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(HR. Muslim, Ahmad dan Hakim).

Sabtu, 28 November 2009

Atrioventricular Block


Atrioventricular (AV) block occurs when the atrial depolarization fail to reach the ventricles or when atrial depolarization is conducted with a delay. Three degrees of AV block are recognized.

First-degree AV block consists of prolongation of the PR interval on the electrocardiogram (ECG) (>0.20 s in adults and >0.16 s in young children). The upper limit of the reference range for the PR interval is age-dependent in children. All atrial impulses reach the ventricles in first-degree AV block, however, conduction is delayed within the AV node

Second-degree AV block is characterized by atrial impulses (generally occurring at a regular rate) failing to conduct to the ventricles in one of the following 4 ways.

Mobitz I second-degree AV block (Wenckebach block) consists of progressive prolongation of the PR interval with the subsequent occurrence of a single nonconducted P wave that results in a pause. The pause is shorter than the sum of any 2 consecutive conducted beats (R-R interval). An episode of Mobitz I AV block usually consists of 3-5 beats, with a ratio of nonconducted to conducted beats of 4:3, 3:2, and so on (see Media file 2). The block is generally in the AV node but can occasionally occur in the His-Purkinje system and is termed infrahisian Wenckebach.

Mobitz II second-degree AV block is characterized by a constant PR interval followed by sudden failure of a P wave to be conducted to the ventricles, such that either an occasional dropped P wave or a regular conduction pattern of 2:1 (2 conducted and 1 blocked), 3:1 (3 conducted and 1 blocked), and so on is observed

High-grade AV block consists of multiple P waves in a row that should conduct, but do not. The conduction ratio can be 3:1 or more and the PR interval of conducted beats is constant. It is a distinct form of complete AV block in that the P waves that conduct to the QRS complexes occur at fixed intervals. For complete AV block, no relationship exists between the P waves and QRS complexes.
2:1 AV block could be Mobitz I or Mobitz II, but distinguishing one form from the other is nearly impossible.

Third-degree AV block is diagnosed when no supraventricular impulses are conducted to the ventricles. P waves on the rhythm strip reflect a sinus node rhythm independent from QRS electrocardiographic wave complexes. The QRS complexes represent an escape rhythm, either junctional or ventricular. The escape rhythm originating from the junctional or high septal region is characterized by narrow QRS complexes at a rate of 40-50 beats per minute, whereas escape rhythm from low ventricular sites is characterized by broad QRS complexes at a rate of 30-40 beats per minute. No relationship exists between the rhythm of P waves and the rhythm of QRS complexes. The frequency of P waves (atrial rate) is higher than the frequency of QRS complexes (ventricular rate)

AV dissociation is a rhythm identified by atrial and ventricular activation occurring from different pacemakers. AV dissociation does not indicate the presence of AV block and is distinctly different. Ventricular activation may be from either junctional pacemakers or infranodal. AV dissociation can occur in the presence of intact AV conduction, especially when rates of the pacemaker, either junctional or ventricular, exceed the atrial rate. Third-degree AV block can occur with AV dissociation. However, in AV dissociation without AV block, the ventricular rate can exceed the atrial rate and conduction can occasionally occur dependent on the timing between the P wave and the QRS complex.

AV block may also occur in patients with atrial fibrillation. Regular R-R intervals are possible in the presence of AV block (generally at slow regular rates).

Read more on atrial fibrillation at Medscape's Atrial Fibrillation Resource Center.


The atrioventricular node (AVN) is part of the conduction system of the heart that allows electrical impulses to be transmitted from the sinus node via atrial tissue (intra-atrial fascicles) to the ventricles. The AV node consists of 3 parts—atrionodal (transitional zone), nodal (compact portion), and nodal-His (penetrating His bundle). The nodal part causes the slowest conduction. The AV node is supplied by the right coronary artery (90%) or by the circumflex artery (10%) and is innervated by both sympathetic and parasympathetic fibers. The AVN receives impulses anteriorly via the intra-atrial fibers in the septum and posteriorly via the crista terminalis. Impulses arriving at the AVN are transmitted to the ventricle 1:1. As faster impulses arrive, the conduction to the ventricles slows; this is called decremental conduction.

The His-Purkinje system is composed of 2 bundles of Purkinje fibers (the left and right bundle) that conduct electrical impulses to allow rapid ventricular activation. The His-Purkinje system is yet another location where AV block may occur.

First-degree heart block and second-degree Mobitz I AV block are usually caused by a delay at the AV node level, whereas second-degree Mobitz II AV block is generally caused by blockage in the His bundle or lower in the conduction system. Third-degree AV block is caused by conduction disturbances in the AV node or the His-Purkinje system. In most cases of complete AV block, an escape rhythm originates from the ventricles, with wide QRS complexes at a low regular rate of 30-40 beats per minute. A higher anatomic location of the block results in a higher location of the escape rhythm pacemaker, a faster escape rhythm (40-60 beats per min in the region of His bundle), and a narrower QRS duration.
United States

First-degree AV block can be found in healthy adults, and its incidence increases with age. At 20 years of age, the PR interval may exceed 0.20 seconds in 0.5-2% of healthy people. At age 60 years, more than 5% of healthy individuals have PR intervals exceeding 0.20 seconds.

Type II second-degree AV block (Mobitz II) is rare in healthy individuals, whereas type I second-degree AV block (Wenckebach) is observed in 1-2% of healthy young people, especially during sleep.

Congenital third-degree AV block is rare—1 case per 20,000 births. This form of heart block, in the absence of major structural abnormalities, is associated with maternal antibodies to Ro (SS-A) and La (SS-B) and secondary to maternal lupus. It is most commonly diagnosed between 18 and 24 weeks' gestation, and may be first, second, or third degree (complete). Mortality approaches approximately 20%; most surviving children require pacemakers.

AV blocks occur more frequently in people older than 70 years, especially in those who have structural heart disease. Approximately 5% of patients with heart disease have first-degree AV block, and about 2% have second-degree AV block. The incidence of third-degree AV block peaks after age 70 years (approximately 5-10%).


The international incidence is the same as incidence in the United States.

Progressive degrees of AV block carry increasing morbidity and mortality.

AV blocks generally are not associated with major morbidity. However, the low heart rate observed in third-degree or Mobitz II AV block may lead to syncopal episodes with major injuries (eg, head trauma, hip fracture), exacerbation of congestive heart failure, or exacerbation of ischemic heart disease symptoms due to low cardiac output.

Cheng et al found that first-degree AV block (ie, PR interval >200 milliseconds) is associated with an increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality. In a prospective, community-based cohort of 7,575 individuals from the Framingham Heart Study (mean age, 47 y; 54% women) who underwent routine 12-lead electrocardiography in 1968-1974, 124 individuals had PR intervals >200 msec on the baseline examination. On follow-up of the cohort through 2007, individuals with first-degree AV block had a 2-fold adjusted risk of atrial fibrillation (hazard ratio [HR], 2.06; 95% CI, 1.36-3.12; P < .001), a 3-fold adjusted risk of pacemaker implantation (HR, 2.89; 95% CI, 1.83-4.57; P < .001), and a 1.4-fold adjusted risk of all-cause mortality (HR, 1.44; 95% CI, 1.09-1.91; P = .01). For all 3 outcomes, each 20-msec increment in PR was associated with an increase in risk.1

No racial proclivity exists in AV blocks.
A 60% female preponderance exists in congenital third-degree AV block.
For acquired third-degree AV block, a 60% male preponderance exists.

The incidence of AV block increases with age. The incidence of third-degree AV block is highest in people older than 70 years (approximately 5-10% of patients with heart disease).
First-degree AV block is generally not associated with any symptoms and is usually an incidental finding on ECG. People with newly diagnosed first-degree AV block may be healthy individuals with high vagal tone (eg, well-conditioned athletes), or they may have a history of myocardial infarction or myocarditis. First-degree AV block also may represent the first sign of a degenerative process of the AV conduction system.
Second-degree AV block usually is asymptomatic. However, in some patients, sensed irregularities of the heartbeat, presyncope, or syncope may occur. The latter usually is observed in more advanced conduction disturbances such as Mobitz II AV block. A history of medications that affect AV node function (eg, digitalis, beta-blockers, calcium channel blockers) may be contributory and should be obtained.
Third-degree AV block frequently is symptomatic with fatigue, dizziness, lightheadedness, presyncope, and syncope being reported most commonly. Syncopal episodes due to slow heart rates are called Morgagni-Adams-Stokes (MAS) episodes in recognition of the pioneer work on syncope by these researchers in the 19th century. Patients with third-degree AV block may have associated symptoms of acute myocardial infarction either causing the block or related to reduced cardiac output from bradycardia in the setting of advanced atherosclerotic coronary artery disease.
Routine physical examination does not lead to the diagnosis of first-degree AV block.
Second-degree AV block may manifest on physical examination as bradycardia (especially Mobitz type II) and/or irregularity of heart rate (especially type I, Wenckebach).
Third-degree AV block is associated with profound bradycardia unless the site of the block is located in the proximal portion of the AV node. Exacerbation of ischemic heart disease or congestive heart failure caused by AV block related bradycardia and reduced cardiac output may lead to specific clinically recognizable symptoms (eg, chest pain, dyspnea, confusion, pulmonary edema). Cannon a waves may be observed intermittently in the jugular venous pulsation when the right atrium contracts against a closed tricuspid valve due to atrioventricular dissociation.

Delay or lack of conduction through the AV node has multiple causes.

First-degree and second-degree Mobitz I (Wenckebach) AV blocks may occur in healthy, well-conditioned people as a physiologic manifestation of high vagal tone. Mobitz I (Wenckebach) block also may occur physiologically at high heart rates (especially with pacing) due to increased refractoriness of the AV node, which protects against conducting a fast rhythm to the ventricles.
AV block may be caused by acute myocardial ischemia or infarction. Inferior myocardial infarction may lead to third-degree block, usually at the AV node level, and by other mechanisms via the Bezold-Jarisch reflex. Anterior myocardial infarction usually is associated with third-degree block due to ischemia or infarction of bundle branches.
Degenerative changes in the AV node or bundle branches (eg, fibrosis, calcification, infiltration) are the most common cause of nonischemic AV block. Lenegre-Lev syndrome is an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. It is most commonly seen in the elderly and is often described as senile degeneration of the conduction system and may lead to third-degree AV block. In 1999, degenerative changes in the AV conduction system were linked to mutations of the SCN5A sodium channel gene (mutations of the same gene may lead to congenital long QT syndrome type 3 and to Brugada syndrome).2
Infiltrative myocardial diseases resulting in AV block include sarcoidosis, myxedema, hemochromatosis, and progressive calcification related to mitral or aortic valve annular calcification.
Endocarditis and other infections of the myocardium, such as Lyme disease with active infiltration of the AV conduction system, may lead to varying degrees of AV block.
Systemic diseases, such as ankylosing spondylitis and Reiter syndrome, may affect the AV nodal conducting tissue.
Surgical (eg, aortic valve replacement, congenital defect repair) or other therapeutic procedures (eg, AV ablation in patients with supraventricular arrhythmias, alcohol septal ablation in patients with obstructive hypertrophic cardiomyopathy) may cause AV block. Patients with corrected transposition of the great vessels have anterior displacement of the AV node and are prone to develop complete heart block during right heart catheterization or surgical manipulation.
A variety of drugs may affect AV conduction. The most common drugs include digitalis glycosides, beta-blockers, calcium channel blockers, and other antiarrhythmic agents.


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