Level 2 of 6Must-remember

Acute heart failure and pulmonary oedema

Assess, manage and stay safe — enough on its own

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The card — assess, manage, caution

Assessment— look, ask, measure

Recognise the patient from the doorway: sitting bolt upright or leaning forward, sweating, grey or cyanosed, using accessory muscles, tachypnoeic and frightened. Acute cardiogenic pulmonary oedema is defined clinically by tachypnoea, orthopnoea, bilateral inspiratory crackles, an oxygen saturation below 90% breathing air, and pulmonary oedema on the chest radiograph.
Name which of the six syndromes is in front of you before choosing a drug: acute decompensated heart failure; hypertensive (flash) oedema with systolic often > 180 mmHg; acute pulmonary oedema; cardiogenic shock; high-output failure with warm peripheries and a wide pulse pressure; and isolated right heart failure with a raised JVP and clear lung fields.
The cardinal symptom is breathlessness, and its qualifiers are diagnostic. Orthopnoea — quantified by pillows, or by an admission that the patient has been sleeping in a chair. Paroxysmal nocturnal dyspnoea — waking two hours into sleep gasping and going to an open window. A patient who lies flat comfortably almost certainly does not have frank pulmonary oedema.
Other symptoms: cough, sometimes with pink frothy sputum, fatigue, ankle or abdominal swelling, weight gain, nocturia, and — with right-sided congestion — anorexia, nausea and right upper quadrant discomfort. Chest pain may indicate a precipitating acute coronary syndrome; its absence does not exclude one.
Respiratory signs: bilateral inspiratory crackles, classically basal and rising as oedema worsens. Wheeze and rhonchi are common — cardiac asthma, from bronchial mucosal congestion — and are a frequent source of misdiagnosis as asthma or COPD. Basal dullness with reduced breath sounds means pleural effusions, usually bilateral.
Cardiovascular signs establish that the wet lung is the heart's fault. A raised jugular venous pressure is the key sign: examine at 45 degrees, measure the height of the venous column above the sternal angle in centimetres and add 5 to give the pressure in cmH2O; 8 cmH2O or less is normal. Where equivocal, elicit the hepatojugular reflux — firm continuous pressure over the liver for 15–30 seconds while the patient breathes normally and does not strain; a sustained rise of more than 1 cm correlates with an elevated wedge pressure.
Add a third heart sound (S3) gallop, strong evidence of raised filling pressures; pulsus alternans; a displaced, sustained apex beat; and any murmur, particularly a new pansystolic one.
Separate congestion from hypoperfusion, because that is what chooses the drug. Congestion: dependent pitting oedema of the ankles or sacrum, tender hepatomegaly, ascites. Hypoperfusion: cold, mottled peripheries with prolonged capillary refill, narrow pulse pressure, urine output below 0.5 mL/kg/hour, confusion, rising lactate.
Red flags — immediate risk of death: systolic BP below 90 mmHg (or a fall in mean arterial pressure > 30 mmHg) with cold peripheries; lactate above 2 mmol/L with cold peripheries even when the pressure looks acceptable — occult shock; urine output below 0.5 mL/kg/hour; new confusion; SpO2 persistently below 90% despite high-flow oxygen and adequate non-invasive ventilation; ST elevation, new left bundle branch block or ongoing ischaemic pain; a new loud pansystolic murmur with abrupt deterioration; and any sustained arrhythmia or heart block driving the failure.
The most treacherous sign is a respiratory rate that begins to fall in a previously tachypnoeic patient, with rising PaCO2, falling pH and drowsiness — exhaustion, not improvement, immediately preceding respiratory arrest.
Ask what has changed in the last week where chronic failure is established: non-adherence or tablets running out, dietary salt, ischaemia, tachyarrhythmia, infection, anaemia, thyrotoxicosis, alcohol — and the iatrogenic causes, worth memorising because they are preventable: NSAIDs, verapamil and diltiazem, thiazolidinediones, corticosteroids, beta-blockers up-titrated too fast, excessive intravenous fluid, intravenous sodium bicarbonate, and transfusion given too rapidly.
A chronic heart-failure patient may have a quiet chest despite severe congestion. Lymphatic adaptation allows pulmonary venous pressure to exceed 30 mmHg before alveolar flooding, and crackles may be entirely absent — the commonest diagnostic error in the condition is dismissing pulmonary oedema because the chest sounds clear. The history — orthopnoea, a night spent in a chair, 3 kg gained in four days — outranks auscultation.
The elderly present with confusion, functional decline, falls or simply being off legs; fatigue may dominate over breathlessness, silent infarction is common, and coexistent lung disease, obesity, anaemia and renal impairment confound every sign and biomarker.
Infants and children present differently again: feeding difficulty — sweating during feeds, taking longer than about 20 minutes, breaking off to breathe — poor weight gain, tachypnoea, grunting, recession and irritability, not orthopnoea. The most reliable sign of congestion in an infant is hepatomegaly (a liver edge more than 2 cm below the costal margin, or one enlarging on serial examination); the JVP is unusable below about five years, and crackles are frequently absent even in a very wet child.
The paediatric differential is not the adult one: in the neonate a duct-dependent congenital lesion (coarctation, interrupted arch, critical aortic stenosis, hypoplastic left heart), suggested by collapse in the first weeks with weak femoral pulses or a pre-ductal/post-ductal saturation gap; later viral myocarditis, supraventricular tachycardia (above 220/min in infants, above 180/min in children), rheumatic carditis, severe anaemia, post-streptococcal glomerulonephritis and sepsis.
A raised JVP with clear lung fields and hypotension is not left heart failure — think right ventricular infarction (inferior ECG changes; preload-dependent), pulmonary embolism or cardiac tamponade. All are worsened by nitrates and diuretics.
Investigate in parallel with treatment, never before it: 12-lead ECG within 10 minutes (a completely normal ECG makes acute heart failure considerably less likely), sitting chest radiograph, arterial blood gas, natriuretic peptides, troponin, urea and electrolytes with magnesium and full blood count, and echocardiography — urgent where the answer changes management now.Not available at your setup — Arterial blood gas, Cardiac troponin, Ultrasound.

Management— do this, in order

Treat and investigate simultaneously, and let the blood pressure and the peripheral perfusion — not the crackles — choose the drug. Two patients may have identical wet lungs, one needing a vasodilator and the other a vasopressor, and giving the wrong one is lethal. Reassess at every review, because the category can change.
Sit the patient upright with the legs dependent. This facilitates respiration and reduces venous return, works within seconds and costs nothing. Patients with frank oedema should not be laid flat — not for a radiograph, not for a line.
Oxygen: high flow immediately to the hypoxaemic patient, then titrate. Published targets are an inspired oxygen concentration of 35–50% with a saturation of 95–98%, a PaO2 above 60 mmHg (8 kPa), and in shock SpO2 92–95%; in practice titrate to 94–98%, or 88–92% in a confirmed carbon dioxide retainer. Oxygen is not indicated in the non-hypoxaemic patient, in whom hyperoxia causes vasoconstriction — but hypoxia kills faster than hypercapnia, so it is never withheld from a hypoxaemic patient with chronic lung disease.
Establish continuous oximetry and cardiac monitoring, frequent blood pressure measurement, two large-bore cannulae, and urinary catheterisation with hourly measurement.
Ventilatory support for the patient failing to maintain saturation on high-flow oxygen, with a respiratory rate persistently above about 25/min, or visibly tiring. CPAP or bilevel non-invasive ventilation increases pulmonary recruitment and functional residual capacity, reduces the work of breathing, and decreases both preload and afterload. Begin at 5 cmH2O and titrate to about 10 cmH2O with the highest available inspired oxygen fraction. Set a time limit before the mask goes on: if respiratory rate, saturation, pH and PaCO2 are not improving within about 30 minutes, the patient needs intubation.Doctor / NurseNot available at your setup — Mechanical ventilator.
Pathway A — adequate perfusion, systolic BP ≥ 100 mmHg (wet and warm). Nitrates first. Sublingual glyceryl trinitrate 0.4 mg (one 400 microgram spray or tablet) repeated every 5 minutes for up to three doses, checking the blood pressure before each repeat and stopping below a systolic of 100 mmHg. Nitrates ameliorate dyspnoea rapidly, before the onset of diuresis. If breathlessness persists, or with concomitant ischaemia or severe hypertension, an intravenous infusion of 10–200 micrograms/minute, increasing by 10–20 micrograms/minute every 5 minutes and keeping the systolic pressure above 85–90 mmHg. Isosorbide dinitrate 5 mg sublingually is an alternative; transdermal patches have no place.Doctor / Nurse
Loop diuretic: furosemide 40–80 mg by slow intravenous injection (published range 40–100 mg as a bolus, or an infusion of 5–40 mg/hour), or bumetanide 1 mg intravenously (1 mg is roughly equivalent to 40 mg furosemide). It is usually indicated even without prior fluid retention, because these agents venodilate and lower wedge pressure before the onset of diuresis. Dose to the patient, not to the textbook: a patient already on a loop diuretic should receive at least their total daily oral dose intravenously, and up to 2.5 times it. Monitor sodium, potassium and creatinine.Doctor / NurseNot available at your setup — Serum electrolytes.
Pathway B — hypertensive (flash) oedema is an afterload problem, and a large diuretic dose is the characteristic error, because these patients are often not volume-overloaded. Treat with sublingual then intravenous glyceryl trinitrate titrated more aggressively, furosemide 40 mg intravenously or none where there is no evidence of overload, and early non-invasive ventilation, which frequently works faster than any injectable agent. Sodium nitroprusside 0.3–5 micrograms/kg/minute is the textbook agent where afterload predominates, but it needs invasive arterial pressure monitoring and risks cyanide accumulation. Reduce mean arterial pressure by no more than about 25% in the first hour unless there is concurrent ischaemia or dissection.Doctor
Pathway C — cardiogenic shock (wet and cold): withhold nitrates and, initially, diuretics. Both will lower the pressure further and convert survivable shock into oliguric death.
Assess volume before assuming overload. Where the JVP is not raised and the chest is clear — suggesting concomitant hypovolaemia or right ventricular infarction — give 250 mL of balanced crystalloid or 0.9% sodium chloride over 10 minutes, then re-examine the JVP and chest before repeating. A routine 500–1000 mL bolus has no place in heart failure.
Noradrenaline is the first-line vasopressor: 0.1–0.5 micrograms/kg/minute (a working range up to 1.0 microgram/kg/minute is quoted), titrated to a mean arterial pressure of 65 mmHg or above, a warming periphery and rising urine output. Central administration is preferred; peripherally, use the largest, most proximal cannula and inspect the site frequently, because extravasation causes tissue necrosis.Doctor / NurseNot available at your setup — Infusion pump.
Dobutamine is the first-line inotrope where pump failure dominates: 2–20 micrograms/kg/minute, with the upper end often needed in patients on a beta-blocker; in frank shock it is given with noradrenaline, not instead of it. Adrenaline 0.05–0.5 micrograms/kg/minute is an alternative where bradycardia or peri-arrest physiology dominates. Only once the systolic pressure is restored above 90 mmHg and the periphery is warming should the loop diuretic be given.Doctor / NurseNot available at your setup — Infusion pump.
Morphine is not a routine treatment but has a place in the genuinely distressed or pain-driven patient, at the smallest useful dose with naloxone available: 2–8 mg intravenously initially, repeated after 2–4 hours, or 2.5–5 mg by slow intravenous injection with metoclopramide 10 mg intravenously. In opioid-induced oedema treat with naloxone 400 micrograms intravenously, repeated.Doctor / Nurse
Treat the precipitant. Rate and rhythm: rapid atrial fibrillation is a common driver and may require emergency synchronised cardioversion in the peri-arrest patient. Beta-blockers, verapamil and diltiazem should be avoided in acute decompensation because of their negative inotropy. Digoxin 0.5 mg intravenously over at least 30 minutes, repeated after 2–6 hours (total loading 1–1.5 mg over 24 hours) slows atrioventricular conduction without negative inotropy; check the potassium first and avoid it in acute coronary syndrome. Amiodarone 300 mg intravenously over 20–60 minutes into a large vein is the alternative.DoctorNot available at your setup — Defibrillator.
Reperfusion: where acute heart failure or cardiogenic shock complicates ST-elevation myocardial infarction, immediate revascularisation has the greatest single effect on survival, and should not be delayed for haemodynamic stabilisation.Doctor
Thromboprophylaxis for all, unless contraindicated: enoxaparin 40 mg subcutaneously daily, reduced or replaced by unfractionated heparin 5000 units subcutaneously 12-hourly if creatinine clearance is below 30 mL/min; treatment dosing (1 mg/kg twice daily) where a concurrent acute coronary syndrome or atrial fibrillation requires it. Correct infection, acidaemia, anaemia and electrolyte depletion at the same time as the oedema.Doctor / Nurse
When first-line treatment fails: convert bolus diuretic to infusion, or add sequential nephron blockade with metolazone 2.5–10 mg orally daily; escalate ventilatory support; and consider renal replacement therapy or ultrafiltration for refractory volume overload, metabolic acidosis (pH around 7.15–7.25 or lower), refractory hypoxaemia and persistent hyperkalaemia. A patient who has received large cumulative doses of loop diuretic and passed almost no urine needs renal replacement, not another dose.DoctorNot available at your setup — Dialysis / renal replacement.
Paediatric. Target SpO2 94–98%, but in known cyanotic congenital heart disease target the child's documented baseline. Furosemide 1 mg/kg by slow intravenous injection (maximum 2 mg/kg per dose), repeated 6–12-hourly according to urine output. Fluid challenge in suspected cardiogenic shock: 5–10 mL/kg over 15–20 minutes, then re-examine liver edge, chest and heart rate — never 20 mL/kg. Dobutamine 5–20 micrograms/kg/minute is the usual first-line inotrope; adrenaline 0.05–0.5 micrograms/kg/minute is often preferred to noradrenaline in small children; noradrenaline 0.1–0.5 micrograms/kg/minute where vasodilatation predominates.Doctor / Nurse
Paediatric analgesia and the duct. Morphine 100 micrograms/kg (0.1 mg/kg) intravenously, slowly, only in the genuinely distressed child, with naloxone available, using ondansetron 100 micrograms/kg (maximum 4 mg) rather than metoclopramide. Prostaglandin E1 (alprostadil) by infusion for the neonate with a suspected duct-dependent lesion — apnoea is a recognised effect and airway support must be immediately available. Estimate weight as (age in years + 4) × 2 kg for children aged 1–10 years.Doctor
Once decongested and stable, start or resume disease-modifying therapy: renin–angiotensin blockade, beta-blockers, mineralocorticoid receptor antagonists (spironolactone or eplerenone 25–50 mg daily) and SGLT-2 inhibitors.Doctor

Caution— what harms

Never let the crackles choose the drug. The blood pressure and the peripheral perfusion decide — vasodilator for the warm, vasopressor for the cold — and giving the wrong one is lethal.
Never give a nitrate or a diuretic to the hypotensive, preload-dependent patient. Nitrates are contraindicated in systolic BP below 90–100 mmHg, right ventricular infarction, severe aortic stenosis, hypertrophic obstructive cardiomyopathy, and within 24 hours of sildenafil or vardenafil or 48 hours of tadalafil.
Never lay a patient with frank pulmonary oedema flat — not for a radiograph, not for a line.
Never assume the oedema is cardiogenic. Cardiogenic oedema is hydrostatic with a wedge pressure invariably raised, usually above 25 mmHg; non-cardiogenic oedema is a permeability problem with a normal or low wedge pressure. The two look almost identical, only one responds to a diuretic, and in the other a diuretic merely renders the patient hypovolaemic.
Never dismiss pulmonary oedema because the chest sounds clear. In long-standing failure the pulmonary lymphatics hypertrophy, pulmonary venous pressure may exceed 30 mmHg before frank alveolar oedema appears, and crackles may be entirely absent — this is the commonest diagnostic error in the condition.
Never mistake a falling respiratory rate for improvement. A previously tachypnoeic patient whose rate falls, with rising PaCO2, falling pH and drowsiness, is exhausted and about to arrest.
Never give a routine 500–1000 mL fluid bolus in heart failure, and never give 20 mL/kg to a child with known or suspected cardiac disease — 5–10 mL/kg over 15–20 minutes, reassessing the liver edge, chest and heart rate after each.
Never rate-control acute decompensation with a beta-blocker, verapamil or diltiazem because of their negative inotropy; and check the potassium before digoxin, avoiding it in acute coronary syndrome.
Never treat flash oedema as a volume problem. A large diuretic dose is the characteristic error — these patients are frequently not fluid-overloaded at all, and the target is afterload.
Never give morphine reflexly: it may cause carbon dioxide retention by reducing ventilatory drive, registry analyses associate its use with increased ventilation and mortality, and it is withheld entirely in the drowsy patient, in systolic pressure below 100 mmHg, in a rising PaCO2, in opioid-induced oedema and in neurogenic oedema.
Never run a peripheral vasopressor carelessly: extravasation causes tissue necrosis, so use the largest, most proximal cannula and inspect the site frequently. Dopamine should not be first line — it produced more arrhythmias in a randomised trial of all-cause circulatory shock, and in the cardiogenic shock subgroup mortality was increased.
Never treat a normal ejection fraction as excluding heart failure — about half of patients have a preserved ejection fraction — and never treat a normal chest radiograph heart size as excluding cardiogenic oedema, though it should raise suspicion of a non-cardiogenic cause.
Never keep giving loop diuretic to a patient who has passed almost no urine after large cumulative doses; that patient needs renal replacement therapy, not another dose.
Never forget the preventable iatrogenic precipitants: NSAIDs, verapamil and diltiazem, thiazolidinediones, corticosteroids, beta-blockers up-titrated too fast, excessive intravenous fluid, intravenous sodium bicarbonate (the sodium load alone can precipitate oedema), and transfusion given too rapidly. Hypokalaemia and hypomagnesaemia after diuresis are preventable causes of a preventable arrest.

Refer / escalate

Escalate immediately to critical care for non-invasive ventilation failing within about 30 minutes, a rising PaCO2 with falling pH, exhaustion with a falling respiratory rate, a falling conscious level or cardiac arrest; to cardiology for immediate revascularisation where acute heart failure or cardiogenic shock complicates ST-elevation myocardial infarction, since that has the greatest single effect on survival and must not wait for haemodynamic stabilisation; to cardiac surgery for any acute mechanical complication, because medical therapy only stabilises; to renal services for refractory volume overload, metabolic acidosis, refractory hypoxaemia or persistent hyperkalaemia; and to paediatric cardiology for any infant with suspected duct-dependent disease, before or while starting prostaglandin E1.

The card — assess, manage, caution

Acute heart failure and pulmonary oedema — Level 1: CorePrevious Acute heart failure and pulmonary oedema — Level 3: Core practiceNext

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