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Third-Degree Atrioventricular Block

  • Author: Adam S Budzikowski, MD, PhD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Dec 31, 2015


Third-degree atrioventricular (AV) block, also referred to as third-degree heart block or complete heart block, is a disorder of the cardiac conduction system where there is no conduction through the atrioventricular node (AVN). Therefore, complete dissociation of the atrial and ventricular activity exists.[1] The ventricular escape mechanism can occur anywhere from the AVN to the bundle-branch Purkinje system.[2]

It is important to realize that not all patients with AV dissociation have complete heart block. For example, patients with ventricular tachycardia have AV dissociation, but not complete heart block; in this example, AV dissociation is due to the ventricular rate being faster than the intrinsic sinus rate. On electrocardiography (ECG), complete heart block is represented by QRS complexes being conducted at their own rate and totally independent of the P waves (see the image below).

Electrocardiogram from patient in complete heart b Electrocardiogram from patient in complete heart block.

AV block results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block can be either congenital or acquired. (See Etiology.)

Initial triage of patients with complete heart block consists of determining symptoms, assessing vital signs, and looking for evidence of compromised peripheral perfusion. In particular, the physical examination findings of patients with third-degree AV block will be notable for bradycardia, which can be severe. (See Clinical.)

Treatment of third-degree AV block is based on the level of the block. The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Medical treatment of complete heart block is limited to patients with conduction disease in the AVN. (See Treatment.)

Initial treatment efforts should focus on assessing the need for temporary pacing and initiating the pacing. Most patients whose heart block is not otherwise treatable will require a permanent pacemaker or an implantable cardioverter defibrillator (ICD).



In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface ECG recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the AVN. The AVN then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles.

During atrial, AVN, and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, AV block can be divided into first-, second-, and third-degree block.

First-degree AV block

First-degree AV block is a condition in which a 1:1 relationship exists between P waves and QRS complexes, but the PR interval is longer than 200 msec. Thus, first-degree AV block represents delay or slowing of conduction. Occasionally, first-degree AV block may be associated with other conduction disturbances, including bundle-branch block and fascicular blocks (bifascicular or trifascicular block).

Second-degree AV block

Second-degree AV block exists when more P waves than QRS complexes are seen on the ECG, but a relationship between P waves and QRS complexes still exists. In other words, not all P waves are followed by QRS complexes (conducted). Traditionally, this type of AV block is divided into 2 main subcategories, Mobitz type I (Wenckebach) and Mobitz type II.

In the Mobitz I second-degree AV block, the PR interval prolonging until the P wave is not followed by a QRS complex. In a typical Mobitz I block, the PR interval prolongation from beat to beat is greatest in the first interval and progressively less with subsequent intervals. This is reflected in shortening of the R-R interval and the overall PR interval increases. Also, the R-R interval enveloping the pause is less than twice the duration of the first R-R interval following the pause.

On the ECG tracing, Mobitz I second-degree AV block results in the characteristic appearance of grouping beats; conversely, the presence of grouped beating should prompt a careful evaluation for Wenckebach conduction (though it should be noted that not all such conduction is pathologic).

In Mobitz II second-degree AV block, the PR interval is constant, but occasional P waves are not followed by the QRS complexes (nonconducted). Occasionally, the first PR interval following nonconducted P waves may be shorter by as much as 20 msec.

To differentiate between Mobitz I block and Mobitz II block, at least 3 consecutive P waves must be present in the tracing. If only every other P wave is conducted (2:1), a second-degree block cannot be classified into either of these categories and thus is best described as a 2:1 AV block, unless the mechanism can be inferred from surrounding patterns of atrial-to-ventricular conduction.

An AV block resembling second-degree AV block has been reported with sudden surges of vagal tone associated with cough, hiccups, swallowing, carbonated beverages, pain, micturition, or airway manipulation in otherwise healthy subjects. The distinguishing feature is simultaneous slowing of the sinus rate. This condition is paroxysmal and benign but must be carefully differentiated from a true second-degree AV block because the prognosis is very different.

Third-degree AV block

Third-degree AV block (ie, complete heart block) exists when there are more P waves than QRS complexes and there is no relationship between them (ie, no conduction). The conduction block may be at the level of the AVN, the bundle of His, or the bundle-branch Purkinje system. In most cases (approximately 61%), the block occurs below the His bundle. Block within the AV node accounts for approximately one fifth of all cases, whereas block within the His bundle accounts for slightly fewer than one fifth of all cases.[2]

The duration of the escape QRS complex depends on the site of the block and the site of the escape rhythm pacemaker. Pacemakers above the His bundle produce a narrow QRS complex escape rhythm, whereas those at or below the His bundle produce a wide QRS complex.

When the block is at the level of the AVN, the escape rhythm generally arises from a junctional pacemaker with a rate of 45-60 beats/min. Patients with a junctional pacemaker frequently are hemodynamically stable, and their heart rate increases in response to exercise and atropine. When the block is below the AVN, the escape rhythm arises from the His bundle or the bundle-branch Purkinje system at rates slower than 45 beats/min. These patients generally are hemodynamically unstable, and their heart rate is unresponsive to exercise and atropine.

AV dissociation

AV dissociation is present when atrial and ventricular activation are independent of each other. It can result from complete heart block or from physiologic refractoriness of conduction tissue. It can also occur in a situation when the atrial/sinus rate is slower than the ventricular rate (eg, with accelerated junctional tachycardia and ventricular tachycardia).

Occasionally, the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; only careful examination of the long rhythm strip may reveal a variation in PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of atrial/sinus rate will result in restoration of normal conduction.



AV block results from various pathologic states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Third-degree AV block can be either congenital or acquired.

The congenital form of complete heart block usually occurs at the level of the AVN. Patients are relatively asymptomatic at rest but later develop symptoms because the fixed heart rate is not able to adjust for exertion. In the absence of major structural abnormalities, congenital heart block is often associated with maternal antibodies to SS-A (Ro) and SS-B (La).[3]

The common causes of acquired AV block are as follows:

  • Drugs (see below)
  • Degenerative diseases – Lenègre disease (sclerodegenerative process involving only the conduction system) and Lev disease (calcification of the conduction system and valves), noncompaction cardiomyopathy, nail-patella syndrome, mitochondrial myopathy [4]
  • Infectious causes - Lyme borreliosis (particularly in endemic areas), Trypanosoma cruzi infection, [5] rheumatic fever, myocarditis, Chagas disease, Aspergillus myocarditis, varicella-zoster virus infection, [6] valve ring abscess
  • Rheumatic diseases - Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma
  • Infiltrative processes - Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myeloma
  • Neuromuscular disorders - Becker muscular dystrophy, myotonic muscular dystrophy
  • Ischemic or infarctive causes - AVN block associated with inferior wall myocardial infarction (MI), His-Purkinje block associated with anterior wall MI (see below)
  • Metabolic causes - Hypoxia, hyperkalemia, hypothyroidism
  • Toxins – “Mad” honey (grayanotoxin), cardiac glycosides (eg, oleandrin), and others
  • Phase IV block (also known as bradycardia-related block)
  • Iatrogenic causes (see below)


Complete heart block can develop from isolated single-agent overdose or—as is often the case—from combined or iatrogenic coadministration of AV nodal, beta-adrenergic, and calcium channel blocking agents. Drugs or toxins associated with heart block include the following:

  • Class Ia antiarrhythmics (eg, quinidine, procainamide, disopyramide)
  • Class Ic antiarrhythmics (eg, flecainide, encainide, propafenone)
  • Class II antiarrhythmics (beta-blockers)
  • Class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide, ibutilide)
  • Class IV antiarrhythmics (calcium channel blockers)
  • Digoxin or other cardiac glycosides; patients who are on digoxin should be educated about possible early symptoms of digoxin toxicity

Myocardial infarction

Anterior wall MI can be associated with an infranodal complete AV block; this is an ominous finding. Complete heart block develops in slightly less than 10% of cases of acute inferior MI and is much less dangerous, often resolving within hours to a few days.

Studies suggest that AV block rarely complicates MI.[7, 8] With an early revascularization strategy, the incidence of AV block decreased from 5.3 to 3.7%. Occlusion of each of the coronary arteries can result in development of conduction disease despite redundant vascular supply to the AVN from all coronary arteries.

Most commonly, occlusion of the right coronary artery (RCA) is accompanied by AV block. In particular, the proximal RCA occlusion has a high incidence of AV block (24%) because there is involvement not only of the AV nodal artery is involved but also of the right superior descending artery, which originates from the very proximal part of the RCA.

In most cases, AV block resolves promptly after revascularization, but sometimes the course is prolonged. Overall, the prognosis is favorable. AV block in the setting of occlusion of the left anterior descending artery (particularly proximal to the first septal perforator) has a more ominous prognosis and usually calls for pacemaker implantation. Second-degree AV block associated with bundle-branch block and in particular with alternating bundle-branch block is an indication for permanent pacing.


AV block may be associated with aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention to the left anterior descending artery, or ablation of the slow or fast pathway of the AVN. Placement of catheters that mechanically interfere with one fascicle when conduction is already impaired in the remaining conduction system (eg, bumping the right bundle with a pulmonary artery catheter in a patient with existing left bundle-branch block) almost always resolves spontaneously.

AV block after cardiac surgery is seen in 1-5.7% of patients.[9] Major risks factors identified for the need for permanent pacing are aortic valve surgery,[10] preexisting conduction disease (either right or left bundle-branch block), bicuspid aortic valve, annular calcification, and female gender. The time course for recovery varies widely, with a significant portion of patients recovering during the 48 hours following surgery. Available evidence suggests that if no recovery in AV conduction is seen by postoperative day 4 or 5, a pacemaker should be implanted.



In the United States, the prevalence of third-degree AV block is 0.02%. Worldwide, the prevalence of third-degree AV block is 0.04%.[11]

The incidence of AV conduction abnormalities increases with advancing age, resembling the age-related incidence of ischemic heart disease. An early peak in incidence occurs in infancy and early childhood due to congenital complete AV block, which is sometimes not recognized until childhood or even adolescence.



Patients with complete heart block are frequently hemodynamically unstable, and as a result, they may experience syncope, hypotension, cardiovascular collapse, or death. Other patients can be relatively asymptomatic and have minimal symptoms other than dizziness, weakness, or malaise.

Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. The cause of death may often be tachyarrhythmias precipitated by the secondary changes in ventricular repolarization (QT prolongation) secondary to the abrupt changes in rate.

Some patients may develop polymorphic ventricular tachycardia when significant bradycardia is present. This is related to prolongation of repolarization with extremely slow rates. This mechanism is also mostly responsible for death in these patients.

When treated with permanent pacing, the prognosis is excellent. The complications related to pacemaker insertion are rare (< 1%). Ventricular arrhythmias from atropine or catecholamines may occur. Common complications include those related to line and/or transvenous pacemaker placement. These complications include arterial injury, hemothorax, pneumothorax, or cardiac tamponade.

Contributor Information and Disclosures

Adam S Budzikowski, MD, PhD, FHRS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn

Adam S Budzikowski, MD, PhD, FHRS is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society

Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching.


Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, Society for Academic Emergency Medicine, Council of Emergency Medicine Residency Directors, Clerkship Directors in Emergency Medicine, Alliance for Clinical Education

Disclosure: Nothing to disclose.

James P Daubert, MD Professor of Medicine, Cardiology Division, Duke University School of Medicine

James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society

Disclosure: Partner received equity interest from Medtronic for none; Received honoraria from Boston Scientific for speaking and teaching; Received consulting fee from CV Therapeutics for consulting; Received consulting fee from Cryocor for consulting.

Andrew C Corsello, MD Consulting Staff, Department of Internal Medicine, Division of Cardiology, Cardiovascular Consultants of Maine, PA

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

Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Abrar H Shah, MD Clinical Assistant Professor, Department of Medicine, University of Rochester Medical Center; Consulting Staff, Department of Medicine (Cardiology), Strong Memorial Hospital, Geneva General Hospital; Consulting Staff, Department of Cardiology, Highland Hospital; Consulting Staff, Department of Cardiology and Electrophysiology, Park Ridge Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Additional Contributors

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

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ECG before and after complete heart block at the AV nodal level.
Complete heart block with wide complex escape.
Electrocardiogram from patient in complete heart block.
Transcutaneous cardiac pacing in a patient with third-degree heart block. Video courtesy of Therese Canares, MD; Marleny Franco, MD; and Jonathan Valente, MD (Rhode Island Hospital, Brown University).
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