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Not one thing. That’s the first thing to understand. Arrhythmia in children covers a whole family of conditions where the heart beats too fast, too slow or just plain irregularly and each type has a different cause, a different risk level and a completely different treatment path that needs to be mapped out carefully.

“Parents hear the word arrhythmia and immediately imagine the worst. But some of these rhythm problems are completely benign and some genuinely need treatment fast and knowing which one you’re dealing with changes everything about what happens next,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

Most arrhythmias in children don’t come with a dramatic presentation. A child complains of a fluttering in the chest. A parent notices the heart racing for no obvious reason at rest.

• SVT: Supraventricular tachycardia is the single most common significant arrhythmia in children. The heart suddenly races to 200 or even 300 beats per minute out of nowhere, episodes start and stop abruptly and children often describe a pounding sensation in the chest or throat that’s hard to put into words.
• Sinus bradycardia: The heart beats slower than normal for the child’s age. In fit athletic teenagers this is often completely normal but in younger children or those with underlying cardiac conditions a persistently low rate needs proper evaluation rather than casual reassurance.
• Heart block: The electrical signal from the upper chambers to the lower ones gets delayed or completely interrupted somewhere along its path. Some degrees of heart block need no treatment and others eventually need a pacemaker depending entirely on how severely the conduction is affected.
• Ventricular tachycardia: Rarer in children than SVT but significantly more serious when it appears. The rhythm originates from the lower chambers and can compromise cardiac output rapidly so this one never gets the watchful waiting approach that some others can afford.

If your child has been told they have an abnormal heart rhythm, a full evaluation at a dedicated pediatric arrhythmia centre is what gives you a real understanding of the type, the risk and the best next step.

Yes. And that’s the part families most need to hear. Some rhythm abnormalities sit quietly for years, behave themselves on every routine ECG and then show up differently under physical or emotional stress. 

• Long QT syndrome: The ECG shows a prolonged interval between two specific waveforms and on paper it can look like almost nothing. But in the wrong circumstances, exercise, a sudden loud noise, even swimming, it can trigger a dangerous rhythm that produces sudden cardiac arrest without any prior warning at all.
• WPW syndrome: An extra electrical pathway exists between the upper and lower chambers that wasn’t there by design. Most children with WPW live completely normally and never know it’s there until an ECG catches it but a subset can develop very fast rhythms under certain conditions that do need catheter ablation to fix properly.
• Ectopic beats: Isolated extra beats that feel like a thump or a skip in the chest are extremely common in children, often completely benign and frequently more distressing to the parent than to the cardiac conduction system. But frequent ectopics deserve at least one proper evaluation to confirm there’s no structural issue sitting underneath them.
• Junctional rhythm: The heart’s pacemaker activity shifts from the sinus node to the junction between chambers, usually because the sinus node is firing too slowly. Often discovered incidentally, rarely symptomatic on its own but always worth understanding in the context of whether it’s truly isolated or a signal of something else.

Parents wondering what cardiac warning signs sometimes precede an arrhythmia diagnosis in children should read this piece on how to spot the early signs of heart disease in neonates because the patterns that show up in newborns are often the earliest version of what gets formally identified years later.

You want someone who has seen every version of this. Not just the textbook ones but the child whose SVT only triggers during school exams and the teenager whose WPW sat silently for three years before one football match changed the picture entirely. Dr. Prashant Bobhate has spent over 12 years working across the full spectrum of paediatric cardiac conditions including complex arrhythmia presentations at every age from newborn through adolescence. Trained at Escorts Heart Institute New Delhi and completed advanced fellowship at the University of Alberta Canada with focused exposure to paediatric electrophysiology alongside structural disease.

• Ventricular Septal Defect, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/001099.htm
• Ventricular Septal Defect, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects

The signs most parents miss are the quiet ones. Bluish skin around the lips, a baby who tires during feeds, breathing that seems too fast even at rest and weight that just won’t come on the way it should. These aren’t always obvious in the first days home. But they’re there if you know what you’re actually looking at.

“Most cardiac signs in newborns don’t announce themselves dramatically. They show up in how the baby feeds, breathes and grows and parents often sense something is off long before anyone puts a name to it,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

The earliest signs don’t look cardiac to most people. They look like a difficult baby. A fussy feeder. 

• Blue colour: A persistent bluish tint around the lips, tongue or fingertips especially during feeding, crying or any kind of effort is the clearest cardiac red flag a newborn can show you and it needs same day assessment not a wait and see.
• Fast breathing: A resting respiratory rate consistently above 60 breaths per minute in a calm settled baby means the lungs are handling more than they should and the heart behind them deserves a proper look without delay.
• Feeding trouble: A baby who sweats during feeds, pulls away repeatedly, takes over 30 minutes to finish a small amount or falls asleep exhausted mid-feed is burning calories the heart can’t keep replacing under the extra circulatory load it’s carrying.
• Poor weight gain: A newborn dropping off their growth curve in the first weeks despite seemingly adequate feeding and no obvious gut reason is often showing you chronic cardiac strain from the outside before any other sign has made itself obvious.

Getting an echocardiogram done properly by someone who knows exactly what a newborn heart should look like is what a proper congenital heart disease assessment does before the window for the easiest intervention quietly closes.

Because there’s a difference between a baby who needs to be seen this week and one who needs to be seen today. Some signs sit in the background for weeks. 

• Grey or mottled skin: A newborn whose skin looks grey, blotchy or mottled rather than just pale is showing you that circulation has already become compromised and that’s a same hour emergency not a tomorrow morning phone call.
• Grunting with every breath: A baby who grunts audibly at the end of each breath is working so hard to keep their lungs open that the body is recruiting every mechanism it has left and that kind of effort can’t be sustained for long.
• Rapid heart rate at rest: A resting heart rate persistently above 160 in a quiet sleeping newborn without fever or obvious cause is the heart telling you it’s compensating for something it can’t keep compensating for indefinitely on its own.
• Puffy face or limbs: Swelling around the eyes, face or feet in a newborn that isn’t positional or feeding related can mean the heart is already failing to manage fluid in the way a newborn heart should and that needs immediate evaluation.

Parents who want to understand exactly what the newborn cardiac warning signs look like in those first fragile weeks should read this piece on how to spot the early signs of heart disease in neonates because the earlier someone identifies what’s happening the more options there are for what comes next.

A newborn with a suspected heart problem needs someone who has read hundreds of neonatal echos, knows what critical pulmonary stenosis looks like on day two of life and can make a management call without waiting for a committee. Dr. Prashant Bobhate spent over 12 years working across every age and complexity of congenital heart disease from fetal diagnosis through neonatal critical presentations through long term follow up into adulthood. Trained at Escorts Heart Institute in New Delhi then went deliberately to the University of Alberta in Canada for advanced paediatric cardiac fellowship training

• Congenital Heart Defects, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/congenitalheartdefects.html

Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects

Nobody knows. That’s the real answer. Idiopathic pulmonary hypertension means the lung arteries narrow and stiffen for reasons medicine still can’t fully explain and the right heart quietly pays the price for it every single day. Symptoms show up late. By then the damage has usually been building for a long time already.

“I tell families the same thing every time. We don’t yet know exactly why this started. But I also tell them that not knowing the cause doesn’t stop us from treating the disease aggressively and that part we’re very good at,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

The cause is a blank. But what happens inside those vessels once the disease starts is well mapped and understanding it is what actually drives every treatment decision. It’s not mysterious. It’s just slow, silent and relentlessly progressive if nobody catches it in time.

• Walls closing in: The smooth muscle inside small lung arteries grows in a way it absolutely shouldn’t, walls thicken from the inside out and the space blood has left to travel through shrinks with every week that passes without intervention.
• Lining stops cooperating: The inner surface of those arteries switches from producing chemicals that keep vessels open and relaxed to producing the ones that constrict and stiffen them. That switch happens silently and nobody feels it while it’s happening.
• Clots pile on: Tiny clots form inside vessels that are already narrowed, blocking what little flow was getting through and adding resistance the right ventricle now has to push against on top of everything else it’s already fighting.
• Right heart hits its limit: The right ventricle was never built for high pressure work. It thickens trying to cope, then enlarges, then eventually fails because nothing pushed that hard for that long comes out the other side undamaged.

What your pressures look like right now and what that’s already done to your right heart is exactly what a thorough pulmonary hypertension evaluation puts on the table before any treatment decision gets made.

Idiopathic doesn’t mean random. There are real patterns. Certain genes, certain biological profiles, certain triggers all seem to push some people’s lung vessels into disease while everyone around them stays fine. The why behind that isn’t fully solved yet. But the patterns are real and they matter.

• BMPR2 mutations: This gene normally tells pulmonary vessel cells when to stop growing. When it’s mutated that signal breaks down and cells grow where and when they shouldn’t. It shows up in enough idiopathic cases that anyone newly diagnosed deserves genetic counselling.
• Mostly women: The numbers are stark. Women develop idiopathic PH at significantly higher rates than men. Hormones are almost certainly involved but the exact mechanism is still being worked out and that research is ongoing.
• Immune system gone quiet and wrong: Some patients have subtle immune abnormalities alongside their PH. Nothing dramatic enough to flag on its own. But enough to suggest their immune system may be quietly contributing to inflammation inside vessels nobody can see without a catheter.
• Wrong drug at the wrong time: Certain older appetite suppressants and stimulants triggered PH in people whose pulmonary vasculature was already sitting on a genetic edge. The external trigger didn’t cause the susceptibility. It just pushed it over.

If you want to see where untreated pulmonary pressure eventually lands people, this piece on when is lung transplant necessary for pulmonary hypertension is worth reading because that outcome is preventable when the right assessment happens early enough.

Idiopathic PH is not a condition that rewards generalist management or cautious watching from a distance. It rewards expertise, urgency and a team that’s been doing this long enough to know what aggressive early treatment actually buys a patient in years of better function. Dr. Prashant Bobhate built his practice around pulmonary hypertension specifically. Over 12 years managing every form it arrives in, idiopathic, genetic, congenital, across children and adults at every disease stage. He founded Western India’s only dedicated multidisciplinary paediatric PH clinic at Kokilaben Hospital. Over 400 patients are actively on advanced therapy under his care right now.

• Pulmonary Hypertension, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/pulmonaryhypertension.html
• Pulmonary Arterial Hypertension, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/pulmonary-hypertension

Balloon pulmonary valvuloplasty opens a narrowed pulmonary valve using a thin catheter guided through a vein in the groin. No chest opening. No surgical scar. A small balloon inflated across the tight valve splits it open and lets blood flow properly from the right ventricle to the lungs again. Most children go home the next morning like nothing major happened.

“Families come in expecting surgery and leave realising they don’t need it. For pulmonary stenosis, the balloon procedure is genuinely smaller than the diagnosis feels and the results speak for themselves,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

There’s no operating theatre involved. No incision. The whole thing happens through a small puncture in the groin vein and the child is usually up and asking for food by the next morning. That’s genuinely what recovery looks like for most families who come in braced for something far heavier.

• Vein access: A thin catheter goes in through the femoral vein in the groin and travels up through the right side of the heart under live X-ray until it sits right at the narrowed pulmonary valve waiting to be opened.
• Balloon inflation: The deflated balloon on the catheter tip gets positioned carefully across the tight valve, inflated briefly to split the fused leaflets apart and then deflated and removed once the job is done.
• Pressure check: Before and after inflation the team measures the pressure gradient directly across the valve to confirm the narrowing is genuinely gone and the right ventricle isn’t still straining against anything.
• Quick recovery: Most kids are observed overnight and home the next day with no stitches, no wound care, no surgical recovery and parents who can’t quite believe it went that smoothly.

Whether your child’s valve is suitable for balloon treatment or needs something different is exactly what a proper pediatric balloon valvuloplasty assessment figures out with echo and catheter data before anyone touches anything.

The procedure itself takes a couple of hours. What happens to the right heart over the next few months is what families actually want to know. And honestly it’s one of the better answers in paediatric cardiology when the timing was right and the valve responds the way it should.

• Pressure drop: The moment that valve opens properly the right ventricle stops fighting against it and the pressure it was generating to push blood through drops significantly within days of a successful procedure.
• Muscle recovery: The right ventricular wall that thickened trying to push through a tight valve for months or years slowly normalises once it’s no longer working under that kind of strain.
• Better stamina: Kids who were tired, breathless or just noticeably slower than their peers often show real change within weeks as the right heart starts working the way it was supposed to all along.
• Echo follow up: Regular echos in the year after track how completely the gradient has resolved and catch any early restenosis before it becomes significant enough to need another procedure.

Parents wanting to understand what an overworked right heart actually looks like before it reaches crisis point should read this piece on top 5 warning signs of pediatric heart failure because catching pressure overload early is what keeps the balloon procedure an option rather than something more complex.

Catheter procedures on children’s hearts aren’t something you want done by someone who does them occasionally. Balloon sizing, inflation pressure, reading the gradient tracings in real time and knowing when enough is enough comes from doing this regularly and doing it well. Dr. Prashant Bobhate spent over 12 years performing catheter-based interventions across every age from newborns with critical pulmonary stenosis through older children who came in late with moderate gradients nobody had acted on. Trained at Escorts Heart Institute in New Delhi then went specifically to the University of Alberta in Canada for advanced paediatric cardiac fellowship training.

• Pulmonary Valve Stenosis, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/001096.htm
• Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects

Fetal echo is the most detailed cardiac scan available before birth and detects the majority of significant structural heart defects when performed between 18 and 24 weeks by an experienced specialist. But it doesn’t catch everything. Some defects are simply too small to see in utero, others only develop or become visible after birth when the circulation changes.

“Fetal echo done well gives families a remarkable head start. But it’s an honest tool not a perfect one and parents deserve to understand both what it finds reliably and what it can sometimes miss,” says Dr. Prashant Bobhate, Pediatric Cardiologist in Mumbai, India.

The conditions fetal echo picks up most consistently are the ones that change the heart’s structure in ways visible on ultrasound at 18 to 24 weeks.

• Large VSDs: A significant hole between the lower chambers changes the appearance of the ventricular septum in a way that’s visible on a careful fetal echo sweep at the right gestational age.
• TOF: The overriding aorta and outflow tract abnormality that defines Tetralogy of Fallot can be picked up on fetal echo when the operator specifically examines the outflow tract views rather than relying on the four chamber view alone.
• Hypoplastic left heart: This severe underdevelopment of the left side of the heart creates such a striking asymmetry between the two ventricles that it’s one of the most reliably detected defects in prenatal screening.
• Major valve defects: Severe pulmonary or aortic valve stenosis, Ebstein’s anomaly and other significant valve abnormalities that alter chamber size or blood flow patterns show up clearly on a detailed fetal cardiac assessment.

Getting that assessment done properly by someone who knows exactly what all the outflow views look like is exactly what fetal echocardiography in the right hands is built to deliver before birth changes everything about the options available.

This is the part most parents don’t get told clearly enough. Not because doctors are hiding anything but because the honest answer is more complicated than a simple yes or no. Some defects are genuinely invisible before birth. Others look normal at 20 weeks and only declare themselves after delivery when the newborn circulation shifts.

• Small VSDs: Tiny muscular holes in the ventricular septum are often below the resolution of prenatal ultrasound and are picked up for the first time on a postnatal echo done because a murmur was heard after birth.
• Small ASDs: Most ASDs are functionally normal in fetal life because the foramen ovale is supposed to be open in utero which makes distinguishing a normal structure from a pathological one genuinely difficult before birth.
• Coarctation: Narrowing of the aorta can be suggested on fetal echo but is notoriously difficult to confirm definitively before birth because fetal circulation patterns make the aortic arch look different than it will postnatally.
• Arrhythmias: Electrical rhythm problems in the fetal heart aren’t structural findings and need specific fetal cardiac rhythm assessment which is a separate layer of evaluation beyond the standard anatomy scan.

Parents who want to understand why early fetal cardiac diagnosis changes outcomes so significantly should read this detailed piece on the importance of fetal diagnosis of critical congenital heart disease which explains exactly what early detection makes possible that a postnatal surprise doesn’t.

A fetal echo is only as good as the person reading it. The scan takes the right equipment and the right gestational timing but what actually determines what gets found and what gets missed is the experience sitting behind the probe. Dr. Prashant Bobhate spent over 12 years working across the full arc of congenital heart disease from fetal diagnosis through neonatal presentation through surgical planning and long term follow up. That means when he reads a fetal echo he already knows what the postnatal heart looks like and exactly what a subtle prenatal finding means for the delivery plan, the nursery team and the family sitting in front of him.

• Fetal Echocardiography, MedlinePlus, U.S. National Library of Medicine — https://medlineplus.gov/ency/article/003405.htm
• Congenital Heart Defects, National Heart Lung and Blood Institute — https://www.nhlbi.nih.gov/health/congenital-heart-defects