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

Third-Degree Atrioventricular Block


In the heart, normal impulse initiation begins in the sinoatrial node. The excitation wave then travels through the atrium. During this time, surface ECG recordings show the P wave. Following intra-atrial conduction to the area of the lower intra-atrial septum, this wavefront reaches the inputs to the atrioventricular (AV) node. The AV node then conducts the impulse to the His bundle. The His bundle divides into the right and left bundles, which distribute this impulse to the ventricles. During atrial, AV node and His-Purkinje conduction, the PR segment is observed. Heart block occurs when slowing or complete block of this conduction occurs. Traditionally, heart block can be divided into first-, second-, and third-degree block.

First-degree AV block is a condition in which a one-to-one relationship exists between P waves and QRS complexes, but the PR interval is longer than 200 milliseconds (ms). Thus, first-degree AV block represents delay or slowing of conduction. Occasionally, first-degree AV block may be associated with other conduction disturbances, including bundle-branch block and fascicular blocks (bifascicular or trifascicular block).

First-degree block is generally not an indication for permanent pacing, but may become an indication for permanent pacing when patients develop symptoms attributable to the AV delay typically, when the PR interval is markedly prolonged (>300 ms) and the patient has documented left ventricular systolic dysfunction and symptoms of heart failure. In patients with muscular dystrophies and any degree of AV block, implantation of a pacemaker should be promptly considered. For more information, see eMedicine's article First-Degree Atrioventricular Block.

Second-degree AV block exists when more P waves than QRS complexes are seen on the ECG, but a relationship between P waves and QRS complexes still exists. In other words, not all P waves are followed by QRS complexes (conducted). Traditionally, this type of AV block is divided into subcategories as type I and type II.

Type I second-degree AV block is also known as Wenckebach block. In type I block, the PR interval is changing (prolonging) with each P wave to the point when the P wave is no longer conducted (followed by QRS complexes). In a typical Wenckebach block, the prolongation of PR interval from beat-to-beat is greatest in the first interval and progressively less with subsequent intervals. This is reflected in shortening of the R-R interval and the overall PR interval increases. Also, the R-R interval enveloping the pause is less than twice the duration of the first R-R interval following the pause.

Upon examination of the ECG tracing, type I second-degree block results in the characteristic appearance of grouping beats, and conversely, the presence of grouped beating should prompt a careful evaluation for Wenckebach conduction. Not all Wenckebach conduction is pathologic. For example, this type of AV block is often seen at rest in athletes or with sleep most likely resulting from increased vagal tone. It resolves spontaneously after physical deconditioning, and is less likely with advancing age.

Type II second-degree AV block is also known as Mobitz II block. In type II block, the PR interval is constant, but occasional P waves are not followed by the QRS complexes (nonconducted). Occasionally, the first PR interval following nonconducted P waves may be shorter by £ 20 ms. For more information, see eMedicine's article Second-Degree Atrioventricular Block.

To differentiate between type I block and type II block, at least 3 consecutive P waves must be present in the tracing. If only every other P wave is conducted (2:1), this block cannot be classified into either of these categories and is best described as 2:1 conduction, unless the mechanism can be inferred from surrounding patterns of atrial-to-ventricular conduction. Generally, Wenckebach block is related to a disease process within the proximal portion of the AV node, tends to respond to atropine, and may resolve. On the other hand, Mobitz II block usually results from the infrahisian block (process involving the His-Purkinje system), does not respond to atropine, and has more ominous clinical consequences.

Although the morphological criteria are somewhat helpful in ascertaining the location of the block in the conduction system, only an invasive electrophysiologic study is able to precisely determine the location of the block. All blocks resulting from prolongation of the HV interval on intracardiac tracing carry a poor prognosis and are an indication for permanent pacing.

An AV block resembling second-degree AV block has been reported with sudden surges of vagal tone associated with cough, hiccups, swallowing, carbonated beverages, pain, micturition, or airway manipulation in otherwise healthy subjects. The distinguishing feature is simultaneous slowing of the sinus rate. This condition is paroxysmal and benign but must be carefully differentiated from a true second-degree AV block because the prognosis is very different.

Third-degree AV block (also called complete heart block) exists when more P waves than the QRS complexes exist and no relationship exists between them (no conduction). The escape rhythm may arise within the AV node (narrow complex) or lower in the conduction system (wide complex). The ventricular rate, and thus the pulse, varies from 30-40 bpm. Characteristically in this block, the atrial rate is rapid, presumably in response to the hemodynamic consequences of block. In most cases of persistent third-degree AV block, permanent pacing is required.

Atrioventricular dissociation is present when atrial and ventricular activation are independent of each other. It can result from complete heart block or physiological refractoriness of conduction tissue. It can also occur in a situation when the atrial/sinus rate is slower than the ventricular rate, namely with accelerated junctional tachycardia and ventricular tachycardia. Occasionally, the atrial and ventricular rates are so close that the tracing would suggest normal AV conduction; only careful examination of the long rhythm strip may reveal a variation in PR interval. This form of AV dissociation is called isorhythmic AV dissociation. Maneuvers or medications resulting in acceleration of atrial/sinus rate will result in restoration of normal conduction.


Heart block results from various pathological states causing infiltration, fibrosis, or loss of connection in portions of the healthy conduction system. Acute myocardial infarction (MI) can cause complete AV block. Common causes of heart block are listed in Causes.
United States

The prevalence of third-degree AV block is 0.02%.

The prevalence of third-degree AV block is 0.04%.1

Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. The cause of death may often be tachyarrhythmias precipitated by the secondary changes in ventricular repolarization (QT prolongation) secondary to the abrupt changes in rate.

The incidence of AV conduction abnormalities increases with advancing age, resembling the age-related incidence of ischemic heart disease. An early peak in incidence occurs in infancy and early childhood due to congenital complete AV block, which is sometimes not recognized until childhood or even adolescence.
Symptoms attributable to complete AV block include syncope, near-syncope, lightheadedness, fatigue, dyspnea, and angina.
Some patients are asymptomatic.
Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death.
History of cardiac interventions should be carefully investigated since aortic valve surgery, septal alcohol ablation, proximal anterior descending artery stenting (complicated by compromised flow in the first septal perforator branch), or ablation of slow or fast pathway of the AV node all may result in the complete heart block.
Initial triage of patients with complete heart block consists of determining symptoms, assessing vitals signs, and looking for evidence of compromised peripheral perfusion.
Careful examination of the neck veins can often show evidence of cannon a waves. A variable intensity S1 may be heard. In addition, the pulse rate may be slow.
If the slow rate or loss of atrial contraction prior to ventricular contraction has caused heart failure, then venous pressures will be elevated, including the jugular venous pressure.
Any new murmurs or gallops should be noted because strong associations exist between cardiomyopathies, mitral calcification, aortic calcification, or endocarditis and complete AV block.
If heart failure is present as evidenced by rales, an S3 gallop, peripheral edema, or hepatomegaly, then a more compelling need for immediate pacing exists.
Because endocarditis, rheumatic fever, and Lyme disease cause heart block, pay attention to any signs of infection or skin rashes during the general examination. This is particularly true in endemic areas for Lyme disease.
Neurologic examination may provide clues to the etiology of AV block because neuromuscular disease, especially myotonic dystrophy and Duchenne muscular dystrophy, can cause AV block.
A phenomenon known as ventriculophasic sinus arrhythmia (P-P intervals) refers to the P-P interval enveloping a QRS complex being slightly shorter than the other P-P intervals.
Lev disease (calcification of the conduction system and valves) has been found to have an inherited component.
The common causes of AV heart block are as follows:
Drugs - Calcium channel blockers, beta-blockers, quinidine, procainamide, lithium, digoxin, tricyclic antidepressant
Degenerative diseases – Lenègre disease (sclerodegenerative process involving only the conduction system) and Lev disease, noncompaction cardiomyopathy, nail-patella syndrome, mitochondrial myopathy2
Infectious causes - Lyme borreliosis (particularly in endemic areas), rheumatic fever, myocarditis, Chagas disease (Central America and South America), Aspergillus myocarditis, varicella zoster virus3 , valve ring abscess
Rheumatic diseases - Ankylosing spondylitis, Reiter syndrome, relapsing polychondritis, rheumatoid arthritis, scleroderma
Infiltrative processes - Amyloidosis, sarcoidosis, tumors, Hodgkin disease, multiple myeloma
Neuromuscular disorders - Becker muscular dystrophy, myotonic muscular dystrophy
Ischemic or infarctive causes - AV nodal block associated with interior wall myocardial infarction, His-Purkinje block associated with anterior wall myocardial infarction
Metabolic causes - Hypoxia, hyperkalemia, hypothyroidism
Toxins – "Mad" honey
Phase IV block (also known as bradycardia-related block)
Iatrogenic – Complicating aortic valve surgery, septal alcohol ablation, percutaneous coronary intervention to the left anterior descending artery, or ablation of slow or fast pathway of the AV node. Placement of catheters mechanically interfering with one fascicle when conduction is already impaired in the remaining conduction system (eg, bumping the right bundle with a PA catheter in a patient with existing left bundle branch block) almost always resolves spontaneously.
Special Circumstances

Heart block during myocardial infarction4,5

Contemporary AV block rarely complicates myocardial infarction. With early revascularization strategy, the incidence of AV block decreased from 5.3 to 3.7%. Occlusion of each of the coronary arteries can result in development of conduction disease despite redundant vascular supply to the AV node from all coronary arteries. Most commonly, the occlusion of the right coronary artery (RCA) is accompanied by AV block. In particular, the proximal RCA occlusion has high incidence of AV block (24%) since not only the AV nodal artery is involved but also right superior descending artery, which originates from the very proximal part of the RCA.

In most cases, AV block resolves promptly after revascularization but sometimes the course is prolonged. Overall the prognosis is favorable. AV block in a setting of occlusion of the left anterior descending artery (particularly proximal to the first septal perforator) has more ominous prognosis and usually requires pacemaker implantation. Second-degree AV block associated with bundle branch block and in particular with alternating bundle branch block is an indication for permanent pacing.

Heart block following cardiac surgery6

Heart block following cardiac surgery is seen in 1-5.7% of patients. Major risks factors identified for the need for permanent pacing are aortic valve surgery, preexisting conduction disease (either right or left bundle branch block), bicuspid aortic valve, annular calcification, and female gender. The time course for recovery varies widely with a significant portion of patients recovering during the 48 hours following surgery. Available evidence suggests that if no recovery in AV conduction is seen by the fourth or fifth day following surgery, a pacemaker should be implanted.


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