Common Respiratory Conditions: A Year 2 Deep Dive

Upper airway differences

• Larger tongue in proportion to the mouth
• Smaller pharynx – less room for swelling/secretions
• Floppier, larger epiglottis
• Larynx sits more anterior – harder to visualise/intubate

Lower airway & lung differences

• Narrower airway diameter throughout
• Less rigid trachea – can collapse under pressure
• Fewer/underdeveloped alveoli – alveoli keep forming through childhood
• Less respiratory reserve overall

Positioning & behaviour

• Larger head, poor head control in babies
• Neck flexion from poor positioning can compromise the airway
• Predominantly nasal breathing in young babies
• A blocked nose can seriously increase work of breathing and feeding difficulty

The physics that matters

• Airway resistance rises sharply as radius falls (Poiseuille’s principle)
• A small amount of oedema or mucus in a narrow airway = big resistance jump
• This is why a child can look like they are coping, then suddenly tire

Effort signs

• Recession: negative pressure pulls soft tissue in – breathing is hard work
• Tracheal tug: strong inspiratory effort pulling tissue around the trachea
• Nasal flaring: widening nostrils to reduce airway resistance
• Grunting: back-pressure to keep small airways/alveoli open – concerning

Sound signs

• Wheeze: air squeezed through narrowed lower airways (asthma, bronchiolitis, CF)
• Stridor: air squeezed through a narrowed upper airway (croup, foreign body, epiglottitis)
• Crackles: small airways/alveoli popping open through fluid or mucus

Late/danger signs

• Low SpO₂: oxygen not reaching or crossing into the blood effectively
• Silent chest: air entry so poor that wheeze disappears – not improvement
• Altered consciousness: brain affected by hypoxia, CO₂ retention, or exhaustion

The core reasoning chain

• Airway swelling/mucus/infection/bronchoconstriction
• → air movement or gas exchange affected
• → increased work of breathing or hypoxia
• → signs appear → A–E assessment → trend → escalate early

The mechanism chain

• Trigger exposure (exercise, pollen, smoke, vaping, infection)
• Mast cells activate → histamine/prostaglandins released
• Bronchoconstriction → wheeze as air is squeezed through
• Mucus increases → air trapping → fatigue and hypoxia

Severity: moderate vs severe

• Moderate: SpO₂ ≥ 92%, PEF ≥ 50% best/predicted
• Severe: SpO₂ < 92%, PEF 33–50%, HR > 125, RR > 30, accessory muscle use
• Life-threatening: PEF < 33%, silent chest, poor effort, altered consciousness

Treatment ladder

• Salbutamol – short-acting beta-2 agonist, relaxes airway muscle
• Ipratropium bromide – added in severe attacks
• Steroids – oral prednisolone or IV hydrocortisone, reduces inflammation (not instant)
• Escalation: IV magnesium sulfate, IV salbutamol, IV aminophylline

Before stepping up treatment

• Check inhaler technique and adherence first
• Consider smoking/vaping, allergens, pollution, mould exposure
• Increasing medication will not fix a technique or environment problem

The mechanism chain

• Virus (commonly RSV) infects bronchiolar epithelium
• Oedema narrows tiny airways → tachypnoea, recession, nasal flaring
• Mucus and cell debris plug airways → crackles, wheeze, air trapping
• Feeding becomes unsafe → baby tires → apnoea risk in severe cases

Typical trajectory

• Usually affects babies/children under 2
• Often peaks around days 3–5 of illness
• A baby unwell on day 1–2 may still get worse before better
• A baby on day 5 may be at or near the peak

Supportive management

• Oxygen if SpO₂ falls below local threshold (often ~90–92%)
• HFNC/Optiflow – warmed, humidified high-flow, splints airways open
• CPAP – positive pressure, keeps small airways/alveoli open
• Suction/secretion management – babies rely heavily on nasal breathing

Why treatment is mainly supportive

• It is viral – no routine antibiotics
• Not classic bronchoconstriction – salbutamol/steroids/ipratropium not routine
• NG feeds or IV fluids protect energy when feeding becomes exhausting
• Clustering cares lets the baby rest between interventions

Croup mechanism

• Usually viral, common under age 5, worse at night
• Swelling around larynx/trachea → barking cough, hoarse voice, stridor
• Agitation worsens obstruction – keeping the child calm matters clinically

Croup severity

• Mild: barking cough, no stridor/recession at rest
• Moderate: stridor + recession at rest, no agitation/lethargy
• Severe: stridor + recession + agitation or lethargy
• Impending failure: fatigue, pallor/cyanosis, reduced consciousness

Pneumonia mechanism

• Alveoli inflamed, fill with fluid/exudate
• Oxygen cannot cross into blood efficiently → low SpO₂
• Community-acquired, hospital-acquired, or aspiration pneumonia
• Likely organism shifts with age – viral in toddlers, Mycoplasma in school age

Pneumonia complications

• Pleurisy, pleural effusion, lung abscess
• Sepsis and respiratory failure – this can become a circulation problem too
• Immunosuppressed children carry higher risk

The mechanism chain

• Faulty CFTR gene (chromosome 7) disrupts chloride/sodium/water movement
• Secretions become dehydrated, thick, and sticky
• Mucociliary clearance fails → bacteria are not cleared properly
• Recurrent infection → airway damage → bronchiectasis over time

Genetics

• Autosomal recessive inheritance
• Two carrier parents: 1 in 4 chance of an affected child
• Around 1 in 25 people may be unaffected carriers

Diagnosis & monitoring

• UK newborn blood spot around day 5–8 screens for common mutations
• Sweat test: CFTR dysfunction raises sweat chloride concentration
• Ongoing monitoring: bone health, liver function, CF-related diabetes

Why sweat is salty

• CFTR normally reabsorbs chloride/sodium in sweat glands
• When CFTR is faulty, this reabsorption fails
• More salt stays in the sweat – the basis of the diagnostic test