Pulmonary oedema
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Pulmonary Oedema
Pulmonary oedema is defined as an excess of extravascular (interstitial and/or alveolar) lung water. It is a life-threatening condition that demands rapid recognition and treatment.
Pathophysiology
Fluid homeostasis in the lung follows Starling forces. Under normal conditions, pulmonary capillary hydrostatic pressure (~7 mmHg) is well below plasma colloid osmotic pressure (~28 mmHg), keeping the lungs dry. Lymphatics continuously drain small amounts of filtered fluid.
Oedema develops when any of the following tips the balance toward net fluid accumulation:
- Increased capillary hydrostatic pressure - exceeds plasma colloid osmotic pressure
- Increased capillary permeability - microvascular/epithelial injury
- Decreased plasma oncotic pressure - hypoalbuminaemia
- Lymphatic obstruction - rare but potent
Safety factor (Guyton): Pulmonary capillary pressure must rise to at least the level of colloid osmotic pressure (~25-28 mmHg) before significant oedema forms - giving an acute safety factor of ~21 mmHg. In chronic conditions (e.g., mitral stenosis), lymphatic expansion over 2 weeks can tolerate pressures up to 40-45 mmHg without lethal oedema. However, when capillary pressure exceeds the safety factor acutely, death may occur within 20-30 minutes if pressure rises 25-30 mmHg above that threshold. - Guyton and Hall Textbook of Medical Physiology
Classification & Causes
1. Cardiogenic (Haemodynamic) - High-pressure oedema
| Mechanism | Examples |
|---|---|
| Increased hydrostatic pressure | Left heart failure (most common), acute MI, hypertensive crisis, mitral stenosis/regurgitation, volume overload |
| Decreased oncotic pressure | Hypoalbuminaemia (nephrotic syndrome, liver disease, protein-losing enteropathy) |
| Lymphatic obstruction | Lymphangitic carcinomatosis |
2. Non-Cardiogenic (Increased Permeability) - Normal-pressure oedema
| Type | Examples |
|---|---|
| Direct lung injury | Bacterial pneumonia, inhaled toxins (chlorine, SO₂, smoke), aspiration of gastric contents, near-drowning, radiation, lung trauma |
| Indirect/systemic injury | Sepsis, burns, pancreatitis, major trauma (SIRS), blood transfusion-related (TRALI) |
| Drugs/toxins | Bleomycin, heroin, cocaine, methadone, amphotericin B, paraquat |
3. Uncertain Origin
- High-altitude pulmonary oedema (HAPE)
- Neurogenic pulmonary oedema (CNS trauma)
- Robbins, Cotran & Kumar Pathologic Basis of Disease
Pathology
Acute cardiogenic: Alveolar capillaries are engorged; interstitial and alveolar spaces contain pale pink granular transudate on histology. Oedema accumulates first in basal regions of lower lobes (dependent pattern) due to hydrostatic effects.
Chronic cardiogenic: Haemosiderin-laden macrophages ("heart failure cells" - result of microhaemorrhages) are abundant. Over time, alveolar wall thickening and fibrosis produce "brown induration" of the lung - this reduces respiratory function and increases infection susceptibility.
Non-cardiogenic / ARDS: Injury to vascular endothelium or alveolar epithelium produces an inflammatory exudate. The histological pattern is diffuse alveolar damage (DAD). - Robbins
Clinical Features
Acute pulmonary oedema presents with:
- Dyspnoea at rest - rapid onset
- Tachypnoea and tachycardia
- Severe hypoxaemia
- Crackles (alveolar flooding) and wheeze (peribronchial cuffing compressing airways, "cardiac asthma")
- Hypertension from endogenous catecholamine release (common in acute decompensation)
- Frothy, blood-tinged sputum in severe cases
Symptoms of the underlying cause (chest pain in MI, fever in pneumonia, etc.) may accompany the above. - Harrison's Principles of Internal Medicine 22E
Investigations
| Test | Findings |
|---|---|
| CXR | Bilateral airspace opacification, interstitial shadowing, Kerley B lines, upper lobe blood diversion, cardiomegaly (cardiogenic), pleural effusions |
| ECG | ST elevation (acute MI), arrhythmias, LVH |
| BNP/NT-proBNP | Substantially elevated in heart failure; helps distinguish cardiogenic from non-cardiogenic |
| Echocardiography | Systolic/diastolic dysfunction, valvular lesions |
| Pulmonary artery catheter (PAC) | PCWP >18 mmHg = cardiogenic; normal PCWP = non-cardiogenic; indicated when aetiology uncertain or oedema refractory to treatment |
| ABG | Hypoxaemia, hypocapnia early; hypercapnia signals respiratory failure |
Chest X-ray Appearances
Serial CXRs show rapid fluctuation in airspace opacification over 48 hours, reflecting fluid shifts between intravascular compartment and air spaces:
Serial chest radiographs over ~48 hours showing rapid fluctuation in airspace opacification - Grainger & Allison's Diagnostic Radiology
Treatment
Treatment depends on the underlying aetiology. Immediate priorities run in parallel: support oxygenation/ventilation, reduce preload, treat the precipitant, and manage complications (infection, acidaemia, anaemia, AKI).
1. Position
- Sit the patient upright, legs dangling (reduces venous return). - Harrison's
2. Oxygenation & Ventilation
| Modality | Notes |
|---|---|
| High-flow nasal cannula (HFNC) | Better outcomes than BiPAP for non-cardiogenic shock (non-CS) acute hypoxaemic failure with normal PaCO₂ |
| NIV (CPAP/BiPAP) | Rests respiratory muscles, improves oxygenation and cardiac function; reduces intubation need in cardiogenic pulmonary oedema |
| Mechanical ventilation with PEEP | For refractory cases. PEEP (1) decreases preload and afterload, (2) redistributes lung water from intraalveolar to extraalveolar space, (3) increases lung volume and prevents atelectasis |
| Target SpO₂ | ≥92% - very high saturation (>98%) may be detrimental |
- Harrison's 22E
3. Preload Reduction
| Agent | Key Points |
|---|---|
| Furosemide (loop diuretic) | First-line. Also acts as a venodilator, reducing preload before diuresis begins. Initial dose ≤0.5 mg/kg; higher (1 mg/kg) for renal insufficiency, chronic diuretic use, or hypervolaemia |
| Sublingual nitroglycerin | 0.4 mg × 3 every 5 min - first-line in acute cardiogenic oedema. Rapidly reduces preload and afterload |
| IV nitroglycerin | 5-10 µg/min if oedema persists without hypotension |
| IV nitroprusside | 0.1-5 µg/kg/min; potent venous and arterial vasodilator; useful with hypertension; avoid in reduced coronary perfusion states |
| ACE inhibitors | Reduce preload and afterload; recommended in hypertensive patients and acute MI with heart failure |
| Nesiritide (BNP) | Potent arterial/venous vasodilator with diuretic properties; reserved for refractory cases; avoid with ischaemia/MI |
4. Inotropes / Inodilators (when cardiac output is low)
| Agent | Notes |
|---|---|
| Dopamine / Dobutamine | Potent inotropic sympathomimetics |
| Milrinone | PDE-3 inhibitor (inodilator); 50 µg/kg bolus then 0.25-0.75 µg/kg/min; stimulates contractility + causes peripheral/pulmonary vasodilation |
| Digitalis glycosides | Rarely used now; useful for rate control in AF with LV dysfunction and pulmonary oedema |
5. Treat the Precipitant
- Acute MI - immediate revascularisation (PCI/thrombolysis)
- Arrhythmia - cardioversion if primary tachyarrhythmia
- Hypertensive emergency - IV vasodilators
- Sepsis / ARDS - treat underlying source, lung-protective ventilation
- Mitral stenosis - consider balloon valvuloplasty
6. Renal Replacement Therapy
- Consider in refractory volume overload, metabolic acidosis (pH <7.15-7.25), refractory hypoxaemia, or persistent hyperkalaemia
- Continuous renal replacement therapy (CRRT) preferred over intermittent HD if hypotensive or requiring inotropes
- In CKD patients with pulmonary oedema, dialysis is often the most rapidly effective intervention - Rosen's Emergency Medicine
7. Special Consideration - Iatrogenic Cardiogenic Shock
Vasodilator combinations in oedema treatment can cause hypotension and coronary hypoperfusion. Patients with hypertensive response to oedema tolerate and benefit most from vasodilators. - Harrison's 22E
Recent Evidence
A 2025 systematic review and meta-analysis (PMID 40506079) specifically examined low-dose vs. high-dose IV nitroglycerin in sympathetic crashing acute pulmonary oedema (SCAPO), an important area of active investigation.
Summary Mnemonic: LMNOP
A bedside aide-memoire for acute cardiogenic pulmonary oedema:
| Letter | Intervention |
|---|---|
| L | Lasix (furosemide) |
| M | Morphine (reduces anxiety/preload - note: evidence questioned in recent practice) |
| N | Nitrates (sublingual/IV GTN) |
| O | Oxygen (target SpO₂ ≥92%), NIV/CPAP |
| P | Position (upright, legs down) |
Sources: Guyton and Hall Textbook of Medical Physiology | Harrison's Principles of Internal Medicine 22E | Robbins, Cotran & Kumar Pathologic Basis of Disease | Grainger & Allison's Diagnostic Radiology | Rosen's Emergency Medicine
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