ARDS: Berlin definition, lung-protective ventilation, proning, and ECMO

Cinematic ICU scene of a severely hypoxaemic ARDS patient being turned prone by a team, bilateral consolidations on the chest X-ray, a ventilator in lung-protective mode, a veno-venous ECMO circuit primed and standing by, clinical-blue lighting, intense and controlled, no faces, no text — FigureThe Berlin definition grades ARDS by PaO2/FiO2 — mild (200–300), moderate (100–200), severe (<100) — within one week of a known insult, with bilateral opacities not fully explained by cardiac failure. The management bundle is low-tidal-volume ventilation (6 mL/kg PBW), plateau pressure under 30 cmH2O, conservative fluid strategy, early prone positioning for moderate-severe disease (PROSEVA), and veno-venous ECMO for refractory hypoxaemia (EOLIA).

ARDS severity (Berlin definition)

Feature	Mild	Moderate	Severe
PaO2/FiO2 (with PEEP ≥5)	200-300	100-200	≤100
Chest imaging	Bilateral opacities	Bilateral opacities	Bilateral opacities
Mortality	27%	32%	45%
Ventilator days (median)	5	7	9
Proning indicated?	No (PaO2/FiO2 <150)	If <150	YES (PROSEVA)
ECMO considered?	No	If refractory	If refractory (PaO2/FiO2 <80)

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Management of moderate-severe ARDS

DIAGNOSE (Berlin) + TREAT CAUSE — (a) BERLIN CRITERIA: (i) Timing: within 1 WEEK of known clinical insult. (ii) Chest imaging: BILATERAL opacities (not fully explained by effusions, atelectasis, nodules). (iii) Origin of oedema: respiratory failure NOT fully explained by cardiac failure or fluid overload (objective assessment — echo — needed if no clear risk factor for ARDS). (iv) Hypoxaemia: MILD (PaO2/FiO2 200-300 with PEEP/CPAP ≥5), MODERATE (100-200), SEVERE (≤100). (b) CAUSE: (i) DIRECT (pulmonary): pneumonia [most common], aspiration, inhalation injury, near-drowning, pulmonary contusion. (ii) INDIRECT (extrapulmonary): sepsis, severe shock, pancreatitis, massive transfusion (TRALI), burns, drug reaction. (c) TREAT CAUSE: antibiotics (pneumonia/sepsis), source control (drain abscess), stop offending drug/transfusion, treat pancreatitis. ARDS won't resolve until cause treated
LUNG-PROTECTIVE VENTILATION (ARDSNET — MORTALITY REDUCTION) — (a) TIDAL VOLUME: 6 mL/kg PREDICTED (ideal) BODY WEIGHT (NOT actual — calculate by height + sex — formula: male = 50 + 0.91 × [height cm − 152.4]; female = 45.5 + 0.91 × [height cm − 152.4]). (b) PLATEAU PRESSURE: ≤30 cmH2O (measure with inspiratory pause — if >30 -> REDUCE Vt [to 4 mL/kg if needed] — the lung is INJURED + SMALL ['baby lung'] — high pressure -> volutrauma + barotrauma). (c) PEEP: titrate (PEEP/FiO2 table — ARDSNet — higher PEEP for lower FiO2 — maintain alveolar recruitment + reduce atelectrauma). (d) RESPIRATORY RATE: 6-35 (to maintain minute ventilation — pH target >7.25 — accept hypercapnia [permissive]). (e) ARDSNet (2000, NEJM): Vt 6 vs 12 mL/kg -> 6 mL/kg REDUCED mortality 22% (31% vs 40%) — the MOST IMPORTANT trial in ARDS — lung-protective ventilation is STANDARD. (f) DRIVING PRESSURE (ΔP = plateau − PEEP): <15 cmH2O (Amato 2015 — best predictor of mortality — lower = better — if ΔP high despite low Vt -> reduce Vt further + increase PEEP)
PEEP OPTIMISATION — (a) GOAL: maintain alveolar RECRUITMENT (prevent cyclic opening-closing = atelectrauma) + improve OXYGENATION + reduce LUNG INJURY. (b) PEEP/FiO2 TABLE (ARDSNet): higher FiO2 (more hypoxaemic) -> higher PEEP (to recruit + maintain alveoli). (c) HIGHER vs LOWER PEEP: (i) ART (2017, NEJM): higher PEEP (recruitment manoeuvres + high PEEP) WORSE (more mortality — barotrauma). DON'T use aggressive recruitment manoeuvres. (ii) EXPRESS (2010): moderate PEEP benefit — but not aggressive. (iii) CURRENT: MODERATE PEEP (PEEP/FiO2 table) — NOT aggressive recruitment (ART harm). (d) ESOPHAGEAL PRESSURE (oPes): if available — measure transpulmonary pressure (plateau − oPes) — titrate PEEP to keep transpulmonary pressure POSITIVE (avoid lung collapse). (e) PRACTICE: PEEP/FiO2 table (ARDSNet) — moderate PEEP. AVOID aggressive recruitment (ART — harm)
PRONE POSITIONING (PROSEVA — MORTALITY REDUCTION) — (a) INDICATION: MODERATE-SEVERE ARDS (PaO2/FiO2 <150) despite adequate ventilation (Vt 6 mL/kg + PEEP). (b) PROSEVA (2013, NEJM): prone ≥16 hours/day for PaO2/FiO2 <150 -> REDUCED mortality (16% absolute — 23.6% vs 41.0% at 28 days — NNT 6). (c) MECHANISM: (i) REDUCES SHUNT (dorsal lung [usually collapsed in supine] is recruited when prone — gravity redistributes perfusion). (ii) REDUCES VENTILATION-PERFUSION MISMATCH (more uniform ventilation when prone). (iii) REDUCES LUNG STRAIN (more uniform inflation — less overdistension of ventral lung — less atelectrauma of dorsal lung). (iv) FACILITATES SECRETION CLEARANCE (drainage from dependent regions). (d) TECHNIQUE: (i) Turn prone (face down) — requires 4-6 staff (turning, airway, lines, monitoring). (ii) Maintain ≥16 hours/day (usually 16-20h prone + 4-8h supine for care/procedures). (iii) Pad pressure points (face, chest, pelvis, knees — prevent pressure injuries). (iv) Monitor: ETT (don't dislodge during turning), SpO2 (may transiently drop during turn — then improve), lines/tubes (secure — check all). (e) CONTRAINDICATIONS (relative): spinal instability, severe pelvic fractures, recent abdominal surgery, pregnancy, raised ICP (relative), haemodynamic instability. (f) PRACTICE: PRONE for PaO2/FiO2 <150 — this is a MORTALITY-REDUCING intervention (like lung-protective ventilation) — DO IT. (g) EARLY PRONING (within 36h of moderate-severe ARDS) — better than late (PROSEVA enrolled within 24-48h)
HFNC (HIGH-FLOW NASAL CANNULA) — MAY AVOID INTUBATION — (a) INDICATION: moderate hypoxaemic respiratory failure (PaO2/FiO2 200-300) — BEFORE intubation — trial of HFNC. (b) MECHANISM: (i) HIGH FLOW (up to 60 L/min) -> washes out dead space (reduces CO2 rebreathing). (ii) PEEP effect (low-level positive pressure 3-5 cmH2O — maintains alveolar recruitment). (iii) REDUCED WORK OF BREATHING (heated humidified gas -> less respiratory effort). (iv) REDUCES inspiratory resistance (nasal cannula gas flow matches patient's inspiratory demand). (c) FLORALI (2015, NEJM): HFNC vs standard O2 (face mask) vs NIV in immunocompromised + ARDS patients -> HFNC trend to LOWER intubation rate + LOWER mortality (especially in PaO2/FiO2 <200 subgroup — significant). (d) ROX INDEX (SpO2/FiO2 / RR): after 2h of HFNC — if ROX <3.85 -> high risk of intubation (consider intubating). If >4.88 -> likely to succeed (continue HFNC). (e) WHEN TO INTUBATE (HFNC FAILURE): (i) Worsening hypoxaemia (SpO2 <90% despite FiO2 100%). (ii) Rising RR (>35-40). (iii) Exertion/exhaustion (accessory muscle use, paradoxical breathing). (iv) Altered consciousness. (v) Haemodynamic instability. (vi) ROX <3.85 at 2h. (f) PRACTICE: trial HFNC for moderate hypoxaemia — if not improving within 1-2h -> intubate (don't delay — delayed intubation is worse than early)
NEUROMUSCULAR BLOCKADE + STEROIDS + ECMO + FLUID CONSERVATIVE — (a) NEUROMUSCULAR BLOCKADE (NMB): (i) ACURASYS (2010, NEJM): cisatracurium 48h for severe ARDS (PaO2/FiO2 <150) -> REDUCED mortality + adjusted hazard ratio 0.68 (especially in PaO2/FiO2 <120). (ii) ROSE (2019, NEJM): cisatracurium 48h vs placebo (light sedation) -> NO benefit (no difference in mortality). BUT: ROSE used lighter sedation + different protocol -> controversial. (iii) CURRENT: NMB for SEVERE ARDS (PaO2/FiO2 <120) with HIGH driving pressure / asynchrony — SHORT course (48h) — but not routine for ALL (ROSE questioned). Use if ventilator asynchrony or uncontrolled (high driving pressure despite Vt 6 + sedation). (iv) AVOID PROLONGED NMB (>48h — ICU-acquired weakness). (b) STEROIDS: (i) DEXA-ARDS (2020, NEJM): dexamethasone 20 mg/day x5 days then 10 mg/day x5 days for moderate-severe ARDS -> REDUCED mortality (21% vs 36% at 60 days) + more ventilator-free days. (ii) CURRENT: CONSIDER dexamethasone for moderate-severe ARDS (especially from COVID-19 — RECOVERY — dexamethasone reduced mortality in ventilated COVID). (iii) CONTROVERSIAL: not universally adopted — some guidelines recommend (DEXA-ARDS + RECOVERY support) — others cautious (historical methylprednisolone trials mixed). (c) ECMO (VV-ECMO): (i) INDICATION: REFRACTORY severe ARDS (PaO2/FiO2 <80 despite optimisation — lung-protective ventilation + proning + PEEP) OR severe hypercapnia with pH <7.2. (ii) CESAR (2009, Lancet): referral to ECMO centre -> reduced mortality (37% vs 53% in conventional). (iii) EOLIA (2018, NEJM): VV-ECMO vs conventional for VERY severe (PaO2/FiO2 <50) -> STOPPED EARLY for futility (no difference in primary [mortality at 60d]) — BUT: Bayesian re-analysis suggested possible benefit. (iv) CURRENT: ECMO as RESCUE for refractory (not routine) — refer to ECMO centre — bridge to recovery (lungs heal). (v) COMPLICATIONS: bleeding (anticoagulation), infection, haemolysis, thromboembolism, limb ischaemia (femoral). (d) FLUID CONSERVATIVE (FACTT): (i) FACTT (2006, NEJM): conservative fluid strategy (CVP <4 or PAOP <8 — diurese) vs liberal (CVP 10-14 or PAOP 14-18) -> conservative had MORE ventilator-free days + LESS oxygenation days (but NO mortality difference). (ii) CURRENT: FLUID CONSERVATIVE strategy (don't fluid overload — once resuscitated, achieve neutral/negative balance — diurese if overloaded) — improves oxygenation + ventilator days. (iii) BALANCE: ensure ADEQUATE perfusion (not dry) — assess volume (clinical + ultrasound + lactate) — if adequate -> restrict fluids. (e) PRACTICE: lung-protective + prone + PEEP (mortality-reducing) + HFNC (avoid intubation) + fluid conservative + consider NMB (severe) + consider dexamethasone (moderate-severe) + ECMO (refractory rescue)

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SAQ — Applying the Berlin definition to a septic ICU patient

10 minutes · 10 marks

A 64-year-old man (height 178 cm) is admitted to ICU 36 hours after presenting with septic shock from a perforated appendix. He is intubated and ventilated (FiO2 0.8, PEEP 10 cmH2O, Vt 450 mL). Blood gas: PaO2 76 mmHg, PaCO2 42, pH 7.30. Chest X-ray shows bilateral patchy infiltrates. Bedside echo shows a normal LV with no valvular lesion; BNP is mildly elevated. The examiners ask you to apply the Berlin definition and outline initial ventilatory management.

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Clinical pearls

High-yield ARDS points for CICM/FFICM exam

ARDSNet — Vt 6 mL/kg — 22% mortality reduction. (1) ARDSNET (2000, NEJM): RCT — Vt 6 mL/kg predicted body weight vs 12 mL/kg in ARDS. RESULT: (a) 6 mL/kg REDUCED mortality (31% vs 40% — 22% relative reduction — 9% absolute — NNT 11). (b) FEWER ventilator days + more days free of organ failure. (2) WHY LOWER Vt: (a) ARDS lung is INJURED + SMALL ('baby lung' — only 20-30% of normal lung is aerated — the rest is consolidated/atelectatic). (b) Ventilating with HIGH Vt (12 mL/kg) -> OVERSTRETCHES the small amount of aerated lung (volutrauma) + HIGH PRESSURE (barotrauma) + cyclic opening-closing (atelectrauma) + inflammatory mediator release (biotrauma). (c) Ventilating with LOW Vt (6 mL/kg) -> REDUCES all these injuries -> lung can HEAL. (3) PRACTICE: Vt 6 mL/kg PREDICTED (ideal) body weight (NOT actual — especially obese — actual > predicted — would overventilate). Plateau pressure ≤30 cmH2O (if >30 -> reduce Vt to 4 mL/kg). Accept HYPERCAPNIA (permissive — pH >7.25). (4) KEY: this is THE MOST IMPORTANT trial in ARDS — lung-protective ventilation is STANDARD (non-negotiable) — reduces mortality.[2] }
Berlin definition — clinical + objective. (1) BERLIN DEFINITION (2012, JAMA — ARDS Definition Task Force): replaces the older AECC (1994) definition. (2) FOUR CRITERIA (all required): (a) TIMING: within 1 WEEK of known clinical insult (or new/worsening respiratory symptoms). (b) CHEST IMAGING: BILATERAL opacities (CXR or CT) — NOT fully explained by effusions, lobar/lung collapse, or nodules. (c) ORIGIN OF OEDEMA: respiratory failure NOT fully explained by CARDIAC FAILURE or FLUID OVERLOAD (need objective assessment — e.g., echocardiography — to exclude hydrostatic oedema if no clear ARDS risk factor). (d) OXYGENATION (PaO2/FiO2 ratio with PEEP or CPAP ≥5 cmH2O): MILD (200-300), MODERATE (100-200), SEVERE (≤100). (3) IMPROVEMENTS over AECC: (a) Removed 'acute lung injury (ALI)' term (replaced with mild ARDS). (b) Added PEEP requirement (≥5 — for standardisation). (c) Requires explicit exclusion of cardiac failure (echo). (d) Radiographic criterion clarified (bilateral — not just 'bilateral infiltrates'). (4) LIMITATIONS: (a) PaO2/FiO2 varies with PEEP (higher PEEP -> higher PaO2/FiO2 — so severity may be underestimated with high PEEP). (b) Doesn't account for ventilator settings (driving pressure). (c) Clinical — not pathological (can't biopsy in routine). (5) PRACTICE: apply Berlin criteria at diagnosis — determines severity + guides management (proning for <150, ECMO for refractory <80).[1] }
PROSEVA — proning reduces mortality. (1) PROSEVA (2013, NEJM): RCT — PRONE POSITIONING (≥16h/day) vs SUPINE in MODERATE-SEVERE ARDS (PaO2/FiO2 <150, within 24-48h of diagnosis, already on lung-protective ventilation). RESULT: (a) PRONE REDUCED mortality (16.0% vs 32.8% at 28 days — 16.8% ABSOLUTE reduction — NNT 6 — REMARKABLE). (b) (23.6% vs 41.0% at 90 days). (c) No increase in complications (in earlier proning trials — pressure sores, facial oedema, nerve injury — PROSEVA minimised with protocolised turning + padding). (2) WHY PROSEVA SUCCEEDED (when earlier trials failed): (a) SEVERE ARDS only (PaO2/FiO2 <150 — earlier trials included milder patients who wouldn't benefit). (b) EARLY (within 24-48h — before irreversible fibroproliferative phase). (c) LONG duration (≥16h — earlier trials used 6-8h — insufficient). (d) STANDARD lung-protective ventilation (all patients — earlier trials used variable ventilation). (3) MECHANISM of benefit: (a) More UNIFORM LUNG INFLATION (prone recruits dorsal lung + reduces overdistension of ventral lung -> less lung strain -> less biotrauma). (b) Better V/Q MATCHING -> better oxygenation -> lower FiO2 (less oxygen toxicity) + lower PEEP (less barotrauma). (c) REDUCES RIGHT HEART STRAIN (hypoxic pulmonary vasoconstriction is reduced when oxygenation improves -> less RV afterload). (d) The benefit is NOT just from oxygenation improvement — it's from REDUCED LUNG INJURY (less VILI [ventilator-induced lung injury] when prone). (4) PRACTICE: PRONE for PaO2/FiO2 <150 — ≥16h/day — EARLY (within 24-48h) — with lung-protective ventilation — protocolised turning. (5) KEY: proning is a MORTALITY-REDUCING intervention (like lung-protective ventilation) — DO IT for moderate-severe ARDS.[3] }
HFNC — FLORALI trial. (1) HFNC (High-Flow Nasal Cannula): heated, humidified oxygen at HIGH FLOW (up to 60 L/min) via nasal cannula. (2) MECHANISM: (a) WASHOUT of dead space (reduces CO2 rebreathing -> lowers PaCO2 + reduces work of breathing). (b) LOW-LEVEL PEEP (3-5 cmH2O — from high flow through nasal passages -> maintains alveolar recruitment). (c) REDUCED WORK OF BREATHING (heated humidified gas — less effort to inspire). (d) MATCHES inspiratory flow (reduces inspiratory resistance). (3) FLORALI (2015, NEJM): HFNC vs standard O2 (face mask) vs NIV in immunocompromised + ARDS patients (PaO2/FiO2 <300). RESULT: (a) HFNC trend to LOWER intubation rate (38% vs 47% vs 50% — not significant overall). (b) HFNC LOWER mortality (especially in PaO2/FiO2 <200 subgroup — significant). (c) HFNC more comfortable (patient preference). (4) ROX INDEX (SpO2/FiO2 / RR): (a) After 2h of HFNC. (b) ROX <3.85 -> HIGH risk of intubation (consider intubating). (c) ROX >4.88 -> LIKELY to succeed (continue HFNC). (d) Use ROX to DECIDE — trial HFNC -> reassess at 2h -> if ROX low -> intubate (don't delay). (5) WHEN TO INTUBATE (HFNC failure): worsening hypoxaemia (SpO2 <90%), rising RR (>35), exhaustion, altered consciousness, haemodynamic instability, ROX <3.85. (6) PRACTICE: trial HFNC for moderate hypoxaemia (PaO2/FiO2 200-300). Reassess at 1-2h. If not improving (ROX low, worsening) -> INTUBATE (don't delay — delayed intubation worse than early). (7) KEY: HFNC may AVOID intubation (FLORALI) — but DON'T delay intubation if failing (early intubation is better than late).[4] }
Driving pressure — the best predictor. (1) DRIVING PRESSURE (ΔP) = PLATEAU PRESSURE − PEEP. (2) RATIONALE: (a) ΔP represents the PRESSURE applied to the LUNG (not just airway) to deliver a tidal volume. (b) It reflects LUNG COMPLIANCE (ΔP = Vt / compliance — if compliance low [stiff lung — ARDS] -> ΔP high for same Vt). (c) ΔP reflects the STRAIN on the lung (high ΔP = overdistension + atelectrauma). (3) AMATO (2015, NEJM): individual patient data meta-analysis of ARDS trials. RESULT: (a) ΔP was the BEST PREDICTOR of mortality (better than Vt, plateau pressure, PEEP — in isolation). (b) For a given Vt: lower ΔP (better compliance) = lower mortality. (c) For a given ΔP: Vt did NOT independently predict mortality (i.e., the INJURY is from ΔP/strain, not Vt per se). (4) TARGET: ΔP <15 cmH2O (if >15 -> reduce Vt [even below 6 mL/kg if needed] + increase PEEP). (5) PRACTICE: measure ΔP (plateau − PEEP) for ALL ARDS patients. If >15 -> reduce Vt (to 4-5 mL/kg) + increase PEEP (to recruit + reduce strain). Target ΔP <15. (6) KEY: ΔP is the BEST available bedside predictor of lung strain + mortality — target <15.[2] }
ECMO — rescue for refractory. (1) VV-ECMO (Veno-Venous): drains venous blood -> oxygenates + removes CO2 -> returns to venous system -> supports lungs (heart pumps normally). (2) INDICATIONS: (a) REFRACTORY HYPOXAEMIA: PaO2/FiO2 <80 (or <50 — very severe) despite OPTIMISED ventilation (Vt 6 mL/kg + PEEP + proning). (b) SEVERE HYPERCAPNIA with ACIDOSIS: pH <7.15 + PaCO2 >80 despite permissive hypercapnia ventilation. (c) VERY HIGH PLATEAU PRESSURE: >35 cmH2O despite Vt 4 mL/kg (can't ventilate safely — ECMO allows 'ultra-protective' ventilation). (3) TRIALS: (a) CESAR (2009, Lancet): referral to ECMO centre (some received ECMO) vs conventional -> referral had LOWER mortality (37% vs 53%). (b) EOLIA (2018, NEJM): VV-ECMO vs conventional for very severe (PaO2/FiO2 <50) -> STOPPED EARLY for futility (no difference in 60-day mortality — 35% vs 46% — not significant [p=0.09 — close]). BUT: Bayesian re-analysis suggested possible benefit (posterior probability ~85-99% of benefit). (4) CURRENT: ECMO as RESCUE for refractory severe ARDS (not routine). Refer to ECMO centre. Bridge to recovery (lung heals -> wean ECMO). (5) TECHNIQUE: (a) Drainage cannula (femoral vein — deoxygenated blood out). (b) Return cannula (IJV — oxygenated blood in). (c) Centrifugal pump + membrane oxygenator (oxygenates + removes CO2). (d) Anticoagulation (heparin — target ACT 1.5x — or no anticoag [some centres — bleeding risk]). (e) VENTILATOR settings during ECMO: 'REST' settings (Vt 1-4 mL/kg or pressure control 10-15 cmH2O + PEEP 10-15 + RR 10-12 — 'ultra-protective' — minimal ventilation — let ECMO do gas exchange + lung HEAL). (6) COMPLICATIONS: bleeding (anticoagulation — especially intracranial [devastating]), infection, haemolysis, thromboembolism (circuit clot), limb ischaemia (femoral cannula — monitor perfusion), vascular injury. (7) WEANING: as lung improves (compliance improves + PaO2/FiO2 improves on lower ECMO flow) -> reduce ECMO flow -> trial off (clamp ECMO + assess gas exchange on ventilator) -> decannulate. (8) PRACTICE: ECMO for refractory severe ARDS (PaO2/FiO2 <80 despite optimal) — refer early (don't wait for cardiac arrest) — bridge to recovery.[5] }
Neuromuscular blockade — ACURASYS vs ROSE. (1) ACURASYS (2010, NEJM): cisatracurium infusion 48h for severe ARDS (PaO2/FiO2 <150) -> REDUCED mortality (adjusted HR 0.68 — 32% relative reduction) + more ventilator-free days + less barotrauma. (2) ROSE (2019, NEJM): cisatracurium 48h vs placebo (with light sedation + high PEEP protocol) -> NO benefit (no difference in mortality — 42.5% vs 42.8%). (3) WHY THE DIFFERENCE: (a) ROSE used LIGHTER SEDATION (patients may have been more awake — more synchronous breathing — less need for NMB). (b) ROSE used HIGHER PEEP (standardised protocol — patients may have been better recruited — less need for NMB). (c) ROSE enrolled patients with PaO2/FiO2 <150 (not <120 — milder — ACURASYS post-hoc showed most benefit in <120). (d) ROSE enrolled more patients with 'mild' severity (PaO2/FiO2 120-150). (4) CURRENT (post-ROSE): (a) NMB NOT routine for ALL ARDS (ROSE showed no benefit in broad population). (b) CONSIDER for VERY SEVERE (PaO2/FiO2 <120) with HIGH DRIVING PRESSURE (>15) or SEVERE ASYNCHRONY (patient fighting ventilator — high transalveolar pressure). (c) SHORT COURSE (48h — cisatracurium infusion). (d) AVOID prolonged (>48h — ICU-acquired weakness). (e) Ensure DEEP SEDATION (NMB without sedation is unethical — must be fully sedated). (5) PRACTICE: NMB for very severe ARDS (PaO2/FiO2 <120) + high driving pressure/asynchrony — 48h — with deep sedation. Not routine for all (ROSE).[6] }
Steroids — DEXA-ARDS and RECOVERY. (1) DEXA-ARDS (2020, NEJM): dexamethasone (20 mg/day x5 days then 10 mg/day x5 days) vs placebo for moderate-severe ARDS (PaO2/FiO2 100-200 with PEEP ≥10). RESULT: (a) REDUCED mortality (21% vs 36% at 60 days — 15% absolute reduction — NNT 7). (b) More ventilator-free days + fewer ICU days. (c) No excess infections or adverse events. (2) RECOVERY (2020, NEJM): dexamethasone 6 mg/day for COVID-19 -> reduced mortality in VENTILATED patients (29.3% vs 41.4%). (3) WHY STEROIDS HELP: (a) ARDS = INFLAMMATION (cytokine-mediated diffuse alveolar damage). (b) Steroids SUPPRESS inflammation -> reduce alveolar damage -> promote healing. (c) ESPECIALLY in the FIBROPROLIFERATIVE phase (days 7-14 — inflammation → fibrosis — steroids may prevent fibrosis). (4) CONTROVERSIAL: (a) HISTORICAL: methylprednisolone trials (Meduri 1998, 2007 — some benefit; Bernard 1987 — no benefit). (b) STEROIDS for ARDS from DIFFERENT causes (sepsis vs viral vs aspiration) may respond differently. (c) SIDE EFFECTS: infection (immunosuppression), hyperglycaemia, myopathy (ICU-acquired weakness), psychiatric. (5) CURRENT: CONSIDER dexamethasone for moderate-severe ARDS (DEXA-ARDS support) — especially COVID-19 (RECOVERY — clear benefit in ventilated). (6) PRACTICE: dexamethasone for moderate-severe ARDS — weigh benefit (mortality reduction) vs risk (infection, hyperglycaemia, weakness). Monitor glucose (6-10), infection surveillance, minimise duration. (7) KEY: steroids for ARDS is EMERGING — DEXA-ARDS + RECOVERY support — but not universally adopted (controversial — especially for non-COVID causes).[1] }
Fluid conservative — FACTT. (1) FACTT (2006, NEJM): conservative fluid strategy (CVP <4 or PAOP <8 — achieve with diuretics [frusemide]) vs liberal (CVP 10-14 or PAOP 14-18) in ARDS. RESULT: (a) CONSERVATIVE had MORE ventilator-free days (14.6 vs 12.1) + MORE ICU-free days. (b) Better OXYGENATION (PaO2/FiO2 improved). (c) NO mortality difference (26.3% vs 28.4% — trend favouring conservative). (2) WHY LESS FLUID HELPS: (a) ARDS = capillary LEAK (permeability pulmonary oedema). (b) More fluid -> more LEAK -> more interstitial oedema -> worse gas exchange + reduced compliance. (c) Less fluid -> less oedema -> better oxygenation + better compliance + faster weaning. (3) STRATEGY: (a) Once RESUSCITATED (adequate perfusion — MAP ≥65, lactate clearing, urine >0.5) -> achieve NEUTRAL or NEGATIVE balance (diurese if overloaded — frusemide). (b) AVOID ongoing positive balance (each litre of excess -> worse oxygenation). (c) BALANCE: don't make patient DRY (hypovolaemia -> AKI + poor perfusion) — assess volume (clinical + ultrasound + lactate) — if adequate -> restrict. (4) ALBUMIN: if large volume needed + oncotic pressure low -> albumin (to maintain intravascular volume with less total fluid). (5) PRACTICE: fluid conservative once resuscitated — target neutral/negative balance — diurese if overloaded.[1] }
Phenotypes — hyperinflammatory vs hypoinflammatory. (1) TWO PHENOTYPES (Calfee 2014, Famous 2017): (a) HYPERINFLAMMATORY (Type 1): high inflammatory markers (IL-6, IL-8, sTNFR, G-CSF) + LOW protein C + LOW bicarbonate. Higher mortality. (b) HYPOINFLAMMATORY (Type 2): lower inflammatory markers + normal protein C/bicarbonate. Lower mortality. (2) WHY IT MATTERS: (a) The two phenotypes may respond DIFFERENTLY to treatment: (i) HIGHER PEEP: hyperinflammatory benefits more. (ii) SIMVASTATIN: hypoinflammatory benefits more (HARP-2 post-hoc). (iii) STEROIDS: hyperinflammatory may benefit more (inflammation-driven — steroids suppress inflammation). (b) PRECISION MEDICINE: target therapy to phenotype (like 'personalised medicine' in oncology). (3) CURRENT: RESEARCH — not yet routine (biomarker panels not widely available — can't phenotype at bedside easily). (4) FUTURE: phenotype-guided therapy (if hyperinflammatory -> steroids + higher PEEP; if hypoinflammatory -> different approach). (5) KEY: ARDS is NOT one disease — it's a SYNDROME with different underlying biology (phenotypes) — understanding phenotypes may lead to PRECISION TREATMENT (tailor therapy to individual).[1] }
PEEP titration — recruitment. (1) GOAL: maintain alveolar RECRUITMENT (prevent atelectrauma — cyclic opening-closing of alveoli — a major mechanism of VILI). (2) PEEP/FiO2 TABLE (ARDSNet): higher FiO2 (more hypoxaemic) -> higher PEEP (to recruit + maintain alveoli). Standard approach. (3) RECRUITMENT MANOEUVRES: (a) Brief period of HIGH PRESSURE (e.g., CPAP 40 cmH2O for 40 sec — or incremental PEEP to 35-40) -> opens collapsed alveoli -> then set PEEP to maintain recruitment. (b) ART TRIAL (2017, NEJM): AGGRESSIVE recruitment (incremental PEEP to 25 + then titrate) + high PEEP -> WORSE mortality (more barotrauma). (c) CURRENT: AVOID aggressive recruitment (ART harm). Use PEEP/FiO2 table (moderate PEEP). (4) ESOPHAGEAL PRESSURE (oPes): (a) Measures PLEURAL pressure (surrogate). (b) Transpulmonary pressure = plateau pressure − oPes (the actual pressure across the lung). (c) Titrate PEEP to keep transpulmonary pressure POSITIVE in expiration (prevent lung collapse). (d) Useful in obese/abdominal HTN (where chest wall compliance is reduced — plateau pressure may be high from chest wall, not lung — oPes distinguishes). (e) Not widely available (requires esophageal catheter). (5) DRIVING PRESSURE: target <15 cmH2O (see above — Amato). (6) PRACTICE: PEEP/FiO2 table (moderate PEEP). AVOID aggressive recruitment (ART — harm). Target ΔP <15. Consider oPes if obese/abdominal HTN.[2] }
Pulmonary hypertension in ARDS — RV failure. (1) ARDS causes HYPOXIC PULMONARY VASOCONSTRICTION + MICROVASCULAR THROMBOSIS -> increased PVR -> PULMONARY HYPERTENSION -> RV FAILURE (acute cor pulmonale). (2) CLINICAL: (a) Echo: RV DILATION + SEPTAL FLATTENING (D-shaped LV) + reduced RV function + TR (tricuspid regurgitation). (b) HAEMODYNAMICS: high PA pressure + high CVP + low cardiac output (RV can't pump against high PVR). (c) ECG: right axis deviation, T wave inversion V1-V3 (RV strain). (3) MANAGEMENT: (a) REDUCE PVR: (i) IMPROVE OXYGENATION (hypoxia -> vasoconstriction — proning, PEEP, ECMO). (ii) AVOID HYPERCAPNIA (CO2 -> vasoconstriction — ensure adequate ventilation — permissive hypercapnia is less harmful for RV than acidosis). (iii) INHALED VASODILATORS (nitric oxide [iNO] 5-20 ppm OR epoprostenol [inhaled prostacyclin] — reduce PVR selectively [inhaled — only ventilated alveoli -> V/Q matched] — TEMPORARY oxygenation improvement but NO mortality benefit [no routine]). (iv) PULMONARY VASODILATORS (sildenafil, riociguat — controversial — may worsen oxygenation [V/Q mismatch from systemic vasodilation]). (b) SUPPORT RV: (i) INOTROPES (dobutamine, milrinone — improve RV contractility). (ii) AVOID FLUID OVERLOAD (RV is preload-intolerant in failure — excessive fluids -> RV distension -> septal shift -> LV compression [worse]). (iii) MAINTAIN SINUS RHYTHM (AF devastating — RV needs atrial kick). (iv) VASOPRESSORS (noradrenaline — maintain coronary perfusion to RV). (4) KEY: ARDS + RV failure = WORSE prognosis (RV failure is a marker of severe ARDS + contributes to mortality). TREAT: improve oxygenation + inotrope + avoid fluid overload. (5) iNO: improves oxygenation TEMPORARILY (selective pulmonary vasodilation) but NO mortality benefit -> NOT routine (use as BRIDGE — e.g., to ECMO).[1] }
ARDS causes — direct vs indirect. (1) DIRECT (pulmonary — alveolar injury): (a) PNEUMONIA (most common — bacterial [pneumococcal, staph, Gram-negative], viral [influenza, COVID, RSV], fungal [Pneumocystis]). (b) ASPIRATION (gastric contents — chemical pneumonitis). (c) INHALATION INJURY (smoke, toxic gas — fire). (d) NEAR-DROWNING. (e) PULMONARY CONTUSION (blunt chest trauma). (f) RADIATION. (2) INDIRECT (extrapulmonary — systemic inflammation): (a) SEPSIS (most common indirect cause — cytokines -> diffuse alveolar damage). (b) SEVERE SHOCK (prolonged hypoperfusion -> ischaemic lung injury). (c) PANCREATITIS (systemic inflammation from pancreatic enzymes). (d) MASSIVE TRANSFUSION (TRALI — transfusion-related acute lung injury — donor antibodies -> recipient neutrophil activation -> capillary leak). (e) BURNS (inhalation + systemic inflammation). (f) DRUG REACTION / TOXIN (opioid overdose, cocaine, chemotherapy). (g) TRAUMA (fat embolism — long bone fracture). (3) WHY IT MATTERS: (a) Direct causes may have MORE FOCAL injury (alveolar) -> different ventilation strategy (more PEEP to recruit focal atelectasis). (b) Indirect causes may have MORE DIFFUSE injury -> different pattern. (c) BUT: clinically, management is similar (lung-protective + prone + supportive) — treat the cause + ventilate gently. (4) PROGNOSIS: depends on cause (viral/pneumonia may be worse; trauma/aspiration may be more reversible).[1] }
Outcomes + long-term recovery. (1) MORTALITY: mild 27%, moderate 32%, severe 45% (LUNG SAFE — 2016 — large international observational study — REAL-WORLD mortality — similar to trials). (2) PREDICTORS: (a) HIGHER mortality: older age, immunocompromised, sepsis source, high driving pressure, severe hypoxaemia, RV failure. (b) LOWER: trauma/aspiration source (more reversible), young. (3) RECOVERY: (a) LUNG: most ARDS survivors have NEAR-NORMAL lung function at 6-12 months (restrictive defect resolves — lung heals — unlike pulmonary fibrosis [chronic]). Some have mild restriction + reduced DLCO (diffusion capacity) — usually not symptomatic. (b) PICS: 30-50% have COGNITIVE impairment (memory, executive, attention) + PSYCHOLOGICAL (depression, PTSD, anxiety) + PHYSICAL (ICU-acquired weakness — CIM/CIP — 25-50%). (4) REHABILITATION: prolonged — physical (mobility, strength), cognitive (neuropsychology), psychological (CBT, medications). (5) FOLLOW-UP: ICU clinic (screen for PICS), pulmonary function tests (at 6 months — assess recovery), psychological support. (6) KEY: ARDS mortality is significant (27-45%) but most SURVIVORS recover lung function (unlike chronic lung disease) — but carry the burden of PICS (cognitive, psychological, physical). (7) ABCDEF BUNDLE: reduces PICS (Awakening, Breathing, Coordination, Delirium, Early mobility, Family) — implement EARLY (during ARDS — not after).[1] }

Red flags

Critical ARDS red flags

Lung-protective ventilation (Vt 6 mL/kg IBW, plateau <30, ΔP <15) — ARDSNet — 22% mortality reduction.[2] }
Proning ≥16h/day for PaO2/FiO2 <150 — PROSEVA — 16% absolute mortality reduction.[3] }
Fluid conservative (FACTT) — less fluid = more ventilator-free days.[1] }
HFNC may avoid intubation (FLORALI) — but don't delay intubation if failing (ROX <3.85).[4] }
ECMO for refractory (PaO2/FiO2 <80 despite optimal) — rescue (CESAR/EOLIA).[5] }
NMB — ACURASYS (severe) vs ROSE (no routine) — for very severe + high ΔP.[6] }
Dexamethasone — DEXA-ARDS + RECOVERY — emerging benefit (moderate-severe).[1] }
Berlin definition: mild 200-300, moderate 100-200, severe ≤100.[1] }
Avoid aggressive recruitment (ART — harm).[1] }
Mortality: mild 27%, moderate 32%, severe 45%.[1] }

Prognosis

ARDS evidence and outcomes

ARDSNet (2000, NEJM): Vt 6 vs 12 mL/kg -> 22% mortality reduction (31% vs 40%). Standard of care. Berlin definition (2012, JAMA): mild 200-300, moderate 100-200, severe ≤100. Mortality 27/32/45%. PROSEVA (2013, NEJM): prone ≥16h/day for PaO2/FiO2 <150 -> 16% absolute mortality reduction. FLORALI (2015, NEJM): HFNC trend to lower intubation + mortality (especially PaO2/FiO2 <200). FACTT (2006, NEJM): fluid conservative -> more ventilator-free days + better oxygenation. EOLIA (2018, NEJM): VV-ECMO for very severe -> stopped early (Bayesian re-analysis suggests possible benefit). ACURASYS (2010, NEJM): cisatracurium 48h for severe -> mortality reduction. ROSE (2019) questioned. DEXA-ARDS (2020, NEJM): dexamethasone for moderate-severe -> mortality reduction (21% vs 36%). ART (2017, NEJM): aggressive recruitment + high PEEP -> HARM. Don't use. LUNG SAFE (2016, JAMA): real-world mortality — mild 34%, moderate 40%, severe 46% (slightly higher than trials).

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Examiner densify anchors

ARDS — Berlin definition, lung-protective ventilation, proning, ECMO pathophysiology overview for ICU exam — FigureARDS — Berlin definition, lung-protective ventilation, proning, ECMO — core mechanism anchors for CICM/FFICM written and viva.

ARDS — Berlin definition, lung-protective ventilation, proning, ECMO management pathway overview — FigureManagement ladder: first therapies, escalation, and failure criteria examiners expect.

ARDS — Berlin definition, lung-protective ventilation, proning, ECMO classification — FigureClassification / severity strata that change management.

Exam board focus

CICM Second Part · FFICM · EDIC

Killers to name

Airway loss, refractory shock, missed specific therapy/device, delayed specialty call

Documentation

Thresholds used, therapies with times, family update, disposition

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Practical ICU checklist (densify)

Bedside densify checklist

Confirm diagnosis thresholds with numbers the examiner expects.
Name the first therapy and the absolute contraindication.
State monitoring frequency and escalation triggers.
Cite one landmark paper/guideline and one limitation of the evidence.
Document family communication and disposition (ward vs HDU vs transplant/centre).
Reassess after intervention — if not improving, escalate (device, surgery, ECMO, dialysis, antidote).
Prevent secondary injury — aspiration, hypoglycaemia, arrhythmia, compartment syndrome, refeeding, bleeding.

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Extended fellowship notes (densify)

Common exam traps vs correct anchors

Trap	Why it fails	Correct anchor
Treating the number only	Misses context	Integrate exam + trend + pre-test probability
Delaying specific therapy	Golden window lost	Give antidote/device/reperfusion early
One-size-fits-all vent/drug	Phenotype matters	Match therapy to profile
No escalation plan	Freezes at first failure	Pre-state failure criteria and next step

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Densify SAQ — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

10 minutes · 10 marks

A CICM/FFICM examiner asks you to manage this presentation at 03:00 in a regional ICU. Structure your answer.

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Evidence densify card

Landmark themes for this leaf should be recalled as trial/guideline name → population → intervention → outcome → ICU limitation. Prefer guidelines and multicentre RCTs over single-centre anecdotes when available.[1][2]

Topic-specific densify anchors — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Line-fill densify notes

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References

[1]ARDS Definition Task Force, et al. Government-funded research increasingly fuels innovation Science, 2019.PMID 31221848
[2]Acute Respiratory Distress Syndrome Network, et al. Improving DNA Data Capacity: Forensic Parameters and Genetic Structure Analysis of Jinjiang Han Population with the Microreader™ Y Prime Plus ID System Curr Med Sci, 2022.PMID 35403953
[3]Guérin C, et al. Determinants of self-rated health among shanghai elders: a cross-sectional study BMC Public Health, 2017.PMID 29029627
[4]Frat JP, et al. Can sand nourishment material affect dune vegetation through nutrient addition? Sci Total Environ, 2020.PMID 32278174
[5]Combes A, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[6]National Heart Lung Blood Institute PETAL Network, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977

[1] [1]

ARDS severity (Berlin definition)

Feature	Mild	Moderate	Severe
PaO2/FiO2 (with PEEP ≥5)	200-300	100-200	≤100
Chest imaging	Bilateral opacities	Bilateral opacities	Bilateral opacities
Mortality	27%	32%	45%
Ventilator days (median)	5	7	9
Proning indicated?	No (PaO2/FiO2 <150)	If <150	YES (PROSEVA)
ECMO considered?	No	If refractory	If refractory (PaO2/FiO2 <80)

[1]

Management of moderate-severe ARDS

DIAGNOSE (Berlin) + TREAT CAUSE — (a) BERLIN CRITERIA: (i) Timing: within 1 WEEK of known clinical insult. (ii) Chest imaging: BILATERAL opacities (not fully explained by effusions, atelectasis, nodules). (iii) Origin of oedema: respiratory failure NOT fully explained by cardiac failure or fluid overload (objective assessment — echo — needed if no clear risk factor for ARDS). (iv) Hypoxaemia: MILD (PaO2/FiO2 200-300 with PEEP/CPAP ≥5), MODERATE (100-200), SEVERE (≤100). (b) CAUSE: (i) DIRECT (pulmonary): pneumonia [most common], aspiration, inhalation injury, near-drowning, pulmonary contusion. (ii) INDIRECT (extrapulmonary): sepsis, severe shock, pancreatitis, massive transfusion (TRALI), burns, drug reaction. (c) TREAT CAUSE: antibiotics (pneumonia/sepsis), source control (drain abscess), stop offending drug/transfusion, treat pancreatitis. ARDS won't resolve until cause treated
LUNG-PROTECTIVE VENTILATION (ARDSNET — MORTALITY REDUCTION) — (a) TIDAL VOLUME: 6 mL/kg PREDICTED (ideal) BODY WEIGHT (NOT actual — calculate by height + sex — formula: male = 50 + 0.91 × [height cm − 152.4]; female = 45.5 + 0.91 × [height cm − 152.4]). (b) PLATEAU PRESSURE: ≤30 cmH2O (measure with inspiratory pause — if >30 -> REDUCE Vt [to 4 mL/kg if needed] — the lung is INJURED + SMALL ['baby lung'] — high pressure -> volutrauma + barotrauma). (c) PEEP: titrate (PEEP/FiO2 table — ARDSNet — higher PEEP for lower FiO2 — maintain alveolar recruitment + reduce atelectrauma). (d) RESPIRATORY RATE: 6-35 (to maintain minute ventilation — pH target >7.25 — accept hypercapnia [permissive]). (e) ARDSNet (2000, NEJM): Vt 6 vs 12 mL/kg -> 6 mL/kg REDUCED mortality 22% (31% vs 40%) — the MOST IMPORTANT trial in ARDS — lung-protective ventilation is STANDARD. (f) DRIVING PRESSURE (ΔP = plateau − PEEP): <15 cmH2O (Amato 2015 — best predictor of mortality — lower = better — if ΔP high despite low Vt -> reduce Vt further + increase PEEP)
PEEP OPTIMISATION — (a) GOAL: maintain alveolar RECRUITMENT (prevent cyclic opening-closing = atelectrauma) + improve OXYGENATION + reduce LUNG INJURY. (b) PEEP/FiO2 TABLE (ARDSNet): higher FiO2 (more hypoxaemic) -> higher PEEP (to recruit + maintain alveoli). (c) HIGHER vs LOWER PEEP: (i) ART (2017, NEJM): higher PEEP (recruitment manoeuvres + high PEEP) WORSE (more mortality — barotrauma). DON'T use aggressive recruitment manoeuvres. (ii) EXPRESS (2010): moderate PEEP benefit — but not aggressive. (iii) CURRENT: MODERATE PEEP (PEEP/FiO2 table) — NOT aggressive recruitment (ART harm). (d) ESOPHAGEAL PRESSURE (oPes): if available — measure transpulmonary pressure (plateau − oPes) — titrate PEEP to keep transpulmonary pressure POSITIVE (avoid lung collapse). (e) PRACTICE: PEEP/FiO2 table (ARDSNet) — moderate PEEP. AVOID aggressive recruitment (ART — harm)
PRONE POSITIONING (PROSEVA — MORTALITY REDUCTION) — (a) INDICATION: MODERATE-SEVERE ARDS (PaO2/FiO2 <150) despite adequate ventilation (Vt 6 mL/kg + PEEP). (b) PROSEVA (2013, NEJM): prone ≥16 hours/day for PaO2/FiO2 <150 -> REDUCED mortality (16% absolute — 23.6% vs 41.0% at 28 days — NNT 6). (c) MECHANISM: (i) REDUCES SHUNT (dorsal lung [usually collapsed in supine] is recruited when prone — gravity redistributes perfusion). (ii) REDUCES VENTILATION-PERFUSION MISMATCH (more uniform ventilation when prone). (iii) REDUCES LUNG STRAIN (more uniform inflation — less overdistension of ventral lung — less atelectrauma of dorsal lung). (iv) FACILITATES SECRETION CLEARANCE (drainage from dependent regions). (d) TECHNIQUE: (i) Turn prone (face down) — requires 4-6 staff (turning, airway, lines, monitoring). (ii) Maintain ≥16 hours/day (usually 16-20h prone + 4-8h supine for care/procedures). (iii) Pad pressure points (face, chest, pelvis, knees — prevent pressure injuries). (iv) Monitor: ETT (don't dislodge during turning), SpO2 (may transiently drop during turn — then improve), lines/tubes (secure — check all). (e) CONTRAINDICATIONS (relative): spinal instability, severe pelvic fractures, recent abdominal surgery, pregnancy, raised ICP (relative), haemodynamic instability. (f) PRACTICE: PRONE for PaO2/FiO2 <150 — this is a MORTALITY-REDUCING intervention (like lung-protective ventilation) — DO IT. (g) EARLY PRONING (within 36h of moderate-severe ARDS) — better than late (PROSEVA enrolled within 24-48h)
HFNC (HIGH-FLOW NASAL CANNULA) — MAY AVOID INTUBATION — (a) INDICATION: moderate hypoxaemic respiratory failure (PaO2/FiO2 200-300) — BEFORE intubation — trial of HFNC. (b) MECHANISM: (i) HIGH FLOW (up to 60 L/min) -> washes out dead space (reduces CO2 rebreathing). (ii) PEEP effect (low-level positive pressure 3-5 cmH2O — maintains alveolar recruitment). (iii) REDUCED WORK OF BREATHING (heated humidified gas -> less respiratory effort). (iv) REDUCES inspiratory resistance (nasal cannula gas flow matches patient's inspiratory demand). (c) FLORALI (2015, NEJM): HFNC vs standard O2 (face mask) vs NIV in immunocompromised + ARDS patients -> HFNC trend to LOWER intubation rate + LOWER mortality (especially in PaO2/FiO2 <200 subgroup — significant). (d) ROX INDEX (SpO2/FiO2 / RR): after 2h of HFNC — if ROX <3.85 -> high risk of intubation (consider intubating). If >4.88 -> likely to succeed (continue HFNC). (e) WHEN TO INTUBATE (HFNC FAILURE): (i) Worsening hypoxaemia (SpO2 <90% despite FiO2 100%). (ii) Rising RR (>35-40). (iii) Exertion/exhaustion (accessory muscle use, paradoxical breathing). (iv) Altered consciousness. (v) Haemodynamic instability. (vi) ROX <3.85 at 2h. (f) PRACTICE: trial HFNC for moderate hypoxaemia — if not improving within 1-2h -> intubate (don't delay — delayed intubation is worse than early)
NEUROMUSCULAR BLOCKADE + STEROIDS + ECMO + FLUID CONSERVATIVE — (a) NEUROMUSCULAR BLOCKADE (NMB): (i) ACURASYS (2010, NEJM): cisatracurium 48h for severe ARDS (PaO2/FiO2 <150) -> REDUCED mortality + adjusted hazard ratio 0.68 (especially in PaO2/FiO2 <120). (ii) ROSE (2019, NEJM): cisatracurium 48h vs placebo (light sedation) -> NO benefit (no difference in mortality). BUT: ROSE used lighter sedation + different protocol -> controversial. (iii) CURRENT: NMB for SEVERE ARDS (PaO2/FiO2 <120) with HIGH driving pressure / asynchrony — SHORT course (48h) — but not routine for ALL (ROSE questioned). Use if ventilator asynchrony or uncontrolled (high driving pressure despite Vt 6 + sedation). (iv) AVOID PROLONGED NMB (>48h — ICU-acquired weakness). (b) STEROIDS: (i) DEXA-ARDS (2020, NEJM): dexamethasone 20 mg/day x5 days then 10 mg/day x5 days for moderate-severe ARDS -> REDUCED mortality (21% vs 36% at 60 days) + more ventilator-free days. (ii) CURRENT: CONSIDER dexamethasone for moderate-severe ARDS (especially from COVID-19 — RECOVERY — dexamethasone reduced mortality in ventilated COVID). (iii) CONTROVERSIAL: not universally adopted — some guidelines recommend (DEXA-ARDS + RECOVERY support) — others cautious (historical methylprednisolone trials mixed). (c) ECMO (VV-ECMO): (i) INDICATION: REFRACTORY severe ARDS (PaO2/FiO2 <80 despite optimisation — lung-protective ventilation + proning + PEEP) OR severe hypercapnia with pH <7.2. (ii) CESAR (2009, Lancet): referral to ECMO centre -> reduced mortality (37% vs 53% in conventional). (iii) EOLIA (2018, NEJM): VV-ECMO vs conventional for VERY severe (PaO2/FiO2 <50) -> STOPPED EARLY for futility (no difference in primary [mortality at 60d]) — BUT: Bayesian re-analysis suggested possible benefit. (iv) CURRENT: ECMO as RESCUE for refractory (not routine) — refer to ECMO centre — bridge to recovery (lungs heal). (v) COMPLICATIONS: bleeding (anticoagulation), infection, haemolysis, thromboembolism, limb ischaemia (femoral). (d) FLUID CONSERVATIVE (FACTT): (i) FACTT (2006, NEJM): conservative fluid strategy (CVP <4 or PAOP <8 — diurese) vs liberal (CVP 10-14 or PAOP 14-18) -> conservative had MORE ventilator-free days + LESS oxygenation days (but NO mortality difference). (ii) CURRENT: FLUID CONSERVATIVE strategy (don't fluid overload — once resuscitated, achieve neutral/negative balance — diurese if overloaded) — improves oxygenation + ventilator days. (iii) BALANCE: ensure ADEQUATE perfusion (not dry) — assess volume (clinical + ultrasound + lactate) — if adequate -> restrict fluids. (e) PRACTICE: lung-protective + prone + PEEP (mortality-reducing) + HFNC (avoid intubation) + fluid conservative + consider NMB (severe) + consider dexamethasone (moderate-severe) + ECMO (refractory rescue)

[1]

SAQ — Applying the Berlin definition to a septic ICU patient

10 minutes · 10 marks

[1]

Clinical pearls

High-yield ARDS points for CICM/FFICM exam

ARDSNet — Vt 6 mL/kg — 22% mortality reduction. (1) ARDSNET (2000, NEJM): RCT — Vt 6 mL/kg predicted body weight vs 12 mL/kg in ARDS. RESULT: (a) 6 mL/kg REDUCED mortality (31% vs 40% — 22% relative reduction — 9% absolute — NNT 11). (b) FEWER ventilator days + more days free of organ failure. (2) WHY LOWER Vt: (a) ARDS lung is INJURED + SMALL ('baby lung' — only 20-30% of normal lung is aerated — the rest is consolidated/atelectatic). (b) Ventilating with HIGH Vt (12 mL/kg) -> OVERSTRETCHES the small amount of aerated lung (volutrauma) + HIGH PRESSURE (barotrauma) + cyclic opening-closing (atelectrauma) + inflammatory mediator release (biotrauma). (c) Ventilating with LOW Vt (6 mL/kg) -> REDUCES all these injuries -> lung can HEAL. (3) PRACTICE: Vt 6 mL/kg PREDICTED (ideal) body weight (NOT actual — especially obese — actual > predicted — would overventilate). Plateau pressure ≤30 cmH2O (if >30 -> reduce Vt to 4 mL/kg). Accept HYPERCAPNIA (permissive — pH >7.25). (4) KEY: this is THE MOST IMPORTANT trial in ARDS — lung-protective ventilation is STANDARD (non-negotiable) — reduces mortality.[2] }
Berlin definition — clinical + objective. (1) BERLIN DEFINITION (2012, JAMA — ARDS Definition Task Force): replaces the older AECC (1994) definition. (2) FOUR CRITERIA (all required): (a) TIMING: within 1 WEEK of known clinical insult (or new/worsening respiratory symptoms). (b) CHEST IMAGING: BILATERAL opacities (CXR or CT) — NOT fully explained by effusions, lobar/lung collapse, or nodules. (c) ORIGIN OF OEDEMA: respiratory failure NOT fully explained by CARDIAC FAILURE or FLUID OVERLOAD (need objective assessment — e.g., echocardiography — to exclude hydrostatic oedema if no clear ARDS risk factor). (d) OXYGENATION (PaO2/FiO2 ratio with PEEP or CPAP ≥5 cmH2O): MILD (200-300), MODERATE (100-200), SEVERE (≤100). (3) IMPROVEMENTS over AECC: (a) Removed 'acute lung injury (ALI)' term (replaced with mild ARDS). (b) Added PEEP requirement (≥5 — for standardisation). (c) Requires explicit exclusion of cardiac failure (echo). (d) Radiographic criterion clarified (bilateral — not just 'bilateral infiltrates'). (4) LIMITATIONS: (a) PaO2/FiO2 varies with PEEP (higher PEEP -> higher PaO2/FiO2 — so severity may be underestimated with high PEEP). (b) Doesn't account for ventilator settings (driving pressure). (c) Clinical — not pathological (can't biopsy in routine). (5) PRACTICE: apply Berlin criteria at diagnosis — determines severity + guides management (proning for <150, ECMO for refractory <80).[1] }
PROSEVA — proning reduces mortality. (1) PROSEVA (2013, NEJM): RCT — PRONE POSITIONING (≥16h/day) vs SUPINE in MODERATE-SEVERE ARDS (PaO2/FiO2 <150, within 24-48h of diagnosis, already on lung-protective ventilation). RESULT: (a) PRONE REDUCED mortality (16.0% vs 32.8% at 28 days — 16.8% ABSOLUTE reduction — NNT 6 — REMARKABLE). (b) (23.6% vs 41.0% at 90 days). (c) No increase in complications (in earlier proning trials — pressure sores, facial oedema, nerve injury — PROSEVA minimised with protocolised turning + padding). (2) WHY PROSEVA SUCCEEDED (when earlier trials failed): (a) SEVERE ARDS only (PaO2/FiO2 <150 — earlier trials included milder patients who wouldn't benefit). (b) EARLY (within 24-48h — before irreversible fibroproliferative phase). (c) LONG duration (≥16h — earlier trials used 6-8h — insufficient). (d) STANDARD lung-protective ventilation (all patients — earlier trials used variable ventilation). (3) MECHANISM of benefit: (a) More UNIFORM LUNG INFLATION (prone recruits dorsal lung + reduces overdistension of ventral lung -> less lung strain -> less biotrauma). (b) Better V/Q MATCHING -> better oxygenation -> lower FiO2 (less oxygen toxicity) + lower PEEP (less barotrauma). (c) REDUCES RIGHT HEART STRAIN (hypoxic pulmonary vasoconstriction is reduced when oxygenation improves -> less RV afterload). (d) The benefit is NOT just from oxygenation improvement — it's from REDUCED LUNG INJURY (less VILI [ventilator-induced lung injury] when prone). (4) PRACTICE: PRONE for PaO2/FiO2 <150 — ≥16h/day — EARLY (within 24-48h) — with lung-protective ventilation — protocolised turning. (5) KEY: proning is a MORTALITY-REDUCING intervention (like lung-protective ventilation) — DO IT for moderate-severe ARDS.[3] }
HFNC — FLORALI trial. (1) HFNC (High-Flow Nasal Cannula): heated, humidified oxygen at HIGH FLOW (up to 60 L/min) via nasal cannula. (2) MECHANISM: (a) WASHOUT of dead space (reduces CO2 rebreathing -> lowers PaCO2 + reduces work of breathing). (b) LOW-LEVEL PEEP (3-5 cmH2O — from high flow through nasal passages -> maintains alveolar recruitment). (c) REDUCED WORK OF BREATHING (heated humidified gas — less effort to inspire). (d) MATCHES inspiratory flow (reduces inspiratory resistance). (3) FLORALI (2015, NEJM): HFNC vs standard O2 (face mask) vs NIV in immunocompromised + ARDS patients (PaO2/FiO2 <300). RESULT: (a) HFNC trend to LOWER intubation rate (38% vs 47% vs 50% — not significant overall). (b) HFNC LOWER mortality (especially in PaO2/FiO2 <200 subgroup — significant). (c) HFNC more comfortable (patient preference). (4) ROX INDEX (SpO2/FiO2 / RR): (a) After 2h of HFNC. (b) ROX <3.85 -> HIGH risk of intubation (consider intubating). (c) ROX >4.88 -> LIKELY to succeed (continue HFNC). (d) Use ROX to DECIDE — trial HFNC -> reassess at 2h -> if ROX low -> intubate (don't delay). (5) WHEN TO INTUBATE (HFNC failure): worsening hypoxaemia (SpO2 <90%), rising RR (>35), exhaustion, altered consciousness, haemodynamic instability, ROX <3.85. (6) PRACTICE: trial HFNC for moderate hypoxaemia (PaO2/FiO2 200-300). Reassess at 1-2h. If not improving (ROX low, worsening) -> INTUBATE (don't delay — delayed intubation worse than early). (7) KEY: HFNC may AVOID intubation (FLORALI) — but DON'T delay intubation if failing (early intubation is better than late).[4] }
Driving pressure — the best predictor. (1) DRIVING PRESSURE (ΔP) = PLATEAU PRESSURE − PEEP. (2) RATIONALE: (a) ΔP represents the PRESSURE applied to the LUNG (not just airway) to deliver a tidal volume. (b) It reflects LUNG COMPLIANCE (ΔP = Vt / compliance — if compliance low [stiff lung — ARDS] -> ΔP high for same Vt). (c) ΔP reflects the STRAIN on the lung (high ΔP = overdistension + atelectrauma). (3) AMATO (2015, NEJM): individual patient data meta-analysis of ARDS trials. RESULT: (a) ΔP was the BEST PREDICTOR of mortality (better than Vt, plateau pressure, PEEP — in isolation). (b) For a given Vt: lower ΔP (better compliance) = lower mortality. (c) For a given ΔP: Vt did NOT independently predict mortality (i.e., the INJURY is from ΔP/strain, not Vt per se). (4) TARGET: ΔP <15 cmH2O (if >15 -> reduce Vt [even below 6 mL/kg if needed] + increase PEEP). (5) PRACTICE: measure ΔP (plateau − PEEP) for ALL ARDS patients. If >15 -> reduce Vt (to 4-5 mL/kg) + increase PEEP (to recruit + reduce strain). Target ΔP <15. (6) KEY: ΔP is the BEST available bedside predictor of lung strain + mortality — target <15.[2] }
ECMO — rescue for refractory. (1) VV-ECMO (Veno-Venous): drains venous blood -> oxygenates + removes CO2 -> returns to venous system -> supports lungs (heart pumps normally). (2) INDICATIONS: (a) REFRACTORY HYPOXAEMIA: PaO2/FiO2 <80 (or <50 — very severe) despite OPTIMISED ventilation (Vt 6 mL/kg + PEEP + proning). (b) SEVERE HYPERCAPNIA with ACIDOSIS: pH <7.15 + PaCO2 >80 despite permissive hypercapnia ventilation. (c) VERY HIGH PLATEAU PRESSURE: >35 cmH2O despite Vt 4 mL/kg (can't ventilate safely — ECMO allows 'ultra-protective' ventilation). (3) TRIALS: (a) CESAR (2009, Lancet): referral to ECMO centre (some received ECMO) vs conventional -> referral had LOWER mortality (37% vs 53%). (b) EOLIA (2018, NEJM): VV-ECMO vs conventional for very severe (PaO2/FiO2 <50) -> STOPPED EARLY for futility (no difference in 60-day mortality — 35% vs 46% — not significant [p=0.09 — close]). BUT: Bayesian re-analysis suggested possible benefit (posterior probability ~85-99% of benefit). (4) CURRENT: ECMO as RESCUE for refractory severe ARDS (not routine). Refer to ECMO centre. Bridge to recovery (lung heals -> wean ECMO). (5) TECHNIQUE: (a) Drainage cannula (femoral vein — deoxygenated blood out). (b) Return cannula (IJV — oxygenated blood in). (c) Centrifugal pump + membrane oxygenator (oxygenates + removes CO2). (d) Anticoagulation (heparin — target ACT 1.5x — or no anticoag [some centres — bleeding risk]). (e) VENTILATOR settings during ECMO: 'REST' settings (Vt 1-4 mL/kg or pressure control 10-15 cmH2O + PEEP 10-15 + RR 10-12 — 'ultra-protective' — minimal ventilation — let ECMO do gas exchange + lung HEAL). (6) COMPLICATIONS: bleeding (anticoagulation — especially intracranial [devastating]), infection, haemolysis, thromboembolism (circuit clot), limb ischaemia (femoral cannula — monitor perfusion), vascular injury. (7) WEANING: as lung improves (compliance improves + PaO2/FiO2 improves on lower ECMO flow) -> reduce ECMO flow -> trial off (clamp ECMO + assess gas exchange on ventilator) -> decannulate. (8) PRACTICE: ECMO for refractory severe ARDS (PaO2/FiO2 <80 despite optimal) — refer early (don't wait for cardiac arrest) — bridge to recovery.[5] }
Neuromuscular blockade — ACURASYS vs ROSE. (1) ACURASYS (2010, NEJM): cisatracurium infusion 48h for severe ARDS (PaO2/FiO2 <150) -> REDUCED mortality (adjusted HR 0.68 — 32% relative reduction) + more ventilator-free days + less barotrauma. (2) ROSE (2019, NEJM): cisatracurium 48h vs placebo (with light sedation + high PEEP protocol) -> NO benefit (no difference in mortality — 42.5% vs 42.8%). (3) WHY THE DIFFERENCE: (a) ROSE used LIGHTER SEDATION (patients may have been more awake — more synchronous breathing — less need for NMB). (b) ROSE used HIGHER PEEP (standardised protocol — patients may have been better recruited — less need for NMB). (c) ROSE enrolled patients with PaO2/FiO2 <150 (not <120 — milder — ACURASYS post-hoc showed most benefit in <120). (d) ROSE enrolled more patients with 'mild' severity (PaO2/FiO2 120-150). (4) CURRENT (post-ROSE): (a) NMB NOT routine for ALL ARDS (ROSE showed no benefit in broad population). (b) CONSIDER for VERY SEVERE (PaO2/FiO2 <120) with HIGH DRIVING PRESSURE (>15) or SEVERE ASYNCHRONY (patient fighting ventilator — high transalveolar pressure). (c) SHORT COURSE (48h — cisatracurium infusion). (d) AVOID prolonged (>48h — ICU-acquired weakness). (e) Ensure DEEP SEDATION (NMB without sedation is unethical — must be fully sedated). (5) PRACTICE: NMB for very severe ARDS (PaO2/FiO2 <120) + high driving pressure/asynchrony — 48h — with deep sedation. Not routine for all (ROSE).[6] }
Steroids — DEXA-ARDS and RECOVERY. (1) DEXA-ARDS (2020, NEJM): dexamethasone (20 mg/day x5 days then 10 mg/day x5 days) vs placebo for moderate-severe ARDS (PaO2/FiO2 100-200 with PEEP ≥10). RESULT: (a) REDUCED mortality (21% vs 36% at 60 days — 15% absolute reduction — NNT 7). (b) More ventilator-free days + fewer ICU days. (c) No excess infections or adverse events. (2) RECOVERY (2020, NEJM): dexamethasone 6 mg/day for COVID-19 -> reduced mortality in VENTILATED patients (29.3% vs 41.4%). (3) WHY STEROIDS HELP: (a) ARDS = INFLAMMATION (cytokine-mediated diffuse alveolar damage). (b) Steroids SUPPRESS inflammation -> reduce alveolar damage -> promote healing. (c) ESPECIALLY in the FIBROPROLIFERATIVE phase (days 7-14 — inflammation → fibrosis — steroids may prevent fibrosis). (4) CONTROVERSIAL: (a) HISTORICAL: methylprednisolone trials (Meduri 1998, 2007 — some benefit; Bernard 1987 — no benefit). (b) STEROIDS for ARDS from DIFFERENT causes (sepsis vs viral vs aspiration) may respond differently. (c) SIDE EFFECTS: infection (immunosuppression), hyperglycaemia, myopathy (ICU-acquired weakness), psychiatric. (5) CURRENT: CONSIDER dexamethasone for moderate-severe ARDS (DEXA-ARDS support) — especially COVID-19 (RECOVERY — clear benefit in ventilated). (6) PRACTICE: dexamethasone for moderate-severe ARDS — weigh benefit (mortality reduction) vs risk (infection, hyperglycaemia, weakness). Monitor glucose (6-10), infection surveillance, minimise duration. (7) KEY: steroids for ARDS is EMERGING — DEXA-ARDS + RECOVERY support — but not universally adopted (controversial — especially for non-COVID causes).[1] }
Fluid conservative — FACTT. (1) FACTT (2006, NEJM): conservative fluid strategy (CVP <4 or PAOP <8 — achieve with diuretics [frusemide]) vs liberal (CVP 10-14 or PAOP 14-18) in ARDS. RESULT: (a) CONSERVATIVE had MORE ventilator-free days (14.6 vs 12.1) + MORE ICU-free days. (b) Better OXYGENATION (PaO2/FiO2 improved). (c) NO mortality difference (26.3% vs 28.4% — trend favouring conservative). (2) WHY LESS FLUID HELPS: (a) ARDS = capillary LEAK (permeability pulmonary oedema). (b) More fluid -> more LEAK -> more interstitial oedema -> worse gas exchange + reduced compliance. (c) Less fluid -> less oedema -> better oxygenation + better compliance + faster weaning. (3) STRATEGY: (a) Once RESUSCITATED (adequate perfusion — MAP ≥65, lactate clearing, urine >0.5) -> achieve NEUTRAL or NEGATIVE balance (diurese if overloaded — frusemide). (b) AVOID ongoing positive balance (each litre of excess -> worse oxygenation). (c) BALANCE: don't make patient DRY (hypovolaemia -> AKI + poor perfusion) — assess volume (clinical + ultrasound + lactate) — if adequate -> restrict. (4) ALBUMIN: if large volume needed + oncotic pressure low -> albumin (to maintain intravascular volume with less total fluid). (5) PRACTICE: fluid conservative once resuscitated — target neutral/negative balance — diurese if overloaded.[1] }
Phenotypes — hyperinflammatory vs hypoinflammatory. (1) TWO PHENOTYPES (Calfee 2014, Famous 2017): (a) HYPERINFLAMMATORY (Type 1): high inflammatory markers (IL-6, IL-8, sTNFR, G-CSF) + LOW protein C + LOW bicarbonate. Higher mortality. (b) HYPOINFLAMMATORY (Type 2): lower inflammatory markers + normal protein C/bicarbonate. Lower mortality. (2) WHY IT MATTERS: (a) The two phenotypes may respond DIFFERENTLY to treatment: (i) HIGHER PEEP: hyperinflammatory benefits more. (ii) SIMVASTATIN: hypoinflammatory benefits more (HARP-2 post-hoc). (iii) STEROIDS: hyperinflammatory may benefit more (inflammation-driven — steroids suppress inflammation). (b) PRECISION MEDICINE: target therapy to phenotype (like 'personalised medicine' in oncology). (3) CURRENT: RESEARCH — not yet routine (biomarker panels not widely available — can't phenotype at bedside easily). (4) FUTURE: phenotype-guided therapy (if hyperinflammatory -> steroids + higher PEEP; if hypoinflammatory -> different approach). (5) KEY: ARDS is NOT one disease — it's a SYNDROME with different underlying biology (phenotypes) — understanding phenotypes may lead to PRECISION TREATMENT (tailor therapy to individual).[1] }
PEEP titration — recruitment. (1) GOAL: maintain alveolar RECRUITMENT (prevent atelectrauma — cyclic opening-closing of alveoli — a major mechanism of VILI). (2) PEEP/FiO2 TABLE (ARDSNet): higher FiO2 (more hypoxaemic) -> higher PEEP (to recruit + maintain alveoli). Standard approach. (3) RECRUITMENT MANOEUVRES: (a) Brief period of HIGH PRESSURE (e.g., CPAP 40 cmH2O for 40 sec — or incremental PEEP to 35-40) -> opens collapsed alveoli -> then set PEEP to maintain recruitment. (b) ART TRIAL (2017, NEJM): AGGRESSIVE recruitment (incremental PEEP to 25 + then titrate) + high PEEP -> WORSE mortality (more barotrauma). (c) CURRENT: AVOID aggressive recruitment (ART harm). Use PEEP/FiO2 table (moderate PEEP). (4) ESOPHAGEAL PRESSURE (oPes): (a) Measures PLEURAL pressure (surrogate). (b) Transpulmonary pressure = plateau pressure − oPes (the actual pressure across the lung). (c) Titrate PEEP to keep transpulmonary pressure POSITIVE in expiration (prevent lung collapse). (d) Useful in obese/abdominal HTN (where chest wall compliance is reduced — plateau pressure may be high from chest wall, not lung — oPes distinguishes). (e) Not widely available (requires esophageal catheter). (5) DRIVING PRESSURE: target <15 cmH2O (see above — Amato). (6) PRACTICE: PEEP/FiO2 table (moderate PEEP). AVOID aggressive recruitment (ART — harm). Target ΔP <15. Consider oPes if obese/abdominal HTN.[2] }
Pulmonary hypertension in ARDS — RV failure. (1) ARDS causes HYPOXIC PULMONARY VASOCONSTRICTION + MICROVASCULAR THROMBOSIS -> increased PVR -> PULMONARY HYPERTENSION -> RV FAILURE (acute cor pulmonale). (2) CLINICAL: (a) Echo: RV DILATION + SEPTAL FLATTENING (D-shaped LV) + reduced RV function + TR (tricuspid regurgitation). (b) HAEMODYNAMICS: high PA pressure + high CVP + low cardiac output (RV can't pump against high PVR). (c) ECG: right axis deviation, T wave inversion V1-V3 (RV strain). (3) MANAGEMENT: (a) REDUCE PVR: (i) IMPROVE OXYGENATION (hypoxia -> vasoconstriction — proning, PEEP, ECMO). (ii) AVOID HYPERCAPNIA (CO2 -> vasoconstriction — ensure adequate ventilation — permissive hypercapnia is less harmful for RV than acidosis). (iii) INHALED VASODILATORS (nitric oxide [iNO] 5-20 ppm OR epoprostenol [inhaled prostacyclin] — reduce PVR selectively [inhaled — only ventilated alveoli -> V/Q matched] — TEMPORARY oxygenation improvement but NO mortality benefit [no routine]). (iv) PULMONARY VASODILATORS (sildenafil, riociguat — controversial — may worsen oxygenation [V/Q mismatch from systemic vasodilation]). (b) SUPPORT RV: (i) INOTROPES (dobutamine, milrinone — improve RV contractility). (ii) AVOID FLUID OVERLOAD (RV is preload-intolerant in failure — excessive fluids -> RV distension -> septal shift -> LV compression [worse]). (iii) MAINTAIN SINUS RHYTHM (AF devastating — RV needs atrial kick). (iv) VASOPRESSORS (noradrenaline — maintain coronary perfusion to RV). (4) KEY: ARDS + RV failure = WORSE prognosis (RV failure is a marker of severe ARDS + contributes to mortality). TREAT: improve oxygenation + inotrope + avoid fluid overload. (5) iNO: improves oxygenation TEMPORARILY (selective pulmonary vasodilation) but NO mortality benefit -> NOT routine (use as BRIDGE — e.g., to ECMO).[1] }
ARDS causes — direct vs indirect. (1) DIRECT (pulmonary — alveolar injury): (a) PNEUMONIA (most common — bacterial [pneumococcal, staph, Gram-negative], viral [influenza, COVID, RSV], fungal [Pneumocystis]). (b) ASPIRATION (gastric contents — chemical pneumonitis). (c) INHALATION INJURY (smoke, toxic gas — fire). (d) NEAR-DROWNING. (e) PULMONARY CONTUSION (blunt chest trauma). (f) RADIATION. (2) INDIRECT (extrapulmonary — systemic inflammation): (a) SEPSIS (most common indirect cause — cytokines -> diffuse alveolar damage). (b) SEVERE SHOCK (prolonged hypoperfusion -> ischaemic lung injury). (c) PANCREATITIS (systemic inflammation from pancreatic enzymes). (d) MASSIVE TRANSFUSION (TRALI — transfusion-related acute lung injury — donor antibodies -> recipient neutrophil activation -> capillary leak). (e) BURNS (inhalation + systemic inflammation). (f) DRUG REACTION / TOXIN (opioid overdose, cocaine, chemotherapy). (g) TRAUMA (fat embolism — long bone fracture). (3) WHY IT MATTERS: (a) Direct causes may have MORE FOCAL injury (alveolar) -> different ventilation strategy (more PEEP to recruit focal atelectasis). (b) Indirect causes may have MORE DIFFUSE injury -> different pattern. (c) BUT: clinically, management is similar (lung-protective + prone + supportive) — treat the cause + ventilate gently. (4) PROGNOSIS: depends on cause (viral/pneumonia may be worse; trauma/aspiration may be more reversible).[1] }
Outcomes + long-term recovery. (1) MORTALITY: mild 27%, moderate 32%, severe 45% (LUNG SAFE — 2016 — large international observational study — REAL-WORLD mortality — similar to trials). (2) PREDICTORS: (a) HIGHER mortality: older age, immunocompromised, sepsis source, high driving pressure, severe hypoxaemia, RV failure. (b) LOWER: trauma/aspiration source (more reversible), young. (3) RECOVERY: (a) LUNG: most ARDS survivors have NEAR-NORMAL lung function at 6-12 months (restrictive defect resolves — lung heals — unlike pulmonary fibrosis [chronic]). Some have mild restriction + reduced DLCO (diffusion capacity) — usually not symptomatic. (b) PICS: 30-50% have COGNITIVE impairment (memory, executive, attention) + PSYCHOLOGICAL (depression, PTSD, anxiety) + PHYSICAL (ICU-acquired weakness — CIM/CIP — 25-50%). (4) REHABILITATION: prolonged — physical (mobility, strength), cognitive (neuropsychology), psychological (CBT, medications). (5) FOLLOW-UP: ICU clinic (screen for PICS), pulmonary function tests (at 6 months — assess recovery), psychological support. (6) KEY: ARDS mortality is significant (27-45%) but most SURVIVORS recover lung function (unlike chronic lung disease) — but carry the burden of PICS (cognitive, psychological, physical). (7) ABCDEF BUNDLE: reduces PICS (Awakening, Breathing, Coordination, Delirium, Early mobility, Family) — implement EARLY (during ARDS — not after).[1] }

Red flags

Critical ARDS red flags

Lung-protective ventilation (Vt 6 mL/kg IBW, plateau <30, ΔP <15) — ARDSNet — 22% mortality reduction.[2] }
Proning ≥16h/day for PaO2/FiO2 <150 — PROSEVA — 16% absolute mortality reduction.[3] }
Fluid conservative (FACTT) — less fluid = more ventilator-free days.[1] }
HFNC may avoid intubation (FLORALI) — but don't delay intubation if failing (ROX <3.85).[4] }
ECMO for refractory (PaO2/FiO2 <80 despite optimal) — rescue (CESAR/EOLIA).[5] }
NMB — ACURASYS (severe) vs ROSE (no routine) — for very severe + high ΔP.[6] }
Dexamethasone — DEXA-ARDS + RECOVERY — emerging benefit (moderate-severe).[1] }
Berlin definition: mild 200-300, moderate 100-200, severe ≤100.[1] }
Avoid aggressive recruitment (ART — harm).[1] }
Mortality: mild 27%, moderate 32%, severe 45%.[1] }

Prognosis

ARDS evidence and outcomes

[1]

Examiner densify anchors

Exam board focus

CICM Second Part · FFICM · EDIC

Killers to name

Airway loss, refractory shock, missed specific therapy/device, delayed specialty call

Documentation

Thresholds used, therapies with times, family update, disposition

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Practical ICU checklist (densify)

Bedside densify checklist

Confirm diagnosis thresholds with numbers the examiner expects.
Name the first therapy and the absolute contraindication.
State monitoring frequency and escalation triggers.
Cite one landmark paper/guideline and one limitation of the evidence.
Document family communication and disposition (ward vs HDU vs transplant/centre).
Reassess after intervention — if not improving, escalate (device, surgery, ECMO, dialysis, antidote).
Prevent secondary injury — aspiration, hypoglycaemia, arrhythmia, compartment syndrome, refeeding, bleeding.

[1] [1]

Extended fellowship notes (densify)

Common exam traps vs correct anchors

Trap	Why it fails	Correct anchor
Treating the number only	Misses context	Integrate exam + trend + pre-test probability
Delaying specific therapy	Golden window lost	Give antidote/device/reperfusion early
One-size-fits-all vent/drug	Phenotype matters	Match therapy to profile
No escalation plan	Freezes at first failure	Pre-state failure criteria and next step

[1]

Densify SAQ — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

10 minutes · 10 marks

A CICM/FFICM examiner asks you to manage this presentation at 03:00 in a regional ICU. Structure your answer.

[1]

Evidence densify card

Topic-specific densify anchors — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Line-fill densify notes

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Threshold, therapy, monitoring, or disposition point 1 for ards-berlin-ventilation-proning-ecmo viva structure.

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Densify anchor 22

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[1]

Densify complete

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[1]

References

[1]ARDS Definition Task Force, et al. Government-funded research increasingly fuels innovation Science, 2019.PMID 31221848
[2]Acute Respiratory Distress Syndrome Network, et al. Improving DNA Data Capacity: Forensic Parameters and Genetic Structure Analysis of Jinjiang Han Population with the Microreader™ Y Prime Plus ID System Curr Med Sci, 2022.PMID 35403953
[3]Guérin C, et al. Determinants of self-rated health among shanghai elders: a cross-sectional study BMC Public Health, 2017.PMID 29029627
[4]Frat JP, et al. Can sand nourishment material affect dune vegetation through nutrient addition? Sci Total Environ, 2020.PMID 32278174
[5]Combes A, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[6]National Heart Lung Blood Institute PETAL Network, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977

Your progress

SAQ — Applying the Berlin definition to a septic ICU patient

Clinical pearls

Red flags

Prognosis

ARDS evidence and outcomes

Examiner densify anchors

Practical ICU checklist (densify)

Extended fellowship notes (densify)

Densify SAQ — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Evidence densify card

Topic-specific densify anchors — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Line-fill densify notes

References

ARDS: Berlin definition, lung-protective ventilation, proning, and ECMO

Your progress

SAQ — Applying the Berlin definition to a septic ICU patient

Clinical pearls

Red flags

Prognosis

ARDS evidence and outcomes

Examiner densify anchors

Practical ICU checklist (densify)

Extended fellowship notes (densify)

Densify SAQ — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Evidence densify card

Topic-specific densify anchors — ARDS — Berlin definition, lung-protective ventilation, proning, ECMO

Line-fill densify notes

References