Overview
Atrioventricular nodal refractory tachycardia (AVNRT), also known as atrioventricular junctional refractory tachycardia (AVJRT), can be divided into two types of AVNRT: slow-fast type and fast-slow type, which are more common in children at the age of 5-6 years old, and in adults before the age of 40 years old, and in young and middle-aged people. Patients may show palpitations, irritability, nervousness, fatigue, angina pectoris, cardiac insufficiency, syncope and even shock.
Causes
Atrioventricular nodal refractory tachycardia (AVNRT) can be seen at any age, from infants of a few months to adults and the elderly, and is more common in children at the age of 5-6 years old, and in adults before the age of 40 years old, and in young and middle-aged people, with a similar incidence in men and women. It is most common in patients without organic heart disease, and can also be caused by drugs or lesions.
Symptoms
Patients may show palpitations, irritability, nervousness, fatigue, angina pectoris, cardiac insufficiency, syncope and even shock. Syncope is caused by a rapid ventricular rate that reduces cardiac output and cerebral circulating blood volume; or in combination with sick sinus node syndrome, when tachycardia is terminated, the sinus node function is suppressed due to overdrive inhibition, and a long interval occurs before sinus rhythm is restored.
AVNRT episodes result in a significant reduction in left ventricular end-diastolic volume and stroke volume per beat due to too fast a frequency and too short a diastolic period. If the patient has normal cardiac function, cardiac output and ejection fraction can be maintained in the normal range. If there is organic heart disease or if the tachycardia is too rapid in frequency and too long in duration, the ejection fraction can be markedly reduced, leading to significant hemodynamic disturbances.
A sudden onset of narrow QRS tachycardia should be considered as a possibility, especially if it occurs in middle-aged, obese women.
Examination
1. Electrocardiography
AVNRT has two different clinical ECG types:
(1) ECG characteristics of slow-fast type AVNRT Slow-fast type AVNRT, also known as typical AVNRT, is most common in adults, accounting for about 90% of AVNRT, which is anterograde in the slow pathway and retrograde in the fast pathway. ①Sudden onset and abrupt termination. P wave is retrograde: during tachycardia, atria and ventricles are excited almost simultaneously. Most of the patients can not see the P wave because it is buried in the QRS wave group. About 30% of the patients have P wave immediately after the QRS wave (R after P), and there is a small r wave in the terminal part of the QRS wave in lead 1 of the R-P interval/P-R interval, which is actually a part of the P wave. ③ Normal QRS waveform: the frequency is 140 to 220 beats/minute, and most of the episodes are 150 to 160 beats/minute, mostly below 200 beats/minute, with regular rhythm. ④ The atrial pre-systole that induces the onset of the tachycardia episode is transmitted down through the slow pathway, so the prolongation of the P-R interval of the first beat of AVNRT shows a double pathway feature. ⑤ Timely electrical stimulation of atrial pre-systole can induce and terminate AVNRT episodes, as can sinus pre-systole, sympathetic zone pre-systole, and ventricular pre-systole (in a few cases). (vi) Carotid sinus compression stimulating vagal nerve method: can terminate the attack in some patients; or only slow down the tachycardia frequency. (7) Accompanied by atrioventricular or ventriculo-atrial block which makes the atrial-ventricular frequency incongruent is rare.
(2) Electrocardiographic features of fast-slow AVNRT Fast-slow AVNRT, also known as atypical AVNRT or rare AVNRT, is characterized by fast-path anterograde and slow-path retrograde, i.e., the slow pathway should not be used for a longer period than the fast pathway. The order of atrial retrograde excitation is different from that of typical AVNRT, and the earliest atrial excitation is often at the coronary venous sinus orifice. It is rare. Episodes are of longer duration and are more common in children. Mostly pathologic or caused by drugs. ① P-wave: because of the slow retrograde transmission of excitation along the slow pathway, the retrograde P-wave follows the T-wave of the previous cardiac cycle and precedes the next QRS wave. It is easily recognized on the surface ECG. p-wave is inverted or biphasic in leads II, III, and aVF, and upright in leads aVR and V1. The P wave is inverted or biphasic in leads II, III, and aVF, and is upright in leads aVR and V1. ② The P-R interval is short and fixed: the R-P interval is long P-R1/2R-R. ③ The QRS wave is mostly supraventricular: in a few cases, with bundle branch block, the QRS wave may also be wide and abnormal. ③ The R-R interval is regular, and the heart rhythm is absolutely regular. The R-R interval is regular, and the heart rate is absolutely regular. The heart rate is 100 to 150 beats per minute. ④There is no P-R interval prolongation of the preterm contraction that induces fast-slow AVNRT. ⑤ It can be induced by atrial pre-systole or by a mildly accelerated heart rate. Fast-slow AVNRT can be seen to begin secondary to sinus tachycardia, often with a gradual increase in sinus heart rate, followed by AVNRT. How fast can AVNRT occur? AVNRT can end with either a P or R wave. (6) Tachycardia is not easily terminated naturally: drugs are poorly effective, esophageal left atrial pacing is more difficult to induce successfully, and programmed electrical stimulation is less likely to show dual-pathway (dual-channel) features.
(3) Special types of AV nodal refractory tachycardia ① AV nodal refractory tachycardia with lower common pathway 2:1 conduction block: It has been found that AV nodal refractory tachycardia can continue to exist even when there is a 2:1 atrioventricular block above the Hirschsprung’s bundle, which indicates that the lower common pathway is located in the proximal part of the Hirschsprung’s bundle. Five cases of AVNRT with 2:1 AV block have been reported in which only inverted P waves between the R-R were seen on the surface ECG. AVNRT with 2:1 AV block: AVNRT can be accompanied by both anterograde and retrograde block without aborting the tachycardia, and the incidence of the former is about 15% in electrophysiologic examination. The incidence of the former is about 15% in electrophysiologic examination, while the reverse block is rare, mostly second-degree type I and 2:1 reverse conduction block, and there is no cure. (iii) AV node refractory tachycardia with frequency-dependent alternating bundle branch block. (iv) Coexistence of atrioventricular nodal refractory tachycardia and atrioventricular refractory tachycardia: When the patient has a preexcitation syndrome in which the paracrine and atrioventricular nodal double-path pathways coexist, AVNRT and AVRT can be induced by esophageal atrial pacing, respectively, and they can be shifted to each other in the pacing. When the excitation “collision” occurs in the refractory loop, the drag phenomenon can be generated.
2. Characteristics of electrophysiologic examination
(1) The electrophysiological characteristics of slow-fast AV nodal refractory tachycardia (1) It can be induced by atrial pre-systole, atrial pre-stimulation and ventricular pre-stimulation, or by the Vinzel’s cycle caused by the slowing down of AV nodal conduction (prolongation of the A-H interval) during the stimulation of the atrial pacing [atrial programmed pre-stimulation (S2) or short bursts of sudden-onset stimulation (S2)]. (ii) The AV node dual-pathway conduction curve response to atrial presynchronous stimulation or atrial pacing stimulation is manifested as a disruption of the conduction curve, i.e., a prolonged “jump” (≥50 ms) in the A2-H2 interval, a jump of ≥60 ms in the S2-R interval, and an RPE of ≤70 ms. (iii) Tachycardia is induced and terminated by the slow pathway from which it is transmitted. The tachycardia is induced and terminated by a slow pathway with critical A-H prolongation (within the critical frequency range) and intra-atrioventricular nodal conduction. In tachycardia, retrograde atrial excitation occurs in a foot-to-cranial sequence: the A-wave leads in the atrioventricular junction (VA interval values from -42 to +70 ms). In tachycardia, the retrograde P wave overlaps the QRS wave, and the terminal part of the QRS wave is distorted. The V wave (ventricular wave) in tachycardia often overlaps with retrograde Ae wave with prolonged R-P-(V-Ae) interval. (6) The Hirschsprung’s bundle and the ventricle do not participate in the refractory loop, and it is controversial whether the atria participate in the refractory loop. (7) Stimulation of the vagus nerve slows the tachycardia frequency and then terminates the tachycardia.
(2) Electrophysiological characteristics of fast-slow AV nodal refractory tachycardia (1) It can be induced by atrial and ventricular pre-stimulation, or by VA retrograde Vernier cycle during ventricular pacing stimulation (2) There is a retrograde AV nodal dual pathway conduction curve. (iii) Tachycardia is induced by retrograde conduction from the slow pathway accompanied by critical HA prolongation. In tachycardia, the retrograde atrial excitation is in the order from foot to head, and the A wave at the coronary sinus leads, suggesting that the slow pathway is the retrograde branch. ⑤ Long R-P interval, i.e., R-P>P-R. ⑥ Hitchcock’s bundle and ventricle do not participate in the refractory loop, and it is controversial whether atria participate in the refractory loop. (7) Stimulation of the vagus nerve slows the tachycardia frequency and then abruptly terminates the tachycardia, blocking the slow pathway retrograde transmission.
Diagnosis
The definitive diagnosis of this syndrome depends on intracardiac electrophysiologic examination. The main manifestations are AH interval jumps and a tachycardia centered on retrograde transmission of the Hirschsprung bundle during atrial pacing and atrial programmed stimulation, and failure of ventricular presynchronous stimulation to prematurely agitate the atria during Hirschsprung bundle inopportune periods. The possibility of a sudden onset of narrow QRS tachycardia needs to be considered, and is more likely to occur in middle-aged, obese women. The absence of P waves on the ECG, or the presence of false Q or S waves in the inferior wall leads, or false r waves in the V1 lead, is helpful in making the diagnosis. If the tachycardia occurs after atrial pre-systole, this strongly supports the diagnosis of the syndrome.
Treatment
1. During treatment of chronic patients, pharmacologic therapy may be administered either by direct action on the refractory loops or by inhibiting triggers. Indications for pharmacologic therapy include patients with frequent episodes, disruption of normal life, or severe symptoms who are unwilling or unable to undergo catheter-based radiofrequency ablation therapy. Patients with episodic, brief, or mild episodes of tachycardia may be treated without medication or given medication when needed for tachycardia episodes. Catheter radiofrequency ablation can be curative and should be the treatment of choice for patients with recurrent, symptomatic episodes.
2. The inhibitory effect of drugs on refractoriness can be counteracted by sympathetic excitation, and the effect of drugs nearly disappears during physical activity and anxiety. Therefore, in daily life and work to avoid mental tension or excessive fatigue, to do regular life, regular living, mental optimism, emotional stability can reduce the recurrence of the disease.
3. Avoid spicy and stimulating food; quit smoking, alcohol and coffee; eat light food.
Hazards
AV nodal refractory tachycardia may lead to angina pectoris, heart failure, shock and other complications, and even cause sudden death.