Acute Pulmonary Oedema
Summary
Acute pulmonary oedema is a medical emergency where fluid rapidly accumulates in the lungs' air sacs, causing severe breathlessness and oxygen deprivation. Picture your lungs as sponges that suddenly fill with water—that's what happens when the heart's pumping mechanism fails, forcing fluid backward into the lungs instead of forward to the body. This condition affects approximately 1-2% of hospital admissions and carries a 30-day mortality of 10-15%. The key to survival is rapid recognition and immediate treatment: oxygen, diuretics, and vasodilators to relieve the pressure, often within minutes of presentation. Most cases stem from acute decompensation of chronic heart failure, but can also occur de novo in acute myocardial infarction, severe hypertension, or valvular emergencies.
Key Facts
- Definition: Rapid accumulation of fluid in pulmonary interstitium and alveoli due to elevated pulmonary capillary pressure
- Incidence: 1-2% of all hospital admissions; ~150,000 cases/year in UK
- Mortality: 10-15% at 30 days; 30-40% at 1 year
- Time to treatment: First-line therapy should begin within 15 minutes of presentation
- Critical threshold: Pulmonary capillary wedge pressure >18 mmHg (normal: 8-12 mmHg)
- Key investigation: Chest X-ray (bilateral infiltrates, Kerley B lines, cardiomegaly)
- First-line treatment: High-flow oxygen, IV furosemide 40-80mg, GTN spray/sublingual
Clinical Pearls
"Think FAST" — Fluid Accumulation, Airway, Sit Upright, Treatment. The patient's position matters: sitting upright uses gravity to reduce preload and improve breathing.
"Pink froth = Flash" — Pink, frothy sputum is pathognomonic of acute pulmonary oedema. It's not just sputum—it's plasma that's leaked into the alveoli, mixed with air, creating that characteristic appearance.
"Not all breathlessness is asthma" — In the elderly or those with cardiac risk factors, always consider cardiac causes first. Wheeze can occur in pulmonary oedema ("cardiac asthma") and mislead clinicians.
"BP guides therapy" — Systolic BP >140 mmHg? Use vasodilators (GTN). BP 90-140 mmHg? Use diuretics + cautious vasodilators. BP <90 mmHg? This is cardiogenic shock—avoid vasodilators, consider inotropes.
Why This Matters Clinically
Acute pulmonary oedema is a true medical emergency where minutes count. Every hour of delay increases mortality by 2-3%. It's the most common cause of acute respiratory failure in patients over 65, and misdiagnosis (often confused with asthma or pneumonia) leads to inappropriate treatment and worse outcomes. Rapid, protocol-driven management can turn a life-threatening situation into a manageable one within 30-60 minutes.
Incidence & Prevalence
- Incidence: 1-2% of all hospital admissions globally
- UK: ~150,000 hospital admissions/year for acute heart failure (of which 60-70% present as pulmonary oedema)
- US: ~1 million hospitalizations/year for heart failure
- Trend: Increasing incidence (aging population, improved survival from MI)
- Peak age: 70-80 years (but can occur at any age)
Demographics
| Factor | Details |
|---|---|
| Age | Median age 75 years; rare <50 years unless acute MI or valvular disease |
| Sex | Slight male predominance (55:45) in younger patients; equal in elderly |
| Ethnicity | Higher rates in Black and Hispanic populations (1.5-2x); earlier onset |
| Geography | Higher in urban areas (access to care); seasonal variation (winter peaks) |
| Socioeconomic | Higher rates in lower socioeconomic groups (2x risk) |
Risk Factors
Non-Modifiable:
- Age >65 years (exponential increase with age)
- Male sex (younger patients)
- Family history of cardiomyopathy or sudden cardiac death
- Genetic cardiomyopathies (hypertrophic, dilated)
Modifiable:
| Risk Factor | Relative Risk | Population Attributable Risk |
|---|---|---|
| Hypertension | 2.5x | 25% |
| Coronary artery disease | 3.0x | 30% |
| Diabetes mellitus | 2.0x | 15% |
| Atrial fibrillation | 2.5x | 20% |
| Chronic kidney disease | 2.0x | 15% |
| Obesity (BMI >0) | 1.5x | 10% |
| Smoking | 1.8x | 12% |
| Excessive alcohol | 1.5x | 8% |
| Valvular heart disease | 2.5x | 10% |
Precipitating Factors (What Triggers Acute Episodes)
| Precipitant | Frequency | Mechanism |
|---|---|---|
| Non-adherence to medications | 30-40% | Loss of diuretic/ACE inhibitor effect |
| Dietary indiscretion (salt/fluid) | 25-30% | Volume overload |
| Arrhythmias (new AF, VT) | 15-20% | Loss of atrial kick, tachycardia |
| Acute coronary syndrome | 10-15% | New myocardial dysfunction |
| Infections (pneumonia, UTI) | 10-15% | Increased metabolic demand |
| Hypertension crisis | 5-10% | Afterload increase |
| Medications (NSAIDs, steroids) | 5-10% | Fluid retention |
| Anemia | 5% | Increased cardiac output demand |
| Pregnancy/thyrotoxicosis | Rare | High-output failure |
The Fluid Cascade: From Heart Failure to Lung Flooding
Think of your heart as a pump and your lungs as a delicate filter. When the pump fails, pressure builds up in the pipes (blood vessels) behind it, forcing fluid through the filter's membrane into spaces where it shouldn't be.
Step 1: Cardiac Dysfunction
- Left ventricular failure: The heart's main pumping chamber (left ventricle) can't eject blood effectively
- Causes: Ischaemia (reduced blood supply), pressure overload (hypertension, aortic stenosis), volume overload (mitral regurgitation), or muscle disease (cardiomyopathy)
- Result: Blood backs up into the left atrium, then pulmonary veins
Step 2: Increased Pulmonary Venous Pressure
- Normal pulmonary capillary pressure: 8-12 mmHg
- In pulmonary oedema: >18 mmHg (often 25-30 mmHg)
- Starling's Law: When capillary pressure exceeds oncotic pressure (25-30 mmHg), fluid leaks out
- The pulmonary capillaries become "leaky pipes"
Step 3: Fluid Transudation
- Fluid first accumulates in the interstitium (space between alveoli and capillaries)
- This causes reduced lung compliance ("stiff lungs") and increased work of breathing
- As pressure increases further, fluid floods into alveoli (air sacs)
- Alveoli fill with fluid → reduced gas exchange → hypoxia
Step 4: Clinical Manifestation
- Dyspnoea: Fluid in alveoli triggers stretch receptors → sensation of breathlessness
- Hypoxia: Reduced oxygen diffusion → low SpO2, cyanosis
- Cough/frothy sputum: Fluid mixes with air in alveoli → pink froth
- Wheeze: "Cardiac asthma" from bronchial wall oedema
Classification by Mechanism
| Type | Mechanism | Common Causes | Clinical Features |
|---|---|---|---|
| Cardiogenic | Increased pulmonary capillary pressure | LV failure, MI, valvular disease | Elevated JVP, S3 gallop, cardiomegaly on CXR |
| Non-cardiogenic (ARDS) | Increased capillary permeability | Sepsis, aspiration, trauma | Normal cardiac size, no S3, different CXR pattern |
| High-output failure | Increased venous return | Anemia, thyrotoxicosis, AV fistula | Bounding pulse, warm extremities |
| Flash pulmonary oedema | Sudden severe hypertension | Renal artery stenosis, phaeochromocytoma | Very rapid onset (<1 hour), severe hypertension |
Anatomical Considerations: Why Lungs Are Vulnerable
Pulmonary Capillary Structure
- Pulmonary capillaries are extremely thin (0.1-0.2 μm) to allow gas exchange
- This thinness makes them vulnerable to pressure changes
- Unlike systemic capillaries, pulmonary capillaries have lower baseline pressure
- They're designed for low pressure, high flow—when pressure increases, they leak easily
Gravity-Dependent Distribution
- In upright patients, fluid accumulates in lower lobes first (gravity effect)
- This explains why CXR shows bilateral lower zone infiltrates
- In supine patients (ICU), distribution is more uniform
Lymphatic Drainage
- Lungs have extensive lymphatic system to clear excess fluid
- In chronic heart failure, lymphatics hypertrophy (compensatory)
- In acute failure, lymphatics can't keep up → rapid fluid accumulation
The Vicious Cycle
Cardiac Dysfunction
↓
Increased LV End-Diastolic Pressure
↓
Increased Left Atrial Pressure
↓
Increased Pulmonary Venous Pressure
↓
Increased Pulmonary Capillary Pressure (>18 mmHg)
↓
Fluid Leaks into Interstitium → Alveoli
↓
Reduced Oxygenation → Hypoxia
↓
Increased Sympathetic Drive → Tachycardia
↓
Increased Myocardial Oxygen Demand
↓
Worsening Cardiac Function
↓
(Back to start - VICIOUS CYCLE)
Breaking the Cycle: Treatment targets multiple points:
- Diuretics: Reduce circulating volume → reduce preload
- Vasodilators: Reduce afterload → improve forward flow
- Oxygen: Improve oxygenation → reduce sympathetic drive
- Inotropes (if needed): Improve contractility → break the cycle
Symptoms: The Patient's Story
Typical Presentation (80-90% of cases):
1. Severe Breathlessness (Dyspnoea)
2. Cough
3. Anxiety and Restlessness
4. Chest Discomfort
5. Fatigue and Weakness
Atypical Presentations (10-20% of cases):
Elderly Patients:
Diabetics:
Chronic Heart Failure Patients:
Signs: What You See and Hear
Vital Signs (Critical to Assess Immediately):
| Sign | Finding | Significance |
|---|---|---|
| Respiratory rate | >5/min (often 30-40/min) | Tachypnoea indicates severe respiratory distress |
| SpO2 | <90% on room air (often 75-85%) | Severe hypoxia; needs immediate oxygen |
| Heart rate | Tachycardia (100-140 bpm) | Compensatory response; may indicate arrhythmia |
| Blood pressure | Variable: High (180+), normal, or low (<90 = shock) | Guides treatment choice |
| Temperature | Usually normal (unless precipitant is infection) | Fever suggests infection as trigger |
General Appearance:
Cardiovascular Examination:
| Finding | What It Means | Frequency |
|---|---|---|
| Elevated JVP | Right heart failure or fluid overload | 60-70% |
| Displaced apex beat | Cardiomegaly | 50-60% |
| S3 gallop | Ventricular dysfunction (pathognomonic) | 40-50% |
| S4 gallop | Stiff, hypertrophied ventricle | 30-40% |
| Murmurs | Valvular disease (MR, AS, MS) | 30-40% |
| Peripheral oedema | Fluid overload (ankles, sacrum) | 40-50% |
| Cool extremities | Poor perfusion (if cardiogenic shock) | 10-20% |
Respiratory Examination:
| Finding | What It Means | Clinical Note |
|---|---|---|
| Tachypnoea | Respiratory distress | >5/min is significant |
| Use of accessory muscles | Increased work of breathing | Neck, intercostal muscles |
| Wheeze | "Cardiac asthma" (bronchial oedema) | Can mimic asthma |
| Crepitations (crackles) | Fluid in alveoli | Bilateral, lower zones, fine to medium |
| Reduced air entry | Severe oedema fills alveoli | Lower zones most affected |
| Pink frothy sputum | Pathognomonic | Plasma + air in alveoli |
Abdominal Examination:
Red Flags
[!CAUTION] Red Flags — Immediate Escalation Required:
- Respiratory rate >30/min or <8/min — Impending respiratory failure
- SpO2 <90% despite high-flow oxygen — Needs CPAP/BiPAP or intubation
- Systolic BP <90 mmHg — Cardiogenic shock; avoid vasodilators
- Altered mental status or confusion — Severe hypoxia or hypercapnia
- Pink frothy sputum — Confirms diagnosis; indicates severe oedema
- Unable to speak in full sentences — Severe respiratory distress
- New arrhythmia (AF, VT) — May be cause or consequence; needs urgent management
- Cardiac arrest — Immediate CPR + consider reversible causes
Structured Approach: The ABCDE Framework
A - Airway
- Assessment: Can patient speak? Is airway patent?
- Findings: Usually patent (unless severe); may have stridor if upper airway oedema (rare)
- Action: If compromised → consider intubation
B - Breathing
- Look: Respiratory rate, use of accessory muscles, cyanosis, position
- Listen: Wheeze, crepitations, reduced air entry
- Feel: Chest expansion, percussion (usually resonant)
- Measure: SpO2, respiratory rate
- Action: High-flow oxygen immediately; consider CPAP if SpO2 <90%
C - Circulation
- Look: Skin colour, capillary refill, JVP, peripheral oedema
- Feel: Pulse (rate, rhythm, volume), BP (both arms)
- Listen: Heart sounds (S3, S4, murmurs)
- Measure: HR, BP, ECG
- Action: IV access x2 (large bore), monitor continuously
D - Disability
- Assessment: GCS, pupil response, blood glucose
- Findings: May be confused if hypoxic
- Action: Check glucose; consider if hypoxia is causing confusion
E - Exposure
- Look: Full body examination for oedema, rashes, signs of infection
- Feel: Temperature, peripheral pulses
- Action: Keep warm, maintain dignity
Specific System Examination
Cardiovascular System:
Inspection:
- Elevated JVP (if visible, indicates right heart failure)
- Displaced apex beat (cardiomegaly)
- Visible pulsations (if severe)
Palpation:
- Apex beat: Displaced laterally (if cardiomegaly), may be weak (if poor LV function)
- Heaves: Left parasternal heave suggests RV hypertrophy
- Thrills: May indicate valvular disease
Auscultation:
- S1: Usually normal; may be soft if poor LV function
- S2: May be loud P2 if pulmonary hypertension
- S3: Pathognomonic of LV dysfunction ("Kentucky" gallop)
- S4: Indicates stiff, hypertrophied ventricle ("Tennessee" gallop)
- Murmurs:
- Mitral regurgitation (pansystolic, apex)
- Aortic stenosis (ejection systolic, aortic area)
- Mitral stenosis (diastolic, apex) - rare but can cause pulmonary oedema
Respiratory System:
Inspection:
- Tachypnoea (>25/min)
- Use of accessory muscles (sternocleidomastoid, intercostals)
- Central cyanosis (if severe hypoxia)
- Pursed-lip breathing (attempt to maintain positive pressure)
Palpation:
- Reduced chest expansion (if severe)
- Tactile fremitus: Usually normal (fluid conducts sound)
Percussion:
- Usually resonant (unless pleural effusion present)
- Dullness at bases if pleural effusion
Auscultation:
- Wheeze: "Cardiac asthma" - expiratory wheeze from bronchial oedema
- Crepitations (crackles):
- Fine: Early oedema (interstitium)
- Medium: Established oedema (alveoli)
- Coarse: Severe oedema or resolving
- Distribution: Bilateral, lower zones (gravity-dependent)
- Reduced air entry: Lower zones if severe
- Pleural rub: If associated pleural effusion
Special Tests
| Test | Technique | Positive Finding | Sensitivity/Specificity | Clinical Use |
|---|---|---|---|---|
| Hepatojugular reflux | Firm pressure on liver for 10-15 seconds | JVP rises >cm | 60%/90% | Indicates right heart failure |
| Valsalva manoeuvre | Patient strains against closed glottis | Abnormal BP response | 70%/85% | Suggests heart failure (not diagnostic) |
| Pulsus alternans | Regular pulse with alternating strong/weak beats | Alternating pulse volume | 30%/95% | Severe LV dysfunction (rare) |
| Kussmaul's sign | JVP rises on inspiration (paradoxical) | JVP increases instead of decreases | 40%/90% | Constrictive pericarditis (rare cause) |
First-Line (Bedside) - Do These Immediately
1. Pulse Oximetry
- Purpose: Assess oxygenation
- Finding: SpO2 <90% indicates severe hypoxia
- Action: Start high-flow oxygen; monitor continuously
- Note: May be falsely reassuring if patient on oxygen already
2. 12-Lead ECG
- Purpose: Identify arrhythmias, ischaemia, or other cardiac causes
- Key Findings:
- Acute MI: ST elevation/depression, new LBBB
- Atrial fibrillation: Irregularly irregular rhythm
- LV hypertrophy: Voltage criteria + strain pattern
- Arrhythmias: VT, SVT (may be cause or consequence)
- Action: Treat identified abnormalities; repeat if unstable
3. Blood Pressure Measurement
- Purpose: Guide treatment choice
- Finding:
- High (>140): Use vasodilators
- Normal (90-140): Standard therapy
- Low (<90): Cardiogenic shock - avoid vasodilators
- Action: Monitor every 5-15 minutes initially
4. Capillary Blood Glucose
- Purpose: Rule out hypoglycaemia (can cause confusion)
- Finding: Normal or elevated (stress response)
- Action: Treat if low; consider if confused
Laboratory Tests
| Test | Expected Finding | Purpose | Timing |
|---|---|---|---|
| BNP/NT-proBNP | Elevated (>400 pg/mL BNP or >000 pg/mL NT-proBNP) | Confirm heart failure diagnosis | Within 1 hour if available |
| Troponin | May be elevated (myocardial strain or MI) | Rule out acute MI as cause | Immediate |
| Urea & Creatinine | May be elevated (pre-renal AKI or CKD) | Assess renal function (affects diuretic dosing) | Immediate |
| Full Blood Count | May show anaemia (precipitant) | Identify anaemia as cause | Within 2 hours |
| Liver Function Tests | May be elevated (hepatic congestion) | Assess for right heart failure | Within 2 hours |
| Arterial Blood Gas | Hypoxia, respiratory alkalosis (early) or acidosis (late) | Assess gas exchange and acid-base status | If SpO2 <90% or concern about ventilation |
| D-dimer | Usually negative (unless PE as cause) | Rule out PE if clinical suspicion | If PE suspected |
BNP Interpretation:
- <100 pg/mL: Heart failure unlikely (negative predictive value 90%)
- 100-400 pg/mL: Grey zone (consider other causes)
- >400 pg/mL: Heart failure likely (positive predictive value 90%)
- Note: BNP can be elevated in other conditions (PE, renal failure, advanced age)
Imaging
Chest X-Ray (Essential - Do Within 1 Hour)
| Finding | What It Shows | Frequency |
|---|---|---|
| Bilateral lower zone infiltrates | Fluid in alveoli (gravity-dependent) | 80-90% |
| Kerley B lines | Interstitial oedema (horizontal lines at lung bases) | 30-40% |
| Cardiomegaly | Enlarged heart (cardiothoracic ratio >0%) | 60-70% |
| Upper lobe diversion | Redistribution of blood flow to upper lobes | 40-50% |
| Pleural effusions | Bilateral small effusions | 30-40% |
| Peribronchial cuffing | Fluid around bronchi | 20-30% |
| Bat wing appearance | Bilateral perihilar infiltrates (severe) | 10-20% |
Echocardiogram (Within 48 Hours)
| Finding | Significance | Clinical Impact |
|---|---|---|
| Reduced LVEF (<40%) | Systolic dysfunction | Indicates need for ACE inhibitor/ARB, beta-blocker |
| Preserved LVEF (>0%) | Diastolic dysfunction (HFpEF) | Different management (diuretics, control BP/HR) |
| Regional wall motion abnormalities | Ischaemic cardiomyopathy | May need revascularization |
| Valvular abnormalities | MR, AS, MS | May need valve surgery |
| LV hypertrophy | Hypertension-related | Control BP aggressively |
CT Pulmonary Angiogram (If PE Suspected)
- Indication: If clinical features suggest PE (sudden onset, pleuritic pain, risk factors)
- Finding: Pulmonary emboli (rare cause of pulmonary oedema)
- Note: Don't delay treatment for imaging if classic presentation
Diagnostic Criteria
Framingham Criteria for Heart Failure (Used for Chronic HF Diagnosis):
Major Criteria (Need 2):
- Paroxysmal nocturnal dyspnoea
- Orthopnoea
- Elevated JVP
- Rales (crepitations)
- Cardiomegaly on CXR
- S3 gallop
- Hepatojugular reflux
Minor Criteria (Need 1 major + 2 minor):
- Bilateral ankle oedema
- Nocturnal cough
- Dyspnoea on exertion
- Hepatomegaly
- Pleural effusion
- Heart rate >120 bpm
- Weight loss >4.5 kg in 5 days
For Acute Pulmonary Oedema:
- Clinical diagnosis (classic presentation + CXR findings)
- BNP/NT-proBNP supports diagnosis but not required
- Echocardiogram confirms underlying cardiac dysfunction
Management Algorithm
ACUTE PULMONARY OEDEMA PRESENTATION
(Severe breathlessness + cardiac risk factors)
↓
┌─────────────────────────────────────────────────┐
│ IMMEDIATE ASSESSMENT (<5 mins) │
│ • ABCDE approach │
│ • Sit patient upright (90°) │
│ • High-flow oxygen (15L/min via reservoir) │
│ • SpO2, BP, HR, RR monitoring │
│ • 12-lead ECG │
│ • IV access (large bore x2) │
│ • Check for pink frothy sputum │
└─────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────┐
│ BLOOD PRESSURE ASSESSMENT │
├─────────────────────────────────────────────────┤
│ SBP >140 mmHg │
│ → GTN spray 2 puffs (repeat q5min) │
│ → GTN infusion 10-200 mcg/min │
│ → IV furosemide 40-80mg │
│ → Monitor BP every 5 mins │
│ │
│ SBP 90-140 mmHg │
│ → IV furosemide 40-80mg │
│ → Cautious GTN (if no hypotension) │
│ → Consider CPAP/BiPAP if SpO2 <90% │
│ │
│ SBP <90 mmHg (CARDIOGENIC SHOCK) │
│ → NO vasodilators │
│ → IV furosemide 20-40mg (cautious) │
│ → Consider inotropes (dobutamine) │
│ → Urgent echo + consider IABP/mechanical support│
└─────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────┐
│ RESPONSE TO INITIAL THERAPY │
├─────────────────────────────────────────────────┤
│ Improving (SpO2 ↑, RR ↓, less breathless) │
│ → Continue current therapy │
│ → Consider CPAP if still distressed │
│ → Monitor for 2-4 hours │
│ → Investigate underlying cause │
│ │
│ Not improving or deteriorating │
│ → Escalate to CPAP/BiPAP │
│ → Consider intubation if: │
│ - SpO2 <85% despite CPAP │
│ - Exhaustion/falling GCS │
│ - Respiratory acidosis (pH <7.25) │
│ → Urgent echo to assess LV function │
│ → Consider transfer to ICU │
└─────────────────────────────────────────────────┘
↓
┌─────────────────────────────────────────────────┐
│ SECONDARY MANAGEMENT │
│ • Chest X-ray (confirm diagnosis) │
│ • BNP/NT-proBNP (if available) │
│ • U&Es (baseline renal function) │
│ • FBC, LFTs, troponin │
│ • Echocardiogram (within 48h) │
│ • Identify and treat precipitant │
└─────────────────────────────────────────────────┘
Acute/Emergency Management - The First 15 Minutes
Immediate Actions (Do Simultaneously):
-
Position Patient
- Sit upright (90°) with legs dangling
- This reduces preload (venous return) and improves breathing
- Don't lay patient flat (worsens symptoms)
-
High-Flow Oxygen
- 15 L/min via non-rebreather mask (reservoir bag)
- Target SpO2 >90% (ideally 94-98%)
- If SpO2 <90% despite oxygen → consider CPAP/BiPAP
-
IV Access
- Large bore cannulae x2 (16-18G)
- One for diuretics, one for other medications
- Consider central line if multiple infusions needed
-
Monitoring
- Continuous SpO2, BP, HR monitoring
- 12-lead ECG
- Consider arterial line if unstable
-
Initial Medications (Based on BP):
If SBP >140 mmHg:
- GTN spray: 2 puffs sublingually (repeat q5min)
- GTN infusion: 10-200 mcg/min (start low, titrate up)
- IV furosemide: 40-80mg IV (higher dose if on chronic diuretics)
- Monitor BP every 5 minutes (avoid hypotension)
If SBP 90-140 mmHg:
- IV furosemide: 40-80mg IV
- Cautious GTN: Only if BP stable and no hypotension risk
- Consider CPAP/BiPAP if SpO2 <90%
If SBP <90 mmHg (Cardiogenic Shock):
- NO vasodilators (will worsen shock)
- IV furosemide: 20-40mg (cautious, may worsen renal function)
- Consider inotropes: Dobutamine 2.5-15 mcg/kg/min
- Urgent echo: Assess LV function
- Consider mechanical support: IABP, ECMO (if available)
Medical Management
Diuretics (First-Line):
| Drug | Dose | Route | Frequency | Notes |
|---|---|---|---|---|
| Furosemide | 40-80mg (higher if on chronic diuretics) | IV | Single dose, repeat q4-6h | First-line; works within 30-60 mins |
| Bumetanide | 1-2mg | IV | Single dose | Alternative if furosemide unavailable |
| Torasemide | 10-20mg | IV | Single dose | Longer-acting alternative |
Mechanism: Blocks Na+/K+/Cl- reabsorption in loop of Henle → increased urine output → reduced circulating volume → reduced preload
Monitoring:
- Urine output (should see diuresis within 1-2 hours)
- U&Es (risk of AKI if over-diuresis)
- Daily weights (target 0.5-1kg/day loss)
Vasodilators (If BP Permits):
| Drug | Dose | Route | Frequency | Notes |
|---|---|---|---|---|
| GTN (Glyceryl trinitrate) | 10-200 mcg/min | IV infusion | Continuous | First-line vasodilator; titrate to BP |
| GTN spray | 400 mcg (2 puffs) | Sublingual | q5min PRN | Quick onset; use while setting up infusion |
| Isosorbide dinitrate | 1-10 mg/hour | IV infusion | Continuous | Alternative to GTN |
| Nitroprusside | 0.3-5 mcg/kg/min | IV infusion | Continuous | Reserved for severe hypertension; requires ICU |
Mechanism:
- Venodilation → reduced preload (reduces venous return)
- Arteriodilation → reduced afterload (improves forward flow)
- Net effect: Reduced cardiac workload + improved forward flow
Contraindications:
- SBP <90 mmHg
- Severe aortic stenosis (reduces coronary perfusion)
- Recent phosphodiesterase inhibitor use (sildenafil, tadalafil) - risk of severe hypotension
Morphine (If Severe Distress):
| Drug | Dose | Route | Frequency | Notes |
|---|---|---|---|---|
| Morphine | 2.5-5mg | IV | q5-10min PRN | Use cautiously; can cause respiratory depression |
Mechanism:
- Venodilation → reduced preload
- Anxiolysis → reduces sympathetic drive
- Analgesia → if chest discomfort present
Caution:
- Can cause respiratory depression (monitor closely)
- Avoid if altered mental status or respiratory depression risk
- Have naloxone available
Non-Invasive Ventilation (CPAP/BiPAP):
Indications:
- SpO2 <90% despite high-flow oxygen
- Respiratory rate >30/min
- Signs of respiratory muscle fatigue
- pH <7.35 (respiratory acidosis)
Settings:
- CPAP: 5-10 cmH2O (start at 5, titrate up)
- BiPAP: IPAP 8-12, EPAP 4-6 cmH2O
Mechanism:
- Positive pressure → reduces preload (like "internal tourniquet")
- Improves oxygenation → reduces work of breathing
- Can avoid intubation in 60-70% of cases
Contraindications:
- Vomiting (aspiration risk)
- Altered mental status (can't protect airway)
- Facial trauma
- Undrained pneumothorax
Inotropes (If Cardiogenic Shock):
| Drug | Dose | Route | Frequency | Notes |
|---|---|---|---|---|
| Dobutamine | 2.5-15 mcg/kg/min | IV infusion | Continuous | First-line inotrope; increases contractility |
| Dopamine | 2-20 mcg/kg/min | IV infusion | Continuous | Less preferred (more arrhythmogenic) |
| Milrinone | 0.375-0.75 mcg/kg/min | IV infusion | Continuous | Phosphodiesterase inhibitor; use if beta-blocker on board |
Mechanism: Increases myocardial contractility → improves cardiac output
Use Only If:
- Cardiogenic shock (SBP <90 with signs of poor perfusion)
- Not responding to diuretics/vasodilators
- Requires ICU monitoring (arrhythmia risk)
Conservative Management
Positioning:
- Upright position: Reduces preload via gravity
- Legs dangling: Further reduces venous return
- Avoid supine: Worsens symptoms
Oxygen Therapy:
- Start with high-flow oxygen
- Escalate to CPAP/BiPAP if needed
- Consider intubation if failing
Fluid Restriction:
- Acute phase: 1-1.5 L/day
- Chronic phase: 1.5-2 L/day (individualize)
- Monitor daily weights
Salt Restriction:
- Acute phase: <2g/day
- Chronic phase: <3g/day
- Educate patient and family
Surgical Management (If Indicated)
Indications for Urgent Intervention:
-
Acute MI with Cardiogenic Shock
- Primary PCI: Restore coronary blood flow
- Timing: Within 90 minutes of presentation
- Outcome: Can dramatically improve LV function
-
Acute Severe Mitral Regurgitation
- Mitral valve surgery: Urgent repair or replacement
- Timing: Within 24-48 hours if stable
- Consider: Transcatheter mitral valve repair (MitraClip) if high surgical risk
-
Acute Aortic Stenosis
- Aortic valve replacement: Surgical or TAVI
- Timing: Urgent if causing pulmonary oedema
- Bridge: Consider balloon valvuloplasty if unstable
-
Mechanical Complications of MI
- Ventricular septal rupture: Urgent surgical repair
- Papillary muscle rupture: Urgent mitral valve surgery
- Free wall rupture: Usually fatal (pericardiocentesis if tamponade)
Mechanical Circulatory Support:
| Device | Indication | Mechanism | Duration |
|---|---|---|---|
| IABP (Intra-aortic balloon pump) | Cardiogenic shock, bridge to surgery | Reduces afterload, improves coronary perfusion | Days to weeks |
| ECMO (Extracorporeal membrane oxygenation) | Refractory cardiogenic shock | Provides complete circulatory support | Days to weeks |
| LVAD (Left ventricular assist device) | End-stage heart failure | Long-term mechanical support | Months to years |
Disposition
Admit to ICU/HDU If:
- Cardiogenic shock (SBP <90)
- Requires inotropes
- Requires CPAP/BiPAP or intubation
- Severe hypoxia (SpO2 <85% despite oxygen)
- Arrhythmias requiring monitoring
- Not responding to initial therapy
Admit to Cardiology Ward If:
- Responding to therapy
- Stable on oxygen/CPAP
- Needs further investigation (echo, angiography)
- Requires optimization of medications
Discharge Criteria (Rare in Acute Phase):
- Complete resolution of symptoms
- SpO2 >94% on room air
- Normal respiratory rate (<20/min)
- Stable BP and HR
- Clear plan for follow-up
- Patient/family understands warning signs
Follow-Up:
- Cardiology clinic: Within 1-2 weeks
- Echocardiogram: Within 48 hours if not done
- Medication review: Optimize ACE inhibitor, beta-blocker, diuretics
- Education: Diet, fluid restriction, medication adherence, warning signs
Immediate (Minutes-Hours)
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Respiratory failure | 20-30% | SpO2 <85%, exhaustion, rising CO2 | Intubation + mechanical ventilation |
| Cardiogenic shock | 5-10% | SBP <90, cool extremities, reduced urine output | Inotropes, consider mechanical support |
| Arrhythmias | 15-25% | VT, VF, AF, bradycardia | DC cardioversion (if unstable), antiarrhythmics |
| Cardiac arrest | 2-5% | Loss of consciousness, no pulse | CPR, reversible causes (4Hs, 4Ts) |
| Acute kidney injury | 20-30% | Rising creatinine, reduced urine output | Careful diuresis, avoid nephrotoxins |
Respiratory Failure:
- Mechanism: Severe oedema → complete alveolar flooding → no gas exchange
- Signs: SpO2 <85% despite CPAP, rising CO2, exhaustion
- Management: Intubation + mechanical ventilation
- Prognosis: Poor if requires intubation (mortality 30-40%)
Cardiogenic Shock:
- Mechanism: Severe LV dysfunction → inadequate cardiac output
- Signs: SBP <90, cool extremities, reduced urine output, altered mental status
- Management: Inotropes (dobutamine), consider IABP/ECMO
- Prognosis: Very poor (mortality 50-70%)
Early (Days)
1. Acute Kidney Injury (20-30%)
- Cause: Reduced renal perfusion + diuretic-induced volume depletion
- Risk factors: Pre-existing CKD, high diuretic doses, low BP
- Management: Careful diuresis, monitor U&Es daily, may need to reduce diuretics
- Prevention: Avoid over-diuresis, maintain adequate BP
2. Electrolyte Imbalances
- Hypokalaemia: Diuretic-induced (furosemide)
- Hyponatraemia: Syndrome of inappropriate diuresis or over-diuresis
- Hypomagnesaemia: Diuretic-induced
- Management: Replace electrolytes, monitor daily
3. Thromboembolism
- Deep vein thrombosis: Immobility + hypercoagulable state
- Pulmonary embolism: Can worsen pulmonary oedema
- Management: Prophylactic LMWH if immobile
4. Hospital-Acquired Infections
- Pneumonia: Intubation, immobility
- UTI: Catheterization
- Management: Aseptic technique, early removal of lines/catheters
5. Delirium
- Cause: Hypoxia, medications (morphine), electrolyte imbalances
- Management: Treat underlying cause, avoid sedatives if possible
Late (Weeks-Months)
1. Chronic Heart Failure
- Mechanism: Persistent LV dysfunction despite treatment
- Management: Long-term medications (ACE inhibitor, beta-blocker, diuretics)
- Prognosis: 30-40% 1-year mortality
2. Recurrent Episodes
- Frequency: 30-50% readmission rate at 6 months
- Causes: Non-adherence, dietary indiscretion, progression of disease
- Prevention: Patient education, close follow-up, medication optimization
3. Reduced Quality of Life
- Symptoms: Persistent breathlessness, fatigue, reduced exercise tolerance
- Management: Cardiac rehabilitation, psychological support
- Impact: Significant on daily activities
4. End-Stage Heart Failure
- Progression: Despite optimal medical therapy
- Options: Heart transplantation, LVAD, palliative care
- Timing: Consider when frequent admissions, poor quality of life
Natural History (Without Treatment)
Untreated Acute Pulmonary Oedema:
- Mortality: 50-70% within hours to days
- Cause of death: Respiratory failure, cardiogenic shock, arrhythmias
- Progression: Rapid deterioration → cardiac arrest
- Time course: Death often within 24-48 hours if untreated
Why So Poor?
- Severe hypoxia → multi-organ failure
- Cardiogenic shock → inadequate perfusion
- Arrhythmias → sudden cardiac death
- This is why rapid treatment is critical
Outcomes with Treatment
| Variable | Outcome | Notes |
|---|---|---|
| In-hospital mortality | 5-10% | Improved with rapid treatment |
| 30-day mortality | 10-15% | Higher in elderly, comorbidities |
| 1-year mortality | 30-40% | Reflects underlying heart failure |
| 5-year survival | 30-50% | Depends on cause and treatment |
| Readmission rate (30 days) | 20-25% | Often due to non-adherence |
| Readmission rate (6 months) | 40-50% | High risk of recurrence |
Factors Affecting Outcomes:
Good Prognosis:
- Younger age (<65 years)
- Reversible cause (e.g., acute MI with successful PCI)
- Preserved LVEF (>50% - HFpEF)
- Rapid response to treatment (<2 hours)
- No comorbidities (no CKD, diabetes, etc.)
- Good medication adherence post-discharge
Poor Prognosis:
- Older age (>80 years)
- Severe LV dysfunction (LVEF <30%)
- Multiple comorbidities (CKD, diabetes, COPD)
- Cardiogenic shock at presentation
- Requires intubation (mortality 30-40%)
- Non-adherence to medications
- Recurrent episodes (>2 admissions/year)
Prognostic Factors
Clinical Factors:
| Factor | Impact on Prognosis | Evidence Level |
|---|---|---|
| Age | Each decade increases mortality 1.5x | High |
| LVEF | <30% = 2x mortality vs >0% | High |
| BNP level | >000 pg/mL = worse prognosis | High |
| Renal function | eGFR <30 = 2x mortality | High |
| Blood pressure | Low BP (<90) = worse (shock) | High |
| Response to treatment | Rapid response = better | Moderate |
Laboratory Markers:
| Marker | Prognostic Value | Clinical Use |
|---|---|---|
| BNP/NT-proBNP | Higher = worse prognosis | Monitor trends |
| Troponin | Elevated = worse (myocardial injury) | Assess for MI |
| Creatinine | Higher = worse (renal dysfunction) | Monitor daily |
| Sodium | Lower = worse (hyponatraemia) | Correct if low |
Treatment Response:
| Response Time | Prognosis | Clinical Meaning |
|---|---|---|
| <2 hours | Good | Rapid improvement suggests reversible cause |
| 2-6 hours | Moderate | May need escalation (CPAP, inotropes) |
| > hours | Poor | Suggests severe underlying dysfunction |
Key Guidelines
1. ESC Heart Failure Guidelines (2021) — Comprehensive European guidelines covering acute and chronic heart failure. European Society of Cardiology
Key Recommendations:
- Immediate oxygen therapy if SpO2 <90%
- IV loop diuretics (furosemide 40-80mg) as first-line
- Vasodilators (GTN) if SBP >110 mmHg
- Non-invasive ventilation (CPAP/BiPAP) if respiratory failure
- Echocardiogram within 48 hours
- Evidence Level: 1A (Strong recommendation, high-quality evidence)
2. NICE Heart Failure Guidelines (2018) — UK national guidelines for diagnosis and management. National Institute for Health and Care Excellence
Key Recommendations:
- BNP/NT-proBNP to confirm diagnosis
- Echocardiogram to assess LV function
- ACE inhibitor or ARB for LVSD
- Beta-blocker for LVSD (once stable)
- Evidence Level: 1A
3. AHA/ACC Heart Failure Guidelines (2022) — US guidelines with comprehensive management algorithms. American Heart Association
Key Recommendations:
- Rapid assessment and treatment (<1 hour)
- Diuretics + vasodilators as first-line
- Consider SGLT2 inhibitors (dapagliflozin, empagliflozin) for chronic management
- Evidence Level: 1A
Landmark Trials
ADHERE Registry (2005) — Acute Decompensated Heart Failure National Registry
- Patients: 105,000+ patients with acute heart failure
- Key Finding: In-hospital mortality 4.2% overall; higher with low BP, high BUN, low sodium
- Clinical Impact: Identified risk factors for poor outcomes; led to risk stratification tools
- PMID: 15753268
EVEREST Trial (2007) — Efficacy of Vasopressin Antagonism in Heart Failure
- Patients: 4,133 patients with acute heart failure
- Intervention: Tolvaptan (vasopressin antagonist) vs. placebo
- Key Finding: Improved symptoms but no mortality benefit
- Clinical Impact: Established role of vasopressin antagonists for hyponatraemia
- PMID: 17452608
ASCEND-HF Trial (2011) — Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure
- Patients: 7,141 patients with acute heart failure
- Intervention: Nesiritide (BNP analogue) vs. placebo
- Key Finding: No mortality benefit; modest symptom improvement
- Clinical Impact: Limited role for nesiritide; diuretics remain first-line
- PMID: 21179059
RELAX-AHF Trial (2013) — Relaxin in Acute Heart Failure
- Patients: 1,161 patients with acute heart failure
- Intervention: Serelaxin (relaxin hormone) vs. placebo
- Key Finding: Reduced 180-day mortality (hazard ratio 0.63)
- Clinical Impact: Promising but not yet approved; needs further study
- PMID: 23992601
TRUE-AHF Trial (2017) — Trial of Ularitide Efficacy and Safety in Acute Heart Failure
- Patients: 2,157 patients with acute heart failure
- Intervention: Ularitide (natriuretic peptide) vs. placebo
- Key Finding: Improved symptoms but no mortality benefit
- Clinical Impact: Confirmed that symptom improvement doesn't always translate to survival benefit
- PMID: 28177811
Evidence Strength
| Intervention | Level | Key Evidence | Clinical Recommendation |
|---|---|---|---|
| Oxygen therapy | 1A | ESC Guidelines 2021 | Use if SpO2 <90% |
| IV loop diuretics | 1A | Multiple RCTs, guidelines | First-line treatment (40-80mg furosemide) |
| Vasodilators (GTN) | 1B | Observational studies, guidelines | Use if SBP >10 mmHg |
| CPAP/BiPAP | 1B | RCTs showing reduced intubation | Use if SpO2 <90% despite oxygen |
| ACE inhibitors | 1A | Multiple RCTs (SOLVD, CONSENSUS) | Start once stable (chronic management) |
| Beta-blockers | 1A | Multiple RCTs (CIBIS, MERIT-HF) | Start once stable (chronic management) |
| Inotropes | 2B | Limited evidence, guidelines | Use only if cardiogenic shock |
| Morphine | 2C | Expert opinion, limited evidence | Use cautiously if severe distress |
What is Acute Pulmonary Oedema?
Imagine your heart as a water pump that sends blood around your body. When this pump gets weak or blocked, it can't push blood forward properly. Instead, blood backs up like water in a blocked pipe. When this happens, fluid gets pushed into your lungs—the air sacs that should only contain air. This fluid makes it incredibly hard to breathe, like trying to breathe through a wet sponge.
In simple terms: Your lungs fill with fluid instead of air, making breathing nearly impossible without help.
Why does it matter?
Acute pulmonary oedema is a medical emergency. Without quick treatment, you can't get enough oxygen, which can damage your brain, heart, and other organs. People can die within hours if not treated. The good news? With rapid treatment (usually within 15-30 minutes), most people recover and can go home within a few days.
Think of it like this: If your car's engine overheats, you need to stop and fix it immediately. Same with your heart—when it's struggling, you need medical help right away.
How is it treated?
1. Oxygen: You'll get extra oxygen through a mask to help you breathe easier. Sometimes a special machine (CPAP) helps push air into your lungs.
2. Medications to remove fluid: Doctors give you medicine (diuretics) that makes you urinate more, getting rid of the extra fluid in your body. You might pass a lot of urine in the first few hours—this is good! It means the treatment is working.
3. Medications to help your heart: Other medicines relax your blood vessels, making it easier for your heart to pump. These are given through a drip in your arm.
4. Position: Sitting upright helps—gravity pulls fluid away from your lungs, making breathing easier.
The goal: Get the fluid out of your lungs and help your heart pump better, usually within 30-60 minutes.
What to expect
In the Hospital:
- First few hours: You'll be closely monitored. You might need to stay in intensive care if you're very unwell.
- First day: You'll feel much better as the fluid comes off. You'll urinate a lot—this is normal and expected.
- Days 2-3: If you're improving, you'll move to a regular ward. Doctors will do tests (like an ultrasound of your heart) to find out why it happened.
- Going home: Usually after 3-5 days if you're stable. You'll go home with new medications to prevent it happening again.
After Going Home:
- Medications: You'll need to take medicines every day to keep your heart strong and prevent fluid buildup. These are usually lifelong.
- Diet changes: Less salt (salt makes your body hold onto water) and sometimes less fluid.
- Weighing yourself: Daily weighing helps catch problems early—if you gain weight quickly, it might mean fluid is building up again.
- Follow-up: You'll see your doctor regularly to check how you're doing and adjust medications.
Recovery Time:
- Breathlessness: Usually much better within hours of treatment
- Full recovery: 1-2 weeks to feel back to normal
- Long-term: Most people can live normal lives with the right medications
When to seek help
Call 999 (or your emergency number) immediately if:
- You suddenly can't catch your breath
- You're breathing very fast (more than 25 breaths per minute)
- Your lips or fingers turn blue
- You're coughing up pink or frothy sputum
- You feel like you're suffocating
- You can't speak in full sentences
See your doctor urgently if:
- You're gaining weight quickly (more than 2kg in 2-3 days)
- Your ankles or legs are swelling
- You're more breathless than usual, especially when lying flat
- You're waking up at night short of breath
- You're more tired than usual
Remember: Don't wait if you're worried. It's always better to get checked early than to wait until it's an emergency.
Primary Guidelines
-
McDonagh TA, Metra M, Adamo M, 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
-
National Institute for Health and Care Excellence. Chronic heart failure in adults: diagnosis and management. NICE guideline [NG106]. 2018. NICE
-
Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145(18):e895-e1032. PMID: 35363499
Key Trials
-
Fonarow GC, Adams KF Jr, Abraham WT, et al. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA. 2005;293(5):572-580. PMID: 15753268
-
Gheorghiade M, Konstam MA, Burnett JC Jr, et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heart failure: the EVEREST Clinical Status Trials. JAMA. 2007;297(12):1332-1343. PMID: 17452608
-
O'Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med. 2011;365(1):32-43. PMID: 21179059
-
Teerlink JR, Cotter G, Davison BA, et al. Serelaxin, recombinant human relaxin-2, for treatment of acute heart failure (RELAX-AHF): a randomised, placebo-controlled trial. Lancet. 2013;381(9860):29-39. PMID: 23992601
-
Packer M, O'Connor C, McMurray JJV, et al. Effect of ularitide on cardiovascular mortality in acute heart failure. N Engl J Med. 2017;376(20):1956-1964. PMID: 28177811
Systematic Reviews
-
Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database Syst Rev. 2013;(5):CD005351. PMID: 23728654
-
Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797-805. PMID: 21366472
Further Resources
- British Heart Foundation: Heart Failure Information
- American Heart Association: Heart Failure Resources
- ESC Heart Failure Association: Patient Resources
Last Reviewed: 2025-12-25 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists. This information is not a substitute for professional medical advice, diagnosis, or treatment.