An one-year old girl presented a persistent tachycardia during a routine visit at the local pediatrician and was immediately transferred to KUNO university hospital. There had been a benign febrile infection 1 week prior to admission. Personal and family history was non-contributory to the tachycardia. Six months before, the previous check at the pediatrician had been uneventful. On admission she had mild signs of heart failure with delayed capillary refill time (3 s) and an enlarged liver. She had a tachycardia with 240 beats/min. Echocardiography showed structural normal anatomy with moderately reduced contractility while tachycardia. Laboratory studies including blood count, inflammatory biomarkers and cardiac troponin were normal but NT-proBNP was significantly elevated (maximum 2,685 pg/ml, lab reference <130 pg/ml).\nThe initial 12-lead electrocardiogram (ECG) showed a regular, sustained small-QRS-complex-tachycardia (mean heart-rate 240 beats/min). The tachycardia demonstrated a 1:1 atrio-ventricular conduction (P-P cycle length 250 ms) with a monomorphic P-wave configuration characterized by a superior axis (P-vector of −60°) and sinus tachycardia was therefore not possible. RP interval was significantly longer than PR—interval (i.e., long-RP-tachycardia) and we thought about a permanent orthodromic supraventricular tachycardia first (such as permanent junctional reciprocating tachycardia) () and gave Adenosine intravenously. This did not stop atrial tachycardia and ruled out a reentry-tachycardia dependent on the AV-node. We therefore hypothesized a focal ectopic atrial tachycardia. Infusion of Flecainide (1 mg/kg/30 min) did not affect the atrial rate or atrioventricular conduction. Synchronized electric cardioversion with 0.5 and 1 J/kg was performed due to signs of hemodynamic instability but this just interrupted the tachycardia for seconds. Medical cardioversion and rate control were attempted starting Amiodarone with a bolus. After 30 min the girl developed a second-degree AV-block (type Wenckebach) with ongoing QRS-amplitude alternans, eventually resulting in a bradycardia with 70 beats/min. Amiodarone infusion was stopped and the AV-block resolved. While persisting EAT, Esmolol infusion was started and slowly increased to a maximum rate of 75 mcg/kg/min. This lowered the atrial tachycardia rate to 160 beats/min without affecting the blood pressure. Ivabradine was started with a dose of 0.25 mg (0.025 mg/kg) every 12 h and increased to 0.5 mg (0.05 mg/kg) per dose on the second day. This led to a persistent heart rate reduction to a physiologic level (80–100 beats/min at rest) with alternating periods of restored sinus rhythm and ectopic atrial rhythm. Subsequent ECG recordings showed sinus rhythms with regular AV conduction and no abnormalities of de- or repolarization (). No adverse effects attributable to Ivabradine were registered. After stabilization Esmolol infusion was discontinued and the beta-blocker therapy was switched to Metoprolol administered orally (1 mg/kg/d). Holter evaluation before discharge (1 week after admission) showed sinus rhythm with short times of ectopic atrial rhythm and a regular diurnal pattern and heart rate.\nIn the follow up visits 2 and 10 weeks later echocardiography showed normal left-ventricular function and dimension. The 12-lead-ECG and Holter evaluation showed alternating ectopic atrial and sinus rhythm with a physiologic diurnal heart rate spectrum and a regular response to physical activity (). Combination of Metoprolol and Ivabradine did not cause bradycardia and no other side effects attributable to medication were noticed.
A 30 day old boy weighing 3 kg was referred to our pediatric intensive care unit in view of significant respiratory distress and cardiogenic shock. Physical examination revealed tachycardia (200bpm), and tachypnoea with decreased pulses and poor peripheral perfusion. Blood gas showed severe metabolic acidosis (pH 6.9; HCO3 3.6 mol/L; PCO2 15mmHg). The baby was resuscitated with intravenous fluid and sodium bicarbonate correction.The 12-lead electrocardiogram (ECG) showed a regular narrow QRS tachycardia with a rapid ventricular rate of 187 bpm with long RP interval and abnormal peaked P wave morphology.The P waves were biphasic in V1 and positive in leads II, III and aVF suggestive of EAT []. Chest radiograph showed a cardiothoracic ratio of 75%. Echocardiography showed severe left ventricular (LV) dysfunction [ejection fraction (EF) 19%] with significant LV dilatation [LVIDd 2.5cm (Z score +3.18)]. SARS-CoV-2 PCR was negative and antibodies levels were normal. Adenosine given during the tachycardia, resulted in transient termination of the tachyarrhythmia followed by reappearance []. Enteral ivabradine (0.15mg/kg) was given resulting in gradual reduction of heart rate one hour after initiation and the rhythm became sinus after 4 hours. Enteral digoxin (10mcg/kg/day) was added one hour after ivabradine. There was significant improvement in the hemodynamics and perfusion (mean BP 25 mmHg). Blood gas after stabilization revealed improvement in the metabolic acidosis (pH 7.49; HCO3 16.6 mol/L; PCO2 22mmHg). However the respiratory distress and LV dysfunction persisted. Supportive care including bubble continuous positive airway pressure, milrinone and furosemide infusion were provided for the LV dysfunction. He symptomatically improved with supportive care and it was weaned off after 24 hours. LV dimension [LVIDd 1.6cm (Z score -1.29)] and function (EF 55%) improved significantly after 72 hours. He was discharged after 5 days of hospitalization on oral ivabradine (0.15mg/kg twice a day), and digoxin (5mcg/kg twice a day). The timeline of events which happened during the first 72 hours isshown in the .