Classification: acute heart failure in the emergency setting
Acute cardiogenic pulmonary oedema is the most dramatic manifestation of acute heart failure. Raised left ventricular filling pressures cause fluid to shift into the interstitium and the alveoli. This results in hypoxaemia, increased work of breathing and a self-perpetuating cycle of sympathetic activation, increased afterload and further congestion.
For acute treatment, the haemodynamic phenotype matters more than the aetiology:
- Hypertensive pulmonary oedema ("flash" pulmonary oedema): sudden onset and high blood pressure, often reflecting redistribution rather than absolute volume overload. Vasodilatation is the priority.
- Normotensive decompensation with volume overload: slower development, peripheral oedema and weight gain. Diuretics are central.
- Hypotensive decompensation progressing to cardiogenic shock: hypoperfusion predominates. Nitrates are contraindicated, and diuretics should be given only if congestion is clearly present.
The trigger should be sought in parallel with stabilisation: acute coronary syndrome, arrhythmia, hypertensive crisis, acute valvular pathology, infection or discontinuation of therapy.
Initial measures and diagnostic work-up
- Sit the patient upright with the legs lowered. Do not lay the patient flat.
- Start monitoring (ECG, blood pressure, SpO₂), establish venous access and obtain a 12-lead ECG early.
- Give oxygen if the patient is hypoxaemic. Use target ranges from the current guideline and avoid routine hyperoxia.
- Perform point-of-care ultrasound where available. Bilateral, diffuse B-lines suggest interstitial oedema. Focused echocardiography provides information on left ventricular function, pericardial effusion and relevant valvular disease.
- In the emergency department, add blood gas analysis (hypercapnia, lactate), laboratory tests including natriuretic peptides, troponin and electrolytes, and a chest radiograph.
The ESC guideline does not recommend routine opioid administration for anxiolysis. Respiratory depression and vomiting during mask ventilation are relevant risks.
Prehospital CPAP and NIV in the emergency department
Mechanism of action
Positive end-expiratory pressure recruits fluid-filled alveoli and improves oxygenation. It reduces the work of breathing. The raised intrathoracic pressure lowers both preload and transmural left ventricular afterload. In hypertensive pulmonary oedema in particular, CPAP therefore has both respiratory and haemodynamic effects.
Evidence and role
The ESC guideline recommends that non-invasive ventilation be considered early in respiratory failure due to acute heart failure. Faster symptom relief and a lower intubation rate are well documented. A mortality benefit, however, has not been shown consistently, and the evidence on this point is limited.
Prehospital CPAP is technically simple and available with many emergency ventilators or disposable systems. It bridges the period until drug therapy takes effect.
CPAP or NIV with pressure support?
- CPAP: standard approach in hypoxaemic cardiogenic pulmonary oedema.
- NIV with pressure support: in relevant hypercapnia, respiratory muscle fatigue or overlap with COPD.
Ventilation pressures are titrated stepwise according to the clinical picture, SpO₂ and blood pressure. Specific pressure settings should be taken from the current guideline or the local SOP.
Contraindications and criteria for discontinuation
- Impaired consciousness, absent protective reflexes, risk of aspiration or vomiting
- Lack of cooperation despite coaching
- Facial injuries or pneumothorax
- Shock or marked hypotension, because preload reduction may further destabilise the circulation
If respiratory rate, oxygenation and level of consciousness do not improve within a short time, timely intubation by experienced clinicians is preferable to delayed emergency intubation under hypoxia.
Vasodilatation: glyceryl trinitrate
Nitrates mainly reduce venous preload and, at higher doses, also afterload. They are used principally in pulmonary oedema with raised blood pressure.
Dosing in acute heart failure/pulmonary oedema with raised blood pressure (ESC 2021/2023):
- Syringe driver 50 mg/50 ml = 1 mg/ml
- Start at 10–20 µg/min i.v. (0.6–1.2 ml/h)
- Increase stepwise up to max. 200 µg/min (12 ml/h)
- Consider if systolic BP > 110 mmHg
- Monitor blood pressure closely and avoid lowering it too abruptly
In the prehospital setting, glyceryl trinitrate is frequently given sublingually (spray 0.4 mg per actuation). The sublingual dose listed in the compendium refers to acute coronary syndrome and angina pectoris (summary of product characteristics). For pulmonary oedema, follow the local SOP and the current summary of product characteristics.
Contraindications:
- Hypotension (systolic BP < 90 mmHg), shock or marked hypovolaemia
- PDE-5 inhibitors: sildenafil or vardenafil within 24 h, or tadalafil within 48 h (risk of severe hypotension)
- Right ventricular infarction (inferior STEMI with RV involvement)
- Use caution in severe aortic stenosis and hypertrophic obstructive cardiomyopathy
Notes:
- Common adverse effects include headache, flushing, reflex tachycardia and hypotension.
- Tolerance develops with continuous infusion over 24–48 h.
- Glyceryl trinitrate adsorbs to PVC, so PVC-free lines are preferred.
- In concomitant ischaemia, nitrates relieve symptoms but do not improve prognosis. They must not delay diagnostic work-up or reperfusion (ESC ACS guideline 2023).
Diuretics: furosemide
Loop diuretics are indicated when signs of fluid overload or congestion are present.
Dosing in acute heart failure with congestion (ESC 2021/2023), preparation 10 mg/ml:
- No prior diuretic therapy: 20–40 mg i.v. (2–4 ml)
- On long-term oral diuretic therapy: 1 to 2 times the oral daily dose i.v.
Assessing response:
- At 2 h by urinary sodium
- At 6 h by urine output
- If diuresis is inadequate, double the dose
Monitoring of diuresis applies mainly to the emergency department. In the prehospital setting, the key point is to give furosemide early and with a clear indication.
Important: Do not give a diuretic in the absence of congestion, for example in hypovolaemia or shock.
Contraindications:
- Anuria or renal failure not responding to furosemide
- Hepatic coma or precoma
- Severe hypokalaemia or hyponatraemia
- Hypovolaemia or dehydration
- Hypersensitivity to furosemide or sulfonamides
Practical notes:
- Inject slowly i.v., at no more than 4 mg/min. Rapid administration, high doses and renal impairment increase the risk of ototoxicity.
- Monitor electrolytes and blood pressure.
- Urinary retention may occur in prostatic hyperplasia, and a urinary catheter may be required.
In children, the dose according to the summary of product characteristics is 1 mg/kg i.v. given slowly, maximum 20 mg (parenteral max. 20 mg/day).
Differential diagnosis: cardiogenic shock
Cardiogenic shock differs fundamentally from hypertensive pulmonary oedema. Its key feature is hypoperfusion, for example cold, mottled skin, altered mental status, oliguria and rising lactate, usually with hypotension. This has different consequences:
- No nitrates if systolic BP < 90 mmHg or in shock
- Diuretics only if congestion is clearly present, and with great restraint
- Use NIV with caution, because positive pressure ventilation further reduces preload; plan controlled intubation early
- Circulatory support with vasopressors and inotropes according to the current guideline
- Establish the cause: ST elevation requires immediate coronary angiography, so refer early to a centre with cardiac catheterisation and intensive care capacity
Differential diagnosis: pneumonia and mixed presentations
Dyspnoea, crackles and hypoxaemia also occur in pneumonia. Features that help to distinguish them:
- Suggests pneumonia: fever, signs of infection, productive cough, unilateral or focal findings, and consolidation with focal B-lines on ultrasound.
- Suggests cardiogenic pulmonary oedema: acute onset, orthopnoea, bilateral diffuse B-lines, pleural effusions, impaired LV function, raised natriuretic peptides and a hypertensive presentation.
Mixed presentations are common, because infection can trigger acute heart failure. Indiscriminate diuretic use in septic hypovolaemia should be avoided, as should missing cardiac decompensation. Treatment is guided by the predominant findings and adjusted according to the patient's course.
Summary
- Treatment of acute pulmonary oedema means identifying the phenotype first, then combining respiratory support, vasodilatation and diuresis in a targeted way.
- Prehospital CPAP improves oxygenation and work of breathing and reduces the intubation rate. A mortality benefit has not been reliably demonstrated.
- Glyceryl trinitrate is the first-choice vasodilator in the hypertensive presentation: start at 10–20 µg/min i.v., up to max. 200 µg/min, and consider if systolic BP > 110 mmHg.
- Furosemide belongs only in the treatment of congestion: 20–40 mg i.v. or 1 to 2 times the oral daily dose. Do not give a diuretic without congestion.
- Acute heart failure in the emergency setting with hypoperfusion is cardiogenic shock: no nitrates, restraint with NIV and diuretics, and early transfer to a specialist centre.
References
- McDonagh TA et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42:3599–3726; 2023 Focused Update, Eur Heart J 2023;44:3627–3639.
- Byrne RA, Rossello X, Coughlan JJ et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J 2023;44:3720–3826.
- Fachinformation Furosemid 20 mg/2 ml bzw. 40 mg/4 ml Injektionslösung – aktuelle Fassung.
- Fachinformation Glyceroltrinitrat-Spray 0,4 mg/Sprühstoß – aktuelle Fassung prüfen.
- Nolan JP, Sandroni C et al. European Resuscitation Council and European Society of Intensive Care Medicine Guidelines 2025 Post-Resuscitation Care. Resuscitation 2025 / Intensive Care Med 2025;51:2213–2288.
This article does not replace clinical judgement in the individual case or the current summary of product characteristics and guidelines.
