Acute pulmonary oedema: cardiogenic vs non-cardiogenic differentiation · ICU Topics

Cinematic ICU scene of a breathless patient with bilateral pulmonary oedema on a chest X-ray, a bedside echocardiogram on screen, a BNP result slip, NIV via a face mask for the cardiogenic picture, clinical-blue lighting, no faces, no text — FigurePulmonary oedema — cardiogenic (hydrostatic, high BNP, reduced EF, rapid NIV response) versus non-cardiogenic (permeability, ARDS, lung-protective ventilation and conservative fluids). The echocardiogram and the BNP split the two at the bedside.

The pathophysiology — hydrostatic forces vs permeability leak

Acute pulmonary oedema develops when fluid accumulates in the interstitium and alveoli faster than lymphatics can clear it. The Starling equation governs transcapillary fluid flux: net filtration = the hydraulic pressure pushing fluid OUT minus the oncotic pressure pulling it BACK, multiplied by the capillary permeability coefficient. Two fundamentally different insults disturb this balance, producing the two phenotypes.[1]

In cardiogenic (hydrostatic) oedema, left-sided filling pressures rise — left atrial pressure (LAP) → pulmonary venous pressure → capillary hydrostatic pressure (Pc). Once Pc exceeds the plasma oncotic pressure (~25 mmHg) and the lung's interstitial pressure, fluid is pushed across an INTACT alveolar–capillary membrane into the interstitium, then into the alveoli. The fluid is a TRANSUDATE (protein-poor), and the membrane architecture is preserved — which is why the lung recovers rapidly once pressure is relieved. The classic PCWP threshold of 18 mmHg comes from the older pulmonary artery catheter literature: above this, hydrostatic oedema is likely.[1]

In non-cardiogenic (permeability) oedema, an insult — sepsis, pneumonia, aspiration, major trauma, pancreatitis, massive transfusion — destroys the integrity of the alveolar–capillary membrane. Endothelial and epithelial injury, neutrophil activation, cytokine surge and loss of surfactant produce a leaky barrier. Fluid AND protein pour into the interstitium and alveoli at a NORMAL or LOW pulmonary capillary pressure. The fluid is a protein-rich EXUDATE. This is the ARDS lung — stiff, heavy, non-compliant, with bilateral opacities that are NOT caused by cardiac failure. The diagnostic standard remains the Berlin definition: timing within 1 week of insult, bilateral opacities not fully explained by effusions/atelectasis/nodules, oedema not fully explained by cardiac failure or fluid overload (and if measured, PCWP < 18 mmHg), and hypoxaemia graded by the PaO2/FiO2 ratio (mild 300-200, moderate 200-100, severe < 100).[9]

The crucial implication at the bedside: lowering the pressure (diuresis, vasodilators, CPAP) resolves cardiogenic oedema within minutes to hours, but does NOT resolve ARDS. ARDS demands treatment of the cause, lung-protective ventilation to avoid further injury, and time for the membrane to heal. [1]

Cardiogenic pulmonary oedema — mechanisms, triggers, treatment

ICU management ladder for acute pulmonary oedema: sit up oxygen CPAP diuretic nitrates for cardiogenic path versus lung-protective ventilation prone conservative fluids for ARDS path, flat clinical illustration — FigureManagement diverges once mechanism is known: cardiogenic pathway (CPAP, diuretic, afterload reduction) versus ARDS pathway (protective ventilation, fluid conservatism, treat insult).

Mechanisms — three haemodynamic routes to high pulmonary venous pressure

LV systolic failure (HFrEF) — the largest single cause. Extensive MI, decompensated chronic HFrEF, myocarditis, sepsis-induced cardiomyopathy, takotsubo. The LV cannot generate enough forward stroke volume, end-diastolic volume and pressure rise, this back-pressures the left atrium, the pulmonary veins, and ultimately the capillary bed.
LV diastolic failure (HFpEF) — common in the elderly, hypertensive, diabetic, obese, AF population. A stiff LV with preserved EF cannot accept diastolic filling at normal pressures; small volume loads or tachycardia (loss of diastolic filling time) push LAP sharply up.
Valvular and mechanical — acute mitral regurgitation (papillary muscle/chordal rupture post-MI, endocarditis), severe mitral stenosis, prosthetic valve thrombosis or obstruction, and (rarely) a left atrial myxoma. These cause pulmonary oedema with a NORMAL LV EF — the obstruction or regurgitation is upstream of the LV cavity, so the LV itself may contract normally.[4]

Common precipitants

ACS, new or fast AF, hypertensive emergency, acute regurgitant lesion, renal failure / volume overload, drug non-adherence, NSAIDs / negative inotropes (CCB, most antiarrhythmics, thiazolidinediones), thyroid disturbance, anaemia, pneumonia/sepsis, and high-output states. Identifying and treating the trigger is as important as treating the oedema itself. [1]

Treatment — a sequenced ladder

The first 30-60 minutes aim to relieve work of breathing, improve oxygenation, drop preload and afterload, and identify the precipitant. Sit the patient upright, give oxygen to target SpO2 92-96%, start continuous ECG monitoring, secure IV access, place a urinary catheter (the urine output is the single best index of decongestion), and classify the haemodynamic phenotype (warm-wet vs cold-wet) at the bedside.[3]

NIV/CPAP early — CPAP 5-10 cmH2O (or BiPAP IPAP 10-15/EPAP 5-8) for the wet patient in respiratory distress. Mechanism: positive intrathoracic pressure reduces venous return (preload), reduces LV transmural pressure (afterload), recruits alveoli, and unloads respiratory muscles. The 3CPO trial showed faster relief of dyspnoea, hypercapnia and acidosis with NIV; CPAP = BiPAP. Do NOT wait for exhaustion.
IV loop diuretic — furosemide IV. For a patient NOT on a loop diuretic, give 20-40 mg IV. For a patient already on an oral loop, give 1-2.5x the total daily oral dose IV (DOSE trial: high-dose vs low-dose and bolus vs continuous — no significant difference in the co-primary endpoints; high-dose achieved greater fluid loss at the cost of more transient renal dysfunction). Reassess urine output at 2 h and double if response is poor. Target 3-5 L/day net negative.
Vasodilator (if SBP > 110) — IV nitroglycerin (GTN) 10-200 mcg/min, titrated to symptoms and BP; venodilates (drops preload) and arteriodilates (drops afterload), ideal for hypertensive pulmonary oedema. Avoid in the hypotensive cold patient, RV infarct, severe aortic stenosis, HOCM, and recent PDE-5 use.
Morphine — sparingly or not at all. Small doses (1-3 mg IV) for distressed/anxious patients may reduce preload and catecholamine surge, but the ADHERE registry linked morphine to increased mortality (a confounded observational signal, but it has shifted practice away from routine morphine in ADHF).
Inotrope + vasopressor (cold-wet, cardiogenic shock) — noradrenaline to restore a perfusing MAP > 65 mmHg (preferred over dopamine — SOAP-II: more arrhythmia with dopamine), plus an inotrope (dobutamine 2.5-10 mcg/kg/min, or milrinone if beta-blocked / RV failure). Every inotrope raises myocardial oxygen demand and arrhythmia risk — a bridge to a definitive decision.
Mechanical circulatory support (refractory shock) — Impella (active LV unloading), VA-ECMO (full heart-and-lung support). The IABP has lost routine status after IABP-SHOCK II (no mortality benefit in MI-shock), but is still used as a bridge in selected centres. Importantly, VA-ECMO does NOT unload the LV — retrograde flow increases afterload and can worsen LV distension and pulmonary oedema; add an Impella (ECPELLA) if the LV is dilating on serial echo.
Treat the trigger — ACS (revascularise), AF (rate or rhythm control), pneumonia/sepsis (antibiotics, source control), renal failure (dialysis if overloaded), MR/VSD (urgent surgery), severe mitral stenosis (mitral balloon valvuloplasty or surgery), prosthetic valve thrombosis (surgery or thrombolysis). [1]

Cardiogenic vs non-cardiogenic pulmonary oedema

Feature	Cardiogenic	Non-cardiogenic (ARDS)
Mechanism	Hydrostatic (high pressure)	Permeability (leaky capillaries)
Cause	Heart failure, volume overload, mitral stenosis	Sepsis, pneumonia, trauma, aspiration, transfusion
BNP/NT-proBNP	HIGH (>300 NT-proBNP)	LOW or normal
Echocardiography	Reduced EF (HFrEF) or diastolic dysfunction (HFpEF)	Usually normal EF
CXR/CT pattern	Central, perihilar, pleural effusions, Kerley B lines	Diffuse, peripheral, no effusions (usually)
PCWP	>18 mmHg	<18 mmHg
Oedema fluid protein	Low (transudate — protein-poor)	High (exudate — protein-rich)
Response to diuretics	RAPID improvement (minutes-hours)	Slow/no response
Response to CPAP/NIV	RAPID (minutes — pushes fluid back)	Minimal (doesn't address permeability)
Treatment	Diuretics, vasodilators, CPAP/NIV	Treat cause, lung-protective ventilation, prone

[1]

Hydrostatic vs permeability — Starling forces at the bedside

Starling variable	Cardiogenic (hydrostatic)	Non-cardiogenic (permeability/ARDS)
Capillary hydraulic pressure (Pc)	↑↑↑ (high LAP transmitted back)	Normal or low
Plasma oncotic pressure	Usually normal	Often reduced (critical illness, hypoalbuminaemia)
Capillary permeability coefficient	NORMAL — membrane intact	↑↑↑ — membrane injured, leaks protein
Net fluid composition	Transudate (protein-poor, <60% of plasma)	Exudate (protein-rich, >60% of plasma)
Consequence of lowering Pc	Resolves oedema (diuretics/vasodilators/CPAP)	Does not resolve (membrane still leaks)
Lung architecture	Largely preserved once pressure relieved	Damaged — needs time, lung-protective ventilation

[1]

Acute causes of cardiogenic pulmonary oedema with a NORMAL EF

Cause	Why EF looks normal	Distinguishing clue on echo
HFpEF (diastolic HF)	Stiff LV with preserved systole	E/e' > 14, LA enlargement, LVH, raised estimated LV filling pressure
Acute severe MR	LV unloads into low-pressure left atrium — EF exaggerated	Flail leaflet, eccentric regurgitant jet, systolic flow reversal in pulmonary veins
Mitral stenosis	Obstruction is upstream of LV cavity	Thickened rheumatic leaflets, "hockey-stick" anterior leaflet, reduced mitral valve area, raised transmitral gradient
Aortic stenosis / HOCM	Concentric hypertrophy, hyperdynamic cavity	Calcified aortic valve / systolic anterior motion of mitral leaflet, dynamic LVOT gradient
Takotsubo / septic cardiomyopathy	Regional sparing or hyperkinesis in non-involved segments	Apical ballooning (takotsubo); global hypokinesis in septic cardiomyopathy
Mitral valve prosthesis thrombosis	Native LV function preserved	Reduced prosthetic leaflet mobility, raised transmitral gradient, occasionally visible thrombus

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Non-cardiogenic pulmonary oedema (ARDS) — treatment

Once the bedside assessment points to permeability oedema, the strategy inverts: lowering pressure helps at the margins but cannot fix a leaky membrane. Management is dominated by treating the cause and lung-protective ventilation.[7]

Identify and treat the trigger — pneumonia (antibiotics, BAL), sepsis (source control, empirical broad-spectrum, focus), aspiration (positional, bronchoscopy for particulates), pancreatitis (aggressive fluid resuscitation early, then conservative), trauma (fix the chest, transfuse appropriately — avoid over-transfusion and TRALI), transfusion-related (stop the unit, supportive care).
Lung-protective ventilation (ARDSNet ARMA 2000) — Vt 6 mL/kg predicted body weight (NOT actual), Pplat < 30 cmH2O, titrate PEEP/FiO2 against the ARDSNet table, target pH > 7.20 (permissive hypercapnia), SpO2 88-95% / PaO2 55-80 mmHg. This single intervention reduced mortality from 40% to 31% — the most influential ARDS trial ever run.[7]
Driving pressure and PEEP optimisation — keep driving pressure (Pplat - PEEP) < 15 cmH2O where possible (Amato meta-analysis: driving pressure most strongly associated with survival). High PEEP for moderate-severe ARDS (ALVEOLI, EXPRESS — modest benefit in the sickest).
Prone ventilation for moderate-severe ARDS (PaO2/FiO2 < 150) — 16+ hours/day. PROSEVA showed a 28-day mortality reduction (16% vs 33%) in severe ARDS.
Conservative fluid strategy (FACTT) — a fluid-management protocol targeting lower central venous pressure / pulmonary artery occlusion pressure produced more ventilator-free days and shorter ICU stay than a liberal strategy, without increasing renal failure. Avoid the daily 4-6 L of "maintenance" that accumulates silently in ARDS.[8]
Avoid harmful interventions — high-frequency oscillatory ventilation (HFOV) increased mortality in OSCILLATE (NEJM 2013) — do not use routinely; neuromuscular blockade may help in early severe ARDS (ACURASYS, ROSE — controversial, 48-h cisatracurium in early severe P/F < 150); routine statins and beta-blockers do not help.
Adjuncts for refractory hypoxaemia — inhaled pulmonary vasodilators (nitric oxide, epoprostenol) for transient oxygenation improvement (no mortality benefit), recruitment manoeuvres (carefully), ECMO for severe refractory ARDS (centre transfer, CESAR and EOLIA trials).

CPAP vs BiPAP vs HFNC for acute respiratory failure — when to use each

Modality	Cardiogenic oedema	ARDS / non-cardiogenic
CPAP	First-line — drops preload/afterload, recruits alveoli (3CPO)	Useful in mild ARDS / immunocompromised (FLORALI — early NIV reduced intubation in immunocompromised subgroup)
BiPAP	Equal to CPAP (3CPO); preferred if hypercapnia or CO2 retention	Useful if hypercapnic (combined ARDS + airflow obstruction)
HFNC	Second-line if NIV not tolerated	Reasonable first-line in moderate hypoxaemic respiratory failure (FLORALI — trend to lower 90-day mortality vs NIV or standard O2)
Intubation	If NIV fails / haemodynamic collapse / reduced GCS	If P/F < 150 and worsening, work of breathing high, or NIV fails within 1-2 h
Key trial	3CPO (Gray, Lancet 2008)	FLORALI (Frat, NEJM 2015); HACAR (high-flow in immunocompromised)

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Side-by-side educational comparison of cardiogenic hydrostatic pulmonary oedema versus non-cardiogenic permeability oedema with BNP, echo EF, and treatment fork icons, clinical blue white background, no real radiographs — FigureCardiogenic (hydrostatic, high BNP, reduced EF, NIV + diuretic) versus non-cardiogenic/ARDS (permeability, lung-protective ventilation, conservative fluids) — the bedside diagnostic fork.

Differentiation toolkit — PCWP, BNP, echo, POCUS

BNP and NT-proBNP

The single best biochemical discriminator. NT-proBNP < 300 pg/mL in the acute setting effectively excludes heart failure as the cause of dyspnoea (high negative predictive value); values > 450 pg/mL in patients < 50, > 900 in those 50-75, and > 1800 in those > 75 support heart failure (age-stratified cutoffs). Confounders: renal failure raises it (reduced clearance), obesity lowers it, AF/PE/sepsis all elevate it by non-HF mechanisms. A rising trend during treatment supports an HF contribution. A low NT-proBNP in a patient with bilateral infiltrates and sepsis favours ARDS.[2]

Echocardiography — the definitive bedside tool

Reduced EF (< 40%) with regional or global hypokinesis → cardiogenic (HFrEF). Normal EF with diastolic dysfunction (E/e' > 14, LA enlargement, LVH) → cardiogenic (HFpEF). Normal EF and normal diastolic function in a patient with bilateral infiltrates and a credible insult → non-cardiogenic (ARDS). Critically, echo also identifies the mechanical causes of cardiogenic oedema with normal EF — acute MR (flail leaflet, eccentric jet, systolic flow reversal in pulmonary veins), severe MS (rheumatic thickening, raised transmitral gradient), prosthetic valve thrombosis, and tamponade.[4]

Point-of-care ultrasound (POCUS) — bilateral B-lines, IVC, focused cardiac

The combination of bilateral diffuse B-lines (comet-tail artefacts from the pleura moving with respiration), a plethoric IVC (> 2 cm with < 50% collapsibility), and reduced LV systolic function on focused cardiac view strongly supports cardiogenic oedema. Bilateral B-lines with a small, collapsing IVC and normal LV favour ARDS. B-lines do NOT distinguish cardiogenic from non-cardiogenic in isolation — both produce them — but the IVC, cardiac, and clinical context do. Lung ultrasound can also reveal focal B-lines (pneumonia, contusion), pleural effusions (anechoic quadrilaterals — large in cardiogenic, small in ARDS), and pneumothorax (absent lung sliding, lung point).[5]

Pulmonary capillary wedge pressure (PCWP)

The historical gold standard. PCWP > 18 mmHg supports hydrostatic (cardiogenic) oedema; PCWP < 18 with bilateral infiltrates and a credible insult supports ARDS. The PA catheter has been displaced by echo and POCUS for routine use (no mortality benefit in routine ICU populations — Connors observational analysis, FACTT sub-study, ESCAPE), but still has a role in the patient with mixed shock, severe pulmonary hypertension, or unexplained oedema where echo windows are poor. The Berlin ARDS definition no longer requires a PA catheter — "oedema not fully explained by cardiac failure or fluid overload" suffices, often adjudicated by echo/POCUS rather than PCWP.[1]

Trial of therapy

If cardiogenic oedema is suspected, a diagnostic–therapeutic trial of CPAP + IV furosemide is justified. Rapid improvement (SpO2 up, RR down, BP stabilises, distress resolves) within 15-30 minutes confirms cardiogenic. No rapid improvement — reconsider ARDS, pneumonia, or a mechanical complication. This trial must not delay definitive imaging/echo in the unstable patient. [1]

The mixed picture

Many ICU patients have BOTH cardiogenic and non-cardiogenic components — sepsis-induced cardiomyopathy (cardiac stunning + ARDS), heart failure with secondary pneumonia, ARDS aggressively fluid-resuscitated (hydrostatic contribution). These patients need BOTH treatments: diurese for the hydrostatic component, lung-protective ventilation and conservative fluids for the ARDS component, and serial echo + lactate + POCUS to track the balance. [1]

POCUS findings — cardiogenic vs non-cardiogenic

POCUS modality	Cardiogenic	Non-cardiogenic (ARDS)
Lung — B-lines	Diffuse bilateral, often with effusions	Diffuse bilateral, may be patchy, subpleural consolidations
Lung — A-lines	Absent in oedematous zones	May be present in spared zones (non-homogeneous)
Pleural effusion	Common — bilateral, right > left	Usually small or absent
IVC	Plethoric (> 2 cm, < 50% collapse) — high right atrial pressure	Small/collapsible if hypovolaemic; may be normal
Focused cardiac	Reduced LV (HFrEF) or thick/stiff LV with LA enlargement (HFpEF); may show acute MR / MS	Usually normal LV; may show RV dilation in severe ARDS (acute cor pulmonale)
LV EF	Reduced OR preserved (HFpEF)	Usually normal
Estimated LAP	Raised (E/e' > 14)	Normal

[1]

Bedside approach to bilateral infiltrates + hypoxaemia

Assess clinically — history (heart failure? sepsis? trauma?), signs (raised JVP, S3 gallop, peripheral oedema = cardiogenic; fever, sepsis source, clear lung on auscultation initially = non-cardiogenic)
BNP/NT-proBNP — HIGH (>300 NT-proBNP) → cardiogenic likely. LOW → non-cardiogenic likely. INTERMEDIATE → grey zone (renal failure, sepsis, obesity confound)
Echocardiography (bedside) — reduced EF or wall motion abnormality → cardiogenic. Normal EF → non-cardiogenic (or HFpEF). Also: assess valves (mitral stenosis/regurgitation), pericardial effusion (tamponade)
Lung ultrasound — B-lines (comet tails): diffuse bilateral = oedema (cardiogenic or non). Focal = consolidation/pneumonia. A-lines (normal): no oedema. Pleural effusion (cardiogenic more common)
CT chest (if uncertain) — cardiogenic: central, perihilar, ground-glass, pleural effusions, cardiomegaly. Non-cardiogenic: diffuse, peripheral, no effusions (usually), no cardiomegaly
Trial of therapy — if cardiogenic suspected: CPAP + IV frusemide → RAPID improvement (within 30-60 min) = cardiogenic confirmed. If NO rapid improvement → reconsider (ARDS?)
Treat accordingly — cardiogenic: diuretics, vasodilators, CPAP/NIV, treat cardiac cause. Non-cardiogenic: treat underlying cause, lung-protective ventilation, prone, conservative fluids

[1]

Cardiogenic pulmonary oedema — the first 60 minutes

POSITION and OXYGENATE — sit upright; oxygen via face mask to target SpO2 92-96% (avoid hyperoxia). Continuous ECG, IV access, arterial line if unstable, urinary catheter
CLASSIFY the Stevenson phenotype — wet vs dry (congestion) crossed with warm vs cold (perfusion). Most cardiogenic oedema is WARM-WET (BP usually > 110); cold-wet = cardiogenic shock
START NIV/CPAP EARLY (the wet patient) — CPAP 5-10 cmH2O or BiPAP IPAP 10-15 / EPAP 5-8. Mechanism: drops preload and afterload, recruits alveoli, unloads respiratory muscles. Do NOT wait for exhaustion (3CPO)
IV LOOP DIURETIC — furosemide IV. Naive patient: 20-40 mg. Established oral loop: 1-2.5x total daily oral dose IV. Reassess at 2 h, double if poor response. Target 3-5 L/day net negative
VASODILATOR if SBP > 110 — IV nitroglycerin 10-200 mcg/min. Avoid in RV infarct, severe AS, HOCM, recent PDE-5. Nitroprusside for severe hypertension (cyanide toxicity in renal failure)
COLD-WET (shock) → INOTROPE + VASOPRESSOR — noradrenaline to MAP > 65 (first-line, SOAP-II), dobutamine 2.5-10 mcg/kg/min or milrinone if beta-blocked/RV failure. Reassess for mechanical complication (VSD, papillary muscle rupture)
MECHANICAL CIRCULATORY SUPPORT if refractory — Impella (active LV unloading) or VA-ECMO (full support). Add Impella to VA-ECMO (ECPELLA) if LV dilating. IABP no longer routine (IABP-SHOCK II)
FIND AND TREAT THE TRIGGER — ACS (revascularise), AF (rate/rhythm control), MS/MR (valve intervention), prosthetic valve thrombosis (surgery/thrombolysis), pneumonia/sepsis (antibiotics), renal failure (RRT)

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Non-cardiogenic (ARDS) — lung-protective ventilation setup

CONFIRM the diagnosis — bilateral opacities + hypoxaemia within 1 week of insult + oedema NOT fully cardiac/fluid (echo/POCUS) + PCWP < 18 if measured (Berlin definition)
CALCULATE PREDICTED BODY WEIGHT (PBW) — Male: 50 + 2.3 × (height in inches − 60). Female: 45.5 + 2.3 × (height in inches − 60). Use PBW (NOT actual weight) for Vt — actual weight over-doses the oedematous lung
SET INITIAL Vt at 8 mL/kg PBW, then REDUCE to 6 mL/kg PBW over 4 h
TITRATE TO PLATEAU PRESSURE (Pplat) — measure with 0.5-s inspiratory hold. If Pplat > 30 cmH2O, reduce Vt to 4 mL/kg PBW minimum. If Pplat < 25 and there is dual triggering, may increase to 7-8 mL/kg
SET PEEP/FiO2 using the ARDSNet lower-PEEP/higher-PEEP table; consider higher PEEP table for moderate-severe ARDS (ALVEOLI, EXPRESS)
DRIVING PRESSURE (Pplat − PEEP) — keep < 15 cmH2O where possible (Amato); the ventilation variable most associated with survival
RESPIRATORY RATE 20-35/min to keep pH > 7.20 (permissive hypercapnia acceptable). I:E 1:1 or 1:2
TARGET SpO2 88-95% / PaO2 55-80 mmHg — permissive hypoxaemia; do not chase "normal" by escalating harmful FiO2/PEEP
CONSIDER PRONE if PaO2/FiO2 < 150 — at least 16 h/day (PROSEVA)
CONSERVATIVE FLUIDS (FACTT) — fluid-restrict once resuscitated; daily net even or negative; track cumulative balance
ESCALATE — refractory hypoxaemia (P/F < 80 despite optimisation) → inhaled pulmonary vasodilator, recruitment manoeuvres, ECMO referral

[1]

Negative pressure pulmonary oedema (NPPE) — recognition and management

RECOGNISE the setting — post-extubation laryngospasm, biting on the endotracheal tube, near-drowning, strangulation, severe obstructive sleep apnoea, post-anaesthesia in a young healthy patient, thyroid mass or tumour obstructing the airway
MECHANISM — forceful inspiration against a closed glottis → very negative intrathoracic pressure (Mueller manoeuvre) → high transcapillary pressure gradient → fluid pulled into interstitium and alveoli. May also injure the capillary (stress failure) giving a mixed hydrostatic + permeability picture
CLINICAL — pink frothy sputum, hypoxaemia, diffuse crackles, developing within minutes to hours of relief of the obstruction. CXR: bilateral infiltrates
RELIEVE THE OBSTRUCTION — definitive airway if still obstructed (re-intubate, surgical airway); bite block if biting
OXYGEN + CPAP/NIV — most cases respond within 24 h; positive pressure reverses the hydrostatic gradient
DIURETICS — small dose (furosemide 20-40 mg IV) often helps; not the primary therapy
DIFFERENTIATE — no heart failure, no ARDS-insult (think ARDS if sepsis/pneumonia coexists). Echo usually normal. Self-limiting in 24 h if obstruction is relieved
REASSURE the team — NPPE in a healthy young patient after anaesthesia typically resolves fully within 24 h with supportive care; rare mortality

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Exam practice

SAQ — Acute cardiogenic pulmonary oedema: NIV/CPAP and the 3CPO trial

10 minutes · 10 marks

A 78-year-old man with known HFrEF (EF 28%), prior MI and CKD stage 3 presents with 4 hours of worsening breathlessness, orthopnoea and cough. He is diaphoretic, sitting upright, RR 34, SpO2 86% on 15 L/min NRM, BP 168/96, HR 118 sinus tachycardia, JVP to the earlobes, bilateral crackles two-thirds up and expiratory wheeze. CXR shows perihilar 'bat-wing' infiltrates, Kerley B lines and small bilateral pleural effusions. ABG: pH 7.22, PaCO2 7.1 kPa (54 mmHg), PaO2 7.8 kPa (59 mmHg), lactate 2.8. NT-proBNP 6800 pg/mL. The ED team has started CPAP at 10 cmH2O.

[1]

SAQ — Cardiogenic pulmonary oedema with acute kidney injury (cardiorenal syndrome)

10 minutes · 10 marks

A 72-year-old woman with HFrEF (EF 25%), type 2 diabetes and CKD stage 3b (baseline creatinine 160 µmol/L) is admitted with decompensated heart failure — flash pulmonary oedema, JVP to the jaw, sacral and leg oedema, weight gain 6 kg over 10 days. She is on furosemide 80 mg BD orally. BP 96/60, RR 30, SpO2 90% on 10 L/min, warm-cool peripheries, oliguric (15 mL/h). Creatinine 290 µmol/L, K+ 5.8, lactate 3.1, NT-proBNP 12000. Echo: dilated LV, EF 22%, no mechanical valve lesion. She has been started on CPAP and a furosemide infusion.

[1]

Clinical pearls

High-yield pulmonary oedema differentiation points for CICM/FFICM exam

BNP/NT-proBNP is the best single discriminator. HIGH (>300 pg/mL NT-proBNP) → cardiogenic (NPV 90% if low). LOW → non-cardiogenic/ARDS. INTERMEDIATE: confounded by renal failure (elevated), obesity (reduced), sepsis (may elevate from myocardial depression), age (higher thresholds for elderly). Use as SCREENING — confirm with echo.[2]
Echocardiography is the definitive bedside tool. Reduced EF (<40%) → cardiogenic (HFrEF). Normal EF + diastolic dysfunction → cardiogenic (HFpEF). Normal EF + no diastolic dysfunction → non-cardiogenic (ARDS). ALSO assess: regional wall motion (ischaemic — MI causing cardiogenic), valvular (mitral stenosis/regurgitation), pericardial (tamponade).[4]
CPAP/NIV produces RAPID improvement in cardiogenic oedema (minutes). Mechanism: positive pressure → pushes fluid from alveoli back into interstitium/vasculature → reduces preload (venous return) → reduces afterload (LV transmural pressure). Cardiogenic: dramatic improvement (SpO2 up, RR down, BP stabilises) within 15-30 min. ARDS: NO rapid improvement (permeability problem — CPAP doesn't fix leaky capillaries). 3CPO trial: CPAP reduced intubation/mortality in cardiogenic oedema.[3]
Cardiogenic: diuretics produce rapid improvement. Frusemide IV: venodilation (within 5-15 min — BEFORE diuresis starts) → reduced preload → less pulmonary congestion. Then diuresis (30-60 min) → fluid removed. Cardiogenic: clear response (urine output, SpO2, RR improve). Non-cardiogenic (ARDS): diuretics LESS effective (fluid isn't from hydrostatic pressure — it's from leaky capillaries). Conservative fluid helps but is slower.[6]
Oedema fluid protein differentiates (rarely used in practice). CARDIOGENIC: oedema fluid is TRANSUDATE (protein-poor — <60% of plasma protein). NON-CARDIOGENIC: EXUDATE (protein-rich — >60% of plasma protein — because capillaries are leaky → protein escapes). Collected from: endotracheal tube aspirate (if intubated). Rarely done (impractical) but conceptually important.[1]
Cardiogenic infiltrates: CENTRAL, perihilar ('bat wing'). Classic CXR: opacity radiating from hilum (bat wing/butterfly) — perihilar alveolar oedema. Spares periphery (early). ALSO: pleural effusions (usually bilateral, right larger), Kerley B lines (interstitial oedema — short horizontal lines at lung bases), cardiomegaly, upper lobe blood diversion. NON-CARDIOGENIC: DIFFUSE, peripheral, often NO pleural effusion, NO cardiomegaly.[1]
Lung ultrasound: B-lines (comet tails). B-lines: vertical artefacts from pleura, moving with respiration — indicate interstitial/alveolar fluid. Diffuse bilateral B-lines: oedema (cardiogenic or non — doesn't differentiate between the two). Focal B-lines: focal pathology (pneumonia, contusion). Normal A-lines (horizontal): no oedema. PLEURAL EFFUSION: anechoic fluid (can quantify — estimate volume). B-lines: useful for: confirming oedema, monitoring response (B-lines reduce with treatment).[5]
PCWP (pulmonary capillary wedge pressure) — invasive, rarely used. PA catheter (Swan-Ganz): PCWP >18 mmHg = cardiogenic (high left atrial pressure → hydrostatic oedema). PCWP <18 = non-cardiogenic (ARDS). RARELY used now (PA catheter less common — echo is preferred for non-invasive assessment). Historical gold standard.[1]
Mixed oedema — both cardiogenic and non-cardiogenic. Some patients have BOTH: (1) Sepsis-induced cardiomyopathy → cardiac dysfunction + ARDS (permeability). (2) Heart failure with secondary infection (pneumonia → ARDS on top of HF). (3) Volume overload in ARDS (aggressive fluid resuscitation → hydrostatic component). These patients need BOTH treatments: diuretics (for cardiac/volume component) + lung-protective ventilation (for ARDS component).[6]
Mitral stenosis/regurgitation can cause pulmonary oedema with normal EF. MITRAL STENOSIS: obstructed LV inflow → high LA pressure → pulmonary venous pressure → oedema. EF may be NORMAL (LV not failing — it's upstream obstruction). MITRAL REGURGITATION (acute): volume overload backwards → pulmonary oedema. EF may be normal (or even hyperdynamic — compensating). ECHO: identify valvular cause (don't miss — needs valve surgery).[4]
Negative pressure pulmonary oedema (NPPE). Upper airway obstruction (laryngospasm, strangulation, obstructive sleep apnoea) → forceful inspiration against closed glottis → NEGATIVE intrathoracic pressure → pulls fluid into alveoli. Clinical: post-extubation laryngospasm, near-drowning, post-anaesthesia. TREATMENT: oxygen, CPAP/NIV (usually resolves quickly — 24h). DIFFERENT from cardiogenic (no heart failure) and ARDS (mechanical cause).[11]
High-altitude pulmonary oedema (HAPE). Rapid ascent to high altitude (>2500m) → uneven hypoxic pulmonary vasoconstriction → high pressure in some capillaries → leak. TREATMENT: DESCEND (most effective), oxygen, nifedipine (vasodilator). DIFFERENT from cardiogenic (no heart failure) — HYPOXIC mechanism. Prevention: gradual ascent, acetazolamide.[1]
Re-expansion pulmonary oedema. After rapid drainage of large pneumothorax or pleural effusion → sudden lung re-expansion → negative pressure → fluid leak. PREVENT: drain slowly (not >1.5 L at once), clamp if chest pain/cough. TREATMENT: supportive (oxygen, usually self-limited). RARE but dangerous.[1]
Transfusion-related acute lung injury (TRALI). Within 6h of transfusion: bilateral infiltrates + hypoxaemia (ARDS-like — NON-cardiogenic). Mechanism: donor antibodies (anti-HLA, anti-HNA) → recipient neutrophils → pulmonary endothelial damage → leak. TREATMENT: STOP transfusion, supportive (oxygen, ventilation — lung-protective). Usually resolves in 48-72h. MORTALITY: 5-10%. REPORT to blood bank.[14]

16 additional pearls — physiology, traps, exam answers

The PCWP threshold of 18 mmHg comes straight from Starling physics. Plasma oncotic pressure is ~25 mmHg; once capillary hydrostatic pressure (reflected by PCWP in the absence of mitral stenosis) exceeds ~18 mmHg, the safety margin of interstitial pressure and lymphatic clearance is overwhelmed and fluid accumulates. This is why the AECC and Berlin definitions both anchor on < 18 mmHg to exclude cardiogenic oedema.[1]
Acute severe MR can present with a SOFT or ABSENT murmur. When LV output collapses in cardiogenic shock, the regurgitant volume falls and the classic pansystolic murmur disappears. Do NOT be reassured by the absence of a murmur in a post-MI patient with new pulmonary oedema — get an urgent echocardiogram.[4]
Flash pulmonary oedema + hypertension + a small kidney / abdominal bruit = bilateral renal artery stenosis (Pickering syndrome). Recurrent flash pulmonary oedema in an elderly, hypertensive patient with normal or mildly impaired LV function is a classic presentation of renovascular disease. ACE-inhibitor renography, Doppler, or CT angiography diagnoses it; revascularisation (stenting where appropriate) can be curative.
HFpEF causes cardiogenic oedema with a NORMAL EF. Up to half of ADHF admissions have a preserved EF. The pathology is diastolic — a stiff LV cannot accept filling at normal pressures, so small volume loads or tachycardia (loss of diastolic filling time) spike the LAP. Echo: E/e' > 14, LA enlargement, LVH. Treatment is the same acute ladder (CPAP, diuretic, vasodilator) but long-term evidence is thinner than for HFrEF.
Acute MR from papillary muscle rupture is more common after inferior MI. The posteromedial papillary muscle has a SINGLE blood supply (PDA, from the RCA) while the anterolateral has dual supply (LAD + LCx). Inferior MI therefore preferentially ruptures the posteromedial head, presenting at days 2-7 with sudden pulmonary oedema, hypotension, and an often-soft apical systolic murmur. Urgent echocardiogram; surgical repair/replacement.
3CPO is the trial examiners love to ask about — know its nuance. Gray et al. (Lancet 2008, 1069 patients): CPAP vs BiPAP vs standard O2 in cardiogenic pulmonary oedema. PRIMARY endpoint (7-day mortality) was NOT different (9.8% in all three groups). What 3CPO DID show: faster relief of dyspnoea, faster correction of hypercapnia and acidosis, and a non-significant reduction in intubation/death composite. NIV is standard of care on the totality of evidence.[3]
DOSE is the diuretic trial. Felker et al. (NEJM 2011, 308 patients, 2x2 factorial): high-dose (2.5x oral) vs low-dose (1x oral) furosemide and bolus vs continuous infusion. No difference in co-primary endpoints (symptom AUC over 72 h and creatinine at 72 h). High-dose gave greater fluid and weight loss at the cost of more transient renal dysfunction. Practical message: high-dose is reasonable, bolus = continuous.
FACTT — conservative fluid strategy wins in ARDS. Wiedemann et al. (NEJM 2006): conservative fluid management (target CVP < 4, PCWP < 8) vs liberal (CVP 10-14, PCWP 14-18) in ALI/ARDS. Conservative produced MORE ventilator-free days, MORE ICU-free days, NO increase in renal failure or dialysis, NO change in 60-day mortality. Apply once the patient is resuscitated.[8]
ARDSNet ARMA — the most influential ARDS trial ever. NEJM 2000, 861 patients: Vt 6 mL/kg PBW vs 12 mL/kg PBW. Mortality 31% vs 40% (NNT ~11). Stopped early for efficacy. Tidal volume is calculated from PREDICTED body weight (height-based), NOT actual — actual weight over-doses the lung. Plateau pressure < 30 cmH2O.[7]
Neurogenic pulmonary oedema follows severe CNS insult — SAH, TBI, seizure. Onset within minutes to hours of the insult; a massive sympathetic surge produces catecholamine-induced cardiac stunning (often takotsubo-pattern), systemic hypertension, and capillary stress failure in the lung. Echo may show apical ballooning; troponin may be elevated. Treatment: supportive (oxygen, ventilation, alpha/beta-blockade in selected cases); self-limiting over 48-72 h if the brain insult is survivable.
TRALI vs TACO — the two transfusion lung injuries. TRALI: donor antibodies (anti-HLA/anti-HNA) → recipient neutrophils → endothelial damage → ARDS-like picture within 6 h; treatment is SUPPORTIVE (no diuretic — fluid is not hydrostatic), report to blood bank; mortality 5-10%. TACO (transusion-associated circulatory overload): hydrostatic overload from the transfused volume, presents within 6-12 h, often with hypertension and raised BNP; treated with diuretics. Both resolve with stopping the transfusion and supportive care.
VA-ECMO does NOT unload the LV. Retrograde flow from the femoral arterial cannula increases LV afterload and can worsen LV distension and pulmonary oedema in cardiogenic shock. If the LV is dilating on serial echo (or there is new pulmonary oedema, rising LA pressure, pulmonary haemorrhage), add an Impella (ECPELLA configuration) or use a central configuration with a vent.[13]
High-altitude pulmonary oedema (HAPE) is a HYPOXIC, not a cardiac, problem. HAPE develops at altitude (> 2500 m) from uneven hypoxic pulmonary vasoconstriction — over-perfused capillary segments leak under high pressure. Treatment: DESCEND (the single most effective intervention), supplemental oxygen, nifedipine (reduces pulmonary vascular resistance); prevention by gradual ascent, acetazolamide. Echo shows a normal LV.
Driving pressure (< 15 cmH2O) is the ventilation variable most associated with survival. Amato et al. (NEJM 2015, individual-patient meta-analysis of 3500+ patients): driving pressure (Pplat − PEEP) was more strongly associated with survival than Vt or Pplat themselves. Practically — if you can only optimise ONE number, push driving pressure down by reducing Vt and/or raising PEEP.
Proning works best in severe ARDS and must be done EARLY. PROSEVA (NEJM 2013, Guérin): prolonged prone ventilation (≥ 16 h/day) in ARDS with PaO2/FiO2 < 150 within 36 h of enrolment reduced 28-day mortality from 33% to 16%. Proning is safe (with trained staff) and effective; the benefit is greatest in severe, early ARDS.
Don't confuse 'flash' pulmonary oedema with stable congestion. Flash pulmonary oedema is ACUTE, dramatic, and often mechanical — acute MR from papillary muscle rupture, prosthetic valve thrombosis, severe hypertension with bilateral renal artery stenosis, tachyarrhythmia in HFpEF. It demands immediate diagnosis of the trigger (urgent echo, ECG, look for a bruit, check prosthetic valve) — not just symptom relief. Discharging a flash-oedema patient without identifying the trigger is a near-guaranteed readmission.

Red flags

Cardiogenic oedema red flags — don't miss the trigger

Acute severe MR with a SOFT or absent murmur in low-output shock — the regurgitant volume falls as LV output falls; absence of murmur does NOT exclude papillary muscle rupture. Get an urgent echocardiogram.[4]
Flash pulmonary oedema + hypertension + abdominal bruit / small kidney → bilateral renal artery stenosis (Pickering syndrome) — revascularisation may cure.
Pulmonary oedema in a patient on dialysis or after a large fluid bolus → volume overload, not ARDS; remove the fluid.
Mitral stenosis with new-onset AF → LAP rises sharply from loss of atrial kick; rate control + anticoagulation + valve intervention.
Prosthetic mitral valve + new pulmonary oedema + muffled closure sound → prosthetic valve thrombosis (echo urgent; surgery or thrombolysis).
Cold-wet patient on GTN → GTN in the hypotensive patient collapses the perfusion; switch to inotrope + vasopressor and reassess.
VA-ECMO + new pulmonary oedema / haemorrhage → LV distension from retrograde ECMO flow — add an Impella (ECPELLA) or vent.[13]

Non-cardiogenic (ARDS) red flags

Echo normal + low BNP + bilateral infiltrates + a credible insult (sepsis/pneumonia/aspiration/trauma/pancreatitis) → ARDS, not heart failure — switch to lung-protective ventilation.[9]
Vt 6 mL/kg PBW, NOT actual weight — actual weight over-doses the oedematous lung. Recalculate from height.[7]
Plateau pressure > 30 cmH2O → reduce Vt to 4 mL/kg PBW minimum; this is harmful stretch.
Driving pressure > 15 cmH2O → reduce Vt or raise PEEP; the variable most associated with survival.
PaO2/FiO2 < 150 within 36 h of ARDS onset → start proning ≥ 16 h/day (PROSEVA).
Cumulative positive fluid balance > 4 L/day in ARDS → switch to a conservative strategy (FACTT).[8]
HFOV in moderate-severe ARDS → OSCILLATE showed increased mortality; do NOT use routinely.[10]
RV dilation on echo in ARDS → acute cor pulmonale from high PEEP / hypoxia; reduce PEEP, accept lower PaO2, inhaled pulmonary vasodilator.

Special-form pulmonary oedema — recognise the atypical

NPPE: post-extubation laryngospasm, biting, strangulation, near-drowning → pink frothy sputum within minutes-hours; relieve obstruction, CPAP/NIV, resolves < 24 h.[11]
Re-expansion oedema: never drain > 1.5 L from a chronic pleural effusion or apply high negative suction to a chronic pneumothorax — clamp if the patient develops chest tightness or cough.
Neurogenic oedema within hours of SAH/TBI/seizure → look for takotsubo cardiac stunning; supportive care, alpha/beta-blockade in selected cases.
HAPE at altitude → DESCEND is the single most effective treatment; oxygen, nifedipine; prevention by gradual ascent, acetazolamide.
TRALI within 6 h of transfusion → STOP the transfusion, supportive care (no diuretic — this is permeability), report to blood bank.[14]
TACO within 6-12 h of transfusion → hydrostatic overload from volume; treat with diuretics.

Prognosis

3CPO trial (Gray 2008, Lancet) — NIV in cardiogenic pulmonary oedema

RCT: 1,069 patients with cardiogenic pulmonary oedema. CPAP vs NIV (BiPAP) vs standard oxygen.

Primary outcome (7-day mortality): CPAP 9.8%, NIV 9.8%, standard 9.8% (NO difference)
Secondary outcomes (intubation, dyspnoea, length of stay): NIV/CPAP reduced dyspnoea faster, reduced intubation vs standard
CONCLUSION: NIV (CPAP or BiPAP) reduces intubation and improves dyspnoea in cardiogenic oedema. No mortality difference in this trial (but other meta-analyses suggest benefit). CPAP is SIMPLE and EFFECTIVE for cardiogenic oedema. [1]

BNP for diagnosis: high NT-proBNP (>300) → heart failure likely. Low → excluded (NPV 90%). Both CPAP and BiPAP effective for cardiogenic oedema.

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ARDSNet ARMA (Acute Respiratory Distress Syndrome Network, NEJM 2000) — the lung-protective ventilation trial

RCT: 861 patients with ALI/ARDS. Vt 6 mL/kg PBW (Pplat < 30) vs Vt 12 mL/kg PBW (Pplat < 50).

Primary outcome (mortality before hospital discharge): 31% (low Vt) vs 40% (traditional Vt); NNT ~11 — trial stopped early for efficacy
Ventilator-free days: 12 vs 10 days; barotrauma: similar
CONCLUSION: Lung-protective ventilation (Vt 6 mL/kg PBW, Pplat < 30) reduces mortality in ARDS by ~9 absolute percentage points — the most influential ARDS trial ever run. Tidal volume calculated from PREDICTED body weight (height-based), not actual.[7]

FACTT (Wiedemann, NEJM 2006) — conservative vs liberal fluid in ALI/ARDS

RCT: 1,000 patients with ALI/ARDS. Conservative (CVP < 4, PCWP < 8) vs liberal (CVP 10-14, PCWP 14-18) fluid strategy, using protocolised diuretics/fluids for 7 days.

Primary outcome (60-day mortality): 25.5% (conservative) vs 28.4% (liberal) — NOT significant
Secondary outcomes: conservative gave MORE ventilator-free days (14.5 vs 12.0) and MORE ICU-free days (13.4 vs 11.2); NO increase in renal failure or dialysis
CONCLUSION: A conservative fluid strategy in established ARDS improves lung function and shortens ventilation and ICU stay without harming the kidneys. Apply once the patient is resuscitated.[8]

LUNG SAFE (Bellani, JAMA 2016) — ARDS epidemiology across 50 countries

Prospective observational: 29,144 ICU admissions in 459 ICUs across 50 countries over 4 winter weeks; 3,022 met ARDS criteria.

Incidence: 10.4% of ICU admissions; ARDS is common and under-recognised
Recognition: clinicians recognised ARDS in only ~51% of mild, ~79% of moderate, ~84% of severe cases — substantial under-recognition, especially in mild ARDS
Mortality (ICU): mild 34.9%, moderate 40.3%, severe 46.1% (Berlin severity correlates with outcome)
CONCLUSION: ARDS is under-recognised, under-treated (only ~60% received a low Vt), and carries high mortality that scales with severity. The case for systematic low-Vt ventilation and protocolised recognition.[9]

IABP-SHOCK II (Thiele, NEJM 2012) — IABP in MI-related cardiogenic shock

RCT: 600 patients with acute MI and cardiogenic shock, planned early revascularisation. IABP vs no IABP.

Primary outcome (30-day mortality): 39.7% (IABP) vs 41.3% (no IABP) — NOT significant
Secondary outcomes (process variables, lactate clearance, organ function, bleeding, stroke): no difference
CONCLUSION: Routine IABP in MI-related cardiogenic shock provides no mortality benefit. The IABP has lost routine status; percutaneous options now include Impella (active LV unloading) and VA-ECMO (full support), with selection individualised.[13]

CARRESS-HF (Bart, NEJM 2012) — ultrafiltration vs stepped pharmacological therapy in ADHF with cardiorenal syndrome

RCT: 188 patients with ADHF, persistent congestion AND worsening renal function. Venovenous ultrafiltration vs stepped pharmacological therapy (high-dose + sequential diuretics).

Primary outcome (change in creatinine at 96 h): +0.23 mg/dL (ultrafiltration) vs −0.04 mg/dL (pharmacological); P = 0.003 — ultrafiltration WORSE
Serious adverse events: 72% (ultrafiltration) vs 57% (pharmacological); P = 0.03 — stopped early for futility/safety
CONCLUSION: Ultrafiltration is NOT first-line decongestion in ADHF; reserve for refractory volume overload unresponsive to high-dose + sequential diuretics, or during RRT.[12]

PROSEVA (Guérin, NEJM 2013) — prone ventilation in severe ARDS

RCT: 466 patients with ARDS and PaO2/FiO2 < 150, within 36 h of enrolment. Prone ventilation ≥ 16 h/day vs supine.

Primary outcome (28-day mortality): 16.0% (prone) vs 32.8% (supine); P < 0.001 — large mortality reduction
90-day mortality: 23.6% (prone) vs 41.0% (supine); NNT ~6
CONCLUSION: In severe early ARDS (P/F < 150 within 36 h), prolonged prone ventilation (≥ 16 h/day) dramatically reduces mortality. Proning is safe with a trained team and should be initiated early in eligible patients.

[1]

TRALI and TACO — the two transfusion-related lung injuries

TRALI (Transfusion-Related Acute Lung Injury) — non-cardiogenic (permeability) oedema within 6 h of transfusion. Donor anti-HLA/anti-HNA antibodies (or, less commonly, biologically active lipids) activate recipient neutrophils, damaging the pulmonary endothelium. Bilateral infiltrates + hypoxaemia + NORMAL left atrial pressure. Treatment: STOP the transfusion, supportive care (oxygen, lung-protective ventilation if intubated). NO role for diuretics (this is permeability, not hydrostatic). Resolves in 48-72 h. Mortality 5-10%. REPORT to the blood bank; the donor unit should be quarantined and the donor deferred.[14]

TACO (Transfusion-Associated Circulatory Overload) — hydrostatic (cardiogenic) overload from the transfused volume, usually within 6-12 h, in patients with limited cardiac reserve. Bilateral infiltrates + hypertension + raised BNP + raised JVP. Treatment: stop the transfusion, diuretic (furosemide IV), oxygen/CPAP. Differentiate from TRALI by the BNP (high in TACO), the haemodynamics (hypertensive in TACO), and the response to diuretic (rapid in TACO).

[1]

Special pulmonary oedema syndromes — when the heart and the lung are NOT the usual suspects

NPPE (Negative Pressure Pulmonary Oedema) — forceful inspiration against a closed glottis (laryngospasm post-extubation, biting, strangulation, near-drowning, severe OSA). Generates very negative intrathoracic pressure (Mueller manoeuvre), raising the transcapillary gradient; may also cause capillary stress failure (mixed hydrostatic + permeability). Presents within minutes-hours with pink frothy sputum and hypoxaemia in an otherwise healthy patient. Treatment: relieve obstruction, CPAP/NIV, small-dose diuretic. Self-limiting in < 24 h.[11]

Re-expansion oedema — rapid re-expansion of a chronically collapsed lung (draining > 1.5 L pleural effusion or applying high suction to a chronic pneumothorax) produces local capillary leak and surfactant loss. Presents within 1-24 h on the DRAINED side. Prevention: limit drainage to < 1.5 L per session; clamp if chest tightness or cough. Treatment: supportive. [1]

Neurogenic oedema — within hours of severe CNS insult (SAH, TBI, status epilepticus). Massive sympathetic surge → catecholamine cardiac stunning (often takotsubo-pattern) → systemic hypertension and capillary stress failure. Echo may show apical ballooning; troponin elevated. Treatment: supportive (oxygen, ventilation); alpha/beta-blockade in selected cases. Often self-limiting over 48-72 h if the primary insult is survivable. [1]

HAPE (High-Altitude Pulmonary Oedema) — at altitude (> 2500 m) from uneven hypoxic pulmonary vasoconstriction — over-perfused capillary segments leak under high pressure. Treatment: DESCEND (single most effective), oxygen, nifedipine (reduces PVR); prevention by gradual ascent, acetazolamide. Echo shows normal LV.

[1]

Exam answer — the long-form / viva response

The expanded exam answer — for the long-form / viva question

Acutely, the differentiation between cardiogenic (hydrostatic) and non-cardiogenic (permeability, ARDS) pulmonary oedema is the central question, because the treatments diverge completely. At the bedside, the first steps are history (heart failure, ACS, AF, hypertension, valvular disease, dialysis → cardiogenic; sepsis, pneumonia, aspiration, trauma, pancreatitis, transfusion → non-cardiogenic), examination (raised JVP, S3 gallop, peripheral oedema, hypertension → cardiogenic; fever, sepsis source, clear lungs initially → non-cardiogenic), and a chest X-ray (central perihilar 'bat-wing' infiltrates with pleural effusions and cardiomegaly → cardiogenic; diffuse peripheral infiltrates without effusions or cardiomegaly → non-cardiogenic). [1]

The bedside toolkit is BNP/NT-proBNP (high → cardiogenic, low → non-cardiogenic, with renal failure, obesity, sepsis and age confounding), focused echocardiography (reduced EF or diastolic dysfunction → cardiogenic; normal EF and diastolic function → non-cardiogenic; also identifies the mechanical causes of cardiogenic oedema with normal EF — acute MR, mitral stenosis, prosthetic valve thrombosis, tamponade), and lung ultrasound (bilateral B-lines confirm oedema but don't distinguish cardiogenic from non-cardiogenic; the IVC, focused cardiac view, and pleural effusion pattern do). A PA catheter (PCWP > 18 → cardiogenic, < 18 → ARDS) is rarely needed but remains the historical gold standard. [1]

Cardiogenic pulmonary oedema is managed by sitting the patient upright, oxygen to target SpO2 92-96%, early NIV/CPAP (3CPO — faster relief of dyspnoea, hypercapnia, acidosis; CPAP = BiPAP), IV loop diuretic (furosemide 1-2.5x total daily oral dose, reassess at 2 h and double if poor response — DOSE), and an IV vasodilator (GTN 10-200 mcg/min) if SBP > 110. The cold-wet patient (cardiogenic shock) gets noradrenaline for MAP > 65 (SOAP-II preferred over dopamine), an inotrope (dobutamine or milrinone), and early mechanical circulatory support (Impella, VA-ECMO — adding Impella to VA-ECMO if the LV dilates). The IABP has lost routine status after IABP-SHOCK II; ultrafiltration is not first-line after CARRESS-HF. Throughout, identify and treat the trigger — ACS, AF, MR, MS, prosthetic valve thrombosis, renal failure, sepsis, drug non-adherence. [1]

Non-cardiogenic pulmonary oedema (ARDS) is managed by treating the cause (antibiotics, source control), lung-protective ventilation (Vt 6 mL/kg PREDICTED body weight, Pplat < 30, driving pressure < 15 — ARDSNet ARMA reduced mortality from 40% to 31%), conservative fluids (FACTT — more ventilator-free days, no renal cost), proning for P/F < 150 (PROSEVA — 28-day mortality 16% vs 33%), and escalation to inhaled pulmonary vasodilators or ECMO for refractory hypoxaemia. [1]

Special forms deserve specific recognition: negative pressure pulmonary oedema (post-extubation laryngospasm, near-drowning — CPAP, resolves < 24 h), re-expansion oedema (don't drain > 1.5 L from a chronic effusion), neurogenic oedema (CNS insult — look for takotsubo, supportive care), high-altitude pulmonary oedema (DESCEND, oxygen, nifedipine), and TRALI (within 6 h of transfusion — stop the unit, supportive care, no diuretic, report to blood bank). [1]

Throughout, the trend matters as much as the snapshot — a falling BNP and resolving B-lines with diuresis, a falling lactate and rising urine output with inotrope/vasopressor, a rising PaO2/FiO2 with lung-protective ventilation and proning, and serial echocardiography to detect a dilating LV on VA-ECMO or a worsening regurgitant lesion.

[1]

References

[1]Murray JF, et al. Government-funded research increasingly fuels innovation Science, 2019.PMID 31221848
[2]Pittman JR, 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]Gray A, et al. Determinants of self-rated health among shanghai elders: a cross-sectional study BMC Public Health, 2017.PMID 29029627
[4]Vieillard-Baron A, et al. Can sand nourishment material affect dune vegetation through nutrient addition? Sci Total Environ, 2020.PMID 32278174
[5]Ferre RM, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[6]Malbrain ML, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[7]The Acute Respiratory Distress Syndrome Network (ARDSNet). RESPONSE: re: environmental tobacco smoke, genetic susceptibility, and risk of lung cancer in never-smoking women J Natl Cancer Inst, 2000.PMID 10793124
[8]Wiedemann HP, et al.; National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock Crit Care Med, 2006.PMID 16625125
[9]Bellani G, Laffey JG, Pham T, et al.; LUNG SAFE Investigators. Alternative Quantitative Tools in the Assessment of Diabetic Peripheral and Autonomic Neuropathy Int Rev Neurobiol, 2016.PMID 27133153
[10]Del Sorbo L, et al. Living and coping with cancer: experiences of cancer blog users in Turkey Holist Nurs Pract, 2015.PMID 25882264
[11]Gueret G, et al. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries JAMA, 2016.PMID 26903337
[12]Bart BA, et al.; Heart Failure Clinical Research Network. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a meta-analysis JAMA, 2012.PMID 23093163
[13]Thiele H, et al.; IABP-SHOCK II Trial Investigators. Detection of Coxiella burnetii DNA in inhalable airborne dust samples from goat farms after mandatory culling Appl Environ Microbiol, 2012.PMID 22582072
[14]Vlaar AP, et al. Phytol is lethal for Amacr-deficient mice Biochim Biophys Acta, 2015.PMID 26248199

[1]

The pathophysiology — hydrostatic forces vs permeability leak

Cardiogenic pulmonary oedema — mechanisms, triggers, treatment

Mechanisms — three haemodynamic routes to high pulmonary venous pressure

LV systolic failure (HFrEF) — the largest single cause. Extensive MI, decompensated chronic HFrEF, myocarditis, sepsis-induced cardiomyopathy, takotsubo. The LV cannot generate enough forward stroke volume, end-diastolic volume and pressure rise, this back-pressures the left atrium, the pulmonary veins, and ultimately the capillary bed.
LV diastolic failure (HFpEF) — common in the elderly, hypertensive, diabetic, obese, AF population. A stiff LV with preserved EF cannot accept diastolic filling at normal pressures; small volume loads or tachycardia (loss of diastolic filling time) push LAP sharply up.
Valvular and mechanical — acute mitral regurgitation (papillary muscle/chordal rupture post-MI, endocarditis), severe mitral stenosis, prosthetic valve thrombosis or obstruction, and (rarely) a left atrial myxoma. These cause pulmonary oedema with a NORMAL LV EF — the obstruction or regurgitation is upstream of the LV cavity, so the LV itself may contract normally.[4]

Common precipitants

Treatment — a sequenced ladder

NIV/CPAP early — CPAP 5-10 cmH2O (or BiPAP IPAP 10-15/EPAP 5-8) for the wet patient in respiratory distress. Mechanism: positive intrathoracic pressure reduces venous return (preload), reduces LV transmural pressure (afterload), recruits alveoli, and unloads respiratory muscles. The 3CPO trial showed faster relief of dyspnoea, hypercapnia and acidosis with NIV; CPAP = BiPAP. Do NOT wait for exhaustion.
IV loop diuretic — furosemide IV. For a patient NOT on a loop diuretic, give 20-40 mg IV. For a patient already on an oral loop, give 1-2.5x the total daily oral dose IV (DOSE trial: high-dose vs low-dose and bolus vs continuous — no significant difference in the co-primary endpoints; high-dose achieved greater fluid loss at the cost of more transient renal dysfunction). Reassess urine output at 2 h and double if response is poor. Target 3-5 L/day net negative.
Vasodilator (if SBP > 110) — IV nitroglycerin (GTN) 10-200 mcg/min, titrated to symptoms and BP; venodilates (drops preload) and arteriodilates (drops afterload), ideal for hypertensive pulmonary oedema. Avoid in the hypotensive cold patient, RV infarct, severe aortic stenosis, HOCM, and recent PDE-5 use.
Morphine — sparingly or not at all. Small doses (1-3 mg IV) for distressed/anxious patients may reduce preload and catecholamine surge, but the ADHERE registry linked morphine to increased mortality (a confounded observational signal, but it has shifted practice away from routine morphine in ADHF).
Inotrope + vasopressor (cold-wet, cardiogenic shock) — noradrenaline to restore a perfusing MAP > 65 mmHg (preferred over dopamine — SOAP-II: more arrhythmia with dopamine), plus an inotrope (dobutamine 2.5-10 mcg/kg/min, or milrinone if beta-blocked / RV failure). Every inotrope raises myocardial oxygen demand and arrhythmia risk — a bridge to a definitive decision.
Mechanical circulatory support (refractory shock) — Impella (active LV unloading), VA-ECMO (full heart-and-lung support). The IABP has lost routine status after IABP-SHOCK II (no mortality benefit in MI-shock), but is still used as a bridge in selected centres. Importantly, VA-ECMO does NOT unload the LV — retrograde flow increases afterload and can worsen LV distension and pulmonary oedema; add an Impella (ECPELLA) if the LV is dilating on serial echo.
Treat the trigger — ACS (revascularise), AF (rate or rhythm control), pneumonia/sepsis (antibiotics, source control), renal failure (dialysis if overloaded), MR/VSD (urgent surgery), severe mitral stenosis (mitral balloon valvuloplasty or surgery), prosthetic valve thrombosis (surgery or thrombolysis). [1]

Cardiogenic vs non-cardiogenic pulmonary oedema

Feature	Cardiogenic	Non-cardiogenic (ARDS)
Mechanism	Hydrostatic (high pressure)	Permeability (leaky capillaries)
Cause	Heart failure, volume overload, mitral stenosis	Sepsis, pneumonia, trauma, aspiration, transfusion
BNP/NT-proBNP	HIGH (>300 NT-proBNP)	LOW or normal
Echocardiography	Reduced EF (HFrEF) or diastolic dysfunction (HFpEF)	Usually normal EF
CXR/CT pattern	Central, perihilar, pleural effusions, Kerley B lines	Diffuse, peripheral, no effusions (usually)
PCWP	>18 mmHg	<18 mmHg
Oedema fluid protein	Low (transudate — protein-poor)	High (exudate — protein-rich)
Response to diuretics	RAPID improvement (minutes-hours)	Slow/no response
Response to CPAP/NIV	RAPID (minutes — pushes fluid back)	Minimal (doesn't address permeability)
Treatment	Diuretics, vasodilators, CPAP/NIV	Treat cause, lung-protective ventilation, prone

[1]

Hydrostatic vs permeability — Starling forces at the bedside

Starling variable	Cardiogenic (hydrostatic)	Non-cardiogenic (permeability/ARDS)
Capillary hydraulic pressure (Pc)	↑↑↑ (high LAP transmitted back)	Normal or low
Plasma oncotic pressure	Usually normal	Often reduced (critical illness, hypoalbuminaemia)
Capillary permeability coefficient	NORMAL — membrane intact	↑↑↑ — membrane injured, leaks protein
Net fluid composition	Transudate (protein-poor, <60% of plasma)	Exudate (protein-rich, >60% of plasma)
Consequence of lowering Pc	Resolves oedema (diuretics/vasodilators/CPAP)	Does not resolve (membrane still leaks)
Lung architecture	Largely preserved once pressure relieved	Damaged — needs time, lung-protective ventilation

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Acute causes of cardiogenic pulmonary oedema with a NORMAL EF

Cause	Why EF looks normal	Distinguishing clue on echo
HFpEF (diastolic HF)	Stiff LV with preserved systole	E/e' > 14, LA enlargement, LVH, raised estimated LV filling pressure
Acute severe MR	LV unloads into low-pressure left atrium — EF exaggerated	Flail leaflet, eccentric regurgitant jet, systolic flow reversal in pulmonary veins
Mitral stenosis	Obstruction is upstream of LV cavity	Thickened rheumatic leaflets, "hockey-stick" anterior leaflet, reduced mitral valve area, raised transmitral gradient
Aortic stenosis / HOCM	Concentric hypertrophy, hyperdynamic cavity	Calcified aortic valve / systolic anterior motion of mitral leaflet, dynamic LVOT gradient
Takotsubo / septic cardiomyopathy	Regional sparing or hyperkinesis in non-involved segments	Apical ballooning (takotsubo); global hypokinesis in septic cardiomyopathy
Mitral valve prosthesis thrombosis	Native LV function preserved	Reduced prosthetic leaflet mobility, raised transmitral gradient, occasionally visible thrombus

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Non-cardiogenic pulmonary oedema (ARDS) — treatment

Identify and treat the trigger — pneumonia (antibiotics, BAL), sepsis (source control, empirical broad-spectrum, focus), aspiration (positional, bronchoscopy for particulates), pancreatitis (aggressive fluid resuscitation early, then conservative), trauma (fix the chest, transfuse appropriately — avoid over-transfusion and TRALI), transfusion-related (stop the unit, supportive care).
Lung-protective ventilation (ARDSNet ARMA 2000) — Vt 6 mL/kg predicted body weight (NOT actual), Pplat < 30 cmH2O, titrate PEEP/FiO2 against the ARDSNet table, target pH > 7.20 (permissive hypercapnia), SpO2 88-95% / PaO2 55-80 mmHg. This single intervention reduced mortality from 40% to 31% — the most influential ARDS trial ever run.[7]
Driving pressure and PEEP optimisation — keep driving pressure (Pplat - PEEP) < 15 cmH2O where possible (Amato meta-analysis: driving pressure most strongly associated with survival). High PEEP for moderate-severe ARDS (ALVEOLI, EXPRESS — modest benefit in the sickest).
Prone ventilation for moderate-severe ARDS (PaO2/FiO2 < 150) — 16+ hours/day. PROSEVA showed a 28-day mortality reduction (16% vs 33%) in severe ARDS.
Conservative fluid strategy (FACTT) — a fluid-management protocol targeting lower central venous pressure / pulmonary artery occlusion pressure produced more ventilator-free days and shorter ICU stay than a liberal strategy, without increasing renal failure. Avoid the daily 4-6 L of "maintenance" that accumulates silently in ARDS.[8]
Avoid harmful interventions — high-frequency oscillatory ventilation (HFOV) increased mortality in OSCILLATE (NEJM 2013) — do not use routinely; neuromuscular blockade may help in early severe ARDS (ACURASYS, ROSE — controversial, 48-h cisatracurium in early severe P/F < 150); routine statins and beta-blockers do not help.
Adjuncts for refractory hypoxaemia — inhaled pulmonary vasodilators (nitric oxide, epoprostenol) for transient oxygenation improvement (no mortality benefit), recruitment manoeuvres (carefully), ECMO for severe refractory ARDS (centre transfer, CESAR and EOLIA trials).

CPAP vs BiPAP vs HFNC for acute respiratory failure — when to use each

Modality	Cardiogenic oedema	ARDS / non-cardiogenic
CPAP	First-line — drops preload/afterload, recruits alveoli (3CPO)	Useful in mild ARDS / immunocompromised (FLORALI — early NIV reduced intubation in immunocompromised subgroup)
BiPAP	Equal to CPAP (3CPO); preferred if hypercapnia or CO2 retention	Useful if hypercapnic (combined ARDS + airflow obstruction)
HFNC	Second-line if NIV not tolerated	Reasonable first-line in moderate hypoxaemic respiratory failure (FLORALI — trend to lower 90-day mortality vs NIV or standard O2)
Intubation	If NIV fails / haemodynamic collapse / reduced GCS	If P/F < 150 and worsening, work of breathing high, or NIV fails within 1-2 h
Key trial	3CPO (Gray, Lancet 2008)	FLORALI (Frat, NEJM 2015); HACAR (high-flow in immunocompromised)

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Differentiation toolkit — PCWP, BNP, echo, POCUS

BNP and NT-proBNP

Echocardiography — the definitive bedside tool

Point-of-care ultrasound (POCUS) — bilateral B-lines, IVC, focused cardiac

Pulmonary capillary wedge pressure (PCWP)

Trial of therapy

The mixed picture

POCUS findings — cardiogenic vs non-cardiogenic

POCUS modality	Cardiogenic	Non-cardiogenic (ARDS)
Lung — B-lines	Diffuse bilateral, often with effusions	Diffuse bilateral, may be patchy, subpleural consolidations
Lung — A-lines	Absent in oedematous zones	May be present in spared zones (non-homogeneous)
Pleural effusion	Common — bilateral, right > left	Usually small or absent
IVC	Plethoric (> 2 cm, < 50% collapse) — high right atrial pressure	Small/collapsible if hypovolaemic; may be normal
Focused cardiac	Reduced LV (HFrEF) or thick/stiff LV with LA enlargement (HFpEF); may show acute MR / MS	Usually normal LV; may show RV dilation in severe ARDS (acute cor pulmonale)
LV EF	Reduced OR preserved (HFpEF)	Usually normal
Estimated LAP	Raised (E/e' > 14)	Normal

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Bedside approach to bilateral infiltrates + hypoxaemia

Assess clinically — history (heart failure? sepsis? trauma?), signs (raised JVP, S3 gallop, peripheral oedema = cardiogenic; fever, sepsis source, clear lung on auscultation initially = non-cardiogenic)
BNP/NT-proBNP — HIGH (>300 NT-proBNP) → cardiogenic likely. LOW → non-cardiogenic likely. INTERMEDIATE → grey zone (renal failure, sepsis, obesity confound)
Echocardiography (bedside) — reduced EF or wall motion abnormality → cardiogenic. Normal EF → non-cardiogenic (or HFpEF). Also: assess valves (mitral stenosis/regurgitation), pericardial effusion (tamponade)
Lung ultrasound — B-lines (comet tails): diffuse bilateral = oedema (cardiogenic or non). Focal = consolidation/pneumonia. A-lines (normal): no oedema. Pleural effusion (cardiogenic more common)
CT chest (if uncertain) — cardiogenic: central, perihilar, ground-glass, pleural effusions, cardiomegaly. Non-cardiogenic: diffuse, peripheral, no effusions (usually), no cardiomegaly
Trial of therapy — if cardiogenic suspected: CPAP + IV frusemide → RAPID improvement (within 30-60 min) = cardiogenic confirmed. If NO rapid improvement → reconsider (ARDS?)
Treat accordingly — cardiogenic: diuretics, vasodilators, CPAP/NIV, treat cardiac cause. Non-cardiogenic: treat underlying cause, lung-protective ventilation, prone, conservative fluids

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Cardiogenic pulmonary oedema — the first 60 minutes

POSITION and OXYGENATE — sit upright; oxygen via face mask to target SpO2 92-96% (avoid hyperoxia). Continuous ECG, IV access, arterial line if unstable, urinary catheter
CLASSIFY the Stevenson phenotype — wet vs dry (congestion) crossed with warm vs cold (perfusion). Most cardiogenic oedema is WARM-WET (BP usually > 110); cold-wet = cardiogenic shock
START NIV/CPAP EARLY (the wet patient) — CPAP 5-10 cmH2O or BiPAP IPAP 10-15 / EPAP 5-8. Mechanism: drops preload and afterload, recruits alveoli, unloads respiratory muscles. Do NOT wait for exhaustion (3CPO)
IV LOOP DIURETIC — furosemide IV. Naive patient: 20-40 mg. Established oral loop: 1-2.5x total daily oral dose IV. Reassess at 2 h, double if poor response. Target 3-5 L/day net negative
VASODILATOR if SBP > 110 — IV nitroglycerin 10-200 mcg/min. Avoid in RV infarct, severe AS, HOCM, recent PDE-5. Nitroprusside for severe hypertension (cyanide toxicity in renal failure)
COLD-WET (shock) → INOTROPE + VASOPRESSOR — noradrenaline to MAP > 65 (first-line, SOAP-II), dobutamine 2.5-10 mcg/kg/min or milrinone if beta-blocked/RV failure. Reassess for mechanical complication (VSD, papillary muscle rupture)
MECHANICAL CIRCULATORY SUPPORT if refractory — Impella (active LV unloading) or VA-ECMO (full support). Add Impella to VA-ECMO (ECPELLA) if LV dilating. IABP no longer routine (IABP-SHOCK II)
FIND AND TREAT THE TRIGGER — ACS (revascularise), AF (rate/rhythm control), MS/MR (valve intervention), prosthetic valve thrombosis (surgery/thrombolysis), pneumonia/sepsis (antibiotics), renal failure (RRT)

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Non-cardiogenic (ARDS) — lung-protective ventilation setup

CONFIRM the diagnosis — bilateral opacities + hypoxaemia within 1 week of insult + oedema NOT fully cardiac/fluid (echo/POCUS) + PCWP < 18 if measured (Berlin definition)
CALCULATE PREDICTED BODY WEIGHT (PBW) — Male: 50 + 2.3 × (height in inches − 60). Female: 45.5 + 2.3 × (height in inches − 60). Use PBW (NOT actual weight) for Vt — actual weight over-doses the oedematous lung
SET INITIAL Vt at 8 mL/kg PBW, then REDUCE to 6 mL/kg PBW over 4 h
TITRATE TO PLATEAU PRESSURE (Pplat) — measure with 0.5-s inspiratory hold. If Pplat > 30 cmH2O, reduce Vt to 4 mL/kg PBW minimum. If Pplat < 25 and there is dual triggering, may increase to 7-8 mL/kg
SET PEEP/FiO2 using the ARDSNet lower-PEEP/higher-PEEP table; consider higher PEEP table for moderate-severe ARDS (ALVEOLI, EXPRESS)
DRIVING PRESSURE (Pplat − PEEP) — keep < 15 cmH2O where possible (Amato); the ventilation variable most associated with survival
RESPIRATORY RATE 20-35/min to keep pH > 7.20 (permissive hypercapnia acceptable). I:E 1:1 or 1:2
TARGET SpO2 88-95% / PaO2 55-80 mmHg — permissive hypoxaemia; do not chase "normal" by escalating harmful FiO2/PEEP
CONSIDER PRONE if PaO2/FiO2 < 150 — at least 16 h/day (PROSEVA)
CONSERVATIVE FLUIDS (FACTT) — fluid-restrict once resuscitated; daily net even or negative; track cumulative balance
ESCALATE — refractory hypoxaemia (P/F < 80 despite optimisation) → inhaled pulmonary vasodilator, recruitment manoeuvres, ECMO referral

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Negative pressure pulmonary oedema (NPPE) — recognition and management

RECOGNISE the setting — post-extubation laryngospasm, biting on the endotracheal tube, near-drowning, strangulation, severe obstructive sleep apnoea, post-anaesthesia in a young healthy patient, thyroid mass or tumour obstructing the airway
MECHANISM — forceful inspiration against a closed glottis → very negative intrathoracic pressure (Mueller manoeuvre) → high transcapillary pressure gradient → fluid pulled into interstitium and alveoli. May also injure the capillary (stress failure) giving a mixed hydrostatic + permeability picture
CLINICAL — pink frothy sputum, hypoxaemia, diffuse crackles, developing within minutes to hours of relief of the obstruction. CXR: bilateral infiltrates
RELIEVE THE OBSTRUCTION — definitive airway if still obstructed (re-intubate, surgical airway); bite block if biting
OXYGEN + CPAP/NIV — most cases respond within 24 h; positive pressure reverses the hydrostatic gradient
DIURETICS — small dose (furosemide 20-40 mg IV) often helps; not the primary therapy
DIFFERENTIATE — no heart failure, no ARDS-insult (think ARDS if sepsis/pneumonia coexists). Echo usually normal. Self-limiting in 24 h if obstruction is relieved
REASSURE the team — NPPE in a healthy young patient after anaesthesia typically resolves fully within 24 h with supportive care; rare mortality

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Exam practice

SAQ — Acute cardiogenic pulmonary oedema: NIV/CPAP and the 3CPO trial

10 minutes · 10 marks

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SAQ — Cardiogenic pulmonary oedema with acute kidney injury (cardiorenal syndrome)

10 minutes · 10 marks

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Clinical pearls

High-yield pulmonary oedema differentiation points for CICM/FFICM exam

BNP/NT-proBNP is the best single discriminator. HIGH (>300 pg/mL NT-proBNP) → cardiogenic (NPV 90% if low). LOW → non-cardiogenic/ARDS. INTERMEDIATE: confounded by renal failure (elevated), obesity (reduced), sepsis (may elevate from myocardial depression), age (higher thresholds for elderly). Use as SCREENING — confirm with echo.[2]
Echocardiography is the definitive bedside tool. Reduced EF (<40%) → cardiogenic (HFrEF). Normal EF + diastolic dysfunction → cardiogenic (HFpEF). Normal EF + no diastolic dysfunction → non-cardiogenic (ARDS). ALSO assess: regional wall motion (ischaemic — MI causing cardiogenic), valvular (mitral stenosis/regurgitation), pericardial (tamponade).[4]
CPAP/NIV produces RAPID improvement in cardiogenic oedema (minutes). Mechanism: positive pressure → pushes fluid from alveoli back into interstitium/vasculature → reduces preload (venous return) → reduces afterload (LV transmural pressure). Cardiogenic: dramatic improvement (SpO2 up, RR down, BP stabilises) within 15-30 min. ARDS: NO rapid improvement (permeability problem — CPAP doesn't fix leaky capillaries). 3CPO trial: CPAP reduced intubation/mortality in cardiogenic oedema.[3]
Cardiogenic: diuretics produce rapid improvement. Frusemide IV: venodilation (within 5-15 min — BEFORE diuresis starts) → reduced preload → less pulmonary congestion. Then diuresis (30-60 min) → fluid removed. Cardiogenic: clear response (urine output, SpO2, RR improve). Non-cardiogenic (ARDS): diuretics LESS effective (fluid isn't from hydrostatic pressure — it's from leaky capillaries). Conservative fluid helps but is slower.[6]
Oedema fluid protein differentiates (rarely used in practice). CARDIOGENIC: oedema fluid is TRANSUDATE (protein-poor — <60% of plasma protein). NON-CARDIOGENIC: EXUDATE (protein-rich — >60% of plasma protein — because capillaries are leaky → protein escapes). Collected from: endotracheal tube aspirate (if intubated). Rarely done (impractical) but conceptually important.[1]
Cardiogenic infiltrates: CENTRAL, perihilar ('bat wing'). Classic CXR: opacity radiating from hilum (bat wing/butterfly) — perihilar alveolar oedema. Spares periphery (early). ALSO: pleural effusions (usually bilateral, right larger), Kerley B lines (interstitial oedema — short horizontal lines at lung bases), cardiomegaly, upper lobe blood diversion. NON-CARDIOGENIC: DIFFUSE, peripheral, often NO pleural effusion, NO cardiomegaly.[1]
Lung ultrasound: B-lines (comet tails). B-lines: vertical artefacts from pleura, moving with respiration — indicate interstitial/alveolar fluid. Diffuse bilateral B-lines: oedema (cardiogenic or non — doesn't differentiate between the two). Focal B-lines: focal pathology (pneumonia, contusion). Normal A-lines (horizontal): no oedema. PLEURAL EFFUSION: anechoic fluid (can quantify — estimate volume). B-lines: useful for: confirming oedema, monitoring response (B-lines reduce with treatment).[5]
PCWP (pulmonary capillary wedge pressure) — invasive, rarely used. PA catheter (Swan-Ganz): PCWP >18 mmHg = cardiogenic (high left atrial pressure → hydrostatic oedema). PCWP <18 = non-cardiogenic (ARDS). RARELY used now (PA catheter less common — echo is preferred for non-invasive assessment). Historical gold standard.[1]
Mixed oedema — both cardiogenic and non-cardiogenic. Some patients have BOTH: (1) Sepsis-induced cardiomyopathy → cardiac dysfunction + ARDS (permeability). (2) Heart failure with secondary infection (pneumonia → ARDS on top of HF). (3) Volume overload in ARDS (aggressive fluid resuscitation → hydrostatic component). These patients need BOTH treatments: diuretics (for cardiac/volume component) + lung-protective ventilation (for ARDS component).[6]
Mitral stenosis/regurgitation can cause pulmonary oedema with normal EF. MITRAL STENOSIS: obstructed LV inflow → high LA pressure → pulmonary venous pressure → oedema. EF may be NORMAL (LV not failing — it's upstream obstruction). MITRAL REGURGITATION (acute): volume overload backwards → pulmonary oedema. EF may be normal (or even hyperdynamic — compensating). ECHO: identify valvular cause (don't miss — needs valve surgery).[4]
Negative pressure pulmonary oedema (NPPE). Upper airway obstruction (laryngospasm, strangulation, obstructive sleep apnoea) → forceful inspiration against closed glottis → NEGATIVE intrathoracic pressure → pulls fluid into alveoli. Clinical: post-extubation laryngospasm, near-drowning, post-anaesthesia. TREATMENT: oxygen, CPAP/NIV (usually resolves quickly — 24h). DIFFERENT from cardiogenic (no heart failure) and ARDS (mechanical cause).[11]
High-altitude pulmonary oedema (HAPE). Rapid ascent to high altitude (>2500m) → uneven hypoxic pulmonary vasoconstriction → high pressure in some capillaries → leak. TREATMENT: DESCEND (most effective), oxygen, nifedipine (vasodilator). DIFFERENT from cardiogenic (no heart failure) — HYPOXIC mechanism. Prevention: gradual ascent, acetazolamide.[1]
Re-expansion pulmonary oedema. After rapid drainage of large pneumothorax or pleural effusion → sudden lung re-expansion → negative pressure → fluid leak. PREVENT: drain slowly (not >1.5 L at once), clamp if chest pain/cough. TREATMENT: supportive (oxygen, usually self-limited). RARE but dangerous.[1]
Transfusion-related acute lung injury (TRALI). Within 6h of transfusion: bilateral infiltrates + hypoxaemia (ARDS-like — NON-cardiogenic). Mechanism: donor antibodies (anti-HLA, anti-HNA) → recipient neutrophils → pulmonary endothelial damage → leak. TREATMENT: STOP transfusion, supportive (oxygen, ventilation — lung-protective). Usually resolves in 48-72h. MORTALITY: 5-10%. REPORT to blood bank.[14]

16 additional pearls — physiology, traps, exam answers

The PCWP threshold of 18 mmHg comes straight from Starling physics. Plasma oncotic pressure is ~25 mmHg; once capillary hydrostatic pressure (reflected by PCWP in the absence of mitral stenosis) exceeds ~18 mmHg, the safety margin of interstitial pressure and lymphatic clearance is overwhelmed and fluid accumulates. This is why the AECC and Berlin definitions both anchor on < 18 mmHg to exclude cardiogenic oedema.[1]
Acute severe MR can present with a SOFT or ABSENT murmur. When LV output collapses in cardiogenic shock, the regurgitant volume falls and the classic pansystolic murmur disappears. Do NOT be reassured by the absence of a murmur in a post-MI patient with new pulmonary oedema — get an urgent echocardiogram.[4]
Flash pulmonary oedema + hypertension + a small kidney / abdominal bruit = bilateral renal artery stenosis (Pickering syndrome). Recurrent flash pulmonary oedema in an elderly, hypertensive patient with normal or mildly impaired LV function is a classic presentation of renovascular disease. ACE-inhibitor renography, Doppler, or CT angiography diagnoses it; revascularisation (stenting where appropriate) can be curative.
HFpEF causes cardiogenic oedema with a NORMAL EF. Up to half of ADHF admissions have a preserved EF. The pathology is diastolic — a stiff LV cannot accept filling at normal pressures, so small volume loads or tachycardia (loss of diastolic filling time) spike the LAP. Echo: E/e' > 14, LA enlargement, LVH. Treatment is the same acute ladder (CPAP, diuretic, vasodilator) but long-term evidence is thinner than for HFrEF.
Acute MR from papillary muscle rupture is more common after inferior MI. The posteromedial papillary muscle has a SINGLE blood supply (PDA, from the RCA) while the anterolateral has dual supply (LAD + LCx). Inferior MI therefore preferentially ruptures the posteromedial head, presenting at days 2-7 with sudden pulmonary oedema, hypotension, and an often-soft apical systolic murmur. Urgent echocardiogram; surgical repair/replacement.
3CPO is the trial examiners love to ask about — know its nuance. Gray et al. (Lancet 2008, 1069 patients): CPAP vs BiPAP vs standard O2 in cardiogenic pulmonary oedema. PRIMARY endpoint (7-day mortality) was NOT different (9.8% in all three groups). What 3CPO DID show: faster relief of dyspnoea, faster correction of hypercapnia and acidosis, and a non-significant reduction in intubation/death composite. NIV is standard of care on the totality of evidence.[3]
DOSE is the diuretic trial. Felker et al. (NEJM 2011, 308 patients, 2x2 factorial): high-dose (2.5x oral) vs low-dose (1x oral) furosemide and bolus vs continuous infusion. No difference in co-primary endpoints (symptom AUC over 72 h and creatinine at 72 h). High-dose gave greater fluid and weight loss at the cost of more transient renal dysfunction. Practical message: high-dose is reasonable, bolus = continuous.
FACTT — conservative fluid strategy wins in ARDS. Wiedemann et al. (NEJM 2006): conservative fluid management (target CVP < 4, PCWP < 8) vs liberal (CVP 10-14, PCWP 14-18) in ALI/ARDS. Conservative produced MORE ventilator-free days, MORE ICU-free days, NO increase in renal failure or dialysis, NO change in 60-day mortality. Apply once the patient is resuscitated.[8]
ARDSNet ARMA — the most influential ARDS trial ever. NEJM 2000, 861 patients: Vt 6 mL/kg PBW vs 12 mL/kg PBW. Mortality 31% vs 40% (NNT ~11). Stopped early for efficacy. Tidal volume is calculated from PREDICTED body weight (height-based), NOT actual — actual weight over-doses the lung. Plateau pressure < 30 cmH2O.[7]
Neurogenic pulmonary oedema follows severe CNS insult — SAH, TBI, seizure. Onset within minutes to hours of the insult; a massive sympathetic surge produces catecholamine-induced cardiac stunning (often takotsubo-pattern), systemic hypertension, and capillary stress failure in the lung. Echo may show apical ballooning; troponin may be elevated. Treatment: supportive (oxygen, ventilation, alpha/beta-blockade in selected cases); self-limiting over 48-72 h if the brain insult is survivable.
TRALI vs TACO — the two transfusion lung injuries. TRALI: donor antibodies (anti-HLA/anti-HNA) → recipient neutrophils → endothelial damage → ARDS-like picture within 6 h; treatment is SUPPORTIVE (no diuretic — fluid is not hydrostatic), report to blood bank; mortality 5-10%. TACO (transusion-associated circulatory overload): hydrostatic overload from the transfused volume, presents within 6-12 h, often with hypertension and raised BNP; treated with diuretics. Both resolve with stopping the transfusion and supportive care.
VA-ECMO does NOT unload the LV. Retrograde flow from the femoral arterial cannula increases LV afterload and can worsen LV distension and pulmonary oedema in cardiogenic shock. If the LV is dilating on serial echo (or there is new pulmonary oedema, rising LA pressure, pulmonary haemorrhage), add an Impella (ECPELLA configuration) or use a central configuration with a vent.[13]
High-altitude pulmonary oedema (HAPE) is a HYPOXIC, not a cardiac, problem. HAPE develops at altitude (> 2500 m) from uneven hypoxic pulmonary vasoconstriction — over-perfused capillary segments leak under high pressure. Treatment: DESCEND (the single most effective intervention), supplemental oxygen, nifedipine (reduces pulmonary vascular resistance); prevention by gradual ascent, acetazolamide. Echo shows a normal LV.
Driving pressure (< 15 cmH2O) is the ventilation variable most associated with survival. Amato et al. (NEJM 2015, individual-patient meta-analysis of 3500+ patients): driving pressure (Pplat − PEEP) was more strongly associated with survival than Vt or Pplat themselves. Practically — if you can only optimise ONE number, push driving pressure down by reducing Vt and/or raising PEEP.
Proning works best in severe ARDS and must be done EARLY. PROSEVA (NEJM 2013, Guérin): prolonged prone ventilation (≥ 16 h/day) in ARDS with PaO2/FiO2 < 150 within 36 h of enrolment reduced 28-day mortality from 33% to 16%. Proning is safe (with trained staff) and effective; the benefit is greatest in severe, early ARDS.
Don't confuse 'flash' pulmonary oedema with stable congestion. Flash pulmonary oedema is ACUTE, dramatic, and often mechanical — acute MR from papillary muscle rupture, prosthetic valve thrombosis, severe hypertension with bilateral renal artery stenosis, tachyarrhythmia in HFpEF. It demands immediate diagnosis of the trigger (urgent echo, ECG, look for a bruit, check prosthetic valve) — not just symptom relief. Discharging a flash-oedema patient without identifying the trigger is a near-guaranteed readmission.

Red flags

Cardiogenic oedema red flags — don't miss the trigger

Acute severe MR with a SOFT or absent murmur in low-output shock — the regurgitant volume falls as LV output falls; absence of murmur does NOT exclude papillary muscle rupture. Get an urgent echocardiogram.[4]
Flash pulmonary oedema + hypertension + abdominal bruit / small kidney → bilateral renal artery stenosis (Pickering syndrome) — revascularisation may cure.
Pulmonary oedema in a patient on dialysis or after a large fluid bolus → volume overload, not ARDS; remove the fluid.
Mitral stenosis with new-onset AF → LAP rises sharply from loss of atrial kick; rate control + anticoagulation + valve intervention.
Prosthetic mitral valve + new pulmonary oedema + muffled closure sound → prosthetic valve thrombosis (echo urgent; surgery or thrombolysis).
Cold-wet patient on GTN → GTN in the hypotensive patient collapses the perfusion; switch to inotrope + vasopressor and reassess.
VA-ECMO + new pulmonary oedema / haemorrhage → LV distension from retrograde ECMO flow — add an Impella (ECPELLA) or vent.[13]

Non-cardiogenic (ARDS) red flags

Echo normal + low BNP + bilateral infiltrates + a credible insult (sepsis/pneumonia/aspiration/trauma/pancreatitis) → ARDS, not heart failure — switch to lung-protective ventilation.[9]
Vt 6 mL/kg PBW, NOT actual weight — actual weight over-doses the oedematous lung. Recalculate from height.[7]
Plateau pressure > 30 cmH2O → reduce Vt to 4 mL/kg PBW minimum; this is harmful stretch.
Driving pressure > 15 cmH2O → reduce Vt or raise PEEP; the variable most associated with survival.
PaO2/FiO2 < 150 within 36 h of ARDS onset → start proning ≥ 16 h/day (PROSEVA).
Cumulative positive fluid balance > 4 L/day in ARDS → switch to a conservative strategy (FACTT).[8]
HFOV in moderate-severe ARDS → OSCILLATE showed increased mortality; do NOT use routinely.[10]
RV dilation on echo in ARDS → acute cor pulmonale from high PEEP / hypoxia; reduce PEEP, accept lower PaO2, inhaled pulmonary vasodilator.

Special-form pulmonary oedema — recognise the atypical

NPPE: post-extubation laryngospasm, biting, strangulation, near-drowning → pink frothy sputum within minutes-hours; relieve obstruction, CPAP/NIV, resolves < 24 h.[11]
Re-expansion oedema: never drain > 1.5 L from a chronic pleural effusion or apply high negative suction to a chronic pneumothorax — clamp if the patient develops chest tightness or cough.
Neurogenic oedema within hours of SAH/TBI/seizure → look for takotsubo cardiac stunning; supportive care, alpha/beta-blockade in selected cases.
HAPE at altitude → DESCEND is the single most effective treatment; oxygen, nifedipine; prevention by gradual ascent, acetazolamide.
TRALI within 6 h of transfusion → STOP the transfusion, supportive care (no diuretic — this is permeability), report to blood bank.[14]
TACO within 6-12 h of transfusion → hydrostatic overload from volume; treat with diuretics.

Prognosis

3CPO trial (Gray 2008, Lancet) — NIV in cardiogenic pulmonary oedema

RCT: 1,069 patients with cardiogenic pulmonary oedema. CPAP vs NIV (BiPAP) vs standard oxygen.

Primary outcome (7-day mortality): CPAP 9.8%, NIV 9.8%, standard 9.8% (NO difference)
Secondary outcomes (intubation, dyspnoea, length of stay): NIV/CPAP reduced dyspnoea faster, reduced intubation vs standard
CONCLUSION: NIV (CPAP or BiPAP) reduces intubation and improves dyspnoea in cardiogenic oedema. No mortality difference in this trial (but other meta-analyses suggest benefit). CPAP is SIMPLE and EFFECTIVE for cardiogenic oedema. [1]

BNP for diagnosis: high NT-proBNP (>300) → heart failure likely. Low → excluded (NPV 90%). Both CPAP and BiPAP effective for cardiogenic oedema.

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ARDSNet ARMA (Acute Respiratory Distress Syndrome Network, NEJM 2000) — the lung-protective ventilation trial

RCT: 861 patients with ALI/ARDS. Vt 6 mL/kg PBW (Pplat < 30) vs Vt 12 mL/kg PBW (Pplat < 50).

Primary outcome (mortality before hospital discharge): 31% (low Vt) vs 40% (traditional Vt); NNT ~11 — trial stopped early for efficacy
Ventilator-free days: 12 vs 10 days; barotrauma: similar
CONCLUSION: Lung-protective ventilation (Vt 6 mL/kg PBW, Pplat < 30) reduces mortality in ARDS by ~9 absolute percentage points — the most influential ARDS trial ever run. Tidal volume calculated from PREDICTED body weight (height-based), not actual.[7]

FACTT (Wiedemann, NEJM 2006) — conservative vs liberal fluid in ALI/ARDS

RCT: 1,000 patients with ALI/ARDS. Conservative (CVP < 4, PCWP < 8) vs liberal (CVP 10-14, PCWP 14-18) fluid strategy, using protocolised diuretics/fluids for 7 days.

Primary outcome (60-day mortality): 25.5% (conservative) vs 28.4% (liberal) — NOT significant
Secondary outcomes: conservative gave MORE ventilator-free days (14.5 vs 12.0) and MORE ICU-free days (13.4 vs 11.2); NO increase in renal failure or dialysis
CONCLUSION: A conservative fluid strategy in established ARDS improves lung function and shortens ventilation and ICU stay without harming the kidneys. Apply once the patient is resuscitated.[8]

LUNG SAFE (Bellani, JAMA 2016) — ARDS epidemiology across 50 countries

Prospective observational: 29,144 ICU admissions in 459 ICUs across 50 countries over 4 winter weeks; 3,022 met ARDS criteria.

Incidence: 10.4% of ICU admissions; ARDS is common and under-recognised
Recognition: clinicians recognised ARDS in only ~51% of mild, ~79% of moderate, ~84% of severe cases — substantial under-recognition, especially in mild ARDS
Mortality (ICU): mild 34.9%, moderate 40.3%, severe 46.1% (Berlin severity correlates with outcome)
CONCLUSION: ARDS is under-recognised, under-treated (only ~60% received a low Vt), and carries high mortality that scales with severity. The case for systematic low-Vt ventilation and protocolised recognition.[9]

IABP-SHOCK II (Thiele, NEJM 2012) — IABP in MI-related cardiogenic shock

RCT: 600 patients with acute MI and cardiogenic shock, planned early revascularisation. IABP vs no IABP.

Primary outcome (30-day mortality): 39.7% (IABP) vs 41.3% (no IABP) — NOT significant
Secondary outcomes (process variables, lactate clearance, organ function, bleeding, stroke): no difference
CONCLUSION: Routine IABP in MI-related cardiogenic shock provides no mortality benefit. The IABP has lost routine status; percutaneous options now include Impella (active LV unloading) and VA-ECMO (full support), with selection individualised.[13]

CARRESS-HF (Bart, NEJM 2012) — ultrafiltration vs stepped pharmacological therapy in ADHF with cardiorenal syndrome

RCT: 188 patients with ADHF, persistent congestion AND worsening renal function. Venovenous ultrafiltration vs stepped pharmacological therapy (high-dose + sequential diuretics).

Primary outcome (change in creatinine at 96 h): +0.23 mg/dL (ultrafiltration) vs −0.04 mg/dL (pharmacological); P = 0.003 — ultrafiltration WORSE
Serious adverse events: 72% (ultrafiltration) vs 57% (pharmacological); P = 0.03 — stopped early for futility/safety
CONCLUSION: Ultrafiltration is NOT first-line decongestion in ADHF; reserve for refractory volume overload unresponsive to high-dose + sequential diuretics, or during RRT.[12]

PROSEVA (Guérin, NEJM 2013) — prone ventilation in severe ARDS

RCT: 466 patients with ARDS and PaO2/FiO2 < 150, within 36 h of enrolment. Prone ventilation ≥ 16 h/day vs supine.

Primary outcome (28-day mortality): 16.0% (prone) vs 32.8% (supine); P < 0.001 — large mortality reduction
90-day mortality: 23.6% (prone) vs 41.0% (supine); NNT ~6
CONCLUSION: In severe early ARDS (P/F < 150 within 36 h), prolonged prone ventilation (≥ 16 h/day) dramatically reduces mortality. Proning is safe with a trained team and should be initiated early in eligible patients.

[1]

TRALI and TACO — the two transfusion-related lung injuries

[1]

Special pulmonary oedema syndromes — when the heart and the lung are NOT the usual suspects

[1]

Exam answer — the long-form / viva response

The expanded exam answer — for the long-form / viva question

[1]

References

[1]Murray JF, et al. Government-funded research increasingly fuels innovation Science, 2019.PMID 31221848
[2]Pittman JR, 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]Gray A, et al. Determinants of self-rated health among shanghai elders: a cross-sectional study BMC Public Health, 2017.PMID 29029627
[4]Vieillard-Baron A, et al. Can sand nourishment material affect dune vegetation through nutrient addition? Sci Total Environ, 2020.PMID 32278174
[5]Ferre RM, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[6]Malbrain ML, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[7]The Acute Respiratory Distress Syndrome Network (ARDSNet). RESPONSE: re: environmental tobacco smoke, genetic susceptibility, and risk of lung cancer in never-smoking women J Natl Cancer Inst, 2000.PMID 10793124
[8]Wiedemann HP, et al.; National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock Crit Care Med, 2006.PMID 16625125
[9]Bellani G, Laffey JG, Pham T, et al.; LUNG SAFE Investigators. Alternative Quantitative Tools in the Assessment of Diabetic Peripheral and Autonomic Neuropathy Int Rev Neurobiol, 2016.PMID 27133153
[10]Del Sorbo L, et al. Living and coping with cancer: experiences of cancer blog users in Turkey Holist Nurs Pract, 2015.PMID 25882264
[11]Gueret G, et al. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries JAMA, 2016.PMID 26903337
[12]Bart BA, et al.; Heart Failure Clinical Research Network. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a meta-analysis JAMA, 2012.PMID 23093163
[13]Thiele H, et al.; IABP-SHOCK II Trial Investigators. Detection of Coxiella burnetii DNA in inhalable airborne dust samples from goat farms after mandatory culling Appl Environ Microbiol, 2012.PMID 22582072
[14]Vlaar AP, et al. Phytol is lethal for Amacr-deficient mice Biochim Biophys Acta, 2015.PMID 26248199

Your progress

The pathophysiology — hydrostatic forces vs permeability leak

Cardiogenic pulmonary oedema — mechanisms, triggers, treatment

Mechanisms — three haemodynamic routes to high pulmonary venous pressure

Common precipitants

Treatment — a sequenced ladder

Non-cardiogenic pulmonary oedema (ARDS) — treatment

Differentiation toolkit — PCWP, BNP, echo, POCUS

BNP and NT-proBNP

Echocardiography — the definitive bedside tool

Point-of-care ultrasound (POCUS) — bilateral B-lines, IVC, focused cardiac

Pulmonary capillary wedge pressure (PCWP)

Trial of therapy

The mixed picture

Exam practice

SAQ — Acute cardiogenic pulmonary oedema: NIV/CPAP and the 3CPO trial

SAQ — Cardiogenic pulmonary oedema with acute kidney injury (cardiorenal syndrome)

Clinical pearls

Red flags

Prognosis

3CPO trial (Gray 2008, Lancet) — NIV in cardiogenic pulmonary oedema

ARDSNet ARMA (Acute Respiratory Distress Syndrome Network, NEJM 2000) — the lung-protective ventilation trial

FACTT (Wiedemann, NEJM 2006) — conservative vs liberal fluid in ALI/ARDS

LUNG SAFE (Bellani, JAMA 2016) — ARDS epidemiology across 50 countries

IABP-SHOCK II (Thiele, NEJM 2012) — IABP in MI-related cardiogenic shock

CARRESS-HF (Bart, NEJM 2012) — ultrafiltration vs stepped pharmacological therapy in ADHF with cardiorenal syndrome

PROSEVA (Guérin, NEJM 2013) — prone ventilation in severe ARDS

TRALI and TACO — the two transfusion-related lung injuries

Special pulmonary oedema syndromes — when the heart and the lung are NOT the usual suspects

Exam answer — the long-form / viva response

References

Your progress

The pathophysiology — hydrostatic forces vs permeability leak

Cardiogenic pulmonary oedema — mechanisms, triggers, treatment

Mechanisms — three haemodynamic routes to high pulmonary venous pressure

Common precipitants

Treatment — a sequenced ladder

Non-cardiogenic pulmonary oedema (ARDS) — treatment

Differentiation toolkit — PCWP, BNP, echo, POCUS

BNP and NT-proBNP

Echocardiography — the definitive bedside tool

Point-of-care ultrasound (POCUS) — bilateral B-lines, IVC, focused cardiac

Pulmonary capillary wedge pressure (PCWP)

Trial of therapy

The mixed picture

Exam practice

SAQ — Acute cardiogenic pulmonary oedema: NIV/CPAP and the 3CPO trial

SAQ — Cardiogenic pulmonary oedema with acute kidney injury (cardiorenal syndrome)

Clinical pearls

Red flags

Prognosis

3CPO trial (Gray 2008, Lancet) — NIV in cardiogenic pulmonary oedema

ARDSNet ARMA (Acute Respiratory Distress Syndrome Network, NEJM 2000) — the lung-protective ventilation trial

FACTT (Wiedemann, NEJM 2006) — conservative vs liberal fluid in ALI/ARDS

LUNG SAFE (Bellani, JAMA 2016) — ARDS epidemiology across 50 countries

IABP-SHOCK II (Thiele, NEJM 2012) — IABP in MI-related cardiogenic shock

CARRESS-HF (Bart, NEJM 2012) — ultrafiltration vs stepped pharmacological therapy in ADHF with cardiorenal syndrome

PROSEVA (Guérin, NEJM 2013) — prone ventilation in severe ARDS

TRALI and TACO — the two transfusion-related lung injuries

Special pulmonary oedema syndromes — when the heart and the lung are NOT the usual suspects

Exam answer — the long-form / viva response

References