Introduction to the diagnosis and treatment of cardiac arrhythmias

  Normal heart impulses originate in the sinoatrial node and propagate through the inter-nodal bundle, atrioventricular node area, atrioventricular bundle, left and right bundle branches and Purkinje fibers at a certain frequency, sequence and speed, causing the heart to contract and diastolic in a regular manner, which is called normal sinus rhythm. Abnormalities in the origin, frequency, or conduction of the heart impulses are called arrhythmias. The most common arrhythmias are various types of premature beats, followed by supraventricular tachycardia (supraventricular tachycardia), ventricular tachycardia, atrial flutter, fibrillation, and various types of bradycardia. This section only describes premature heart beats, supraventricular tachycardia, and atrioventricular block.
  I. Premature heart beats
  (cardiac presystole)
  Diagnosis
  (a) Electrocardiographic diagnosis.
  1. Premature ventricular contractions.
  (1) Early appearance of ORS waves without ectopic P waves before them.
  (2) ORS waves with wide distortion and prolonged time, more than 0.10 sec in children and more than 0.08 sec in infants. the T wave is opposite to the main wave direction of QRS wave.
  (3) Ventricular premature beats are mostly accompanied by complete compensatory intervals.
  2. Atrial premature contractions.
  (1) Atrial ectopic P waves appearing early, with a morphology different from that of sinus P waves.
  (2) P’-R interval in the normal range, ≥0.12 seconds in adults and ≥0.10 seconds in pediatric patients.
  (3) QRS wave morphology can have three forms.
①The same as sinus QRS wave;
(2) abnormal QRS waves with intraventricular differential conduction;
(3) Atrial premature beats without downward conduction have no QRS wave after the ectopic P’ wave.
  (4) The compensatory intervals of atrial premature beats are mostly incomplete and occasionally complete.
  3. Premature atrioventricular junctional contractions.
  (1) The morphology of the prematurely appearing QRS waves is the same as that of sinus, or it is distorted by differential intraventricular conduction.
  (2) The P’ wave of junctional premature beats is retrograde (P II, III, avF inverted, PI, aVR often upright, and the mean electrical axis of P’ wave is between 600 and 900), and the relationship with QRS wave can still have three forms.
① Retrograde P’wave appears before the QRS wave group, its P’-R interval can be less than the normal range, <0.12 seconds in adults, ≤0.10 seconds in pediatric patients, or slightly shorter than the sinus P-R interval;
(ii) Retrograde P’ wave appears after the QRS wave, and the R-P’ interval is <0.20 seconds;
(3) There is no P’ wave before or after the ORS wave.
  (3) Complete compensatory interval is often present.
  4. Premature sinus beats.
  (1) Early appearance of P-QRS-T waves with the same morphology as sinus ones.
  (2) There is a fixed pairing interval.
  (3) Incomplete compensatory intervals.
  (4) It is not related to respiration.
  (ii) Simple versus pathological premature beats.
  1. The basis for determining the nature of premature beats.
  (1) Whether there is a basis of organic heart disease.
  (2) Whether there are combined ECG abnormalities: prolonged Q-T interval, ST-T changes, atrial hypertrophy, conduction block (intra-atrial, atrioventricular, intraventricular), abnormal Q waves, etc.
  (3) Characteristics of premature beats.
①Ventricular premature beats are not as clinically significant as supraventricular ones; sinus premature beats are rare and of little clinical significance.
(2) Premature beats are frequent, in association, paired or repeated with more than three premature beats.
(iii) Polymorphic premature contractions and premature contractions of multiple origin.
④Wide QRS deformity with time limit >0.14 seconds or amplitude <10mm or lower than the amplitude of R wave in the same lead.
⑤ Various types of premature beats (ventricular, supraventricular), co-existing. (6) RonT or RonP.
  (4) Increased premature beats after exercise or during rapid heart rhythm.
  The presence of one of the four items or one of the three points other than ① can be considered as organic premature heartbeat.
  2. Further tests to determine the nature of premature beats.
  (1) Electrocardiographic stress test.
  (2) Ambulatory electrocardiographic monitoring.
  (3) Ultrasound examination of the heart.
  (4) Clinical electrophysiological examination.
  [Treatment].
  (I) Anti-arrhythmic drugs may be dispensed with in the following cases.
  1. Asymptomatic, normal activity or detected by physical examination;
  2. Premature beats are more frequent at night or at rest, and less frequent during activity;
  3. The heart is not large and normal in shape on chest radiograph, and the cardiac ultrasonography shows normal intracardiac structures;
  4. ECG is not abnormal except for premature beats, cardiac function is normal, and cardiac enzyme values are within normal range.
  (II) Treatment of pathological premature beats.
  1. Treatment of etiology and causative factors.
  2. Appropriate sedation.
  3. The following antiarrhythmic drugs are generally considered to be used for premature beats ≥10 beats/min or symptomatic pathological premature beats.
  Propafenone (cardioplegia), the most commonly used first-line broad-spectrum anti-premature drug in pediatrics, is administered orally 5-7 mg/(kg.times) every 6-8 hours, and the number of premature beats is reduced by more than 50% and maintained at 3-4 mg/(kg.times) for a period of 3-6 months. The total amount is not more than 6mg/kg. Use with caution for bradycardia, conduction block and heart failure.
  Propranolol (insulin), for premature beats caused by sympathetic excitation, oral 1 mg/(kg.d), divided into 3 oral doses, 0.1-0.2mg/(kg.times), not more than 3mg/time, add 10% glucose 10-15ml, 10-15 minutes slow injection, mainly for supraventricular tachycardia. Forbidden to be used in children with asthma and in combination with calcium antagonists.
  Verapamil (Isoptin), a calcium antagonist, 1-1.5 mg/(kg.dose) 3 times daily. It is contraindicated in pre-excitation syndrome and should be used with caution in <1 year of age, as it may cause a drop in blood pressure, cardiac arrest, and worsening heart failure.
  Morelcizine (etomoxetine) is a broad-spectrum drug for premature beats, mainly used for intractable ventricular premature beats. It can also be used for supraventricular tachycardia and short bouts of ventricular tachycardia. 4-5 mg/(kg.dose) 3 times daily.
  Amiodarone, a broad-spectrum anti-premature drug, was previously used as a second-line drug because of its perceived adverse effects, but recent domestic and international studies have shown that its adverse effects on the thyroid and lung are uncommon in childhood, and the American College of Cardiology has recommended it as the drug of choice for post-resuscitation ventricular arrhythmias in pediatrics. Oral 10mg/(kg.d) in 2 divided doses, reduced to 5mg/(kg.d) after 7-10 days, 1 oral dose, 5 days off 2 days.
  Intravenous injection 2.5~5 mg/(kg.d), add to glucose solution and inject slowly or drip. It is particularly suitable for children with cardiac insufficiency because of its weak negative cardiac effect. It is generally not used in combination with other antiarrhythmic drugs. Intravenous amiodarone can increase the mass concentration of digoxin, and the dosage of digoxin should be reduced when the two drugs are used together.
  Sotalol, a broad-spectrum anti-premature drug, is indicated for premature beats, ventricular tachycardia, ventricular fibrillation, and supraventricular tachycardia associated with pre-excitation. 2-4 mg/(kg.d) orally in 2 to 3 doses. IV 0.5-1.5 mg/(kg.d), 5-10 minutes slow injection, note that it may cause tip-twisting ventricular tachycardia individually.
  Mecillin (slow rhythm), a membrane stabilizer, is mainly used for ventricular premature, peak blood dose 3 hours after oral administration, maintained for more than 8 hours, 15-20 mg/(kg.d), divided into 3-4 times; 1-2 minutes after sedation onset, 1-3 mg/(kg.d), 5 minutes slow injection, mainly used for ventricular tachycardia, ventricular fibrillation and arrhythmias caused by digitalis poisoning and maintenance treatment after lidocaine resuscitation.
  Amproliquid, mainly for intractable ventricular premature, 1~3 mg/(kg.d) orally in 3 doses, maintenance 0.5~1.5 mg/(kg.d).
  Phenytoin sodium, for digitalis intoxication causing premature ventricularization, 5-10 mg/(kg.d) orally in 3 doses; 2-3 mg/(kg.d) by sedation, may be repeated once in 5-10 minutes.
  Lidocaine (Serocaine), can not be taken orally, intravenous treatment of ventricular tachycardia, ventricular fibrillation and severe ventricular premature. 1 to 2 mg/(kg.d), may be repeated after 5 to 10 minutes, after seeing the effect, change to intravenous drip, 20 to 40 µg/kg, the total amount does not exceed 5 mg/kg.
  Digoxin, which can be used for supraventricular tachycardia in cardiac arrhythmias.
  It is generally recommended to apply one kind of medicine for premature beats, and when it must be used in combination, it should not be more than two kinds.
  4. For complex ventricular premature with poor drug efficacy, electrophysiological examination should be performed and catheter interventional radiofrequency ablation treatment can be considered.
  SVT is one of the emergencies of pediatric heart disease, and the incidence has increased significantly in recent years with the improvement of electrophysiological research and detection means, which is 1/1000~1/250. The most common cause of pediatric supraventricular tachycardia is the atrioventricular bypass regurgitation SVT, which accounts for 52%, and the atrioventricular node double pathway regurgitation, which accounts for 20%-30%.
  The younger the age, the faster the heart rate, and the longer the duration, the more likely it is to be combined with heart failure, and should be actively managed.
  Diagnosis
  (A) sudden onset and sudden stop; panic, chest tightness, pallor, cold sweat, infant moaning, irritability, refusal of milk, vomiting, etc. during the attack.
  (B) History of recurrent attacks.
  (iii) ECG changes: heart rate: infants >230 beats/min, children >180 beats/min, adults >160 beats/min; ventricular rhythm is absolutely regular, R-R homogeneous; P-T fusion, junctional visible retrograde P′ wave; QRS morphology is normal, if there is intraventricular differential conduction, WPW, bundle branch conduction block can be wide aberration; ST segment depression, T wave inversion.
  (D) chronic supraventricular tachycardia: no sudden onset and sudden stop characteristics, chronic passage, lasting > 1 month; heart rate 120-180 beats/min, more than 50 beats difference between the heart rate during wakefulness and sleep; common ectopic P waves, P II, III, aVF abnormal upright or inverted; mostly asymptomatic, poor efficacy, most can recover on their own after several years.
  【Treatment】
  (a) Treat the original disease and the trigger.
  (B) Terminate the acute attack.
  1. Excite the vagus nerve.
  (1)Stimulate the posterior pharyngeal wall with tongue depressor etc. to induce nausea and vomiting; exhale after deep inhalation and then do the inhalation movement forcefully (Valsalva method); squatting position and forcefully lowering the head, immersing the face in cold water or ice water towel covering the face for 10-15 seconds each time to induce diving reflex; press the eyeball and carotid sinus, it is not easy to grasp the scale in children, and generally not used.
  (2) Application of antihypertensive drugs, producing a pressurized reflex, to monitor blood pressure and ECG, pediatrics is used sparingly.
  (3) Adenosine triphosphate (ATP), this drug has a strong excitatory vagus nerve effect, rapid action, can terminate SVT within 30 seconds, the first dose of 0.1mg/kg (not more than 12mg/time), rapid sedation. There are recommendations: 3-5 mg/dose for infants and children, 5-15 mg/dose for older children, if the rhythm is not turned in 10 minutes, increase the dose and repeat once as appropriate. Sinus bradycardia, transient AVB, sinus arrest may occur, should be performed under cardiac monitoring, may provoke asthma attacks, and should be used with caution in those with a history of allergy.
  At present, some scholars believe that ATP termination of SVT is not related to the vagus nerve, but rapidly binds to the adenosine receptors on the atrioventricular node cell membrane to delay AV node conduction and temporary AVB, thus terminating AVNRT and AVRT.
  2.Drug transrhythmics.
  (1)Cardioplegia: Apply to all types of SVT. 1~2mg/(kg.times) dissolved in 10% glucose 10 ml, slow intravenous injection for 10-15 minutes, repeat 1~2 times after 20 minutes of ineffectiveness.
  (2) Methocarbamol: Used for SVT caused by digitalis poisoning or WPW. see chapter on premature pacing for dose and usage. children with combined asthma can be treated with methocarbamol.
  (3)Amiodarone: effective for all types of SVT, especially for WPW combined with SVT: 2.5~5mg/(kg.times), slow intravenous injection for 10~15 minutes.
  (4) Rapid digitalis preparation: preferred for SVT that has combined heart failure and cardiogenic shock, and should not be used for reverse type bypass foldback. Cidilan 0.02-0.04mg/kg, half amount of the first dose, and then 1/4 amount after 6 hours, slow onset of action, median time 6 hours.
  3. Electrophysiological treatment.
  (1) Esophageal atrial pacing.
  (2) Direct current shock transient rhythm: 5-10 J for newborns, 20-40 J for infants, 60-100 J for children, with no more than 3 repeated shocks.
  (3) Radiofrequency catheter ablation method (RFCA).
  4.Surgical treatment: cut off the bypass or eliminate the ectopic excitation foci.
  5.Prevention of recurrence treatment: 3-6 months of maintenance treatment with insulin, 3-6 months of cardioplegia and 1-3 months of digoxin.
  3.Atrioventricular conduction block
  (cardiac A-V block)
  Diagnosis
  (a) First degree AV block.
  1. Prolonged atrioventricular conduction time, but each atrial excitation can be transmitted to the ventricle without conscious symptoms, and the first heart sound at the apical part of the heart is diminished on auscultation.
  2, ECG changes: according to age and heart rate, PR interval exceeds the highest normal value, generally above 0.16 seconds in preschool, above 0.18 seconds in school-age children, and above 0.21 seconds in adults; PR interval does not exceed the normal range, but when the heart rate is unchanged or faster, PR interval is prolonged by more than 0.04 seconds compared with the original.
  (II) Second degree AV block.
  1. Partial failure of atrial excitation to transmit to the ventricle, intermittent ventricular shedding. When the ventricular rate is slower and there are more missed beats, there may be dizziness, weakness and palpitations.
  2. Electrocardiographic changes.
  (1) Mohs type I (Wen’s type).
  ① PR interval is gradually prolonged until one P wave is blocked and ventricular dislodgement occurs;
  (2) Progressive prolongation of the PR interval with progressive shortening of the R-R interval until ventricular dislodgement occurs;
  (3) The RR interval with ventricular dislodgement is less than 2 PP intervals.
  (2) Mohs type II.
  ①PR interval is fixed;
  ②P waves appear regularly, and some P waves are not followed by QRS waves.
  (3) High degree AV block: In second degree AV block, the AV conduction is more than 3:1, such as 4:1, 5:1, etc. It is called high degree AV block, only a few P waves can be transmitted downward, the ventricular rate is very slow, and junctional or ventricular escape or escape rhythm often appears.
  (3) Third degree AV block.
  The ventricular rate is slow and regular, mostly in the range of 35 to 55 beats/min. The first heart sound varies in strength and can be heard as “big gun sound”, and the child may have dizziness, weakness, chest tightness, and Asymmetry may occur.
  2.Electrocardiographic changes.
  P waves are not related to QRS waves;
  The atrial rate is faster than the ventricular rate, and the atrial rhythm is mostly sinus rhythm or atrial flutter or atrial fibrillation;
  The ventricular rhythm is junctional or ventricular escape rhythm;
  QRS pattern: if the block site is above the AV bundle, the QRS wave is the same as normal sinus; if the block is in the ventricle or with bundle branch block, the ORS wave is deformed and the time limit is >0.10 seconds.
  Treatment
  (I) Etiological treatment: First degree and second degree I AV block are mainly treated etiologically.
  (B) Treatment to increase heart rate: Generally, if the heart rate is <50 beats/min or there are self-conscious symptoms, one of the following drugs is used
  1.Atropine, 0.01-0.03mg/(kg.times), once in 1-6 hours, subcutaneously or intravenously if necessary.
  2.654-2, 1~2.5mg/time for infants, 3~5mg/time for preschoolers, 5~10 mg/time for children.
  3.Isoprenaline, 5~10 mg/dose inclusive, 3~4 times a day, 0.5~1mg added to 10% glucose 250~500ml intravenously if necessary, adjust the drip rate according to the heart rate.
  (C) Promote the recovery of conduction system function drugs.
  1, 5% NaHCO3 3-5ml/kg, intravenous infusion, once a day.
  2.Dexamethasone, 0.1~0.3 mg/(kg.times), intravenous infusion, 1~2 times a day.
  (iv) Symptomatic treatment: treat heart failure, cardiogenic cerebral hypoxia syndrome, cardiogenic shock, etc.
  (v) Placement of pacemakers: In pediatric and adolescent requiring permanent cardiac pacing are mostly seen in.
  1. symptomatic bradycardia;
  2. Recurrent bradycardia-tachycardia syndrome;
  3. Congenital complete atrioventricular block;
  4. Surgical/acquired high second or third degree atrioventricular block.
  Attachment: Non-pharmacological treatment of arrhythmias
  In the past decade, radiofrequency catheter ablation has been used to treat tachyarrhythmias such as pre-excitation syndrome, atrioventricular node regurgitation tachycardia (AVRT), atrial tachycardia, atrial flutter, idiopathic ventricular tachycardia and frequent premature ventricular beats with good results, and has become the preferred method for the treatment of these arrhythmias; and the indications tend to be younger.
  Implantable pacemakers for the treatment of pediatric slow-onset arrhythmias are also gradually being developed, covering not only the common high atrioventricular block and sinus node dysfunction, but also severe vasovagal syncope and congenital long QT syndrome with bradycardia. The treatment of malignant ventricular arrhythmias with buried cardioverter-defibrillators (ICDs) has been widely performed in adults, but is currently a gap in the field of pediatrics in China.