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)

ARRHYTHMIA – DIVISION

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)

Etiologyectopic 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)

Diagnosisabnormal 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)

Therapyusually 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)

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)

Atrial Ectopic Tachycardia (AET)

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

Diagnosisabnormal 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)

Etiologythe most common (incidence 1:25 000) symptomatic arrhythmia (paroxysmal supraventricular tachycardia = SVT) in newbornsSVT 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

Diagnosisventricular 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 SVY 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)

Etiologyreentry pathway in the atria => reentrant tachycardia; typical for fetal and neonatal period => cardiac failure => hydrops fetalis

Atrial fibrillation is rare in newborns

Diagnosisatrial frequency 300-400/minutesawtooth 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)

Etiologychronic form of AVRT – only retrograde conduction through the accessory pathway

Diagnosisnegative P waves in II, III, aVF leadsnormal QRSlong 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)

Etiologyrare arrhythmia based on abnormal automation of cells within AV junctioncongenital (requires chronic medication in order to prevent cardiac failure) and acquired form (after cardio surgery)

Diagnosisnormal QRSventricular 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)

Etiologyrare 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

Diagnosisprolonged 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)

Etiologyectopic 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

Diagnosiswide 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)

Etiologyrare 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)

Diagnosiswide QRS; atrioventricular dissociation; ventricular frequency > atrial

Therapysymptomatic VT => electric cardioversionAdenosine is useful as it can differentiate between SVT (the most common arrhythmia) and true VT

BRADYARRHYTHMIA

Atrioventricular Block – First Degree (AV block I)

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

DiagnosisPR interval > 110 ms

Therapynot required (or based on the primary diagnosis)

Atrioventricular Block – Second Degree (AV block II)

Etiologyabsence 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

Therapynot required (or based on the primary diagnosis); cardiostimulator can be indicated in Mobitz II

Atrioventricular Block – Third Degree (AV block III)

Etiologycomplete 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

DRUGINTERMITTENTCONTINUOUS
Adenosine0.1 – 0.3 mg/kg IVNA
Amiodarone2.5 – 5.0 mg/kg IV10 – 15 μg/kg/min IV
Atropine0.02 – 0.03 mg/kg IVNA
Digoxin0.02 mg/kg/day PO0.005 mg/kg/day PO
IsoprenalineNA0.01 – 0.50 μg/kg/min IV
Lidocaine1 mg/kg IV20 – 50 μg/kg/min IV
Propafenone0.5 – 1.0 mg/kg IVNA
Sotalol60-180 mg/m²/day PONA

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

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