Atrioventricular block causes
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- Degenerative (Lev’s and Lenegre’s)
- Infiltrative (Sarcoidosis, Amyloidosis, Hemochromatosis)
- Inflammatory (Systemic lupus erythematosus (SLE), scleroderma, rheumatoid arthritis (RA))
- Myopathic (Myotonic Dystrophy, Erb's palsy)
- Infectious (Lyme disease, endocarditis, Chagas disease)
- Trauma (Valve replacement, intravenous therapy)
- Autonomic (Carotid sinus hypersensitivity, situational syncope, vagal reaction)
- Medications (Beta blockers, calcium-channel blocker (CCB), digoxin, clonidine, antiarrhythmics)
- Electrolytes (Hyperkalemia, hypokalemia)
- PR prolongation can be found in 0.5% of healthy patients
- Second degree block type I may be seen in healthy patients during sleep
- Transient AV block can occur with vagal maneuvers
ST Elevation MI
In acute ST elevation MI:
- First degree block occurs in 8% to 13%
- Second degree block in 3.5% to 10%
- Complete heart block in 2.5% to 8%
Inferior ST Elevation MI
- In 90% of patients the inferior wall is supplied by the RCA which gives off a branch to the AV node
- As a rule, the AV block is transient and normal function returns within a week of the acute episode
Anterior ST Elevation MI
- Incidence of second degree AV block and third degree AV block is 5 to 7%
- 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.
- 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
- 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.
- 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
- Acute rheumatic fever: PR prolongation is a common (25 to 95% of cases) sign in patients with acute rheumatic fever
- Ankylosing spondylitis
- Chagas disease
- Dilated cardiomyopathy results in various degrees of heart block are seen in 15% of patients
- HCM: 3% of patients with HCM will develop heart block
- Lyme disease
- Muscular dystrophy
- Tumors, primary and secondary
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 ageing process may cause AV block
- May also be seen in bacterial endocarditis, especially of the aortic valve
- When second degree AV block is induced, it is always of the Type I variety.
- When complete block occurs, the QRS complexes are narrow because the block is of the AV node.
- 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.
- Laxatives like sodium sulfate, potassium sulfate and magnesium sulfate.
- 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
- 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
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