Arrhythmia in infants and children is caused by structural heart defects, genetic ion channel disorders, heart muscle inflammation, electrolyte imbalances and in some cases no identifiable cause at all. Some are present from birth. Others develop after cardiac surgery, viral illness or as the child grows and a substrate that was always there finally declares itself under the right trigger.

“The cause matters enormously because the treatment for an arrhythmia from a repaired congenital heart is completely different to one from a channelopathy and getting that distinction right early is what stops families spending years on the wrong management,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

The cause varies significantly by age, cardiac history and whether the heart is structurally normal or not.

• Congenital heart disease: Structural defects and post-surgical scar tissue create arrhythmia substrates in chambers that were never built to manage the pressures and volumes they ended up carrying across years of abnormal haemodynamics.
• Channelopathies: Long QT syndrome, Brugada syndrome and CPVT are genetic ion channel disorders that leave the heart structurally normal on echo but electrically unstable enough to trigger ventricular fibrillation under specific physiological conditions.
• Myocarditis: Viral inflammation of the heart muscle disrupts normal conduction and creates zones of electrical instability that persist for months after the child looks and feels completely well again.
• Post-surgical substrate: Scar tissue from atrial and ventricular incisions, patches and suture lines acts as the anatomical substrate for macro re-entrant arrhythmias including incisional atrial flutter that can develop years after a technically successful repair.

Every child with a documented or suspected arrhythmia needs a systematic assessment and pediatric arrhythmia evaluation maps the structural, electrical and genetic picture before any management decision is made.

Newborn arrhythmias have distinct causes that differ substantially from those seen in older children and each carries its own urgency and treatment path.

• Accessory pathways: WPW and other accessory pathway tachycardias are among the most common causes of SVT in infants and the very fast rates they generate can cause heart failure within hours in a baby whose parents had no idea anything was wrong.
• Congenital heart block: Maternal anti-Ro and anti-La antibodies cross the placenta and damage the fetal AV node causing complete heart block that needs pacemaker implantation in symptomatic neonates who can’t sustain adequate cardiac output at the slow ventricular rate.
• Metabolic causes: Hypoglycaemia, hypocalcaemia and hyperkalaemia in sick neonates alter the electrical environment of the heart enough to produce rhythm disturbances that resolve completely once the metabolic abnormality is corrected without any antiarrhythmic treatment.
• Idiopathic neonatal SVT: Many infants develop SVT in the first months of life with no identifiable structural genetic or metabolic cause and while these often resolve by twelve months the initial presentation can be dramatic enough to need emergency cardioversion.

Parents wanting to understand how cardiac abnormalities including arrhythmia substrates are detected in the newborn period before any symptomatic episode occurs should read this piece on newborn pulse oximetry heart screening because early detection changes what management options are available before a rhythm problem declares itself with a frightening episode.

Finding the cause of arrhythmia in a child means reading the ECG in context, interpreting the Holter against the clinical history, deciding whether the echo is enough or whether genetic testing changes the management and putting all of that together into a plan that matches what this specific child’s rhythm problem actually requires. Not a protocol. A real assessment built around that one child. Dr. Prashant Bobhate has spent over 12 years managing paediatric arrhythmia across its full causal spectrum from structural post-surgical substrates through channelopathies through neonatal accessory pathway tachycardias at the Children’s Heart Centre, Kokilaben Dhirubhai Ambani Hospital.

• Arrhythmia, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/arrhythmia.html
• Arrhythmia, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/arrhythmias

Yes, a  normal resting ECG misses arrhythmias that are intermittent, exercise-triggered or only present during specific physiological states because it captures seconds of electrical activity from a heart that may only misbehave for minutes a day. A normal ECG tells you the rhythm was normal when the stickers were on. It says nothing about what happens the rest of the time.

“Parents bring in a normal ECG and think that’s the end of the investigation and I understand why but a child who faints during sport and has a normal resting ECG has not been cleared. They’ve had one test that was normal at rest. Those are completely different statements,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

More than most families realise. The ECG is twelve seconds long and arrhythmias don’t follow appointment schedules.

• Intermittent SVT: Supraventricular tachycardia episodes in children start and stop abruptly and can be completely absent at the time of an ECG meaning a child who had three episodes last week can have a perfectly normal tracing today and nobody would know from the paper alone.
• Long QT syndrome: Some long QT variants are borderline on a resting ECG especially in children whose QTc sits in the grey zone and the syndrome only declares itself as dangerous under adrenergic stress during exercise, sudden noise or emotional arousal that a resting trace never produces.
• Exercise-induced arrhythmia: Ventricular ectopics, sustained ventricular tachycardia and certain outflow tract arrhythmias only appear when heart rate rises with physical exertion and a resting ECG performed on a calm child lying still captures none of the electrical instability that exercise would immediately reveal.
• WPW with intermittent pre-excitation: In some children with Wolff-Parkinson-White syndrome the delta wave that indicates an accessory pathway is intermittent and can be absent on a resting ECG taken at a moment when normal conduction is dominant making the pathway invisible to a single snapshot investigation.

Every child with unexplained syncope, palpitations or exertional symptoms deserves more than a resting ECG and pediatric arrhythmia evaluation uses the right combination of investigations to catch what a single trace misses.

Once Tetralogy of Fallot is confirmed, the next steps focus on assessing severity, associated conditions, and planning the most appropriate treatment approach

• Severity determines urgency: A newborn with severe outflow obstruction and low saturations needs prostaglandin to keep the ductus open and urgent surgical planning while a baby with moderate obstruction and adequate saturations can be monitored and planned for elective repair in the first few months of life.
• Cardiac MRI in complex cases: When the pulmonary artery anatomy is complex or the echo leaves questions about branch pulmonary artery size or confluence a cardiac MRI or CT angiogram provides three-dimensional anatomy that guides the surgical approach in ways a two-dimensional echo can’t always match.
• Genetic testing: TOF is associated with 22q11 deletion syndrome and other chromosomal abnormalities often enough that genetic testing is recommended for every confirmed TOF newborn because the genetic result affects surgical risk, long term development planning and family counselling in ways that are missed entirely without testing.
• Surgical planning discussion: The timing, type of repair whether complete correction or a staged approach and the centre where surgery will be performed are all discussed with the family after the full diagnostic workup is complete and not before because the anatomy determines the plan not the diagnosis alone.

Parents wanting to understand what the earliest warning signs of critical cardiac disease look like in the newborn period before any formal diagnosis is made should read this piece on how to spot the early signs of heart disease in neonates because the earlier TOF is identified the more surgical options remain on the table and the less compromised the baby is when the operation happens.

A child with unexplained syncope and a normal ECG needs a cardiologist who looks at the clinical history and immediately asks what the heart is doing when it isn’t in a clinic room and who knows which of the available investigations is most likely to capture the problem given how the symptoms present. Not a repeat resting ECG. The right next test. Dr. Prashant Bobhate has spent over 12 years managing paediatric arrhythmia across the full spectrum from benign ectopics through Long QT, WPW and complex ventricular arrhythmias requiring electrophysiology study at the Children’s Heart Centre, Kokilaben Dhirubhai Ambani Hospital. Escorts Heart Institute New Delhi.

• Arrhythmia, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/arrhythmia.html
• Arrhythmia, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/arrhythmias

Tetralogy of Fallot in a newborn is confirmed primarily through echocardiography which maps all four components of the defect including the VSD, right ventricular outflow tract obstruction, overriding aorta and right ventricular hypertrophy in detail. Supporting investigations include ECG, chest X-ray and pulse oximetry and together these give the cardiac team everything needed to plan surgical timing before the baby deteriorates.

“TOF in a newborn doesn’t always present dramatically. Some babies are pink enough to pass a routine examination and the diagnosis only comes when someone does an echo because the saturations were borderline or the murmur was unusual. That’s exactly why pulse oximetry screening in every newborn matters so much,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

Each investigation adds a different layer and together they build the full picture the surgical team needs before any planning conversation happens.

• Echocardiography: The definitive test that maps the VSD size and location, measures the degree of right ventricular outflow tract obstruction, assesses pulmonary valve and artery anatomy and confirms the aortic override in enough detail to plan the surgical approach entirely from echo alone in most cases.
• Chest X-ray: The classic boot-shaped cardiac silhouette from right ventricular enlargement and a concave pulmonary artery segment is often visible and reduced pulmonary vascular markings indicate reduced pulmonary blood flow that tells the team how obstructed the outflow actually is before the echo even begins.
• ECG: Shows right ventricular hypertrophy with right axis deviation in most TOF cases and while it doesn’t confirm the anatomy it adds supporting electrical evidence and helps the team assess rhythm and conduction before planning anaesthesia and surgery.
• Pulse oximetry: A pre and post-ductal saturation screen flags the oxygen desaturation pattern that TOF produces and in newborns where cyanosis isn’t yet visually obvious pulse oximetry is often the first investigation that pushes the neonatal team toward urgent cardiology referral rather than watchful observation.

Every newborn with a suspected or confirmed TOF diagnosis needs a detailed structural assessment and tetralogy of fallot evaluation maps the anatomy, the haemodynamic severity and the surgical timeline before any management decision is made.

Once Tetralogy of Fallot is confirmed, the next steps focus on assessing severity, associated conditions, and planning the most appropriate treatment approach

• Severity determines urgency: A newborn with severe outflow obstruction and low saturations needs prostaglandin to keep the ductus open and urgent surgical planning while a baby with moderate obstruction and adequate saturations can be monitored and planned for elective repair in the first few months of life.
• Cardiac MRI in complex cases: When the pulmonary artery anatomy is complex or the echo leaves questions about branch pulmonary artery size or confluence a cardiac MRI or CT angiogram provides three-dimensional anatomy that guides the surgical approach in ways a two-dimensional echo can’t always match.
• Genetic testing: TOF is associated with 22q11 deletion syndrome and other chromosomal abnormalities often enough that genetic testing is recommended for every confirmed TOF newborn because the genetic result affects surgical risk, long term development planning and family counselling in ways that are missed entirely without testing.
• Surgical planning discussion: The timing, type of repair whether complete correction or a staged approach and the centre where surgery will be performed are all discussed with the family after the full diagnostic workup is complete and not before because the anatomy determines the plan not the diagnosis alone.

Parents wanting to understand what the earliest warning signs of critical cardiac disease look like in the newborn period before any formal diagnosis is made should read this piece on how to spot the early signs of heart disease in neonates because the earlier TOF is identified the more surgical options remain on the table and the less compromised the baby is when the operation happens.

A pre-travel cardiac assessment for a child with CHD isn’t a rubber stamp. It’s a look at the current echo, the current saturations, the specific destination, the flight duration and the medical facilities available at the other end and then an honest answer about whether this trip is safe as planned or needs modification. Dr. Prashant Bobhate has spent over 12 years advising families with paediatric cardiac conditions on travel safety, pre-travel oxygen assessment and emergency planning across the full spectrum of congenital and pulmonary vascular disease at the Children’s Heart Centre, Kokilaben Dhirubhai Ambani Hospital.

• Tetralogy of Fallot, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/001567.htm
• Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects

In premature babies a patent ductus arteriosus causes a left-to-right shunt that floods the lungs with excess blood flow and strains a heart not yet ready to manage it. Common symptoms include fast breathing, difficulty weaning off ventilator support, poor feeding, bounding pulses and a heart murmur picked up on routine neonatal examination.

“PDA in a term baby is often a watch and wait situation. PDA in a 28-weeker who can’t come off respiratory support is a completely different clinical problem and the urgency of the decision is something families and neonatal teams sometimes underestimate until they’re already in trouble,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

They overlap with everything else a premature baby is dealing with and that overlap is exactly what makes PDA the diagnosis that gets attributed to prematurity alone until someone looks specifically for it.

• Respiratory difficulty: A premature baby with a significant PDA struggles to wean off oxygen or ventilator support because pulmonary overcirculation keeps the lungs fluid-loaded and the respiratory team keeps waiting for improvement that isn’t coming from ventilator adjustments alone.
• Bounding pulses: The widened pulse pressure from a large left-to-right PDA shunt produces strong bounding peripheral pulses that feel distinctly different on clinical examination from the normal pulses of a baby without a significant shunt running.
• Heart murmur: A continuous machinery-type murmur audible at the left upper sternal border is the classic PDA finding though in very premature babies the murmur can be soft, intermittent or absent entirely even when the shunt is haemodynamically significant.
• Poor weight gain: A premature baby working harder than expected to breathe because of pulmonary overcirculation burns calories the body can’t keep replacing and persistent poor weight gain despite apparently adequate nutrition is one of the signs that prompts a cardiac look in the NICU.

Every premature baby with suspected PDA needs a formal echocardiographic assessment and patent ductus arteriosus evaluation maps the shunt size, the pulmonary blood flow and the haemodynamic impact before any treatment decision gets made.

It depends entirely on size, gestational age, and haemodynamic significance

• Watchful waiting: Small PDAs in more mature premature babies with minimal symptoms are often managed conservatively because spontaneous closure remains possible and unnecessary treatment in a borderline case carries its own risks that conservative management avoids.
• Medications: Indomethacin and ibuprofen promote ductal closure through prostaglandin inhibition and are used in premature babies with haemodynamically significant PDAs before considering any procedural intervention when the clinical picture and gestational age make pharmacological closure appropriate.
• Catheter closure: Transcatheter device closure is now feasible in very small premature infants at experienced centres and avoids the risks of open surgical ligation in a baby already compromised by prematurity, respiratory disease and the other complications of very early birth.
• Surgical ligation: Still used when catheter closure isn’t feasible due to anatomy or weight and when the haemodynamic burden of the PDA is causing enough pulmonary and cardiac compromise that waiting for spontaneous closure or medication response is no longer clinically appropriate.

Parents wanting to understand what cardiac warning signs in neonates look like beyond what the NICU team has already identified should read this piece on how to spot the early signs of heart disease in neonates because the overlap between prematurity symptoms and cardiac symptoms is exactly what delays PDA diagnosis in babies who needed earlier intervention.

A premature baby with a significant PDA needs a neonatologist and paediatric cardiologist working together not separately and the cardiologist needs to have read enough neonatal echos to know what a haemodynamically significant PDA looks like in a 900-gram baby on high-frequency ventilation rather than in a textbook diagram. Dr. Prashant Bobhate has spent over 12 years performing neonatal echocardiography and managing PDA in premature infants across every gestational age and every level of haemodynamic compromise at the Children’s Heart Centre, Kokilaben Dhirubhai Ambani Hospital.

• Patent Ductus Arteriosus, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/001560.htm
• Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects

Cardiac catheterization in children is a minimally invasive and generally safe procedure performed under sedation or general anaesthesia, in which a thin tube called a catheter is guided through blood vessels into the heart for diagnosis or treatment. It usually allows faster recovery than surgery, with most children discharged within 24 hours, while the main risks involve minor bleeding or infection at the insertion site.

“Most parents hear the word catheterization and imagine something close to open heart surgery and the relief when I explain what it actually involves is something I see at almost every pre-procedure appointment. It’s a very different conversation to the one they were bracing for” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

Structured, precise and very different from the open surgical procedures most families confuse it with when they first hear the recommendation.

• Access site preparation: A needle punctures the femoral vein or artery in the groin under sterile conditions and a sheath is placed through which catheters of different sizes can be exchanged throughout the procedure without repeated punctures at the access site.
• Catheter navigation: The catheter is advanced through the vascular system into the right or left heart chambers under continuous fluoroscopic X-ray guidance and the operator steers it to specific locations inside the heart to take the measurements or perform the intervention the procedure was planned for.
• Pressure and oxygen measurements: In a diagnostic catheterization pressures in each cardiac chamber and the great vessels are recorded alongside oxygen saturations to calculate pulmonary vascular resistance, identify shunts and determine whether intervention is indicated and at what timing.
• Therapeutic interventions: In an interventional catheterization the same access allows balloon dilatation of a narrowed valve, deployment of a device to close an ASD or VSD, coil embolisation of an abnormal vessel or stenting of a narrowed pulmonary artery all without touching the chest wall.

Understanding the full range of what catheter-based procedures can achieve in children and when they are the right approach over surgery is exactly what a thorough interventional pediatric cardiology assessment maps out before any procedure date is set.

Lower risk than surgery, but not zero risk, which is why it is important to understand it clearly before the procedure day

• Access site complications: Bruising, minor bleeding and in rare cases a haematoma or arterial spasm at the femoral puncture site are the most common post-procedure issues and are managed conservatively with pressure and rest in almost every case without additional intervention.
• Arrhythmia during the procedure: The catheter moving through heart chambers can trigger transient rhythm disturbances that the monitoring team manages immediately and which almost always resolve spontaneously once the catheter is repositioned away from the area that triggered them.
• Radiation exposure: Fluoroscopic guidance uses X-ray and paediatric catheterization laboratories use dose minimisation protocols specifically designed for children but families should know that radiation exposure is part of the procedure and the clinical benefit is always weighed against it before recommending catheterization.
• Recovery timeline: Most children spend four to six hours in a monitored recovery area after an uncomplicated catheterization, go home the same day or the following morning and return to normal activity within three to five days with the access site avoiding significant physical strain for one week.

Parents wanting to understand what cardiac warning signs look like in children in the days after any cardiac procedure should read this piece on top 5 warning signs of pediatric heart failure because knowing what to watch for at home is as important as understanding what happened in the catheterization laboratory.

A paediatric cardiac catheterization in the right hands is a precise, low-risk procedure that achieves things in an hour that would otherwise require open heart surgery and weeks of recovery. In less experienced hands the same procedure carries higher complication rates, longer procedure times and outcomes that don’t justify the risk. The operator matters as much as the indication. Dr. Prashant Bobhate has spent over 12 years performing diagnostic and interventional cardiac catheterizations across the full range of congenital defects including ASD and VSD device closure, balloon valvuloplasty, pulmonary artery stenting and India’s first transcatheter Potts shunt at the Children’s Heart Centre, Kokilaben Dhirubhai Ambani Hospital. Escorts Heart Institute New Delhi.

• Cardiac Catheterization, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/003419.htm
• Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects