Paediatric cardiac arrest sits in SLO3 (resuscitation) and is written at day-one consultant level — you are the clinician the resus room turns to. So the testable question is rarely “what is the paediatric ALS algorithm?” It is the modification: the cause that changes the drugs, the threshold that switches a treatment on or off, and the one fact that separates a child’s arrest from an adult’s. The single most important of those facts is that most paediatric arrests are hypoxic — respiratory or circulatory failure that was missed or under-treated, ending in a bradycardic, then asystolic, collapse. The shockable rhythm is the exception, not the rule. Reverse the hypoxia early and you often prevent the arrest entirely.

This guide follows the Resuscitation Council UK (RCUK) 2025 Paediatric Life Support framework, organised by the way the exam asks it. For each topic we give the modification, the doses and thresholds worth knowing, and the consultant-level point — the reason it matters and the trap it sets. It is a high-yield working set, not the entire syllabus.

The RCUK 2025 Paediatric Life Support guidance is evolutionary, not revolutionary — it reinforces the things that change outcomes rather than overturning the algorithm. The themes worth knowing at a high level:

• Early reversal of hypoxia — most paediatric arrests are hypoxic, so high-quality oxygenation and ventilation lead the response, and the airway and breathing are prioritised before the arrest is even confirmed.
• Age-specific ventilation rates during CPR once an advanced airway is in — 25 per minute in infants, 20 over 1 year, 15 over 8 years, 10 over 12 years (the full set is in the next section).
• Waveform capnography (EtCO₂) — used throughout the arrest to confirm tracheal tube placement, gauge CPR quality, and flag ROSC by a sudden rise in EtCO₂.
• Structured use of the 4 Hs and 4 Ts to drive the search for a reversible cause, with the paediatric-specific causes (the undiagnosed metabolic or congenital child) folded in.
• Considering ECPR early in selected children — especially an in-hospital arrest with a reversible cause — rather than as a last resort.

Always revise from the current guideline. FRCEM Final questions are written and validated well ahead of each sitting (and reviewed again afterwards), but the safest approach — for the exam and for your patients — is to know the latest RCUK guidance: the doses, the thresholds, and the hypoxia-first logic.

The algorithm itself is assumed knowledge, but the exam lives in the detail around it — the numbers that define good CPR, the drug timing, the access rule, and the structured response to a child who suddenly deteriorates. Hold these as a working set.

CPR quality — the numbers that earn the mark:

• Rate 100–120 per minute.
• Depth at least one third of the AP chest diameter, and do not exceed 6 cm.
• Change the compressor at least every 2 minutes, and reassess the rhythm every 2 minutes with pauses under 5 seconds.

Compression–ventilation ratio:

• 15:2 for trained paediatric providers — in hospital that is you, so this is your ratio.
• 30:2 for those trained only in adult BLS, or untrained.
• Once an advanced airway is in, give continuous compressions with ventilation at a low-normal rate for age.

Ventilation rates with an advanced airway — an examinable list (note they fall as the child grows older):

For mechanical ventilation, use a tidal volume of 6–8 mL/kg ideal body weight at a low-normal rate for age.

Access — go intraosseous early: do not spend more than 5 minutes or two attempts on IV access before switching to intraosseous (IO) — any drug or fluid can go down it. The examinable detail is where to site it: the proximal tibia (anteromedial, just below the tuberosity) is first-line, with the distal femur, distal tibia (above the medial malleolus) or proximal humerus as alternatives.

Drug and shock timing:

In a shockable arrest the drugs go in after the 3rd shock and again after the 5th: adrenaline 10 micrograms/kg with amiodarone 5 mg/kg each time. The amiodarone is 5 mg/kg on both occasions — unlike the adult dose of 300 mg after the 3rd shock, then 150 mg.

For refractory VF/pVT, the ALS algorithm allows a stepwise increase in defibrillation energy from the 5th shock, up to a maximum of 8 J/kg (not exceeding 360 J).

The reversible causes — the 4 Hs and 4 Ts:

In a special-circumstances stem, identifying the H or T is the key. You still run the standard algorithm — but alongside it you must anticipate and treat the underlying cause. The marks are in delivering the cause-specific treatment in parallel, not just cycling the algorithm and waiting.

ECPR — consider it early. Extracorporeal CPR (extracorporeal life support during arrest) is for selected children: a witnessed in-hospital arrest, with ongoing high-quality CPR and a reversible or treatable cause, in a centre with ECMO capability. The classic candidates are a cardiac cause (post-cardiac surgery, myocarditis, an arrhythmia), refractory hypothermia, or a poisoning where the drug will clear with time. Think of it as a bridge to a definitive fix, activated early — not a last resort.

The special circumstances are the situations where the standard paediatric algorithm is deliberately modified by the cause. RCUK groups them as drowning, hypothermia, severe asthma, anaphylaxis, hyperkalaemia and metabolic causes, poisoning, and traumatic cardiac arrest — with the paediatric-specific addition of the undiagnosed child presenting in an inborn metabolic crisis or with a duct-dependent congenital heart lesion. Each is its own section below.

The common thread is the four-step read at the end of this guide: the stem signposts the cause, the observations tell you how close to arrest the child is, and the modification — the dose, the threshold, the manoeuvre — is the answer. A few worked patterns set the level:

• Child pulled from a lake, not breathing → 5 rescue breaths and 100% oxygen first — this is a hypoxic arrest.
• Core 28°C, three shocks given, still VF → hold further shocks until above 30°C, and give only a single dose of adrenaline.
• Anaphylaxis, two IM adrenaline doses, now no output → switch to IV/IO adrenaline 10 micrograms/kg on the arrest protocol; stop the IM.
• Day-7 neonate, grey, absent femoral pulses → duct-dependent lesion — prostaglandin to re-open the duct.

None of those is the standard algorithm. Each is a defensible deviation driven by the cause — and that is the level the exam is pitched at.

Drowning is a hypoxic arrest, and every modification follows from that one fact: the heart stopped from hypoxia, so the priority is to reverse it — oxygenation and ventilation lead, airway and breathing before the rhythm.

• Start with ventilation/oxygenation — give rescue breaths first (paediatric BLS starts with 5 rescue breaths) as soon as it is safe, on land or in the boat, with 100% oxygen when available.
• Apply the AED after drying the chest, and rewarm simultaneously — most drowned children are also cold.
• If arrest occurs, follow PALS modified for hypothermia (see the next section for the temperature thresholds).
• No routine abdominal thrusts — there is no role unless there is a foreign-body obstruction — and no routine c-spine immobilisation unless the mechanism suggests it (for example a dive).

Because most drownings are out-of-hospital arrests, much of the work that earns marks comes after ROSC: aspiration drives acute lung injury, so ventilate lung-protectively — start PEEP at 5 cmH₂O and titrate PEEP and FiO₂ to oxygenation, with a tidal volume of 6–8 mL/kg ideal body weight at a low-normal rate for age. And always ask why the child drowned — seizure, arrhythmia, intoxication or trauma. An untreated underlying cause may be the reason there is no ROSC.

In hypothermic arrest the drug and shock rules change with the core temperature, so the temperature itself tells you what to do — which is exactly why a question can be built around it. Measure it with a low-reading thermometer.

If you cannot measure the core temperature, the Swiss staging system grades it clinically — HT I (35–32°C, conscious and shivering), HT II (32–28°C, impaired, not shivering), HT III (28–24°C, unconscious with vital signs present), HT IV (below 24°C, vital signs absent).

Rewarm, and don’t stop until rewarmed. Use active truncal rewarming (the trunk, not the limbs), aiming for at least 1°C per hour, with warmed humidified oxygen and warmed IV/IO fluids (around 39–42°C); handle the child extremely gently and keep them horizontal — a cold, irritable myocardium can tip into VF with rough movement, so anticipate that it may arrest again, especially during rewarming. ECLS/ECPR is the route when CPR is failing or there is no ROSC in the field — transfer to an ECPR centre, and transfer the at-risk child too (P or U on AVPU, trauma, ventricular arrhythmia, hypotension).

Rewarming techniques — and roughly how fast each is (the exam may ask which is quickest):

Both are reversible causes you can often treat before the arrest — and both have a clean before/after-arrest switch the exam likes to test.

Anaphylaxis — run the algorithm in order. Recognise it (ABCDE), call for help, remove the trigger, position the patient (lie flat with legs raised; sit up if it eases breathing; a pregnant patient on her left side — and remember an adolescent can be pregnant), then give IM adrenaline.

The key move after that is that the route and dose change the instant the pulse goes. While the child still has output, give IM adrenaline by age (1 mg/mL), repeated after 5 minutes if there is no improvement, with aggressive fluids (10 mL/kg boluses, reassessing after each):

Treat the symptoms alongside (APLS): stridor → nebulised adrenaline; wheeze → nebulised salbutamol; shock → IV/IO fluid 10 mL/kg. Reassess ABCDE and repeat IM adrenaline after 5–10 minutes if there is no improvement. Steroids and antihistamines are second-line, given once the patient has stabilised.

If the child is deteriorating after two IM doses — refractory anaphylaxis but not yet arrested — establish IV/IO access, seek expert help (critical care / anaesthetics) early, and start a low-dose IV adrenaline infusion with continuous monitoring (not IV boluses, which are hazardous while there is still output), with repeated fluid boluses. Add glucagon if the child is on a beta-blocker and not responding — whether it is their own prescribed medication or an accidental overdose (a beta-blocker blunts the response to adrenaline).

Once the child arrests, switch to PALS: give IV/IO adrenaline 10 micrograms/kg on the arrest protocol — do not keep giving IM, because IM absorption is now unreliable — with aggressive fluid boluses and early CPR. These children arrest from a sudden, reversible cause having been previously well, so consider prolonged CPR and ECPR: they are exactly the group who can be salvaged.

Asthma — a hypoxic arrest with a mechanical trap. In severe or critical asthma the standard treatment should already be running: 100% oxygen, a short-acting beta-2 agonist, inhaled ipratropium, and corticosteroids; for refractory cases give IV magnesium sulphate 40 mg/kg (maximum 2 g) over 20 minutes, and escalate to NIV or intubation in near-fatal asthma.

In the asthmatic arrest two things dominate:

• Dynamic hyperinflation / gas-trapping — the “S” of DOPES. Obstructed lungs cannot empty, intrathoracic pressure climbs, venous return falls, and the child drops into PEA. Disconnect from the ventilator and manually compress the chest laterally to let the trapped air out, and reduce the rate. Ventilate slowly — a low rate of around 8–10 per minute, accepting permissive hypercapnia.
• Tension pneumothorax — high inflation pressures make it common, and often bilateral. Keep a high index of suspicion and decompress (needle or thoracostomy).

Choking — foreign-body airway obstruction (FBAO) — is a common, reversible cause of paediatric arrest with its own algorithm, and the manoeuvre differs between an infant and a child.

• Effective cough — encourage coughing and watch closely; do not intervene.
• Ineffective cough, still conscious — 5 back blows, then: an infant gets 5 chest thrusts (never abdominal — injury risk); a child over 1 year gets 5 abdominal thrusts. Reassess and repeat.
• Ineffective cough, unconscious — open the airway and look for the object (remove it if you can see it, but no blind finger sweep), then start CPR (5 rescue breaths, then compressions); check the mouth each cycle.

Once it has obstructed and arrested, this is a hypoxic arrest — oxygenation and clearing the obstruction are the priority, and laryngoscopy with Magill forceps may be needed to retrieve the object.

Severe hyperkalaemia is a potassium above 6.5 mmol/L, and the paediatric triggers differ from the adult — neonatal haemolysis, tumour lysis, crush injury, renal failure, congenital adrenal hyperplasia. The treatment runs alongside high-quality PALS and follows the same protect–shift–remove logic:

• Calcium gluconate 10% 0.5 mL/kg — protects the myocardium (does not lower potassium).
• Insulin 0.1 unit/kg (maximum 10 units) with 10% glucose 5 mL/kg — shifts potassium into cells.
• Nebulised salbutamol — further shift.
• Dialysis — the route that actually removes potassium; arrange it for the refractory or recurrent case.

The other metabolic causes sit in the same group. The one to check in every collapsed child is glucose: treat hypoglycaemia with 10% glucose 2 mL/kg, and consider a first presentation of an inborn metabolic error (the undiagnosed child, below). Briefly: hypokalaemia (D&V losses, pyloric stenosis, DKA treatment) needs IV potassium with magnesium correction; disorders of calcium and magnesium are corrected to the cause; and malignant hyperthermia means stop the trigger, cool actively, and give dantrolene.

Poisoning is an infrequent cause of paediatric arrest — suspect it once the common reversible causes are excluded — and TOXBASE/NPIS is the authority. Two rules govern it: resuscitate for a prolonged period (drug levels fall as the toxin is metabolised or excreted), and protect yourself and the team — some toxins (cyanide, hydrogen sulphide, corrosives, organophosphates) need PPE and decontamination. Support ABCDE, secure the airway early, and give antidotes where they exist.

Beta-blocker and calcium-channel-blocker toxicity is the high-yield one, and the sequence is testable: atropine, then glucagon, then HIET; add sodium bicarbonate if the QRS broadens. Two traps to avoid:

• Lipid emulsion is NOT evidence-based for beta-blocker poisoning — reserve it for local-anaesthetic toxicity. In an SBA it is the wrong answer whenever a better option (atropine, glucagon, HIET) is on the list; it is only a last-ditch consideration once everything else has failed.
• Beta-blockers cause hypoglycaemia in children, so check the glucose — it is easy to miss and easy to treat.

Expect a prolonged resuscitation and contact an ECMO/ECPR centre early — a poisoned child with a falling drug level is a candidate for bridging to recovery.

Traumatic arrest inverts the usual priority: fixing the reversible cause comes before anything else, because compressing an empty heart achieves little. Work the reversible causes — HOTT — in parallel: Hypovolaemia, Oxygenation/hypoxia, Tension pneumothorax, Tamponade.

• Tension pneumothorax — needle thoracocentesis in the 4th/5th intercostal space, anterior axillary line; but in trauma do a finger thoracostomy (bilateral in traumatic arrest), then a chest drain.
• Cardiac tamponade — urgent pericardiocentesis or resuscitative thoracotomy depending on the setting and available expertise.
• Haemorrhage — limit crystalloid (maximum 20 mL/kg), give tranexamic acid 15–20 mg/kg (maximum 1 g) IV over 10 minutes, and move to blood products.
• Hypoxia — a jaw-thrust airway and oxygenation; minimise spinal movement without hampering CPR.

Point-of-care ultrasound guides the whole sequence without interrupting compressions.

This is the section with no adult equivalent. A previously well infant or child can arrest from a first presentation of a condition you have to think of to treat — and the clue is almost always in the history.

The inborn metabolic crisis. Poor feeding, a fasting or intercurrent illness, a first presentation — check the glucose in every collapsed child and treat hypoglycaemia with 10% glucose 2 mL/kg. An undiagnosed inborn error of metabolism (or new diabetes) can present as collapse, and the glucose is the cheapest, fastest reversible cause to exclude.

The duct-dependent congenital heart lesion. A neonate who collapses as the arterial duct closes — classically around day 3 to 14 — with cyanosis not corrected by oxygen, or absent/weak femoral pulses, has a duct-dependent lesion until proven otherwise. The clues in the stem: known congenital heart disease or cardiac surgery, a family history of sudden death, a syndrome, or a cyanosis that an oxygen challenge does not fix. The peri-arrest move is prostaglandin (alprostadil) to re-open the duct — watch for apnoea — alongside cardiology and ABCDE support.

A word on PE. Pulmonary embolism is easily missed in a child but does occur — think of it with a central line, malignancy, nephrotic syndrome, or an adolescent on the combined oral contraceptive pill; thrombolyse if peri-arrest, resuscitate for a prolonged period, and consider ECMO/ECPR.

Status epilepticus — the stepwise algorithm. A prolonged seizure is a peri-arrest emergency in its own right, and it has its own algorithm (APLS / NICE):

• 0–5 min: ABC, high-flow O₂, and check the glucose — treat hypoglycaemia (10% glucose 2 mL/kg) and look for a treatable cause.
• First dose (~5 min): IV/IO lorazepam 0.1 mg/kg (max 4 mg). No IV access → buccal midazolam 0.3 mg/kg or rectal diazepam.
• Second dose (~10 min): repeat lorazepam 0.1 mg/kg — a maximum of two benzodiazepine doses (including any given pre-hospital). Get anaesthetics and specialist help (PICU / paediatric neurology) involved.
• Second-line: levetiracetam 40–60 mg/kg (max 4.5 g), or phenytoin 20 mg/kg over 20 min, or sodium valproate.
• Refractory (~20 min): rapid-sequence induction / general anaesthesia (e.g. thiopental) and intubation — call anaesthetics and PICU.

Because every step is defined, status epilepticus is reliably examinable — the exam can ask for the next drug, the exact dose, or the point at which you escalate to anaesthetics, and there is always a defensible answer.

The 2025 RCUK arrhythmia guidance asks two questions: is the rhythm fast or slow, and is the child compensated or decompensated (shocked)? Assess ABCDE, get continuous monitoring and a 12-lead ECG, and treat reversible causes.

Bradycardia in a child is usually hypoxic, so oxygenate and ventilate first — most resolve. If the heart rate stays below 60 with poor perfusion despite adequate oxygenation and ventilation, start CPR. Give adrenaline 10 micrograms/kg IV/IO; atropine 20 micrograms/kg for increased vagal tone or AV block; consider pacing for heart block; and treat the reversible cause.

Tachycardia — decide narrow-complex (SVT) versus broad-complex (VT), and compensated versus decompensated:

SVT clues: a very fast, fixed rate (>220 in an infant, >180 in a child), little beat-to-beat variability, and abnormal or absent P waves — versus sinus tachycardia, which varies and has a cause (fever, hypovolaemia, pain).

The exam hands you a paediatric scenario and asks for the next step. A reproducible four-step read gets you there reliably:

• 1. Read the stem — find the diagnosis being signposted (the cause, the H or T, the special circumstance).
• 2. Read the child’s condition — stable, deteriorating or crashing — from the observations, and read for a child, not an adult. Use age-specific ranges; bradycardia is pre-terminal in a child; look for the paediatric signs — tracheal tug, recession, grunting, the child’s appearance/colour/tone, capillary refill, and the fontanelle.
• 3. Place them on the algorithm — this gives you the immediate next step.
• 4. Read the question — what is the lead-in actually asking? Usually it is treatment; sometimes it is disposition.

A classic trap is reading the obs as if they belonged to an adult. A heart rate that is reassuring in a 40-year-old can be pre-terminal in an infant, and a falling rate in a sick child is a peri-arrest emergency, not a sign of improvement.

If you want the method behind building revision around how this specific exam works — rather than how you revised for everything else — see how I rebuilt my guideline revision for the FRCEM Final. For the adult counterpart to this guide, see adult cardiac arrest in special circumstances; and for the poisoning that underlies the toxin-driven arrests above, see our guide to toxidromes and the unknown poisoning.

Sources: Resuscitation Council UK 2025 Paediatric Life Support guidelines and the RCUK Paediatric emergency algorithms & resources (Feb 2026); APLS; TOXBASE / National Poisons Information Service (NPIS) for poisoning. Doses are a high-yield revision guide — always confirm against the BNFc.