Overview
Acute Pulmonary Oedema (Cardiogenic)
Topic Overview
Summary
Acute pulmonary oedema (APO) is a life-threatening emergency caused by acute fluid accumulation in the lungs, most commonly due to left ventricular failure. It presents with sudden severe dyspnoea, orthopnoea, pink frothy sputum, and bilateral crackles. Treatment prioritises oxygenation (CPAP/NIV), vasodilation (GTN), and diuresis (furosemide). Identify and treat the precipitant (ACS, arrhythmia, medication non-compliance).
Key Facts
- Pathophysiology: ↑ LV filling pressure → pulmonary venous congestion → alveolar oedema
- Presentation: Acute dyspnoea, orthopnoea, pink frothy sputum, bilateral crackles, S3 gallop
- Initial management: Sit upright, O₂, NIV/CPAP, IV GTN, IV furosemide
- Avoid: Excessive morphine (respiratory depression), over-diuresis in hypotensive patients
- Key precipitants: ACS, arrhythmia (especially AF), non-compliance, sepsis, hypertensive crisis
Clinical Pearls
NIV/CPAP reduces mortality and need for intubation — start early if SpO₂ under 90% despite O₂
GTN is the cornerstone of treatment in normotensive/hypertensive APO — vasodilation is more important than diuresis early on
Morphine is no longer routinely recommended — increases mortality in some studies
Why This Matters Clinically
APO is one of the most common medical emergencies and is terrifying for patients and staff. Rapid, systematic treatment saves lives. Identifying and treating the precipitant is as important as managing the pulmonary oedema itself.
Visual Summary
Visual assets to be added:
- CXR showing pulmonary oedema (bat's wings, Kerley B lines)
- APO management algorithm flowchart
- Frank-Starling curve with APO marked
- CPAP/NIV setup photograph
Epidemiology
Incidence
- Acute heart failure hospitalisations: ~100,000/year in UK
- APO as presenting feature: ~50% of acute HF presentations
- Mortality: In-hospital 5-10%; 1-year mortality 30%
Demographics
- Age: Predominantly elderly (over 65)
- Sex: Equal or slight male predominance
- Comorbidities: IHD, hypertension, AF, diabetes, CKD
Common Precipitants
| Precipitant | Notes |
|---|---|
| ACS | Most important to exclude — may need urgent PCI |
| Arrhythmia | Fast AF, VT |
| Hypertensive crisis | Flash pulmonary oedema |
| Medication non-compliance | Stopped diuretics, HF meds |
| Dietary indiscretion | Excess salt/fluid intake |
| Infection/sepsis | Increased metabolic demand |
| Renal deterioration | Volume overload |
| Anaemia | High output failure |
Pathophysiology
Normal Physiology
- Pulmonary capillary wedge pressure (PCWP) normally 6-12 mmHg
- Oncotic pressure ~25 mmHg keeps fluid in capillaries
- Lymphatic drainage handles small transudation
APO Cascade
1. ↑ LV Filling Pressure
- LV dysfunction (systolic or diastolic) → ↑ LVEDP
- Mitral regurgitation, AS can contribute
2. ↑ LA Pressure → ↑ Pulmonary Venous Pressure
- Transmitted backwards to pulmonary veins
3. ↑ Pulmonary Capillary Hydrostatic Pressure
- Exceeds oncotic pressure (>25 mmHg)
- Starling forces favour transudation
4. Interstitial Oedema → Alveolar Flooding
- Initially interstitial (Kerley B lines)
- Progresses to alveolar flooding (bat's wing CXR)
5. Impaired Gas Exchange
- V/Q mismatch
- Hypoxaemia
- Increased work of breathing
Flash Pulmonary Oedema
- Rapid onset, often in hypertensive crisis
- May occur with renal artery stenosis + ACEi initiation
- Dramatic presentation, often responds rapidly to treatment
Clinical Presentation
Symptoms
Signs
Profiles by Blood Pressure
| Profile | BP | Features | Treatment Priority |
|---|---|---|---|
| Warm & Wet | Normal/high | Congested, good perfusion | Vasodilator + diuretic |
| Cold & Wet | Low | Congested + hypoperfused | Inotrope + careful diuretic |
| Warm & Dry | Normal | Compensated | Investigation, optimise meds |
| Cold & Dry | Low | Hypoperfused, dehydrated | Fluids + inotrope |
Severe dyspnoea — sudden onset
Common presentation.
Orthopnoea — cannot lie flat
Common presentation.
Paroxysmal nocturnal dyspnoea — wakes from sleep
Common presentation.
Pink frothy sputum — alveolar flooding
Common presentation.
Chest tightness — may suggest ACS
Common presentation.
Clinical Examination
Focused Assessment
Vital Signs:
- Respiratory rate (often over 25)
- SpO₂ (may be under 90%)
- BP (guides treatment — vasodilators vs inotropes)
- HR (look for arrhythmia)
Cardiovascular:
- JVP (elevated)
- Heart sounds (S3 gallop, murmurs)
- Peripheral perfusion (cool = low output)
Respiratory:
- Work of breathing
- Crackles (bilateral, basal → mid-zones)
- Wheeze ("cardiac asthma")
Peripheries:
- Oedema (if chronic)
- Cyanosis
Investigations
Immediate
| Investigation | Purpose |
|---|---|
| ECG | ACS, arrhythmia, LVH |
| SpO₂ / ABG | Hypoxia, type 1 vs 2 resp failure |
| CXR | Confirm pulmonary oedema, exclude pneumonia |
Laboratory
| Test | Findings |
|---|---|
| BNP / NT-proBNP | Elevated (over 400 pg/ml highly likely HF) |
| Troponin | May be elevated (ACS or demand ischaemia) |
| U&E | Renal function, electrolytes |
| FBC | Anaemia as precipitant |
| LFTs | Congestive hepatopathy |
Echocardiography
- LV function (HFrEF vs HFpEF)
- Valvular disease
- Wall motion abnormalities (ACS)
- Pericardial effusion
CXR Features of APO
| Feature | Description |
|---|---|
| Upper lobe diversion | Earliest sign |
| Kerley B lines | Interstitial oedema |
| Bat's wing/butterfly | Alveolar oedema |
| Cardiomegaly | Often present |
| Pleural effusions | Usually bilateral |
Classification & Staging
By Predominant Phenotype
| Type | LVEF | Description |
|---|---|---|
| HFrEF | Under 40% | Systolic dysfunction — reduced contractility |
| HFmrEF | 40-49% | Mildly reduced EF |
| HFpEF | Over 50% | Diastolic dysfunction — preserved EF |
Killip Classification (AMI with HF)
| Class | Features |
|---|---|
| I | No HF |
| II | Crackles, S3 |
| III | Frank pulmonary oedema |
| IV | Cardiogenic shock |
Management
Immediate Management (LMNOP + Position)
Position:
- Sit upright (legs dependent reduces preload)
L — Lasix (Furosemide):
- 40-80mg IV (higher if already on oral furosemide)
- Onset 5-15 min (diuresis) + immediate venodilatation
M — Morphine:
- No longer routinely recommended — associated with increased intubation and mortality
- May use 2.5-5mg IV cautiously if very agitated and not hypoxic
N — Nitrates (GTN):
- First-line in normotensive/hypertensive APO
- IV GTN infusion: Start 10-20 mcg/min, titrate to BP
- Buccal GTN / sublingual spray as bridge
- Do NOT use if SBP under 90
O — Oxygen:
- If SpO₂ under 94%
- Target 94-98%
P — Positive Pressure Ventilation:
- CPAP/NIV — first-line for moderate-severe APO
- Reduces work of breathing, improves oxygenation, reduces preload
- Reduces mortality and need for intubation
- Contraindicated if GCS reduced, vomiting
Management by BP Profile
| BP | First-Line Treatment |
|---|---|
| SBP over 110 | GTN + furosemide + NIV |
| SBP 90-110 | Cautious GTN, diuretic, NIV |
| SBP under 90 | Inotrope (dobutamine), cautious diuretic, consider mechanical support |
Identify and Treat Precipitant
- ACS: Urgent PCI if STEMI
- Fast AF: Rate control (digoxin/amiodarone); cardioversion if unstable
- Hypertensive crisis: IV GTN/labetalol
- Sepsis: Antibiotics, source control
- Medicine non-compliance: Re-educate, restart
Refractory APO
- Escalate NIV to invasive ventilation
- Inotropes (dobutamine)
- Ultrafiltration/dialysis
- Mechanical support (IABP, LVAD, ECMO)
Complications
Immediate
- Respiratory failure requiring intubation
- Cardiogenic shock
- Arrhythmias
- Death
Hospital Complications
- AKI (over-diuresis or low output)
- Infection (HAP if intubated)
- Thromboembolic events
Long-Term
- Recurrent admissions (30-40% at 1 year)
- Progressive HF
- QoL impairment
Prognosis & Outcomes
Mortality
- In-hospital: 5-10%
- 30-day: 10-15%
- 1-year: 30%
- Higher with hypotension, ACS, advanced age, renal impairment
Good Outcomes Associated With
- Early NIV
- Rapid treatment
- Identification and treatment of precipitant
- Optimised HF therapy on discharge
Evidence & Guidelines
Key Guidelines
- ESC Guidelines for Acute and Chronic Heart Failure (2021)
- NICE NG106: Acute Heart Failure (2014, updated)
- Resuscitation Council UK: Acute Pulmonary Oedema
Key Evidence
- 3CPO Trial: NIV reduces intubation and mortality in APO
- DOSE Trial: High-dose furosemide safe; no significant outcome difference vs low dose
- Morphine: Observational data suggest harm — no longer routinely recommended
Patient & Family Information
What is Acute Pulmonary Oedema?
APO is when fluid suddenly builds up in your lungs, making it very hard to breathe. It is usually caused by the heart not pumping well.
Symptoms
- Severe shortness of breath
- Cannot lie flat
- Coughing up pink foamy liquid
- Feeling like you're "drowning"
Treatment
- Oxygen and breathing support
- Medicines to remove fluid (water tablets)
- Medicines to open blood vessels
- Finding and treating the cause
What Can I Do?
- Take your heart medicines as prescribed
- Limit salt and fluid if advised
- Weigh yourself daily — report weight gain
- Call 999 if you feel suddenly breathless
Resources
References
Primary Guidelines
- McDonagh TA, et al. 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure. Eur Heart J. 2021;42(36):3599-3726. PMID: 34447992
- NICE. Acute Heart Failure: Diagnosis and Management (NG106). 2014/2021. nice.org.uk
Key Trials
- Gray A, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema (3CPO). N Engl J Med. 2008;359(2):142-151. PMID: 18614781
- Felker GM, et al. Diuretic Strategies in Patients with Acute Decompensated Heart Failure (DOSE). N Engl J Med. 2011;364(9):797-805. PMID: 21366472