Level 1 of 6Core
Acute heart failure and pulmonary oedema
The core to-do list — diagnose and manage, at a glance
Diagnose— recognise it
- Recognise the patient from the doorway: sitting bolt upright, sweating, grey or cyanosed, using accessory muscles, tachypnoeic and frightened — acute cardiogenic pulmonary oedema is defined by tachypnoea, orthopnoea, bilateral inspiratory crackles, SpO₂ below 90% on air and 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 above 180 mmHg; acute pulmonary oedema; cardiogenic shock; high-output failure with warm peripheries; and isolated right heart failure with raised JVP and clear lung fields.
- Separate congestion from hypoperfusion, because that is what chooses the drug: congestion — pitting oedema, tender hepatomegaly, ascites; hypoperfusion — cold mottled peripheries, narrow pulse pressure, urine output below 0.5 mL/kg/hour, confusion, rising lactate. A raised JVP is the key sign that the wet lung is the heart's fault (8 cmH₂O or less is normal), with an S3 gallop and any new murmur.
- A quiet chest does not exclude pulmonary oedema: in chronic failure lymphatic adaptation lets pulmonary venous pressure exceed 30 mmHg before alveolar flooding and crackles may be entirely absent — the commonest diagnostic error is dismissing oedema because the chest sounds clear; the history (orthopnoea, a night in a chair, 3 kg gained in four days) outranks auscultation.
- A raised JVP with clear lung fields and hypotension is not left heart failure — think right ventricular infarction, pulmonary embolism or tamponade, all preload-dependent and all worsened by nitrates and diuretics. And the most treacherous sign is a falling respiratory rate in a previously tachypnoeic patient, with rising PaCO₂ and drowsiness — exhaustion immediately preceding respiratory arrest.
- Infants present differently: feeding difficulty — sweating during feeds, taking longer than about 20 minutes, breaking off to breathe — poor weight gain, tachypnoea, grunting and irritability; the most reliable sign of congestion in an infant is hepatomegaly, the JVP is unusable below about five years, and crackles are frequently absent even in a very wet child.
Manage now— do this, in order
- Let the blood pressure and the peripheral perfusion — not the crackles — choose the drug, and reassess at every review because the category can change; two patients may have identical wet lungs, one needing a vasodilator and the other a vasopressor, and giving the wrong one is lethal.
- Sit the patient upright with the legs dependent — works within seconds and costs nothing; never lay a patient with frank oedema flat, not for a radiograph, not for a line.
- Oxygen high flow to the hypoxaemic patient, then titrate to 94–98% (88–92% in a confirmed CO₂ retainer); oxygen is not indicated in the non-hypoxaemic patient. Continuous oximetry and cardiac monitoring, frequent blood pressure, two large-bore cannulae, urinary catheter with hourly measurement, and a 12-lead ECG within 10 minutes.Doctor / Nurse
- Pathway A — warm and wet, systolic BP 100 mmHg or more: nitrates first. Sublingual GTN 0.4 mg (one 400 microgram spray or tablet) every 5 minutes up to three doses, checking BP before each repeat and stopping below systolic 100; if breathlessness persists, IV infusion 10–200 micrograms/minute keeping systolic above 85–90 mmHg. Then furosemide 40–80 mg by slow IV injection — a patient already on a loop diuretic gets at least their total daily oral dose IV, up to 2.5 times it.Doctor / Nurse
- Pathway B — hypertensive (flash) oedema is an afterload problem, and a large diuretic dose is the characteristic error: GTN titrated more aggressively, furosemide 40 mg IV or none where there is no overload, and early non-invasive ventilation — reduce mean arterial pressure by no more than about 25% in the first hour.Doctor / Nurse
- Pathway C — cold and wet (cardiogenic shock): withhold nitrates and, initially, diuretics. If the JVP is not raised and the chest is clear, give 250 mL of crystalloid over 10 minutes and re-examine — a routine 500–1000 mL bolus has no place in heart failure. Noradrenaline 0.1–0.5 micrograms/kg/minute to MAP 65 mmHg or above; dobutamine 2–20 micrograms/kg/minute with noradrenaline, not instead of it; only once the systolic is above 90 mmHg and the periphery warming is the loop diuretic given.Doctor / NurseNot available at your setup — Infusion pump.
- Ventilatory support for the patient failing on high-flow oxygen, respiratory rate persistently above about 25/min, or visibly tiring: begin CPAP or bilevel at 5 cmH₂O and titrate to about 10 cmH₂O — and set the time limit before the mask goes on: if rate, saturation, pH and PaCO₂ are not improving within about 30 minutes, the patient needs intubation.Doctor / NurseNot available at your setup — Mechanical ventilator.
- Treat the precipitant: rapid atrial fibrillation may need emergency synchronised cardioversion in the peri-arrest patient; avoid beta-blockers, verapamil and diltiazem in acute decompensation; digoxin 0.5 mg IV over at least 30 minutes (check potassium first, avoid in ACS) or amiodarone 300 mg IV over 20–60 minutes into a large vein. Where AHF or shock complicates STEMI, immediate revascularisation has the greatest single effect on survival and must not wait for stabilisation.Doctor / NurseNot available at your setup — Defibrillator.
- Paediatric: furosemide 1 mg/kg by slow IV injection (maximum 2 mg/kg per dose); fluid challenge in suspected cardiogenic shock 5–10 mL/kg over 15–20 minutes — never 20 mL/kg — re-examining liver edge, chest and heart rate; dobutamine 5–20 micrograms/kg/minute is the usual first-line inotrope; prostaglandin E1 by infusion for the neonate with a suspected duct-dependent lesion, with airway support immediately available because apnoea is a recognised effect.Doctor / Nurse
Choose the pathway on BP and perfusion — not the crackles
| Pathway | Picture | First moves |
|---|---|---|
| A | Warm and wet, SBP ≥ 100 | GTN 0.4 mg SL q5min ×3, then furosemide 40–80 mg IV |
| B | Hypertensive flash oedema, SBP often > 180 | Aggressive GTN, furosemide 40 mg or none, early NIV |
| C | Cold and wet (cardiogenic shock) | No nitrates; 250 mL fluid if JVP flat; noradrenaline + dobutamine; diuretic only once SBP > 90 |
Refer / escalate
Escalate immediately to critical care for NIV failing within about 30 minutes, rising PaCO₂ with falling pH, exhaustion or a falling conscious level; to cardiology for immediate revascularisation where AHF or cardiogenic shock complicates STEMI; to cardiac surgery for any acute mechanical complication; to renal services for refractory overload, acidosis, hypoxaemia or hyperkalaemia; and to paediatric cardiology for any infant with suspected duct-dependent disease, before or while starting prostaglandin E1.
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