Atrioventricular block causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]

Overview

Causes

Intrinsic Etiology

Extrinsic Etiology

Normal Variants

  1. PR prolongation can be found in 0.5% of healthy patients
  2. Second degree block type I may be seen in healthy patients during sleep
  3. Transient AV block can occur with vagal maneuvers

ST Elevation MI

In acute ST elevation MI:

Inferior ST Elevation MI

  • Inferior ST elevation MI: AV block is more common in patients with inferior MIs (1/3rd of patients)
  1. In 90% of patients the inferior wall is supplied by the RCA which gives off a branch to the AV node
  2. As a rule, the AV block is transient and normal function returns within a week of the acute episode

Anterior ST Elevation MI

  • Anterior ST elevation MI: AV block may be seen in up to 21%
  1. Incidence of second degree AV block and third degree AV block is 5 to 7%
  2. Block is the result of damage to the interventricular septum supplied by the LAD
  3. There is damage to the bundle branches either in the form of bilateral bundle branch block or trifascicular block
  4. RBBB, RBBB + LAHB, RBBB + LPHB or LBBB often appear before the development of AV block
  5. The PR is normal or minimally prolonged before the onset of second degree AV block or third degree AV block
  6. Although the AV block is usually transient, there is a relatively high incidence of recurrence or high-degree AV block after the acute event
  7. In addition to ischemia, fibrosis and calcification of the summit of the ventricular septum that involve the branching part of the bundle branches, may play a role in the genesis of the conduction defect.
  8. It used to be thought that CAD was the most frequent cause of chronic complete AV block, but it actually causes only 15% of cases

Degenerative Diseases

  • Sclero-degenerative disease of the bundle branches first described by Lenegre
  • The pathologic process is called idiopathic bilateral bundle branch fibrosis and the heart block is called primary heart block
  • This is the most common cause of chronic AV block (46%)
  • Lev described similar degenerative lesions, which he referred to as sclerosis of the left side of the cardiac skeleton. There is progressive fibrosis and calcification of the mitral annulus, the central fibrous body, the pars membranacea, the base of the aorta, and the summit of the muscular ventricular septum. Various portions of the His bundle or the bundle branches may be involved, resulting in AV block.

Hypertension

  • Chronic AV block in patients with HTN is thought to be due to CAD or sclerosis of the left side of the cardiac skeleton exacerbated by hypertension

Diseases of the Myocardium

  1. Type I second degree AV block may occur, but complete AV block is uncommon
  2. Usually transient, disappears when the patient recovers

Valvular Heart Disease

Valvular Diseases

  • Calcific aortic stenosis may be accompanied by chronic partial or complete AV block
  • There is an extension of the calcification to involve the main bundle or its bifurcation, resulting in degeneration and necrosis of the conduction tissue
  • May also occur in rheumatic mitral valve disease, but is less common
  • Occasionally, massive calcification of the mitral annulus as an ageing process may cause AV block
  • May also be seen in bacterial endocarditis, especially of the aortic valve

Drugs

  1. When second degree AV block is induced, it is always of the Type I variety.
  2. When complete block occurs, the QRS complexes are narrow because the block is of the AV node.
  3. The ventricular response rate is more rapid than that due to organic lesions, and increased automaticity of the AV junctional pacemaker may be responsible.

Congenital

Trauma

  • May be induced during open heart surgery in the area of AV conduction tissue
  • Seen in patients operated on for the correction of VSD, tetralogy of Fallot, and endocardial cushion defect.
  • May be due to edema, transient ischemia, or actual disruption of the conduction tissue. The block may therefore be permanent or transient.
  • Also reported with both penetrating and non-penetrating trauma of the chest

Causes by Organ System

Cardiovascular Aortic valve stenosis, Atrial septal defect, Cardiomyopathy, Carotid hypersensitivity, Congenitally corrected transposition of great arteries, Ebstein anomaly, Endocarditis, Hypertension, Ischaemic heart disease, Myocardial infarction, Myocarditis, Rheumatic heart disease, Kearns-Sayre syndrome, Lenegre-Lev disease
Chemical / poisoning Chlorpyrifos, Coumaphos, Oleander, Propoxur
Dermatologic Dermatomyositis
Drug Side Effect Acetylcholinesterase inhibitors, Amiodarone, Articaine, Atenolol, Beta blockers, Bupivacaine, Calcium channel blockers, Clonidine, Digoxin, Diltiazem, Disopyramide, Dolasetron, Donepezil, Eslicarbazepine acetate, Fesoterodine, Fingolimod, Ibutilide, Labetalol, Lacosamide, Lanatoside C, Paliperidone, Pergolide, Phenylephrine, Pilocarpine, Propoxyphene, Propranolol, Ritonavir, Quinidine, Quinine, Terodiline, Tolterodine, Verapamil
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic Emery-Dreifuss muscular dystrophy, X-linked, Fabry disease, Glycogenosis type 2b, Hemochromatosis, Kearns-Sayre syndrome, Lenegre-Lev disease, Myotonic dystrophy, Singleton-Merten syndrome
Hematologic No underlying causes
Iatrogenic Cardiac surgery, Intravenous therapy, Valve replacement
Infectious Disease Borrelia burgdorferi, Chagas disease, Diphtheria, Lyme disease, Rheumatic fever
Musculoskeletal / Ortho Dermatomyositis, Ankylosing spondylitis, Rheumatoid arthritis, Myotonic dystrophy, Emery-Dreifuss muscular dystrophy, X-linked
Neurologic Neurogenic, Vagal reaction
Nutritional / Metabolic Fabry disease, Glycogenosis type 2b, Hemochromatosis
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic Kearns-Sayre syndrome
Overdose / Toxicity Acetylcholinesterase inhibitors, Amiodarone, Atenolol, Beta blockers, Bupivacaine, Calcium channel blockers, Clonidine, Digoxin, Diltiazem, Disopyramide, Dolasetron, Donepezil, Eslicarbazepine acetate, Fesoterodine, Fingolimod, Ibutilide, Labetalol, Lacosamide, Lanatoside C, Paliperidone, Propoxyphene, Propranolol, Quinidine, Quinine, Terodiline, Tolterodine, Verapamil
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal / Electrolyte Hyperkalaemia, Hypokalaemia
Rheum / Immune / Allergy Amyloidosis, Rheumatoid arthritis, Sarcoidosis, Scleroderma, Systemic lupus erythematosus, Systemic sclerosis
Sexual No underlying causes
Trauma Chest trauma
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Athletes, Hypothermia, Situational syncope, Valsalva manouevre

Causes in Alphabetical Order


References

  1. LENEGRE J (1964). "ETIOLOGY AND PATHOLOGY OF BILATERAL BUNDLE BRANCH BLOCK IN RELATION TO COMPLETE HEART BLOCK". Prog Cardiovasc Dis. 6: 409–44. doi:10.1016/s0033-0620(64)80001-3. PMID 14153648.
  2. LEV M (1964). "ANATOMIC BASIS FOR ATRIOVENTRICULAR BLOCK". Am J Med. 37: 742–8. doi:10.1016/0002-9343(64)90022-1. PMID 14237429.
  3. Deng GH, Wang AX (1991). "[Clinical analysis of 130 patients with fever of unknown origin]". Zhonghua Nei Ke Za Zhi. 30 (3): 157–9, 188–9. PMID 1874084.
  4. Yada H, Soejima K (2019). "Management of Arrhythmias Associated with Cardiac Sarcoidosis". Korean Circ J. 49 (2): 119–133. doi:10.4070/kcj.2018.0432. PMC 6351276. PMID 30693680.
  5. Tselios K, Gladman DD, Harvey P, Su J, Urowitz MB (2018). "Severe brady-arrhythmias in systemic lupus erythematosus: prevalence, etiology and associated factors". Lupus. 27 (9): 1415–1423. doi:10.1177/0961203318770526. PMID 29665757.
  6. Yeung C, Baranchuk A (2019). "Diagnosis and Treatment of Lyme Carditis: JACC Review Topic of the Week". J Am Coll Cardiol. 73 (6): 717–726. doi:10.1016/j.jacc.2018.11.035. PMID 30765038.
  7. Umapathy S, Saxena A (2018). "Acute rheumatic fever presenting as complete heart block: report of an adolescent case and review of literature". BMJ Case Rep. 2018. doi:10.1136/bcr-2017-223792. PMC 5836695. PMID 29440244.

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