Atrioventricular Block

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Practice Essentials

Signs and symptoms

Signs and symptoms of atrioventricular (AV) block include the following:

In third-degree AV block, exacerbation of ischemic heart disease or congestive heart failure caused by AV block–related bradycardia and reduced cardiac output may lead to specific, clinically recognizable symptoms, such as the following:

See Clinical Presentation for more specific information on the signs and symptoms of AV block.

Diagnosis

Laboratory studies

Although laboratory studies are not usually indicated in patients with AV block, the following may be helpful in certain cases:

Electrocardiography

Routine electrocardiographic (ECG) recording and cardiac monitoring with careful evaluation of the relationship between P waves and QRS complexes are the standard tests leading to proper diagnosis of AV blocks. Identifying episodes of transient AV block with sudden pauses and/or low heart rate causing syncopal episodes may require any of the following:

Additional modalities

Other means of evaluating patients for AV block can include the following:

See Clinical Presentation and Workup for more specific information on the diagnosis of atrioventricular block.

Management

Pacemaker implantation

Implantation of a permanent pacemaker is the therapy of choice in advanced AV block. Recommendations for the implantation of pacemakers and arrhythmia devices, as devised by the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS), include the following[1] :

A large, randomized study, the BLOCK-HF (Biventricular Versus Right Ventricular Pacing in Patients With Left Ventricular Dysfunction and Atrioventricular Block) trial, indicated that biventricular pacing may be superior to the use of right-ventricle-only pacemakers in terms of hospitalization and survival in heart-failure patients with AV block. Biventricular pacing may have led to improved outcomes in the study because, unlike right ventricular (RV) pacing, it did not cause ventricular function to deteriorate .[2]

Pharmacologic therapy

Considerations regarding the administration of anticholinergic agents include the following:

See Treatment and Medication for more specific information on the treatment of atrioventricular block.

Image library


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First-degree atrioventricular block. PR interval is constant and is 280 msec.

Background

Atrioventricular (AV) block occurs when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized.

First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (> 200 msec in adults and > 160 msec in young children). The upper limit of the reference range for the PR interval is age-dependent in children. All atrial impulses reach the ventricles in first-degree AV block; however, conduction is delayed within the AV node (see the image below).


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First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) that fail to conduct to the ventricles in 1 of the following 4 ways.

The first form of second-degree AV block is Mobitz I second-degree AV block (Wenckebach block), which consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval).

An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so forth (see the image below). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed intrahisian or infrahisian Wenckebach (depending if the block occurs within or below the His-Purkinje system).


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Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortene....

The second form is Mobitz II second-degree AV block, which is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, so that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed (see the image below).


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Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is ....

The third form is high-grade AV block, which consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or higher, and the PR interval of conducted beats is constant. This is a distinct form of complete AV block, in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.

The fourth form is 2:1 AV block. This could be either Mobitz I or Mobitz II, but distinguishing one variety from the other is nearly impossible.

Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats/min, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats/min.

No relationship exists between the rhythm of P waves and the rhythm of QRS complexes in third-degree AV block. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate) (see the image below).


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Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the....

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal.

AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex.

AV block may also occur in patients with atrial fibrillation (see the Atrial Fibrillation Center). Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

Pathophysiology

The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. This node consists of 3 parts—atrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal portion causes the slowest conduction.

The AVN is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. It receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle in a 1:1 ratio. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction.

The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur.

First-degree AV block and second-degree Mobitz I AV block usually involve a delay at the level of the AVN, whereas second-degree Mobitz II AV block generally involves blockage in the His bundle or lower regions of the conduction system. Third-degree AV block involves conduction disturbances in the AV node or the His-Purkinje system.

In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats/min. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats/min in the region of His bundle), and a narrower QRS duration.

Etiology

Delay or lack of conduction through the AV node has multiple causes.

First-degree AV block and Mobitz I (Wenckebach) second-degree AV block may occur in healthy, well-conditioned people as a physiologic manifestation of high vagal tone. Mobitz I AV block also may occur physiologically at high heart rates (especially with pacing) as a result of increased refractoriness of the AVN, which protects against conducting an accelerated arrhythmia to the ventricles.

AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AVN level; this may occur through other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block resulting from ischemia or infarction of bundle branches.

Degenerative changes in the AVN or bundle branches (eg, fibrosis, calcification, or infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block.

In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).[3]

Infiltrative myocardial diseases resulting in AV block include sarcoidosis, myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification. Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block. Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue.

Surgical procedures (eg, aortic valve replacement and congenital defect repair) may cause AV block, as may other therapeutic procedures (eg, AV node ablation and alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy). Patients with corrected transposition of the great vessels have anterior displacement of the AVN and are prone to develop complete heart block during right heart catheterization or surgical manipulation.

A variety of drugs may affect AV conduction. The most common of these include digitalis glycosides, beta-blockers, calcium channel blockers, adenosine, and other antiarrhythmic agents.

Epidemiology

First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Mobitz II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas Mobitz I (Wenckebach) second-degree AV block is observed in 1-2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare, at 1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks’ gestation and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers.

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block.

The international incidence is similar to that of the United States.

Age-, sex-, and race-related demographics

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease). A 60% female preponderance exists in congenital third-degree AV block. For acquired third-degree AV block, a 60% male preponderance exists. No racial proclivity exists in AV blocks.

Prognosis

Patients treated with permanent pacing to treat AV blocks have an excellent prognosis. Patients with advanced AV blocks who are not treated with permanent pacing remain at high risk of sudden cardiac death.

Although AV block generally is not associated with major morbidity, progressive degrees of AV block carry increasing morbidity and mortality.

Cheng et al found that first-degree AV block (ie, PR interval > 200 msec) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality.[4] In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12-lead ECG in 1968-1974, 124 individuals had PR intervals > 200 msec on the baseline examination.

On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation, a 3-fold adjusted risk of pacemaker implantation, and a 1.4-fold adjusted risk of all-cause mortality.[4] For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk.

A prospective cohort study of 938 patients with stable coronary artery disease were examined to assess if first-degree AV block was associated with an increased risk of heart failure and mortality. Patients were classified as a PR interval of 220 ms or less. Patients with first-degree AV block were at increased risk for heart failure hospitalization (age-adjusted heart rate, 2.33; 95% CI, 1.49-3.65; P = 0.0002), mortality (age-adjusted heart rate, 1.58; 95% CI, 1.13-2.20; P = 0.008], cardiovascular mortality (age-adjusted heart rate 2.33; 95% CI, 1.28-4.22; P = 0.005], and the combined endpoint of heart failure hospitalization or cardiovascular mortality (age-adjusted heart rate, 2.43: 95% CI, 1.64–3.61; P ≤ 0.0001). These associations persisted after multivariable adjustment for heart rate, medication use, ischemic burden, and QRS duration. Despite adjusting for systolic and diastolic dysfunction, first-degree AV block wasassociated with anincreased risk for heart failure or cardiovascular death (heart rate, 1.61; 95% CI, 1.02–2.54; P = 0.04).[5]

The low heart rate observed in third-degree or Mobitz II second-degree AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

Patient Education

Patients with implanted pacemakers require additional education, with particular emphasis on situations involving exposure to magnetic and electrical fields (eg, airport security gates) and training regarding transtelephonic monitoring of pacemaker function.

History

First-degree atrioventricular (AV) block is generally not associated with any symptoms and is usually an incidental finding on electrocardiography (ECG). People with newly diagnosed first-degree AV block may be healthy individuals with high vagal tone (eg, well-conditioned athletes), or they may have a history of myocardial infarction or myocarditis. First-degree AV block also may represent the first sign of a degenerative process of the AV conduction system.

Second-degree AV block usually is asymptomatic. However, in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur. The latter usually is observed in more advanced conduction disturbances, such as Mobitz II second-degree AV block. A history of medications that affect atrioventricular node (AVN) function (eg, digitalis, beta-blockers, and calcium channel blockers) may be contributory and should be obtained.

Third-degree AV block frequently is associated with symptoms such as fatigue, dizziness, lightheadedness, presyncope, and syncope most commonly. Syncopal episodes due to slow heart rates are called Morgagni-Adams-Stokes (MAS) episodes, in recognition of the pioneering work of these researchers on syncope. Patients with third-degree AV block may have associated symptoms of acute myocardial infarction either causing the block or related to reduced cardiac output from bradycardia in the setting of advanced atherosclerotic coronary artery disease.

Any level of atrioventricular block leading to profound bradycardia may also lead to life-threatening torsades de pointes.

Physical Examination

Routine physical examination does not lead to the diagnosis of first-degree AV block. Second-degree AV block may manifest on physical examination as bradycardia (especially Mobitz II), irregularity of heart rate (especially Mobitz I [Wenckebach]), or both.

Third-degree AV block is associated with profound bradycardia unless the site of the block is located in the proximal portion of the AVN. Exacerbation of ischemic heart disease or congestive heart failure caused by AV block–related bradycardia and reduced cardiac output may lead to specific clinically recognizable symptoms (eg, chest pain, dyspnea, confusion, and pulmonary edema). Cannon a waves may be observed intermittently in the jugular venous pulsation when the right atrium contracts against a closed tricuspid valve due to atrioventricular dissociation.

Complications

Complications include the following:

Laboratory Studies

Laboratory testing is not usually indicated in patients with atrioventricular (AV) block. Levels of electrolytes and drugs (eg, digitalis) can be checked in the case of second-degree or third-degree AV block when suspicion of increased potassium level or drug toxicity exists. In cases when second-degree and third-degree AV block might be a manifestation of acute myocardial infarction, cardiac enzymes should be measured.

If clinical evaluation suggests systemic illness, appropriate directed laboratory studies for infection, myxedema, or connective tissue disease should be performed.

Electrocardiography

Routine electrocardiographic (ECG) recording and cardiac monitoring with careful evaluation of the relationship between P waves and QRS complexes are the standard tests leading to proper diagnosis of AV blocks.

Identifying episodes of transient AV block with sudden pauses and/or low heart rate causing syncopal episodes may require 24-hour Holter monitoring, multiple ECG recordings, event (loop) ECG recordings, or, in selected cases, monitoring with implantable loop recorders (Reveal, Medtronic, Inc; Confirm, St Jude Medical, Inc).

Electrophysiologic Testing

Electrophysiologic testing is indicated in a patient with suspected AV block as the cause of syncope. The invasive recording of AH (atrium-His) and HV (His-ventricle) intervals may determine the degree of conduction abnormality and may guide decision making for pacemaker therapy. As noted, in selected cases, invasive diagnostic procedures may include implantation of a loop recorder.

Imaging Studies

In general, routine imaging studies are not helpful in diagnosing AV blocks.

However, imaging studies (eg, echocardiography) might be useful in diagnosing underlying comorbid conditions, such as aortic valve stenosis with calcification, wall motion abnormalities in acute ischemia, cardiomyopathy, and congenital heart disease (eg, congenitally corrected transposition of the great vessels).

Exercise

Advanced heart block, such as Mobitz II or third-degree AV block, may become more symptomatic with increased activity, where an actual increase in block and decrease in effective heart rate may occur.

Exercise may be used to evaluate 2:1 heart block and differentiate Mobitz I second-degree AV block (where the conducted rate increases) from Mobitz II AV block (where the block becomes more significant and often symptomatic).

Approach Considerations

Long-term medical therapy is not indicated in atrioventricular (AV) block. Permanent pacing is the therapy of choice in advanced AV block, and it does not require concomitant medical therapy. AV nodal blocking medications contributing to heart block should be discontinued if not necessary.

Pacemaker implantation is a routine surgical procedure, generally performed with conscious sedation and local anesthesia in the electrophysiology laboratory. The procedure usually requires an overnight observation period in the hospital.

Temporary transcutaneous or transvenous pacing is the treatment of choice for an emergency involving a slow heart rate (and for asystole) caused by AV blocks. Transfer to a specialized medical center may be advisable. Atropine administration (0.5-1.0 mg) may improve AV conduction in emergencies where bradycardia is caused by a proximal AV block (located in the atrioventricular node [AVN]) but may worsen conduction if the block is in the His-Purkinje system.

Pacemaker Implantation

In general, the decision regarding implantation of a pacemaker must be considered with respect to whether or not AV block is permanent. Reversible causes of AV block, such as electrolyte abnormalities, if present, should be corrected first. Some diseases may follow a natural history to resolution (eg, Lyme disease), and some AV block can be expected to reverse (eg, hypervagotonia due to recognizable and avoidable physiologic factors, perioperative AV block due to hypothermia, or inflammation near the AV conduction system after surgery in this region).

Conversely, some conditions may warrant pacemaker implantation owing to the possibility of disease progression even if the AV block reverses transiently (eg, sarcoidosis, amyloidosis, neuromuscular diseases). Finally, permanent pacing for AV block after valve surgery follows a variable natural history, and, therefore the decision for permanent pacing is at the physician’s discretion.

Types of cardiac pacemakers implanted in patients with heart block may include ventricular (usually VVI) or dual chamber (usually DDD) modes of pacing. The cardiologist or electrophysiologist should make the decision regarding the optimal mode of pacing.

ACC/AHA/NASPE guidelines

The following recommendations are based on the 2008 guidelines for implantation of cardiac pacemakers and antiarrhythmia devices formulated by the American College of Cardiology (ACC), the American Heart Association (AHA), and the Heart Rhythm Society (HRS).[1]

First-degree AV block and Mobitz I second-degree AV block do not generally require treatment unless they cause symptoms and are not due to a reversible cause. If a drug overdose is a possible cause, the drug must be withheld (and its future use or dosage subsequently should be decreased or reconsidered).

Small, uncontrolled trials have suggested that some symptomatic and functional improvement may be achieved in pacing patients with PR intervals longer than 300 msec by decreasing the time for AV conduction. This is rare. Although echocardiographic or invasive techniques may be used to assess hemodynamic improvement before permanent pacemaker implantation, such studies are not required for evaluation of symptoms due to first-degree and Mobitz I second-degree AV block.

Mobitz II second-degree AV block and third-degree AV block usually require temporary and/or permanent cardiac pacing. Mobitz II second-degree AV block and a wide QRS complex indicate diffuse conduction system disease and constitute an indication for pacing even in the absence of symptoms. Mobitz II with a wide QRS may degenerate into third-degree AV block, and this is another reason to consider permanent pacing. In the setting of acute anterior myocardial infarction, transcutaneous pacing initially and transvenous pacing subsequently are warranted.

With inferior myocardial infarction, the block usually resolves spontaneously within several days, and only a small percentage of patients require temporary or permanent pacing. Patients with persistent bundle branch block and transient third-degree AV block may benefit from permanent pacing therapy, especially after anterior myocardial infarction. Nonrandomized studies strongly suggest that permanent pacing does improve survival in patients with third-degree AV block, especially if syncope has occurred.

Indications/contraindications for treatment may be summarized according to the following ACC/AHA/HRS class I, II, and III recommendations:

With respect to pacemaker implantation in the setting of AV block, class I is defined as third-degree and advanced second-degree AV block at any anatomic level, associated with any 1 of the following conditions:

Class IIa is defined as follows:

Class IIb is defined as follows:

Class III is defined as follows:

Complications of pacing

Pacing therapy (temporary or permanent) may be complicated acutely by tamponade, hemothorax, or pneumothorax. Dysfunction of the pacemaker, lead fracture, and malfunction (eg, inappropriate capture or sensing) are infrequent complications of pacing therapy. Infection of the pacemaker or lead wires is a rare, but important, short-term and long-term complication of pacemaker implantation.

Activity Restriction

Restrictions after permanent pacemaker implantation include restricted weight lifting with the ipsilateral hand/arm to the pacemaker until healing occurs (approximately 4-6 wk). Contact sports are restricted unless a protective shield is worn over the implanted pacemaker. Electromagnetic interference—from power lines and arc welding, for example—may cause inhibition of pacing. This is problematic for patients who are pacemaker dependent.

Consultations

Consultation with a cardiologist or cardiac electrophysiologist is indicated in the case of advanced heart block or unexplained syncope. An electrophysiologist must be consulted when invasive electrophysiology testing is needed to determine the level and/or magnitude of conduction disturbance.

Long-Term Monitoring

Patients with first-degree and benign Mobitz I second-degree AV block do not require hospitalization. Patients with symptomatic second- or third-degree AV block require hospitalization with telemetry monitoring. Transcutaneous or transvenous pacing should be utilized, and indications for permanent pacing need to be determined.

Patients with first- and second-degree Mobitz I AV block may require follow-up ECG or Holter monitoring to determine the likelihood and rate of progression of the AV conduction disorder. Patients with implanted pacemakers require routine follow-up to monitor pacemaker function.

Medication Summary

Long-term medical therapy is not indicated in atrioventricular (AV) block. Permanent pacing is the therapy of choice in advanced AV block, and it does not require concomitant medical therapy. Sometimes AV nodal blocking medications that contribute to heart block can be discontinued if not necessary. Atropine administration (0.5-1.0 mg) or isoproterenol infusion may improve AV conduction in emergencies where bradycardia is caused by a proximal AV block (located in the atrioventricular node [AVN]) but may worsen conduction if the block is in the His-Purkinje system.

Atropine IV/IM (Atropair, Atropisol)

Clinical Context:  Atropine increases AV conduction. An insufficient dose may cause paradoxical slowing of the heart rate.

Isoproterenol (Isuprel)

Clinical Context:  Isoproterenol has beta1- and beta2-adrenergic receptor activity. It binds the beta-receptors of the heart, smooth muscle of bronchi, skeletal muscle, the vasculature, and the alimentary tract. It has positive inotropic and chronotropic actions.

Class Summary

The goal of administering anticholinergic agents is to improve conduction through the AVN by reducing vagal tone via muscarinic receptor blockade. This is only effective if the site of block is within the AVN. For patients with suspected infranodal block, this therapy is ineffective and may make the level of the block worse if it is in the His bundle or below.

Author

Chirag M Sandesara, MD, FACC, Virginia Cardiovascular Associates, Cardiac Rhythm Care

Disclosure: Nothing to disclose.

Coauthor(s)

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

Specialty Editors

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

Steven J Compton, MD, FACC, FACP, FHRS, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

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

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Wojciech Zareba, MD, PhD, FACC, and Stacy D Fisher, MD, to the development and writing of the source article.

References

  1. Epstein AE, Dimarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: executive summary. Heart Rhythm. Jun 2008;5(6):934-55. [View Abstract]
  2. Stiles S. BLOCK-HF: replace RV pacing with BiV in AV-block heart failure. Heartwire [serial online]. Nov 8, 2012;Available from: Medscape. Accessed Nov 19, 2012. Available at http://www.medscape.com/viewarticle/774145
  3. Schott JJ, Alshinawi C, Kyndt F, et al. Cardiac conduction defects associate with mutations in SCN5A. Nat Genet. Sep 1999;23(1):20-1. [View Abstract]
  4. Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. Jun 24 2009;301(24):2571-7. [View Abstract]
  5. Crisel RK, Farzaneh-Far R, Na B, Whooley MA. First-degree atrioventricular block is associated with heart failure and death in persons with stable coronary artery disease: data from the Heart and Soul Study. Eur Heart J. Aug 2011;32(15):1875-80. [View Abstract]

First-degree atrioventricular block. PR interval is constant and is 280 msec.

First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortened PR interval following the dropped beat.

Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.

Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the atrial and ventricular activity.

First-degree atrioventricular block. PR interval is constant and is 280 msec.

Second-degree atrioventricular block, Mobitz type I (Wenckebach). Note the prolongation of the PR interval preceding the dropped beat and the shortened PR interval following the dropped beat.

Second-degree atrioventricular block, Mobitz type II. A constant PR interval in conducted beats is present. Intraventricular conduction delay also is present.

Third-degree atrioventricular block (complete heart block). The atrial rate is faster than the ventricular rate, and no association exists between the atrial and ventricular activity.