atrioventricular nodal reentrant tachycardia
Introduction
Introduction to atrioventricular nodal reentry tachycardia Atrioventricular nodal reentrant tachycardia (AVNRT) can be divided into slow-fast, fast-slow two AVNRT. basic knowledge The proportion of sickness: 0.01% Susceptible people: no special people Mode of infection: non-infectious Complications: syncope, cardiogenic shock, hypotension
Cause
The cause of atrioventricular nodal reentry tachycardia
(1) Causes of the disease
Atrioventricular nodal reentrant tachycardia (AVNRT) can be seen at any age, from months to babies to adults, the elderly, children are more common 5 to 6 years old, adults often occur before the age of 40, more common in young and middle-aged, male and female The rate is similar, more common in patients with no structural heart disease, can also be caused by drugs or lesions.
(two) pathogenesis
The electrophysiological basis of AVNRT is that there are two different performance conduction paths in the atrioventricular node with functional longitudinal separation, that is, the atrioventricular node double path (multipath path can also exist in the atrioventricular node), and one is a fast path. The characteristic is that the conduction speed is fast and the refractory period is long; the other is the slow path, which is characterized by slow conduction speed and short refractory period. The proximal end and the distal end of the double-path have a common channel, forming a complete return loop. AVNRT's return loop is not limited to a very small atrioventricular node, but actually involves the atrioventricular junction, so some people call the atrioventricular junction reentrant tachycardia (AVJRT), under normal circumstances, sinus rhythm atrial The impulse is transmitted to the ventricle along a fast path with a fast conduction velocity, and a normal QRS wave is generated. At the same time, the atrial impulse is also slowly transmitted from the slow path. When passing to the His bundle, the His bundle has been transmitted from the fast path. The impulse is excited and in refractory period, so it is no longer excited, and can no longer produce QRS waves. If sinus agitation is transmitted to the ventricle along the fast path, the timely pre-atrial contraction just happens to meet the refractory period of the fast path. Only along the slow path in the reaction period Slowly transmitted, there is a prolongation of the PR interval on the surface electrocardiogram. If the conduction in the slow path is slow, enough to reach the distal end after the fast path is detached, the excitement can be reversed to the atria caused by the fast path. Atrial echo, when the slow path has been detached from the refractory period, the excitement can be transmitted along the slow path, and then the rapid path is reversed, so repeated, the circular motion in the atrioventricular node is formed, which is characterized by supraventricular tachycardia. The rapid onset, this is the most common slow-fast atrioventricular nodal reentry tachycardia.
Another rare type is the opposite. The refractory period of the fast path is shorter than the refractory period of the slow path, and the direction of tachycardia is reversed. It is transmitted from the fast path and reversed from the slow path, resulting in a rare atrioventricular node. Foldback form fast-slow AVNRT.
Timely ventricular premature contraction can also induce AVNRT, sometimes ventricular premature contraction is retarded in the slow path, and then reversed from the fast path, and then slowly transmitted from the slow path, can also make the forward double Pathway patients induce slow-fast atrioventricular nodal reentry tachycardia, but ventricular premature contraction-induced AVNRT must have:
1 The retrograde refractory period of the Xi-Pu system is shorter than the retrograde refractory period of the slow pathway, so that the ventricular premature contraction is not blocked in the Xi-Pu system;
2 The retrograde refractory period of the fast path must be shorter than the retrograde refractory period of the slow path. Otherwise, the excitement will be reversed from the fast and slow path at the same time, and interference will occur in the slow path. The above conditions cause the ventricular premature contraction to induce slowness - Fast AVNRT is subject to certain restrictions.
Prevention
Atrioventricular nodal reentry tachycardia prevention
1. During chronic treatment, drug therapy may control recurrence by directly acting on the reentry loop, or by inhibiting triggering factors, such as spontaneous premature contraction. The indications for chronic drug treatment include frequent episodes, affecting normal life or severe symptoms. Patients who are unwilling or unable to receive catheter radiofrequency ablation may be treated with medication for occasional, episodes of short-lived, or mild symptoms, or medication when needed for a tachycardia episode.
2. The inhibitory effect of drugs on reentry can be offset by sympathetic excitation. In physical activity and anxiety, the effects of drugs almost disappear, so avoid mental stress or excessive fatigue in daily life and work, and make life rules Regular living, mental optimism, and emotional stability can reduce the recurrence of the disease.
3. Avoid spicy food, stimulate food; quit smoking, coffee, food should be light.
Complication
Atrioventricular nodal reentry tachycardia complications Complications, syncope, cardiogenic shock, hypotension
Atrioventricular nodal reentry tachycardia occurs in people with organic heart disease, especially in the ventricular rate, long-term patients with syncope, cardiogenic shock, hypotension, and can induce complications such as heart failure.
Symptom
Atrioventricular nodal reentrant tachycardia symptoms common symptoms tachycardia fatigue palpitations syncope irritability shock
Depending on the frequency of tachycardia, duration of time, and the presence or absence of organic heart disease and the extent of its condition, patients can express palpitations, irritability, nervousness, fatigue, angina, cardiac insufficiency, syncope, and even shock. Because the ventricular rate is too fast, the cardiac output and cerebral circulation blood volume are reduced; or the sick sinus syndrome is combined. When the tachycardia is terminated, the sinus node function is suppressed due to the overspeed inhibition, and the sinus rhythm is restored. Long intermittent before.
Due to the frequency of AVNRT and the short diastolic period, the left ventricular end-diastolic volume and stroke volume are significantly reduced. If the patient's heart function is normal, the cardiac output and ejection fraction can be maintained in the normal range. Sexual heart disease or tachycardia frequency is too fast, and when the duration is too long, the ejection fraction can be significantly reduced, resulting in significant hemodynamic disorder.
Examine
Examination of atrioventricular nodal reentry tachycardia
1. ECG examination AVNRT has two different types of clinical ECG:
(1) Electrocardiogram characteristics of slow-fast AVNRT: slow-fast form AVNRT (also known as slow-fast form AVNRT) is the most common type of AVNRT. It is the most common in adults, accounting for 90% of AVNRT. It is a slow path and a fast path. .
1 typical ECG features:
A. Sudden onset, abrupt termination.
B. The P' wave is retrograde: when the tachycardia is over, the atrium and the ventricle are almost simultaneously excited. About 66% of the patients are not seen because the P' wave is buried in the QRS complex. About 30% of the patients have a P' wave. Following the QRS wave (R-P-), the RP-interval/P--R interval is <1, and the P' wave is inverted in the II, III, aVF leads. The aVR leads are erect, and some cases are in the V1 lead. The QRS wave has a small r-wave at the end, which is actually part of the P' wave.
C.QRS waveform is normal: the frequency is 140 ~ 220 times / min, most of the attacks are 150 ~ 160 times / min, more than 200 times / min, rhythm rules.
D. The atrial premature contraction that initiates the onset of tachycardia is transmitted through the slow path, so the P--R interval of the first heart beat of AVNRT is prolonged, indicating that there is a dual path feature.
E. Timely atrial premature contraction electrical stimulation can induce and terminate the onset of AVNRT, pre-systolic contraction, premature contraction of the anterior junction, and ventricular premature contraction can also be induced (in a few cases).
F. Carotid sinus compression Stimulation of the vagus nerve method: some patients may be terminated; or only the tachycardia frequency may be slowed down.
G. It is rare to have atrial or ventricular conduction block that makes the atrial ventricular frequency inconsistent.
2 detailed description of typical ECG features:
A. Because the reentry loop is small, the P' wave can be in front of the QRS wave, and then there is a partial overlap between the two. The typical atrial agitation start point of a typical AVNRT patient (the earliest activation of the atrial electrocardiogram) Point) is located before the start of the QRS wave, or at the same time, sometimes P-starts very early, so that the QRS wave of the lower wall II, III, aVF leads "false q wave", "false q wave" is rare, However, it is very specific for AVNRT. The rapid retrograde atrial agitation is due to the retrograde branch. The atrial activation in 25% of patients begins within the QRS wave. About 95% of patients have a surface electrocardiogram or no clear P' wave. 50%), or the terminal part of the QRS wave is slightly distorted, may be a "false s wave" in the inferior leads, or a "false r wave" in the V1 lead, or at the end of the QRS wave Non-specific notch, the remaining patients can see the P' wave followed by the end of the QRS wave, the RP-interval time of AVNRT is <70ms.
B.QRS waveform is normal: When the tachycardia is too fast, the heart rate may be in the relative refractory period, and the bundle branch block type indoor differential conduction, mostly right bundle branch block type, is considered to be AVNRT patient. There is little time-differential indoor differential conduction, because the atrial premature contraction of AVNRT induces a significantly prolonged PR interval, which causes the heartbeat to have a longer H1-H2 interval, exceeding the functional refractory period of the bundle branch. Therefore, functional bundle branch block (intraventricular differential conduction) is rarely caused. Among the 141 consecutively observed AVNRT patients, 7 patients have sustained bundle branch block after AVNRT induction after atrial premature stimulation. 5 cases were right bundle branch block, 2 cases were left bundle branch block, and no case of tachycardia perimeter or HH interval was affected by bundle branch block.
C. Frequency of tachycardia: mostly 140-220 times/min, the lowest can be 110-130 times/min, up to 240 times/min.
D. When RP-interval>1/2R-R interval, 90% belong to AVNRT, and RP-<1/2R-R also have 54% belong to AVNRT. In esophageal lead, RP-interval is often 70ms. .
E. In rare cases, because the autonomic nerve changes the conduction velocity and refractory period of the two-pathway in the atrioventricular node, a simultaneous transmission representing two different velocities appears on the electrocardiogram, presenting a P' wave, which is transmitted. Two QRS complexes, the P--R interval is one short and one long, and it is easy to be mistaken for premature contraction. In addition, there is also atrial agitation from the fast path and the slow path to the ventricle, forming P-- The interval between the R interval is short and short, and even due to the ecstasy, the occult retrograde conduction can occur in another path, so that the next P' wave is detached and misdiagnosed as a second degree atrioventricular block.
F. Since the initial pulsation (such as atrial contraction) is transmitted through the slow path, the first heart beat PR-interval of AVNRT is prolonged.
G. In a few cases, tachycardia can be induced by ventricular premature contraction or sinus premature contraction.
H. The onset of slow-fast AVNRT has nothing to do with the speed of sinus rhythm.
I. About 10% of patients with slow-fast AVNRT may have QRS electrical alternation.
(2) Electrocardiogram characteristics of fast-slow AVNRT: fast-slow form AVNRT (also known as atypical AVNRT or rare AVNRT), characterized by fast path pre-transmission, slow path reversal, that is, slow path should not The period is longer than the fast path. The atrial reversal agitation order is different from the typical AVNRT. The earliest atrial agitation is often in the coronary sinus ostium. It is rare, only 5% to 10% of the atrioventricular nodal reentry tachycardia. The seizure lasts for a long time and is more common in children, mostly pathological or caused by drugs.
AP' wave: Since the reversal of the slow path is slow, the retrograde P' wave is after the T wave of the previous cardiac cycle, and the surface electrocardiogram is easily recognized before the next QRS wave. The P' wave is at II, III, aVF. The lead is inverted or in two phases, and in the aVR, the V1 lead is upright.
The BP--R interval is short and fixed: RP-interval length P--R1/2R-R (Fig. 5).
C.QRS wave is supraventricular: a few with bundle branch block, QRS wave can also be a wide deformity, RR interval rules, the heart rhythm is absolutely neat, heart rate is 100 ~ 150 times / min.
D. Induction of pre-systolic contraction of fast-slow AVNRT without prolongation of P--R interval.
E. Can be induced by atrial premature contraction, mildly increased heart rate can also be induced, it can be seen that fast-slow AVNRT begins to be secondary to sinus tachycardia, often the sinus heart rate gradually becomes faster, then AVNRT occurs The frequency is as fast as AVNRT, which varies from person to person, some are 80 to 90 times/min; some are 100 to 130 times/min, and the end of AVNRT can be the end of P or R wave.
F. tachycardia is not easy to terminate naturally: the drug effect is poor, the left atrial pacing of the esophagus is difficult to induce success, and the program electrical stimulation is not easy to show the characteristics of the dual path (dual channel).
(3) Special types of atrioventricular nodal reentry tachycardia:
1 atrioventricular nodal reentry tachycardia with lower common path 2:1 conduction block: Some people found that at 2:1 atrioventricular block above the His bundle, atrioventricular nodal reentry tachycardia can still exist. It is indicated that the common path at the lower end is located at the proximal end of the His bundle. Five cases of AVNRT with 2:1 atrioventricular block have been reported, and the surface electrocardiogram shows only the inverted P' wave located between the RRs.
2 atrioventricular nodal reentry tachycardia with secondary type I nodule reverse conduction block: AVNRT can be associated with anterior and posterior block without tachycardia, the incidence of the former is about 15% in electrophysiological examination However, the reverse block is rare, mostly second degree I and 2:1 retrograde block, and no cure.
3 atrioventricular nodal reentry tachycardia with frequency-dependent alternating bundle branch block.
4 atrioventricular nodal reentry tachycardia and atrioventricular reentry tachycardia coexist: when the patient has a pre-excitation syndrome bypass and a double-pathway in the atrioventricular node, the esophageal atrial pacing can be induced separately AVNRT and AVRT can change each other during pacing. When the excitement "collision" occurs in the reentry loop, the towing phenomenon can occur.
2. Electrophysiological examination features
(1) Electrophysiological examination features of slow-fast atrioventricular nodal reentry tachycardia:
1 can be induced by pre-atrial contraction, pre-atrial stimulation and ventricular pre-stimulation, or in the atrial pacing stimulation [atrial pre-control stimulation (S2) or short-term burst stimulation (S2)] Induced by the Venturi cycle caused by delayed junction conduction (longed AH interval).
2 For atrial pre-stimulation or atrial pacing stimulation, there is a conduction curve of the atrioventricular nodal pathway. The conduction curve is interrupted, that is, the A2-H2 interval is extended by jumping (maximum increase 50ms), and the S2-R interval is increased. 60ms, RPE70ms.
3 The induction and termination of tachycardia depends on the extension of the critical AH (within the critical frequency range) and the conduction of the atrioventricular node from the slow path.
4 When the tachycardia is over-speed, the atrial agitation is from the foot to the head: the A-wave leading in the atrioventricular junction (the VA interval is from -42 to +70 ms).
5 When the tachycardia is overspeed, the reverse P wave overlaps the QRS wave, and the terminal part of the QRS wave is deformed. The V wave (ventricular wave) at the tachycardia often overlaps with the retrograde Ae wave with RP-(V-Ae). The period is extended.
6 His bundle, the ventricle does not participate in the reentry loop, and there is still disagreement about whether the atrium participates in the reentry loop.
7 Stimulating the vagus nerve slows the tachycardia frequency and then terminates the tachycardia.
(2) Electrophysiological examination features of fast-slow atrioventricular nodal reentry tachycardia:
1 can be induced by atrial stimulation and ventricular pre-stimulation, or induced by VA retrograde ventricle during ventricular pacing stimulation.
2 There is a retrograde conduction curve of the atrioventricular node.
3 The induction of tachycardia relies on retrograde transmission from the slow path with a critical HA extension.
4 When the tachycardia is over-speed, the atrial agitation is from the foot to the head, and the A-wave of the coronary sinus is leading, suggesting that the slow path is a retrograde branch.
5 long RP-interval, ie RP->P--R.
6 His bundle, the ventricle does not participate in the reentry loop, and there is still disagreement about whether the atrium participates in the reentry loop.
7 Stimulating the vagus nerve to slow down the tachycardia frequency, and then suddenly stop the tachycardia, always blocking the slow path reversal.
Diagnosis
Diagnosis and diagnosis of atrioventricular nodal reentry tachycardia
Seeing the sudden narrowing of the QRS tachycardia requires consideration of the possibility of this disease. If it occurs in middle age, it is more likely to be overweight, and most of the ECG will not see P wave, or see the lower wall lead. It is helpful for diagnosis to a false Q or a fake S wave, or a false r wave in the V1 lead. If the tachycardia occurs after the atrial contraction, it strongly supports the diagnosis of this disease.
The diagnosis of this disease depends on intracardiac electrophysiological examination, which is mainly characterized by AH interval hopping during atrial pacing and atrial stimulation, and tachycardia centered on His bundle back. The pre-ventricular stimulation does not excite the atrium in advance.
Differential diagnosis
Identification of atrioventricular nodal reentry tachycardia and atrioventricular reentry tachycardia:
1 The former has a slightly more incidence of women, and the latter is 2 times higher than female patients;
2 The frequency of tachycardia is about 170 beats/min (160-180 beats/min more common), and only a few adults exceed 200 beats/min, while the latter is faster, and most of them have episodes of more than 200 beats/min. 3 In the tachycardia, the retrograde P' wave overlaps with the QRS wave, and the minority overlaps with the QRS wave terminal, and the RP-interval is <70ms. The latter retrograde P' wave is more clearly visible, and the RP' interval is >70ms. .
