Spontaneous atrial tachycardia

Introduction to autonomous atrial tachycardia Automated atrial tachycardia (AAT) refers to atrial tachycardia caused by a moderately high triggering mechanism of ectopic pacemakers in the atrium. basic knowledge The proportion of illness: 0.003%--0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: syncope, hypotension, shock

The cause of autonomous atrial tachycardia

Cause:

Acute autonomic atrial tachycardia can occur in any age group, but occurs mostly in adults, often on the basis of organic heart disease, such as acute myocardial infarction, cardiomyopathy, chronic obstructive pulmonary disease (especially with Acute infection), pulmonary heart disease, etc., digitalis overdose, hypokalemia is often an important cause of autonomic atrial tachycardia, in addition, myocardial ischemia, metabolic disorders, drinking, hypoxia, etc. are often induced factors, Autonomic atrial tachycardia with atrioventricular block is often associated with digitalis poisoning. Clinically, many supraventricular tachycardia with atrioventricular block may be due to increased self-discipline (including digitalis poisoning). Individually seen in normal people without structural heart disease.

Pathogenesis

The mechanism of AAT is the increased self-discipline of ectopic pacemakers in the atrium. The intensity of the AAT is moderately increased in grade 4, and the frequency of stimulating is accelerated. The rapid depolarization rate of the atrial myocytes may be accelerated, or the atrial muscles of the lesions may be removed. Due to the extreme and/or diastolic oscillating potential, the 4-phase auto-depolarization action potential of the atrial conduction beam increases rapidly, the slope becomes steep, or the atrial myopathy changes the fast response potential to a slow response potential and anomalous self-discipline. Atrial tachycardia is produced. It is believed that the trigger mechanism is a muscle atrial arrhythmia. Autonomous atrial tachycardia is a rapid atrial transition between accelerated atrial escape rhythm and atrial flutter. Arrhythmia.

Autonomic atrial 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.

Autonomic atrial tachycardia complications Complications, syncope, hypotension, shock

If tachycardia occurs on the basis of organic heart disease or if the attack time is too long, complications such as syncope, hypotension, cardiogenic shock or heart failure may occur.

Autonomic atrial tachycardia symptoms Common symptoms Warm waking tachycardia chest tightness palpitations dizziness

AAT has the characteristics of sudden onset and sudden termination. Patients have chest tightness discomfort, palpitations, dizziness and other symptoms at the time of onset. A few patients have hypotension, cardiogenic shock, etc. The heart rate is 100-180 beats/min, mostly 160 times/ Min, <250 times/min.

Self-regulatory atrial tachycardia

1. ECG characteristics

(1) Typical ECG features:

The 1P' wave morphology is different from the sinus P wave, and is similar to the P wave shape in the subsequent tachycardia, and the P'-R interval is >0.12 s.

The frequency of 2 atrial tachycardia: generally 100 ~ 180 times / min, <250 times / min.

The 3P' wave appears before the QRS wave: RP'/P'R>1, which can also be seen in the atrial tachycardia of the P' wave after R, and the QRS wave is a supraventricular pattern.

4 The tachycardia begins to see a phenomenon in which the rate gradually increases. This is the phenomenon of warm up of the ectopic stove.

The onset of 5AAT is sudden, sudden, and often occurs automatically. The contraction of atrial tachycardia is formed by the early atrial contraction of the diastolic period. The timely atrial premature contraction electrical stimulation can not induce and terminate the episode. The sinus can not terminate the episode, nor can it be suppressed by electrical stimulation, or even overspeed.

6 can be combined with atrioventricular block to make the ventricular rate slower than the atrial rate, but the tachycardia does not end.

(2) A detailed description of typical ECG features:

1 The frequency of atrial tachycardia at different times in the same AAT patient can vary significantly.

2 At the onset of tachycardia, the initial P'-P' spacing is gradually shortened (warm-up phenomenon), then stabilized at a level, fixed, usually P'-P' spacing does not differ by more than 20ms, gradually before termination Deceleration, there is a longer compensatory interval at the end.

3 tachycardia is a paroxysmal attack that can last for a few seconds, minutes, hours, days or even more than 10 days.

4 The tachycardia is not fixed at the first P' wave and the previous sinus P wave at each episode.

5 If there is an atrial premature contraction during the onset of tachycardia, the frequency of atrial tachycardia can be accelerated.

6 tachycardia episodes may be accompanied by atrioventricular block, can be 2:1, 3:1 or 3:2 or Venturi block, especially when using digitalis, quinidine and other drugs are more likely to occur .

7 Because the lesion is in the room, the tissue below the atrium is not involved, so the frequency of tachycardia does not affect the atrioventricular block, or the P'-R interval does not change when the bundle branch block occurs. Or RP' interval, unless accompanied by an extension of the HV interval.

8 compression of the carotid sinus or oppression of the eyeball and other methods of stimulation of the vagus nerve can not terminate the atrial tachycardia, but can cause atrioventricular block, drug treatment of AAT can slow the tachycardia, but it is not easy to terminate its attack, electric shock is not easy It works.

9 According to the results of the radiofrequency ablation target of the ectopic pacemaker in the atrium, the position of the ectopic pacemaker is initially determined from the 12-lead electrocardiogram, and its location is similar to the reentry tachycardia in the room.

(1) Atrial premature contraction stimulation usually cannot induce and terminate autonomic atrial tachycardia, but can re-regulate its frequency.

(2) The onset of tachycardia has nothing to do with the delay in the conduction of the room or the atrioventricular.

(3) The atrial activation sequence is different from the sinus rhythm.

(4) The AH interval is related to the frequency of tachycardia.

(5) The first P' wave of the tachycardia is the same as the continuous P' wave after the tachycardia.

(6) Autonomous atrial tachycardia is not inhibited by overspeed pacing, but pacing stimulation usually cannot terminate tachycardia. Some people think that it can speed up the frequency.

Diagnosis and diagnosis of autonomous atrial tachycardia

diagnosis

Diagnosis can be based on clinical manifestations.

1. Timely atrial premature contractions cannot induce or terminate seizures.

2. Frequency <250 times / min, generally 100 ~ 180 times / min.

3. The P' wave appears before the QRS wave, RP'/P'R>1, and the atrial tachycardia of the P' wave after R is also seen.

4. When the tachycardia starts, there is a frequency acceleration phenomenon, that is, the phenomenon of "warm up", but the frequency does not change when the tachycardia continues.

5. Excited vagus nerve methods such as carotid sinus compression, can not terminate tachycardia.

6. Can be combined with atrioventricular block to make the ventricular rate slower than the atrial rate, but the tachycardia does not end.

Differential diagnosis

Identification of sinus P wave and ectopic atrial P wave: high atrial P wave can fully meet the sinus P wave ECG diagnostic criteria (P wave is positive in II, negative in aVR lead, PR0.12 s), careful comparison of the morphology of the P-wave and sinus rhythm on each lead on the ECG helps to identify, sometimes the atrial P-wave can be similar to the sinus P-wave in some leads and the other in the simultaneous recording Some leads have differences. Multi-channel recording to distinguish sinus P waves from atrial P waves helps to improve the reliability of sinus node refractory period and sinus node recovery time. In supraventricular tachycardia The P wave often overlaps with other components and cannot be compared with the morphological comparison of sinus rhythm. In this case, two methods can be used:

1 using the atrial activation timing of PEP-PED-Pv1 to compare (ie, observe the phase relationship of P wave peaks in two unipolar esophageal leads and V1 simultaneous recording);

2 Using the morphology of the P wave in the unipolar and bipolar esophageal leads compared with the sinus rhythm, both methods can more clearly distinguish the ectopic atrial P wave from the sinus P wave, thus Helps with reentry (or self-regulation) tachycardia and sinus reentry tachycardia (or differential non-paroxysmal sinus tachycardia), also contributes to sinus reentry and intraventricular reentry The identification of atrial echoes.

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