Acute heart failure

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Urgent

Request urgent cardiology/critical care support for any patient with:[1]

Respiratory distress/failure[22]
Reduced consciousness
Use of accessory muscles for breathing, respiratory rate >25/minute[22]
Oxygen saturation (SpO₂) <90% despite supplemental oxygen
Heart rate <40 or >130 bpm[22]
Systolic blood pressure persistently <90 mmHg[22]
- Unless known to be usually hypotensive (based on the opinion of our expert adviser)
Signs or symptoms of hypoperfusion (see Shock)[1]
Haemodynamic instability[1]
Acute heart failure due to an acute coronary syndrome (ACS)[4]
Persistent life-threatening arrhythmia.

Urgently identify and treat any underlying precipitants/causes of acute heart failure that must be managed immediately to prevent further rapid deterioration (while recognising that any acute heart failure is potentially life-threatening). Causes to consider include:[1]

ACS. See Unstable angina, Non-ST elevation myocardial infarction, and ST-elevation myocardial infarction[4]
Hypertensive emergency. See Hypertensive emergencies
Rapid arrhythmias or severe bradycardia/conduction disturbance. See Assessment of tachycardia and Bradycardia
An acute mechanical cause (e.g., myocardial rupture as a complication of ACS, chest trauma)
Acute pulmonary embolism. See Pulmonary embolism
Infections (including myocarditis)
Tamponade.

Practical tip

You should initiate management of acute heart failure in tandem with investigation and treatment of underlying precipitants/causes. However, depending on the clinical setting and circumstances, addressing the underlying cause may take immediate priority: for example, if primary percutaneous coronary intervention is available and indicated for a patient with acute ST-elevation myocardial infarction, this should not be delayed by continued efforts to stabilise the patient.

Organise rapid transfer to hospital for any patient in the community with suspected acute heart failure.[1] Transfer to the most appropriate setting.[1]

Key Recommendations

Determine acute drug treatment based on the patient’s clinical presentation, including haemodynamic status and the presence of shock; drug treatment options include vasoactive drugs, diuretics, and vasodilators.[1][4][23]

After stabilisation, start an oral diuretic if the patient has symptoms or signs of congestion, or switch from an intravenous to an oral diuretic once a patient who was started on an intravenous diuretic in the acute phase is euvolaemic.[1]

Plan subsequent treatment based on measurement of the patient’s left ventricular ejection fraction (LVEF) using echocardiography and their level of symptoms.[1][6]

Start an ACE inhibitor (or an angiotensin-II receptor antagonist if unable to tolerate an ACE inhibitor) and a beta-blocker in patients with reduced LVEF (≤40%).[1][4] If the patient is already taking a beta-blocker for a comorbidity (e.g., angina, hypertension), switch to a beta-blocker that is licensed for heart failure.[24]
Start an aldosterone antagonist in addition to an ACE inhibitor (or angiotensin-II receptor antagonist) and a beta-blocker in patients with acute heart failure and reduced LVEF.[6][23]
Sacubitril/valsartan is recommended as a replacement for an ACE inhibitor in suitable patients with heart failure with reduced ejection fraction who remain symptomatic despite optimal treatment with an ACE inhibitor (or an angiotensin-II receptor antagonist), a beta-blocker, and an aldosterone antagonist.[1] Sacubitril/valsartan may also be considered as a first-line therapy instead of an ACE inhibitor.[1] Treatment with sacubitril/valsartan should be started by a heart failure specialist.[23]
Aim to provide symptomatic relief (e.g., reducing symptoms of congestion with diuretics) and improve general overall health and well-being for any patient with preserved LVEF (>40%).[1]

Do not give oxygen routinely; it should be used only if the patient has oxygen saturations <90% or PaO₂ <8 kPa (<60 mmHg).[1]

Ensure the patient has input from the heart failure specialist team within 24 hours of admission to hospital.[29]

Full recommendations

VIEW ALL

Treatment goals

The goals of initial treatment of the patient with acute heart failure are to:[1]

Identify and treat any underlying cause
Alleviate symptoms
Improve congestion and organ perfusion
Restore oxygenation
Limit organ damage (cardiac, renal, hepatic, gut).

Subsequent treatment aims to:[1]

Improve symptoms and quality of life
Control symptoms and fully relieve congestion, prevent early readmission, and improve survival.

More info: Using the type of clinical presentation to guide management decisions

The European Society of Cardiology describes four major clinical presentations of acute heart failure. Although these presentations may overlap, each requires different treatment. This classification therefore offers a practical framework to help guide management decisions.[1]

Acute decompensated heart failure

symptoms associated with peripheral fluid accumulation, increased intraventricular pressure
gradual onset (days)
normal or low systolic blood pressure
Treatment: diuretics, vasoactive drugs if peripheral hypoperfusion/hypotension (an inotrope and/or a vasopressor), short-term mechanical ventilatory support or renal replacement therapy if needed.

Acute pulmonary oedema

symptoms associated with fluid redistribution to the lungs and acute respiratory failure
rapid onset (hours)
normal to high systolic blood pressure
Treatment: oxygen (given as continuous positive airway pressure, non-invasive positive pressure-ventilation, and/or high-flow nasal cannula), diuretics, vasodilators.

Isolated right ventricular failure

symptoms from increased central venous pressure and often systemic hypoperfusion
gradual or rapid onset
low systolic blood pressure
Treatment: diuretics for peripheral congestion, vasoactive drugs if peripheral hypoperfusion/hypotension (an inotrope and/or a vasopressor), short-term mechanical ventilatory support or renal replacement therapy if needed.

Cardiogenic shock

symptoms from systemic hypoperfusion (severe cardiac dysfunction)
gradual or rapid onset
low systolic blood pressure
Treatment: vasoactive drugs (an inotrope and/or a vasopressor), short-term mechanical ventilatory support, and/or renal replacement therapy, together with early identification and treatment of the underlying cause.

Initial supportive care

Request urgent cardiology/critical care support for any patient with:[1]

Respiratory distress/failure[22]
Reduced consciousness
Use of accessory muscles for breathing, respiratory rate >25/minute[22]
Oxygen saturation (SpO₂) <90% despite supplemental oxygen
Heart rate <40 or >130 bpm[22]
Systolic blood pressure persistently <90 mmHg[22]
- Unless known to be usually hypotensive (based on the opinion of our expert adviser)
Signs or symptoms of hypoperfusion (see Shock)[1]
Haemodynamic instability
Acute heart failure due to an acute coronary syndrome (ACS)[4]
Persistent life-threatening arrhythmia.

Seek expert help on any use of intravenous fluids in patients with known underlying cardiac impairment such as heart failure.[30]

Monitor transcutaneous arterial oxygen saturation (SpO₂).[1]

Give oxygen if the patient has oxygen saturations <90% or PaO₂ <8 kPa (<60 mmHg).[1]
Monitor controlled oxygen therapy. An upper SpO₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
- Evidence suggests that liberal use of supplemental oxygen (target SpO₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[31]
- A lower target SpO₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[32]
Do not use oxygen routinely in non-hypoxaemic patients with acute heart failure because it causes vasoconstriction and a reduction in cardiac output.[1]

Consider non-invasive positive pressure ventilation (continuous positive airway pressure [CPAP], bilevel positive airway pressure [BiPAP]) in patients with respiratory distress (respiratory rate >25 breaths/minute, SpO₂ <90%); start as soon as possible to decrease respiratory distress and reduce the rate of mechanical endotracheal intubation. Use with caution in patients with hypotension, monitoring blood pressure regularly.[1]

Consider invasive ventilation if the patient has respiratory failure leading to hypoxaemia (PaO₂ <8 kPa [<60 mmHg]), hypercapnia (PaCo₂ >6.65 kPa [>50 mmHg]), and acidosis (pH <7.35) that cannot be managed non-invasively.[1]

Evidence: Target oxygen saturation in acutely ill adults

Too much supplemental oxygen increases mortality.

Evidence from a large systematic review and meta-analysis supports conservative/controlled oxygen therapy versus liberal oxygen therapy in acutely ill adults who are not at risk of hypercapnia.

Guidelines differ in their recommendations on target oxygen saturation in acutely unwell adults who are receiving supplemental oxygen.
- The 2017 British Thoracic Society (BTS) guideline recommends a target SpO₂ range of 94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[32][33]
- The 2022 Global Initiative For Asthma (GINA) guidelines recommend a target SpO₂ range of 93% to 96% in the context of acute asthma exacerbations.[34]
One systematic review including a meta-analysis of data from 25 randomised controlled trials, published in 2018, found that, in adults with acute illness, liberal oxygen therapy (broadly equivalent to a target saturation >96%) is associated with higher mortality than conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[31]
- In-hospital mortality was 11 per 1000 higher for the liberal oxygen therapy versus conservative therapy group (95% CI 2 to 22 per 1000 more).
- Mortality at 30 days was also higher in the group who had received liberal oxygen (RR 1.14, 95% CI 1.01 to 1.29).
- The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction, and cardiac arrest, and patients who had emergency surgery. Studies that were limited to people with chronic respiratory illness or psychiatric illness, and patients on extracorporeal life support, receiving hyperbaric oxygen therapy, or having elective surgery, were all excluded from the review.
An upper SpO₂ limit of 96% is therefore reasonable when administering supplemental oxygen to medical patients with acute illness who are not at risk of hypercapnia. However, a higher target may be appropriate for some specific conditions (e.g., pneumothorax, carbon monoxide poisoning, cluster headache, and sickle cell crisis).[35]
In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis and decided an interim update was not required.[36]
- The committee noted that the systematic review supported the use of controlled oxygen therapy to a target.
- While the systematic review showed an association between higher oxygen saturations and higher mortality, the BTS committee felt the review was not definitive on what the optimal target range should be. The suggested range of 94% to 96% in the review was based on the lower 95% confidence interval and the median baseline SpO₂ from the liberal oxygen groups, along with the earlier 2015 TSANZ guideline recommendation.
Subsequently, experience during the coronavirus disease 2019 (COVID-19) pandemic has also made clinicians more aware of the feasibility of permissive hypoxaemia.[37]
Management of oxygen therapy in patients in intensive care is specialised and informed by further evidence (not covered in this summary) that is more specific to this setting.[38][39][40]

Urgently identify and treat any underlying precipitants/causes of acute heart failure that must be managed immediately to prevent further rapid deterioration (while recognising that any acute heart failure is potentially life-threatening). Causes to consider include:[1]

ACS.[4] See Unstable angina, Non-ST elevation myocardial infarction, and ST-elevation myocardial infarction
Hypertensive emergency. See Hypertensive emergencies
Rapid arrhythmias or severe bradycardia/conduction disturbance (see Assessment of tachycardia and Bradycardia)
An acute mechanical cause (e.g., myocardial rupture as a complication of ACS, acute valvular regurgitation, chest trauma)
Acute pulmonary embolism. See Pulmonary embolism
Infections (including myocarditis)
Tamponade.

Practical tip

Organise rapid transfer to hospital for any patient in the community with suspected acute heart failure.[1] Transfer to the most appropriate setting.[1]

Ensure the patient has input from the heart failure specialist team within 24 hours of admission to hospital.[29]

Evidence: Specialist review

Access to a heart failure specialist during admission with acute heart failure improves prescription of disease-modifying heart failure treatment and reduces mortality rates both in hospital and post discharge.

The UK National Institute for Health and Care Excellence (NICE) guideline on acute heart failure recommends that “all people admitted to hospital with suspected acute heart failure have early and continuing input from a dedicated specialist heart failure team”.[23]

This is based on evidence of reduced mortality from six observational studies, of which data from the 2012 and 2013 National Institute for Cardiovascular Outcomes Research (NICOR) heart failure audits in England and Wales were felt to be the most relevant.
'Early' is defined as 24 hours in the linked NICE quality standard.[41]

The UK National Confidential Enquiry into Patient Outcome and Death (NCEPOD) in people who died following a hospital admission for acute heart failure found that specialist review could have been improved for 23.7% of the patients included.[4]

The enquiry included all adult patients admitted as an emergency with a primary diagnosis of heart failure and who died in hospital (between 1 January 2016 and 31 December 2016); a subset of those who died within 7 days was used for more detailed analysis.
At some point in their admission 197/585 patients (33.7%) were transferred to a specialist ward (cardiology, coronary care, or critical care).
199/603 patients (33.0%) were reviewed by a specialist heart failure team.
273/561 patients (48.7%) were reviewed by a cardiologist.
- Cardiology review frequently resulted in changes to treatment (90/134; 67.2% of patients).
- Where information on timing of cardiology review was available, 61 patients (37.7%) were reviewed within 12 hours of admission, 102 (63%) within 24 hours, and 136 (84%) within 48 hours.
  - 38/133 cardiology reviews (28.6%) assessed by NCEPOD peer reviewers were judged as not having taken place within an appropriate time frame.
52/218 patients (23.9%) who did not have any specialist review died within 24 hours of admission to hospital.
Care was more likely to be rated as ‘good’ for those patients who had specialist review (53.8% vs. 12.4%).
- People under the age of 80 and those with newly diagnosed heart failure were more likely to have specialist review.

The NICOR heart failure audit (England and Wales) has shown consistently that specialist review is associated with reduced inpatient mortality. Figures from the 2022 audit (based on 2020-2021 data) showed there is still room for improvement in specialist review of patients admitted with heart failure; this applies both during acute admission and post-discharge.[6]

Approximately 88% of patients had a specialist review during hospital admission.
- Overall, 53% saw a consultant cardiologist and 49% saw a specialist nurse.
- Patients admitted to cardiology wards were more likely to see a specialist than those on general medical wards (99% vs. 74%).
- There was huge variation, with only 65% of hospitals achieving review rates over 80%.
The percentage of patients with heart failure with reduced ejection fraction being prescribed a combination of all three disease-modifying medicines (ACE inhibitors, beta-blockers, and aldosterone antagonists) at discharge was 52% irrespective of the ward setting and specialist review. This increased to 58% for patients managed on a cardiology ward and 55% for patients who had specialist review.
- Over a 5-year period prescription rates improved for specialist review, while prescription rates were generally static for patients not undergoing specialist review.
In-hospital mortality was 9.2% for all patients admitted to hospital.
- Mortality was reduced for patients who were reviewed by a specialist or managed on a cardiology ward (7.9% and 6.0%, respectively).
- Age-adjusted multivariable analyses showed that not being admitted to a cardiology ward (hazard ratio 1.75, P <0.001) was an independent predictor of increased mortality when other common markers of disease severity are included in the model.

Do not routinely offer opioids to a patient with acute heart failure.[23]

Acute drug treatment

Determine acute drug treatment based on the patient’s haemodynamic status and the presence or absence of shock.[1][4][23]

Haemodynamically unstable: hypotensive (systolic blood pressure <90 mmHg) or other signs of cardiogenic shock

Get urgent cardiology or critical care support; treatment should be provided in a specialist environment.

Vasoactive drugs (an inotrope and/or a vasopressor) should only be considered in patients with acute heart failure with potentially reversible cardiogenic shock or those who are potential candidates for a heart transplant. They should only be administered in a cardiac care unit or high-dependency unit or an alternative setting with at least level 2 care.[23][42] Selection of appropriate vasoactive agents may vary according to clinician preference and local practice guidelines.
Short-term intravenous infusion of inotropic drugs may be considered in this group of patients to increase cardiac output, increase blood pressure, improve peripheral perfusion, and maintain end-organ function.[1] This should be given in a specialist setting.
Use of short-term mechanical circulatory support devices (e.g., intra-aortic balloon pumps, impella devices, short-term ventricular assist devices) may be considered by specialists.[43]
For more information on the assessment and management of patients with cardiogenic shock, see Shock.

Haemodynamically unstable: hypertensive crisis

Consider giving a vasodilator intravenously if the patient has hypertension, in addition to usual care.[1][23] This may also be used for relief of dyspnoea in this group of patients.[1][4][23]

Monitor the patient’s symptoms and blood pressure in a critical care environment to ensure systolic blood pressure remains >90 mmHg.[1][23]
Sodium nitroprusside may be given in clinical practice but the UK National Institute for Health and Care Excellence recommends that it should not be given to patients with acute heart failure.[23] However, it is approved for use in acute heart failure in the UK and it is suggested as an intravenous vasodilator option for acute heart failure by the European Society of Cardiology guidelines.[1] Monitor blood pressure (including intra-arterial blood pressure) and blood cyanide concentration.
Although evidence for survival benefit from the use of vasodilators in patients with acute heart failure is lacking, they remain in widespread use for symptom relief and blood pressure control.[1][23]

Evidence: Vasodilators

Guidelines recommend using vasodilators in selected patients with acute heart failure, but this is based on clinical experience and there is no evidence to support their use. Use of vasodilators is associated with an increased risk of adverse events: in particular, headache and hypotension.

Although vasodilators are commonly used in adults with acute heart failure, the UK National Institute for Health and Care Excellence (NICE) reviewed the evidence for their use in 2014 due to variation in practice both in the UK and across Europe. The reviewers identified five relevant randomised controlled trials (RCTs) (n=1369).[23]

The interventions were: intravenous glyceryl trinitrate (two RCTs, n=529), oral isosorbide dinitrate (two RCTs, n=28), and intravenous sodium nitroprusside (one RCT, n=812). All were compared with placebo.
Only the study with sodium nitroprusside reported mortality as an outcome.
- For men with acute left ventricular failure and presumed myocardial infarction there was no difference in all-cause mortality at 48 hours, 21 days, or 13 weeks with sodium nitroprusside compared with placebo (n=812, very low-quality evidence assessed using GRADE).
Haemodynamic outcomes were reported as favourable for all interventions (four studies); however, as it was unclear whether/how these relate to longer-term clinical benefit, they were not used by NICE to formulate its recommendations.
There was no difference in global symptomatic improvement or patient-reported dyspnoea with glyceryl trinitrate compared with placebo (follow-up 3 hours, GRADE moderate to low).
Two studies reported adverse events, of which headache and hypotension were considered the most important.
- More people had headache with glyceryl trinitrate compared with placebo (follow-up 3 hours, risk ratio [RR] 5.63, 95% CI 1.69 to 18.78; GRADE moderate).[23] In the first 24 hours after administration headache occurred in 44 people (20%) and hypotension occurred in 27 people (13%), although only one person had severe hypotension.[44] Hypotension was not reported for the placebo group; therefore, NICE did not report this outcome.
- With sodium nitroprusside, significantly more patients reached the hypotensive limit compared with placebo (RR 26.87, 95% CI 6.59 to 109.46; absolute effect 128 more per 1000 [from 28 more to 536 more], GRADE low). Headache and severe headache were also more common in the sodium nitroprusside group (GRADE low to very low).
While there was limited evidence of any benefit, the guideline group noted that, based on its clinical experience, nitrates may help some patients: for example, those with myocardial ischaemia or severe hypertension.

Key evidence since the 2014 NICE guideline evidence review

Two subsequent RCTs, the Goal-directed Afterload Reduction in Acute Congestive Cardiac Decompensation (GALACTIC) study (published 2019, n=788) and the Effect of an Emergency Department Care Bundle on 30-Day Hospital Discharge and Survival Among Elderly Patients With Acute Heart Failure (ELISABETH) trial (published 2020, n=503), compared interventions that included early use of vasodilation with usual care without early vasodilation.

Neither study demonstrated a survival/hospitalisation benefit from early use of intravenous vasodilators compared with usual care (including high-dose diuretics).[45][46]
Consequently, the European Society of Cardiology did not issue any recommendation for a regimen favouring vasodilator-based treatment versus usual care in its 2021 guideline for the diagnosis and treatment of acute and chronic heart failure.[1]

Give an intravenous loop diuretic to all patients with acute heart failure including those with severe hypertension.[23]

If the patient is already on long-term diuretic therapy, give an initial intravenous dose that is at least equal to the pre-existing oral dose (some experts recommend approximately twice the equivalent oral dose) unless you have significant concerns about the patient’s adherence to their diuretic therapy before admission.[1][23][47]
Give the diuretic as either intermittent boluses or a continuous infusion.[1][23]
Adjust the dose according to the patient’s symptoms and clinical status.[1]
Closely monitor the patient’s weight, renal function, and urine output while they are taking diuretics.[1][23]
Discuss with the patient the best strategies of coping with an increased urine output.[23]

Practical tip

Avoid excessive diuresis; this is more dangerous than oedema.[1]

Consider adding a thiazide-type diuretic or an aldosterone antagonist if the patient has resistant oedema or symptoms or signs of congestion despite treatment with a loop diuretic.[1]

Carefully monitor the patient for hypokalaemia or hyperkalaemia, renal impairment, and hypovolaemia.[1]

Haemodynamically stable: normal blood pressure

Give an intravenous loop diuretic to a haemodynamically stable patient if there are symptoms or signs of congestion.[1]

If the patient is already on long-term diuretic therapy, give an initial intravenous dose that is at least equal to the pre-existing oral dose (some experts recommend approximately twice the equivalent oral dose) unless you have significant concerns about the patient’s adherence to their diuretic therapy before admission.[1][23]
[1]Give the diuretic as either intermittent boluses or a continuous infusion.[23]
Adjust the dose according to the patient’s symptoms and clinical status.[1]
Monitor the patient’s weight, renal function, and urine output carefully while they are taking diuretics.[1][23]
- Aim to achieve positive diuresis with a reduction of body weight by 0.75 to 1.0 kg/day.[1]

Practical tip

Avoid excessive diuresis; this is more dangerous than oedema.[1]

Consider adding an aldosterone antagonist or a thiazide-type diuretic if the patient has resistant oedema or symptoms or signs of congestion despite treatment with a loop diuretic.[1]

Carefully monitor the patient for hypokalaemia or hyperkalaemia, renal impairment, and hypovolaemia.[1]

Do not give intravenous vasodilators routinely in patients with normal blood pressure. Consider them in specific circumstances: for example, for concomitant myocardial ischaemia or aortic/mitral regurgitation.[1][4][23]

If vasodilators are given, monitor the patient’s symptoms and blood pressure in a critical care environment to ensure systolic blood pressure remains >90 mmHg.[1][23]

Evidence: Vasodilators

The interventions were: intravenous glyceryl trinitrate (two RCTs, n=529), oral isosorbide dinitrate (two RCTs, n=28), and intravenous sodium nitroprusside (one RCT, n=812). All were compared with placebo.
Only the study with sodium nitroprusside reported mortality as an outcome.
- For men with acute left ventricular failure and presumed myocardial infarction there was no difference in all-cause mortality at 48 hours, 21 days, or 13 weeks with sodium nitroprusside compared with placebo (n=812, very low-quality evidence assessed using GRADE).
Haemodynamic outcomes were reported as favourable for all interventions (four studies); however, as it was unclear whether/how these relate to longer-term clinical benefit, they were not used by NICE to formulate its recommendations.
There was no difference in global symptomatic improvement or patient-reported dyspnoea with glyceryl trinitrate compared with placebo (follow-up 3 hours, GRADE moderate to low).
Two studies reported adverse events, of which headache and hypotension were considered the most important.
- More people had headache with glyceryl trinitrate compared with placebo (follow-up 3 hours, risk ratio [RR] 5.63, 95% CI 1.69 to 18.78; GRADE moderate).[23] In the first 24 hours after administration headache occurred in 44 people (20%) and hypotension occurred in 27 people (13%), although only one person had severe hypotension.[44] Hypotension was not reported for the placebo group; therefore, NICE did not report this outcome.
- With sodium nitroprusside, significantly more patients reached the hypotensive limit compared with placebo (RR 26.87, 95% CI 6.59 to 109.46; absolute effect 128 more per 1000 [from 28 more to 536 more], GRADE low). Headache and severe headache were also more common in the sodium nitroprusside group (GRADE low to very low).
While there was limited evidence of any benefit, the guideline group noted that, based on its clinical experience, nitrates may help some patients: for example, those with myocardial ischaemia or severe hypertension.

Key evidence since the 2014 NICE guideline evidence review

Neither study demonstrated a survival/hospitalisation benefit from early use of intravenous vasodilators compared with usual care (including high-dose diuretics).[45][46]
Consequently, the European Society of Cardiology did not issue any recommendation for a regimen favouring vasodilator-based treatment versus usual care in its 2021 guideline for the diagnosis and treatment of acute and chronic heart failure.[1]

Continue a beta-blocker if the patient is already taking this, unless they have:[23]

Heart rate <50 bpm
Second- or third-degree atrioventricular block
Shock.

Treatment after stabilisation

Start an oral diuretic if the patient has symptoms or signs of congestion, or switch from an intravenous to an oral diuretic once a patient who was started on an intravenous diuretic in the acute phase is euvolaemic.[1]

Most patients will require a loop diuretic due to severe symptoms of congestion and worsening renal function. Use a combination of a loop and a thiazide-type diuretic if the patient has resistant oedema.[1]
Adjust the dose according to the patient’s symptoms and clinical status.[1]
Monitor the patient’s weight, renal function, and urine output carefully while they are taking a diuretic.[1][23]
- Aim to achieve positive diuresis with a reduction of body weight by 0.75 to 1.0 kg/day.[1]

Practical tip

Avoid excessive diuresis; this is more dangerous than oedema.[1] In practice, convert the patient from an intravenous to an oral diuretic when there is significant reduction in peripheral oedema (i.e., oedema to ankles only).

Heart failure with reduced ejection fraction (LVEF ≤40%)

Start an ACE inhibitor (or an angiotensin-II receptor antagonist if unable to tolerate an ACE inhibitor) and a beta-blocker.[1][4][6][23] [ ]

In general, start with low doses and titrate upwards to maximally tolerated doses, taking into account any contraindications.[1]
If the patient is already taking a beta-blocker for a comorbidity (e.g., angina, hypertension), switch to a beta-blocker that is licensed for heart failure.[24]
Make sure the patient has remained stable for at least 48 hours after starting or restarting a beta-blocker before they are discharged.[23]

Give an aldosterone antagonist in addition to an ACE inhibitor (or an angiotensin-II receptor antagonist if unable to tolerate an ACE inhibitor) and a beta-blocker.[23]

Sacubitril/valsartan is recommended as a replacement for an ACE inhibitor in suitable patients with heart failure with reduced ejection fraction who remain symptomatic despite optimal treatment with an ACE inhibitor, a beta-blocker, and an aldosterone antagonist; however, it may also be considered for first-line therapy instead of an ACE inhibitor.[1]

Treatment with sacubitril/valsartan should be started by a heart failure specialist.[24]

Start a sodium-glucose co-transporter 2 (SGLT2) inhibitor (dapagliflozin or empagliflozin) in patients with heart failure with reduced ejection fraction in addition to an ACE inhibitor (or angiotensin-II receptor antagonist), a beta-blocker, and an aldosterone antagonist, regardless of whether they have diabetes or not (unless contraindicated or not tolerated).[1]

Early involvement of the specialist heart failure team for all patients admitted with acute heart failure enables consideration of additional treatments to optimise outcomes.[6] For patients with heart failure with reduced ejection fraction these may include:[1][24]

Ivabradine
Isosorbide dinitrate plus hydralazine
Digoxin
Cardiac resynchronisation therapy
Implantable cardioverter defibrillator
Transplantation or mechanical circulatory support device.

Heart failure with mildly reduced ejection fraction (LVEF 41% to 49%)

Formulate an individualised care plan for patients with mildly reduced ejection fraction (HFmrEF), which should depend on clinical characteristics, risk factors, patterns of cardiac remodelling, and the patient’s comorbidities and prognosis.

Offer symptomatic relief and measures to improve general overall health and well-being. This should include screening for and treating any comorbidities.
Consider therapies recommended for patients with HFrEF (e.g., ACE inhibitor, angiotensin-II receptor antagonist, beta-blocker, aldosterone antagonist, sacubitril/valsartan).[1] Treatment with a SGLT2 inhibitor may also be beneficial for this group, regardless of the presence of diabetes.[48]

Heart failure with preserved ejection fraction (LVEF ≥50%)

Aim to provide symptomatic relief (e.g., by starting a diuretic) and improve general overall health by identifying and treating the underlying risk factors, aetiology, and coexisting comorbidities.[1][2]

These patients tend to be older with more comorbidities (cardiovascular and non-cardiovascular) compared with patients with HFrEF.[1]
The European Society of Cardiology states that no specific treatment has been shown to convincingly reduce morbidity or mortality; however, one subsequent randomised controlled trial suggests that these patients may benefit from a SGLT2 inhibitor (empagliflozin), regardless of the presence of diabetes.[48]

Discharge

Consider discharging the patient if:

They have an up-to-date echocardiogram (in practice, within the last year if considered unnecessary during this hospital visit)
They have been reviewed by the heart failure specialist team[6][29]
They are stable and euvolaemic (persistent congestion before discharge is associated with a higher risk of readmission and mortality)[1]
They have been established on recommended oral medication[1]
Their condition has been stable for typically 48 hours after starting or restarting beta-blockers.[23]

Ensure the patient has the following before discharge:

A follow-up appointment with a member of the multidisciplinary heart failure team within 2 weeks[4][6][23]
Offer of referral to cardiac rehabilitation.[4][24] Cardiac rehabilitation should be personalised and exercise-based. It should also address psychological and educational aspects.[4][24]

Use of this content is subject to our disclaimer