Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Respiratory failure and escalation
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Decompensated respiratory failure
Bradypnoea, irregular breathing, apnoea, a silent or poorly moving chest, severe hypoxaemia, hypercapnia, cyanosis, exhaustion, bradycardia or reduced consciousness indicates inadequate gas exchange and imminent arrest.
Action: Call the paediatric resuscitation, anaesthetic and critical-care team, open and maintain the airway, give 100% oxygen initially and support inadequate ventilation with a two-person bag-mask technique. Treat immediately reversible obstruction or tension pneumothorax, attach continuous oximetry and ECG, and prepare a supraglottic or tracheal airway without allowing an intubation attempt to interrupt effective oxygenation.
Overview
Distinguish respiratory distress from failing oxygenation or ventilation, identify the anatomical and physiological cause, support breathing in an ordered sequence, and escalate from oxygen to bag-mask ventilation, non-invasive support or a protected advanced airway before exhaustion becomes arrest.
Observe before upsetting the child. Note interaction, voice or cry, position, audible sounds, respiratory rate, recession, nasal flare and colour. Then assess chest movement, symmetry, air entry and added sounds, oxygen saturation, heart rate and consciousness. A young child may not describe dyspnoea; poor feeding, pauses, head bobbing, weak cry and reduced responsiveness can be the decisive features.
Distress and failure are physiological stages rather than diagnoses. A tachypnoeic wheezing child who remains alert with good chest excursion may compensate; one who becomes drowsy with a silent chest is failing even if recession appears less dramatic. RCUK advises using multiple variables and trends because no isolated saturation, carbon dioxide or respiratory rate defines failure in every child.
Practice
Two practice questions
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Paediatrics and child healthOriginal SBA
Apparent improvement with fatigue
A child with severe respiratory distress becomes quieter. Recession is less visible, but air entry is now minimal, respiratory rate is falling and the child is drowsy. What is the best interpretation?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Airway comes first. Let a conscious child choose the easiest position. Open the airway with head tilt and chin lift or jaw thrust when appropriate, clear only visible material and suction secretions carefully. Use an oropharyngeal or nasopharyngeal adjunct for reduced consciousness when suitable. Stridor, drooling or swelling requires early anaesthetic and ENT help with minimal agitation.
Give 100% oxygen initially in respiratory, circulatory or neurological failure. If breathing is ineffective, do not wait for a gas: use bag-mask ventilation as the first-line method. A two-person technique improves seal and jaw position. Deliver a long enough inspiration for mild visible chest rise, then allow exhalation; excessive rate or volume causes air trapping, gastric distension and reduced venous return.
Escalation is based on response. Conventional oxygen that does not achieve adequate oxygenation can progress to high-flow nasal oxygen or non-invasive ventilation when drive, airway protection and haemodynamics remain adequate. Deteriorating consciousness, apnoea, severe fatigue, refractory hypoxaemia, uncontrolled hypercapnia or an unprotected airway usually needs invasive support with PICU and anaesthesia.
Tracheal intubation is a high-risk physiological procedure. Pre-oxygenate, prepare drugs and a difficult-airway rescue plan, use video or direct laryngoscopy according to competence and stop an attempt immediately for desaturation or bradycardia. RCUK limits attempts to four and each attempt to 30–60 seconds. Return to bag-mask or a supraglottic device between attempts rather than persisting without oxygenation.
After stabilisation, identify the mechanism through focused history, blood gas and cause-directed imaging or tests. Review medication exposure, neuromuscular function, infection, aspiration and trauma. In chronic respiratory or cyanotic cardiac disease, use the child's baseline and specialist target rather than imposing a generic saturation. Renal and hepatic dysfunction affect sedative and opioid clearance and heighten post-procedure monitoring needs.
Recovery includes more than extubation. Reassess swallowing, voice, mobility, sleep, feeding and school participation, and review the family emergency plan for tracheostomy, neuromuscular or chronic lung disease. A critical-care admission can be traumatic; explain the escalation sequence and offer psychological and rehabilitation follow-up where function has changed.
Key points
Respiratory distress has increased effort with preserved effectiveness; failure has inadequate oxygenation or ventilation, fatigue, altered consciousness or cardiovascular compromise.
Assess work, effectiveness and systemic effect: rate, recession, sounds, position, chest excursion, air entry, saturation, colour, heart rate and consciousness.
Falling respiratory effort is dangerous when chest movement, air entry or alertness also declines.
First-line emergency management is airway positioning, suction of visible secretions when needed, 100% oxygen for failure and immediate support of inadequate ventilation.
Bag-mask ventilation is the first-line ventilation method; use correct head position, a suitable mask, airway adjunct and preferably a two-person seal.
Aim for mild visible chest rise at an age-appropriate rate and avoid excessive volume, pressure and gastric inflation.
Once saturation is reliable, titrate oxygen to 94–98% in a previously healthy child using the lowest FiO2 that achieves the target.
High-flow nasal oxygen or non-invasive ventilation can be considered when conventional oxygen is inadequate and respiratory drive is still sufficient.
Use a supraglottic airway or tracheal tube early when bag-mask support is ineffective or prolonged ventilation is expected; oxygenation remains the priority during airway attempts.
Aetiology
01
Airway obstruction
Foreign body, croup, anaphylaxis, infection, secretions, trauma and tracheostomy blockage restrict airflow and can deteriorate abruptly.
02
Lower-airway or parenchymal disease
Asthma, bronchiolitis, pneumonia, pulmonary oedema and acute lung injury cause ventilation-perfusion mismatch, air trapping or diffusion failure.
03
Respiratory-pump failure
Neuromuscular weakness, spinal disease, fatigue, sedative or opioid toxicity and central neurological injury reduce effective tidal volume or drive.
04
Mechanical or vascular cause
Pneumothorax, pleural fluid, diaphragmatic dysfunction, pulmonary hypertension and embolic disease can significantly impair ventilation or pulmonary circulation.
Pathophysiology
1
Oxygenation failure
Ventilation-perfusion mismatch, shunt or diffusion impairment lowers arterial oxygen; supplemental oxygen may help mismatch but has limited effect on a large true shunt.
2
Ventilation failure
Inadequate minute ventilation causes carbon dioxide retention and respiratory acidosis; oxygen can improve saturation without correcting this process.
3
Increased work and fatigue
High resistance or reduced compliance raises the energy cost of each breath until muscle fatigue reduces tidal volume, chest movement and respiratory rate.
4
Cardiovascular interaction
Hypoxia and acidosis depress myocardium, while high intrathoracic pressure can reduce venous return; severe respiratory failure therefore progresses to bradycardia and circulatory collapse.
Clinical features and red flags
Compensated distress
Tachypnoea and increased work occur with preserved chest excursion, interaction, air entry and circulation.
Oxygenation failure
Cyanosis or persistent low saturation despite oxygen, with increased effort or altered consciousness, indicates inadequate arterial oxygenation.
Stridor, hoarse or weak voice, drooling, swelling and preferred upright posture can precede complete obstruction.
Peri-arrest respiratory failure
Apnoea, gasping, silent chest, bradycardia or unresponsiveness requires ventilation and paediatric life support immediately.
Red flags requiring action
A child who becomes quieter with less recession can be deteriorating if air entry, respiratory rate or alertness is falling.
Bradypnoea, irregular breathing, apnoea, grunting, cyanosis, a silent chest or reduced consciousness indicates respiratory failure rather than compensated distress.
Investigations
01First-line continuous oximetry and clinical breathing assessmentFirst stepFirst line
Why
Measure oxygenation while repeatedly assessing work, chest excursion, air entry and consciousness.
Interpretation and limitations
A reliable saturation trend is useful, but supplemental oxygen can conceal ventilation failure and poor perfusion can impair the signal.
02First-line blood gasFirst line
Why
Assess pH, carbon dioxide, oxygen where arterial, lactate, glucose and electrolytes when failure is suspected.
Interpretation and limitations
Rising carbon dioxide with acidosis and fatigue supports ventilatory failure; a normal early value does not override a deteriorating child.
03Waveform capnography
Why
Confirm and monitor a tracheal or supraglottic airway and trend ventilation.
Interpretation and limitations
Absent waveform prompts immediate airway and circulation review; compare end-tidal with blood carbon dioxide after stabilisation.
04Cause-directed chest imaging
Why
Identify pneumonia, collapse, oedema, foreign body, pneumothorax or device position when imaging will change care.
Interpretation and limitations
Do not
Differential diagnosis
01
Metabolic acidosis with compensation
DKA, sepsis or renal failure can cause deep rapid breathing with relatively clear lungs; the primary treatment is metabolic and circulatory while breathing is supported.
02
Shock-driven tachypnoea
Poor perfusion and acidosis raise respiratory rate, so circulation must be assessed alongside the chest rather than assuming primary lung disease.
03
Upper-airway noise without failure
Mild croup or chronic stertor may preserve air entry, colour and interaction; trajectory and work distinguish compensated disease from a threatened airway.
04
Anxiety or pain
Distress can cause tachypnoea, but hypoxia, asymmetric air entry, recession, grunting or altered alertness cannot be attributed to anxiety without full assessment.
Management
01DistressSupport and treat the causeFirst stepEffort is increased but gas exchange and interaction remain adequate.+
1Position comfortably, minimise distress and apply continuous observations.
2Give cause-appropriate oxygen and treatment and reassess response frequently.
3EscalationEscalate early if work rises, air entry falls or systemic signs develop.
02FailureOxygenate and ventilateOxygenation, ventilation, consciousness or circulation is failing.+
1Call resuscitation, anaesthetic and PICU help and give 100% oxygen.
2Open the airway and start two-person bag-mask ventilation with mild chest rise.
3Treat obstruction, anaphylaxis, bronchospasm or pneumothorax immediately.
4
Complications
01
Cardiorespiratory arrest
Progressive hypoxia, hypercapnia, acidosis and fatigue lead to bradycardia, pulseless electrical activity and hypoxic brain injury.
02
Airway and ventilation injury
Repeated intubation, excessive pressure, gastric inflation, aspiration, barotrauma and ventilator-associated lung injury can add avoidable harm.
03
Treatment-related haemodynamic collapse
Induction, positive-pressure ventilation and excessive PEEP reduce venous return and can precipitate arrest in shock or obstructive physiology.
04
Functional and psychological sequelae
Critical illness can produce weakness, feeding problems, voice or airway injury, sleep disturbance and traumatic stress requiring multidisciplinary follow-up.
Monitoring and follow-up
Trend respiratory rate, work, chest excursion, air entry, oxygen requirement, saturation, heart rate and consciousness together.
Repeat blood gas according to clinical trajectory and after a material ventilation change; never wait for it when bedside failure is clear.
Use continuous waveform capnography with any advanced airway and consider it during non-invasive ventilation where available.
During airway attempts monitor saturation, ECG and blood pressure and stop immediately for bradycardia or clinically important desaturation.
After starting high-flow or non-invasive support, document a short review time and explicit failure criteria rather than continuing by inertia.
Review fluid balance and cardiac signs because overload and positive pressure can worsen respiratory and circulatory performance.
After critical illness, assess voice, swallowing, feeding, mobility, cognition, sleep and family distress and refer to the appropriate MDT.
Special situations
Quieter can mean weaker
As muscle power fails, wheeze, recession and rate may lessen even while gas exchange deteriorates.
Saturation is not ventilation
Oxygen can produce a normal displayed saturation while carbon dioxide and acidosis continue to rise.
Bag-mask is the first advanced skill
A well-performed two-person technique often restores gas exchange faster than a rushed intubation.
Every support trial needs an exit
High-flow or NIV is safe only with a target, review interval and prompt plan for failure.
DOPES is immediate troubleshooting
Sudden deterioration after intubation is first assumed to be airway, lung or equipment failure until proven otherwise.
Common pitfalls
01
Equating reduced recession with recovery without checking air entry and alertness.
02
Using oxygen saturation alone to exclude ventilatory failure.
03
Waiting for a blood gas before supporting inadequate breathing.
04
Forcing a child with an upper-airway threat to lie flat.
05
Using high-flow or NIV indefinitely despite worsening fatigue.
06
Continuing an intubation attempt through bradycardia or desaturation.
07
Failing to use capnography with an advanced airway.
08
Ordering imaging before treating a clinical tension pneumothorax.
09
Ignoring sedative accumulation in renal or hepatic dysfunction.
Confirm and continuously monitor every advanced airway with waveform capnography, as well as clinical chest movement and bilateral air entry.
Use DOPES for sudden deterioration after an airway is placed: displacement, obstruction, pneumothorax or pathology, equipment, and stomach, stacking or sedation.
Treat the cause in parallel, including foreign-body relief, anaphylaxis adrenaline, bronchodilator therapy, antibiotics, naloxone or decompression as indicated.
Bradycardia in an unwell child usually reflects severe hypoxia and requires immediate effective oxygenation and ventilation.
Stridor at rest, drooling, inability to swallow, tripod positioning or rapidly increasing neck swelling signals a threatened upper airway; do not force the child supine or inspect the throat with distressing instruments.
Sudden unilateral loss of air entry with shock during positive-pressure ventilation suggests tension pneumothorax and is treated clinically before imaging.
A tracheostomy child in distress with an impassable suction catheter may have a blocked tube requiring immediate removal and replacement under the emergency algorithm.
Normal oxygen saturation while receiving supplemental oxygen does not exclude rising carbon dioxide, exhaustion or inadequate minute ventilation.
transfer an unstable child or delay decompression of a clinical tension pneumothorax for a radiograph.
05Lung or cardiac point-of-care ultrasound
Why
Support rapid recognition of pleural air or fluid, consolidation, oedema and cardiac contribution.
Interpretation and limitations
Findings are operator dependent and complement rather than replace definitive imaging and echocardiography.
06Reference-standard airway or cause assessment
Why
Use specialist endoscopy, bronchoscopy, CT, MRI, formal lung function or neurophysiology when the suspected cause requires confirmation.
Interpretation and limitations
The reference test is condition specific and follows physiological stabilisation; bronchoscopy may be both diagnostic and therapeutic for a foreign body.
Prepare advanced support while continuous effective ventilation continues.
03Non-invasive escalationBridge while drive remainsEscalationConventional oxygen is inadequate but the child protects the airway and breathes effectively.+
1Select high-flow nasal oxygen or non-invasive ventilation with critical-care guidance.
2Set a defined physiological target and short reassessment interval.
3Monitor effort, gas exchange, consciousness and haemodynamics continuously.
4Move to invasive support promptly if the trial fails rather than prolonging exhaustion.
04Advanced airwayOxygenation over intubationBag-mask support is ineffective or prolonged ventilation and airway protection are required.+
1Pre-oxygenate and prepare a checklist, rescue device, drugs and skilled team.
2Limit attempts and resume bag-mask or supraglottic oxygenation at deterioration.
3Confirm placement with waveform capnography and clinical checks.
4Use lung-protective settings, analgesia and sedation with continuous PICU monitoring.