Acute Heart Failure

Acute heart failure
Straight to the point of care
Last updated: Mar 16, 2021

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Risk factors 4
Aetiology 5
Pathophysiology 6
Classification 7
Case history 8
Diagnosis 9
Recommendations 9
History and exam 18
Investigations 22
Differentials 27
Criteria 27
Management 29
Recommendations 29
Treatment algorithm overview 40
Treatment algorithm 43
Emerging 59
Primary prevention 59
Secondary prevention 59
Patient discussions 60
Follow up 61
Monitoring 61
Complications 62
Prognosis 62
Guidelines 64
Diagnostic guidelines 64
Treatment guidelines 64
References 66
Images 77
Disclaimer 81
Acute heart failure Overview
Summary
Suspect acute heart failure in any patient with: breathlessness, ankle swelling, reduced exercise tolerance,
fatigue, tiredness, increased time to recover after exercise, and nocturnal cough.
OVERVIEW
Urgently assess for any signs or symptoms related to the underlying cause of acute heart failure.
Arrange immediate bedside echocardiography (requires specialist expertise) and ECG for any patient who is
haemodynamically unstable (low blood pressure or shock) or in respiratory failure with suspected acute heart
failure as part of looking for life-threatening causes.
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).
Request urgent cardiology/critical care support for any patient with: respiratory distress/failure; reduced
consciousness or physical exhaustion; use of accessory muscles for breathing, respiratory rate >25/
minute; oxygen saturation (SpO 2 ) <90% despite supplemental oxygen; heart rate <40 or >130 beats per
minute; systolic blood pressure <90 mmHg (unless known to be usually hypotensive); signs or symptoms of
hypoperfusion; haemodynamic instability; acute heart failure due to an acute coronary syndrome; recurrent
arrhythmia.
For any patient with suspected heart failure always record and interpret a 12-lead ECG; monitor this
continuously.
Also always order a chest x-ray, N-terminal-proB-type natriuretic peptide (NT-proBNP), or BNP as well other
standard blood tests, and echocardiography to establish the presence or absence of cardiac abnormalities.
Determine acute drug treatment based on the patient’s haemodynamic status and the presence of shock;
drug treatment options include vasoactive drugs, diuretics, and vasodilators.
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.
Plan subsequent treatment based on measurement of the patient’s left ventricular ejection fraction using
echocardiography and their level of symptoms.
Ensure the patient has input from the heart failure specialist team within 24 hours of admission to hospital.
Definition
Heart failure is defined clinically as a syndrome in which patients have symptoms and signs resulting from
an abnormality of cardiac structure and/or function.[1] Acute heart failure refers to rapid onset or worsening
of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment.[1] This topic does not
cover children or pregnant women.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 16, 2021.
BMJ Best Practice topics are regularly updated and the most recent version
3
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2021. All rights reserved.
Acute heart failure Theory
Epidemiology
Approximately 900,000 people in the UK have heart failure; 5% of all adult emergency hospital admissions
in the UK are caused or complicated by acute heart failure.[2] [3] Outside of the UK, prevalence of heart
THEORY
disease is about 1.3% in China, 6.7% in Malaysia, 1% in Japan, 4.5% in Singapore, 0.12% to 0.44% in India,
1% in South America, and 1% to 2% in Australia.[4]
The National Heart Failure Audit 2018/2019, which included 89% of patients admitted to hospital with acute
heart failure in England and Wales, showed a mean age of 78 years overall; this was slightly lower for men
and higher for women. There were more men at all ages, apart from the ≥85 years group in which women
were a majority.[5]
Risk factors
Strong
previous cardiovascular disease
Coronary heart disease is the most common cause of heart failure.[9]
older age
Prevalence of heart failure is ≥10% in people >70 years of age.[1]
prior episode of heart failure

In patients hospitalised for acute heart failure, around 75% have a history of prior heart failure.[10]
diabetes mellitus
Related directly to ischaemia and renal failure.
family history of ischaemic heart disease or cardiomyopathy

A risk factor for acute heart failure.[9]
excessive alcohol intake

The association between alcohol intake and the risk of developing new-onset heart failure is U-
shaped; the lowest risk is with modest alcohol consumption (up to 7 drinks/week).[1]
smoking
The epidemiological associations of smoking with the development of cardiovascular disease suggest
that smoking cessation would be beneficial.[1]
cardiac arrhythmias
Cardiac arrhythmias, including tachyarrhythmia and bradyarrhythmia, are risk factors for acute heart
failure.
history of systemic conditions associated with heart failure

Conditions that are associated with heart failure include sarcoidosis and haemochromatosis.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 16, 2021.
previous chemotherapy
A risk factor for heart failure.
medication
THEORY
Non-adherence to medication is a precipitating factor in patients with chronic heart failure. Drugs that
may exacerbate heart failure include non-steroidal anti-inflammatory drugs, steroids, diltiazem, and
verapamil.[9]
hypertension
Hypertension is associated with an increased risk of developing heart failure. Antihypertensive therapy
markedly reduces the incidence of heart failure; however, alpha-adrenoceptor blockers are less
effective than other antihypertensives in preventing heart failure.[1]
Weak
valvular heart disease
Both significant stenotic and regurgitate lesions can lead to heart failure.
Although rheumatic valvular disease is now rarely found in western countries, calcific valvular heart
disease (in particular, aortic stenosis) is commonly encountered.
In patients with significant valvular disease, the heart failure will not improve until the underlying
valvular disease has been corrected.
pericardial disease
A large pericardial effusion can present with symptoms or signs of acute heart failure.
Pericardial constriction, such as tuberculosis pericarditis or the effects of radiotherapy, can also
present with acute heart failure.
myocarditis
There are many causes of myocarditis, of which a viral aetiology appears to be the most common.
There is usually a prodrome of a non-specific illness characterised by fatigue, mild dyspnoea, and
myalgias.
excessive salt intake

Noted in 22% of people with heart failure.[11]
excessive catecholamine stimulation

Can be caused by phaeochromocytoma or subarachnoid haemorrhage.[12]
abnormal thyroid function

Both hypothyroidism and thyrotoxicosis can be associated with heart failure.[13] [14]
Aetiology
Causes and precipitating factors are:
• Acute coronary syndrome (ACS)
5
• Hypertensive emergency
• Rapid arrhythmias or severe bradycardia/conduction disturbance
• An acute mechanical cause (e.g., myocardial rupture as a complication of ACS [such as free wall
rupture], ventricular septal defect or acute mitral regurgitation, chest trauma)
THEORY
• Acute pulmonary embolism

• Valve disease
• Myocarditis
• Decompensation of pre-existing chronic heart failure
• Cardiac tamponade
• Aortic dissection
• Postpartum cardiomyopathy
• Lack of adherence with medical treatment
• Volume overload
• Infections
• Severe brain insult
• After major surgery
• Reduction of renal function
• Drug abuse
• Phaeochromocytoma
• High output syndromes
• Septicaemia
• Thyrotoxic crisis
• Anaemia
• Shunt syndromes.
The most common concurrent conditions present in patients with acute heart failure are coronary artery
disease, hypertension, diabetes mellitus, atrial fibrillation, and renal insufficiency.[6] [7]
Pathophysiology
During an episode of acute heart failure, the majority of patients will have evidence of volume overload with
pulmonary and/or venous congestion. Haemodynamic measurements in these cases usually show increased
right- and left-sided ventricular filling pressures with depressed cardiac index and cardiac output. However, if
there is associated infection, the cardiac output may be normal or, in some cases, increased.
Activation of the sympathetic nervous system causes tachycardia, increased myocardial contractility,
increased myocardial oxygen consumption, peripheral vasoconstriction, and activation of renin-angiotensin
system with salt and water retention. There is also activation of vasoconstrictor neurohormones, which leads
to sodium and fluid retention, increased myocardial wall stress, and decreased renal perfusion.[8]
If the condition is not treated effectively, the myocardium becomes unable to maintain a cardiac output
sufficient to meet the demands of the peripheral circulation. In order for patients with acute heart failure to
respond quickly to treatment, the increased myocardial stress must be reversed: for example, correction of
acute severe hypertension. This is particularly important in acute heart failure caused by ischaemia, as a
dysfunctional myocardium can return to normal when appropriately treated.
Classification
There have been several attempts to classify acute heart failure based on different criteria. According to
the European Society of Cardiology, the most useful classifications in practice are those based on clinical
THEORY
presentation at admission. These not only allow the identification of patients at high risk of complications but
also help to inform individualised management directed at specific targets.[1]
Systolic blood pressure

In most cases, patients with acute heart failure present with either:[1]
• Preserved (90-140 mmHg) systolic blood pressure (SBP)
or
• Elevated (>140 mmHg; hypertensive acute heart failure) SBP.
Only 5% to 8% of all patients present with low SBP (i.e., <90 mmHg; hypotensive acute heart failure).[1]
Precipitants
An alternative approach is to classify patients according to the presence of factors leading to
decompensation (which need to be treated urgently):[1]
• Acute coronary syndrome

• Acute mechanical cause underlying acute heart failure
• Acute pulmonary embolism.
Physical examination
Another way to classify acute heart failure is based on the presence of clinical symptoms/signs of:[1]
• Congestion (‘wet’ vs. ‘dry’ if present vs. absent)
and/or
• Peripheral hypoperfusion (‘cold’ vs. ‘warm’ if present vs. absent).
Combining these options identifies four groups:
• Warm and wet (well-perfused and congested); most common

• Cold and wet (hypoperfused and congested)
• Cold and dry (hypoperfused without congestion)
• Warm and dry (compensated, well-perfused without congestion).
Types of heart failure

Traditionally heart failure is classified as:
• Systolic - associated with left ventricular dysfunction and characterised by cardiomegaly, third heart
sound, and volume overload with pulmonary congestion. Left ventricular ejection fraction (LVEF) is
decreased
7
• Diastolic - typically associated with normal cardiac size, hypertension, pulmonary congestion, and a
fourth heart sound. LVEF is preserved.
Based on measurement of LVEF, heart failure is classified as:[1]
THEORY
• Heart failure with reduced ejection fraction (HFrEF) - symptoms and signs and LVEF <40%
• Heart failure with mid-range ejection fraction (HFmrEF) - symptoms and signs and LVEF 40% to 49%
• Heart failure with preserved ejection fraction (HFpEF) - symptoms and signs and LVEF >50%.
Case history
Case history #1
A 70-year-old woman describes increasing exertional dyspnoea for the last 2 days and now has dyspnoea
at rest. She has a history of hypertension for the last 5 years and a 35 pack-year smoking history, but no
other established illnesses. Current medications are a diuretic daily for the last 3 years. She has been
prescribed an ACE inhibitor but failed to fill the prescription. On examination her BP is 190/90 mmHg, and
her heart rate is 104 bpm. There is an audible S4 and the jugular venous pressure is elevated 2 cm above
normal. Lung examination reveals fine bibasal crepitations. There is no ankle oedema. Echocardiogram
shows an ejection fraction of 60%.
Case history #2
A 73-year-old woman with a history of myocardial infarction presents to the accident and emergency
department. She is breathless and finding it difficult to talk in full sentences. On examination she is
centrally cyanosed with cool extremities. Her pulse is 110 bpm and systolic BP only just recordable at 80
mmHg. Jugular venous pressure is elevated 3 cm above normal and the cardiac apex beat is displaced.
Respiratory rate is increased and she has widespread crackles and wheezes on chest examination.
Echocardiogram shows an ejection fraction of 35%
Other presentations
Patients may present with predominant symptoms of the underlying condition such as chest pain with
acute myocardial infarction, syncope with significant valvular stenosis, palpitations with arrhythmias, and
viral prodrome with myocarditis.
Acute heart failure Diagnosis
Recommendations
Urgent
Arrange immediate bedside echocardiography (requires specialist expertise) and ECG for any
patient who is haemodynamically unstable (low blood pressure or shock) or in respiratory failure with
suspected acute heart failure as part of looking for life-threatening causes . Life-threatening causes
include:[1] [3]
• Acute coronary syndrome (ACS)[3]

• An acute mechanical cause (e.g., myocardial rupture as a complication of ACS, chest trauma)
• Acute pulmonary embolism.
Request urgent critical care/cardiology support for any patient with:[1]
• Respiratory distress/failure[19]
• Reduced consciousness or physical exhaustion
• Heart rate <40 or >130 bpm[19]
• Systolic blood pressure <90 mmHg[19]
• Unless known to be usually hypotensive (based on the opinion of our expert adviser)
• Signs or symptoms of hypoperfusion - see our topic Shock
• Haemodynamic instability
• Acute heart failure due to ACS
• Recurrent arrhythmia.
Request serum brain natriuretic peptide (BNP) measurement in the first set of blood tests for all
patients with acute breathlessness who may have new acute heart failure.[3] [20]
• The UK National Institute for Health and Care Excellence recommends use of N-terminal pro-B-
DIAGNOSIS
type natriuretic peptide (NT-proBNP).[21]
• BNP measurement is central to differentiating acute heart failure from non-cardiac causes of acute
dyspnoea.[1]
Organise rapid transfer to hospital (preferably to a site with a cardiology department and/or a
coronary care/intensive care unit) for any patient in the community with suspected acute heart failure.[1]
• Acute heart failure is potentially life-threatening and requires urgent evaluation and treatment.[1]
Key Recommendations
Assess for common symptoms and signs of acute heart failure. These include:[1]
• Dyspnoea
• Orthopnoea
• Paroxysmal nocturnal dyspnoea
• Ankle swelling
• Reduced exercise tolerance
• Fatigue
• Elevated jugular venous pressure
9
• Third heart sound (gallop rhythm)
• Pulmonary crepitations.
Ask about risk factors for heart failure. Heart failure is unusual in a patient with no relevant medical
history.[1]
Establish the patient’s haemodynamic status as this will determine further management. Most patients
present with either normal (90-140 mmHg) or hypertensive (>140 mmHg) systolic blood pressure (SBP).
• Hypotension (SBP <90 mmHg) is associated with poor prognosis, particularly when hypoperfusion
is present.
Always order the following investigations for a patient with new suspected acute heart failure to establish
the presence or absence of cardiac abnormalities:[1] [20]
• ECG[5]
• Chest x-ray
• N-terminal-proB-type natriuretic peptide (NT-proBNP) or BNP and other standard blood tests
• Echocardiography.[5]
Once stabilised, use the patient’s left ventricular ejection fraction to guide disease-modifying treatment.
Address causative aetiology and relevant comorbidities.[1]
Full Recommendations
Clinical presentation
Suspect acute heart failure in any patient with:
• Breathlessness [1]
• This may be acute but also includes orthopnoea and paroxysmal nocturnal dyspnoea[22]
• Ankle swelling [1]
DIAGNOSIS
• This often reduces when the patient’s legs have been elevated for a sustained period of time
(e.g., in bed overnight)
• Reduced exercise tolerance[1]
• Fatigue, tiredness, increased time to recover after exercise[1]
• Less common symptoms, including: wheezing, dizziness, confusion (especially in older patients),
loss of appetite, nocturnal ischaemic pain, nocturnal cough (frothy sputum suggests that it is
alveolar in origin and not bronchial).[1] [22]
Urgently assess for any signs or symptoms related to the underlying cause of acute heart failure.[1] [22]
• It is important to screen for an underlying cause of heart failure as this may be treatable.[1]
• 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) include:[1]
• Acute coronary syndrome (ACS).[3] See our topics Unstable angina, ST-elevation

myocardial infarction, and Non-ST elevation myocardial infarction
• Hypertensive emergency. See our topic Hypertensive emergencies
• Rapid arrhythmias or severe bradycardia/conduction disturbance. See our topics
Assessment of tachycardia and Bradycardia
• An acute mechanical cause (e.g., myocardial rupture as a complication of ACS [such as free
wall rupture], ventricular septal defect or acute mitral regurgitation, chest trauma)
• Acute pulmonary embolism. See our topic Pulmonary embolism
• Valve disease
• Myocarditis. See our topic Myocarditis .
Request urgent critical care/cardiology support for any patient with:[1]
• Signs or symptoms of hypoperfusion. See our topic Assessment of shock
• Acute heart failure due to ACS
History
Check whether the patient has previously been diagnosed and treated for heart failure. If so, ask
about:
• Current treatment for heart failure and the patient's adherence.

Ask about risk factors for heart failure if the patient has not previously been diagnosed, including:
• Previous cardiovascular disease; coronary heart disease is the most common cause of heart
failure[9]
• Older age[1]
• Prevalence of heart failure is ≥10% in people >70 years of age[1]

• Diabetes[9]
DIAGNOSIS
• Family history of ischaemic heart disease or cardiomyopathy[9]
• Excessive alcohol intake or smoking[9]
• Cardiac arrhythmias including tachyarrhythmia or bradyarrhythmia
• History of systemic conditions associated with heart failure (e.g., sarcoidosis and
haemochromatosis)
• Previous chemotherapy.
Ask about recent drug history . Drugs that may exacerbate heart failure include non-steroidal anti-
inflammatory drugs, steroids, diltiazem, and verapamil.[9]
Practical tip
Heart failure is unusual in patients with no relevant medical history.[1]
Physical examination
Assess the degree of dyspnoea,#including:
• Respiratory rate[1]
• Breathlessness when lying flat[19]
• Effort of breathing[19]
11
• Degree of hypoxia.
Look for signs of poor perfusion such as:
• Cold extremities[1]
• Narrow pulse pressure[1]
• Altered mental status[1]
• Oliguria[1]
• Dizziness[1]
• Central cyanosis
• Delayed capillary refill time.
Check for signs of congestion such as:
• Peripheral oedema[1] [3] [5]
• Leg oedema is usually bilateral and pitting

• Pulmonary crepitations
• Dullness to percussion and decreased air entry in lung bases
• Wheezing[23]
• Elevated jugular venous pressure
• Ascites.[1] [3]
Measure the patient’s blood pressure; haemodynamic status will determine further management.
• Most patients present with either normal (90-140 mmHg) or hypertensive (>140 mmHg) systolic
blood pressure (SBP).[1]
• Hypotension (SBP <90 mmHg) is associated with poor prognosis, particularly when hypoperfusion
is present.[1] See our topic Shock .
Listen to the patient’s heart sounds. Signs of acute heart failure include:
• A displaced apex beat[1]

• A gallop rhythm (third heart sound).[1]
Also listen for potential valvular causes such as aortic stenosis or mitral regurgitation.
DIAGNOSIS
Practical tip
The sound of the crackles heard on chest auscultation in heart failure is described as ‘wet’ and
sounding like Velcro. Crackles in heart failure are usually fine and quiet rather than the coarse
sounds that are more commonly heard in lung disease. They can be mistaken for the bilateral
crackles of lung fibrosis, but patients with fibrotic lungs are more likely to be hypoxic with exertional
desaturation.
Always check above the level of the patient’s earlobes for a raised jugular venous pressure because
this is easily missed. However, a raised jugular venous pressure can be difficult to spot, even for a
heart failure specialist.
Investigations
Always order
ECG
Record and interpret a 12-lead ECG for all patients with suspected heart failure; monitor this
continuously .[5]
• Arrange this immediately if the patient is haemodynamically unstable or in respiratory failure to look
for any life-threatening cause of acute heart failure (e.g., acute coronary syndrome, particularly ST-
elevation myocardial infarction). See our topic ST-elevation myocardial infarction .[1]
Check heart rhythm, heart rate, QRS morphology, and QRS duration, as well as looking for specific
abnormalities such as arrhythmias, atrioventricular block, evidence of a previous myocardial infarction
(e.g., Q waves), and evidence of left ventricular hypertrophy.[1]
The ECG is usually abnormal in acute heart failure.[1]
ECG showing left ventricular hypertrophy with sinus tachycardia

From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD
Chest x-ray
Look for:[1]
DIAGNOSIS
• Pulmonary congestion
• Pleural effusion
• Interstitial or alveolar fluid in horizontal fissure
• Cardiomegaly.
Practical tip
13
Be aware that significant left ventricular dysfunction may be present without cardiomegaly on chest
x-ray.[1]
Chest x-ray showing acute pulmonary oedema with increased alveolar

markings, fluid in the horizontal fissure, and blunting of the costophrenic angles
DIAGNOSIS
DIAGNOSIS
Chest x-ray showing acute pulmonary oedema with increased alveolar markings and bilateral pleural effusions
Blood tests
Natriuretic peptides
• Order N-terminal pro-B-type natriuretic peptide (NT-proBNP) if available. Brain natriuretic

peptide (BNP) or mid-regional pro-atrial natriuretic peptide (MR-proANP) (in some countries) are
alternatives.[1] [3] [20]
• Normal levels make the diagnosis of acute heart failure unlikely (normal levels: NT-proBNP <300
ng/L (<300 picograms [pg]/mL); BNP <100 ng/L (<100 pg/mL); MR-proANP <120 ng/L (<120
pg/mL).[1] [20] However, elevated levels of natriuretic peptides do not automatically confirm the
diagnosis of acute heart failure as they may be associated with a wide variety of cardiac and
non-cardiac causes. Low levels of natriuretic peptides can occur in end-stage heart failure, flash
pulmonary oedema, or right-sided acute heart failure.[1]
• Most older patients presenting to hospital with acute breathlessness have an elevated NT-
proBNP so separate ‘rule in’ diagnostic cut-offs are useful in this setting.
15
• If NT-proBNP is significantly elevated (>1800 ng/mL [>1800 pg/mL] in patients >75

years; see table below) acute heart failure is likely and should be confirmed by inpatient
echocardiography. If the NT-proBNP is intermediate (>300 ng/mL [>300 pg/mL] but <1800
ng/mL [<1800 pg/mL]), consider other possible causes of breathlessness, but if these are
excluded and diagnostic suspicion of heart failure remains, request an echocardiogram.[20]
Age (years) <50 50-75 >75
NT-proBNP level >450 >900 >1800

(ng/L or pg/mL)
above which acute
heart failure is
likely [3]
Practical tip
Be aware that natriuretic peptides may be raised due to other causes (e.g., acute coronary
syndrome, myocarditis, pulmonary embolism, older age, and renal or liver impairment), hence the
need for practical ‘rule in’ cut-offs.[1]
Troponin
• Measure troponin in all patients with suspected acute heart failure.[19]

• Most patients with acute heart failure have an elevated troponin level. As well as diagnosis,
troponin may be useful for prognosis; elevated levels are associated with poorer outcomes.[19]
• Be aware that interpretation is not straight forward ; type 2 myocardial infarction and
myocardial injury are common.
Full blood count
• Identify anaemia , which can worsen heart failure and also suggest an alternative cause of
symptoms.[1]
Electrolytes, urea, and creatinine
• Order as a baseline test to inform decisions on drug treatment that may affect renal function (e.g.,
DIAGNOSIS
diuretics, ACE inhibitors), and to exclude concurrent or causative renal failure.

Glucose
• Measure blood glucose in all patients with suspected acute heart failure to screen for diabetes.[19]
• In practice, also request HbA1c (based on the opinion of our expert).
Liver function tests
• Order these for any patient with suspected acute heart failure.
• Liver function tests are often elevated due to reduced cardiac output and increased venous
congestion. Abnormal liver function tests are associated with a worse prognosis.[1]
Thyroid function tests
• Order thyroid-stimulating hormone in any patient with newly diagnosed acute heart failure. Both
hypothyroidism and hyperthyroidism can cause acute heart failure.[1] See our topic Overview of
thyroid dysfunction .
C-reactive protein
• Consider ordering C-reactive protein (based on the opinion of our expert).

• Inflammation is associated with progression of chronic heart failure.
• Levels of high-sensitivity C-reactive protein are raised in patients with acute heart failure.[24]
D-dimer
• Indicated in patients with suspicion of acute pulmonary embolism.[19] See our topic Pulmonary
embolism .
Echocardiography
Arrange immediate bedside echocardiography for any patient who is haemodynamically
unstable or in respiratory failure .[1] [3] Specialist expertise is required.
If a patient is haemodynamically stable , arrange echocardiography within 48 hours if:
• They are not known to have heart failure[5] [20]

• Their cardiac structure or function is unknown or is likely to have changed since previous
echocardiography.[1]
Echocardiography is used to assess myocardial systolic and diastolic function of both left and right
ventricles, assess valvular function, and measure left ventricular ejection fraction (LVEF).[5]
• Evaluating the patient’s LVEF has a key role in assessing the severity of any decrease in systolic
function and is essential in determining your patient’s long-term management.[1]
Practical tip
The diagnosis of heart failure with reduced ejection fraction (HFrEF) requires an LVEF <40%.
Patients with heart failure with preserved ejection fraction (HFpEF) have clinical signs of heart
failure with normal or near-normal LVEF. There is an emerging group of patients with heart failure
with mid-range ejection fraction (40% to 49%) (HFmrEF) and encouraging data with some therapies
recommended for HRrEF, but current guidelines recommend the same management approach as
for HFpEF (so apply to patients with heart failure with LVEF >40%).[1]
Consider ordering
DIAGNOSIS
Venous or arterial blood gas
Perform an arterial blood gas (ABG) if the patient has cardiogenic shock, you cannot measure
oxygenation with pulse oximetry, or an accurate measurement of arterial partial pressure of oxygen (PaO 2
) and arterial partial pressure of carbon dioxide (PaCO 2 ) is needed.[1]
Consider measurement of blood pH and PaCO 2 even if the patient does not have cardiogenic shock,
especially if they have acute pulmonary oedema or known COPD.[1]
• Do not routinely perform an ABG. Venous blood gas may acceptably indicate pH and PaCO 2 .[1]
A blood gas may show:
• Hypoxaemia
• PaO 2 <10.67 kPa (<80 mmHg) on arterial blood gas)

• Metabolic acidosis with raised lactate in a patient with hypoperfusion
• pH <7.35, lactate >2 mmol/L (>18 mg/dL)

• Type I or type II respiratory failure
17
• Type I respiratory failure: PaO 2 <8 kPa (<60 mmHg)

• Type II respiratory failure: PaCO 2 >6.65 kPa (>50 mmHg).
Blood tests screening for myocarditis

Consider blood tests screening for acute myocarditis if you suspect myocarditis as a cause of acute heart
failure. These include screening for viruses that cause acute myocarditis, including coxsackievirus group
B, HIV, cytomegalovirus, Ebstein-Barr virus, hepatitis, echovirus, adenovirus, enterovirus, human herpes
virus 6, parvovirus B19, and influenza viruses. See our topic Myocarditis .
Bedside thoracic ultrasound

Bedside thoracic ultrasound is useful in countries with no access to BNP/NT-proBNP testing for detecting
signs of interstitial oedema and pleural effusion in heart failure if specialist expertise is available.[1] [3]
History and exam

Key diagnostic factors
breathlessness (common)
Assess the degree of dyspnoea, including:
• Respiratory rate[1]
• Breathlessness when lying flat[19]
• Effort of breathing[19]
• Degree of hypoxia.
Dyspnoea may be acute, but also includes orthopnoea and paroxysmal nocturnal dyspnoea.[22]
peripheral oedema (common)

Leg oedema is usually bilateral and pitting.
DIAGNOSIS
Ankle swelling often reduces when the patient’s legs have been elevated for a sustained period of time
(e.g., in bed overnight).
reduced exercise tolerance (common)

Due to poor cardiac functioning.
fatigue (common)
Fatigue, tiredness, and an increased time to recover after exercise are common signs of acute heart
failure.
Due to poor cardiac functioning.
cold extremities (common)

A sign of poor perfusion. Other signs of poor perfusion include:

• Oliguria[1]
• Dizziness[1]
elevated jugular venous pressure (common)

A sign of congestion.
Always check above the level of the patient’s earlobes for an elevated jugular venous pressure
because this is easily missed. However, an elevated jugular venous pressure can be difficult to spot,
even for a heart failure specialist.
risk factors (common)

Ask about risk factors for heart failure if the patient has not previously been diagnosed, including:
• Previous cardiovascular disease; coronary heart disease is the most common cause of heart
failure[9]
• Older age[1]
• Prevalence of heart failure is ≥10% in people >70 years of age[1]

• Diabetes[9]
• Family history of ischaemic heart disease or cardiomyopathy[9]
• Excessive alcohol intake or smoking[9]
• Cardiac arrhythmias including tachyarrhythmia or bradyarrhythmia
• History of systemic conditions associated with heart failure (e.g., sarcoidosis and
haemochromatosis)
• Previous chemotherapy.
Ask about recent drug history. Drugs that may exacerbate heart failure include non-steroidal anti-
inflammatory drugs, steroids, diltiazem, and verapamil.[9]
displaced apex beat (common)
DIAGNOSIS
A common sign of acute heart failure.
gallop rhythm (third heart sound) (common)

A common sign of acute heart failure.
Other diagnostic factors

nocturnal cough (uncommon)
Due to pulmonary congestion.
Frothy sputum suggests that it is alveolar in origin and not bronchial.
wheezing (uncommon)
dizziness (uncommon)
19
• Cold extremities
• Oliguria[1]
confusion (uncommon)
May be a sign of acute heart failure, especially in older people.
loss of appetite (uncommon)

A less common sign of acute heart failure.
nocturnal ischaemic pain (uncommon)

A less common sign of acute heart failure.
ascites (uncommon)
A less common sign of acute heart failure. Due to portal hypertension.
central cyanosis (uncommon)

• Oliguria[1]
• Dizziness[1]
narrow pulse pressure (uncommon)

DIAGNOSIS
• Oliguria[1]
• Dizziness[1]
altered mental status (uncommon)

• Oliguria[1]
• Dizziness[1]
oliguria (uncommon)
• Dizziness[1]
delayed capillary refill time (uncommon)

• Oliguria[1]
• Dizziness[1]
• Central cyanosis.
pulmonary crepitations (uncommon)

The sound of the crackles heard on chest auscultation in heart failure is described as ‘wet’ and
sounding like Velcro. Crackles in heart failure are usually fine and quiet rather than the coarse sounds
that are more commonly heard in lung disease. They can be mistaken for the bilateral crackles of lung
DIAGNOSIS
fibrosis, but patients with fibrotic lungs are more likely to be hypoxic with exertional desaturation.
dullness to percussion/decreased air entry in lung bases#(uncommon)

21
Investigations
1st test to order
Test Result
ECG arrhythmias, ischaemic ST-
Record and interpret a 12-lead ECG for any patient with suspected and T-wave changes
heart failure; monitor this continuously.[5]
• Arrange this immediately if the patient is haemodynamically

unstable or in respiratory failure to look for any life-threatening
cause of acute heart failure such as acute coronary syndrome.
See our topic Non-ST-elevation myocardial infarction .[1]
Check heart rhythm, heart rate, QRS morphology, and QRS duration,
as well as looking for specific abnormalities such as arrhythmias,
atrioventricular block, evidence of a previous myocardial infarction
(e.g., Q waves) and evidence of left ventricular hypertrophy.[1]
The ECG is usually abnormal in acute heart failure.[1]

DIAGNOSIS
ECG showing left ventricular hypertrophy with sinus tachycardia

From the private collections of Syed W. Yusuf,
MBBS, MRCPI, and Daniel Lenihan, MD
chest x-ray pulmonary congestion, pleural
Look for:[1] effusion, pulmonary oedema,
cardiomegaly
• Pulmonary congestion
• Pleural effusion
• Interstitial or alveolar oedema
• Cardiomegaly.
Practical tip
Test Result
Be aware that significant left ventricular dysfunction may be

present without cardiomegaly on chest x-ray.[1]
Chest x-ray showing acute pulmonary oedema with

increased alveolar markings, fluid in the horizontal
fissure, and blunting of the costophrenic angles
DIAGNOSIS
Chest x-ray showing acute pulmonary oedema with

increased alveolar markings and bilateral pleural effusions
23
Test Result
natriuretic peptides NT-proBNP >300 ng/L (>300
Order N-terminal pro-B-type natriuretic peptide (NT-proBNP) if picograms [pg]/mL), BNP
available. Brain natriuretic peptide (BNP) or mid-regional pro- >100 ng/L (>100 pg/mL), MR-
atrial natriuretic peptide (MR-proANP) (in some countries) are
proANP >120 ng/L (>120 pg/
alternatives.[1] [3] [20]
mL)
Normal levels make the diagnosis of acute heart failure unlikely.[1]
[20] However, elevated levels of natriuretic peptides do not
automatically confirm the diagnosis of acute heart failure as they may
be associated with a wide variety of cardiac and non-cardiac causes.
Low levels of natriuretic peptides can occur in end-stage heart failure,
flash pulmonary oedema, or right-sided acute heart failure.[1]
Most older patients presenting to hospital with acute breathlessness

have an elevated NT-proBNP so separate ‘rule in’ diagnostic cut-offs
are useful in this setting.
• If NT-proBNP is significantly elevated (>1800 ng/mL [>1800

pg/mL] in patients >75 years; see table below) acute
heart failure is likely and should be confirmed by inpatient
echocardiography. If the NT-proBNP is intermediate (>300 ng/
mL [>300 pg/mL] but <1800 ng/mL [<1800 pg/mL]), consider
other possible causes of breathlessness, but if these are
excluded and diagnostic suspicion of heart failure remains,
request an echocardiogram.[20]
Age <50 50-75 >75
(years)
NT- >450 >900 >1800

proBNP
level
(ng/L or
pg/mL)
DIAGNOSIS
above
which
acute
heart
failure
is likely
[3]
Practical tip
Be aware that natriuretic peptides may be raised due to other

causes (e.g., acute coronary syndrome, myocarditis, pulmonary
embolism, older age, and renal or liver impairment), hence the
need for practical ‘rule in’ cut-offs.[1]
troponin most patients with acute
Measure troponin in all patients with suspected acute heart heart failure have an elevated
failure.[19] troponin level
Troponin may be useful for prognosis; elevated levels are associated
with poorer outcomes.[19]
Test Result
Be aware that interpretation is not straightforward; type 2 myocardial
infarction and myocardial injury are common.
full blood count may show anaemia

Order a full blood count to identify anaemia, which can worsen heart
failure and also suggest an alternative cause of symptoms.[1]
urea, electrolytes, and creatinine baseline levels
Order as a baseline test to inform decisions on drug treatment that
may affect renal function (e.g., diuretics, ACE inhibitors), and to
exclude concurrent or causative renal failure.
glucose and HbA1c may be elevated
Measure blood glucose in all patients with suspected acute heart
failure to screen for diabetes.[19] In practice, also request HbA1c
(based on the opinion of our expert).
liver function tests may be elevated
Order these for any patient with suspected acute heart failure.
Liver function tests are often elevated due to reduced cardiac output
and increased venous congestion. Abnormal liver function tests are
associated with a worse prognosis.[1]
thyroid function tests may show hypothyroidism or
Order thyroid-stimulating hormone in any patient with newly hyperthyroidism
diagnosed acute heart failure. Both hypothyroidism and
hyperthyroidism can cause acute heart failure.[1] See our topic
Overview of thyroid dysfunction .
C-reactive protein raised in acute heart failure
Consider ordering C-reactive protein (based on the opinion of our
expert).
DIAGNOSIS
Inflammation is associated with progression of chronic heart failure.
Levels of high-sensitivity C-reactive protein are raised in patients with

acute heart failure.[24]
D-dimer raised in acute pulmonary
Indicated in patients with suspicion of acute pulmonary embolism.[19] embolism; see our topic
Pulmonary embolism
echocardiography left ventricular systolic

Arrange immediate bedside echocardiography for any patient who is dysfunction, left ventricular
haemodynamically unstable or in respiratory failure.[1] [3] Specialist diastolic dysfunction,
expertise is required.
constriction, left ventricular
If a patient is haemodynamically stable, arrange echocardiography hypertrophy, valve disease,
within 48 hours if: restrictive heart disease,
right ventricular dysfunction,
• They are not known to have heart failure[5] [20] pulmonary hypertension, may
• Their cardiac structure or function is unknown or is likely to detect the underlying cause
have changed since previous echocardiography.[1]
25
Test Result
Echocardiography is used to assess myocardial systolic and diastolic
function of both left and right ventricles and valvular function and
measure left ventricular ejection fraction (LVEF).[5]
• Evaluating the patient’s LVEF has a key role in assessing the

severity of any decrease in systolic function and is essential in
determining your patient’s long-term management.[1]
Practical tip
The diagnosis of heart failure with reduced ejection fraction

(HFrEF) requires an LVEF <40%. Patients with heart failure
with preserved ejection fraction (HFpEF) have clinical signs
of heart failure with normal or near-normal LVEF. There is an
emerging group of patients with heart failure with mid-range
ejection fraction (40% to 49%) (HFmrEF) and encouraging
data with some therapies recommended for HRrEF, but current
guidelines recommend the same management approach as
for HFpEF (so apply to patients with heart failure with LVEF
>40%).[1]
Other tests to consider
Test Result
venous or arterial blood gas hypoxaemia: PaO 2 <10.67
Perform an arterial blood gas (ABG) if the patient has cardiogenic kPa (<80 mmHg) on arterial
shock, you cannot measure oxygenation with pulse oximetry, or blood gas; metabolic acidosis
an accurate measurement of arterial partial pressure of oxygen with raised lactate: pH <7.35,
(PaO 2 ) and arterial partial pressure of carbon dioxide (PaCO 2 ) is lactate >2 mmol/L (>18 mg/
dL); type I respiratory failure:
needed.[1]
PaO 2 <8 kPa (<60 mmHg);
Consider measurement of blood pH and PaCO 2 even if the patient type II respiratory failure:
does not have cardiogenic shock, especially if they have acute PaCO 2 >6.65 kPa (>50
DIAGNOSIS
pulmonary oedema or known COPD.[1] mmHg)
• Do not routinely perform an ABG. Venous blood gas may

acceptably indicate pH and PaCO 2 .[1]
A blood gas may show:
• Hypoxaemia
• Metabolic acidosis with raised lactate in a patient with
hypoperfusion
• Type I or type II respiratory failure.
blood tests screening for myocarditis may show presence of virus

Consider blood tests screening for acute myocarditis if you suspect
myocarditis as a cause of acute heart failure. These include
screening for viruses that cause acute myocarditis, including
coxsackievirus group B, HIV, cytomegalovirus, Ebstein-Barr virus,
hepatitis, echovirus, adenovirus, enterovirus, human herpes virus 6,
parvovirus B19, and influenza viruses. See our topic Myocarditis .
Test Result
bedside thoracic ultrasound interstitial oedema, pleural
Bedside thoracic ultrasound is useful in countries with no access to effusion
BNP/NT-proBNP testing for detecting signs of interstitial oedema and
pleural effusion in heart failure if specialist expertise is available.[1]
[3]
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Pneumonia • Fever, cough, productive • WBC: elevated.
sputum. • Blood cultures: positive for
• Focal signs of consolidation - organism.
increased vocal fremitus and • Chest x-ray: consolidation.
bronchial breathing.
Pulmonary embolism • Haemoptysis and sharp, • CT pulmonary angiography:

pleuritic chest pain. clot in pulmonary artery.
• Risk factors of
thromboembolism (TE)
include personal history
of TE, family history,
recent trauma, prolonged
immobilisation, smoker,
or combined hormonal
contraception use.
Asthma • Wheezing on physical • Reduced peak flow.

examination. • Spirometry: obstructive
pattern, reversibility with
beta-agonist inhalers
DIAGNOSIS
Interstitial lung disease • Progressively increasing • Chest x-ray: reticular infiltrate
dyspnoea. in the late stages of disease.
• Oxygen desaturation with • High-resolution CT scan:
exercise. ground-glass appearance,
• Fine bibasal crepitations reticular infiltrates,
with no other signs of heart honeycombing, and
failure. architectural distortion.
• Spirometry: restrictive
pattern.
Acute respiratory distress • Severe hypoxia, fine • Chest x-ray: diffuse infiltrates
syndrome crepitations. • Pulmonary artery wedge
pressure: <18 mmHg
Criteria
New York Heart Association (NYHA) functional classification of
heart failure based on severity of symptoms and physical activity[1]
27
• Class I: asymptomatic
• No limitation of physical activity

• Ordinary physical activity does not result in undue breathlessness, fatigue, or palpitations
• Class II: mild symptoms with moderate exertion
• Slight limitation of physical activity

• Comfortable at rest
• Ordinary physical activity causes undue breathlessness, fatigue, or palpitations
• Class III: symptoms with minimal activity
• Marked limitation of physical activity

• Comfortable at rest
• Less than ordinary physical activity causes undue breathlessness, fatigue, or palpitations
• Class IV: symptoms at rest
• Unable to carry on any physical activity without discomfort

• Discomfort increases if any physical activity undertaken
DIAGNOSIS
Acute heart failure Management
Recommendations
Urgent
Request urgent cardiology/critical care support for any patient with:[1]
• Use of accessory muscles for breathing, respiratory rate >25/minute[19]
• Oxygen saturation (SpO 2 ) <90% despite supplemental oxygen
• Signs or symptoms of hypoperfusion (see our topic Shock )
• Acute heart failure due to an acute coronary syndrome (ACS)
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):[1]
• ACS[3]
• See our topics Unstable angina, Non-ST elevation myocardial infarction , and ST-elevation
myocardial infarction
• Rapid arrhythmias or severe bradycardia/conduction disturbance. See our topics Assessment of
tachycardia and Bradycardia
• An acute mechanical cause (e.g., myocardial rupture as a complication of ACS, chest trauma)
• Acute pulmonary embolism. See our topic Pulmonary embolism .
Key Recommendations
Determine acute drug treatment based on the patient’s haemodynamic status and the
presence of shock ; drug treatment options include vasoactive drugs, diuretics, and vasodilators.[1] [3]
[20]
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
MANAGEMENT
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] [5]
29
• 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] [3] [5] 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.[21]
• 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.[5] [20]
• Sacubitril/valsartan is recommended as a replacement for an ACE inhibitor in ambulatory
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] Treatment with sacubitril/valsartan should be started by a heart failure
specialist.[20]
• Aim to provide symptomatic relief and improve general overall health and well-being for
any patient with preserved LVEF (≥40%).[1]
Do not give ox ygen routinely ; it should be used only if the patient has oxygen saturations <90% or
PaO 2 <8 kPa (<60 mmHg).[1]
Ensure the patient has input from the heart failure specialist team within 24 hours of admission to
hospital.[25]
Full Recommendations
Treatment goals
The goals of initial treatment of the patient with acute heart failure are to:[1]
• Improve haemodynamics and organ perfusion

• Restore oxygenation
• Identify and treat any underlying cause
• Alleviate symptoms
• Limit cardiac and renal damage.
Subsequent treatment aims to:[1]
• Control symptoms and congestion and optimise blood pressure

• Initiate and up-titrate disease-modifying drug therapy, or use device therapy where appropriate, to
improve the patient’s clinical status, functional capacity, and quality of life, and to reduce mortality.
Initial supportive care

Request urgent cardiology/critical care support for any patient with:[1]
• Use of accessory muscles for breathing, respiratory rate >25/minute[19]
MANAGEMENT
• Oxygen saturation (SpO 2 ) <90% despite supplemental oxygen

• Signs or symptoms of hypoperfusion (see our topic Shock )
• Acute heart failure due to an acute coronary syndrome (ACS)
Seek expert help on any use of intravenous fluids in patients with known underlying cardiac
impairment such as heart failure.[26]
Monitor transcutaneous arterial oxygen saturation (SpO 2 ).[1]
• Give oxygen if the patient has oxygen saturations <90% or PaO 2 <8 kPa (<60 mmHg).[1]
• Aim for a target ox ygen saturation of 94% to 96% in acutely ill patients who are not at risk of
hypercapnia .
• A lower target SpO 2 of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory
failure.[27]
• Do not use ox ygen 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, SpO 2 <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 (PaO 2 <8
kPa [<60 mmHg]), hypercapnia (PaCo 2 >6.65 kPa [>50 mmHg]), and acidosis (pH <7.35) that cannot be
managed non-invasively.[1]
Evidence: Target ox ygen saturation in acutely ill adults
Too much supplemental oxygen increases mortality.
Evidence from a large systematic review and meta-analysis supports a 96% upper limit for
target ox ygen saturation in non-hypercapnic acutely ill adults.
• 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 SpO 2 range of 94% to 98% for patients not at risk of hypercapnia,
whereas the 2015 Thoracic Society of Australia and New Zealand guideline recommends 92%
to 96%.[27]
• A 2018 systematic review including a meta-analysis of data from 25 randomised controlled trials
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
MANAGEMENT
equivalent to a target saturation ≤96%).[28]
• In-hospital mortality was 11 per 1000 higher with liberal oxygen therapy versus
conservative therapy (95% CI, 2-22 per 1000 more).
31
• Mortality at 30 days was also higher with liberal oxygen (risk ratio 1.14, 95% CI 1.01 to
1.29).
• The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction,
or cardiac arrest, and patients who had emergency surgery. Studies that were limited to
people with chronic respiratory illness or psychiatric illness, patients on extracorporeal life
support, patients receiving hyperbaric oxygen therapy, or those having elective surgery
were all excluded from the review.
• An upper SpO 2 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).[29]
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):[1]
• ACS.[3] See our topics Unstable angina, Non-ST elevation myocardial infarction , and ST-elevation
myocardial infarction
• Rapid arrhythmias (see our topic Assessment of tachycardia ) or severe bradycardia/conduction
disturbance (see our topic Bradycardia )
• An acute mechanical cause (e.g., myocardial rupture as a complication of ACS, acute valvular
regurgitation, chest trauma)
• Acute pulmonary embolism. See our topic Pulmonary embolism .
Ensure the patient has input from the heart failure specialist team within 24 hours of admission to
hospital.[25]
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 2014 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”.[20]
• 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.
MANAGEMENT
• 'Early' is defined as 24 hours in the linked NICE quality standard.[30]

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.[3]
• 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 2020 audit (based on 2018-2019 data)
showed there is still room for improvement in specialist review of patients admitted with heart failure.[5]
• Approximately 82% of patients had a specialist review during hospital admission.
• Overall, 57% 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. 67%).
• There was huge variation, with only 61% 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) was 48% irrespective of the ward setting and specialist review. This
increased to 55% for patients managed on a cardiology ward and 56% for patients who had
specialist review.
• Over a 5-year period prescription rates improved for specialist review, while prescription
rates were generally static or falling for patients not undergoing specialist review.
• In-hospital mortality was 9.3% for all patients admitted to hospital.
MANAGEMENT
• Mortality was reduced for patients who were reviewed by a specialist or managed on a
cardiology ward (8.0% and 6.7%, respectively).
33
• Age-adjusted multivariable analyses showed that not being admitted to a cardiology ward
(hazard ratio 1.67, 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.[20]
Acute drug treatment

Determine acute drug treatment based on the patient’s haemodynamic status and the
presence or absence of shock .[1] [3] [20]
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 set ting with at least level 2 care .[20] [31]
• 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. This should be given in a specialist set ting. [1]
• 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.[32]
Haemodynamically unstable: hypertensive crisis

Give a vasodilator intravenously if the patient has severe hypertension .[1] [20] This may also be
used for relief of dyspnoea in this group of patients.[1] [3] [20]
• Monitor the patient’s symptoms and blood pressure in a critical care environment to ensure
systolic blood pressure remains >90 mmHg.[1] [20]
• 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 .[20] 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.
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
MANAGEMENT
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).[33]
• 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).[33] 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.[34]
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 publication of the 2014 NICE guideline
The Goal-directed Afterload Reduction in Acute Congestive Cardiac Decompensation (GALACTIC)

study (published 2019, n=788) was an open-label, multicentre, pragmatic RCT comparing early
intensive and sustained vasodilatation (n=386) with standard of care (n=402).[35]
• The intervention consisted of a combination of sublingual and transdermal nitrates; oral

hydralazine; and rapid up-titration of ACE inhibitors, angiotensin-II receptor antagonists, or
sacubitril/valsartan. Doses were individualised and target systolic blood pressure was 90 to 110
MANAGEMENT
mmHg.
• Both groups received loop diuretics, beta-blockers, aldosterone antagonists, cardiac devices,
and routine follow-up, as recommended by the European Society of Cardiology guidelines, at
the discretion of the treating physician.
35
• There was no difference in the primary outcome, a composite of all-cause mortality or
rehospitalisation for acute heart failure, at 180 days (n=779, 30.6% with intervention compared
with 27.8% with standard care, adjusted hazard ratio 1.07, 95% CI 0.83 to 1.39).
• There was no difference in dyspnoea at follow-up on day 2 or day 6.
• For adverse events, hypokalaemia and renal function were similar between groups. Other
adverse events occurred more frequently with the intensive intervention: headache (26% vs.
10%), dizziness (15% vs. 10%), and hypotension (8% vs. 2%).
Give an intravenous loop diuretic to all patients with acute heart failure including those with severe
hypertension.[20]
• 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] [20] [36]
• Give the diuretic as either intermittent boluses or a continuous infusion.[1] [20]
• 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] [20]
• Discuss with the patient the best strategies of coping with an increased urine output.[20]
Practical tip
Avoid excessive diuresis; this is more dangerous than oedema.[1]
Consider adding a thia zide-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] [20]
• Give the diuretic as either intermittent boluses or a continuous infusion.[1] [20]
• Monitor the patient’s weight, renal function, and urine output carefully while they are taking
diuretics.[1] [20]
MANAGEMENT
• 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 thia zide-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] [3] [20]
• 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] [20]
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).[33]
• 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
MANAGEMENT
3 hours, risk ratio [RR] 5.63, 95% CI 1.69 to 18.78; GRADE moderate).[33] 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.[34]
37
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 publication of the 2014 NICE guideline
The Goal-directed Afterload Reduction in Acute Congestive Cardiac Decompensation (GALACTIC)

study (published 2019, n=788) was an open-label, multicentre, pragmatic RCT comparing early
intensive and sustained vasodilatation (n=386) with standard of care (n=402).[35]
• The intervention consisted of a combination of sublingual and transdermal nitrates; oral

hydralazine; and rapid up-titration of ACE inhibitors, angiotensin-II receptor antagonists, or
sacubitril/valsartan. Doses were individualised and target systolic blood pressure was 90 to 110
mmHg.
• Both groups received loop diuretics, beta-blockers, aldosterone antagonists, cardiac devices,
and routine follow-up, as recommended by the European Society of Cardiology guidelines, at
the discretion of the treating physician.
• There was no difference in the primary outcome, a composite of all-cause mortality or
rehospitalisation for acute heart failure, at 180 days (n=779, 30.6% with intervention compared
with 27.8% with standard care, adjusted hazard ratio 1.07, 95% CI 0.83 to 1.39).
• There was no difference in dyspnoea at follow-up on day 2 or day 6.
• For adverse events, hypokalaemia and renal function were similar between groups. Other
adverse events occurred more frequently with the intensive intervention: headache (26% vs.
10%), dizziness (15% vs. 10%), and hypotension (8% vs. 2%).
Continue a beta-blocker if the patient is already taking this, unless they have:[20]
• 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
MANAGEMENT
renal function. Use a combination of a loop and a thiazide-type diuretic if the patient has resistant
oedema.[1]
• Monitor the patient’s weight, renal function, and urine output carefully while they are taking a
diuretic.[1] [20]
• 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] [3] [5] [20]
• 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.[21]
• Make sure the patient has remained stable for at least 48 hours after starting or restarting a beta-
blocker before they are discharged.[20]
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.[20]
Sacubitril/valsartan is recommended as a replacement for an ACE inhibitor in ambulatory 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.[1]
• Treatment with sacubitril/valsartan should be started by a heart failure specialist.[21]

Early involvement of the specialist heart failure team for all patients admitted with acute heart
failure enables consideration of additional treatments to optimise outcomes.[5] For patients with heart
failure with reduced ejection fraction these may include:[1] [21]
• Ivabradine
• Isosorbide dinitrate plus hydralazine
• Digoxin
• Cardiac resynchronisation therapy
• Implantable cardioverter defibrillator
• Transplantation or mechanical circulatory support device.
Heart failure with preserved ejection fraction (LVEF ≥40%)

Aim to provide symptomatic relief and improve general overall health and well-being . This
should include screening for and treating any comorbidities.[1]
• These patients tend to be older with more severe symptoms and often have a poor quality of life; no
MANAGEMENT
specific treatment has been shown to significantly reduce morbidity or mortality.[1]

Consider a diuretic for relief of symptoms due to congestion in patients with heart failure with
preserved ejection fraction.[37]
39
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[5] [25]
• They are stable and euvolaemic[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.[20]
Ensure the patient has the following before discharge:
• A follow-up appointment with a member of the multidisciplinary heart failure team within 2 weeks[3]
[5] [20]
• Offer of referral to cardiac rehabilitation.[3] [21] Cardiac rehabilitation should be personalised and
exercise-based. It should also address psychological and educational aspects.[3] [21]
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
Acute ( summary )
haemodynamically unstable:
hypotensive (systolic BP <90 mmHg)
or other signs of cardiogenic shock
1st vasoactive drug
consider respiratory support
plus treatment of underlying cause
consider mechanical support device
plus referral to specialist
hypertensive crisis
1st vasodilator
plus loop diuretic
consider aldosterone antagonist or thia zide-type

diuretic
haemodynamically stable
1st loop diuretic
consider vasodilator

diuretic
consider continue beta-blocker

MANAGEMENT
41
Ongoing ( summary )
acute episode stabilised: LVEF <40%
1st ACE inhibitor or angiotensin-II receptor

antagonist or sacubitril/valsartan
plus beta-blocker
consider aldosterone antagonist
consider diuretic
plus cardiac rehabilitation
acute episode stabilised: LVEF ≥40%
1st referral to specialist
consider diuretic
MANAGEMENT
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
43
Acute
hypotensive (systolic BP <90 mmHg)
or other signs of cardiogenic shock
1st vasoactive drug
» Vasoactive drugs (an inotrope and/or a

vasopressor) should 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
set ting with at least level 2 care .[20] [31]
» Short-term intravenous infusion of

inotropic drugs may be considered in patients
with hypotension (systolic blood pressure <90
mmHg) and/or signs/symptoms of hypoperfusion
despite adequate filling status, to increase
cardiac output, increase blood pressure,
improve peripheral perfusion, and maintain end-
organ function. This should be given in a
specialist set ting. [1]
» Consult a specialist for guidance on suitable

regimens.
Treatment recommended for SOME patients in
selected patient group
» Give ox ygen if the patient has oxygen
saturations <90% or PaO 2 <8 kPa (<60
mmHg).[1]
• Aim for a target oxygen saturation of 94%

to 96% in acutely ill patients who are not
at risk of hypercapnia.
• A lower target SpO 2 of 88% to 92% is
appropriate if the patient is at risk of
hypercapnic respiratory failure.[27]
• Do not use ox ygen 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
MANAGEMENT
(respiratory rate >25 breaths/minute, SpO 2

<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]
Acute
» Consider invasive ventilation if the patient
has respiratory failure leading to hypoxaemia
(PaO 2 <8 kPa [<60 mmHg]), hypercapnia
(PaCo 2 >6.65 kPa [>50 mmHg]), and acidosis
(pH <7.35) that cannot be managed non-
invasively.[1]
Treatment recommended for ALL patients in
» 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):[1]
• Acute coronary syndrome (ACS).[3] See

our topics Unstable angina, Non-ST
elevation myocardial infarction , and ST-
elevation myocardial infarction
• Hypertensive emergency. See our topic
Hypertensive emergencies
• Rapid arrhythmias (see our topic
Assessment of tachycardia ) or severe
bradycardia/conduction disturbance (see
our topic Bradycardia )
• An acute mechanical cause (e.g.,
myocardial rupture as a complication of
ACS, acute valvular regurgitation, chest
trauma)
• Acute pulmonary embolism. See our topic
Pulmonary embolism .
consider mechanical support device

» 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
.[32]
» Ensure the patient has input from the heart
failure specialist team within 24 hours of
MANAGEMENT
admission to hospital.[25]
hypertensive crisis
1st vasodilator
45
Acute
Primary options
» glyceryl trinitrate: 10 micrograms/minute

intravenous infusion initially, adjust dose
according to response, maximum 400
micrograms/minute
OR
» isosorbide dinitrate: 2-10 mg/hour

according to response, maximum 20 mg/hour
Secondary options
» sodium nitroprusside: consult specialist for

guidance on dose
» Give a vasodilator intravenously if there is

severe hypertension.[1] [20] This may also be
used for relief of dyspnoea in this group of
patients.[1] [20]
• Monitor the patient’s symptoms and blood

pressure in a critical care environment
to ensure systolic blood pressure
remains >90 mmHg .[1]
• 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 .[20] 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.
plus loop diuretic

Primary options
» furosemide: 20-50 mg intravenously initially,

increase by 20 mg every 2 hours if required
according to response, maximum 1500 mg/
day
MANAGEMENT
Doses greater than 50 mg should be given by

intravenous infusion only.
» Give an intravenous loop diuretic to all

patients with acute heart failure and severe
hypertension.[20]
Acute
• 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] [20]
• Give the diuretic as either intermittent
boluses or a continuous infusion.[1] [20]
• 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] [20]
• Discuss with the patient the best
strategies of coping with an increased
urine output.[20]

diuretic
Primary options
» spironolactone: 25 mg orally once daily

initially, increase gradually according to
response, maximum 50 mg/day
Doses of up to 200 mg/day may be required
in congestive heart failure.
OR
» eplerenone: 25 mg orally once daily initially,

increase gradually according to response,
maximum 50 mg/day
OR
» metolazone: 5-10 mg orally once daily

» Consider adding an aldosterone antagonist

(e.g., spironolactone, eplerenone) or a thiazide-
type diuretic (e.g., metolazone) if the patient has
resistant oedema or symptoms or signs
of congestion despite treatment with a loop
MANAGEMENT
diuretic.[1]
• Carefully monitor the patient for

hypokalaemia or hyperkalaemia, renal
impairment, and hypovolaemia.[1]
47
Acute
mmHg).[1]

mechanical endotracheal intubation.[1]

invasively.[1]
threatening):[1]

elevation myocardial infarction, and ST-
MANAGEMENT

Acute
trauma)

haemodynamically stable
1st loop diuretic

Primary options
» furosemide: 20-50 mg intravenously initially,

increase by 20 mg every 2 hours if required
according to response, maximum 1500 mg/
day
Doses greater than 50 mg should be given by
intravenous infusion only.
» Give an intravenous loop diuretic 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] [20]
• Give the diuretic as either intermittent
boluses or a continuous infusion.[1] [20]
• Monitor the patient’s weight, renal
function, and urine output carefully while
they are taking diuretics.[1] [20]
• Aim to achieve positive diuresis with

a reduction of body weight by 0.75
to 1.0 kg/day.[1]
MANAGEMENT
consider vasodilator
49
Acute
Primary options
» glyceryl trinitrate: 10 micrograms/minute

according to response, maximum 400
micrograms/minute
OR
» isosorbide dinitrate: 2-10 mg/hour

according to response, maximum 20 mg/hour
Secondary options
» sodium nitroprusside: consult specialist for

guidance on dose
» 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] [3] [20]
• 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] [20]
• 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 .[20] 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.

diuretic
Primary options
MANAGEMENT

Acute
OR

maximum 50 mg/day
OR

» Consider adding an aldosterone antagonist

(e.g., spironolactone, eplerenone) or a thiazide-
type diuretic (e.g., metolazone) 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]
consider continue beta-blocker

» Continue a beta-blocker if the patient is
already taking this, unless they have:[20]
• Heart rate <50 bpm

• Second- or third-degree atrioventricular
block
• Shock.

mmHg).[1]

MANAGEMENT

51
Acute
mechanical endotracheal intubation.[1]

invasively.[1]
threatening):[1]

elevation myocardial infarction and ST-
trauma)

MANAGEMENT
Ongoing
acute episode stabilised: LVEF <40%
1st ACE inhibitor or angiotensin-II receptor

antagonist or sacubitril/valsartan
Primary options
» lisinopril: 2.5 mg orally once daily initially,

maximum 35 mg/day
OR
» ramipril: 1.25 mg orally once daily initially,

maximum 10 mg/day given in 1-2 divided
doses
OR
» enalapril: 2.5 mg orally once daily initially,

maximum 40 mg/day given in 2 divided doses
Secondary options
» candesartan: 4 mg orally once daily initially,

maximum 32 mg/day
OR
» losartan: 12.5 mg orally once daily initially,

maximum 150 mg/day
OR
» valsartan: 40 mg orally twice daily initially,

maximum 320 mg/day
Tertiary options
» sacubitril/valsartan: dose depends on

whether patient is currently stabilised on
an ACE inhibitor (or angiotensin-II receptor
antagonist); consult specialist for guidance on
dose
» Start the patient on an ACE inhibitor (or an

MANAGEMENT
angiotensin-II receptor antagonist if an ACE

inhibitor is not tolerated).[3] [5] [20] In general,
start with low doses and titrate upwards
up to maximally tolerated doses after taking into
account any contraindications.[1]
53
Ongoing
» Sacubitril/valsartan is recommended
as a replacement for an ACE inhibitor
(or angiotensin-II receptor antagonist)
in ambulatory 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] Treatment with sacubitril/
valsartan should be started by a heart failure
specialist.[21]
plus beta-blocker
Primary options
» bisoprolol: 1.25 mg orally once daily initially

for 1 week, increase gradually according to
OR
» carvedilol: 3.125 mg orally twice daily

response, maximum 50 mg/day (body weight
<85 kg) or 100 mg/day (body weight >85 kg)
OR
» nebivolol: 1.25 mg orally once daily initially,

maximum 10 mg/day
» Start a beta-blocker up to maximally tolerated

doses, once the patient’s condition has been
stabilised.[5] [20]
» 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.[21]
» In general, start with low doses and titrate

upwards .[1]
» Make sure the patient has remained stable for

at least 48 hours after starting or restarting a
beta-blocker before they are discharged.[20]
consider aldosterone antagonist
MANAGEMENT

Primary options
Ongoing
OR

maximum 50 mg/day
» Give an aldosterone antagonist in addition

to an ACE inhibitor and a beta-blocker in
patients with acute heart failure and reduced left
ventricular ejection fraction.[5] [20]
» In general, start with low doses and titrate

upwards to maximally tolerated doses after
taking into account any contraindications.[1] [3]
[20]
consider diuretic
Primary options
» furosemide: 40 mg orally once daily initially,

titrate gradually according to response,
maximum 120 mg/day
OR
» torasemide: 5 mg orally once daily initially,

maximum 40 mg/day
OR

maximum 120 mg/day
-or-
maximum 40 mg/day
--AND--
MANAGEMENT
» Start an oral diuretic if the patient has

symptoms or signs of congestion , or switch
from an intravenous to an oral diuretic once
55
Ongoing
a patient who was started on an intravenous
diuretic in the acute phase is euvolaemic .[1]
• Most patients will require a loop diuretic

(e.g., furosemide, torasemide) 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]
• Monitor the patient’s weight, renal
function, and urine output carefully while
they are taking a diuretic.[1] [20]
• 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).
» Early involvement of the specialist heart

failure team for all patients admitted with acute
heart failure enables consideration of additional
treatments to optimise outcomes.[5] For patients
with heart failure with reduced ejection fraction
these may include:[1] [21]
• Ivabradine
• Isosorbide dinitrate plus hydralazine
• Digoxin
• Cardiac resynchronisation therapy
• Implantable cardioverter defibrillator
• Transplantation or mechanical circulatory
MANAGEMENT
support device.

Ongoing
» Offer the patient a referral to cardiac
rehabilitation before they are discharged.[3] [21]
» Cardiac rehabilitation should be personalised

and exercise-based. It should also address
psychological and educational aspects.[3] [21]
acute episode stabilised: LVEF ≥40%
1st referral to specialist

» Early involvement of the specialist heart

failure team for all patients admitted with acute
heart failure enables consideration of additional
treatments to optimise outcomes.[5]
» Offer the patient a referral to cardiac
rehabilitation before they are discharged.[3]
[21]
» Cardiac rehabilitation should be personalised

and exercise-based. It should also address
psychological and educational aspects.[3] [21]
consider diuretic
Primary options

maximum 120 mg/day
OR

maximum 40 mg/day
OR

maximum 120 mg/day
MANAGEMENT
-or-
maximum 40 mg/day
--AND--
57
Ongoing
» Consider a diuretic for relief of symptoms

due to congestion in patients with heart failure
with preserved ejection fraction.[37]
MANAGEMENT
Emerging
Tolvaptan
A vasopressin antagonist that blocks the action of arginine vasopressin at the V 2 receptor in renal tubules
and promotes aquaresis.[1] Tolvaptan may be used to treat patients with volume overload and resistant
hyponatraemia.[1]
Cinepa zide
Cinepazide, a vasodilator, was associated with significantly improving symptoms with less adverse effects in
patients with decompensated heart failure, compared with dobutamine.[130]
Vericiguat
The US Food and Drug Administration has approved vericiguat, an orally administered soluble guanylate
cyclase stimulator, for treatment of chronic heart failure in patients who are hospitalised for heart failure or
need outpatient intravenous diuretics.
Other investigational medications

These include ularitide, tezosentan, istaroxime, perhexiline, relaxin, and cardiac myosin activators. These
agents are investigational and not routinely used to treat acute heart failure. [131] [132] [133] [134]
Adenosine A1- receptor antagonists (e.g., tonapofylline and rolofylline) have failed to show any clinical
benefit in initial studies.[135] [136] When compared with placebo, rolofylline did not show any benefit in
patients with acute heart failure and impaired renal function.[136] In a phase 2 trial of patients with acute
heart failure (ejection fraction <40%), treatment with omecamtiv mecarbil (a selective small-molecule
activator of cardiac myosin) did not improve the primary end point of dyspnoea, or any pre-specified
secondary end point when compared with placebo.[137]
Primary prevention
Consider interventions aimed at modifying risk factors in order to delay or prevent the onset of acute heart
failure, including:[1]
• Coronary artery disease: manage with aspirin, beta-blockers, statins, and ACE inhibitors, as needed
• Optimising treatment of hypertension, smoking cessation, and lipid control provides substantial
benefit in patients with coronary artery disease[1]
• Optimal control of hypertension may require more than one antihypertensive medication.
Different antihypertensive drugs (diuretics, ACE inhibitors, angiotensin receptor blockers, beta-
blockers) have been shown to be effective, especially in older people, both with and without a
history of myocardial infarction[1]
• Diabetes mellitus: in addition to metabolic control, ensure aggressive control of lipids and blood
pressure[15] [16]
• Alcohol consumption and excessive salt and fluid intake: discourage in patients with known left
ventricular dysfunction[17]
• Drugs that can cause or potentiate heart failure: avoid, if safe and possible to do so.[18]
Secondary prevention
MANAGEMENT
All patients with heart failure are recommended to have pneumococcal vaccination and annual influenza
vaccine.
59
Patient discussions
Advise the patient on measures to prevent further episodes, including:
• Restricting fluid intake

• Restricting salt intake
• Limiting alcohol intake
• Continuing medication as prescribed
• Checking of weight daily.
Provide the patient with a self-management plan that outlines when they should seek medical attention.[3]
MANAGEMENT
Acute heart failure Follow up
Monitoring
Monitoring
FOLLOW UP
During the acute phase all patients require cardiac monitoring. Other types of monitoring might also be
indicated, depending on drugs used: for example, renal function, electrolytes, heart rate, blood pressure,
and overall clinical status should be closely monitored during treatment with beta-blockers, aldosterone
antagonists, or angiotensin-converting enzyme inhibitors; renal function, weight, and urine output should
be closely monitored during diuretic therapy.[20]
After discharge from hospital, a follow-up clinical assessment should be undertaken by a member
of the specialist heart failure team within 2 weeks.[20] Follow-up arrangements should be clearly
documented.[3]
Once the acute phase is over and patients are stable and considered to have stable heart failure, they
should be encouraged to do regular aerobic exercise, and it is recommended that they be enrolled in a
multidisciplinary care management programme.[1]
61
Complications
Complications Timeframe Likelihood

FOLLOW UP
arrhythmias short term high
Acute heart failure is frequently precipitated by arrhythmias (in particular, atrial fibrillation), but acute heart
failure may also cause arrhythmias.[140] [141]
complications of glyceryl trinitrate short term high
Commonly causes headache and hypotension. The headache is usually mild to moderate in severity and
either resolves or diminishes in intensity with continued nitrate therapy. If hypotension occurs then the
infusion rate should be decreased. If hypotension persists then the infusion should be discontinued and
restarted when the patient is haemodynamically stable.
complications of treatment: nesiritide short term high
Causes headache and hypotension. If hypotension occurs, then the infusion rate should be decreased.
If hypotension persists, then the infusion should be discontinued and restarted when the patient is
haemodynamically stable.
complications of treatment: diuretics short term medium
Over-diuresis leads to worsening of renal function, hypotension, and hypokalaemia, and also activation
of neurohormones including renin-angiotensin system and the sympathetic system. It may potentiate
the toxicity of other agents like digoxin, either by causing hypokalaemia or by decreasing the glomerular
filtration.
In cases of worsening renal impairment due to over-diuresis, the dose of diuretics should be decreased.
In case of severe renal impairment the diuretic can be withheld and the patients assessed daily, with re-
introduction of diuretic at lower doses.
complications of treatment: inotropes short term medium
Dobutamine and milrinone can cause arrhythmias and worsening of coronary ischaemia.
The occurrence of sustained arrhythmias should lead to discontinuation. In cases where these
medications are absolutely needed, concomitant use of amiodarone may be advisable, although there are
no large-scale data on the use of anti-arrhythmics in this setting. If the patient has symptomatic coronary
ischaemia, these infusions should be discontinued.
Prognosis
Acute heart failure carries an inpatient mortality of 11% overall; in England and Wales there is significant
variation between acute hospitals (lowest 6%; highest 26%).[3]
Predictors of adverse outcomes include: hypotension, renal dysfunction, older age, male sex, ischaemic
congestive heart failure (CHF), previous CHF, respiratory rate on admission >30/minute, anaemia,
hyponatraemia, elevated troponin, elevated B-type natriuretic peptide, and other comorbidities such as
cancer.[138]
FOLLOW UP
The National Heart Failure Audit 2018/2019, which included 89% of patients admitted to hospital with acute
heart failure in England and Wales, showed that mortality was lower for patients admitted to cardiology
(6.7%) compared with general medical (9.3%) wards and for those seen by a specialist (8.0%) compared
with those who didn’t (13.2%).[5]
One study found that among patients hospitalised with heart failure, patients across the ejection fraction
spectrum have a similarly poor 5-year survival with an elevated risk for cardiovascular and heart failure
admission.[139] All patients in this cohort, regardless of ejection fraction, had a remarkably high mortality
rate at 5 years from index admission (75.4%).[139]
63
Acute heart failure Guidelines
Diagnostic guidelines
Europe
ESC guidelines for the diagnosis and treatment of acute and chronic heart
failure
Published by: European Society of Cardiology Last published: 2016
Acute heart failure: diagnosis and management

Published by: National Institute for Health and Care Excellence Last published: 2014
North America
2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the
management of heart failure
GUIDELINES
Published by: American College of Cardiology; American Heart Last published: 2017
Association; Heart Failure Society of America
2017 comprehensive update of the Canadian Cardiovascular Society

guidelines for the management of heart failure
Published by: Canadian Cardiovascular Society Last published: 2017
2013 ACCF/AHA guideline for the management of heart failure

Association
Treatment guidelines
Europe
ESC guidelines for the diagnosis and treatment of acute and chronic heart
failure
Published by: European Society of Cardiology Last published: 2016
Implantable cardioverter defibrillators and cardiac resynchronisation therapy

for arrhythmias and heart failure
Published by: National Institute for Health and Care Excellence Last published: 2014
Acute heart failure Guidelines
North America
Academy of Nutrition and Dietetics evidence-based practice guideline for the

management of heart failure in adults
Published by: Academy of Nutrition and Dietetics Last published: 2018
2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the
management of heart failure
2017 comprehensive update of the Canadian Cardiovascular Society

guidelines for the management of heart failure
Published by: Canadian Cardiovascular Society Last published: 2017
2016 ACC/AHA/HFSA focused update on new pharmacological therapy for
GUIDELINES
heart failure: an update of the 2013 ACCF/AHA guideline for the management
of heart failure
2013 ACCF/AHA guideline for the management of heart failure

Association
Recommendations for the use of mechanical circulatory support: device

strategies and patient selection
Published by: American Heart Association Last published: 2012
2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based

therapy of cardiac rhythm abnormalities
Association; Heart Rhythm Society
Oceania
Guidelines for the prevention, detection, and management of heart failure in

Australia
Published by: National Heart Foundation of Australia; Cardiac Society Last published: 2018
of Australia and New Zealand
65
Acute heart failure References
Key articles
• Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC guidelines for the diagnosis and treatment of
REFERENCES
acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic
heart failure of the European Society of Cardiology (ESC) developed with the special contribution of
the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016 Jul 14;37(27):2129-200. Full text
Abstract
• National Confidential Enquiry into Patient Outcome and Death. Failure to function. 2018
[internet publication]. Full text
• National Institute for Cardiovascular Outcomes Research; British Society For Heart Failure. National
heart failure audit (NHFA) 2020 summary report (2018/19 data). December 2020 [internet publication].
Full text
• National Institute for Health and Care Excellence. Acute heart failure: diagnosis and management.
October 2014 [internet publication]. Full text
References
1. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC guidelines for the diagnosis and treatment of
acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic
heart failure of the European Society of Cardiology (ESC) developed with the special contribution of
the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2016 Jul 14;37(27):2129-200. Full text
Abstract
2. National Institute for Cardiovascular Outcomes Research; British Society For Heart Failure. National
heart failure audit 2019 summary report (2017/18 data). September 2019 [internet publication]. Full
text
3. National Confidential Enquiry into Patient Outcome and Death. Failure to function. 2018
[internet publication]. Full text
4. Savarese G, Lund LH. Global public health burden of heart failure. Card Fail Rev. 2017 Apr;3(1):7-11.
Full text Abstract
5. National Institute for Cardiovascular Outcomes Research; British Society For Heart Failure. National
heart failure audit (NHFA) 2020 summary report (2018/19 data). December 2020 [internet publication].
Full text
6. Alla F, Zannad F, Filippatos G. Epidemiology of acute heart failure syndromes. Heart Fail Rev. 2007
Jun;12(2):91-5. Abstract
7. Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure syndromes: current state and framework
for future research. Circulation. 2005 Dec 20;112(25):3958-68. Full text Abstract
8. Jackson G, Gibbs CR, Davies MK, Lip GY. ABC of heart failure. Pathophysiology. BMJ. 2000 Jan
15;320(7228):167-70. Abstract
REFERENCES
9. Williams RP, Oakeshott P. Diagnosis and management of chronic heart failure. BMJ. 2014 Feb
12;348:g1429. Abstract
10. Fonarow GC. The Acute Decompensated Heart Failure National Registry (ADHERE): opportunities to
improve care of patients hospitalized with acute decompensated heart failure. Rev Cardiovasc Med.
2003;4(suppl 7):S21-30. Abstract
11. Tsuyuki RT, McKelvie RS, Arnold JM, et al. Acute precipitants of congestive heart failure
exacerbations. Arch Intern Med. 2001 Oct 22;161(19):2337-42. Full text Abstract
12. Takizawa M, Kobayakawa N, Uozumi H, et al. A case of transient left ventricular ballooning
with pheochromocytoma, supporting pathogenetic role of catecholamines in stress-induced
cardiomyopathy or takotsubo cardiomyopathy. Int J Cardiol. 2007 Jan 2;114(1):e15-7. Abstract
13. Rodondi N, Newman AB, Vittinghoff E, et al. Subclinical hypothyroidism and the risk of heart failure,
other cardiovascular events, and death. Arch Intern Med. 2006 Mar;8(3):217-8. Full text Abstract
14. Berlin T, Lubina A, Levy Y, et al. Graves' disease presenting as right heart failure. Isr Med Assoc J.
2006 Mar;8(3):217-8. Abstract
15. Snow V, Aronson MD, Hornbake ER, et al. Lipid control in the management of type 2 diabetes mellitus:
a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2004 Apr
20;140(8):644-9. Full text Abstract
16. Yusuf S, Sleight P, Pogue J, et al; the Heart Outcomes Prevention Evaluation Study Investigators.
Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk
patients. N Engl J Med. 2000 Jan 20;342(3):145-53. Full text Abstract
17. Heart Failure Society of America. Executive summary: HFSA 2010 Comprehensive Heart Failure
Practice Guideline. J Card Fail. 2010 Jun;16(6):e1-194. Abstract
18. Page RL, O'Bryant CL, Cheng D, et al. Drugs that may cause or exacerbate heart failure: a scientific
statement from the American Heart Association. Circulation. 2016 Aug 9;134(6):e32-69. Full text
Abstract
19. Mebazaa A, Yilmaz MB, Levy P, et al. Recommendations on pre-hospital & early hospital management
of acute heart failure: a consensus paper from the Heart Failure Association of the European Society
of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency
Medicine. Eur J Heart Fail. 2015 Jun;17(6):544-58. Full text Abstract
20. National Institute for Health and Care Excellence. Acute heart failure: diagnosis and management.
October 2014 [internet publication]. Full text
21. National Institute for Health and Care Excellence. Chronic heart failure in adults: diagnosis and
management. September 2018 [internet publication]. Full text
67
22. Watson RD, Gibbs CR, Lip GY. ABC of heart failure: clinical features and complications. BMJ. 2000
Jan 22;320(7229):236-9. Full text Abstract
REFERENCES
23. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical
presentation and outcome. BMC Cardiovasc Disord. 2007 May 14;7:16. Full text Abstract
24. Kalogeropoulos AP, Tang WH, Hsu A, et al. High-sensitivity C-reactive protein in acute heart failure:
insights from the ASCEND-HF trial. J Card Fail. 2014 May;20(5):319-26. Abstract
25. National Institute for Health and Care Excellence. Acute heart failure: quality standard. December
2015 [internet publication]. Full text
26. National Institute for Health and Care Excellence. Intravenous fluid therapy in adults in hospital. May
2017 [internet publication]. Full text
27. O'Driscoll BR, Howard LS, Earis J, et al. BTS guideline for oxygen use in adults in healthcare and
emergency settings. Thorax. 2017 Jun;72(suppl 1):ii1-90. Full text Abstract
28. Chu DK, Kim LH, Young PJ, et al. Mortality and morbidity in acutely ill adults treated with liberal
versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis. Lancet. 2018 Apr
28;391(10131):1693-705. Abstract
29. Siemieniuk RAC, Chu DK, Kim LH, et al. Oxygen therapy for acutely ill medical patients: a clinical
practice guideline. BMJ. 2018 Oct 24;363:k4169. Abstract
30. National Institute for Health and Care Excellence. Acute heart failure, quality statement 3: organisation
of care – early specialist input. December 2015 [internet publication]. Full text
31. Bistola V, Arfaras-Melainis A, Polyzogopoulou E, et al. Inotropes in acute heart failure: from guidelines
to practical use: therapeutic options and clinical practice. Card Fail Rev. 2019 Nov;5(3):133-9. Full text
Abstract
32. Hajjar LA, Teboul JL. Mechanical circulatory support devices for cardiogenic shock: state of the art.
Crit Care. 2019 Mar 9;23(1):76. Full text Abstract
33. National Institute for Health and Care Excellence. Acute heart failure: diagnosis and management -
evidence. October 2014 [internet publication]. Full text
34. Publication Committee for the VMAC Investigators (Vasodilatation in the Management of Acute CHF).
Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a
randomized controlled trial. JAMA. 2002 Mar 27;287(12):1531-40. Full text Abstract
35. Kozhuharov N, Goudev A, Flores D, et al. Effect of a strategy of comprehensive vasodilation vs

usual care on mortality and heart failure rehospitalization among patients with acute heart failure: the
GALACTIC randomized clinical trial. JAMA. 2019 Dec 17;322(23):2292-302. Full text Abstract
36. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart
failure. N Engl J Med. 2011 Mar 3;364(9):797-805. Full text Abstract
37. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/
AHA guideline for the management of heart failure: a report of the American College of Cardiology/
American Heart Association task force on clinical practice guidelines and the Heart Failure Society of
REFERENCES
America. J Card Fail. 2017 Aug;23(8):628-51. Full text Abstract
38. O'Driscoll BR, Howard LS, Earis J, et al; British Thoracic Society Emergency Oxygen Guideline Group;
BTS Emergency Oxygen Guideline Development Group. BTS guideline for oxygen use in adults in
healthcare and emergency settings. Thorax. 2017 Jun;72(suppl 1):ii1-90 Abstract
39. British Thoracic Society; Scottish Intercollegiate Guidelines Network. British guideline on the
management of asthma: a national clinical guideline. July 2019 [internet publication]. Full text
40. Chu DK, Kim LH, Young PJ, et al. Mortality and morbidity in acutely ill adults treated with liberal
versus conservative oxygen therapy (IOTA): systematic review and meta-analysis. Lancet. 2018 Apr
26;391(10131):1693-1705 Abstract
41. Siemieniuk RAC, Chu DK, Kim LH, et al. Oxygen therapy for acutely ill medical patients: a clinical
practice guideline. BMJ. 2018 Oct 24;363:k4169 Full text Abstract
42. Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC guidelines for the diagnosis and treatment of
acute and chronic heart failure. Eur Heart J. 2016 May 20;37(27):2129-200 Full text Abstract
43. National Institute for Health and Care Excellence. Chronic heart failure in adults: diagnosis and
management. September 2018 [internet publication] Full text
44. Williams RP, Oakeshott P. Diagnosis and management of chronic heart failure. BMJ. 2014 Feb
12;348:g1429 Full text Abstract
45. Cosentino F, Grant PJ, Aboyans V, et al. 2019 ESC guidelines on diabetes, pre-diabetes, and
cardiovascular diseases developed in collaboration with the EASD. Eur Heart J. 2020 Jan
7;41(2):255-323 Full text Abstract
46. DiMatteo MR, Lepper HS, Croghan TW. Depression is a risk factor for noncompliance with medical
treatment: meta-analysis of the effects of anxiety and depression on patient adherence. Arch Intern
Med. 2000 Jul 24;160(14):2101-7 Abstract
47. National Confidential Enquiry into Patient Outcome and Death. Failure to function. 2018 [internet
publication] Full text
48. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic
hypotension, neurally mediated syncope and the postural tachycardia syndrome. Clin Auton Res. 2011
Apr;21(2):69-72 Abstract
49. Kidney Disease Improving Global Outcomes. KDIGO 2012 clinical practice guideline for the evaluation
and management of chronic kidney disease. January 2013 [internet publication] Full text
50. Hsu CY, Ordoñez JD, Chertow GM, et al. The risk of acute renal failure in patients with chronic kidney
disease. Kidney Int. 2008 Apr 2;74(1):101-7 Full text Abstract
69
51. Chowdhury TA, Cheston H, Claydon A. Managing adults with diabetes in hospital during an acute
illness. BMJ. 2017 Jun 22;357:j2551 Full text Abstract
REFERENCES
52. Joint British Diabetes Societies for inpatient care. The use of variable rate intravenous insulin infusion
(VRIII) in medical inpatients. October 2014 [internet publication] Full text
53. Joint British Diabetes Societies for inpatient care. Management of adults with diabetes undergoing
surgery and elective procedures: Improving standards. Revised March 2016 [internet publication] Full
text
54. British National Formulary 77. Metformin hydrochloride. London: BMJ Group, RCPCH Publications Ltd
and the Royal Pharmaceutical Society of Great Britain. July 2020 Full text
55. Medicines and Healthcare products Regulatory Agency. SGLT2 inhibitors: monitor ketones in blood
during treatment interruption for surgical procedures or acute serious medical illness. March 2020
[internet publication] Full text
56. Peters AL, Buschur EO, Buse JB, et al. Euglycemic diabetic ketoacidosis: a potential complication of
treatment with sodium-glucose cotransporter 2 inhibition. Diabetes Care. 2015 Jun 15;38(9):1687-93
Abstract
57. Joint British Diabetes Societies Inpatient Care Group. The management of diabetic ketoacidosis in
adults. 2nd ed. September 2013 [internet publication] Full text
58. Fritz Z, Slowther AM, Perkins GD. Resuscitation policy should focus on the patient, not the decision.
BMJ. 2017 Feb 28;356:j813 Full text Abstract
59. National Institute for Health and Care Excellence. Decision making and mental capacity. October 2018
60. Department of Health. Mental Capacity Act 2005 [internet publication] Full text
61. Social Care Institute for Excellence. Independent mental capacity advocate (IMCA). 2011 [internet
62. Grau AJ, Urbanek C, Palm F. Common infections and the risk of stroke. Nat Rev Neurol. 2010 Nov
9;6(12):681-94 Abstract
63. Eigenbrodt ML, Rose KM, Couper DJ, et al. Orthostatic hypotension as a risk factor for stroke: the
atherosclerosis risk in communities (ARIC) study, 1987-1996. Stroke. 2000 Oct;31(10):2307-13
Abstract
64. Winstein CJ, Stein J, Arena R, et al. Guidelines for adult stroke rehabilitation and recovery: a guideline
for healthcare professionals from the American Heart Association/American Stroke Association.
Stroke. 2016 May 4;47(6):e98-e169 Full text Abstract
65. Pendlebury ST, Klaus SP, Mather M, et al. Routine cognitive screening in older patients admitted
to acute medicine: abbreviated mental test score (AMTS) and subjective memory complaint versus
Montreal Cognitive Assessment and IQCODE. Age Ageing. 2015 Oct 13;44(6):1000-5 Full text
Abstract
REFERENCES
66. Hodkinson HM. Evaluation of a mental test score for assessment of mental impairment in the elderly.
Age Ageing. 1972 Nov;1(4):233-8 Abstract
67. The National Institute for Health and Clinical Excellence. Delirium: diagnosis, prevention and
management. (CG103). March 2019 [internet publication] Full text
68. The National Institute for Health and Clinical Excellence. Dementia: assessment, management and
support for people living with dementia and their carers. June 2018 [internet publication] Full text
69. Scottish Intercollegiate Guidelines Network. Risk reduction and management of delirium. March 2019
70. Nova Scotia Health Authority. This is not my Mom. 2012 [internet publication] Full text
71. Inouye SK, Schlesinger MJ, Lydon TJ. Delirium: a symptom of how hospital care is failing older
persons and a window to improve quality of hospital care. Am J Med. 1999 May;106(5):565-73
Abstract
72. Bellelli G, Morandi A, Davis DH, et al. Validation of the 4AT, a new instrument for rapid delirium
screening: a study in 234 hospitalised older people. Age Ageing. 2014 Mar 2;43(4):496-502 Full text
Abstract
73. MacLullich AM, Shenkin SD, Goodacre S, et al. The 4 'A's test for detecting delirium in acute medical
patients: a diagnostic accuracy study. Health Technol Assess. 2019 Aug;23(40):1-194 Full text
Abstract
74. White S, Griffiths R, Baxter M, et al. Guidelines for the peri-operative care of people with dementia:
guidelines from the Association of Anaesthetists. Anaesthesia. 2019 Jan 11;74(3):357-72 Full text
Abstract
75. Siddiqi N, Harrison JK, Clegg A, et al. Interventions for preventing delirium in hospitalised non-ICU
patients. Cochrane Database Syst Rev. 2016 Mar 11;3:CD005563 Full text Abstract
76. Martinez F, Tobar C, Hill N. Preventing delirium: should non-pharmacological, multicomponent

interventions be used? A systematic review and meta-analysis of the literature. Age Ageing. 2014 Nov
25;44(2):196-204 Full text Abstract
77. Public Health England. Urinary tract infection: diagnostic tools for primary care. September 2019
78. Pryor C, Clarke A. Nursing care for people with delirium superimposed on dementia. Nurs Older
People. 2017 Mar 31;29(3):18-21 Full text Abstract
79. Ma H, Huang Y, Cong Z, et al. The efficacy and safety of atypical antipsychotics for the treatment
of dementia: a meta-analysis of randomized placebo-controlled trials. J Alzheimers Dis.
2014;42(3):915-37 Abstract
71
80. Huybrechts KF, Gerhard T, Crystal S, et al. Differential risk of death in older residents in nursing
homes prescribed specific antipsychotic drugs: population based cohort study. BMJ. 2012 Feb
23;344:e977 Full text Abstract
REFERENCES
81. Van Leeuwen E, Petrovic M, van Driel ML, et al. Withdrawal versus continuation of long-term
antipsychotic drug use for behavioural and psychological symptoms in older people with dementia.
Cochrane Database Syst Rev. 2018 Mar 30;3:CD007726 Full text Abstract
82. American Diabetes Association. 15. Diabetes care in the hospital: standards of medical care in
diabetes - 2020. Diabetes Care. 2020 Jan;43(suppl 1):S193-S202 Full text Abstract
83. NHS Digital. National Diabetes Inpatient Audit (NaDIA) - 2017. March 2018 [internet publication] Full
text
84. Joint British Diabetes Societies for inpatient care. Self-management of diabetes in hospital. March
2012 [internet publication] Full text
85. National Institute for Health and Care Excellence. Type 1 diabetes in adults: diagnosis and
management. July 2016 [internet publication] Full text
86. Moghissi ES, Korytkowski MT, DiNardo M, et al. American Association of Clinical Endocrinologists
and American Diabetes Association consensus statement on inpatient glycemic control. Endocr Pract.
2009 May-Jun;15(4):353-69 Abstract
87. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl
J Med. 2001 Nov 8;345(19):1359-67 Full text Abstract
88. NICE-SUGAR Study Investigators; Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional
glucose control in critically ill patients. N Engl J Med. 2009 Mar 26;360(13):1283-97. Full text
Abstract
89. Marik PE, Preiser JC. Toward understanding tight glycemic control in the ICU: a systematic review and
metaanalysis. Chest. 2009 Dec 16;137(3):544-51 Full text Abstract
90. Joint British Diabetes Societies for inpatient care. The management of the hyperosmolar
hyperglycaemic state (HHS) in adults with diabetes. August 2012 [internet publication] Full text
91. Rehman A, Setter SM, Vue MH. Drug-induced glucose alterations part 2: drug-Induced hyperglycemia.
Diabetes Spect. 2011 Nov;24(4):234-8 Full text
92. Joint British Diabetes Societies for inpatient care. The hospital management of hypoglycaemia in
adults with diabetes mellitus. 4th ed. January 2020 [internet publication] Full text
93. Rowles S, Kilvert A, Sinclair A; on behalf of the Association of British Clinical Diabetologists (ABCD).
ABCD position statement on diabetes and end of life care. Pract Diab Int, 2011;28:26-7 Full text
94. National Institute for Health and Care Excellence. Diabetic foot problems: prevention and
management. October 2019 [internet publication] Full text
95. Rayman G, Vas PR, Baker N, et al. The Ipswich Touch Test: a simple and novel method to identify
inpatients with diabetes at risk of foot ulceration. Diabetes Care. 2011 May 18;34(7):1517-8 Full text
Abstract
REFERENCES
96. Salpeter SR, Ormiston TM, Salpeter EE. Cardiovascular effects of beta-agonists in patients with
asthma and COPD: a meta-analysis. Chest. 2004 Jun;125(6):2309-21 Full text Abstract
97. Au DH, Curtis JR, Every NR, et al. Association between inhaled beta-agonists and the risk of unstable
angina and myocardial infarction. Chest. 2002 Mar;121(3):846-51 Full text Abstract
98. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management
and prevention of chronic obstructive pulmonary disease. 2020 [internet publication] Full text
99. Walters JA, Tan DJ, White CJ, et al. Different durations of corticosteroid therapy for exacerbations of
chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018 Mar 19;3:CD006897 Full
text Abstract
100. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen
Intern Med. 2001 Sep;16(9):606-13 Abstract
101. Boden JM, Fergusson DM. Alcohol and depression. Addiction. 2011 Mar 7;106(5):906-14 Full text
Abstract
102. Taylor DM, Barnes TRE, Young AH. The Maudsley prescribing guidelines in psychiatry. 13th edition.
Chichester: Wiley-Blackwell; 2018
103. Cleare A, Pariante CM, Young AH, et al. Evidence-based guidelines for treating depressive disorders
with antidepressants: a revision of the 2008 British Association for Psychopharmacology guidelines. J
Psychopharmacol. 2015 May 12;29(5):459-525 Full text Abstract
104. National Institute for Health and Care Excellence. Depression in adults with a chronic physical health
problem: recognition and management. October 2009 [internet publication] Full text
105. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005 Mar 17;352(11):1112-20
Abstract
106. Flowers L. Nicotine replacement therapy. Am J Psychiatry Resid. 2016 Jun;11(6)4-7 Full text
107. Desai HD, Seabolt J, Jann MW. Smoking in patients receiving psychotropic medications: a
pharmacokinetic perspective. CNS Drugs. 2001;15(6):469-94 Abstract
108. Oliveira P, Ribeiro J, Donato H, Madeira N. Smoking and antidepressants pharmacokinetics: a

systematic review. Ann Gen Psychiatry. 2017;16:17 Full text Abstract
109. National Centre for Smoking Cessation and Training. Smoking cessation and mental health: a briefing
for front-line staff. 2014 [internet publication] Full text
110. National Institute for Health and Care Excellence. Liaison psychiatry. In: Emergency acute medical
care in over 16s: service delivery and organisation. March 2018 [internet publication] Full text
73
111. National Confidential Enquiry into Patient Outcome and Death (NCEPOD). Treat as one. Bridging the
gap between mental and physical healthcare in general hospitals. 2017 [internet publication] Full text
REFERENCES
112. Clarke DM, Currie KC. Depression, anxiety and their relationship with chronic diseases: a review of the
epidemiology, risk and treatment evidence. Med J Aust. 2009 Apr 6;190(7 suppl):S54-60 Abstract
113. Prina AM, Cosco TD, Dening T, et al. The association between depressive symptoms in the
community, non-psychiatric hospital admission and hospital outcomes: a systematic review. J
Psychosom Res. 2014 Nov 8;78(1):25-33 Full text Abstract
114. World Health Organization. Excess mortality in persons with severe mental disorders. 2016 [internet
115. Clark AL, Kalra PR, Petrie MC, et al. Change in renal function associated with drug treatment in heart
failure: national guidance. Heart. 2019 Jun;105(12):904-10 Abstract
116. Medicines and Healthcare products Regulatory Agency. Spironolactone and renin-angiotensin system
drugs in heart failure: risk of potentially fatal hyperkalaemia. December 2016 [internet publication] Full
text
117. Huang YL, Lai CC, Wang YH, et al. Impact of selective and nonselective beta-blockers on the risk
of severe exacerbations in patients with COPD. Int J Chron Obstruct Pulmon Dis. 2017;12:2987-96
Abstract
118. Salpeter S, Ormiston T, Salpeter E. Cardioselective beta-blockers for chronic obstructive pulmonary
disease. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD003566 Full text Abstract
119. Maltais F, Buhl R, Koch A, et al. β-Blockers in COPD: a cohort study from the TONADO research
program. Chest. 2018 Jun;153(6):1315-25 Full text Abstract
120. Quint JK, Herrett E, Bhaskaran K, et al. Effect of β blockers on mortality after myocardial infarction in
adults with COPD: population based cohort study of UK electronic healthcare records. BMJ. 2013 Nov
22;347:f6650 Full text Abstract
121. Gottlieb SS, McCarter RJ, Vogel RA. Effect of beta-blockade on mortality among high-risk and low-risk
patients after myocardial infarction. N Engl J Med. 1998 Aug 20;339(8):489-97 Full text Abstract
122. Wang WH, Cheng CC, Mar GY, et al. Improving outcomes in chronic obstructive pulmonary disease by
taking beta-blockers after acute myocardial infarction: a nationwide observational study. Heart Vessels.
2019 Jul;34(7):1158-67 Abstract
123. Liao KM, Lin TY, Huang YB, et al. The evaluation of β-adrenoceptor blocking agents in patients
with COPD and congestive heart failure: a nationwide study. Int J Chron Obstruct Pulmon Dis.
2017;12:2573-81 Abstract
124. Lipworth B, Skinner D, Devereux G, et al. Underuse of β-blockers in heart failure and chronic
obstructive pulmonary disease. Heart. 2016 Dec 1;102(23):1909-14 Full text Abstract
125. National Heart, Lung, and Blood Institute. Guidelines for the diagnosis and management of asthma:
expert panel report 3. August 2007 [internet publication] Full text
REFERENCES
126. Global Initiative for Asthma. Global strategy for asthma management and prevention. 2018 [internet
127. Salpeter S, Ormiston T, Salpeter E. Cardioselective beta-blockers for reversible airway disease.
Cochrane Database Syst Rev. 2002;(4):CD002992 Full text Abstract
128. Morales DR, Jackson C, Lipworth BJ, et al. Adverse respiratory effect of acute β-blocker exposure
in asthma: a systematic review and meta-analysis of randomized controlled trials. Chest. 2014
Apr;145(4):779-86 Full text Abstract
129. National Institute for Health and Care Excellence. Smoking: acute, maternity and mental health
services. Public health guideline [PH48]. November 2013 [internet publication] Full text
130. Lu Y, Huang D, Dou C, et al. Clinical efficacy of intravenous cinepazide in the treatment of severe
decompensated heart failure. Biomedical Research (India). 2012;23(4):561-5.
131. De Luca L, Mebazaa A, Filippatos G, et al. Overview of emerging pharmacologic agents for acute
heart failure syndromes. Eur J Heart Fail. 2008 Feb;10(2):201-13. Full text Abstract
132. De Luca L, Fonarow GC, Mebazaa A, et al. Early pharmacological treatment of acute heart failure
syndromes: a systematic review of clinical trials. Acute Card Care. 2007;9(1):10-21. Abstract
133. deGoma EM, Vagelos RH, Fowler MB, et al. Emerging therapies for the management
of decompensated heart failure: from bench to bedside. J Am Coll Cardiol. 2006 Dec
19;48(12):2397-409. Abstract
134. Teerlink JR, Metra M, Felker GM, et al. Relaxin for the treatment of patients with acute heart failure
(Pre-RELAX-AHF): a multicentre, randomised, placebo-controlled, parallel-group, dose-finding phase
IIb study. Lancet. 2009 Apr 25;373(9673):1429-39. Abstract
135. Ensor CR, Russell SD. Tonapofylline: a selective adenosine-1 receptor antagonist for the treatment of
heart failure. Expert Opin Pharmacother. 2010 Oct;11(14):2405-15. Abstract
136. Massie BM, O'Connor CM, Metra M, et al. Rolofylline, an adenosine A1-receptor antagonist, in acute
heart failure. N Engl J Med. 2010 Oct 7;363(15):1419-28. Full text Abstract
137. Teerlink JR, Felker GM, McMurray JJ, et al; ATOMIC-AHF Investigators. Acute treatment with
omecamtiv mecarbil to increase contractility in acute heart failure: the ATOMIC-AHF study. J Am Coll
Cardiol. 2016 Mar 29;67(12):1444-55. Full text Abstract
138. Dec GW. Management of acute decompensated heart failure. Curr Probl Cardiol. 2007
Jun;32(6):321-66. Abstract
139. Shah KS, Xu H, Matsouaka RA, et al. Heart failure with preserved, borderline, and reduced ejection
fraction: 5-year outcomes. J Am Coll Cardiol. 2017 Nov 14;70(20):2476-86. Abstract
75
140. Siurila-Waris K, Lassus J, Melin J, et al. Characteristics, outcomes, and predictors of 1-year mortality
in patients hospitalized for acute heart failure. Eur Heart J. 2006 Dec;27(24):3011-7. Full text
Abstract
REFERENCES
141. Benza RL, Tallaj JA, Felker GM, et al. The impact of arrhythmias in acute heart failure. J Card Fail.
2004 Aug;10(4):279-84. Abstract
Acute heart failure Images
Images
IMAGES
Figure 1: ECG showing left ventricular hypertrophy with sinus tachycardia
Figure 2: Chest x-ray showing acute pulmonary oedema with increased alveolar markings, fluid in the
horizontal fissure, and blunting of the costophrenic angles
77
IMAGES Acute heart failure Images
Figure 3: Chest x-ray showing acute pulmonary oedema with increased alveolar markings and bilateral
pleural effusions
Acute heart failure Images
IMAGES
Figure 4: ECG showing left ventricular hypertrophy with sinus tachycardia
Figure 5: Chest x-ray showing acute pulmonary oedema with increased alveolar markings, fluid in the
horizontal fissure, and blunting of the costophrenic angles
79
IMAGES Acute heart failure Images
Figure 6: Chest x-ray showing acute pulmonary oedema with increased alveolar markings and bilateral
pleural effusions
Acute heart failure Disclaimer
Disclaimer
BMJ Best Practice is intended for licensed medical professionals. BMJ Publishing Group Ltd (BMJ) does not
advocate or endorse the use of any drug or therapy contained within this publication nor does it diagnose
patients. As a medical professional you retain full responsibility for the care and treatment of your patients
and you should use your own clinical judgement and expertise when using this product.
This content is not intended to cover all possible diagnosis methods, treatments, follow up, drugs and any
contraindications or side effects. In addition, since such standards and practices in medicine change as
new data become available, you should consult a variety of sources. We strongly recommend that you
independently verify specified diagnosis, treatments and follow-up and ensure it is appropriate for your
patient within your region. In addition, with respect to prescription medication, you are advised to check the
product information sheet accompanying each drug to verify conditions of use and identify any changes in
dosage schedule or contraindications, particularly if the drug to be administered is new, infrequently used, or
has a narrow therapeutic range. You must always check that drugs referenced are licensed for the specified
use and at the specified doses in your region.
Information included in BMJ Best Practice is provided on an “as is” basis without any representations,
conditions or warranties that it is accurate and up to date. BMJ and its licensors and licensees assume no
responsibility for any aspect of treatment administered to any patients with the aid of this information. To
the fullest extent permitted by law, BMJ and its licensors and licensees shall not incur any liability, including
without limitation, liability for damages, arising from the content. All conditions, warranties and other terms
which might otherwise be implied by the law including, without limitation, the warranties of satisfactory
quality, fitness for a particular purpose, use of reasonable care and skill and non-infringement of proprietary
rights are excluded.
Figure 1 – BMJ Best Practice Numeral Style
5-digit numerals: 10,000
4-digit numerals: 1000
numerals < 1: 0.25
Where BMJ Best Practice has been translated into a language other than English, BMJ does not warrant the
accuracy and reliability of the translations or the content provided by third parties (including but not limited to
local regulations, clinical guidelines, terminology, drug names and drug dosages). BMJ is not responsible for
DISCLAIMER
any errors and omissions arising from translation and adaptation or otherwise.Where BMJ Best Practice lists
drug names, it does so by recommended International Nonproprietary Names (rINNs) only. It is possible that
certain drug formularies might refer to the same drugs using different names.
This approach is in line with the guidance of the International Bureau of Weights and Measures Service.
Contact us
+ 44 (0) 207 111 1105

[email protected]
BMJ
BMA House
Tavistock Square
London
WC1H 9JR
UK
81
Contributors:
// Acknowledgements:
Best Practice would like to gratefully acknowledge the previous expert contributor, whose work is retained
in parts of the content:Syed Wamique Yusuf, MBBS, FACC, FRCPIProfessor of MedicineDepartment of
CardiologyUniversity of TexasMD Anderson Cancer CenterHoustonTX
DISCLOSURES: SWY is a co-director of the American College of Cardiology (ACC) Cardiovascular Board
Review Course, during which he also delivers lectures.
// Peer Reviewers:
Lisa Anderson, BSc, MB, ChB, MD

Consultant Cardiologist
Cardiovascular Clinical Academic Group, Molecular and Clinical Sciences Research Institute, St George's,
University of London, St George's University Hospitals NHS Foundation Trust, London, UK
DISCLOSURES: LA was deputy chair for the British Society of Heart Failure clinical advisory board for
tafamidis, undertook consultancy services for tafamidis (Pfizer), received a research grant from Pfizer, was
on the clinical advisory board for dapagliflozin (AstraZeneca), and received lecture fees from the British
Society of Cardiology/AstraZeneca and Pfizer.
James Gamble, BM, BCh, DM, FRCP

Oxford Heart Centre, John Radcliffe Hospital, Oxford, UK
DISCLOSURES: JG has been reimbursed for delivering educational meetings by: Novartis, the
manufacturer of sacubitril/valsartan; Boerhinger Ingelhiem, the manufacturer of empagliflocin; AstraZeneca,
the manufacturer of dapagliflozin; and Medtronic, the manufacturer of implantable cardioverter defibrillator
(ICD) and cardiac resynchronisation therapy (CRT) devices. He has been supported to attend educational
meetings by Abbott, Medtronic, and Boston Scientific, who all manufacture ICD and CRT devices. All of
these companies produce drugs or devices related to the treatment of heart failure.
// Expert Advisers:
Resham Baruah, MBBS, BSc, MRCP, PhD

Chelsea and Westminster Hospital and the Royal Brompton and Harefield NHS Trust, London, UK
DISCLOSURES: RB has received honorarium/speaker fees from Novartis and Boehringer Ingleheim.
Adam D. Hartley, MBBS, BSc, MRCP

Wellcome Trust Clinical Research Fellow
Imperial College London, Specialist Registrar in Cardiology, Imperial College Healthcare NHS Trust,
London, UK
DISCLOSURES: ADH declares that he has no competing interests.
// Editors:
Susan Mayor,
Contributors:
Lead Section Editor, BMJ Best Practice
DISCLOSURES: SM works as a freelance medical journalist and editor, video editorial director and
presenter, and communications trainer. In this capacity, she has been paid, and continues to be paid,
by a wide range of organisations for providing these skills on a professional basis. These include: NHS
organisations, including the National Institute for Health and Care Excellence, NHS Choices, NHS Kidney
Care, and others; publishers and medical education companies, including the BMJ Group, the Lancet
group, Medscape, and others; professional organisations, including the British Thoracic Oncology Group,
the European Society for Medical Oncology, the National Confidential Enquiry into Patient Outcome and
Death, and others; charities and patients’ organisations, including the Roy Castle Lung Cancer Foundation
and others; pharmaceutical companies, including Bayer, Boehringer Ingelheim, Novartis, and others; and
communications agencies, including Publicis, Red Healthcare and others. She has no stock options or
shares in any pharmaceutical or healthcare companies; however, she invests in a personal pension, which
may invest in these types of companies. She is managing director of Susan Mayor Limited, the company
name under which she provides medical writing and communications services.
Annabel Sidwell,
Section Editor, BMJ Best Practice
DISCLOSURES: AS declares that she has no competing interests.
Rachel Wheeler,
Lead Section Editor, BMJ Best Practice
DISCLOSURES: RW declares that she has no competing interests.
Julie Costello,
Comorbidities Editor, BMJ Best Practice
DISCLOSURES: JC declares that she has no competing interests.
Adam Mitchell,
Drug Editor, BMJ Best Practice
DISCLOSURES: AM declares that he has no competing interests.

Acute Heart Failure

Uploaded by

Document Informationclick to expand document information

Copyright:

Available Formats

Acute Heart Failure

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Acute Heart Failure

Uploaded by

Copyright:

Available Formats

Acute heart failure

Straight to the point of care

Last updated: Mar 16, 2021

prior episode of heart failure

family history of ischaemic heart disease or cardiomyopathy

excessive alcohol intake

history of systemic conditions associated with heart failure

excessive salt intake

excessive catecholamine stimulation

abnormal thyroid function

• Acute coronary syndrome (ACS)

• Acute pulmonary embolism

Systolic blood pressure

• Preserved (90-140 mmHg) systolic blood pressure (SBP)

• Acute coronary syndrome

• Congestion (‘wet’ vs. ‘dry’ if present vs. absent)

• Warm and wet (well-perfused and congested); most common

Types of heart failure

• Acute coronary syndrome (ACS)[3]

• Acute coronary syndrome (ACS).[3] See our topics Unstable angina, ST-elevation

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

• Current treatment for heart failure and the patient's adherence.

• Prevalence of heart failure is ≥10% in people >70 years of age[1]

Heart failure is unusual in patients with no relevant medical history.[1]

• Peripheral oedema[1] [3] [5]

• Leg oedema is usually bilateral and pitting

• A displaced apex beat[1]

The ECG is usually abnormal in acute heart failure.[1]

ECG showing left ventricular hypertrophy with sinus tachycardia

Chest x-ray showing acute pulmonary oedema with increased alveolar

• Order N-terminal pro-B-type natriuretic peptide (NT-proBNP) if available. Brain natriuretic

• If NT-proBNP is significantly elevated (>1800 ng/mL [>1800 pg/mL] in patients >75

Age (years) <50 50-75 >75

NT-proBNP level >450 >900 >1800

• Measure troponin in all patients with suspected acute heart failure.[19]

diuretics, ACE inhibitors), and to exclude concurrent or causative renal failure.

Liver function tests

• Consider ordering C-reactive protein (based on the opinion of our expert).

If a patient is haemodynamically stable , arrange echocardiography within 48 hours if:

• They are not known to have heart failure[5] [20]

• PaO 2 <10.67 kPa (<80 mmHg) on arterial blood gas)

• pH <7.35, lactate >2 mmol/L (>18 mg/dL)

• Type I respiratory failure: PaO 2 <8 kPa (<60 mmHg)

Blood tests screening for myocarditis

Bedside thoracic ultrasound

History and exam

peripheral oedema (common)

reduced exercise tolerance (common)

Due to poor cardiac functioning.

cold extremities (common)

• Narrow pulse pressure[1]

elevated jugular venous pressure (common)

risk factors (common)

• Prevalence of heart failure is ≥10% in people >70 years of age[1]

displaced apex beat (common)

gallop rhythm (third heart sound) (common)

Other diagnostic factors

Frothy sputum suggests that it is alveolar in origin and not bronchial.