Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:

"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".

(HR. Muslim, Ahmad dan Hakim).

Sabtu, 28 November 2009

First-Degree Atrioventricular Block


The PR interval of the surface electrocardiogram (ECG) is measured from the onset of atrial depolarization (P wave) to the beginning of ventricular depolarization (QRS complex). In the adult population, normal PR interval ranges from 0.12-0.20 seconds at normal heart rates. First-degree atrioventricular (AV) block is defined as a PR interval exceeding 0.20 seconds (see Image 1).

The PR interval represents the time needed for an electrical impulse from the sinoatrial (SA) node to conduct through the atria, AV node, bundle of His, bundle branches, and Purkinje fibers. Thus, as shown in electrophysiological studies, PR interval prolongation (ie, first-degree AV block) may be due to conduction delay within the right atrium, the AV node, the His-Purkinje system, or a combination of these. AV nodal dysfunction accounts for the majority of cases. First-degree AV block caused by conduction delay in the His-Purkinje system often is associated with bundle-branch block.

Structure and function of the AV node and His-Purkinje system

The AV node is the only normal electrical connection between atria and ventricles. It is an oval or elliptical structure, measuring 7-8 mm in its longest (anteroposterior) axis, 3 mm in its vertical axis, and 1 mm transversely. The AV node is located beneath the right atrial endocardium, dorsal to the septal leaflet of the tricuspid valve, and about 1 cm superior to the orifice of the coronary sinus. The bundle of His originates from the anteroinferior pole of the AV node and travels through the central fibrous body to reach the dorsal edge of the membranous septum. It then divides into right and left bundle branches. The right bundle continues first intramyocardially, then subendocardially, toward the right ventricular apex. The left bundle continues distally along the membranous septum and then divides into anterior and posterior fascicles.

Blood supply to the AV node is provided by the AV node artery, a branch of the right coronary artery in 90% of individuals and of the left circumflex coronary artery in the remaining 10%. The His bundle has a dual blood supply from branches of anterior and posterior descending coronary arteries. Likewise, the bundle branches are supplied by both left and right coronary arteries.

The AV node has a rich autonomic innervation and is supplied by both sympathetic and parasympathetic nerve fibers. This autonomic innervation has a major role in the time required for the impulse to pass through the AV node.
United States

First-degree AV block is rare in young healthy adults. It is reported in 0.65-1.1% of young adults older than 20 years. Higher prevalence is reported in trained athletes (8.7%). The prevalence also increases with age; first-degree AV block is reported in 5% of men older than 60 years. The overall prevalence is 1.13 cases per 1000 lives.

No mortality or morbidity is related to isolated first-degree AV block. However, in the setting of acute inferior myocardial infarction (MI), first-degree AV block may herald higher degrees of AV block. Markedly prolonged PR interval in patients with left ventricular systolic dysfunction may impair ventricular filling and thus reduce cardiac output.

Incidence of first-degree AV block increases with age.
Patients with first-degree AV block are generally asymptomatic at rest. Markedly prolonged PR interval may reduce exercise tolerance in some patients with left ventricular systolic dysfunction. Syncope may result from transient high-degree AV block, especially in those with infranodal block and wide QRS complex.
The intensity of the first heart sound (S1) is decreased in patients with first-degree AV block.
Patients with first-degree AV block may have a short, soft, blowing, diastolic murmur heard at the cardiac apex. This diastolic murmur is not caused by diastolic mitral regurgitation, because it reaches its peak before the onset of regurgitation. The diastolic murmur is thought to be related to antegrade flow through closing mitral valve leaflets that are stiffer than normal. Administration of atropine may reduce the duration of this murmur by shortening the PR interval.
Athletic training: Well-trained athletes can demonstrate first-degree (and occasionally higher degree) AV block owing to an increase in vagal tone.
Coronary artery disease
Acute MI: First-degree AV block occurs in fewer than 15% of patients with acute MI admitted to coronary care units.
His bundle electrocardiographic studies have shown that, in most of these patients, AV node is the site of conduction block.
AV block is more common in the setting of inferior MI.
In the Thrombolysis in Myocardial Infarction (TIMI) II study, high-degree (second- or third-degree) AV block occurred in 6.3% of patients at the time of presentation and in 5.7% in the first 24 hours after thrombolytic therapy. Patients with AV block at the time of presentation had a higher in-hospital mortality rate than patients without AV block; both groups, however, had similar mortality rates during the following year. Patients who developed AV block after thrombolytic therapy had higher mortality rates both in-hospital and in the following year than patients without AV block. Right coronary artery was more often the site of infarction in patients with heart block than in those without heart block. Patients with AV block are believed to have larger infarct size. However, the prevalence of multivessel disease is not higher in patients with AV block.
Angina pectoris
Prinzmetal angina
Idiopathic degenerative diseases of the conduction system
Lev disease: This is due to progressive degenerative fibrosis and calcification of the neighboring cardiac structures, "sclerosis of the left side of cardiac skeleton," including mitral annulus, central fibrous body, membranous septum, base of the aorta, and crest of the ventricular septum. Lev disease has an onset about the fourth decade and is believed to be secondary to wear and tear on these structures caused by the pull of the left ventricular musculature. It affects the proximal bundle branches and is manifested by bradycardia and varying degrees of AV block.
Lenègre disease: This is an idiopathic, fibrotic degenerative disease restricted to the His-Purkinje system. It is caused by fibrocalcareous changes in mitral annulus, membranous septum, aortic valve, and crest of the ventricular septum. These degenerative and sclerotic changes are not attributed to inflammatory or ischemic involvement of adjacent myocardium. Lenègre disease involves the middle and distal portions of both bundle branches and affects a younger population than Lev disease.
Drugs: Calcium channel blockers, beta-blockers, digoxin, and amiodarone all may cause first-degree AV block. Although first-degree AV block is not an absolute contraindication for administration of these drugs, extreme caution should be exercised in the use of these medications in patients with first-degree AV block, as they carry the risk of developing higher degree AV block on exposure to these drugs.
Mitral or aortic valve annulus calcification: The main penetrating bundle of His is located near the base of the anterior leaflet of the mitral valve and the noncoronary cusp of the aortic valve. Heavy calcium deposits in patients with aortic or mitral annular calcification is associated with increased risk of AV block.
Infectious disease: Infective endocarditis, diphtheria, rheumatic fever, Chagas disease, Lyme disease, and tuberculosis all may be associated with first-degree AV block.
Extension of the infection to the adjacent myocardium in native or prosthetic valve infective endocarditis (ie, ring abscess) can cause AV block.
Acute myocarditis caused by diphtheria, rheumatic fever, or Chagas disease can result in AV block.
Collagen vascular disease: Rheumatoid arthritis, systemic lupus erythematous, and scleroderma all may be associated with first-degree AV block.
Rheumatoid nodules may occur in the central fibrous body and result in AV block.
Fibrosis of the AV node or the adjacent myocardium in patients with systemic lupus erythematous or scleroderma can cause first-degree AV block.
Doppler echocardiographic signs of first-degree AV block have been demonstrated in about 33% of fetuses of pregnant women who are anti-SSA/Ro 52-kd positive. In most of these fetuses, the blocks resolved spontaneously. However, progression to a more severe degree of block was seen in 2 of the fetuses. Serial Doppler echocardiographic measurement of AV-time intervals can be used for surveillance of these high-risk pregnancies.
Infiltrative diseases such as amyloidosis or sarcoidosis
Myotonic dystrophy
First-degree AV block occurs in about 10% of patients who undergo adenosine stress testing and is usually hemodynamically insignificant. Patients with baseline first-degree AV block more often develop higher degrees of AV block during adenosine stress testing. These episodes, however, are generally well tolerated and do not require specific treatment or discontinuation of the adenosine infusion.
Marked first-degree AV block may occur following catheter ablation of the fast AV nodal pathway with resultant conduction of the impulse via the slow pathway. This may result in symptoms similar to the pacemaker syndrome.
First-degree AV block (reversible or permanent) has been reported in about 2% of patients who undergo closure of atrial septal defect using the Amplatzer septal occluder.
First-degree AV block can occur following cardiac surgery. Transient first-degree AV block may result from right heart catheterization.


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