Third degree AV block causes: Difference between revisions
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Third degree heart block may also be congenital and has been linked to the presence of [[lupus erythematosus|lupus]] in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third degree heart block in many patients is unknown. Studies suggest that the prevalence of congenital third degree heart block is between 1 in 15,000 and 1 in 22,000 live births. | Third degree heart block may also be congenital and has been linked to the presence of [[lupus erythematosus|lupus]] in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third degree heart block in many patients is unknown. Studies suggest that the prevalence of congenital third degree heart block is between 1 in 15,000 and 1 in 22,000 live births. | ||
==Causes== | ==Causes== | ||
===Common Causes=== | ===Common Causes=== | ||
The most common causes of first degree heart block are an AV nodal disease, enhanced vagal tone (for example in athletes), [[myocarditis]], acute [[myocardial infarction]] (especially acute inferior MI), electrolyte disturbances and [[drugs]]. The drugs that most commonly cause first degree heart block are those that increase the refractory time of the [[AV node]], thereby slowing AV conduction. These include [[calcium channel blockers]], [[beta-blockers]],[[digitalis]],[[cardiac glycosides]] and anything that increases [[cholinergic]] activity such as [[cholinesterase inhibitor]]s. | The most common causes of first degree heart block are an AV nodal disease, enhanced vagal tone (for example in athletes), [[myocarditis]], acute [[myocardial infarction]] (especially acute inferior MI), electrolyte disturbances and [[drugs]]. The drugs that most commonly cause first degree heart block are those that increase the refractory time of the [[AV node]], thereby slowing AV conduction. These include [[calcium channel blockers]], [[beta-blockers]],[[digitalis]],[[cardiac glycosides]] and anything that increases [[cholinergic]] activity such as [[cholinesterase inhibitor]]s. | ||
* Acute ST elevation MI - [[Complete heart block]] occurs in 2.5% to 8% of patients. | * Acute ST elevation MI - [[Complete heart block]] occurs in 2.5% to 8% of patients. |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Many conditions can cause third degree heart block, but the most common cause is coronary ischemia. Progressive degeneration of the electrical conduction system of the heart can lead to third degree heart block. This may be preceded by first degree AV block, second degree AV block, bundle branch block, or bifascicular block. In addition, acute myocardial infarction may present with third degree AV block.
Third degree heart block may also be congenital and has been linked to the presence of lupus in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third degree heart block in many patients is unknown. Studies suggest that the prevalence of congenital third degree heart block is between 1 in 15,000 and 1 in 22,000 live births.
Causes
Common Causes
The most common causes of first degree heart block are an AV nodal disease, enhanced vagal tone (for example in athletes), myocarditis, acute myocardial infarction (especially acute inferior MI), electrolyte disturbances and drugs. The drugs that most commonly cause first degree heart block are those that increase the refractory time of the AV node, thereby slowing AV conduction. These include calcium channel blockers, beta-blockers,digitalis,cardiac glycosides and anything that increases cholinergic activity such as cholinesterase inhibitors.
- Acute ST elevation MI - Complete heart block occurs in 2.5% to 8% of patients.
- Inferior ST elevation MI: AV block is more common in patients with inferior MIs (1/3rd of patients).
- Anterior ST elevation MI: AV block may be seen in up to 21%.
- Block is the result of damage to the interventricular septum supplied by the LAD
- There is damage to the bundle branches either in the form of bilateral bundle branch block or trifascicular block.
- RBBB, RBBB + LAHB, RBBB + LPHB or LBBB often appear before the development of AV block.
- The PR is normal or minimally prolonged before the onset of second degree AV block or third degree AV block.
- Although the AV block is usually transient, there is a relatively high incidence of recurrence or high-degree AV block after the acute event.
- 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.
- Degenerative diseases
- Sclerodegenerative 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 byhypertension
- Diseases of the myocardium
- Acute rheumatic fever: PR prolongation is a common (25 to 95% of cases) sign in patients with acute rheumatic fever
- Usually transient, disappears when the patient recovers
- Amyloidosis
- Ankylosing spondylitis
- Chagas disease
- Dermatomyositis
- Dilated cardiomyopathy results in various degrees of heart block are seen in 15% of patients
- Diphtheria
- HCM: 3% of patients with HCM will develop heart block
- Hemochromatosis
- Lyme disease
- Muscular dystrophy
- Myocarditis
- Sarcoid
- Scleroderma
- SLE
- Tumors, primary and secondary
- Acute rheumatic fever: PR prolongation is a common (25 to 95% of cases) sign in patients with acute rheumatic fever
- Valvular Heart Disease
- 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 aging process may cause AV block
- May also be seen in bacterial endocarditis, especially of the aortic valve
- Ebstein's anomaly may be associated with first-degree AV block.
- Drugs
- Digoxin is one of the most common causes of reversible AV block
- The ventricular response rate is more rapid than that due to organic lesions, and increased automaticity of the AV junctional pacemaker may be responsible.
- Quinidine and Procainamide may produce slight prolongation of the PR
- β blockers may cause AV block
- Diltiazem and verapamil may cause AV conduction delay and PR interval prolongation
- Digoxin is one of the most common causes of reversible AV block
- Congenital
- Occurs in the absence of other evidence of organic heart disease
- Site is usually proximal to the bifurcation of the His bundle, most often in the AV node
- Narrow QRS with a rate > 40 beats per minute
- Frequently seen in those with corrected transposition of the great vessels, and occasionally in ASDs and Ebstein's anomaly
- 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 | AV nodal disease, Myocarditis, Acute myocardial infarction (especially acute inferior MI), Hypertension, Acute rheumatic fever, Dilated cardiomyopathy, HCM, Myocarditis, Valvular heart disease, Transposition of the great vessels, ASDs, Ebstein's anomaly, VSD, Tetralogy of Fallot, Endocardial cushion defect |
Chemical / poisoning | No underlying causes |
Dermatologic | No underlying causes |
Drug Side Effect | Calcium channel blockers, Beta-blockers, Digitalis, Cardiac glycosides, Cholinesterase inhibitors, Quinidine,Procainamide |
Ear Nose Throat | No underlying causes |
Endocrine | No underlying causes |
Environmental | No underlying causes |
Gastroenterologic | Hemochromatosis |
Genetic | No underlying causes |
Hematologic | No underlying causes |
Iatrogenic | No underlying causes |
Infectious Disease | Acute rheumatic fever, Chagas disease, Diphtheria, Lyme disease, Myocarditis |
Musculoskeletal / Ortho | Ankylosing spondylitis, Muscular dystrophy |
Neurologic | No underlying causes |
Nutritional / Metabolic | No underlying causes |
Obstetric/Gynecologic | No underlying causes |
Oncologic | No underlying causes |
Opthalmologic | No underlying causes |
Overdose / Toxicity | No underlying causes |
Psychiatric | No underlying causes |
Pulmonary | Sarcoidosis |
Renal / Electrolyte | No underlying causes |
Rheum / Immune / Allergy | Ankylosing spondylitis, Dermatomyositis, Scleroderma, SLE |
Sexual | No underlying causes |
Trauma | No underlying causes |
Urologic | No underlying causes |
Dental | No underlying causes |
Miscellaneous | Amyloidosis, Enhanced vagal tone (for example in athletes), Normal variants |
Causes in Alphabetical Order
- Acute myocardial infarction (especially acute inferior MI)
- Acute rheumatic fever
- Amyloidosis
- Ankylosing spondylitis
- ASD
- AV nodal disease
- Beta-blockers
- Calcium channel blockers
- Cardiac glycosides
- Chagas disease
- Cholinesterase inhibitors
- Dermatomyositis
- Digitalis
- Dilated cardiomyopathy
- Diphtheria
- Ebstein's anomaly
- Endocardial cushion defect
- Enhanced vagal tone (for example in athletes)
- HCM
- Hemochromatosis
- Hypertension
- Lyme disease
- Muscular dystrophy
- Myocarditis
- Normal variants
- Procainamide
- Quinidine
- Sarcoidosis
- Scleroderma
- SLE
- Tetralogy of Fallot
- Transposition of the great vessels
- Valvular heart disease
- VSD