Ards

11 min read Last updated April 8, 2026

Surgical approach

  • Not a surgical condition; management is supportive and ICU-based.
  • Procedures sometimes required to facilitate management
    • Source control: e.g. laparotomy/drainage for intra-abdominal sepsis; debridement for necrotising infection
    • Bronchoscopy for airway toileting/diagnostic sampling (selected cases)
    • Central/arterial access; renal replacement therapy access; tracheostomy (prolonged ventilation)
    • ECMO cannulation (VV-ECMO) in specialist centres when refractory hypoxaemia/hypercapnia despite optimal conventional therapy

Anaesthetic management (when ARDS patient requires theatre/procedures)

  • Type of anaesthesia
    • Usually GA with controlled ventilation; regional techniques may be adjuncts to reduce opioid requirement but rarely sole technique in established ARDS
  • Airway
    • ETT almost always (cuffed); avoid SGA in moderate–severe ARDS due to high airway pressures, aspiration risk, need for PEEP and recruitment
  • Duration
    • Procedure dependent; anticipate prolonged time for optimisation, transport, positioning (e.g. prone), and haemodynamic management
  • How painful?
    • Depends on procedure; aim opioid-sparing multimodal analgesia (paracetamol, regional blocks) to facilitate ventilation/weaning; avoid NSAIDs if renal dysfunction/bleeding risk
  • Key intraoperative priorities
    • Maintain lung-protective ventilation (low VT, limit plateau and driving pressure), avoid derecruitment, careful fluid strategy, vasopressors early if needed
    • Pre-brief with ICU: current ventilator settings, PEEP, recent gases, proning status, rescue therapies (iNO, paralysis), haemodynamic targets
    • Transport risks: disconnections → derecruitment; ensure portable ventilator capable of required PEEP/FiO2; clamp ETT briefly if circuit change unavoidable

Definition and diagnostic criteria (Berlin definition)

  • Syndrome of acute inflammatory lung injury causing increased alveolar–capillary permeability, non-cardiogenic pulmonary oedema, reduced aerated lung volume, and severe hypoxaemia.
  • Berlin criteria (all required)
    • Timing: within 1 week of known clinical insult or new/worsening respiratory symptoms
    • Imaging: bilateral opacities on CXR/CT not fully explained by effusions, lobar/lung collapse, or nodules
    • Origin of oedema: respiratory failure not fully explained by cardiac failure or fluid overload; objective assessment (e.g. echo) if no risk factor
    • Oxygenation (with PEEP/CPAP ≥ 5 cmH2O): Mild 200–300, Moderate 100–200, Severe ≤ 100 (PaO2/FiO2 in mmHg)
  • Practical conversion: PaO2/FiO2 300 ≈ 40 kPa/1.0? (use consistent units); in UK often use kPa: 200 mmHg ≈ 26.7 kPa; 100 mmHg ≈ 13.3 kPa.

Aetiology / risk factors

  • Direct (pulmonary) insults
    • Pneumonia (commonest), aspiration of gastric contents, inhalational injury, pulmonary contusion, near drowning
  • Indirect (extrapulmonary) insults
    • Sepsis (non-pulmonary), pancreatitis, major trauma, massive transfusion/TRALI, cardiopulmonary bypass, drug overdose
  • Iatrogenic contributors/worseners
    • Ventilator-induced lung injury (VILI), excessive fluids, high FiO2 for prolonged periods (oxygen toxicity), patient self-inflicted lung injury (P-SILI) with vigorous spontaneous effort

Pathophysiology (high-yield)

  • Exudative phase (days 1–7): diffuse alveolar damage, protein-rich oedema, hyaline membranes, surfactant dysfunction → atelectasis and shunt.
  • Proliferative phase (days 7–21): type II pneumocyte hyperplasia, interstitial inflammation, early fibrosis; improving oxygenation in survivors.
  • Fibrotic phase (variable): fibrosis, reduced compliance, pulmonary hypertension, prolonged ventilator dependence (not universal).
  • Physiology: ↓ compliance (“stiff lung”), ↓ FRC, ↑ shunt and V/Q mismatch, ↑ dead space (microthrombosis), hypoxic pulmonary vasoconstriction may be impaired.
  • ‘Baby lung’ concept: only a small fraction of lung is aerated; normal tidal volumes overdistend remaining units → volutrauma/barotrauma.

Clinical features and investigations

  • Symptoms/signs: acute dyspnoea, tachypnoea, refractory hypoxaemia, increased work of breathing; may have sepsis features.
  • ABG: hypoxaemia; early respiratory alkalosis; later hypercapnia if severe disease/low VT strategy.
  • CXR/CT: bilateral infiltrates; CT shows dependent consolidation with relatively spared non-dependent regions (recruitable lung varies).
  • Echo: assess LV function/valvular disease, RV strain/pulmonary hypertension; helps exclude cardiogenic oedema.
  • Consider differentials: cardiogenic pulmonary oedema, pneumonia, PE, diffuse alveolar haemorrhage, acute eosinophilic pneumonia, ILD exacerbation.

Ventilatory management (core FRCA)

  • Goals: adequate oxygen delivery while minimising VILI (volutrauma, barotrauma, atelectrauma, biotrauma).
  • Lung-protective ventilation (ARDSNet principles)
    • Tidal volume: ~6 mL/kg predicted body weight (PBW) (range 4–8); avoid using actual weight
    • Plateau pressure (Pplat): aim ≤ 30 cmH2O (measure with inspiratory hold)
    • Driving pressure: ΔP = Pplat − PEEP; lower is better; aim ~≤ 15 cmH2O if achievable
    • PEEP: use sufficient PEEP to prevent derecruitment; titrate to oxygenation/compliance; avoid excessive PEEP causing overdistension and hypotension
    • Permissive hypercapnia: accept higher PaCO2 to maintain low VT/pressures (unless contraindicated)
    • Contraindications/relative cautions to permissive hypercapnia: raised ICP, severe pulmonary hypertension/RV failure, severe metabolic acidosis, significant arrhythmias/ischaemia (case-dependent)
  • Oxygenation targets
    • Avoid both hypoxaemia and hyperoxaemia; typical ICU targets: SpO2 92–96% (or PaO2 ~7–10 kPa) depending on local policy/comorbidity
  • Ventilator mode considerations
    • Volume control: ensures VT but may increase pressures as compliance worsens; monitor Pplat/ΔP
    • Pressure control: limits pressure but VT varies; ensure adequate minute ventilation and monitor VT/PaCO2
    • Spontaneous modes: can reduce sedation but risk P-SILI if strong inspiratory effort; consider early controlled ventilation in moderate–severe ARDS
  • Recruitment manoeuvres
    • May transiently improve oxygenation in recruitable lung; risks include hypotension, barotrauma; not routine for all; use case-by-case with monitoring
  • Prone positioning
    • Indication: moderate–severe ARDS (commonly PaO2/FiO2 ≤ 150 mmHg on FiO2 ≥ 0.6 with PEEP ≥ 5–10) despite optimisation
    • Benefits: improved V/Q matching, more homogeneous transpulmonary pressures, reduced VILI; mortality benefit when used early and for prolonged sessions (~16 h/day)
    • Practical issues: secure ETT/lines, eye/pressure area care, enteral feeding considerations, facial oedema; contraindications include unstable spine, open abdomen (relative), raised ICP (relative)
  • Neuromuscular blockade
    • Short course may help synchrony, reduce oxygen consumption and P-SILI in severe ARDS; balance against ICU-acquired weakness; ensure deep sedation/analgesia
  • Inhaled pulmonary vasodilators (e.g. nitric oxide, prostacyclin)
    • Rescue therapy: can improve oxygenation transiently by better V/Q matching; no consistent mortality benefit; consider as bridge to proning/ECMO
  • ECMO (VV-ECMO)
    • Consider in refractory hypoxaemia/hypercapnia despite optimal lung-protective ventilation, proning, and adjuncts; requires specialist centre and careful selection

Haemodynamics and fluids

  • ARDS often coexists with sepsis: vasodilation, capillary leak, myocardial dysfunction; positive pressure ventilation increases RV afterload and reduces venous return.
  • Fluid strategy: conservative (after initial resuscitation) improves lung function and ventilator-free days; avoid fluid overload worsening pulmonary oedema.
  • Vasopressors: noradrenaline first-line in septic shock; consider vasopressin adjunct; aim MAP appropriate to patient (often ≥ 65 mmHg).
  • Right ventricular failure: suspect with rising CVP, hepatomegaly, echo RV dilation, worsening oxygenation/hypercapnia; manage by reducing PVR (correct hypoxia/acidosis, avoid overdistension, consider prone/iNO), optimise preload, use inotropes if needed.

Sedation, analgesia, delirium, and supportive care

  • Sedation: aim for the minimum compatible with synchrony and safety; daily sedation breaks when appropriate; avoid deep sedation unless severe ARDS/proning/paralysis.
  • Analgesia-first approach; consider multimodal and regional techniques where feasible (e.g. epidural/paravertebral for thoracic trauma) to reduce ventilatory impairment.
  • Delirium prevention: sleep hygiene, early mobilisation when feasible, minimise benzodiazepines, treat pain and sepsis.
  • Nutrition: early enteral feeding if possible; avoid overfeeding (excess CO2 production).
  • VTE prophylaxis: pharmacological + mechanical unless contraindicated; ARDS is prothrombotic (microthrombosis).

Complications

  • Ventilation-related: barotrauma (pneumothorax, pneumomediastinum), VILI, ventilator-associated pneumonia.
  • Haemodynamic: hypotension from high intrathoracic pressures/PEEP; RV failure from increased PVR.
  • Systemic: ICU-acquired weakness, delirium, critical illness polyneuropathy/myopathy, AKI, pressure injuries (esp. prone).
  • Long-term: reduced exercise tolerance, neuropsychological sequelae, fibrotic lung disease in a subset.
Define ARDS and give the Berlin diagnostic criteria including severity classification.

Structure your answer as: definition → 4 Berlin criteria → severity by PaO2/FiO2 with PEEP/CPAP requirement.

  • Definition: acute diffuse inflammatory lung injury causing increased permeability pulmonary oedema, reduced aerated lung, and hypoxaemia not fully explained by cardiac failure/fluid overload.
  • Berlin criteria: timing ≤ 1 week; bilateral opacities; respiratory failure not fully explained by cardiac failure/fluid overload; oxygenation impairment with PEEP/CPAP ≥ 5 cmH2O.
  • Severity (PaO2/FiO2, mmHg): Mild 200–300; Moderate 100–200; Severe ≤ 100 (all with PEEP/CPAP ≥ 5).
Explain the pathophysiology of hypoxaemia in ARDS and why it can be refractory to oxygen therapy.

Focus on shunt, V/Q mismatch, atelectasis, diffusion limitation (less important), and impaired HPV.

  • Protein-rich alveolar oedema + surfactant dysfunction → alveolar collapse and consolidation → true shunt (perfused but non-ventilated units).
  • V/Q mismatch from heterogeneous lung units; dependent atelectasis with relatively spared non-dependent regions.
  • Shunt is relatively refractory to increased FiO2 because shunted blood does not contact alveolar gas; recruitment/PEEP/proning can reduce shunt fraction.
  • Microthrombosis and vascular changes increase dead space and may worsen gas exchange and RV load.
Describe lung-protective ventilation in ARDS. Include targets for tidal volume, plateau pressure and driving pressure, and explain why they matter.

Give numbers and the rationale (baby lung, VILI).

  • VT ~6 mL/kg PBW (range 4–8) to reduce volutrauma in the small ‘baby lung’.
  • Keep plateau pressure ≤ 30 cmH2O (measure with inspiratory hold) to limit overdistension/barotrauma.
  • Driving pressure ΔP = Pplat − PEEP; lower ΔP correlates with better outcomes; aim ~≤ 15 cmH2O if feasible.
  • Use adequate PEEP to prevent cyclic opening/closing (atelectrauma) while avoiding overdistension and haemodynamic compromise.
  • Accept permissive hypercapnia if needed to maintain protective pressures, provided no major contraindication (e.g. raised ICP).
A ventilated ARDS patient becomes hypotensive after increasing PEEP. Explain mechanisms and immediate management.

Think: reduced venous return, RV afterload, overdistension, occult pneumothorax, sepsis progression.

  • Mechanisms: increased intrathoracic pressure → reduced venous return and CO; increased PVR → RV strain/failure; overdistension reduces LV preload; possible barotrauma (tension pneumothorax).
  • Immediate actions: check airway pressures, chest movement, auscultation, capnography; exclude pneumothorax (clinical/US) and treat if suspected.
  • Reduce PEEP/mean airway pressure if overdistension suspected; reassess compliance and oxygenation; consider alternative recruitment strategy (e.g. prone).
  • Support circulation: vasopressor (noradrenaline), cautious fluid bolus only if fluid responsive; consider echo for RV/LV assessment.
Discuss prone positioning in ARDS: indications, physiological benefits, contraindications, and complications.

Examiners like: when to prone, why it works, and practical risks.

  • Indications: moderate–severe ARDS with persistent hypoxaemia despite optimisation (often P/F ≤ 150 mmHg on FiO2 ≥ 0.6 with PEEP ≥ 5–10).
  • Benefits: improved V/Q matching; more even distribution of transpulmonary pressure; recruitment of dorsal lung; reduced overdistension of ventral lung; reduced VILI; mortality benefit when used early and for prolonged sessions (~16 h).
  • Contraindications (often relative): unstable spine, open chest/abdomen, uncontrolled shock/arrhythmia, raised ICP, late pregnancy, recent sternotomy (case-dependent).
  • Complications: accidental extubation/line loss, pressure sores, facial/airway oedema, corneal injury, brachial plexus injury, vomiting/aspiration, haemodynamic instability.
Explain permissive hypercapnia: why it is used in ARDS, how you would manage it, and when you would avoid it.

Link to lung-protective ventilation and consequences of respiratory acidosis.

  • Used to allow low VT/low pressures to minimise VILI; accepting higher PaCO2 is preferable to injurious ventilation.
  • Management: ensure adequate oxygenation; increase RR within safe limits; minimise dead space; consider buffering only selectively (severe acidaemia with instability); treat underlying metabolic acidosis; consider extracorporeal CO2 removal/ECMO in refractory cases.
  • Avoid/caution: raised ICP/brain injury, severe pulmonary hypertension or RV failure, severe arrhythmias/ischaemia, profound metabolic acidosis.
How would you differentiate ARDS from cardiogenic pulmonary oedema at the bedside and with investigations?

Use history, exam, imaging, echo, and response to therapy; acknowledge overlap.

  • History/risk factors: ARDS often follows sepsis/aspiration/trauma; cardiogenic relates to MI, valvular disease, fluid overload.
  • Exam: raised JVP, S3, peripheral oedema suggest cardiogenic; but may be confounded in critical illness.
  • Imaging: ARDS bilateral opacities without classic cardiogenic features; cardiogenic may show cardiomegaly, pleural effusions, Kerley B lines (not definitive).
  • Echo: LV systolic/diastolic dysfunction, valvular lesions; ARDS may have normal LV but can have RV strain.
  • Response: cardiogenic improves with diuresis/afterload reduction; ARDS primarily needs lung-protective ventilation and addressing trigger.
You are asked to anaesthetise a patient with severe ARDS for emergency laparotomy. Outline your plan (pre-op, induction, ventilation, haemodynamics, postoperative).

This is a common FRCA-style scenario: prioritise oxygenation, avoid derecruitment, and manage shock.

  • Pre-op: liaise with ICU; review ventilator settings, recent ABG, proning/adjuncts; ensure bloods, crossmatch, antibiotics, source control plan; assess lines and access; plan for transfer with portable ventilator and adequate PEEP.
  • Induction: high aspiration risk; preoxygenate with PEEP/CPAP; RSI with haemodynamically stable agents; have vasopressors running; avoid prolonged apnoea; consider maintaining PEEP during induction if feasible.
  • Ventilation: continue lung-protective strategy (VT ~6 mL/kg PBW, Pplat ≤ 30, low ΔP); titrate PEEP; accept permissive hypercapnia; avoid circuit disconnections; consider recruitment only if safe.
  • Haemodynamics/fluids: treat septic shock; noradrenaline first-line; conservative fluids after initial resuscitation; use dynamic assessment/echo; avoid excessive PEEP causing RV failure; consider iNO if RV failure with hypoxaemia (bridge).
  • Monitoring: arterial line, capnography, temperature, urine output; consider cardiac output monitoring/TOE if unstable; frequent ABGs.
  • Post-op: return to ICU ventilated; ensure handover of intra-op events, ventilator settings, fluids/vasopressors, cultures/source control; plan for proning continuation if indicated.
What is ventilator-induced lung injury (VILI)? Describe the mechanisms and how ARDS ventilation strategies reduce it.

Name the injury patterns and link each to a protective strategy.

  • Volutrauma: overdistension from high VT/transpulmonary pressure → use low VT, limit Pplat/ΔP.
  • Barotrauma: pneumothorax/pneumomediastinum from high pressures → limit pressures, monitor for air leak.
  • Atelectrauma: repetitive opening/closing → use adequate PEEP, avoid disconnections.
  • Biotrauma: inflammatory mediator release from mechanical stress → reduced by overall protective ventilation and avoiding injurious settings.
  • Oxygen toxicity: prolonged high FiO2 → titrate FiO2 to target saturations once stable.

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