Acute heart failure

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

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

ACUTE

haemodynamically unstable: hypotensive (systolic BP <90 mmHg) or other signs of cardiogenic shock

1st line – treatment of underlying cause

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1st line –

treatment of underlying cause

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

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

Practical tip

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

Identify and manage any comorbidity-related precipitant

Consider whether factors relating to any comorbid conditions may have triggered this episode of acute heart failure including any medications associated with a deterioration in cardiac function, arrhythmia, or increased fluid retention. Consider non-adherence to cardiovascular medication as this is strongly associated with increased risk of hospitalisation in heart failure.[62]

The following is a non-exhaustive list of specific potential precipitants to consider in your patient with one or more comorbidity.

Hypertension and/or coronary artery disease

Diltiazem or verapamil, which may have been prescribed for hypertension or angina, in a patient with acute heart failure with a reduced ejection fraction (HFrEF).[63][64][65]
Alpha-blockers (e.g., doxazosin, prazosin) and minoxidil which should be avoided in patients with heart failure.[62]

Stroke

A cerebrovascular insult, such as a new stroke.
A previous stroke may affect swallowing which can lead to difficulty in taking heart failure medication and hence lead to decompensation (based on expert opinion).

Chronic kidney disease (CKD)

Medication adjustments and titration
- In general, medication doses may need adjustment and require particularly careful titration in a patient with CKD.
- Check this is done.

Diabetes

Medications.
- Thiazolidinediones (glitazones) are not recommended in patients with co-existent heart failure.[63][66]
- They can lead to fluid retention.[63][62]
- Dipeptidyl peptidase-4 (DDP-4) inhibitors (e.g., saxagliptin, sitagliptin) should be avoided.[62]
Metabolic derangement.
- For example, diabetic ketoacidosis may be a precipitant.

COPD and/or asthma

Oral corticosteroids may cause sodium and water retention.[63][65] Inhaled corticosteroids are not thought to be associated with the same adverse effect.[63]
Use beta-2 agonists with caution, especially in patients on high doses and/or those with uncontrolled heart rates.[62]
An acute exacerbation or other infection may trigger heart failure decompensation and may require temporary suspension of beta-blockers if there is ongoing bronchospasm and wheeze (based on expert opinion).

Depression

Tricyclic antidepressants may increase arrhythmia risk and are not recommended in a patient with heart failure.[63][62]
Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with depression.[67]

Dementia

Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with cognitive impairment (e.g., with dementia).[68]
Cognitive impairment can also affect adherence to sick-day rules which are necessary for heart failure medications (renin-angiotensin-aldosterone system [RAAS] inhibitors and sodium-glucose cotransporter-2 [SGLT2] inhibitors) (based on expert opinion).

Frailty

Consider referring any patients with higher levels of frailty - assessed for example using the Rockwood clinical frailty scale or the heart failure-specific tool developed by the Heart Failure Association of the European Society of Cardiology - to the specialist heart failure team for more frequent monitoring and follow-up.[69][70] Dalhousie University: Clinical Frailty Scale Opens in new window
Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided as they can lead to sodium and fluid retention and increased systemic vascular resistance.[62]
Frailty may impact medication adherence because of reduced dexterity and difficulty opening medication packaging.[62]

Practical tip

Consider a medication review by a pharmacist with specialist expertise in prescribing for heart failure for your patient with acute heart failure and one or more comorbidities, on admission and at discharge from hospital. Medication regimens can be complex.[69]

Consider – vasoactive drug

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Consider –

vasoactive drug

Additional treatment recommended for SOME patients in selected patient group

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 setting with at least level 2 care.[23][42] Selection of appropriate vasoactive agents may vary according to clinician preference and local practice guidelines. For more information on the assessment and management of patients with cardiogenic shock, see Shock.

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 setting.[1]

Consider – respiratory support

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Consider –

respiratory support

Additional treatment recommended for SOME patients in selected patient group

Give oxygen if the patient has oxygen saturations <90% or PaO ₂ <8 kPa (<60 mmHg). [1]

Monitor controlled oxygen therapy. An upper SpO ₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
Evidence suggests that liberal use of supplemental oxygen (target SpO ₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[31]
A lower target SpO ₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[32]
Do not use oxygen routinely in non-hypoxaemic patients with acute heart failure because it causes vasoconstriction and a reduction in cardiac output.[1]

Consider non-invasive positive pressure ventilation (continuous positive airway pressure [CPAP], bilevel positive airway pressure [BiPAP]) in patients with respiratory distress (respiratory rate >25 breaths/minute, 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]

Oxygen therapy in your patient with asthma

Measure resting oxygen saturation in all acutely unwell patients.[71]

If your patient’s asthma is stable, follow guideline recommendations for oxygen saturation target for the presenting acute condition.
If the acute presenting condition triggers an acute exacerbation of your patient’s asthma, the Global Initiative for Asthma recommends controlled oxygen to maintain saturations between 93% and 95%.[72]
Be aware that pulse oximetry may overestimate oxygen saturation in patients with darker skin tones.[72]
Hypercapnia in asthma is a near fatal sign showing a patient is tiring and needs ventilatory support.[73] Intensive care support is needed immediately.[73]

Oxygen therapy in your patient with COPD

Measure resting oxygen saturations and be aware of additional factors to consider when prescribing oxygen therapy in a patient with COPD who is hypoxaemic.

Any patient with COPD requiring oxygen supplementation needs an arterial blood gas (ABG) measurement.[74]
Re-check ABG after 30 to 60 minutes in all patients.[74]

If a patient with comorbid COPD is critically ill (e.g., shock, sepsis, major head injury, status epilepticus, anaphylaxis, major trauma) and needs high levels of oxygen:

The British Thoracic Society (BTS) recommends an initial target oxygen saturation in line with the recommendation for patients without COPD.[74] Evidence suggests that targeting an upper oxygen saturation level of 96% may be preferred compared with a higher level.[75][76]
Subsequently, you may need to adjust to controlled oxygen therapy with a target oxygen saturation range of 88% to 92% depending on the ABG results.[74]

If a patient with comorbid COPD is acutely but not critically ill and is at risk of hypercapnic failure (including any patient with moderate or severe COPD, particularly if on long-term oxygen therapy, or with an alert card, or with a previous history of hypercapnic respiratory failure):[74]

Use an initial target oxygen saturation of 88% to 92%
Check ABG and recheck after 30 to 60 minutes.

If a patient with comorbid COPD is acutely but not critically ill and is NOT at risk of hypercapnic respiratory failure (e.g., stable, mild COPD with minimal symptoms):

Use an initial target oxygen saturation as recommended by guidelines for the presenting acute condition
- Evidence suggests that for most acutely ill patients, targeting an upper oxygen saturation level of 96% may be preferred compared with a higher level.[75][76]
Measure ABG as soon as possible[74]
Subsequently, you may need to adjust to controlled oxygen therapy with a target oxygen saturation range of 88% to 92% depending on the ABG results.[74]

If your patient is suitable for full escalation of care, refer for consideration of ventilation support if the patient is:

Severely hypoxaemic (PaO₂ <7.3 kPa [<54.8 mmHg]) despite oxygen therapy (based on expert opinion)
Hypercapnic (PaCO₂ >6 kPa [>45 mmHg]) with respiratory acidosis (pH <7.35)[74]
AND/OR
Exhibiting changes in mental status (confusion, coma).

Plus – check baseline kidney function and monitor closely

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Plus –

check baseline kidney function and monitor closely

Treatment recommended for ALL patients in selected patient group

Check baseline kidney function as you would on admission for any acutely ill patient and monitor closely, especially if your patient has risk factors for AKI, including a history of CKD and/or diabetes.[77][78]

Acute illness increases the risk of deterioration in kidney function.[77]
Assess and monitor volume status.[77]
Monitor for and respond to oliguria.[77]

The European Society of Cardiology recommends that all inpatients with acute heart failure should be monitored preferably with daily measurements of blood urea, serum creatinine, and electrolytes after initial stabilisation.[63]

Ongoing monitoring of kidney function during treatment for acute heart failure and CKD

Monitor estimated glomerular filtration rate (eGFR) and serum potassium concentration in conjunction with patient’s volume status particularly closely during any escalation in treatment and/or clinical deterioration.[79]

Consider liaising with a nephrologist early if your patient with heart failure has worsening kidney function, particularly if they have other comorbidities (based on expert opinion).
Be aware when starting renin-angiotensin-aldosterone system (RAAS) inhibitors (ACE inhibitors, angiotensin-II receptor antagonists, mineralocorticoid receptor/aldosterone antagonists, or angiotensin receptor-neprilysin inhibitors) or sodium-glucose cotransporter-2 (SGLT2) inhibitors, you would expect a small reduction in eGFR.[80] There may also be a rise in creatinine due to altered renal haemodynamics.[63][80]
- A transient rise in creatinine can also be seen when a patient is started on diuretics (oral or intravenous). On its own this should not be concerning if the patient's volume status and symptoms are improving on diuretics.[63][81]
- It may be necessary to temporarily reduce or withhold RAAS inhibitor therapy during intravenous offloading, due to symptomatic hypotension, or if a change in kidney function is more than expected.[81]

Weigh the risk of the decline in kidney function against the prognostic benefits of these medications for your patient with heart failure and CKD.

RAAS inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with heart failure with reduced ejection fraction (HFrEF), so have prognostic benefit.[63][81]
The benefit of RAAS inhibitors is greater in a patient with HFrEF compared with heart failure with preserved ejection fraction (HFpEF). Liaise with a cardiologist for advice regarding your patient with HFpEF, as RAAS inhibitor treatment is individualised.[82]
SGLT2 inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with HFrEF and HFpEF, so have prognostic benefit.[81][83]
Be aware of the risk of euglycaemic ketoacidosis for patients with diabetes receiving SGLT2 inhibitors.[84][85] Most consensus guidance for people with diabetes self-managing an intercurrent illness recommends to stop SGLT2 inhibitors when they are acutely ill, unable to eat, or have diarrhoea and/or vomiting and to monitor blood ketones.[86][87]
If your patient does not have diabetes, euglycaemic ketosis is rare, but be aware of the possibility.[88] It is still reasonable to withhold SGLT2 inhibitors during times of prolonged fasting, surgery, or critical medical illness (when people may be at greater risk for ketosis).[79]
Monitor ketones in all situations, whether SGLT2 inhibitors have been stopped or continued (based on expert opinion).
RAAS inhibitors and SGLT2 inhibitors may also slow progression of kidney disease in people with diabetic kidney disease.[82]

In the context of a stable or improving clinical condition, a decline in eGFR on its own is not usually an indication to discontinue disease-modifying therapies.[80]

Remember to communicate to the primary care practitioner about continued monitoring needed post-discharge.

Plus – review diabetes medication (NEVER stop insulin in a person with type 1 diabetes)

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Plus –

review diabetes medication (NEVER stop insulin in a person with type 1 diabetes)

Treatment recommended for ALL patients in selected patient group

Check your patient’s blood glucose and HbA1c on admission.

Exclude hypoglycaemia, diabetic ketoacidosis, and hyperosmolar hyperglycaemic state, which are medical emergencies.
Admission HbA1c may give you an indication of your patient’s previous diabetes control and may influence your treatment on discharge (based on expert opinion).

Never stop basal insulin (long-acting/background insulin [e.g., glargine or degludec]) in a patient with type 1 diabetes who presents with an acute illness.[89]

Insulin deficiency (e.g., due to delayed or missed doses) will rapidly cause ketoacidosis.[89]
Refer any person with diabetes admitted to hospital using an insulin pump to the diabetes specialist team.[90]

Generally, any patient with type 2 diabetes who is on basal insulin should continue to receive it, but this may not always be the case so check with your senior and/or diabetes specialist team (based on expert opinion).

Consider whether there is any need to adjust insulin dose when a patient is admitted to hospital.

If a patient with type 1 or type 2 diabetes is taking insulin, has good glycaemic control, and has not got significant hyperglycaemia on admission, it may be appropriate to reduce the dose of basal insulin by 20%, particularly if they are not eating as much as they would normally at home. Another factor to bear in mind is that hospital meals generally contain less carbohydrate than meals patients would have at home.
Conversely, patients who are acutely ill with an infection sometimes need more insulin.
Regular monitoring of blood glucose (at least four times daily) can help guide appropriate adjustments to insulin dosing. Seek specialist advice if in doubt.

Practical tip

Ask for expert advice from the diabetes inpatient team at an early stage, particularly if care is complex (e.g., there is metabolic derangement, recurrent or severe hypoglycaemia, persistent hyperglycaemia), or your patient needs enteral feeding for a period of time.[91]

Indications for a variable rate intravenous insulin infusion (VRIII) include:[92][93]

Patients with diabetes or hospital-related hyperglycaemia who can’t eat or drink and where it’s not possible to adjust their insulin regimen. For example, when:
- Vomiting
- Nil by mouth and the patient will miss more than one meal
- There is severe illness with a need to achieve good glycaemic control (such as with sepsis).
Patients with diabetes requiring emergency surgery may require a VRIII. Follow local protocols or recommendations from the UK-based Centre for Perioperative Care.[94]

Get specialist advice from the diabetes team in these circumstances.

If a VRIII is started:

Always continue basal insulin[92]
- This reduces the risk of ketosis if the VRIII is accidentally interrupted (e.g., by cannula displacement or blockage) or switched off (e.g., during ward transfer).
Stop the patient’s usual rapid-acting and mixed insulins while on a VRIII[92]
Use the VRIII for as short a time as possible[92]
Follow your hospital protocol for correct processes including discontinuation.

Consider stopping or adjusting oral hypoglycaemic medication in a patient with diabetes admitted to hospital with an acute condition.

Withhold metformin in any patient:[95]
- With contraindications, such as significant renal impairment (eGFR <30 mL/minute/1.73 m²), whether chronic or secondary to the acute illness.
- With metabolic acidosis (including lactic acidosis or diabetic ketoacidosis).
- At risk of lactic acidosis with metformin. This includes conditions associated with acute kidney injury or tissue hypoxia (including acute cardiac or respiratory failure), dehydration, or renal impairment in patients who have, or are to be fasted for a prolonged period or who are due to have a radio-opaque contrast injection as part of an imaging procedure (based on expert opinion). Follow local protocols for guidance on the specific eGFR levels indicating renal impairment for this to be applied.
Be aware that withholding metformin results in hyperglycaemia.
- If your patient is taking other glucose-lowering medications, these may need to be increased in dose; if not, an alternative hypoglycaemic medication may need to be prescribed (based on expert opinion).
- Some patients may need insulin as a temporary measure, but seek diabetes inpatient specialist team advice.
Reduce or omit the dose of gliclazide if the patient has newly impaired or worsening kidney function, or is eating less than usual, to avoid hypoglycaemia at night.
Stop sodium-glucose cotransporter-2 (SGLT2) inhibitors prescribed for diabetes and monitor blood ketones in any patient with acute serious medical illness (including those undergoing major surgery), particularly if dehydrated or with infection, to reduce the risk of euglycaemic ketoacidosis.[96]
- SGLT2 inhibitors (e.g., dapagliflozin, canagliflozin, empagliflozin, ertugliflozin) reduce blood glucose reabsorption in the kidneys (independently of insulin metabolism of glucose).[97]
- They can mask underlying ketoacidosis as the patient may have a normal (or near normal) serum glucose level (euglycaemic ketoacidosis).
- If an SGLT2 inhibitor is continued during illness, for instance where it is being taken for its prognostic benefit for heart failure or to protect against progression of CKD to kidney failure, be aware of the low risk of euglycaemic ketoacidosis.[88] Monitor ketone levels on a daily basis (based on expert opinion). It is still reasonable to withhold SGLT2 inhibitors during times of prolonged fasting, surgery, or critical medical illness (when people may be at greater risk for ketosis).[79] Seek expert advice.
- Check blood ketones as urinary ketone measurement may be unreliable.
- Restart SGLT2 inhibitors when ketone values are normal and your patient’s condition has stabilised.[96]

Treat for diabetic ketoacidosis (DKA) if capillary or blood ketone concentration is >3 mmol/L or there is significant ketonuria (2+ or more on standard urine sticks), and venous pH is <7.3 and/or bicarbonate concentration <15 mmol/L.[98]

Be aware that at a later stage, following stabilisation of acute heart failure, an SGLT2 inhibitor may be recommended for a patient with heart failure, regardless of whether the patient has diabetes or not (unless contraindicated or not tolerated).[63][83] See ONGOING timeframe of this treatment algorithm.

However, although type 1 diabetes is not an absolute contraindication to SGLT2 inhibitors for this indication, they are not recommended for use in patients with type 1 diabetes owing to the risk of DKA and you should seek cardiology and diabetes expert advice.

Plus – set an escalation plan/consider ceiling of intervention

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Plus –

set an escalation plan/consider ceiling of intervention

Treatment recommended for ALL patients in selected patient group

In consultation with your patient (and their family or carers if applicable), agree an escalation plan as early as possible (based on expert opinion). This applies to all patients, but may be particularly relevant to patients living with frailty and/or with certain comorbidities, such as dementia, stroke, heart failure, COPD and late-stage CKD (based on expert opinion).

An escalation plan should include:[99]
- Resuscitation status (i.e., ‘Do Not Attempt Cardiopulmonary Resuscitation’ [DNACPR] decision)
- Ceiling of intervention (e.g., suitability for intubation or intensive care admission).
It should take account of advance care plans, including legally binding advance directives.[99]
It should be guided by your conversations with the patient about their individual wishes, including discussion to help them reach an informed decision about the likely benefit-risk balance of higher intensity interventions.
Review the decision on CPR at intervals, and especially when an individual’s condition or expressed wishes change.[100]

In some situations, a patient with dementia, other significant comorbidities, or learning disabilities (particularly if they are acutely unwell) will lack the mental capacity to make decisions for the escalation plan.

Assess and document mental capacity (the ability to make a specific decision at the specific time that the decision needs to be made).[101] Follow the appropriate legislation in your region.
In England and Wales, health professionals must comply with the 2005 Mental Capacity Act.[102] Assessments should follow the principles in the Act.[102]
If your patient is assessed to lack mental capacity, consult with their next of kin to make ‘best interests’ decisions, bearing in mind what is known about the patient’s own previously expressed preferences.[102] According to the 2005 Mental Capacity Act in England and Wales, if a patient is ‘unbefriended’ (i.e., has nobody to represent their best interests who is not paid to provide care) and a decision is not time-critical, an independent mental capacity advocate (IMCA) should be sought to perform this role.[103]

Consider – mechanical support device

Plus – referral to specialist

Plus – monitor comorbidities during hospital stay

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Plus –

monitor comorbidities during hospital stay

– baseline neurological assessment

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baseline neurological assessment

Treatment recommended for ALL patients in selected patient group

Do a baseline neurological assessment at the earliest appropriate opportunity for any patient with a history of stroke.

A patient with an acute condition (e.g., an infection and illness-related hypotension) is at increased risk of stroke.[104][105][106] This risk is even higher in anyone with a history of stroke.
If there is a change in neurological status during admission, repeat the neurological assessment in case of a new stroke.
Following assessment, ensure the right level of patient supervision (e.g., relating to the risk of confusion at night and the risk of falls associated with frailty). A patient with a history of stroke is at increased risk of falling and injury.[107]

– baseline cognitive and delirium assessments with collateral history

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baseline cognitive and delirium assessments with collateral history

Treatment recommended for ALL patients in selected patient group

Do a baseline cognitive assessment at the earliest opportunity in any patient with dementia or suspected frailty and take a collateral history from family, friend, or carer.[108]

Use a validated scoring system that is feasible in the acute setting, such as the abbreviated mental test score/10 (AMTS/10).[108][109] British Geriatrics Society: Abbreviated Mental Test Score. 2018 Opens in new window
- Be aware that, while highly specific, the AMTS may underestimate the degree of cognitive impairment and more detailed assessment may be required in selected patients.[110]
The collateral history establishes whether the patient’s cognition is stable, or if any decline in cognition and function has been gradual or acute.
A standardised cognitive assessment score is useful for monitoring for any clinical improvement, and for establishing needs on discharge. This score is often best interpreted alongside a functional assessment, usually performed by a trained occupational therapist.
Although the score may not represent the person's usual baseline for cognition due to the impact of the acute condition and its treatment, it is still good practice to record and repeat it when the person has recovered (based on expert opinion).

Delirium

Delirium is an acute deterioration in mental functioning arising over hours or days that is triggered mainly by acute medical illness, surgery, trauma, or drugs.[111] Your patient may also have altered arousal and be experiencing hallucinations or delusions.[111] See Assessment of delirium.

Use a screening tool to detect probable delirium, such as:
- The 4AT.[112][111][113][114]
  - More information on calculating the 4AT has been produced by the Scottish Intercollegiate Guidelines Network. 4AT Calculator Opens in new window
- The Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC) if your patient is in a critical care setting or in the recovery room after surgery.[115]
  - Recommended by the UK National Institute for Health and Care Excellence (NICE) as specifically designed for these settings, but training is needed, which may limit implementation.[113]

Assess for delirium whenever a patient with dementia presents with acute illness.[113] Also assess for delirium in your patient with frailty.[116]

People living with dementia are at increased risk of delirium when they are admitted to hospital and throughout their admission.[111][117]
Frailty increases the risk of delirium threefold during hospital admission.[116]

Consider the following actions as part of a multicomponent intervention to reduce the risk of delirium during a hospital admission in people with dementia or frailty:[111]

Help with orientation; make sure patients have their own glasses and/or hearing aids
Get patients mobilised as soon as possible
Control pain adequately
Monitor for and treat postoperative complications as soon as possible
Keep patients well hydrated and help them to eat adequately
Monitor and maintain regular bowel and bladder function
Use supplementary oxygen according to guideline recommendations
Consider facilitating the patient's usual carer to assist in non-medical care, such as help with meal times, if they desire to do so.

Arrange a medication review with an experienced healthcare professional:[111]

Calculate the anticholinergic burden (ACB) score.[118]
A score of 3 or more may increase the risk of delirium within 24-48 hours of admission.[119]
Consider discontinuing or substituting anticholinergic drugs where possible, but be aware of the need to taper some medications to avoid withdrawal side effects such as nausea and sweating.[120]

Practical tip

Dementia and frailty are risk factors for postoperative delirium.[117][121][122]

Consider contacting the anaesthetist for advice on pain management.[123]

Evidence: Primary prevention of delirium in hospital using non-pharmacological interventions

There is evidence that a non-pharmacological approach reduces the risk of delirium in non-intensive care unit (non-ICU) patients in hospital.

A Cochrane systematic review found non-pharmacological multicomponent interventions were effective in preventing incident delirium in adults in a non-ICU hospital setting.[124]

Meta-analysis of 14 studies on multicomponent interventions found a significant reduction in incident delirium compared with usual care (risk ratio 0.57, 95% CI 0.46 to 0.71).
There is emerging evidence that multicomponent interventions may reduce hospital length of stay (mean difference -1.3 days, 95% CI -2.56 to -0.04 days) but there was significant heterogeneity between the studies.
There was little information specifically on people with dementia as this group were frequently excluded from trials despite their increased risk of developing delirium.

More info: Initial investigations for a patient with delirium

If a patient has delirium, check for and treat life-threatening causes:[111]

Hypoxia
Low blood glucose
Hypotension
Drug intoxication or withdrawal, including alcohol withdrawal.

Other investigations include (based on expert opinion):

Full blood count, electrolytes, renal function, thyroid function tests, liver function tests, calcium, glucose, CRP, folate, and vitamin B12
Blood cultures (if bacteraemia is suspected)
Urine culture
Chest x-ray.

Advanced non-routine investigations such as CT head may be needed, depending on specific clinical findings. Discuss with your senior.[111]

Check for and treat any reversible causes of delirium.[113]

Pain
Infection
Poor nutrition
Constipation
Dehydration
Medications
- Ask about recently prescribed medications, especially opioid analgesics, anxiolytics, sedatives, antipsychotics, or medicines with strong anticholinergic properties.
- Consider calculating a total anticholinergic burden score.
Environment (including immobility; poor sleep; sensory impairment e.g., ear wax or loss of glasses).

The mnemonic PINCH ME may be helpful as an aide memoire for the underlying causes of delirium superimposed on dementia.[125]

More info: Management of a patient with delirium

Manage patients with delirium initially with non-pharmacological treatment.[113]

Reduce disorientation by providing a well-lit room, with a clock and calendar visible (e.g., on the wall).
Encourage and facilitate family, friends, and carers to visit the patient.
Use verbal and non-verbal techniques to de-escalate conflict and distress.

Where non-pharmacological treatments are ineffective, and the patient is distressed or considered a risk to themselves or others, short-term (often only 1-2 days is required) antipsychotic or sedative drugs may be considered, but only as a last resort. Any new antipsychotic prescribed for this purpose must be regularly reviewed, and discontinued as soon as practical (based on expert opinion).

NICE recommends short-term use of haloperidol (usually for less than 1 week), but it is not suitable in all patients and must never be used in patients with Parkinson’s disease or in patients with dementia with Lewy bodies.[113] Check for all contraindications.
Take particular care to closely monitor and regularly review older people with frailty when prescribing haloperidol for acute delirium. They are particularly at risk of adverse neurological and cardiac effects of this drug.[126]
- A baseline ECG and correction of electrolyte abnormalities is recommended before starting haloperidol.
- Prescribe at the lowest dose and for the shortest length of time possible.
- During treatment, cardiac and electrolyte monitoring is recommended, as is monitoring for extrapyramidal adverse effects.
The evidence on the efficacy of antipsychotics for delirium is inconclusive, and hospital protocols may vary.[111] Follow your local hospital protocol for choice of medication.
Always start at the lowest dose for antipsychotic drugs and titrate carefully according to symptoms.[113] Only ever use oral or intramuscular medication (never intravenous) for this purpose.

Provide the family/carers with information so they understand what is happening and how they can work together with the clinical team to help the patient get back to their usual self.[111]

Evidence: Risks and safe withdrawal of antipsychotics in older people

Antipsychotics are associated with increased mortality in people with dementia.

Short-term antipsychotics may sometimes be needed in people with dementia without delirium to enable safe care. However, antipsychotics have various adverse effects in older people and are associated with an increased risk of death in people with dementia.

A Cochrane review found very low certainty evidence that typical antipsychotics such as haloperidol improve agitation, and may improve psychosis slightly in people with Alzheimer’s disease and vascular dementia. Atypical antipsychotics probably reduce agitation. Both types increase the risk of somnolence and extrapyramidal symptoms.[127]
A network meta-analysis found that people who take atypical antipsychotics for behavioural and psychological symptoms of dementia may have a small improvement in behavioural and psychological symptoms but have increased safety risks including cerebrovascular adverse events compared with those taking placebo.[128]
Contrary to popular belief, long-term antipsychotic prescriptions can be safely withdrawn in most people with dementia once behaviour has settled.[129]

If delirium is not responding to initial treatment within 48 hours, refer to a healthcare professional trained and skilled at diagnosing delirium to confirm the diagnosis and treatment plan (based on expert opinion).

Document the diagnosis of delirium clearly.[111][113]

– monitor and manage blood glucose during the hospital admission

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monitor and manage blood glucose during the hospital admission

Treatment recommended for ALL patients in selected patient group

Monitor blood glucose levels at least four times a day (every 4-6 hours or, if eating, pre-meal and before bedtime) in any acutely unwell patient with diabetes mellitus.[130]

The risk of hypo- and hyperglycaemia increases when a person with diabetes is admitted to hospital acutely (based on expert opinion).
Even more frequent monitoring is needed after any episode of hyperglycaemia or hypoglycaemia and after a change in hypoglycaemic medication (based on expert opinion).
If your patient has undergone surgery, follow your local protocol or recommendations from guideline organisations such as the UK-based Centre for Perioperative Care on blood glucose management and frequency of blood glucose monitoring.[94]
Any patient on a variable rate intravenous insulin infusion (VRIII) needs capillary blood glucose (CBG) measurements initially every hour.[92][131] Adjust according to your hospital VRIII protocol.

Support your patient to self-manage their diabetes (including monitoring blood glucose, and insulin dose adjustment and administration in those treated with insulin) during a hospital admission if:[90][132]

It is safe
The patient is willing, and
It conforms to local protocols.

Decide on and monitor target blood glucose levels.

There is no consensus among guideline organisations on target blood glucose levels for people with diabetes who are in hospital.

The Joint British Diabetes Societies for Inpatient Care recommend the following for medical inpatients with diabetes:
- An ideal range of 6 to 10 mmol/L (108-180 mg/dL)[131]
- A range of 4 to 12 mmol/L (72-216 mg/dL) is acceptable in some circumstances.[131] A lower level of 4 mmol/L (72 mg/dL) may be acceptable in people with very well controlled diabetes in hospital who are self-managing (based on expert opinion)
- A target range of 7.5 to 10 mmol/L (135-180 mg/dL) for patients with diabetes in hospital with mild frailty, and up to 12 mmol/L (216 mg/dL) for those with moderate or severe frailty.[133] An upper level of 12 mmol/L may also be appropriate for any patient at high risk of falls or with dementia (based on expert opinion).
The Centre for Perioperative Care recommends maintaining a range of 6 to 10 mmol/L (108-180 mg/dL), with an acceptable upper level of 12 mmol/L (216 mg/dL) in perioperative patients.[94]
The UK National Institute for Health and Care Excellence recommends a target plasma glucose level of 5 to 8 mmol/L (90-144 mg/dL) in adults with type 1 diabetes in hospital with acute illness or undergoing surgery, although this is lower than other guideline recommendations.[132]
The American Diabetes Association recommends a target range of 7.8 to 10 mmol/L (140-180 mg/dL) for most critically ill patients and 5.6 to 10 mmol/L (100-180 mg/dL) for most non-critically ill patients once insulin has been started for persistent hyperglycaemia.[130]

Evidence: Blood glucose targets for critically ill patients with hyperglycaemia

Conflicting evidence has led to variations in recommendations on how tight the blood glucose control should be in critically ill patients (a mixed population with and without a history of diabetes). Follow your local protocol.

Intensive care setting:
- A randomised controlled trial (RCT) of critically ill patients in a primarily surgical intensive care setting found lower patient mortality with tight glucose control, 4.4 to 6.1 mmol/L (80-110 mg/dL), compared with ‘conventional’ more liberal glucose control.[134]
- However, a subsequent multicentre RCT in critically ill medical and surgical patients in other intensive care settings found increased mortality with tighter glucose control, possibly due to more frequent episodes of hypoglycaemia.[135]
- A 2010 systematic review of 6 RCTs and a meta-analysis investigating tight glucose control (4.4-6.1 mmol/L [80-110 mg/dL]) versus less strict glucose control in critically ill patients in the intensive case setting found no significant improvement in mortality with tight glucose control, but it was associated with significantly more hypoglycaemic episodes compared with less strict glucose control.[136]

Hyperglycaemia during the ongoing hospital admission

Hyperglycaemia in patients in hospital, whether with known diabetes or not, is associated with adverse patient outcomes, including increased mortality.[95]

Act promptly to treat hyperglycaemia to avoid diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS), which are medical emergencies.

Follow your local hospital protocol if your patient’s CBG is ≥15 mmol/L (≥270 mg/dL).
- Generally, action is required at this CBG level, but local protocols may have slightly different cut-off levels and it may vary depending on whether the patient has type 1 or type 2 diabetes.
Exclude DKA or HHS, both of which require specific urgent management.[98][137]
Patients who are usually managed with sodium-glucose co-transporter-2 (SGLT2) inhibitors should have blood ketone measurements to exclude euglycaemic ketoacidosis (ketoacidosis in the presence of normal blood glucose concentration) even if the SGLT2 inhibitor has been stopped (based on expert opinion).

If your patient has DKA or HHS, seek advice from the diabetes inpatient specialist team and follow local hospital guidelines or those from the Joint British Diabetes Society for Inpatient Care (JBDS-IP).[98][137]

It is imperative to ensure early senior review of patients with HHS by a clinician familiar with the management of this condition.[137] Patients with additional comorbidities may need to be on a high-dependency unit.[137]
See Diabetic ketoacidosis or Hyperosmolar hyperglycaemic state.

Be aware that the following medications may be associated with hyperglycaemia and may need to be reviewed:[138]

Corticosteroids
Some beta-blockers (e.g., propranolol, atenolol)
Thiazide diuretics (e.g., hydrochlorothiazide)
Some second-generation antipsychotics (e.g., olanzapine, clozapine)
Certain fluoroquinolone antibiotics (e.g., ciprofloxacin)
Calcineurin inhibitors (e.g., ciclosporin, tacrolimus)
Protease inhibitors (e.g., as a component in antiretroviral therapy, such as ritonavir).

Practical tip

Ask for expert advice from the diabetes team in complex patients, or where hyperglycaemia is difficult to control.

Hypoglycaemia during the ongoing hospital admission

Monitor blood glucose and adjust medication in response to illness and hospital meal times, to reduce the risk of hypoglycaemic episodes.

Approximately 1 in 5 inpatients with diabetes in England and Wales were found to have had a hypoglycaemic episode during their hospital stay.[139]
Causes include:[140]
- Recovery from an acute illness
- Insulin or oral hypoglycaemic medication error
- Wrong timing of insulin in relation to meals
- Patients eating less but taking the same amount of diabetes medication
- No bedtime snacks
- Reduced appetite or vomiting.

Consider intervening if the blood glucose falls below 6 mmol/L (108 mg/dL) (‘looming/impending’ hypoglycaemia) if on insulin or on sulfonylureas.

These patients are at high risk of progressing to hypoglycaemia.
Give carbohydrates as recommended in the hypoglycaemia guideline and follow your local protocol (see below).[140]

Treat hypoglycaemia actively if the blood glucose falls below 4 mmol/L (72 mg/dL).[140] Follow hospital protocol or JBDS-IP management of hypoglycaemia algorithm.[140] The JBDS-IP guidelines also recommend that you:[140]

Retest blood glucose at 10-15 minutes to determine response to treatment
Never stop the next scheduled dose of insulin if the hypoglycaemia has been corrected. This can cause rebound hyperglycaemia and DKA in people with type 1 diabetes.
- Seek diabetes inpatient specialist team advice on whether a review of your patient’s insulin regimen is needed.

Take steps to reduce the risk of hypogylcaemia at night. Assuming your patient can swallow, they are likely to have a smaller evening meal in hospital than at home.[139]

In the absence of significant hyperglycaemia, consider reducing the evening basal insulin by 20% on admission (based on expert opinion).

Be aware that hypoglycaemia as an adverse effect of sulfonylurea medication (e.g., glibenclamide, gliclazide, glimepiride, glipizide) is more likely if meals are skipped or doses are excessive.

In the acute hospital setting, meal times may be interrupted or may not always be at exactly the same time each day.
- Give sulfonylurea medication before or with food. Check local drug formulary for more specific guidance on timing of dose in relation to food for specific sulfonylurea.
- Never give sulfonylurea medication at bedtime and, if the patient is taking a dose with their evening meal, consider reducing the evening dose to reduce the risk of nocturnal hypoglycaemia (based on expert opinion).

Practical tip

Bedtime snacks can reduce the risk of early morning hypoglycaemia.[139]

More info: Management of patients with diabetes who are receiving end-of-life care

If a patient with diabetes is receiving end-of-life care:

Reduce hypoglycaemic medication to a minimum, but keep the patient free from symptomatic hyperglycaemia, which can lead to:[141]
- Dehydration
- Ketosis
- Hyperosmolar hyperglycaemia.
Do not stop basal insulin in a person with type 1 diabetes
Refer to local protocols or guidance from diabetes organisations such as the UK-based TREND^TM Diabetes.[141]

– check your patient’s feet

– ensure monitoring is in place to detect any asthma exacerbation during your patient's hospital admission

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–

ensure monitoring is in place to detect any asthma exacerbation during your patient's hospital admission

Treatment recommended for ALL patients in selected patient group

Acute worsening of respiratory symptoms may suggest a patient with comorbid asthma is having an acute exacerbation of their asthma.

Follow guideline recommendations on assessing severity and managing an acute exacerbation of asthma in adults.[73][72]
See Acute asthma exacerbation in adults.

Consider temporarily stopping any long-acting muscarinic antagonist (LAMA) the patient may be on for maintenance therapy (e.g., tiotropium, aclidinium, glycopyrronium, umeclidinium) if you prescribe a nebulised short-acting muscarinic antagonist (e.g., ipratropium) (based on expert opinion).

This is due to concern over possible additive anticholinergic adverse effects.
Ensure to re-prescribe the LAMA once the nebuliser treatment has been stopped.

Be aware that the long-term use of beta-2 agonists to manage asthma may increase the risk of cardiovascular events.

Evidence: Cardiovascular harm with beta-2 agonists

Beta-2 agonists may increase the risk of myocardial infarction and other adverse cardiovascular events.

Beta-2 agonists increase heart rate and reduce potassium levels.[144] They are absorbed into the systemic circulation and there is evidence that long-term regular use may be associated with an increased risk of myocardial infarction, unstable angina, congestive heart failure, and arrhythmias.[144][145]
However, it is not routine practice to discontinue beta-2 agonists if they are needed for comorbid asthma.

– ensure monitoring is in place to detect any COPD exacerbation during your patient's hospital admission

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–

ensure monitoring is in place to detect any COPD exacerbation during your patient's hospital admission

Treatment recommended for ALL patients in selected patient group

Acute worsening of respiratory symptoms may suggest a patient with comorbid COPD is having an acute exacerbation.[146]

Differentiate from other conditions, such as acute coronary syndrome, acute heart failure, and pneumonia.
Follow guideline recommendations. See Acute exacerbation of COPD.

Bronchodilator therapy via a nebuliser should only be used for 24 to 48 hours and then the patient should be switched back onto their usual inhaler(s) (based on expert opinion).

The Global Initiative for Chronic Obstructive Disease recommends continuing inhaled long-acting bronchodilators during an exacerbation, or starting them as soon as possible before discharge from hospital.[146] This is an individualised clinical decision due to limited evidence.

Consider temporarily stopping any long-acting muscarinic receptor antagonist (LAMA) the patient may be on for maintenance therapy (e.g., tiotropium, aclidinium, glycopyrronium, umeclidinium) if you prescribe a nebulised short-acting muscarinic antagonist (e.g., ipratropium) (based on expert opinion).

This is due to concern over possible additive anticholinergic adverse effects.
Ensure the LAMA is re-prescribed once the nebuliser treatment has been stopped.

Be aware that the long-term use of beta-2 agonists to manage COPD may increase the risk of cardiovascular events.

Evidence: Cardiovascular harm with beta-2 agonists

Beta-2 agonists may increase the risk of myocardial infarction and other adverse cardiovascular events.

Beta-2 agonists may increase heart rate and reduce potassium levels.[144] They are absorbed into the systemic circulation and there is evidence that long-term regular use may be associated with an increased risk of myocardial infarction, unstable angina, congestive heart failure, and arrhythmias.[145][144]
However, the Global Initiative for Chronic Obstructive Lung Disease states that there has been no reported association between beta-2-agonist use and increased mortality in people with COPD.[146] It is not routine practice to discontinue beta-2 agonists if they are needed for comorbid COPD.

Evidence: Short duration versus longer duration of corticosteroids for acute exacerbation of COPD

A systematic review found no difference in outcomes (treatment failure, time to next exacerbation, time in hospital, lung function, adverse effects, mortality) between short courses (7 days or less) versus more conventional longer courses (longer than 7 days) of corticosteroids in people with an acute exacerbation of COPD.[147]

The randomised controlled trials included in this Cochrane review were all in hospital settings and only included people with severe to very severe COPD.[147]
The review authors concluded that due to the addition of a new trial, they have increased confidence that a corticosteroid course of around 5 days is likely to be sufficient for the treatment of an acute exacerbation of COPD.[147]
Similarly, a review of the evidence in 2019 resulted in the National Institute for Health and Care Excellence (NICE) recommending to offer prednisolone for 5 days during an exacerbation of COPD.[148]

– continue your patient's inhalers as prescribed for asthma or COPD

– mental state examination

– review current treatment for depression in your patient with cardiac disease

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review current treatment for depression in your patient with cardiac disease

Treatment recommended for ALL patients in selected patient group

Get an up-to-date list of medication used to manage your patient’s mental health, either by asking them directly or retrieving relevant primary care medical records (if available).

Consider that antidepressants may be used in the treatment of conditions other than depression, and drugs other than antidepressants may be used to treat depression. The information here refers to antidepressant medications and important considerations for patients with acute cardiac disease.

Seek expert advice on reviewing existing medication and/or prescribing a new psychotropic for your patient with acute heart failure or acute coronary syndrome and depression. Avoid abruptly stopping antidepressants due to the potential risk of discontinuation symptoms and prescribe new ones with caution.[151][152]
- The unique side-effect profile of the various antidepressants should be taken into consideration; this includes interactions (additive or otherwise) with cardiac medication.[153]
- Selective serotonin-reuptake inhibitors (SSRIs) are considered to be a good first option in the post myocardial infarction (MI) period, though relative caution should be taken. Sertraline is the drug of choice.[154]
- From the newer classes of antidepressants, agomelatine and vortioxetine have a favourable cardiac effect profile and have no specific contraindication in patients who have had an MI.[155][156]
- Tricyclic antidepressants are contraindicated in the immediate period following an MI. Similarly, they should be avoided in patients with coronary artery disease and/or heart failure because they are associated with hypotension, arrhythmias, and worsening heart failure.[157][158][63]
- Monoamine oxidase inhibitors are not recommended in cardiovascular disease (or may be contraindicated in some countries).
- Serotonin-noradrenaline reuptake inhibitors, reboxetine, and trazodone are best avoided in patients with cardiovascular disease.[157]
When reviewing current medication, look out for:
- Current and previous adverse effects
- Recent changes in dose
- Recent switches from a different class of medication
- Pharmacological nuances of specific depression subtypes (e.g., it is likely that patients suffering from psychotic depression would be co-prescribed an antipsychotic)
- Augmenting strategies that may be in use when treating resistant depression (e.g., lithium or quetiapine augmentation of an SSRI).
Consider drug-drug interactions.
- Antidepressant medications may cause pharmacokinetic (by inhibiting the CYP450 pathway) and pharmacodynamic interactions with medications used for other conditions.[157][158]
Consider psychiatric complications when prescribing non-psychotropic drugs.
- Take particular care when prescribing anticonvulsants, antiparkinsonian medication, and corticosteroids.
Consider adverse effects, which may include the following:
- Hyponatraemia, caused by antidepressants, especially SSRIs, and compounded by other co-prescribed drugs (e.g., diuretics). Check your patient’s serum electrolytes.
- Serotonin syndrome (altered mental state, agitation, tremor, hyper-reflexia, clonus, muscle rigidity, diaphoresis, tachycardia, increased bowel sounds, temperature >38℃), especially with polypharmacy and/or overdose of a serotonergic agent.[159][160] See Serotonin syndrome.
  - Be particularly aware of increased risk of serotonin syndrome in patients with end-stage renal disease on SSRIs. Treating depression in patients with renal impairment requires a multidisciplinary approach and demands extra caution.
- Hepatotoxicity. Adjust doses of antidepressants in patients with hepatic impairment if necessary and avoid drugs that are known to be hepatotoxic.
- QTc prolongation, arrhythmias, increased heart rate, postural hypotension with tricyclic antidepressants. Check ECG, especially in people at risk of arrhythmias.
- Gastrointestinal bleeding. SSRIs are associated with an increased risk of gastrointestinal bleeding.[157] Risk is particularly increased when co-prescribed with aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), or oral anticoagulants.[161][162] Try to avoid this combination of drugs.[157] Monitor closely and consider gastroprotection with proton-pump inhibitors if SSRI use cannot be avoided.[157]

This list of adverse effects is not exhaustive - consult local formulary for further information. Consult your liaison psychiatry colleagues and/or a pharmacist for advice.

Ask your patient about non-pharmacological treatments for their depression and check current level of support in the community.

This may include other health professionals involved in their care, charities, family and social networks, and psychological therapy.

Practical tip

Be aware that smoking cessation or switching from tobacco smoking to alternatives (including nicotine replacement therapy) may result in a change to the plasma concentration of any psychotropic medication the patient may be taking (e.g., for depression). This is because nicotine replacement therapy does not impact hepatic enzyme activity like tobacco smoking.[163][164][165] Seek advice on whether any adjustment to the dose of psychotropic medication is appropriate.

– consider referral to the liaison psychiatry team

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consider referral to the liaison psychiatry team

Treatment recommended for ALL patients in selected patient group

Consider a referral to the liaison psychiatry team/service for any patient with comorbid depression who is admitted to hospital with an acute condition.[166][167]

Referral may not be required if there are no concerns that depression and/or its management (e.g., medication) may be affecting the acute condition (based on expert opinion).
Accidents of unclear circumstances, self-injurious behaviours, and/or suicide attempts should trigger clinical suspicion of comorbid mental health disorder (based on expert opinion).

Evidence: Depression and adherence with treatment post-discharge

Comorbid depression is linked to poor adherence with recommended physical health treatments, from medication to rehabilitation.[168]

This may lead to worse clinical outcomes, including higher readmission risk.[169][170][171]
Most importantly, affective symptoms including depression have been linked with excess mortality, though a causal link remains to be proven.[172][173]

haemodynamically unstable: hypertensive crisis

1st line – treatment of underlying cause

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1st line –

treatment of underlying cause

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

Practical tip

Identify and manage any comorbidity-related precipitant

The following is a non-exhaustive list of specific potential precipitants to consider in your patient with one or more comorbidity.

Hypertension and/or coronary artery disease

Diltiazem or verapamil, which may have been prescribed for hypertension or angina, in a patient with acute heart failure with a reduced ejection fraction (HFrEF).[63][64][65]
Alpha-blockers (e.g., doxazosin, prazosin) and minoxidil which should be avoided in patients with heart failure.[62]

Stroke

A cerebrovascular insult, such as a new stroke.
A previous stroke may affect swallowing which can lead to difficulty in taking heart failure medication and hence lead to decompensation (based on expert opinion).

Chronic kidney disease (CKD)

Medication adjustments and titration
- In general, medication doses may need adjustment and require particularly careful titration in a patient with CKD.
- Check this is done.

Diabetes

Medications.
- Thiazolidinediones (glitazones) are not recommended in patients with co-existent heart failure.[63][66]
- They can lead to fluid retention.[63][62]
- Dipeptidyl peptidase-4 (DDP-4) inhibitors (e.g., saxagliptin, sitagliptin) should be avoided.[62]
Metabolic derangement.
- For example, diabetic ketoacidosis may be a precipitant.

COPD and/or asthma

Oral corticosteroids may cause sodium and water retention.[63][65] Inhaled corticosteroids are not thought to be associated with the same adverse effect.[63]
Use beta-2 agonists with caution, especially in patients on high doses and/or those with uncontrolled heart rates.[62]
An acute exacerbation or other infection may trigger heart failure decompensation and may require temporary suspension of beta-blockers if there is ongoing bronchospasm and wheeze (based on expert opinion).

Depression

Tricyclic antidepressants may increase arrhythmia risk and are not recommended in a patient with heart failure.[63][62]
Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with depression.[67]

Dementia

Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with cognitive impairment (e.g., with dementia).[68]
Cognitive impairment can also affect adherence to sick-day rules which are necessary for heart failure medications (renin-angiotensin-aldosterone system [RAAS] inhibitors and sodium-glucose cotransporter-2 [SGLT2] inhibitors) (based on expert opinion).

Frailty

Consider referring any patients with higher levels of frailty - assessed for example using the Rockwood clinical frailty scale or the heart failure-specific tool developed by the Heart Failure Association of the European Society of Cardiology - to the specialist heart failure team for more frequent monitoring and follow-up.[69][70] Dalhousie University: Clinical Frailty Scale Opens in new window
Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided as they can lead to sodium and fluid retention and increased systemic vascular resistance.[62]
Frailty may impact medication adherence because of reduced dexterity and difficulty opening medication packaging.[62]

Practical tip

Consider – vasodilator

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Consider –

vasodilator

Additional treatment recommended for SOME patients in selected patient group

Consider giving a vasodilator intravenously if there is hypertension.[1][23] This may also be used for relief of dyspnoea in this group of patients.[1][23]

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.[23] However, it is approved for use in acute heart failure in the UK and it is suggested as an intravenous vasodilator option for acute heart failure by the European Society of Cardiology guidelines.[1] Monitor blood pressure (including intra-arterial blood pressure) and blood cyanide concentration.
Although evidence for survival benefit from the use of vasodilators in patients with acute heart failure is lacking, they remain in widespread use for symptom relief and blood pressure control.[1][23]

Primary options

glyceryl trinitrate: 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

glyceryl trinitrate : 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

glyceryl trinitrate: 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

isosorbide dinitrate: 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

isosorbide dinitrate : 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

isosorbide dinitrate: 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

Secondary options

sodium nitroprusside: consult specialist for guidance on dose

sodium nitroprusside : consult specialist for guidance on dose

sodium nitroprusside: consult specialist for guidance on dose

Plus – check baseline kidney function and monitor closely

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Plus –

check baseline kidney function and monitor closely

Treatment recommended for ALL patients in selected patient group

Acute illness increases the risk of deterioration in kidney function.[77]
Assess and monitor volume status.[77]
Monitor for and respond to oliguria.[77]

Ongoing monitoring of kidney function during treatment for acute heart failure and CKD

Consider liaising with a nephrologist early if your patient with heart failure has worsening kidney function, particularly if they have other comorbidities (based on expert opinion).
Be aware when starting renin-angiotensin-aldosterone system (RAAS) inhibitors (ACE inhibitors, angiotensin-II receptor antagonists, mineralocorticoid receptor/aldosterone antagonists, or angiotensin receptor-neprilysin inhibitors) or sodium-glucose cotransporter-2 (SGLT2) inhibitors, you would expect a small reduction in eGFR.[80] There may also be a rise in creatinine due to altered renal haemodynamics.[63][80]
- A transient rise in creatinine can also be seen when a patient is started on diuretics (oral or intravenous). On its own this should not be concerning if the patient's volume status and symptoms are improving on diuretics.[63][81]
- It may be necessary to temporarily reduce or withhold RAAS inhibitor therapy during intravenous offloading, due to symptomatic hypotension, or if a change in kidney function is more than expected.[81]

Weigh the risk of the decline in kidney function against the prognostic benefits of these medications for your patient with heart failure and CKD.

RAAS inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with heart failure with reduced ejection fraction (HFrEF), so have prognostic benefit.[63][81]
The benefit of RAAS inhibitors is greater in a patient with HFrEF compared with heart failure with preserved ejection fraction (HFpEF). Liaise with a cardiologist for advice regarding your patient with HFpEF, as RAAS inhibitor treatment is individualised.[82]
SGLT2 inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with HFrEF and HFpEF, so have prognostic benefit.[81][83]
Be aware of the risk of euglycaemic ketoacidosis for patients with diabetes receiving SGLT2 inhibitors.[84][85] Most consensus guidance for people with diabetes self-managing an intercurrent illness recommends to stop SGLT2 inhibitors when they are acutely ill, unable to eat, or have diarrhoea and/or vomiting and to monitor blood ketones.[86][87]
If your patient does not have diabetes, euglycaemic ketosis is rare, but be aware of the possibility.[88] It is still reasonable to withhold SGLT2 inhibitors during times of prolonged fasting, surgery, or critical medical illness (when people may be at greater risk for ketosis).[79]
Monitor ketones in all situations, whether SGLT2 inhibitors have been stopped or continued (based on expert opinion).
RAAS inhibitors and SGLT2 inhibitors may also slow progression of kidney disease in people with diabetic kidney disease.[82]

In the context of a stable or improving clinical condition, a decline in eGFR on its own is not usually an indication to discontinue disease-modifying therapies.[80]

Remember to communicate to the primary care practitioner about continued monitoring needed post-discharge.

Plus – loop diuretic

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Plus –

loop diuretic

Treatment recommended for ALL patients in selected patient group

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

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

Seek senior advice on fluid balance and diuretic dosing

Discuss your patient’s fluid balance and diuretic treatment with your senior, as this may be particularly challenging to manage in patients with CKD and heart failure.[69]

Higher doses of diuretics may be required in a patient with CKD and fluid congestion.[81] Seek expert advice.
Transient deterioration in kidney function may be a consequence of using higher doses of diuretics if they lead to intravascular volume depletion.

Primary options

furosemide: 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

furosemide : 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

furosemide: 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

Consider – aldosterone antagonist or thiazide-type diuretic

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Consider –

aldosterone antagonist or thiazide-type diuretic

Additional treatment recommended for SOME patients in selected patient group

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 risk of hyperkalaemia with aldosterone antagonists

Be aware that there is an increased risk of severe hyperkalaemia when aldosterone antagonists are used in combination with ACE inhibitors or angiotensin-II receptor antagonists (including sacubitril/valsartan), particularly in patients who have impaired kidney function.[174]

Monitor this carefully.

Primary options

spironolactone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

spironolactone : 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

spironolactone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

eplerenone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

eplerenone : 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

eplerenone: 25 mg orally once daily initially, increase gradually according to response, maximum 50 mg/day

metolazone: 5-10 mg orally once daily initially, increase gradually according to response, maximum 80 mg/day

metolazone : 5-10 mg orally once daily initially, increase gradually according to response, maximum 80 mg/day

metolazone: 5-10 mg orally once daily initially, increase gradually according to response, maximum 80 mg/day

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Show drug information for a patient with no comorbidities

Primary options

spironolactone

For patients with CKD, please check your local drug formulary

For patients with CKD see dose in the Renal Drug HandbookFor patients with CKD see dose in the Renal Drug Handbook

eplerenone

For patients with CKD, please check your local drug formulary

For patients with CKD see dose in the Renal Drug HandbookFor patients with CKD see dose in the Renal Drug Handbook

metolazone

For patients with CKD, please check your local drug formulary

For patients with CKD see dose in the Renal Drug HandbookFor patients with CKD see dose in the Renal Drug Handbook

Consider – respiratory support

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Consider –

respiratory support

Additional treatment recommended for SOME patients in selected patient group

Give oxygen if the patient has oxygen saturations <90% or PaO ₂ <8 kPa (<60 mmHg).[1]

Monitor controlled oxygen therapy. An upper SpO ₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.
Evidence suggests that liberal use of supplemental oxygen (target SpO ₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[31]
A lower target SpO ₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[32]
Do not use oxygen routinely in non-hypoxaemic patients with acute heart failure because it causes vasoconstriction and a reduction in cardiac output.[1]

Oxygen therapy in your patient with asthma

Measure resting oxygen saturation in all acutely unwell patients.[71]

If your patient’s asthma is stable, follow guideline recommendations for oxygen saturation target for the presenting acute condition.
If the acute presenting condition triggers an acute exacerbation of your patient’s asthma, the Global Initiative for Asthma recommends controlled oxygen to maintain saturations between 93% and 95%.[72]
Be aware that pulse oximetry may overestimate oxygen saturation in patients with darker skin tones.[72]
Hypercapnia in asthma is a near fatal sign showing a patient is tiring and needs ventilatory support.[73] Intensive care support is needed immediately.[73]

Oxygen therapy in your patient with COPD

Measure resting oxygen saturations and be aware of additional factors to consider when prescribing oxygen therapy in a patient with COPD who is hypoxaemic.

Any patient with COPD requiring oxygen supplementation needs an arterial blood gas (ABG) measurement.[74]
Re-check ABG after 30 to 60 minutes in all patients.[74]

If a patient with comorbid COPD is critically ill (e.g., shock, sepsis, major head injury, status epilepticus, anaphylaxis, major trauma) and needs high levels of oxygen:

The British Thoracic Society (BTS) recommends an initial target oxygen saturation in line with the recommendation for patients without COPD.[74] Evidence suggests that targeting an upper oxygen saturation level of 96% may be preferred compared with a higher level.[75][76]
Subsequently, you may need to adjust to controlled oxygen therapy with a target oxygen saturation range of 88% to 92% depending on the ABG results.[74]

Use an initial target oxygen saturation of 88% to 92%
Check ABG and recheck after 30 to 60 minutes.

If a patient with comorbid COPD is acutely but not critically ill and is NOT at risk of hypercapnic respiratory failure (e.g., stable, mild COPD with minimal symptoms):

Use an initial target oxygen saturation as recommended by guidelines for the presenting acute condition
- Evidence suggests that for most acutely ill patients, targeting an upper oxygen saturation level of 96% may be preferred compared with a higher level.[75][76]
Measure ABG as soon as possible[74]
Subsequently, you may need to adjust to controlled oxygen therapy with a target oxygen saturation range of 88% to 92% depending on the ABG results.[74]

If your patient is suitable for full escalation of care, refer for consideration of ventilation support if the patient is:

Severely hypoxaemic (PaO₂ <7.3 kPa [<54.8 mmHg]) despite oxygen therapy (based on expert opinion)
Hypercapnic (PaCO₂ >6 kPa [>45 mmHg]) with respiratory acidosis (pH <7.35)[74]
AND/OR
Exhibiting changes in mental status (confusion, coma).

Plus – review diabetes medication (NEVER stop insulin in a person with type 1 diabetes)

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Plus –

review diabetes medication (NEVER stop insulin in a person with type 1 diabetes)

Treatment recommended for ALL patients in selected patient group

Check your patient’s blood glucose and HbA1c on admission.

Exclude hypoglycaemia, diabetic ketoacidosis, and hyperosmolar hyperglycaemic state, which are medical emergencies.
Admission HbA1c may give you an indication of your patient’s previous diabetes control and may influence your treatment on discharge (based on expert opinion).

Never stop basal insulin (long-acting/background insulin [e.g., glargine or degludec]) in a patient with type 1 diabetes who presents with an acute illness.[89]

Insulin deficiency (e.g., due to delayed or missed doses) will rapidly cause ketoacidosis.[89]
Refer any person with diabetes admitted to hospital using an insulin pump to the diabetes specialist team.[90]

Consider whether there is any need to adjust insulin dose when a patient is admitted to hospital.

If a patient with type 1 or type 2 diabetes is taking insulin, has good glycaemic control, and has not got significant hyperglycaemia on admission, it may be appropriate to reduce the dose of basal insulin by 20%, particularly if they are not eating as much as they would normally at home. Another factor to bear in mind is that hospital meals generally contain less carbohydrate than meals patients would have at home.
Conversely, patients who are acutely ill with an infection sometimes need more insulin.
Regular monitoring of blood glucose (at least four times daily) can help guide appropriate adjustments to insulin dosing. Seek specialist advice if in doubt.

Practical tip

Indications for a variable rate intravenous insulin infusion (VRIII) include:[92][93]

Patients with diabetes or hospital-related hyperglycaemia who can’t eat or drink and where it’s not possible to adjust their insulin regimen. For example, when:
- Vomiting
- Nil by mouth and the patient will miss more than one meal
- There is severe illness with a need to achieve good glycaemic control (such as with sepsis).
Patients with diabetes requiring emergency surgery may require a VRIII. Follow local protocols or recommendations from the UK-based Centre for Perioperative Care.[94]

Get specialist advice from the diabetes team in these circumstances.

If a VRIII is started:

Always continue basal insulin[92]
- This reduces the risk of ketosis if the VRIII is accidentally interrupted (e.g., by cannula displacement or blockage) or switched off (e.g., during ward transfer).
Stop the patient’s usual rapid-acting and mixed insulins while on a VRIII[92]
Use the VRIII for as short a time as possible[92]
Follow your hospital protocol for correct processes including discontinuation.

Consider stopping or adjusting oral hypoglycaemic medication in a patient with diabetes admitted to hospital with an acute condition.

Withhold metformin in any patient:[95]
- With contraindications, such as significant renal impairment (eGFR <30 mL/minute/1.73 m²), whether chronic or secondary to the acute illness.
- With metabolic acidosis (including lactic acidosis or diabetic ketoacidosis).
- At risk of lactic acidosis with metformin. This includes conditions associated with acute kidney injury or tissue hypoxia (including acute cardiac or respiratory failure), dehydration, or renal impairment in patients who have, or are to be fasted for a prolonged period or who are due to have a radio-opaque contrast injection as part of an imaging procedure (based on expert opinion). Follow local protocols for guidance on the specific eGFR levels indicating renal impairment for this to be applied.
Be aware that withholding metformin results in hyperglycaemia.
- If your patient is taking other glucose-lowering medications, these may need to be increased in dose; if not, an alternative hypoglycaemic medication may need to be prescribed (based on expert opinion).
- Some patients may need insulin as a temporary measure, but seek diabetes inpatient specialist team advice.
Reduce or omit the dose of gliclazide if the patient has newly impaired or worsening kidney function, or is eating less than usual, to avoid hypoglycaemia at night.
Stop sodium-glucose cotransporter-2 (SGLT2) inhibitors prescribed for diabetes and monitor blood ketones in any patient with acute serious medical illness (including those undergoing major surgery), particularly if dehydrated or with infection, to reduce the risk of euglycaemic ketoacidosis.[96]
- SGLT2 inhibitors (e.g., dapagliflozin, canagliflozin, empagliflozin, ertugliflozin) reduce blood glucose reabsorption in the kidneys (independently of insulin metabolism of glucose).[97]
- They can mask underlying ketoacidosis as the patient may have a normal (or near normal) serum glucose level (euglycaemic ketoacidosis).
- If an SGLT2 inhibitor is continued during illness, for instance where it is being taken for its prognostic benefit for heart failure or to protect against progression of CKD to kidney failure, be aware of the low risk of euglycaemic ketoacidosis.[88] Monitor ketone levels on a daily basis (based on expert opinion). It is still reasonable to withhold SGLT2 inhibitors during times of prolonged fasting, surgery, or critical medical illness (when people may be at greater risk for ketosis).[79] Seek expert advice.
- Check blood ketones as urinary ketone measurement may be unreliable.
- Restart SGLT2 inhibitors when ketone values are normal and your patient’s condition has stabilised.[96]

However, although type 1 diabetes is not an absolute contraindication to SGLT2 inhibitors for this indication, they are not recommended for use in patients with type 1 diabetes owing to the risk of DKA and you should seek cardiology and diabetes expert advice.

Plus – set an escalation plan/consider ceiling of intervention

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Plus –

set an escalation plan/consider ceiling of intervention

Treatment recommended for ALL patients in selected patient group

An escalation plan should include:[99]
- Resuscitation status (i.e., ‘Do Not Attempt Cardiopulmonary Resuscitation’ [DNACPR] decision)
- Ceiling of intervention (e.g., suitability for intubation or intensive care admission).
It should take account of advance care plans, including legally binding advance directives.[99]
It should be guided by your conversations with the patient about their individual wishes, including discussion to help them reach an informed decision about the likely benefit-risk balance of higher intensity interventions.
Review the decision on CPR at intervals, and especially when an individual’s condition or expressed wishes change.[100]

Assess and document mental capacity (the ability to make a specific decision at the specific time that the decision needs to be made).[101] Follow the appropriate legislation in your region.
In England and Wales, health professionals must comply with the 2005 Mental Capacity Act.[102] Assessments should follow the principles in the Act.[102]
If your patient is assessed to lack mental capacity, consult with their next of kin to make ‘best interests’ decisions, bearing in mind what is known about the patient’s own previously expressed preferences.[102] According to the 2005 Mental Capacity Act in England and Wales, if a patient is ‘unbefriended’ (i.e., has nobody to represent their best interests who is not paid to provide care) and a decision is not time-critical, an independent mental capacity advocate (IMCA) should be sought to perform this role.[103]

Plus – referral to specialist

Plus – monitor comorbidities during hospital stay

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Plus –

monitor comorbidities during hospital stay

– baseline neurological assessment

– baseline cognitive and delirium assessments with collateral history

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baseline cognitive and delirium assessments with collateral history

Treatment recommended for ALL patients in selected patient group

Do a baseline cognitive assessment at the earliest opportunity in any patient with dementia or suspected frailty and take a collateral history from family, friend, or carer.[108]

Use a validated scoring system that is feasible in the acute setting, such as the abbreviated mental test score/10 (AMTS/10).[108][109] British Geriatrics Society: Abbreviated Mental Test Score. 2018 Opens in new window
- Be aware that, while highly specific, the AMTS may underestimate the degree of cognitive impairment and more detailed assessment may be required in selected patients.[110]
The collateral history establishes whether the patient’s cognition is stable, or if any decline in cognition and function has been gradual or acute.
A standardised cognitive assessment score is useful for monitoring for any clinical improvement, and for establishing needs on discharge. This score is often best interpreted alongside a functional assessment, usually performed by a trained occupational therapist.
Although the score may not represent the person's usual baseline for cognition due to the impact of the acute condition and its treatment, it is still good practice to record and repeat it when the person has recovered (based on expert opinion).

Delirium

Use a screening tool to detect probable delirium, such as:
- The 4AT.[112][111][113][114]
  - More information on calculating the 4AT has been produced by the Scottish Intercollegiate Guidelines Network. 4AT Calculator Opens in new window
- The Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) or the Intensive Care Delirium Screening Checklist (ICDSC) if your patient is in a critical care setting or in the recovery room after surgery.[115]
  - Recommended by the UK National Institute for Health and Care Excellence (NICE) as specifically designed for these settings, but training is needed, which may limit implementation.[113]

Assess for delirium whenever a patient with dementia presents with acute illness.[113] Also assess for delirium in your patient with frailty.[116]

People living with dementia are at increased risk of delirium when they are admitted to hospital and throughout their admission.[111][117]
Frailty increases the risk of delirium threefold during hospital admission.[116]

Consider the following actions as part of a multicomponent intervention to reduce the risk of delirium during a hospital admission in people with dementia or frailty:[111]

Help with orientation; make sure patients have their own glasses and/or hearing aids
Get patients mobilised as soon as possible
Control pain adequately
Monitor for and treat postoperative complications as soon as possible
Keep patients well hydrated and help them to eat adequately
Monitor and maintain regular bowel and bladder function
Use supplementary oxygen according to guideline recommendations
Consider facilitating the patient's usual carer to assist in non-medical care, such as help with meal times, if they desire to do so.

Arrange a medication review with an experienced healthcare professional:[111]

Calculate the anticholinergic burden (ACB) score.[118]
A score of 3 or more may increase the risk of delirium within 24-48 hours of admission.[119]
Consider discontinuing or substituting anticholinergic drugs where possible, but be aware of the need to taper some medications to avoid withdrawal side effects such as nausea and sweating.[120]

Practical tip

Dementia and frailty are risk factors for postoperative delirium.[117][121][122]

Consider contacting the anaesthetist for advice on pain management.[123]

Evidence: Primary prevention of delirium in hospital using non-pharmacological interventions

There is evidence that a non-pharmacological approach reduces the risk of delirium in non-intensive care unit (non-ICU) patients in hospital.

A Cochrane systematic review found non-pharmacological multicomponent interventions were effective in preventing incident delirium in adults in a non-ICU hospital setting.[124]

Meta-analysis of 14 studies on multicomponent interventions found a significant reduction in incident delirium compared with usual care (risk ratio 0.57, 95% CI 0.46 to 0.71).
There is emerging evidence that multicomponent interventions may reduce hospital length of stay (mean difference -1.3 days, 95% CI -2.56 to -0.04 days) but there was significant heterogeneity between the studies.
There was little information specifically on people with dementia as this group were frequently excluded from trials despite their increased risk of developing delirium.

More info: Initial investigations for a patient with delirium

If a patient has delirium, check for and treat life-threatening causes:[111]

Hypoxia
Low blood glucose
Hypotension
Drug intoxication or withdrawal, including alcohol withdrawal.

Other investigations include (based on expert opinion):

Full blood count, electrolytes, renal function, thyroid function tests, liver function tests, calcium, glucose, CRP, folate, and vitamin B12
Blood cultures (if bacteraemia is suspected)
Urine culture
Chest x-ray.

Advanced non-routine investigations such as CT head may be needed, depending on specific clinical findings. Discuss with your senior.[111]

Check for and treat any reversible causes of delirium.[113]

Pain
Infection
Poor nutrition
Constipation
Dehydration
Medications
- Ask about recently prescribed medications, especially opioid analgesics, anxiolytics, sedatives, antipsychotics, or medicines with strong anticholinergic properties.
- Consider calculating a total anticholinergic burden score.
Environment (including immobility; poor sleep; sensory impairment e.g., ear wax or loss of glasses).

The mnemonic PINCH ME may be helpful as an aide memoire for the underlying causes of delirium superimposed on dementia.[125]

More info: Management of a patient with delirium

Manage patients with delirium initially with non-pharmacological treatment.[113]

Reduce disorientation by providing a well-lit room, with a clock and calendar visible (e.g., on the wall).
Encourage and facilitate family, friends, and carers to visit the patient.
Use verbal and non-verbal techniques to de-escalate conflict and distress.

NICE recommends short-term use of haloperidol (usually for less than 1 week), but it is not suitable in all patients and must never be used in patients with Parkinson’s disease or in patients with dementia with Lewy bodies.[113] Check for all contraindications.
Take particular care to closely monitor and regularly review older people with frailty when prescribing haloperidol for acute delirium. They are particularly at risk of adverse neurological and cardiac effects of this drug.[126]
- A baseline ECG and correction of electrolyte abnormalities is recommended before starting haloperidol.
- Prescribe at the lowest dose and for the shortest length of time possible.
- During treatment, cardiac and electrolyte monitoring is recommended, as is monitoring for extrapyramidal adverse effects.
The evidence on the efficacy of antipsychotics for delirium is inconclusive, and hospital protocols may vary.[111] Follow your local hospital protocol for choice of medication.
Always start at the lowest dose for antipsychotic drugs and titrate carefully according to symptoms.[113] Only ever use oral or intramuscular medication (never intravenous) for this purpose.

Provide the family/carers with information so they understand what is happening and how they can work together with the clinical team to help the patient get back to their usual self.[111]

Evidence: Risks and safe withdrawal of antipsychotics in older people

Antipsychotics are associated with increased mortality in people with dementia.

A Cochrane review found very low certainty evidence that typical antipsychotics such as haloperidol improve agitation, and may improve psychosis slightly in people with Alzheimer’s disease and vascular dementia. Atypical antipsychotics probably reduce agitation. Both types increase the risk of somnolence and extrapyramidal symptoms.[127]
A network meta-analysis found that people who take atypical antipsychotics for behavioural and psychological symptoms of dementia may have a small improvement in behavioural and psychological symptoms but have increased safety risks including cerebrovascular adverse events compared with those taking placebo.[128]
Contrary to popular belief, long-term antipsychotic prescriptions can be safely withdrawn in most people with dementia once behaviour has settled.[129]

Document the diagnosis of delirium clearly.[111][113]

– monitor and manage blood glucose during the hospital admission

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monitor and manage blood glucose during the hospital admission

Treatment recommended for ALL patients in selected patient group

Monitor blood glucose levels at least four times a day (every 4-6 hours or, if eating, pre-meal and before bedtime) in any acutely unwell patient with diabetes mellitus.[130]

The risk of hypo- and hyperglycaemia increases when a person with diabetes is admitted to hospital acutely (based on expert opinion).
Even more frequent monitoring is needed after any episode of hyperglycaemia or hypoglycaemia and after a change in hypoglycaemic medication (based on expert opinion).
If your patient has undergone surgery, follow your local protocol or recommendations from guideline organisations such as the UK-based Centre for Perioperative Care on blood glucose management and frequency of blood glucose monitoring.[94]
Any patient on a variable rate intravenous insulin infusion (VRIII) needs capillary blood glucose (CBG) measurements initially every hour.[92][131] Adjust according to your hospital VRIII protocol.

It is safe
The patient is willing, and
It conforms to local protocols.

Decide on and monitor target blood glucose levels.

There is no consensus among guideline organisations on target blood glucose levels for people with diabetes who are in hospital.

The Joint British Diabetes Societies for Inpatient Care recommend the following for medical inpatients with diabetes:
- An ideal range of 6 to 10 mmol/L (108-180 mg/dL)[131]
- A range of 4 to 12 mmol/L (72-216 mg/dL) is acceptable in some circumstances.[131] A lower level of 4 mmol/L (72 mg/dL) may be acceptable in people with very well controlled diabetes in hospital who are self-managing (based on expert opinion)
- A target range of 7.5 to 10 mmol/L (135-180 mg/dL) for patients with diabetes in hospital with mild frailty, and up to 12 mmol/L (216 mg/dL) for those with moderate or severe frailty.[133] An upper level of 12 mmol/L may also be appropriate for any patient at high risk of falls or with dementia (based on expert opinion).
The Centre for Perioperative Care recommends maintaining a range of 6 to 10 mmol/L (108-180 mg/dL), with an acceptable upper level of 12 mmol/L (216 mg/dL) in perioperative patients.[94]
The UK National Institute for Health and Care Excellence recommends a target plasma glucose level of 5 to 8 mmol/L (90-144 mg/dL) in adults with type 1 diabetes in hospital with acute illness or undergoing surgery, although this is lower than other guideline recommendations.[132]
The American Diabetes Association recommends a target range of 7.8 to 10 mmol/L (140-180 mg/dL) for most critically ill patients and 5.6 to 10 mmol/L (100-180 mg/dL) for most non-critically ill patients once insulin has been started for persistent hyperglycaemia.[130]

Evidence: Blood glucose targets for critically ill patients with hyperglycaemia

Intensive care setting:
- A randomised controlled trial (RCT) of critically ill patients in a primarily surgical intensive care setting found lower patient mortality with tight glucose control, 4.4 to 6.1 mmol/L (80-110 mg/dL), compared with ‘conventional’ more liberal glucose control.[134]
- However, a subsequent multicentre RCT in critically ill medical and surgical patients in other intensive care settings found increased mortality with tighter glucose control, possibly due to more frequent episodes of hypoglycaemia.[135]
- A 2010 systematic review of 6 RCTs and a meta-analysis investigating tight glucose control (4.4-6.1 mmol/L [80-110 mg/dL]) versus less strict glucose control in critically ill patients in the intensive case setting found no significant improvement in mortality with tight glucose control, but it was associated with significantly more hypoglycaemic episodes compared with less strict glucose control.[136]

Hyperglycaemia during the ongoing hospital admission

Hyperglycaemia in patients in hospital, whether with known diabetes or not, is associated with adverse patient outcomes, including increased mortality.[95]

Act promptly to treat hyperglycaemia to avoid diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS), which are medical emergencies.

Follow your local hospital protocol if your patient’s CBG is ≥15 mmol/L (≥270 mg/dL).
- Generally, action is required at this CBG level, but local protocols may have slightly different cut-off levels and it may vary depending on whether the patient has type 1 or type 2 diabetes.
Exclude DKA or HHS, both of which require specific urgent management.[98][137]
Patients who are usually managed with sodium-glucose co-transporter-2 (SGLT2) inhibitors should have blood ketone measurements to exclude euglycaemic ketoacidosis (ketoacidosis in the presence of normal blood glucose concentration) even if the SGLT2 inhibitor has been stopped (based on expert opinion).

It is imperative to ensure early senior review of patients with HHS by a clinician familiar with the management of this condition.[137] Patients with additional comorbidities may need to be on a high-dependency unit.[137]
See Diabetic ketoacidosis or Hyperosmolar hyperglycaemic state.

Be aware that the following medications may be associated with hyperglycaemia and may need to be reviewed:[138]

Corticosteroids
Some beta-blockers (e.g., propranolol, atenolol)
Thiazide diuretics (e.g., hydrochlorothiazide)
Some second-generation antipsychotics (e.g., olanzapine, clozapine)
Certain fluoroquinolone antibiotics (e.g., ciprofloxacin)
Calcineurin inhibitors (e.g., ciclosporin, tacrolimus)
Protease inhibitors (e.g., as a component in antiretroviral therapy, such as ritonavir).

Practical tip

Ask for expert advice from the diabetes team in complex patients, or where hyperglycaemia is difficult to control.

Hypoglycaemia during the ongoing hospital admission

Monitor blood glucose and adjust medication in response to illness and hospital meal times, to reduce the risk of hypoglycaemic episodes.

Approximately 1 in 5 inpatients with diabetes in England and Wales were found to have had a hypoglycaemic episode during their hospital stay.[139]
Causes include:[140]
- Recovery from an acute illness
- Insulin or oral hypoglycaemic medication error
- Wrong timing of insulin in relation to meals
- Patients eating less but taking the same amount of diabetes medication
- No bedtime snacks
- Reduced appetite or vomiting.

Consider intervening if the blood glucose falls below 6 mmol/L (108 mg/dL) (‘looming/impending’ hypoglycaemia) if on insulin or on sulfonylureas.

These patients are at high risk of progressing to hypoglycaemia.
Give carbohydrates as recommended in the hypoglycaemia guideline and follow your local protocol (see below).[140]

Retest blood glucose at 10-15 minutes to determine response to treatment
Never stop the next scheduled dose of insulin if the hypoglycaemia has been corrected. This can cause rebound hyperglycaemia and DKA in people with type 1 diabetes.
- Seek diabetes inpatient specialist team advice on whether a review of your patient’s insulin regimen is needed.

Take steps to reduce the risk of hypogylcaemia at night. Assuming your patient can swallow, they are likely to have a smaller evening meal in hospital than at home.[139]

In the absence of significant hyperglycaemia, consider reducing the evening basal insulin by 20% on admission (based on expert opinion).

Be aware that hypoglycaemia as an adverse effect of sulfonylurea medication (e.g., glibenclamide, gliclazide, glimepiride, glipizide) is more likely if meals are skipped or doses are excessive.

In the acute hospital setting, meal times may be interrupted or may not always be at exactly the same time each day.
- Give sulfonylurea medication before or with food. Check local drug formulary for more specific guidance on timing of dose in relation to food for specific sulfonylurea.
- Never give sulfonylurea medication at bedtime and, if the patient is taking a dose with their evening meal, consider reducing the evening dose to reduce the risk of nocturnal hypoglycaemia (based on expert opinion).

Practical tip

Bedtime snacks can reduce the risk of early morning hypoglycaemia.[139]

More info: Management of patients with diabetes who are receiving end-of-life care

If a patient with diabetes is receiving end-of-life care:

Reduce hypoglycaemic medication to a minimum, but keep the patient free from symptomatic hyperglycaemia, which can lead to:[141]
- Dehydration
- Ketosis
- Hyperosmolar hyperglycaemia.
Do not stop basal insulin in a person with type 1 diabetes
Refer to local protocols or guidance from diabetes organisations such as the UK-based TREND^TM Diabetes.[141]

– check your patient’s feet

– ensure monitoring is in place to detect any asthma exacerbation during your patient's hospital admission

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–

ensure monitoring is in place to detect any asthma exacerbation during your patient's hospital admission

Treatment recommended for ALL patients in selected patient group

Acute worsening of respiratory symptoms may suggest a patient with comorbid asthma is having an acute exacerbation of their asthma.

Follow guideline recommendations on assessing severity and managing an acute exacerbation of asthma in adults.[73][72]
See Acute asthma exacerbation in adults.

This is due to concern over possible additive anticholinergic adverse effects.
Ensure to re-prescribe the LAMA once the nebuliser treatment has been stopped.

Be aware that the long-term use of beta-2 agonists to manage asthma may increase the risk of cardiovascular events.

Evidence: Cardiovascular harm with beta-2 agonists

Beta-2 agonists may increase the risk of myocardial infarction and other adverse cardiovascular events.

Beta-2 agonists increase heart rate and reduce potassium levels.[144] They are absorbed into the systemic circulation and there is evidence that long-term regular use may be associated with an increased risk of myocardial infarction, unstable angina, congestive heart failure, and arrhythmias.[144][145]
However, it is not routine practice to discontinue beta-2 agonists if they are needed for comorbid asthma.

– ensure monitoring is in place to detect any COPD exacerbation during your patient's hospital admission

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ensure monitoring is in place to detect any COPD exacerbation during your patient's hospital admission

Treatment recommended for ALL patients in selected patient group

Acute worsening of respiratory symptoms may suggest a patient with comorbid COPD is having an acute exacerbation.[146]

Differentiate from other conditions, such as acute coronary syndrome, acute heart failure, and pneumonia.
Follow guideline recommendations. See Acute exacerbation of COPD.

Bronchodilator therapy via a nebuliser should only be used for 24 to 48 hours and then the patient should be switched back onto their usual inhaler(s) (based on expert opinion).

This is due to concern over possible additive anticholinergic adverse effects.
Ensure the LAMA is re-prescribed once the nebuliser treatment has been stopped.

Be aware that the long-term use of beta-2 agonists to manage COPD may increase the risk of cardiovascular events.

Evidence: Cardiovascular harm with beta-2 agonists

Beta-2 agonists may increase the risk of myocardial infarction and other adverse cardiovascular events.

Beta-2 agonists may increase heart rate and reduce potassium levels.[144] They are absorbed into the systemic circulation and there is evidence that long-term regular use may be associated with an increased risk of myocardial infarction, unstable angina, congestive heart failure, and arrhythmias.[145][144]
However, the Global Initiative for Chronic Obstructive Lung Disease states that there has been no reported association between beta-2-agonist use and increased mortality in people with COPD.[146] It is not routine practice to discontinue beta-2 agonists if they are needed for comorbid COPD.

Evidence: Short duration versus longer duration of corticosteroids for acute exacerbation of COPD

The randomised controlled trials included in this Cochrane review were all in hospital settings and only included people with severe to very severe COPD.[147]
The review authors concluded that due to the addition of a new trial, they have increased confidence that a corticosteroid course of around 5 days is likely to be sufficient for the treatment of an acute exacerbation of COPD.[147]
Similarly, a review of the evidence in 2019 resulted in the National Institute for Health and Care Excellence (NICE) recommending to offer prednisolone for 5 days during an exacerbation of COPD.[148]

– continue your patient's inhalers as prescribed for asthma or COPD

– mental state examination

– review current treatment for depression in your patient with cardiac disease

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review current treatment for depression in your patient with cardiac disease

Treatment recommended for ALL patients in selected patient group

Get an up-to-date list of medication used to manage your patient’s mental health, either by asking them directly or retrieving relevant primary care medical records (if available).

Seek expert advice on reviewing existing medication and/or prescribing a new psychotropic for your patient with acute heart failure or acute coronary syndrome and depression. Avoid abruptly stopping antidepressants due to the potential risk of discontinuation symptoms and prescribe new ones with caution.[151][152]
- The unique side-effect profile of the various antidepressants should be taken into consideration; this includes interactions (additive or otherwise) with cardiac medication.[153]
- Selective serotonin-reuptake inhibitors (SSRIs) are considered to be a good first option in the post myocardial infarction (MI) period, though relative caution should be taken. Sertraline is the drug of choice.[154]
- From the newer classes of antidepressants, agomelatine and vortioxetine have a favourable cardiac effect profile and have no specific contraindication in patients who have had an MI.[155][156]
- Tricyclic antidepressants are contraindicated in the immediate period following an MI. Similarly, they should be avoided in patients with coronary artery disease and/or heart failure because they are associated with hypotension, arrhythmias, and worsening heart failure.[157][158][63]
- Monoamine oxidase inhibitors are not recommended in cardiovascular disease (or may be contraindicated in some countries).
- Serotonin-noradrenaline reuptake inhibitors, reboxetine, and trazodone are best avoided in patients with cardiovascular disease.[157]
When reviewing current medication, look out for:
- Current and previous adverse effects
- Recent changes in dose
- Recent switches from a different class of medication
- Pharmacological nuances of specific depression subtypes (e.g., it is likely that patients suffering from psychotic depression would be co-prescribed an antipsychotic)
- Augmenting strategies that may be in use when treating resistant depression (e.g., lithium or quetiapine augmentation of an SSRI).
Consider drug-drug interactions.
- Antidepressant medications may cause pharmacokinetic (by inhibiting the CYP450 pathway) and pharmacodynamic interactions with medications used for other conditions.[157][158]
Consider psychiatric complications when prescribing non-psychotropic drugs.
- Take particular care when prescribing anticonvulsants, antiparkinsonian medication, and corticosteroids.
Consider adverse effects, which may include the following:
- Hyponatraemia, caused by antidepressants, especially SSRIs, and compounded by other co-prescribed drugs (e.g., diuretics). Check your patient’s serum electrolytes.
- Serotonin syndrome (altered mental state, agitation, tremor, hyper-reflexia, clonus, muscle rigidity, diaphoresis, tachycardia, increased bowel sounds, temperature >38℃), especially with polypharmacy and/or overdose of a serotonergic agent.[159][160] See Serotonin syndrome.
  - Be particularly aware of increased risk of serotonin syndrome in patients with end-stage renal disease on SSRIs. Treating depression in patients with renal impairment requires a multidisciplinary approach and demands extra caution.
- Hepatotoxicity. Adjust doses of antidepressants in patients with hepatic impairment if necessary and avoid drugs that are known to be hepatotoxic.
- QTc prolongation, arrhythmias, increased heart rate, postural hypotension with tricyclic antidepressants. Check ECG, especially in people at risk of arrhythmias.
- Gastrointestinal bleeding. SSRIs are associated with an increased risk of gastrointestinal bleeding.[157] Risk is particularly increased when co-prescribed with aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), or oral anticoagulants.[161][162] Try to avoid this combination of drugs.[157] Monitor closely and consider gastroprotection with proton-pump inhibitors if SSRI use cannot be avoided.[157]

This list of adverse effects is not exhaustive - consult local formulary for further information. Consult your liaison psychiatry colleagues and/or a pharmacist for advice.

Ask your patient about non-pharmacological treatments for their depression and check current level of support in the community.

This may include other health professionals involved in their care, charities, family and social networks, and psychological therapy.

Practical tip

– consider referral to the liaison psychiatry team

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–

consider referral to the liaison psychiatry team

Treatment recommended for ALL patients in selected patient group

Consider a referral to the liaison psychiatry team/service for any patient with comorbid depression who is admitted to hospital with an acute condition.[166][167]

Referral may not be required if there are no concerns that depression and/or its management (e.g., medication) may be affecting the acute condition (based on expert opinion).
Accidents of unclear circumstances, self-injurious behaviours, and/or suicide attempts should trigger clinical suspicion of comorbid mental health disorder (based on expert opinion).

Evidence: Depression and adherence with treatment post-discharge

Comorbid depression is linked to poor adherence with recommended physical health treatments, from medication to rehabilitation.[168]

This may lead to worse clinical outcomes, including higher readmission risk.[169][170][171]
Most importantly, affective symptoms including depression have been linked with excess mortality, though a causal link remains to be proven.[172][173]

haemodynamically stable

1st line – treatment of underlying cause

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1st line –

treatment of underlying cause

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

Practical tip

Identify and manage any comorbidity-related precipitant

The following is a non-exhaustive list of specific potential precipitants to consider in your patient with one or more comorbidity.

Hypertension and/or coronary artery disease

Diltiazem or verapamil, which may have been prescribed for hypertension or angina, in a patient with acute heart failure with a reduced ejection fraction (HFrEF).[63][64][65]
Alpha-blockers (e.g., doxazosin, prazosin) and minoxidil which should be avoided in patients with heart failure.[62]

Stroke

A cerebrovascular insult, such as a new stroke.
A previous stroke may affect swallowing which can lead to difficulty in taking heart failure medication and hence lead to decompensation (based on expert opinion).

Chronic kidney disease (CKD)

Medication adjustments and titration
- In general, medication doses may need adjustment and require particularly careful titration in a patient with CKD.
- Check this is done.

Diabetes

Medications.
- Thiazolidinediones (glitazones) are not recommended in patients with co-existent heart failure.[63][66]
- They can lead to fluid retention.[63][62]
- Dipeptidyl peptidase-4 (DDP-4) inhibitors (e.g., saxagliptin, sitagliptin) should be avoided.[62]
Metabolic derangement.
- For example, diabetic ketoacidosis may be a precipitant.

COPD and/or asthma

Oral corticosteroids may cause sodium and water retention.[63][65] Inhaled corticosteroids are not thought to be associated with the same adverse effect.[63]
Use beta-2 agonists with caution, especially in patients on high doses and/or those with uncontrolled heart rates.[62]
An acute exacerbation or other infection may trigger heart failure decompensation and may require temporary suspension of beta-blockers if there is ongoing bronchospasm and wheeze (based on expert opinion).

Depression

Tricyclic antidepressants may increase arrhythmia risk and are not recommended in a patient with heart failure.[63][62]
Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with depression.[67]

Dementia

Non-adherence to medications or to advice on fluid and salt intake, which may be more common in a person with cognitive impairment (e.g., with dementia).[68]
Cognitive impairment can also affect adherence to sick-day rules which are necessary for heart failure medications (renin-angiotensin-aldosterone system [RAAS] inhibitors and sodium-glucose cotransporter-2 [SGLT2] inhibitors) (based on expert opinion).

Frailty

Consider referring any patients with higher levels of frailty - assessed for example using the Rockwood clinical frailty scale or the heart failure-specific tool developed by the Heart Failure Association of the European Society of Cardiology - to the specialist heart failure team for more frequent monitoring and follow-up.[69][70] Dalhousie University: Clinical Frailty Scale Opens in new window
Non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided as they can lead to sodium and fluid retention and increased systemic vascular resistance.[62]
Frailty may impact medication adherence because of reduced dexterity and difficulty opening medication packaging.[62]

Practical tip

Plus – loop diuretic

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Plus –

loop diuretic

Treatment recommended for ALL patients in selected patient group

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][23]
Give the diuretic as either intermittent boluses or a continuous infusion.[1][23]
Adjust the dose according to the patient’s symptoms and clinical status.[1]
Monitor the patient’s weight, renal function, and urine output carefully while they are taking diuretics.[1][23]
- Aim to achieve positive diuresis with a reduction of body weight by 0.75 to 1.0 kg/day.[1]

Seek senior advice on fluid balance and diuretic dosing

Discuss your patient’s fluid balance and diuretic treatment with your senior, as this may be particularly challenging to manage in patients with CKD and heart failure.[69]

Higher doses of diuretics may be required in a patient with CKD and fluid congestion.[81] Seek expert advice.
Transient deterioration in kidney function may be a consequence of using higher doses of diuretics if they lead to intravascular volume depletion.

Primary options

furosemide: 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

furosemide : 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

furosemide: 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

Plus – check baseline kidney function and monitor closely

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Plus –

check baseline kidney function and monitor closely

Treatment recommended for ALL patients in selected patient group

Acute illness increases the risk of deterioration in kidney function.[77]
Assess and monitor volume status.[77]
Monitor for and respond to oliguria.[77]

Ongoing monitoring of kidney function during treatment for acute heart failure and CKD

Consider liaising with a nephrologist early if your patient with heart failure has worsening kidney function, particularly if they have other comorbidities (based on expert opinion).
Be aware when starting renin-angiotensin-aldosterone system (RAAS) inhibitors (ACE inhibitors, angiotensin-II receptor antagonists, mineralocorticoid receptor/aldosterone antagonists, or angiotensin receptor-neprilysin inhibitors) or sodium-glucose cotransporter-2 (SGLT2) inhibitors, you would expect a small reduction in eGFR.[80] There may also be a rise in creatinine due to altered renal haemodynamics.[63][80]
- A transient rise in creatinine can also be seen when a patient is started on diuretics (oral or intravenous). On its own this should not be concerning if the patient's volume status and symptoms are improving on diuretics.[63][81]
- It may be necessary to temporarily reduce or withhold RAAS inhibitor therapy during intravenous offloading, due to symptomatic hypotension, or if a change in kidney function is more than expected.[81]

Weigh the risk of the decline in kidney function against the prognostic benefits of these medications for your patient with heart failure and CKD.

RAAS inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with heart failure with reduced ejection fraction (HFrEF), so have prognostic benefit.[63][81]
The benefit of RAAS inhibitors is greater in a patient with HFrEF compared with heart failure with preserved ejection fraction (HFpEF). Liaise with a cardiologist for advice regarding your patient with HFpEF, as RAAS inhibitor treatment is individualised.[82]
SGLT2 inhibitors reduce heart failure hospitalisations and mortality compared with placebo in patients with HFrEF and HFpEF, so have prognostic benefit.[81][83]
Be aware of the risk of euglycaemic ketoacidosis for patients with diabetes receiving SGLT2 inhibitors.[84][85] Most consensus guidance for people with diabetes self-managing an intercurrent illness recommends to stop SGLT2 inhibitors when they are acutely ill, unable to eat, or have diarrhoea and/or vomiting and to monitor blood ketones.[86][87]
If your patient does not have diabetes, euglycaemic ketosis is rare, but be aware of the possibility.[88] It is still reasonable to withhold SGLT2 inhibitors during times of prolonged fasting, surgery, or critical medical illness (when people may be at greater risk for ketosis).[79]
Monitor ketones in all situations, whether SGLT2 inhibitors have been stopped or continued (based on expert opinion).
RAAS inhibitors and SGLT2 inhibitors may also slow progression of kidney disease in people with diabetic kidney disease.[82]

In the context of a stable or improving clinical condition, a decline in eGFR on its own is not usually an indication to discontinue disease-modifying therapies.[80]

Remember to communicate to the primary care practitioner about continued monitoring needed post-discharge.

Consider – vasodilator

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Consider –

vasodilator

Additional treatment recommended for SOME patients in selected patient group

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

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

Primary options

glyceryl trinitrate: 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

glyceryl trinitrate : 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

glyceryl trinitrate: 10 micrograms/minute intravenous infusion initially, adjust dose according to response, maximum 400 micrograms/minute

isosorbide dinitrate: 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

isosorbide dinitrate : 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

isosorbide dinitrate: 2-10 mg/hour intravenous infusion initially, adjust dose according to response, maximum 20 mg/hour

Secondary options

sodium nitroprusside: consult specialist for guidance on dose

sodium nitroprusside : consult specialist for guidance on dose

sodium nitroprusside: consult specialist for guidance on dose

Consider – aldosterone antagonist or thiazide-type diuretic

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Consider –

aldosterone antagonist or thiazide-type diuretic

Additional treatment recommended for SOME patients in selected patient group

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

Consider risk of hyperkalaemia with aldosterone antagonists

Monitor this carefully.