossref 8. Pellegrini CN, Scheinman MM. Bradycardia: sinus and AV node dysfunction. Herzschrittmacherther Elektrophysiol. 2015;26(3):175-191.PubMedGoogle ScholarCrossref

Journal

JAMA Internal MedicineAmerican Medical Association

Published: Mar 1, 2016

Keywords: cardiac arrhythmia,electrocardiogram,syncope,second degree atrioventricular block,mobitz type i incomplete atrioventricular block,mobitz type ii atrioventricular block,diagnostic techniques, cardiovascular,cardiac conduction

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