Arrhythmia

Predominant heart rhythm in healthy newborns is sinus rhythm (variant respiratory arrhythmia). Heart rate (HR) can vary 70-190 beats per minute:

• depends on gestational age => the lower the gestational age, the higher the HR
• state of consciousness => lower HR in deep sleep
• concomitant medication => Caffein citrate in high doses can cause tachycardia; anaesthetics are generally cardiotoxic and can cause bradycardia

Arrhythmias (heart rhythm disorders; irregular heartbeat) are found in up to 5% of newborns during the first 10 days of life (abnormal rhythm or speed of rhythm of the heartbeat) – most are premature supraventricular beats that will disappear over the first month of life.

Diagnosis is usually made through 12-lead ECG or using 24-hour Holter ECG measurement. In order to rule out extracardial causes, investigations should be made:

• Arterial blood gas (acid-base balance)
• Electrolytes (sodium, potassium, calcium)
• Inflammatory markers (CRP, procalcitonin, interleukin-6)
• Imaging (Chest X-ray; Cranial Ultrasound)
• Pharmacology (serum levels of medication affecting heart rate and rhythm)

Classification of Arrhythmia

Sinus Tachycardia

Heart rate > 160/min in term infants and > 180/min in preterm infants (or HR above 2 standard deviations for the given gestational age)

• fever
• pain
• shock (hypovolemia, sepsis)
• anemia
• arterial duct (hemodynamically significant ductus arteriosus Botalli)
• hyperthyroidism
• medication (catecholamines, methylxanthines)

Sinus Bradycardia

Heart rate < 80/min in term infants and < 100/min in preterm infants (or HR below 2 standard deviations for the given gestational age)

• vomiting
• airway suctioning / insertion of gastric tube
• hypoxia / apnea
• intracranial hemorrhage / hydrocephalus
• hypothermia
• hyperkalemia
• hypothyroidism
• medication(propranolol, digoxine)

Arrhythmia

Abnormal origin and propagation of action potentials in myocardium

Tachyarrhythmia = based on reentry mechanism

• Triggered activity (abnormal repolarization due to electrolyte transport disorder)
• Abnormal automation (spontaneous depolarization of cells outside the sinoatrial node or the conduction system of the myocardium)

Bradyarrhythmia = based on decreased automation of the sinoatrial node or atrioventricular dissociation

Tachyarrhythmia

Supraventricular Extrasystoles (premature atrial contractions – PAC)

Etiology: ectopic centres in atria generating premature atrial contractions (healthy newborns – the rate of extrasystoles decreases with advancing postnatal age (usually disappear by the end of the first month of life); congenital heart disorders; after cardiac surgery; electrolyte dysbalance)

Diagnosis: abnormal and premature P wave; QRS with normal morphology; if the atrial beat is premature enough, it may reach the atrioventricular node during its refractory period (no QRS complex following the P wave = incomplete compensation pause)

Therapy: usually not required (if needed (frequent PACs; atrial ectopic tachycardia) => beta blockers – Sotalol – see prescription example below)

Sotalol NEO (5 mg/ml)

(for newborns)
Sotaloli hydrochloridi 0,1 g
Aqua pro injectione ad 20,0 g

M.f. sol.
Exp. orig. No. (of packages)
D.S. 80-90 mg/m²/day (divide into 3 daily doses)

Learn More

Sotalol (5 mg/ml)

(for children > 1 month)
Sotaloli hydrochloridi 0,5 g
Acidi citrici 0,08 g
Kalii sorbas 0,1 g
Sirupi simplex 20,0
Aqua purificata ad 105,0 g (= ad 100 ml)

M.f. sol.
Exp. orig. No. (of packages)
D.S. 80-90 mg/m²/day (divide into 3 daily doses)
Note: expiration 3 months (store at 2-8 °C)

Learn More

Atrial Ectopic Tachycardia (AET)

Etiology: the most common arrhythmia based on abnormal automation; often 1:1 conversion to ventricles; can lead to continual tachycardia => cardiomyopathy => cardiac failure

Diagnosis: abnormal P wave; QRS with normal morphology

Therapy:

• Acute => Amiodarone (continuous infusion) => to arrest ectopic focus, slow down AV conduction or reverse continual tachycardia
• Chronic => oral anti-arrhythmic therapy (Sotalol, Propafenone, Digoxin)

Atrioventricular Reentrant Tachycardia (AVRT)

Etiology: the most common (incidence 1:25 000) symptomatic arrhythmia (paroxysmal supraventricular tachycardia = SVT) in newborns; SVT is based on accessory atrioventricular pathway => ventricles are activated through normal conduction pathways and the signal flows retrogradely through the pathological pathway to activate the atria and the cycle repeats (can reach up to 220-300 beats/minute => cardiac failure)

If the pathway allows anterograde signal => pre-excitation (Wolff-Parkinson-White) => paroxysmal AVRT = WPW syndrome

Overall good prognosis as most AVRT episodes will cease by the end of the first year of life; 30% children can experience recurrent episodes of AVRT

Diagnosis: ventricular frequency 220-300/minute; frequency does not change with activity; abnormal P wave and PR interval; WPW = wide QRS, delta wave, shortened PR interval
Clinical presentation is often silent in the beginning => later symptoms include irritability and reluctance to feed => cardiac failure develops in 48 hours in half the patients (antenatally, prolonged paroxysmal SVT can lead to hydrops fetalis)

Therapy:

• Acute
  → Vagal maneuvers (diving reflex = cold cover on the face)
  → Adenosine (0.1 – 0.3 mg/kg IV as a rapid bolus) – caution with WPW syndrome as Adenosine can cause atrial and ventricular fibrillation (requires defibrillation)
  → Amiodarone (2.5 – 5 mg/kg IV for 30 min, followed by continuous infusion as necessary 10 – 15 μg/kg/min)
• Chronic => oral anti-arrhythmic therapy (Sotalol, Propafenone, Digoxin)

Digoxin contraindicated in patients with WPW syndrome (shortening anterograde refractory period of the accessory pathway) !

Atrial Flutter (AFL)

Etiology: reentry pathway in the atria => reentrant tachycardia; typical for fetal and neonatal period => cardiac failure => hydrops fetalis. Atrial fibrillation is rare in newborns

Diagnosis: atrial frequency 300-400/minute; sawtooth pattern P waves; QRS with normal morphology; AV conduction usually 2:1 with resultant ventricular tachycardia of 200-220/min

Therapy: Acute => Esophageal overdrive; Electrical cardioversion (0.5-1 J/kg); Medication is used rarely in children

Permanent Junctional Reciprocating Tachycardia (PJRT)

Etiology: chronic form of AVRT – only retrograde conduction through the accessory pathway

Diagnosis: negative P waves in II, III, aVF leads; normal QRS; long RP interval (retrograde atrial activation through slow-conducting accessory pathway)

Therapy:

• Acute => Adenosine (0.1 – 0.3 mg/kg IV as a rapid bolus)
• Chronic => oral anti-arrhythmic therapy (Sotalol, Propafenone, Digoxin)

Junctional Ectopic Tachycardia (JET)

Etiology: rare arrhythmia based on abnormal automation of cells within AV junction; congenital (requires chronic medication in order to prevent cardiac failure) and acquired form (after cardio surgery)

Diagnosis: normal QRS; ventricular frequency higher than atrial => atrioventricular dissociation

Therapy:

• Acute => Amiodarone (2.5 – 5 mg/kg IV for 30 min, then if necessary continuous infusion 10 – 15 μg/kg/min)
• Chronic => oral anti-arrhythmic therapy (Propafenone)

Long QT Syndrome (LQTS)

Etiology: rare neonatal arrhythmia based on electrolyte channel disorders (inherited/acquired) in the myocardium => prolonged action potential and early depolarizations => polymorphic ventricular tachycardia torsades de pointes or ventricular fibrillation; often coincidental finding on ECG => requires repeat test

Diagnosis: prolonged QTc (> 440 ms); functional AV block II; detailed family history

Therapy: anti-arrhythmic therapy (Beta Blockers)

Medications that prolong QT interval are contraindicated in patients with LQTS) !

Ventricular Extrasystole (VE)

Etiology: ectopic centres in ventricles => premature QRS without preceding P wave; can be monomorphic/polymorphic; bigeminy/trigeminy (ratio of normal QRS complexes to VE)

Differential diagnosis: benign monomorphic VE; myocarditis; congenital heart disorders; cardiac tumors; catecholamines; methylxanthines

Diagnosis: wide QRS without preceding P wave => complete compensation pause

Therapy: none for benign VE (good prognosis); otherwise oral anti-arrhythmic therapy (beta blockers)

Ventricular Tachycardia (VT)

Etiology: rare neonatal arrhythmia (most cases of tachycardia with wide QRS complex fall into supraventricular tachycardia category)

Differential diagnosis: acidosis; hypoxia; electrolyte dysbalance; congenital heart disorders; cardiac tumors; genetic syndromes (LQTS)

Diagnosis: wide QRS; atrioventricular dissociation; ventricular frequency > atrial

Therapy: symptomatic VT => electric cardioversion; Adenosine is useful as it can differentiate between SVT (the most common arrhythmia) and true VT

Bradyarrhythmia

Atrioventricular Block – First Degree (AV block I)

Etiology: prolonged PR interval due to slow-down conduction through AV node; idiopathic/acquired (congenital heart disorders; myocarditis; digoxin overdose)

Diagnosis: PR interval > 110 ms

Therapy: not required (or based on the primary diagnosis)

Atrioventricular Block – Second Degree (AV block II)

Etiology: absence of QRS complexes – some atrial conduction impulses will not pass through to ventricles; idiopathic/acquired (congenital heart disorders; myocarditis; digoxin overdose)

Diagnosis: absence of QRS complex
AV block II – Mobitz I (Wenckebach) = gradual PR prolongation with following absence of QRS (defected conduction at the AV node)
AV block II – Mobitz II (Mobitz) = sudden absence of QRS complex without preceding PR prolongation

Therapy: not required (or based on the primary diagnosis); cardiostimulator can be indicated in Mobitz II

Atrioventricular Block – Third Degree (AV block III)

Etiology: complete disassociation of atrial conduction to ventricles

• congenital (immunologic disorder of mother – systemic lupus erythematodes – IgG <=> Ss-A/Ro and Ss-B/L antigens in the conduction system of fetal myocardium) => fetal cardiac failure if ventricular frequency < 60/min => hydrops fetalis
• acquired (myocarditis; cardiac surgery; congenital heart disorders)

Diagnosis: complete AV disassociation (atrial frequency usually 120-140/minute; ventricular frequency 60-80/minute); normal QRS morphology

Therapy:

• prenatal => corticosteroids; beta-2 adrenergic agonists to mother
• postnatal => cardiostimulator; in acute phase isoprenaline

Anti-arrhythmic medication

References

① Jaeggi E, Öhman A. Fetal and Neonatal Arrhythmias. Clin Perinatol. 2016;43(1):99-112. doi:10.1016/j.clp.2015.11.007