Second-Degree Atrioventricular Block

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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.

Essential update: Prolonging survival in Mobitz type I second degree atrioventricular block

In a retrospective cohort study of older men (average age, 75 years) with Mobitz type I AV block, Coumbe et al found that implantation of a cardiac electronic device prolonged survival. Of the 299 patients in the study, 141 required an implantable cardiac electronic device, 17 of which were implantable cardioverter-defibrillators. After a median of approximately 3 years of follow-up, cardiac electronic device implantation was associated with a 46% reduction in mortality.[4]

Signs and symptoms

In patients with second-degree AV block, symptoms may vary substantially, as follows:

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:

The typical ECG findings in Mobitz II AV block are as follows:

The level of the block, AV nodal or infranodal (ie, in the specialized His-Purkinje conduction system), carries prognostic significance, as follows:

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:

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:

Other indications for electrophysiologic testing are as follows:

Laboratory studies to identify possible underlying causes are as follows:

See Workup for more detail.

Management

Acute treatment of Mobitz type I second-degree AV block is as follows:

Acute treatment of Mobitz type II second-degree AV block is as follows:

Guidelines recommend the following as indications for permanent pacing in second-degree AV block[6, 7] :

In some cases, the following may also be indications for permanent pacemaker insertion:

Permanent pacing may not be required in the following situations:

See Treatment and Medication for more detail.

Image library

See the image below.


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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 prece....

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) 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.

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.

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.[8]

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.[9]

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.

Etiology

Cardioactive drugs are an important cause of AV block.[10, 11, 12] 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.[13]

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.[14] 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.

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.[10]

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.[24] 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.[24] 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.[25] 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.[26]

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.[27]

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.[28]

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.[29]

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.[30] 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.

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.[5] 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.[5, 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.

History and Physical Examination

In patients with Mobitz I second-degree atrioventricular (AV) block, symptoms may vary substantially, ranging from an absence of symptoms in well-trained athletes and persons without structural heart disease to recurrent syncope, presyncope, and bradycardia in patients with heart disease.

Most patients are asymptomatic. Patients may experience light-headedness, dizziness, or syncope, but these symptoms are uncommon. Patients may have chest pain if the heart block is related to myocarditis or ischemia. Patients may have a history of structural heart disease.

In contrast to patients with Mobitz I AV block, those with Mobitz II AV block are more likely to experience light-headedness, dizziness, or syncope, though they may be asymptomatic as well. Patients may have chest pain if the heart block is related to myocarditis or ischemia.

Patients often have a regularly irregular heartbeat. Bradycardia may be present. Symptomatic patients may have signs of hypoperfusion, including hypotension.

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.


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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).


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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 prece....

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.


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Electrocardiogram of patient with Mobitz II second-degree atrioventricular block.


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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....

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.


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Variable-ratio Mobitz I atrioventricular block. Note marked PR-interval prolongation in first beat of each cycle. Maximum prolongation of PR interval ....

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.


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Sinus rhythm with Mobitz I second-degree 3:2 infranodal atrioventricular (AV) block and bifascicular block. Note that AH interval (indicative of AV no....

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.


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Representative 12-lead electrocardiogram in asymptomatic 78-year-old woman during recent noncardiac surgery. Patient was referred for implantation of ....

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:

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).

Approach Considerations

Second-degree atrioventricular (AV) block in the asymptomatic patient does not require any specific therapy in the prehospital setting. If the patient is symptomatic, standard advanced cardiac life support (ACLS) guidelines for bradycardia, including the use of atropine and transcutaneous pacing, are indicated.[12, 31]

No specific therapy is required in the emergency department (ED) for Mobitz I (Wenckebach) second-degree AV block, unless the patient is symptomatic. Patients with suspected myocardial ischemia should be treated with an appropriate anti-ischemic regimen. Second-degree block at the level of the atrioventriocular node (AVN) may be due to digoxin, beta-blockers, or calcium channel blockers. Decreasing the dose and/or discontinuing these medications may restore normal AV conduction.

Mobitz II block is more likely to progress to complete heart block and thus requires a different approach. As with Mobitz I block, AV nodal agents should be avoided, and an anti-ischemic regimen should be instituted if ischemia is suspected.

Permanent pacing is considered in accordance with the relevant guidelines (see Pacemaker Implantation). Except for the use of atropine in selected cases of transient AV block, permanent cardiac pacing has replaced medical interventions in the treatment of patients with symptomatic, otherwise untreatable, AV block.

Atropine and Transcutaneous/Transvenous Pacing

Mobitz I block

Admit patients who have symptoms or who have concomitant acute myocardial ischemia or myocardial infarction (MI). Admission should be to a unit with telemetry monitoring, which has transcutaneous pacing capabilities.

Symptomatic patients should be treated with atropine and transcutaneous pacing. However, atropine should be administered with caution in patients with suspected myocardial ischemia, as ventricular dysrhythmias can occur in this situation.

The goal of atropine administration is to improve conduction through the AVN by reducing vagal tone via atropine-induced receptor blockade. However, this goal will only be effective if the level of the blockade is at the site of the AVN. Patients with infranodal second-degree AV block are unlikely to benefit from atropine. In addition, in patients who have denervated hearts (eg, patients who have undergone a cardiac transplant), atropine is also not likely to be effective.

Mobitz II block

Admit all patients to a unit with monitored beds, where transcutaneous and transvenous pacing capabilities are available. The admitting cardiologist should determine whether permanent pacemaker implantation is indicated.

Transcutaneous pacing pads should be applied to all patients with Mobitz II second-degree AV block, including those who are asymptomatic patients, because such patients have a propensity to progress to complete heart block. The transcutaneous pacemaker should be tested to ensure capture. If capture is not able to be achieved, then insertion of a transvenous pacemaker is indicated, even in asymptomatic patients.

Urgent cardiology consult is indicated for patients who have symptomatic type II block and for those asymptomatic patients who are unable to achieve capture with transcutaneous pacing.

Some institutions recommend insertion of a transvenous pacemaker for all new Mobitz type II blocks, although this practice varies greatly from institution to institution.

Patients who are hemodynamically unstable for whom an emergency cardiology consult is not available should undergo placement of a temporary transvenous pacing wire in the ED. A chest radiograph is required to confirm position of the wire and to exclude complications, including hemothorax or pneumothorax.

2:1 block

In cases where there is a 2:1 block and one is unable to determine if there is a Mobitz I block or Mobitz II block, the patient should be admitted and cardiology consultation should be obtained. In such cases, it is safest to assume that a Mobitz II second-degree AV block exists.

Pacemaker Implantation

Indications for permanent pacing in second-degree AV block are explained in detail in the guidelines published by the American College of Cardiology (ACC), the American Heart Association (AHA), and the North American Society for Pacing and Electrophysiology (NASPE) in 2002[6] and by the ACC, the AHA, and the Heart Rhythm Society (HRS) in 2008.[7] A summary of indications is as follows.

Second-degree AV block may occur after MI, and it may be transient or asymptomatic. In this case, pacemaker placement may not be needed. However, persistent and symptomatic second-degree AV block after MI, especially if it is associated with bundle-branch block, warrants permanent pacemaker placement. High-grade AV block after anterior MI, even if transient, may warrant permanent pacing.

Second-degree AV block after cardiac surgery may be persistent and necessitate pacemaker placement.

Second-degree AV block in patients with drug toxicity, Lyme disease, or hypoxia in sleep apnea is expected to resolve. In any situation where second-degree AV is expected to resolve as a result of correction of the underlying pathology, permanent pacemaker placement is not indicated.

Consultations

For symptomatic patients with Mobitz I AV block, a cardiology consultation is indicated. Asymptomatic patients with a Mobitz I block can be referred to a cardiologist on an outpatient basis.

For any patient with a new Mobitz II AV block, cardiology consultation is indicated, regardless of symptoms.

Long-Term Monitoring

Patients who are discharged from the ED with a Mobitz II AV block should have prompt follow-up arranged with a cardiologist.

If high-grade AV block and, possibly, symptoms due to AV block are present, consider monitoring the patient and then performing Holter monitoring or treadmill testing in the future. If the AV block occurs at night, consider sleep apnea as the cause.

Medication Summary

Atropine can be used for immediate treatment of symptomatic second-degree atrioventricular (AV) block in the atrioventricular node (AVN). For block in the His-Purkinje system, atropine does not improve conduction and can actually precipitate third-degree AV block by increasing the sinus rate and AVN conduction.

Atropine IV/IM (AtroPen)

Clinical Context:  Atropine is used to increase heart rate through vagolytic effects, causing an increase in cardiac output. It enhances sinus node automaticity; in addition, it blocks the effects of acetylcholine at the AVN, thereby decreasing the refractory time and speeding conduction through the AVN. Insufficient doses of atropine can cause paradoxical effects, further slowing the heart rate.

Class Summary

Anticholinergic agents improve AV nodal conduction in second-degree block at the level of the AVN. Drug therapy in second-degree heart block is aimed at vagolysis; atropine is the only currently recommended agent.

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

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

Disclosure: Nothing to disclose.

Specialty Editors

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

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

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; BioControl Consulting fee Consulting; Boehringer Ingelheim Consulting fee Consulting; Amarin Consulting fee Review panel membership; sanofi aventis Review panel membership

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

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

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

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.

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

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.

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.

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.

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.