Third degree AV block


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Overview
Third degree AV block, also known as complete heart block, is a defect of the electrical system of the heart, in which the impulse generated in the atria (typically the SA node on top of the right atrium) does not propagate to the ventricles.

Presentation

 * Because the impulse is blocked, an accessory pacemaker below the level of the block will typically activate the ventricles. This is known as an escape rhythm. Since this accessory pacemaker activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (EKG).


 * One will activate the atria and create the P waves, typically with a regular P to P interval.
 * The second will activate the ventricles and produce the QRS complex, typically with a regular R to R interval. The PR interval will be variable, as the hallmark of complete heart block is no apparent relationship between P waves and QRS complexes.


 * Patients with third degree AV block typically experience a lower overall measured heart rate (as low as 28 beats per minute during sleep), low blood pressure, and poor circulation. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for sustained activity.

Etiology

 * 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.


 * An inferior wall myocardial infarction may cause damage to the AV node, causing third degree heart block. In this case, the damage is usually transitory, and the AV node may recover.  Studies have shown that third degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. The escape rhythm typically originates in the AV junction, producing a narrow complex escape rhythm.


 * An anterior wall myocardial infarction may damage the distal conduction system of the heart, causing third degree heart block. This is typically extensive, permanent damage to the conduction system, necessitating a permanent pacemaker to be placed. The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.


 * 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.

Electrocardiographic Findings

 * 1) There is complete failure of the supraventricular impulse to reach the ventricles.
 * 2) The atrial and the ventricular activities are independent of each other
 * 3) The block may be at the level of the AV node, the His bundle or the bundle branches
 * 4) If the block is in the main bundle branches, it is called bilateral bundle branch block
 * 5) If it involves the right bundle branch and two divisions of the left bundle, then it is called trifascicular block
 * 6) The atrial rate is faster than the ventricular rate
 * 7) The ventricular rhythm is maintained by either a junctional or an idioventricular pacemaker.
 * 8) The PP and RR intervals are regular, but the P waves bear no relation to the QRS complexes (i.e. the PR interval varies)
 * 9) In 30 to 40% of patients with complete AV block, ventriculophasic sinus arrhythmia can be demonstrated. In this case, there is a decrease in the PP interval in those PP intervals containing a QRS.
 * 10) When the underlying rhythm is atrial fibrillation, the presence of complete AV block is manifested by the regularity of the ventricular rhythm.
 * 11) In AV block, the atrial rate is faster than the ventricular rate, in AV dissociation the ventricular rate is faster than the atrial rate (likely due to automaticity of a subsidiary pacemaker).
 * 12) If the subsidiary pacemaker is above the His bundle, then the escape rhythm is of a narrow complex and is likely to be AV junctional in origin.
 * 13) If the subsidiary pacemaker is below the His bundle, then the escape rhythm is wide. Wide complexes can result from a junctional escape rhythm with superimposed bundle branch block.
 * 14) The rate in complete AV block:
 * 15) * AV junctional escape rhythms have a rate between 40 to 60 beats per minute, which may be increased by exercise or vagolytic agents
 * 16) * Idioventricular rhythms have a rate of 30 to 40 beats per minute but may be as low as 20 and as high as 50, and the rate is not affected by exercise or vagolytic agents
 * 17) His bundle recordings:
 * 18) * Allows determination of the site of block
 * 19) * In chronic acquired complete AV block, most cases (@ 50% to 60%) have block located distal to the His bundle, and the QRS complexes are wide.
 * 20) * In acute heart block secondary to an inferior MI, infection, or drugs, the site of the block is usually proximal to the His bundle.
 * 21) * In acute anterior MI, the site of the block is usually distal to the His bundle and reflects the fact that a large territory has been infarcted.

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:
 * 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

 * 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

 * 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 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
 * Type I second degree AV block may occur, but complete AV block is uncommon
 * 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

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 aging process may cause AV block
 * May also be seen in bacterial endocarditis, especially of the aortic valve

Drugs

 * Digoxin is one of the most common causes of reversible AV block
 * 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

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

Treatment
Third degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node and sends a pulse to the AV node at an appropriate interval, essentially completing the connection between the two nodes. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third degree AV block.

Treatment may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.

Treatment in emergency situations is atropine and an external pacer.

Resources

 * ECGpedia: Course for interpretation of ECG
 * The whole ECG - A basic ECG primer
 * 12-lead ECG library
 * Simulation tool to demonstrate and study the relation between the electric activity of the heart and the ECG
 * ECG information from Children's Hospital Heart Center, Seattle
 * ECG Challenge from the ACC D2B Initiative
 * National Heart, Lung, and Blood Institute, Diseases and Conditions Index
 * A history of electrocardiography
 * Interpretation of electrocardiograms in infants and children.