eMedicine Specialties > Cardiology > Arrhythmias

First-Degree Atrioventricular Block

Jamshid Alaeddini, MD, FACC, Clinical Cardiac Electrophysiologist, Inland Cardiology Associates
Jamshid Shirani, MD, FACC, FAHA, Consulting Staff, Director of Cardiovascular Fellowship Program, Department of Medicine, Division of Cardiology, Geisinger Medical Center

Updated: Jan 3, 2007

Introduction

Background

The PR interval of the surface electrocardiogram (ECG) is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). In the adult population, normal PR interval ranges from 0.12-0.20 seconds at normal heart rates. First-degree atrioventricular (AV) block is defined as a PR interval exceeding 0.20 seconds (see Image 1).

Pathophysiology

The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, AV node, bundle of His, bundle branches, and Purkinje fibers. Thus, as shown in electrophysiological studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AV node, the His-Purkinje system, or a combination of these. AV nodal dysfunction accounts for the majority of cases. First-degree AV block caused by conduction delay in the His-Purkinje system often is associated with bundle-branch block.

Structure and function of the AV node and His-Purkinje system

The AV node is the only normal electrical connection between atria and ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AV node is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus. The bundle of His originates from the anteroinferior pole of the AV node and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles.

Blood supply to the AV node is provided by the AV node artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries.

The AV node has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AV node.

Frequency

United States

First-degree AV block is rare in young healthy adults. It is reported in 0.65-1.1% of young adults older than 20 years. Higher prevalence is reported in trained athletes (8.7%). The prevalence also increases with age; first-degree AV block is reported in 5% of men older than 60 years. The overall prevalence is 1.13 cases per 1000 lives.

Mortality/Morbidity

No mortality or morbidity is related to isolated first-degree AV block. However, in the setting of acute inferior myocardial infarction (MI), first-degree AV block may herald higher degrees of AV block. Markedly prolonged PR interval in patients with left ventricular systolic dysfunction may impair ventricular filling and thus reduce cardiac output.

Age

Incidence of first-degree AV block increases with age.

Clinical

History

• Patients with first-degree AV block are generally asymptomatic at rest. Markedly prolonged PR interval may reduce exercise tolerance in some patients with left ventricular systolic dysfunction. Syncope may result from transient high-degree AV block, especially in those with infranodal block and wide QRS complex.

Physical

• The intensity of the first heart sound (S1) is decreased in patients with first-degree AV block.
• Patients with first-degree AV block may have a short, soft, blowing, diastolic murmur heard at the cardiac apex. This diastolic murmur is not caused by diastolic mitral regurgitation, because it reaches its peak before the onset of regurgitation. The diastolic murmur is thought to be related to antegrade flow through closing mitral valve leaflets that are stiffer than normal. Administration of atropine may reduce the duration of this murmur by shortening the PR interval.

Causes

• Athletic training: Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.
• Coronary artery disease
  • Acute MI: First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units.
    • His bundle electrocardiographic studies have shown that, in most of these patients, AV node is the site of conduction block.
    • AV block is more common in the setting of inferior MI.
    • In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy. Patients with AV block at the time of presentation had a higher in-hospital mortality rate than patients without AV block; both groups, however, had similar mortality rates during the following year. Patients who developed AV block after thrombolytic therapy had higher mortality rates both in-hospital and in the following year than patients without AV block. Right coronary artery was more often the site of infarction in patients with heart block than in those without heart block. Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.
  • Angina pectoris
  • Prinzmetal angina
• Idiopathic degenerative diseases of the conduction system
  • Lev disease: This is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, "sclerosis of the left side of cardiac skeleton," including mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum. Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block.
  • Lenègre disease: This is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lenègre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease.
• Drugs: Calcium channel blockers, beta-blockers, digoxin, and amiodarone all may cause first-degree AV block. Although first-degree AV block is not an absolute contraindication for administration of these drugs, extreme caution should be exercised in the use of these medications in patients with first-degree AV block, as they carry the risk of developing higher degree AV block on exposure to these drugs.
• Mitral or aortic valve annulus calcification: The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.
• Infectious disease: Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block.
  • Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block.
  • Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.
• Collagen vascular disease: Rheumatoid arthritis, systemic lupus erythematous, and scleroderma all may be associated with first-degree AV block.
  • Rheumatoid nodules may occur in the central fibrous body and result in AV block.
  • Fibrosis of the AV node or the adjacent myocardium in patients with systemic lupus erythematous or scleroderma can cause first-degree AV block.
  • Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive. In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.
• Infiltrative diseases such as amyloidosis or sarcoidosis
• Myotonic dystrophy
• Iatrogenic
  • First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuation of the adenosine infusion.
  • Marked first-degree AV block may occur following catheter ablation of the fast AV nodal pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to the pacemaker syndrome.
  • First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of atrial septal defect using the Amplatzer septal occluder.
  • First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.

Differential Diagnoses

Atrioventricular Block
Atrioventricular Dissociation
Second-Degree Atrioventricular Block
Third-Degree Atrioventricular Block

Other Problems to Be Considered

In AV dissociation, atrial and ventricular contractions are not related; in patients with first-degree AV block, the PR interval is constant during each cardiac cycle.

Workup

Imaging Studies

• In patients with first-degree AV block and left ventricular systolic dysfunction, Doppler ultrasound may be used to document an improvement in cardiac output during dual-chamber pacing at short AV delay. This may provide evidence for the appropriateness of implanting a permanent pacemaker for hemodynamic support in such patients. More recently, cardiac resynchronization therapy (ie, biventricular pacing) has been applied in patients with cardiomyopathy, congestive heart failure, or intraventricular conduction delay (IVCD). First-degree AV block is frequently present in these patients as well.

Other Tests

• Surface ECG: The PR interval exceeds 0.20 seconds and all P waves conduct to the ventricle with constant but prolonged PR interval.
• His bundle ECG: This is necessary only in patients with symptomatic (ie, presyncope and syncope) first-degree AV block and a wide QRS complex, indicative of bundle-branch block. The study is used to locate the site of the block in these patients. As many as 50% of patients show an infranodal conduction delay.

Histologic Findings

When studied by light microscopy, an AV node is composed of a thick mesh of tiny pale cells, which anastomose with one another via short pluridirectional cytoplasmic projections. Under electron microscopy, 4 types of cells are observed in the AV node: transitional cells, P cells, common myocardial cells, and Purkinje cells. Three functional regions have been described in the AV node based on the differing conductive properties: atrionodal (AV), nodal (N), and nodal-His (NH). Cells in the N region have slower conduction times than the other regions and have no automaticity properties. Cells of the AN and NH regions have faster conduction times and display spontaneous diastolic repolarization activity.

Treatment

Medical Care

Patients with asymptomatic first-degree AV block require no treatment.

• In patients with symptomatic first-degree AV block, the following applies:
  • Discontinue medications with potential for AV block, if possible.
  • Permanent electronic pacemakers may be indicated in those with the following:
    • Severe bradycardia
    • Syncope associated with infranodal block
    • Left ventricular systolic dysfunction when a shorter AV delay has been shown to improve hemodynamic condition
• The American College of Cardiology/American Heart Association considers use of the permanent dual-chamber pacemaker in patients with first-degree AV block with symptoms suggestive of pacemaker syndrome during ventricular pacing and documented alleviation of symptoms with temporary dual-chamber pacing as a class IIa therapy (ie, weight of evidence/opinion is in favor of usefulness/efficacy).
• Use of a permanent pacemaker is considered as class IIb therapy in patients with marked first-degree AV block (PR interval >0.30 s) accompanied by left ventricular dysfunction and symptoms of congestive heart failure in whom a shorter AV interval results in hemodynamic improvement (class IIb: usefulness/efficacy is less well established by evidence/opinion).
• Use of a permanent pacemaker for asymptomatic first-degree AV block is considered a class III therapy (class III: generally not appropriate).

Consultations

Electrophysiology consultation may be indicated for patients with first-degree AV block and symptoms of syncope or heart failure.

Medication

Use of medication is not indicated for treatment of asymptomatic first-degree AV block. However, in patients with severe bradycardia or those with the possibility of progression to higher degree AV block, medications (eg, atropine, isoproterenol) can be used in anticipation of insertion of a cardiac pacemaker.

Parasympathetic blocker

Parasympathetic blockade shortens the PR interval by improving AV nodal conduction.

Atropine (Atropair)

Increases heart rate through vagolytic effects, causing increase in cardiac output.

Dosing

Adult

0.5-1 mg IV push; repeat q3-5min prn; not to exceed total dose of 0.04 mg/kg

Pediatric

Not established

Interactions

Other anticholinergics cause additive effects; may increase pharmacologic effects of atenolol and digoxin; may increase antipsychotic effects of phenothiazines; TCAs, thiazides, and amantadine may increase effects; levodopa can decrease effects

Contraindications

Documented hypersensitivity; thyrotoxicosis; narrow-angle glaucoma; tachycardia

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Avoid in Down syndrome and/or children with brain damage to prevent hyperreactive response; avoid also in coronary heart disease, tachycardia, CHF, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; patients with prostatic hypertrophy, prostatism can have dysuria and may require catheterization; may cause tachycardia, altered mental status, flushing, or blurred vision

Sympathomimetics

Isoproterenol infusion can be used to shorten AV conduction time. Isoproterenol has chronotropic as well as inotropic effects, which result in an increase in cardiac output.

Isoproterenol (Isuprel)

Has beta1- and beta2-adrenergic receptor activity. Binds beta-receptors of heart, smooth muscle of bronchi, skeletal muscle, vasculature, and alimentary tract. Has positive inotropic and chronotropic actions.

Dosing

Adult

2-4 mcg/min IV; titrate to effect

Pediatric

Not established

Interactions

Bretylium and MAOIs increase action of vasopressors on adrenergic receptors, which may result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; TCAs may potentiate pressor response of direct-acting vasopressors

Contraindications

Documented hypersensitivity; tachyarrhythmias, tachycardia, or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

May have deleterious effect on injured or failing heart by increasing myocardial oxygen requirements while decreasing effective coronary perfusion; in some patients, presumably with organic disease of AV node and its branches, may paradoxically worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism; if heart rate >110 beats/min, may be advisable to decrease infusion rate or temporarily discontinue infusion

Follow-up

Further Inpatient Care

• Patients with first-degree AV block started on AV nodal blocking drugs should be monitored to make sure that higher grade AV block does not develop.

Further Outpatient Care

• Patients with first-degree AV block started on AV nodal blocking drugs should be monitored to make sure that higher grade AV block does not develop.

Complications

• Progression to higher degrees of AV block
• Reduction in left ventricular stroke volume and cardiac output
• Pacemaker syndrome

Prognosis

• Isolated first-degree AV block carries no increased risk of mortality.
• Patients with first-degree AV block and infranodal blocks have increased risk of progression to complete AV block.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize and treat symptomatic first-degree AV block

Multimedia

Media file 1: The PR interval is 0.24 seconds (240 ms) in this patient with asymptomatic first-degree atrioventricular block.

References

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3. Bexton RS, Camm AJ. First degree atrioventricular block. Eur Heart J. Mar 1984;5 Suppl A:107-9. [Medline].

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5. Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary--a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). Circulation. Apr 7 1998;97(13):1325-35. [Medline].

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7. Ishikawa T, Kimura K, Nihei T, et al. Relationship between diastolic mitral regurgitation and PQ intervals or cardiac function in patients implanted with DDD pacemakers. Pacing Clin Electrophysiol. Nov 1991;14(11 Pt 2):1797-802. [Medline].

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12. Nair CK, Sketch MH, Desai R, et al. High prevalence of symptomatic bradyarrhythmias due to atrioventricular node-fascicular and sinus node-atrial disease in patients with mitral anular calcification. Am Heart J. Feb 1982;103(2):226-9. [Medline].

13. Panidis IP, Ross J, Munley B, et al. Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: a common finding by Doppler echocardiography. J Am Coll Cardiol. Apr 1986;7(4):768-74. [Medline].

14. Perlman LV, Ostrander LD, Keller JB, Chiang BN. An epidemiologic study of first degree atrioventricular block in Tecumseh, Michigan. Chest. Jan 1971;59(1):40-6. [Medline].

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16. Schnittger I, Appleton CP, Hatle LK, Popp RL. Diastolic mitral and tricuspid regurgitation by Doppler echocardiography in patients with atrioventricular block: new insight into the mechanism of atrioventricular valve closure. J Am Coll Cardiol. Jan 1988;11(1):83-8. [Medline].

17. Sonesson SE, Salomonsson S, Jacobsson LA, et al. Signs of first-degree heart block occur in one-third of fetuses of pregnant women with anti-SSA/Ro 52-kd antibodies. Arthritis Rheum. Apr 2004;50(4):1253-61. [Medline].

18. Suda K, Raboisson MJ, Piette E, et al. Reversible atrioventricular block associated with closure of atrial septal defects using the Amplatzer device. J Am Coll Cardiol. May 5 2004;43(9):1677-82. [Medline].

Keywords

first-degree atrioventricular block, AV block, heart block, Lev disease, Lenègre disease, Lenegre disease, His-Purkinje system, atrial depolarization, ventricular depolarization, P wave, QRS complex, His bundle, acute inferior myocardial infarction, left ventricular systolic dysfunction, infranodal block, wide QRS complex, coronary artery disease, acute myocardial infarction, inferior myocardial infarction, angina pectoris, Prinzmetal angina, idiopathic degenerative diseases of the conduction system, mitral valve annulus calcification, aortic valve annulus calcification, infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, tuberculosis, acute myocarditis, collagen vascular disease, rheumatoid arthritis, systemic lupus erythematous, scleroderma, infiltrative diseases, amyloidosis, sarcoidosis, myotonic dystrophy, pacemaker syndrome, reversible first-degree AV block, permanent first-degree AV block, atrial septal defect closure, Amplatzer septal occluder,bundle-branchblock

Contributor Information and Disclosures

Author

Jamshid Alaeddini, MD, FACC, Clinical Cardiac Electrophysiologist, Inland Cardiology Associates
Jamshid Alaeddini, MD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, and Heart Rhythm Society
Disclosure: Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; St. Jude  Honoraria Speaking and teaching; Reliant Honoraria Speaking and teaching

Coauthor(s)

Jamshid Shirani, MD, FACC, FAHA, Consulting Staff, Director of Cardiovascular Fellowship Program, Department of Medicine, Division of Cardiology, Geisinger Medical Center
Jamshid Shirani, MD, FACC, FAHA is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Echocardiography, and Association of Subspecialty Professors
Disclosure: Nothing to disclose.

Medical Editor

Robert E Fowles, MD, Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic
Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Disclosure: Nothing to disclose.

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