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).

Kamis, 24 Desember 2009

Atrioventricular Nodal Reentry Tachycardia (AVNRT)


Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, more specific nomenclature based on the mechanism of reentry helps in better classifying these arrhythmias and thus helps in choosing appropriate therapies.

The substrate for AVNRT may be functional rather than anatomic. These arrhythmias occur in young, healthy patients and in those with chronic heart disease.

In patients with atrioventricular (AV) nodal reentry, the AV node is functionally divided into 2 longitudinal pathways that form the reentrant circuit. In the majority of patients, during AVNRT, antegrade conduction occurs to the ventricle over the slow (alpha) pathway and retrograde conduction occurs over the fast (beta) pathway (see Media file 1). In most patients with this arrhythmia, the tachycardia is initiated when a fortuitously timed atrial premature complex is blocked in the fast pathway (longer refractory period) and conducts in the slow pathway (shorter refractory period) (see Media file 1). While the impulse conducts to the ventricle in the slow pathway (antegrade conduction), the fast pathway recovers so that the impulse can conduct retrograde up the fast pathway to the atrium and the atrial end of the slow pathway (retrograde conduction).

This sets up the reentrant circuit. In approximately one third of patients, AVNRT is induced by premature ventricular stimulation. In addition to the typical mechanism of AV nodal reentry described above, atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in the fast pathway and retrograde conduction in the slow pathway. Less commonly, the reentrant circuit can be over 2 slow pathways, the so-called slow-slow AV node reentry.

United States

AVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT. The prevalence of SVT in the general population is likely several cases per thousand persons.

Frequency is similar to that in the United States.

AVNRT is usually well tolerated; it often occurs in patients with no structural heart disease. In patients with coronary artery disease, AVNRT may cause angina or myocardial infarction. Prognosis for patients without heart disease is usually good.

More women than men have AVNRT.

AVNRT may occur in persons of any age. It is common in young adults.
AVNRT is characterized by an abrupt onset and termination of episodes.
Episodes may last from seconds to minutes to days.
In the absence of structural heart disease, it is usually well tolerated.
Common symptoms include palpitations, nervousness, anxiety, lightheadedness, neck and chest discomfort, and dyspnea. Polyuria can occur after termination of the episode (due to the release of atrial natriuretic factor).
AVNRT may cause or worsen heart failure in patients with poor left ventricular function.
It may cause angina or myocardial infarction in patients with coronary artery disease.
Syncope may occur in patients with a rapid ventricular rate or prolonged tachycardia due to poor ventricular filling, decreased cardiac output, hypotension, and reduced cerebral circulation. Syncope may also occur because of transient asystole when the tachycardia terminates, owing to tachycardia-induced depression of the sinus node.
The heart rate is usually rapid, ranging from 150-250 beats per minute (bpm). It is usually 180-200 bpm in adults and, in children, may exceed 250 bpm.
Hypotension may occur initially or with rapid ventricular rates and prolonged episodes.
Sometimes, initial hypotension evokes a sympathetic response that increases blood pressure and may terminate the tachycardia by an increase in vagal tone.
Signs of left heart failure may develop or worsen in patients with poor left ventricular function.

The substrate for AVNRT is the presence of dual AV nodal pathways. Age of onset varies from childhood to the teenage years or adulthood. Some patients do not present until their seventh or eighth decade or older. In contrast to a bypass tract, dual AV nodal physiology is often an acquired abnormality.


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