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Level 2 of 6Must-remember

Acute respiratory distress syndrome: recognition and protective ventilation

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Ask what caused it, because ARDS is always secondary: pneumonia (bacterial, viral including influenza and SARS-CoV-2, Pneumocystis), aspiration of gastric contents, sepsis from any source, severe trauma with shock and multiple transfusions, acute pancreatitis, transfusion-related acute lung injury, drug overdose — more than 80% of cases arise from pneumonia and sepsis (together 40-60%), aspiration, major trauma, multiple transfusions and drug overdose.
  • The earliest sign is unexplained tachypnoea, not desaturation: a respiratory rate climbing over hours in a patient with a recognisable insult is ARDS until proved otherwise; profound dyspnoea then develops rapidly, characteristically 12-48 hours after the initiating event and always within 7 days.
  • The hallmark is hypoxaemia refractory to supplemental oxygen: a patient who needed 2 L/min by nasal cannula overnight needs a reservoir mask at 15 L/min by morning for the same saturation — this is shunt, and it does not respond to more FiO2.
  • Examine for the work of breathing: accessory muscle use, intercostal recession, tachypnoea, tachycardia, sweating, inability to speak a full sentence, unwillingness to lie flat, agitation with a falling conscious level; cyanosis is late.
  • Three especially informative patterns: asynchronous respiration (thoracic and abdominal compartments out of time), paradoxical respiration (abdomen moving in as the chest moves out) and respiratory alternans (breath-to-breath alternation between accessory muscles and diaphragm).
  • Auscultate for fine crackles throughout both lung fields, not merely at the bases, and look for failure of the kidneys, liver, gut, nervous system and circulation, which commonly accompany it.
  • Apply the Berlin definition, which needs all four: onset within one week of a known insult or of new or worsening respiratory symptoms; new bilateral opacities on chest radiograph or CT not fully explained by effusion, collapse or nodules; respiratory failure not fully explained by cardiac failure or fluid overload; and a PaO2/FiO2 ratio of 300 mmHg or less measured on at least 5 cmH2O of PEEP or CPAP.Not available at your setup — Arterial blood gas.
  • Calculate the P/F ratio yourself: P/F equals PaO2 in mmHg divided by FiO2 as a decimal, and if the analyser reports kPa multiply by 7.5 — so PaO2 8.0 kPa on a reservoir mask at an FiO2 of about 0.85 is 60 mmHg divided by 0.85, that is 71, severe ARDS.Not available at your setup — Arterial blood gas.
  • Grade severity by the P/F ratio alone: mild 300-200 mmHg (40-26.6 kPa), moderate 200-100 mmHg (26.6-13.3 kPa), severe below 100 mmHg (below 13.3 kPa).Not available at your setup — Arterial blood gas.
  • Record the FiO2 and the device on every gas — a gas without them cannot yield a P/F ratio — and remember respiratory failure is present when PaO2 is below 8 kPa (60 mmHg) or PaCO2 above 7 kPa (55 mmHg).Not available at your setup — Arterial blood gas.
  • Danger signs meaning imminent need for mechanical ventilation: respiratory rate above 40/min, inability to speak, visible exhaustion despite maximal therapy, or a falling respiratory rate in a patient still distressed with increasing drive to breathe, which is exhaustion and pre-arrest.
  • More danger signs: confusion, restlessness or falling conscious level (agitation in a hypoxaemic patient is hypoxia until proved otherwise); cyanosis or SpO2 persistently below 90% despite a reservoir mask at 15 L/min; PaO2 below 8 kPa (60 mmHg) despite maximal oxygen; PaCO2 above 8 kPa (60 mmHg) particularly if rising in a previously hypocapnic patient; haemodynamic instability; a P/F ratio falling despite escalating support.Not available at your setup — Arterial blood gas.
  • Exclude cardiogenic pulmonary oedema, because specific treatment exists for it: look for raised JVP, an S3 gallop, murmur, peripheral oedema and orthopnoea, and on the film cardiomegaly, a widened vascular pedicle, upper-lobe blood diversion, Kerley B lines, bat's wing shadowing and sizeable effusions — in ARDS the heart size is normal and effusions small or absent, with air bronchograms in about 80% and sparing of the costophrenic angles.
  • In the already-ventilated patient none of the above will be seen: the first evidence is a rising FiO2 requirement with falling compliance, the same tidal volume needing a higher plateau pressure.Not available at your setup — Mechanical ventilator.
  • In children judge tachypnoea against normal for age (under 1 year 30-40; 1-2 years 25-35; 2-5 years 25-30; 5-12 years 20-25; over 12 years 15-20 breaths/min) and watch for grunting, nasal flaring, head-bobbing, intercostal and subcostal recession and tracheal tug — a falling respiratory rate in a drowsy child, or bradycardia, is pre-terminal and blood pressure holds until very late.
  • Beware silent hypoxaemia: some patients, particularly with COVID-19 pneumonitis, tolerate very low oxygen tensions with modest distress — a comfortable patient with a P/F of 120 still has severe ARDS.

Management— do this, in order

  • Identify and treat the precipitating condition first: more than 80% of deaths are attributable to sepsis and non-pulmonary organ failure, not hypoxaemia, so give appropriate broad-spectrum antibiotics early where infection is suspected and pursue source control — the ventilator buys time, but only source control and antimicrobial therapy cure.Doctor / Nurse
  • Sit the patient up unless the blood pressure forbids it and give a non-rebreathing reservoir mask at 15 L/min in the unstable, undiagnosed patient: severe hypoxaemia is more dangerous than hypercapnia.
  • Once stable, titrate down to SpO2 88-95% with PaO2 above 55 mmHg (7.3 kPa), using the lowest FiO2 and PEEP that achieve them and reducing FiO2 towards 0.6 or less as fast as is safe, because hyperoxia generates oxygen free radicals and oxidative lung injury.
  • Consider high-flow nasal oxygen or CPAP as a strictly time-limited trial with pre-specified criteria — for example CPAP 8 cmH2O at FiO2 0.6, reassessed at 60 minutes, proceeding to intubation if the respiratory rate remains above 30, SpO2 is below 90%, or the P/F ratio has not improved.Doctor / NurseNot available at your setup — Mechanical ventilator.
  • Intubate for severe distress persisting despite maximal therapy, confusion or falling conscious level, rising PaCO2 above 8 kPa (60 mmHg), PaO2 below 8 kPa (60 mmHg) despite oxygen, inability to protect the airway, or shock — clinical judgement outweighs any single number, and delay in a tiring patient is the commonest avoidable harm in this syndrome.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Induction drugs: ketamine 1-2 mg/kg IV is first choice if shocked (child 1-2 mg/kg IV); etomidate 0.3 mg/kg IV; propofol 1-2 mg/kg IV only if haemodynamically stable (child 2-3 mg/kg IV); midazolam 0.05-0.1 mg/kg IV (child 0.1 mg/kg IV); fentanyl 1-2 micrograms/kg IV if the blood pressure allows.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Paralysis and paediatric adjuncts: suxamethonium 1-1.5 mg/kg IV (child 1-2 mg/kg IV), rocuronium 1-1.2 mg/kg IV (child 1 mg/kg IV), vecuronium 0.1 mg/kg IV (child 0.1 mg/kg IV), and atropine 20 micrograms/kg IV (minimum 100, maximum 600 micrograms) to prevent laryngoscopy bradycardia in infants and small children.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Anticipate hypotension after induction from impeded venous return under positive pressure, loss of endogenous catecholamine drive and the induction agents themselves — have crystalloid running and a vasopressor immediately available, and expect a further fall in right heart dysfunction or pulmonary hypertension.Doctor / Nurse
  • Paediatric tube sizing: over 1 year, uncuffed (age divided by 4) plus 4 mm or cuffed (age divided by 4) plus 3.5 mm; infants 3.5-4.0 mm; neonates 3.0-3.5 mm — confirm with capnography and equal chest movement, since right main bronchus intubation is the commonest error, and obtain a chest radiograph.Doctor / NurseNot available at your setup — Endotracheal intubation kit.
  • Ventilate protectively — the only intervention with a large, reproducible survival benefit: tidal volume 6 mL/kg predicted body weight (range 4-8), plateau pressure 30 cmH2O or less, PEEP at least 5 and usually 5-15 cmH2O titrated against FiO2, respiratory rate 16-20/min initially and up to 30-35/min for CO2, FiO2 1.0 initially reduced to 0.6 or less as tolerated, targeting SpO2 88-95%, pH 7.30 or above and MAP 65 mmHg or above.Doctor / NurseNot available at your setup — Mechanical ventilator.
  • Calculate predicted body weight from height, never from measured weight — male PBW in kg equals 50 plus 0.91 times (height in cm minus 152.4); female PBW equals 45.5 plus 0.91 times (height in cm minus 152.4) — because an oedematous 90 kg man may have a PBW of 65 kg.
  • Measure the plateau pressure with a 0.5-1 second inspiratory hold after every change, and if it exceeds 30 cmH2O reduce the tidal volume in 1 mL/kg steps to a minimum of 4 mL/kg PBW.Doctor / NurseNot available at your setup — Mechanical ventilator.
  • Paediatric ventilation: volume or pressure control, tidal volume 5-8 mL/kg PBW (3-6 where compliance is very poor), plateau pressure 28 cmH2O or less, PEEP 5-10 cmH2O and higher in severe disease, rate set for age, targeting SpO2 92-97% (88-92% accepted on high PEEP) and pH 7.20 or above.Doctor / NurseNot available at your setup — Mechanical ventilator.
  • Accept permissive hypercapnia, managing it with a higher respiratory rate rather than by abandoning the protective volume, aiming for pH 7.30 or above and tolerating down to 7.20 — but in obstructive disease the correct strategy is instead lower rates of 9-12/min with tidal volumes of 7-9 mL/kg and a long expiratory time.Doctor / NurseNot available at your setup — Mechanical ventilator.
  • Sedate and analgese to a documented score: fentanyl 1-2 micrograms/kg/h by infusion, or morphine 2-5 mg IV boluses with an infusion of 1-5 mg/h (child 0.05-0.1 mg/kg IV), with propofol 1-4 mg/kg/h or midazolam 1-5 mg/h — non-benzodiazepine sedatives are preferred, and daily interruption paired with a spontaneous breathing trial shortens ventilation and critical care stay.Doctor / NurseNot available at your setup — Infusion pump.
  • Keep the lung dry once the patient is out of shock: aim for a consistently negative fluid balance with furosemide 20-40 mg IV slowly, repeated or increased against response and renal function, or an infusion of 5-10 mg/h if boluses fail (child 0.5-1 mg/kg IV, maximum 2 mg/kg/dose), limited only by hypotension and hypoperfusion of critical organs such as the kidneys.Doctor / Nurse
  • In hypotensive patients give small aliquots — 250-500 mL in an adult, 10 mL/kg in a child — reassessing after each and reaching for a vasopressor rather than repeating boluses into a leaking lung; in paediatric ARDS without shock restrict fluid to 60-70% of maintenance.Doctor / Nurse
  • Prone the severe patient early: prone positioning is the one rescue manoeuvre with a demonstrated survival benefit, cutting 28-day mortality from 32.8% to 16.0% in severe ARDS with a P/F below 150 mmHg when applied early and for longer periods prone than supine, and needing a secured airway, adequate sedation, several trained staff and meticulous protection of the tube, lines, pressure areas and eyes.Doctor / NurseNot available at your setup — ICU / HDU bed.

Caution— what harms

  • Do not escalate FiO2 and expect it to work: shunt, unlike ventilation-perfusion mismatch, is refractory to supplemental oxygen, so recruiting collapsed alveoli with PEEP is the effective manoeuvre — not more oxygen.
  • Do not push the oxygen target too low either: a trial comparing a conservative PaO2 of 55-70 mmHg with a more physiological 90-105 mmHg found no mortality reduction and more adverse events, including mesenteric ischaemia, in the conservative arm.
  • Never use large tidal volumes: over-distension by large tidal volumes (volutrauma), high inflation pressures (barotrauma) and repeated opening and closing of distal airways (atelectrauma) disrupt the alveolar-capillary membrane and release inflammatory mediators (biotrauma) — large tidal volumes can produce ARDS in patients who did not have it.
  • Never assume improving oxygenation means improving oxygen delivery: raising PEEP impedes venous return, raises pulmonary vascular resistance and can reduce cardiac output, so oxygenation on the monitor can improve while total oxygen delivery falls — check blood pressure and hourly urine output after every increment, not only the saturation.
  • Do not trust the displayed plateau pressure in a spontaneously breathing patient: at PEEP 10 with a driving pressure of 15, a paralysed patient shows a plateau of 25 cmH2O and a tidal volume of 300 mL, whereas a patient generating 10 cmH2O of effort has a net transalveolar pressure of 35 cmH2O and a tidal volume of 700 mL while the ventilator still displays 25.
  • Do not rely on non-invasive ventilation in established ARDS: patients with severely impaired oxygenation are less likely to benefit and should be intubated if they require mechanical ventilation, and a patient breathing hard on CPAP or high-flow oxygen can generate very large spontaneous tidal volumes and injure their own lungs further — non-invasive support is contraindicated by reduced conscious level, inability to protect the airway, copious secretions, haemodynamic instability, facial injury, vomiting and respiratory arrest.
  • Do not trust the pulse oximeter: it is insensitive to changing gas exchange, a normal SpO2 on oxygen does not exclude CO2 retention, it is unreliable with poor perfusion, and it overestimates saturation in darker skin.
  • Do not let a blood gas mislead you: eject air bubbles immediately and analyse at once or ice the syringe, since gas in a bubble equilibrates with blood and falsely raises PO2 and lowers PCO2.
  • Avoid suxamethonium in hyperkalaemia, burns more than 24 hours old, crush injury and chronic neuromuscular disease.
  • Suspect tension pneumothorax in any ventilated patient who deteriorates — new hypoxia and hypercarbia, an unexplained rise in airway pressure, hypotension, unequal chest expansion, tracheal deviation, a displaced apex beat away from the affected side and a hyper-resonant hemithorax; breath sounds are diminished but misleading in ventilated patients, and where deterioration is rapid perform needle decompression in the second intercostal space in the mid-clavicular line followed by a chest drain.Not available at your setup — Chest drain / tube thoracostomy.
  • On sudden deterioration, disconnect and hand-ventilate with 100% oxygen while displacement, obstruction, pneumothorax, equipment failure and breath-stacking are excluded; a peak-to-plateau gradient above 10-15 cmH2O indicates a resistance problem (blocked or kinked tube, secretions, bronchospasm), while both pressures raised with a normal gradient indicates a compliance problem.
  • Do not paralyse without sedation: neuromuscular blocking agents paralyse without altering mental state, so sedative-induced amnesia is mandatory — and blockade does not improve overall outcomes and contributes to critical illness myopathy.
  • Do not give steroids routinely — steroids in persistent ARDS may improve lung function but do not appear to improve outcome; reserve them for septic shock refractory to fluid and vasopressors and severe community-acquired pneumonia (hydrocortisone 200 mg IV over 24 hours, typically 50 mg six-hourly), COVID-19 needing oxygen or ventilation (dexamethasone 6 mg once daily for 10 days), and acute eosinophilic pneumonia or vasculitis presenting as ARDS.
  • Do not treat liberation as a gradual wean — treating removal of support as a wean extends unnecessary ventilation by up to 40%; and after extubation expect up to 10% to develop respiratory distress, remembering that non-invasive ventilation as rescue after failed extubation may give worse outcomes than prompt re-intubation.

Refer / escalate

Escalate to critical care immediately for any patient with a P/F ratio of 300 mmHg or less, respiratory rate above 40/min, SpO2 persistently below 90% on a reservoir mask at 15 L/min, PaO2 below 8 kPa (60 mmHg) or PaCO2 above 8 kPa (60 mmHg) and rising, confusion or falling conscious level, or haemodynamic instability — and refer early to a specialist centre for prone positioning, and for veno-venous ECMO as a salvage option, since delay in a tiring patient is the commonest avoidable harm in this syndrome.

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