AHF accounts for over 67,000 admissions per year and is associated with a high mortalityrate. It is the leading cause of hospital admission in people aged 65 years or older in the UK and is a difficult condition to diagnose and manage.1
AHF involves the acute failure of the heart to pump blood to meet the body’s demand.
As a result, two courses of pathology develop:
Congestion in the pulmonary or systemic circulation. Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia. These patients are ‘WET’.
Hypoperfusion of vital organs as the cardiac output is reduced. These patients are ‘COLD’.
The European Society of Cardiology (ESC) classifies AHF patients according to these presentations into four haemodynamic profiles.
Patients may show signs of congestion, hypoperfusion, or both:2
50% of patients will show signs ofcongestion without signs of hypoperfusion (WET-WARM).
45% of patients will show signs of congestion with signs of hypoperfusion (WET-COLD).
5% of patients will show no signs of congestion (DRY-WARM or DRY-COLD).
Causes of new-onset AHF include:
Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Acute valve dysfunction
Causes of acute decompensation of CHF include:
Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
Worsening chronic valve disease
Non-adherence with drugs/diet
Change in drug regimen
Withdrawal/reduction of heart failure medications inappropriately
Initiation/increase of rate-control medications inappropriately
Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones
Ankle swelling (clarify how high and whether this is progressing)
Pink frothy sputum
Orthopnoea (asl about the number of pillows used)
Paroxysmal nocturnal dyspnoea
Other important areas to cover in the history include:
Chest pain (e.g. precipitating cardiac ischaemia or pulmonary embolism)
Palpitations (e.g. precipitating arrhythmia)
Fever (e.g. precipitating infection)
Medications: assess compliance and ask about recent dose changes
In the context of acute heart failure, a thorough cardiorespiratoryexamination is necessary. See the Geeky Medics guides on cardiovascular and respiratory examinations for further information.
Typical clinical findings in acute heart failure include evidence of pulmonary or systemic congestion and hypoperfusion.
Signs of pulmonary or systemiccongestion include:
Fine basal crackles (bilateral)
Peripheral oedema (bilateral)
Dull percussion at the lung bases
Raised jugular venous pressure (JVP)
Gallop rhythm (S3 or S4 heart sounds)
Signs of hypoperfusion include:
Tachypnoea and accessory muscle use
Cold, pale, and sweaty peripheries
Narrow pulse pressure
Asthma, chronic obstructive pulmonary disease (COPD), pneumonia, and pulmonary oedema due to AHF can be difficult to differentiate, especially where they may coexist in older patients.
When considering a diagnosis of AHF, consider that:
Myocardial infarction is the leading cause of AHF without established CHF.
A presentation of unilateral basal crackles, especially concurrent with cough and fever, is more likely to represent a chest infection.
If there is a global wheeze, consider asthma, although there be a wheeze in pulmonary oedema.
Vital signs: may show hypoxia (often SpO2 < 90%), tachycardia, and tachypnoea. The systolic blood pressure may be normal, elevated, or reduced (hypotension is associated with cardiogenic shock and poor prognosis). The pulse pressure may be narrow (<25% of the sBP).
ECG: the ECG is rarely normal. Abnormalities (e.g. signs of ischaemia or arrhythmias) are very common in AHF and an alternative diagnosis should be considered if the ECG is completely normal.
B‑type natriuretic peptide (BNP): BNP is a sensitive but non-specific marker of heart failure. AHF is unlikely and can be ruled out if:
BNP is less than 100 ng/litre
NT‑proBNP is less than 300 ng/litre
Arterial blood gas: often shows type 1 respiratory failure, or type 2 respiratory failure in those with pre-existing chronic lung conditions.
Baseline blood tests (FBC, U&E, coagulation, CRP): anaemia may be a contributing factor.
Cardiac troponin: to detect myocardial infarction (MI) as the underlying cause, however, troponins are often elevated in AHF patients without myocardial infarction.
Thyroid-stimulating hormone (TSH): thyroid abnormalities may precipitate AHF.
D-dimer: performed if a pulmonary embolism is suspected and Well’s score is low (if Well’s score is high proceed to imaging). Note that D-dimer can be positive in AHF in patients without a pulmonary embolism.
Chest X-ray: abnormalities are present in up to 80% of patients in AHF. If the chest X-ray is normal, consider alternative diagnoses such as a pulmonary embolism or exacerbation of asthma/COPD. It can help exclude other causes of dyspnoea such as pneumonia or pneumothorax.
Echocardiogram (transthoracic ultrasound scan): should be performed early in those with suspected AHF, especially if cardiogenic shock or life-threatening cardiac abnormalities are present. The echocardiogram assesses:
Biventricular systolic and diastolic function for ventricular dilation, reduced ejection fraction, ventricular hypertrophy and poor contractility
Ventricular wall rupture
Intracardiac shunts: the presence of a dilated inferior vena cava with reduced respiratory variation is indicative of high venous pressure
Bedside lung ultrasound: may reveal extracardiac pathology such as pulmonary embolism or B-lines (consistent with interstitial oedema in pulmonary oedema)
Chest X-ray findings in AHF
A mnemonic to remember chest x-ray findings in heart failure is ABCDE:
Early senior involvement is important as the management of these patients is often complex.
Take an ABCDE approach to these patients as they may be acutely unwell.
Investigate underlying cause
Identify conditions early on which may have precipitated AHF and treat these urgently. Look out for CHAMP conditions:
Acute coronary syndrome (ACS)
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
If the patient is hypoxic, titrate oxygen to maintain saturations between 94-98% (or 88-92% in those with COPD). Patients often require 15L/minute with a reservoir mask.
Regularly reassess and down-titrate oxygen to avoid hyper-oxygenation which is associated with worsening myocardial ischaemia and other pathology.8
Diuretics increase sodium excretion causing diuresis and decrease afterload. All ‘WET’ patients will require diuretics as the cornerstone of their management.
Administer 40 milligrams furosemide intravenously initially to improve symptoms of congestion fluid overload.
Patients with chronic kidney disease and those already on oral diuretics will need a greater dose. Monitor renal function and urine output to titrate dose according to clinical response.
Nitrates (sublingual glyceryl trinitrate or intravenous nitrates) are the second most used agents in AHF used for ‘WET’ patients. Do not use nitrates in those with SBP <90mmHg or aortic stenosis, who rely on sufficient preload to overcome their pressure gradient.
Nitrates cause venous and/or arterial dilation to reduce preload and/or afterload. They are given to patients with concomitant myocardial ischaemia or hypertension.
Non-invasive ventilation (NIV)
CPAP or BiPAP are used for those with cardiogenic pulmonary oedema, dyspnoea, and
NIV improves ventilation to reduce respiratory distress and drives fluid out of alveoli and into vasculature in those whose respiratory failure is not controlled with oxygen therapy given via a face mask.
Some ‘COLD’ patients whose AHF has led to a potentially reversible cardiogenic shock may present with haemodynamic instability (systolic blood pressure <90mmHg). These patients require early expert help. Specialists may consider inotropes (e.g. dobutamine) to increase cardiac output and peripheral perfusion, and vasopressors (e.g. adrenaline) to increase blood pressure and vital organ perfusion. The use of these drugs is associated with poorer outcomes.
After the patient is stabilised, pharmacological treatment aims to increase cardiac output by optimising preload and contractility whilst decreasing afterload.
Before discharge, consider offering patients with reduced ejection fraction (LVEF <40%) heart failure a selection of treatments, as discussed below.
Loop diuretics increase sodium excretion causing diuresis and decreased afterload.
Used for symptomatic relief of congestion and fluid retention, and titrated up or down according to needs.
ACE-inhibitor (ACEi) or angiotensin receptor blockers (ARB)
Contraindications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.
Begin therapy once established on a diuretic and ACEi/ARB, and when BP and congestion are controlled.
Beta-blockers decrease heart rate, myocardium oxygen demand and RAAS activation.
Contraindications include asthma, 2nd or 3rd-degree atrioventricular block, sick sinus syndrome and sinus bradycardia.
‘Start low and go slow’
Antagonise aldosterone increasing sodium excretion causing diuresis and decreased afterload.
Other specialist drugs
Ivabradine: for patients who cannot have a beta-blocker or who are on the maximum dose already, if they are in sinus rhythm with a heart rate >75
Sacubitril valsartan: for patients who decompensate on an ACEi/ARB
Hydralazine and nitrate: for patients who cannot tolerate an ACEi/ARB, or who are on the maximum dose
Digoxin: for patients with atrial fibrillation and uncontrolled tachycardia despite a beta-blocker
Follow up the patient within 2 weeks of hospital discharge.
About 40% of people admitted to hospital with heart failure die or are readmitted within 1 year.9
AHF may cause arrhythmias, particularly atrial fibrillation.
There is an increased risk of stroke and other thromboembolic diseases following an episode of AHF.
AHF refers to the rapid onset or worsening of signs and symptoms of heart failure and has a high mortality rate.
AHF can occur as new onset or as decompensation of CHF.
Myocardial infarction is the leading cause of AHF.
Patients may have signs and symptoms of pulmonary oedema, peripheral oedema, and hypoperfusion.
Early senior involvement is key for these complex patients.
The ECG and chest X-ray are rarely normal.
BNP is a sensitive but non-specific marker used to rule out heart failure.
Treat hypoxia with oxygen.
Actively look for underlying causative conditions and treat urgently.
Medical management is mainly with diuretics, with some patients also receiving nitrates.
Dr Bara Erhayiem
Consultant Cardiologist and Nottingham University Hospitals and Clinical Lead for Heart Failure.
Dr Chris Jefferies
National Institute of Health and Care Excellence. Acute heart failure: diagnosis and management. Published in 2014. Available from: [LINK]
European Society of Cardiology. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Published in 2016. Available from: [LINK]
Penn Medicine. Heart Failure Classification – Stages of Heart Failure and Their Treatments. Published in 2014. Available from: [LINK]
Wilkinson, Raine & Wiles. Oxford Handbook of Clinical Medicine (10th). Published in 2017.
The Resus Room. Acute Heart Failure. Published in 2017. Available from: [LINK]
RCEM Learning. Cardiogenic Pulmonary Oedema. Published in 2017. Available from: [LINK]
BMJ Best Practice. Acute exacerbation of congestive heart failure. Last reviewed in 2020. Available from: [LINK]
Chu, Kim, et al. Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis. Published in 2018. Available from: [LINK]
National Institute of Health and Care Excellence. Chronic heart failure in adults: diagnosis and management. Published in 2018. Available from: [LINK]