💔 Cardiogenic Pulmonary Oedema (CPO) is a medical emergency. Often triggered by STEMI, arrhythmia, or mechanical failure. Always exclude these early. A simple bedside echo is invaluable. Acute pulmonary oedema is usually driven by a sudden rise in left-sided filling pressures (LV failure/acute MR/MI, hypertensive crisis), forcing fluid across the alveolar-capillary membrane. Your early wins are: improve oxygenation/ventilation (CPAP), offload the lungs (diuresis), and reduce preload/afterload (vasodilators) while treating the trigger.

💔 Emergency Management: Cardiogenic Pulmonary Oedema (CPO)
🪑 Position → Sit upright, comfort, legs dependent, reassure, may need catheter 🫁 Oxygen → Maintain sats >92% (88–92% if COPD); CPAP if hypoxic 💧 Diuretics → Furosemide 40–80 mg IV bolus often as 4mg/kg but may need more rapid if in extremis. Diuresis and venodilates 💉 Opiates → Morphine 2.5–5 mg IV slow + antiemetic 💊 Nitrates → GTN spray; IV infusion if SBP >110 mmHg 🫀 Arrhythmias/STEMI → Treat Fast AF (Digoxin, Amiodarone) /VT (Amiodarone or DC shock), urgent PCI if STEMI 🔌 Advanced Support → CPAP 5–10 cmH₂O/NIV, balloon pump, dialysis if needed, Papillary rupture / VSD → balloon pump + urgent surgery

💔 Emergency Management: Cardiogenic Pulmonary Oedema (CPO)

🪑 Position → Sit upright, comfort, legs dependent, reassure, may need catheter
🫁 Oxygen → Maintain sats >92% (88–92% if COPD); CPAP if hypoxic
💧 Diuretics → Furosemide 40–80 mg IV bolus often as 4mg/kg but may need more rapid if in extremis. Diuresis and venodilates
💉 Opiates → Morphine 2.5–5 mg IV slow + antiemetic
💊 Nitrates → GTN spray; IV infusion if SBP >110 mmHg
🫀 Arrhythmias/STEMI → Treat Fast AF (Digoxin, Amiodarone) /VT (Amiodarone or DC shock), urgent PCI if STEMI
🔌 Advanced Support → CPAP 5–10 cmH₂O/NIV, balloon pump, dialysis if needed, Papillary rupture / VSD → balloon pump + urgent surgery

💡 Mnemonic: sit up and FONAM = Furosemide, Oxygen Nitrates Arrhythmia Morphine,

📖 About

CPO = acute left ventricular dysfunction → pulmonary venous hypertension → alveolar flooding.
Rapidly leads to respiratory failure ± cardiogenic shock.
30-day mortality ~15% if NT-proBNP >5000 ng/L.
LV systolic function strongly influences prognosis.

⚖️ Pathophysiology

Normally: Plasma oncotic pressure (~25 mmHg) holds water in; Pulmonary capillary pressure (~7–12 mmHg) pushes fluid out.
If PCP > POP → alveolar oedema → hypoxia, ↑ work of breathing.

🔎 Aetiology

Poor systolic function (e.g. MI).
Poor diastolic function (HFpEF).
Valve lesions (MR, AR, AS).
Arrhythmias (AF, VT, bradycardia).
Hypertension, myocarditis, cardiomyopathy.
Fluid overload (blood transfusion, renal failure).

❓ Precipitating Causes

Cause	Clues	Diagnostics
MI	Chest pain, diaphoresis	ECG, troponin, echo
AF	Palpitations, irregular pulse	ECG, echo
HTN	Headache, chest pain	BP, LVH on echo
Valvular disease	Murmur, dyspnoea	Echo, Doppler
PE	Pleuritic pain, haemoptysis	CTPA, D-dimer
Sepsis	Fever, hypotension	Blood cultures, lactate
Drug/alcohol	Recent change	Medication review

📊 Clinical: Left vs Right HF

The patient may be grey cold clammy and dramatically breathless and struggling to breath with a tachycardia and S3 and possibly murmurs, there is a raised JVP and lungs have fine inspiratory crackles. The sats may be low. Urgent management is needed.

Left-sided: Tachypnoea, Tachycardia, S3, Murmurs, Orthopnoea, PND, bibasal creps, “bat-wing” CXR.
Right-sided: Raised JVP, hepatomegaly, ascites, oedema.
Often coexist → congestive HF.

🧪 Investigations (Acute Cardiogenic Pulmonary Oedema)

Bedside (immediate):
- Vitals + monitoring: RR, BP, HR, temperature, continuous SpO₂ + ECG monitoring.
- ECG (12-lead): look for ACS (ST/T changes), arrhythmia (AF, VT), LVH/strain, conduction disease.
- ABG/VBG: pO₂/pCO₂, pH, HCO₃⁻; identify hypercapnia/tiring (important for NIV/ITU decisions).
- Lactate: marker of hypoperfusion/shock and severity.
- Glucose: especially if diabetic/altered mental state.
- Urine output: catheter if severe illness; helps gauge diuretic response and perfusion.
Bloods:
- FBC: anaemia (reduces oxygen delivery), leukocytosis (infection trigger).
- U&E/creatinine: baseline renal function, K⁺/Na⁺ before diuresis/ACEi; guides dosing and safety.
- LFTs: hepatic congestion or hypoperfusion (“shock liver”).
- Troponin: MI/ischemia trigger (interpret in context; may be type 2 rise in severe HF).
- NT-proBNP: supports HF diagnosis if uncertain (less helpful if obvious clinically or known HF).
- CRP: if infection suspected; blood cultures before antibiotics if septic.
- TFTs: not urgent in resus, but useful if AF/new HF or unexplained decompensation.
- Mg/Ca/phosphate: if arrhythmia or on diuretics (electrolytes drive ectopy and rate control success).
Imaging:
- CXR: cardiomegaly, upper lobe diversion, interstitial oedema (Kerley B lines), perihilar “bat-wing” shadowing, pleural effusions; also exclude pneumonia/pneumothorax.
- Point-of-care ultrasound (if available): lung B-lines, pleural effusions, IVC size; rapid bedside support for congestion.
- Echocardiography (urgent if severe/unclear): LV/RV function, regional wall motion (ischaemia), valve lesions (acute MR/AS), pericardial effusion/tamponade, pulmonary pressures.
Advanced / specialist tests (selected cases, not acute resus):
- CT pulmonary angiography: if PE is a realistic alternative/trigger (especially if disproportionate hypoxia, RV strain).
- Coronary angiography: if STEMI/NSTEMI or ongoing ischaemia driving ACPO (cardiology pathway).
- Cardiac MRI: myocarditis/infiltrative disease/scar assessment once stabilised.
- Nuclear imaging (SPECT/PET): viability/ischaemia assessment in chronic planning rather than acute management.

⚡ Complications

Respiratory failure:
- Type 1 (hypoxaemic): alveolar flooding + V/Q mismatch → low pO₂.
- Progression to Type 2 (hypercapnic): fatigue, reduced minute ventilation, worsening alveolar ventilation (red flag for NIV failure/ITU).
Cardiac complications:
- Arrhythmias: AF with fast rate (worsens filling), VT/VF, bradyarrhythmias; risk of sudden cardiac death.
- Myocardial ischaemia/infarction: ACPO can be both a cause and consequence of ACS (type 1 vs demand-mediated injury).
- Cardiogenic shock: “cold + wet” phenotype with hypoperfusion, rising lactate, oliguria.
Renal dysfunction:
- AKI / cardiorenal syndrome: low forward flow + venous congestion + diuretics/ACEi exposure → creatinine rise and diuretic resistance.
Hepatic and splanchnic congestion:
- Congestive hepatopathy: cholestatic LFT pattern; can progress to marked transaminitis if hypoperfusion (“shock liver”).
- Gut oedema: impaired drug absorption (e.g., oral diuretics) and malnutrition.
Electrolyte and acid–base problems:
- Hyponatraemia: dilutional (ADH-driven) and a marker of severe HF; worsens confusion/falls risk.
- Hypokalaemia / hypomagnesaemia: diuretics → ectopy/VT risk and digoxin toxicity risk.
- Hyperkalaemia: renal impairment + RAAS blockade; conduction disturbance risk.
- Metabolic alkalosis: aggressive diuresis; may worsen CO₂ retention in vulnerable patients.
Thromboembolism:
- VTE: immobility, inflammation and haemoconcentration; consider prophylaxis if safe.
- Stroke/systemic embolism: especially if AF or severe LV dysfunction with thrombus.
Functional decline and vulnerability:
- Delirium: hypoxia, infection, metabolic disturbance, opioids.
- Frailty, sarcopenia/cachexia: chronic catabolism + inflammation; strongly predicts readmission and mortality.
- Pressure injury/falls: immobility, hypotension, polypharmacy.

💊 Management

Call for help + monitor: Sit upright, continuous ECG, BP, SpO₂, RR; IV access; strict fluid balance + urine output (catheter if very unwell).
Immediate investigations: ABG/VBG (± lactate), U&E/creatinine, FBC, troponin, glucose; CXR; ECG; bedside echo if available (LV function, MR, tamponade, RV strain).
Oxygen strategy:
- Give O₂ only if hypoxic. Aim SpO₂ 94–98% (or 88–92% if known CO₂ retention).
- Early CPAP/NIV if severe distress/hypoxia despite O₂ (often rapidly reduces work of breathing and improves gas exchange).
- Escalate to CCU/ICU/anaesthetics early if tiring, reduced consciousness, or NIV failing.
Diuretics (decongestion):
- IV loop diuretic (e.g., furosemide 40 mg, 50 mg or 80 mg are all fine as needed or bumetanide 1-2 mg).
- Use higher doses if already on regular diuretics.
- Reassess response (symptoms, RR, crackles, urine output) and check renal function/electrolytes; consider infusion if poor response.
Vasodilators (reduce preload/afterload):
- If SBP ≥ 110 mmHg and ongoing distress, consider GTN (sublingual or IV infusion) to rapidly reduce pulmonary capillary pressure.
- Avoid if hypotensive, severe aortic stenosis, or suspected RV infarct.
Analgesia/anxiolysis:
- Avoid routine morphine; if used, do so cautiously (risk of respiratory depression/hypotension) and treat nausea.
If shock/poor perfusion (cold + wet):
- Urgent senior/ICU input; consider inotropes/vasopressors (e.g., dobutamine ± noradrenaline) guided by echo/BP/perfusion.
- Look hard for reversible causes: MI, acute MR, arrhythmia, tamponade, massive PE.
Treat the trigger (do not miss):
- ACS/MI: follow local ACS pathway; early cardiology review and reperfusion if indicated.
- Hypertensive ACPO: nitrates + CPAP are often key.
- Arrhythmia (AF with fast rate, VT): rate/rhythm control; urgent DC cardioversion if unstable.
- Acute valvular disease (e.g., acute MR): urgent echo + cardiothoracic/cardiology input.
- Fluid overload/renal failure: consider ultrafiltration/dialysis discussion if diuretic-resistant.
When improving (transition to chronic HF care):
- Start/optimise disease-modifying therapy once stable: ACEi/ARB/ARNI, beta-blocker, MRA, and consider SGLT2 inhibitor where appropriate (per local/NICE guidance).
- Plan follow-up, education (daily weights, salt/fluids), and review precipitant + adherence.
Advanced/definitive options (selected patients): CRT, ICD, LVAD, transplant (specialist pathways).

✅ Quick practical timing prompts

0–10 minutes: Sit up, monitoring, ABG/VBG, CPAP/NIV early if needed; if SBP ≥110, start GTN (SL then IV).
10–60 minutes: IV loop diuretic if congested; reassess BP/respiratory effort every 5–15 min; ECG/CXR; start ACS/arrhythmia pathway if indicated.
1–6 hours: Review urine output, repeat gases if severe, check U&E/K/Mg; consider escalation (infusions, inotropes, ICU) or specialist add-ons (metolazone/ultrafiltration) if resistant.

💊 Drug Table

Drug	When to use	Typical dose	Timing / titration	Key cautions
GTN (glyceryl trinitrate) – sublingual spray/tablet	Severe dyspnoea with SBP ≥110 mmHg, especially hypertensive ACPO, while preparing IV infusion	400 micrograms (1 spray) SL	Repeat every 5 minutes as needed while monitoring BP (commonly up to 3 doses)	Avoid/very cautious in hypotension, severe aortic stenosis, suspected RV infarct, recent PDE5 inhibitors
GTN – IV infusion	Ongoing distress despite oxygen/NIV, hypertensive pulmonary oedema	Start 5–10 micrograms/min	Increase by 5–10 micrograms/min every 3–5 min to symptom relief/BP target (often 20–200 micrograms/min; higher in monitored/ICU settings)	Continuous BP monitoring; stop/reduce if SBP falls or headache/hypotension develops
Furosemide – IV bolus	Clinical fluid overload, raised JVP/oedema, or known HF with congestion	40 mg IV (if diuretic-naïve). If already on loop diuretic: same as or up to 2× their usual total daily oral dose as IV equivalent (senior-led)	Assess urine output and symptoms at 30–60 min. Consider repeat dosing if inadequate response	Can worsen hypotension/AKI; check U&E, watch K/Mg; avoid “diuretic-first” if profoundly hypertensive distress where nitrates/NIV are the rapid wins
Bumetanide – IV bolus	Alternative loop diuretic (e.g., poor response to furosemide, significant gut oedema, or local preference)	1 mg IV (roughly ≈ furosemide 40 mg)	Reassess at 30–60 min; repeat/step up guided by response	Same cautions as loop diuretics; electrolyte depletion
Loop diuretic infusion (e.g., furosemide)	Diuretic resistance or repeated boluses needed; ICU/CCU-style pathway	Common approach: loading bolus then 5–10 mg/hour (ranges vary)	Titrate every 1–2 hours to urine output/clinical congestion; close U&E monitoring	Requires careful monitoring; risk of AKI, ototoxicity at very high doses/rapid pushes; senior-led
Morphine – IV (NOT routine)	Only if severe distress/pain/anxiety persists despite NIV and haemodynamic stabilisation, and senior agrees	1–2 mg IV slow, small aliquots	Reassess after 5–10 min; repeat cautiously if needed	Respiratory depression, hypotension, nausea/vomiting; avoid if drowsy/CO₂ retaining/hypotensive
Antiemetic (e.g., ondansetron)	If opioid used or significant nausea/vomiting	4 mg IV	Single dose; reassess	QT prolongation risk (check ECG if concerns)
Dobutamine – IV infusion	Cold + wet (hypoperfusion/shock) with low cardiac output, typically ICU/CCU after echo/senior review	Start 2.5 micrograms/kg/min	Titrate every 10–20 min (typical range 2.5–20 micrograms/kg/min) to perfusion/BP/urine output	Arrhythmias, tachycardia, myocardial ischaemia; needs monitoring and clear diagnosis
Noradrenaline (norepinephrine) – IV infusion	Hypotension/shock to maintain perfusion pressure (often alongside inotrope), ICU pathway	Common starting range 0.05 micrograms/kg/min (local protocols vary)	Titrate every 2–5 min to MAP/BP target	Extravasation risk; ideally central access; treat the cause (MI, MR, tamponade etc.)
Nitroprusside – IV infusion (specialist)	Refractory hypertensive ACPO with severe afterload problem (ICU/CCU only)	Start 0.3 micrograms/kg/min	Titrate every 3–5 min (typical max ~10 micrograms/kg/min short term)	Cyanide/thiocyanate toxicity risk, hypotension; requires invasive monitoring
ACE inhibitor (e.g., captopril – oral) (selected cases)	After initial stabilisation, persistent hypertension with HF once not in shock and no contraindications	6.25 mg PO	Can repeat/uptitrate cautiously after 30–60 min with BP monitoring (senior-led)	Avoid in hypotension, AKI, hyperkalaemia, bilateral RAS, pregnancy; not a “first 10 minutes” drug

⚡ Additional interventions

Trigger / scenario	Drug(s)	Typical dose	Timing / titration	Key cautions / notes
Suspected ACS / MI	Aspirin	300 mg PO (chewed) if not already taken	Give immediately once ACS suspected (per ACS pathway)	Contra: true aspirin allergy, active major bleeding
Suspected ACS / MI	P2Y12 inhibitor (specialist pathway)	Common UK practice: Ticagrelor 180 mg PO loading or Clopidogrel 300–600 mg PO loading (varies by STEMI/NSTEMI pathway)	As per local cardiology/PCI pathway (often after ECG confirmation and discussion)	Bleeding risk; avoid if urgent surgery likely; follow trust protocol
Suspected ACS / ongoing ischaemic pain	GTN (as per core table)	SL 400 micrograms q5 min PRN; IV start 5–10 micrograms/min	Titrate every 3–5 min to pain relief/BP	Avoid in hypotension, severe AS, RV infarct, recent PDE5 inhibitors
AF with fast ventricular response (haemodynamically stable)	Digoxin (rate control in HF)	500 micrograms IV (or PO) then 250 micrograms at 6 hours and again at 12 hours (max 1.0–1.5 mg in 24 h depending on age/renal function)	Slower onset; reassess rate and symptoms over hours	Reduce dose in elderly/renal impairment; toxicity risk (arrhythmias, GI, confusion); check K/Mg
AF with fast rate (stable, BP ok)	Amiodarone (rhythm control / rate control alternative)	300 mg IV over 20–60 min, then infusion 900 mg over 24 h	Use when appropriate (often senior-led/cardiology)	Hypotension/bradycardia; interacts with warfarin/digoxin; needs ECG monitoring
Unstable tachyarrhythmia (AF/VT with hypotension, ischaemia, pulmonary oedema)	DC cardioversion	Energy per ALS protocol (biphasic escalating)	Immediate	Not a drug, but the correct “dose” is electricity; involve resus/anaesthetics
VT / Electrical storm (with ACPO)	Amiodarone	300 mg IV over 20–60 min (can repeat per ALS), then 900 mg/24 h	Early, alongside correction of K/Mg and ischaemia treatment	Consider magnesium; urgent cardiology/ICU for recurrent VT/VF
Torsades / hypomagnesaemia	Magnesium sulfate	2 g IV (8 mmol) over 10–15 min	May repeat once if needed; then consider infusion per protocol	Monitor reflexes/respiration in renal failure; correct K as well
Hypertensive emergency driving ACPO	GTN IV (first-line add-on)	Start 5–10 micrograms/min, titrate rapidly	Increase every 3–5 min to symptom/BP response	Often the “fastest fix” with CPAP; avoid if severe AS/RV infarct/hypotension
Acute severe mitral regurgitation (papillary muscle dysfunction/rupture, endocarditis etc.)	Vasodilator (GTN) ± inotrope (dobutamine)	GTN as above; dobutamine start 2.5 micrograms/kg/min	Titrate GTN every 3–5 min; dobutamine every 10–20 min	Needs urgent echo + cardiology/cardiothoracic; may require mechanical support/urgent surgery
Suspected sepsis/pneumonia precipitant	Antibiotics (per local guideline)	Depends on source and severity	Give within 1 hour if sepsis suspected	Fluid resuscitation must be cautious in ACPO—senior review; use vasopressors if shock rather than large fluids
Thromboembolism risk / immobility	VTE prophylaxis (if no contraindication)	Example: Enoxaparin 40 mg SC OD (adjust for renal function/weight)	Once stable and bleeding risk assessed	Follow local VTE policy; avoid if active bleeding/very high risk
Fluid overload + renal failure / diuretic resistance	Metolazone (specialist add-on)	2.5 mg PO	Often single dose, reassess over 6–12 h; may repeat cautiously (senior-led)	Profound diuresis/hypoNa/hypoK; close U&E monitoring; usually HF specialist decision
Persistent congestion despite loops	Chlorothiazide IV (less common UK) / thiazide-type add-on	Varies by local availability	Specialist/ICU pathway	Electrolyte depletion; monitor Na/K/Mg closely
After stabilisation: start disease-modifying HF therapy	ACEi/ARB/ARNI; beta-blocker; MRA; SGLT2 inhibitor	Start low (agent-specific) once euvolaemic and BP/renal function acceptable	Usually on the ward once off IV nitrates/inotropes and not in AKI	Not “resus drugs”; avoid initiating/up-titrating beta-blocker during acute decompensation/shock

📉 Prognosis

HF prognosis worse than many cancers.
EF <35% = poor marker.
NT-proBNP correlates with survival.
Consider palliative care in end-stage disease.

📚 References

Cases - Acute Heart Failure & Pulmonary Oedema

Case 1 - Hypertensive Emergency 💥: A 72-year-old man with untreated hypertension presents acutely breathless at night, unable to lie flat. Exam: BP 210/110, tachypnoea, widespread crackles, S3 gallop. CXR: bilateral perihilar “bat-wing” shadowing. Diagnosis: Acute pulmonary oedema triggered by hypertensive crisis. Acute Management: Sit upright, oxygen, IV furosemide, IV GTN infusion, morphine if distressed, strict BP control. Monitor U&Es and fluid balance.
Case 2 - Acute MI Complication ❤️: A 64-year-old man presents with acute chest pain followed by severe dyspnoea. Exam: hypotension, crackles to mid-zones, raised JVP, cool peripheries. ECG: anterior STEMI. Echo: severe LV systolic dysfunction. Diagnosis: Acute cardiogenic pulmonary oedema secondary to MI. Acute Management: Sit upright, O₂, IV diuretics, cautious opioids; urgent PCI for MI; inotropes or mechanical support (IABP) if shock persists.
Case 3 - Acute Decompensation in Chronic HF 🌀: A 78-year-old woman with known HFrEF (EF 30%) presents with sudden worsening breathlessness after a chest infection. Exam: tachypnoeic, bibasal crackles, elevated JVP, peripheral oedema. BNP elevated, CXR: pulmonary congestion. Diagnosis: Acute decompensated heart failure with pulmonary oedema, triggered by infection. Acute Management: Sit upright, O₂, IV furosemide; treat infection (antibiotics); optimise chronic therapy (ACEi, beta-blocker, spironolactone) once stable.

Teaching Commentary 🧠

Acute heart failure with pulmonary oedema is a medical emergency. - Pathophysiology: raised LV end-diastolic pressure → pulmonary venous congestion → alveolar fluid → hypoxia. - Precipitants: MI, arrhythmias, hypertensive crisis, infection, fluid overload, non-compliance. - Clinical: severe breathlessness, orthopnoea, crackles, frothy pink sputum, gallop rhythm. - Acute management (“PODMAN”): Position upright, Oxygen, Diuretics (IV loop), Morphine, Afterload reduction (nitrates), Non-invasive ventilation if hypoxic. Long-term: optimise HF therapy (ACEi/ARNI, beta-blockers, MRA, SGLT2 inhibitors); lifestyle and fluid restriction; device therapy (CRT, ICD) in select patients.

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Acute Cardiogenic Pulmonary Oedema (CPO/LVF) ❤️