Жүрек соғудың жылдамдығының бұзылуы: AV торабының қайталама тахикардиясы

AV nodal reentrant tachycardia (AVNRT) is a type of abnormal fast heart rhythm. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medications, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed. AVNRT occurs when a reentrant circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff Parkinson White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to muscular heart tissue of the heart's ventricles.

The main symptom of AVNRT is the sudden development of rapid regular palpitations. These palpitations may be associated with a fluttering sensation in the neck, caused by near simultaneous contraction of the atria and ventricles against a closed tricuspid valve leading to the pressure or atrial contraction being transmitted backwards into the venous system. The rapid heart rate may lead to feelings of anxiety, and may therefore be mistaken for panic attacks. Someone with underlying coronary artery disease (narrowing of the arteries of the heart by atherosclerosis) who has a very rapid heart rate may experience chest pain similar to angina; this pain is band or pressure like around the chest and often radiates to the left arm and angle of the left jaw. This can take several forms. "Typical", "common", or "slow fast" AVNRT uses the slow AV nodal pathway to conduct towards the ventricle (the anterograde limb of the circuit) and the fast AV nodal pathway to conduct to the atria (the retrograde limb). The re entrant circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb, referred to as "atypical", "uncommon", or "fast slow" AVNRT. Atypical AVNRT may also use the slow AV nodal pathway as the anterograde limb and left atrial fibres that approach the AV node from the left side of the inter atrial septum as the retrograde limb, and is sometimes referred to as "slow slow" AVNRT.

In typical AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway ("slow fast" AVNRT). Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) occurs very soon after stimulation of the ventricles (which causes the QRS complex). As a result, the time from the QRS complex to the P wave (the RP interval) is short, less than 50% of the time between consecutive QRS complexes. The RP interval is often so short that the inverted P waves may not be seen on the surface electrocardiogram (ECG) as they are buried within or immediately after the QRS complexes, appearing as a "pseudo R prime" wave in lead V1 or a "pseudo S" wave in the inferior leads.

Treatments for AVNRT aim to terminate episodes of tachycardia, and to prevent further episodes from occurring in the future. These treatments include physical manoeuvres, medication, and invasive procedures such as ablation.

An episode of supraventricular tachycardia due to AVNRT can be terminated by any action that transiently blocks the AV node. Some of those with AVNRT may be able to stop their attack by using physical manoeuvres that increase the activity of the vagus nerve on the heart, specifically on the atrioventricular node. These manoeuvres include carotid sinus massage (pressure on the carotid sinus in the neck) and the Valsalva manoeuvre (increasing the pressure in the chest by attempting to exhale against a closed airway by bearing down or holding one's breath). Medications that slow or briefly halt electrical conduction through the AV node can terminate AVNRT, including adenosine, beta blockers, or non dihydropyridine calcium channel blockers (such as verapamil or diltiazem). The risks and benefits are weighed up before this is performed. Catheter ablation of the slow pathway, if successfully carried out, can potentially cure AVNRT with success rates of >95%, balanced against a small risk of complications including damaging the AV node and subsequently requiring a pacemaker.