Av node reentry tachycardia I47.1

AV node reentry tachycardia (AVNRT) is a form of regular tachycardia that occurs predominantly in healthy individuals.

Note: The reentry mechanism is one of the three main mechanisms in tachycardic arrhythmias. It produces a circular excitation in the myocardium. As in a "roundabout", the electrical excitation in the heart rotates in AV node reentry tachycardia.

Previously, AVNRT and atrioventricular reentry tachycardia (AVRT [see also paroxysmal supraventricular tachycardia]) were grouped together under the generic term "paroxysmal supraventricular tachycardia (PSVT)" (Herold 2020).

The AVNRT is one of the most common forms of PSVT. The prevalence is between 0.1% - 0.2% (Pinger 2019). Mostly younger patients between the ages of 10-12 years (Herold 2020) or 20-50 years (Kasper 2015) are affected.

The disease occurs more frequently in the female sex.

AVNRT is a primarily electrical heart disease. Tachycardia occurs independently of stress or rest situations (Stierle 2017).

There is a dissociation of the AV junction line into two functional pathways called the "fast pathway" and the "slow pathway". This leads to a re-entry of excitation, the so-called "reentry" (Kasper 2015).

The dissociation is not only limited to the region of the AV node. They are also located in the region of the Koch's triangle (the area between the plane of the tricuspid valve, the ostium of the coronary vein sinus and the Todaro tendon).

The "fast pathway" represents a path with fast conduction and slow refractory time, while the "slow pathway" represents a slow conduction with fast refractory time.

These dual functional pathways result in an approximately simultaneous excitation of the atrium and ventricles. This leads to an atrial systole against the closed tricuspid valve (Kasper 2015). The diastolic filling is shortened, which in turn leads to a significant reduction in cardiac output (Paul 2018).

Existing during tachycardia:

• There is normally one antegrade conduction on the slow pathway and one retrograde conduction on the fast pathway, also called slow- fast AVNRT. This form occurs in up to 90% of cases (Hafeez 2020).
• The atypical form, also known as "fast slow AVNRT", has a reverse excitation sequence. The atypical form occurs in 5 % - 10 % of cases (Hafeez 2020)
• AVNRT over two "slow pathway", also known as "slow- slow- AVNRT", occurs in approx. 1 % - 5 % (Hafeez 2020, Pinger 2019)

Typical is the abrupt onset of tachycardia (important to differentiate other forms of tachycardia), which can last minutes to hours and is associated with a frequency between 120 - 250 beats / min (Sattler 2007).

The tachycardia usually ends just as suddenly. In some cases, however, the return to sinus rhythm is gradual. In otherwise heart-healthy patients, there are no other symptoms.

In patients with pre-existing heart failure or coronary artery disease, the critical reduction in cardiac output may cause the following symptoms:

• Hypotension
• Dizziness
• Syncope
• angina pectoris
• rarely cardiogenic shock
• urinary flooding during or after tachycardia triggered by atrial natriuretic peptide ANP)
• Plugging of the jugular veins with visible rapid pulsation of the jugular veins, also known as "frog sign." Occurs with simultaneous contraction of the atrium and ventricle
• Pulmonary edema (Kasper 2015)

ECG: The resting ECG shows during the seizure;

in the typical form the following changes:

• at the beginning of the symptoms often supraventricular extrasystoles (SVES)
• regular tachycardia with a narrow QRS complex
• frequency between 120 - 250 beats / min, mostly between 160 - 200 / min ( Stierle 2017)
• the P wave is superimposed by the QRS complex

in the atypical form:

• negative P- waves (Herold 2020)
• short PQ time (Stierle 2017)

in the "slow pathway":

• late onset P- waves after the QRS complex (appearance like atrial tachycardia) (Hafeez 2020)

• atrioventricular reentry tachycardia (here a hidden accessory pathway is found)
• atrial or sinus tachycardia (here there is a constant 1: 1 transition and a relatively long PQ interval which covers the P wave from the previous QRS complex)
• Ventricular tachycardia (with broad QRS chamber complex, antidromic atrioventricular reentry tachycardia) (Herold 2020)
• junctional ectopic tachycardia
• Atrial tachycardia
• Atrial flutter
• Sinus tachycardia (Hafeez 2020)

Therapeutic measures are differentiated between symptomatic therapy, electrotherapy, and interval treatment (Herold 2020). Among patients undergoing catheter ablation, 60% have AVNRT (Kasper 2015).

1. symptomatic therapy:

Symptomatic treatment should always be performed under ongoing ECG distinction.

• In patients with stable circulation, vagus stimulation is initially performed by e.g.:
• Valsalva pressing (after deep inhalation the patient should press for as long as possible).
• drinking a large, preferably cold and acidic drink in rapid succession
• dipping the face in cold water
• Ice tie
• Drug treatment:
  • Adenosine is 1st choice agent.
    • Mode of action: short-term blocking of the AV conduction in the AV node.
    • Contraindication: atrial tachycardia, atrial fibrillation with WPW syndrome (strongly widened QRS complex), bronchial asthma, atrial fibrillation, atrial flutter, QT prolongation, sick sinus syndrome, AV block > 1st degree
    • Side effect: short term asystole possible, dyspnea, bronchospasm, flush, drop in blood pressure, feeling of pressure in the chest.
    • Dosage: 6 mg rapidly applied i. v.; in case of no response after 3 min. Injection of 12 mg
  • Verapamil 2nd choice agent
    • Mode of action: negative ionotropic effect
    • Contraindication: atrial tachycardia, ventricular tachycardia, atrial fibrillation with WPW syndrome (widened QRS complex), hypotension, sick sinus syndrome with history of bradycardia, manifest heart failure, pretreatment with beta blockers.
    • Side effect: Asystole, drop in blood pressure etc.
    • Dosage: 5 mg slowly i. v. over 10 min, in case of non-response after 15 - 30 min re-injection of 5 mg (Herold 2020).
  • Ajmaline
    • Indication: Ajmaline can be given in both AVNRT and WPW- syndrome. If it is not possible to differentiate the clinical pictures with the help of the ECG, ajmaline is the drug of choice.
    • Mode of action: causes prolongation of depolarization in phase 0 and 4 and prolongs the refractory period. Negative ionotropic effect and blood pressure lowering are mild.
    • Side effect: hypotension, nausea, vomiting, flush, headache etc.
    • Dosage: i. v. injection of 5 mg - 10 mg / min, in pre-damaged heart 2.5 mg - 3 mg / min; maximum dose 50 mg over 5 min. Repeat dose is possible after 30 min (Bäumel 2009).

2. electrotherapy

If the above measures are not successful, electrotherapy is indicated.

A distinction is made between overdrive pacing and electrocardioversion:

• Overdrive pacing: Overdrive pacing involves overstimulation to terminate the circular excitation. It should be performed while the patient is under continuous ECG recording, ready for resuscitation, and under appropriate analgesia (e.g., 2 mg - 5 mg morphine i.v.) (Herold 2020 / Köhler 2018).
• Electrocardioversion:
  • The indication for performing electrocardioversion is:
    • Circulatory unstable patients in whom cardiogenic shock is imminent
    • unconscious patients with hypotension
    • patients in whom drug treatment is failing
  • Contraindication:
    • digitalis intoxication
    • Recurrence of paroxysmal supraventricular tachycardia (PSVT) with previous cardioversion.
  • Treatment is given in resuscitation readiness under short anesthesia (e.g., with propofol i. v.) with e.g., initial 100 J., the dose can be repeated with higher energy doses if unsuccessful. (Herold 2020)

3. interval treatment

If further recurrences occur despite the above measures, slow pathway ablation is recommended, in which the slow pathway is ablated. Ablation of the fast pathway is no longer recommended, since the success rate is equally high, but the risk of complete AV blockis significantly increased (Kuck 2007).

• The success rate is > 95 %,
• the recurrence rate is 5 % - 10 %,
• the risk of 3rd degree AV block< 0.5% (Herold 2020).

The prognosis is generally good once the diagnosis has been confirmed (Hafeez 2020).

Associated cardiac malformations: Accompanying structural heart diseases are usually not present (Kasper 2015).

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