Senior PCN Clinical Pharmacist Robin Mullen provides her top practical tips for performing holistic and effective heart failure reviews
Heart failure (HF) is a complex, progressive condition that demands careful, tailored management and is associated with poor prognosis. As clinical pharmacists in primary care, we are ideally positioned to contribute to HF reviews in general practice, drawing on our expertise in managing complex polypharmacy and multimorbidity through structured medication reviews.
Whether you’re just starting out or looking to fine-tune your approach, these seven top tips will help you deliver effective, evidence-based medication reviews for patients with heart failure.
1. Go beyond breathlessness: assess the true impact on daily life
When assessing symptoms, don’t stop at ‘Are you breathless?’ Understanding how heart failure impacts a patient’s functional status gives essential context for treatment decisions.
Ask questions about activities of daily living (ADLs), for example:
- Can they manage stairs without stopping?
- Do they sleep in a bed or a chair?
- How far can they walk before needing to rest?
Documenting the number of pillows used at night can reveal signs of worsening orthopnoea, and a shift from bed to sleeping upright in a chair may suggest deteriorating pulmonary oedema. Watch for signs like rapid weight gain, reduced appetite (due to abdominal congestion) and a cough with white frothy sputum.
Importantly, always consider differentials – breathlessness may also stem from COPD, anaemia, deconditioning or even undiagnosed sleep apnoea.
Do not forget to consider the impact of heart failure on the patient’s mental health as well.
For some GP practices this all falls under the requirement to assess functional capacity annually in patients with heart failure, as well as conducting yearly medication reviews, as part of the Quality and Outcomes Framework (QOF; see indicator HF007).1 See box 1 for the full list of current QOF HF indicators
Box 1: QOF indicators: HF1
Initial diagnosis
- HF008. The percentage of patients with a diagnosis of heart failure on or after 1 April 2023 which:
- Has been confirmed by an echocardiogram or by specialist assessment in the 6 months before entering on to the register; or
- If registered at the practice after diagnosis, with no record of the diagnosis originally being confirmed either by echocardiogram or by specialist assessment, a record of an echocardiogram or a specialist assessment within 6 months of the date of registration.
Ongoing management
- HF003. In those patients with a diagnosis of HF due to left ventricular systolic dysfunction or whose HF is due to reduced ejection fraction, the percentage of patients who are currently treated with an ACE inhibitor or ARBs.
- HF006. The percentage of patients with a diagnosis of HF due to left ventricular systolic dysfunction or whose HF is due to reduced ejection fraction, who are currently treated with a beta blocker licensed for HF.
- HF007. The percentage of patients with a diagnosis of heart failure on the register, who have had a review in the preceding 12 months, including an assessment of functional capacity and a review of medication to ensure medicines optimisation at maximal tolerated doses
2. Right diagnosis, right treatment: start with classification
Before diving into optimisation, confirm which classification of heart failure the patient has:
- Heart failure with reduced ejection fraction (HFrEF): EF <40%
- Heart failure with mildly reduced ejection fraction (HFmrEF): EF 41-49%
- Heart failure with preserved ejection fraction (HFpEF): EF ≥50%
Review echocardiogram reports carefully to determine: when the last echocardiogram was performed; and whether the type of HF has been clearly coded in the patient’s record. Accurate classification is vital as it directly guides therapeutic options. Documenting these in your consultation notes for reference helps ongoing reviews and saves time in the future.
3. Master the four pillars: a smarter way to start HFrEF therapy
For HFrEF, the goal is rapid introduction of the four pillars of guideline-directed medical therapy (GDMT) tailored to the patient’s clinical history and preferences:2,3
- ACE inhibitor / angiotensin receptor blocker (ARB) / angiotensin receptor-neprilysin inhibitor (ARNI).
- Beta blocker.
- Sodium-glucose cotransporter 2 (SGLT2) inhibitor.
- Mineralocorticoid receptor antagonist (MRA; eg, spironolactone).
As such, there has been a shift away from slow, stepwise initiation of GDMT to the approach of starting these treatments at the same time. If the patient is stable (normal blood pressure [BP], pulse, renal function and not fluid overloaded), low doses of all four drugs can often be started concurrently and uptitrated over time.2,3 It is important to be mindful when starting multiple medicines concurrently and a patient develops side effects, that it may be difficult to determine which agent is responsible. A pragmatic approach to rapid introduction in primary care is to prescribe all four agents but counsel the patient to stagger initiation of each drug every few days. This approach will depend on your patient’s clinical and haemodynamic status and involves a shared decision with the patient. It is important to ensure you have follow-up monitoring arranged within 1-2 weeks and appropriate safety netting in place to ensure patients are advised to seek advice sooner if any adverse effects or deteriorating heart failure symptoms occur.
Tailor therapy based on individual patient clinical status:
- Fluid overloaded? Delay beta blockers and commence SGLT2 inhibitor, MRAs.
- Bradycardic (<60bpm)? Avoid initiating beta blockers and focus on other therapies.
- Low eGFR (<30ml/min/1.73m2)? Avoid initiating ACE inhibitor/ARB/ARNI, MRA and SGLT2 inhibitor – consider beta blockers and seek specialist advice.
- Hyperkalaemic (>5.5 mmol/L)? Avoid ACE inhibitor/ARB/MRA – consider beta blocker plus SGLT2 inhibitor.
- Hypotensive? Initiate with dapagliflozin or spironolactone (minimal BP effect).
If the patient has type 2 diabetes mellitus (T2DM), especially those on insulin or sulfonylureas, be mindful of hypoglycaemia risk and recheck HbA1c after initiating an SGLT2 inhibitor. Avoid SGLT2 inhibitors in type 1 diabetes. Note also that in patients with eGFR <45ml/min/1.73m2, the addition of SGLT2 inhibitor for HF will have minimal impact on HbA1c levels.
4. HFpEF isn’t HFrEF: manage the multimorbidity
There’s no strong evidence for rapid GDMT in HFpEF. The focus here is controlling comorbidities:
- Tackle hypertension, atrial fibrillation, T2DM, chronic kidney disease (CKD), obesity and ischaemic heart disease.
- SGLT2 inhibitors can be considered in line with NICE4,5 (check your local guidance), especially in those with coexisting CKD or T2DM.
- Loop diuretics remain the mainstay to manage symptoms of fluid overload – use the lowest dose needed to maintain euvolaemia.
HFpEF often coexists with frailty and polypharmacy – holistic care and collaborative MDT working is essential.
Similarly, in HFmrEF there are currently no strong recommendations on specific therapies. However, the use of ACE inhibitors/ARBs, beta blockers and MRAs may be considered.6 Diuretics should be used to manage congestion and SGLT2 inhibitors may also be considered in line with NICE guidance.4,5
5. Empower and adjust: smarter loop diuretic use
Loop diuretics are essential for managing fluid overload in HF, but striking the right balance is key. Overuse can lead to dehydration and electrolyte disturbances, while underuse contributes to symptom burden and hospital admissions. It is important that clinicians review and consider reducing diuretics at each encounter to lowest maintenance dose to maintain euvolaemia (a patient’s ‘dry weight’). This is to minimise risk of hypovolaemia, dehydration and risk of renal deterioration/acute kidney injury.
When to consider increasing the dose:
- Sudden weight gain of ≥2kg over 2–3 days.
- Increased oedema, dyspnoea, orthopnoea, paroxysmal dyspnoea (PND) or ascites.
When to consider reducing the dose:
- If patient is clinically stable with only mild dyspnoea and no signs of orthopnoea, oedema or ascites.
- Symptoms suggest dehydration, such as thirst, urinary retention, dry mucous membranes, reduced skin turgor and/or postural hypotension.
Empower patients to monitor their weight and symptoms daily and to self-titrate loop diuretics with a self-management plan and safety netting. This supports proactive self-management and can reduce the need for emergency escalation. Temporary increase of a loop diuretic for 2-3 days does not necessarily warrant a blood test. Ensure patients are counselled to inform you when a sustained increase in loop diuretics approaches 1-2 weeks so that a blood test can be arranged to monitor U&Es.
Dose equivalence:
40mg furosemide = 1mg bumetanide
When to consider switching to bumetanide?
Bumetanide has better bioavailability and may be more effective in patients with resistant oedema despite high-dose furosemide.
Other considerations:
- Loop diuretics can increase the risk of hyperuricaemia and may exacerbate gout.
- Always aim for the lowest dose required to maintain euvolaemia (the patient’s ‘dry weight’) – not necessarily zero fluid retention but an absence of symptoms.
6. Don’t prescribe in isolation: look at the whole regimen
When HF medication optimisation is limited by low blood pressure or dizziness, consider whether other non-HF medicines are contributing:
- Common culprits include amlodipine, doxazosin and other non-essential antihypertensives. Be mindful of whether patients were already being prescribed a thiazide diuretic such as bendroflumethiazide for hypertension, prior to their diagnosis of HF, as the addition of a loop diuretic in such patients will lead to excess diuresis. This combination is often reserved for resistant oedema.
- While amlodipine may be providing anti-anginal relief in patients with ischaemic disease, weigh its value against potential to cause hypotension.
- Also review for medications that can exacerbate HF as outlined in box 2 below.
Box 2. Medications associated with exacerbation of HF symptoms / adverse effects
NSAIDs, COX inhibitors
- Increase fluid retention, increase vascular resistance, decrease response to diuretics.7
Thiazolidinediones (pioglitazone)
- Possible calcium channel blockade, increase fluid retention.6
Saxigliptin
- Potential mechanism unclear.
Doxasozin
- beta-1 stimulation, increase renin and aldosterone.7
Diltiazem/verapamil
- Negative inotropic effects.7
Antimuscarinics (oxybutynin, tolterodine, solifenacin, fesoterodine)
- Increase fluid retention, increase tachycardia.8
Antidepressants (can also cause hyponatraemia)
- Citalopram
- Prolongation of QTc interval (sertraline recommended first-line, while escitalopram has demonstrated safety but can also be associated with QTc prolongation).9
- SNRIs (venlafaxine and duloxetine)
- Associated with dose-dependent increase in BP; venlafaxine my prolong QTc interval.
- Tricyclic antidepressants
- Arrhythmias/QTc prolongation, hypotension.9
7. Treat the patient, not the numbers
Mild changes in bloods are not always a reason to stop therapy. ACE inhibitors, ARBs, ARNIs, MRAs and SGLT2 inhibitors can cause expected rises in creatinine and drops in eGFR when initiated – this doesn’t necessarily signal harm and stopping a patient’s GDMT in HFrEF may be more detrimental to their prognosis:10
- A <30% rise in serum creatinine is generally acceptable.
- Ensure potassium readings are accurate – falsely high values can result from poor sampling technique (tight tourniquet or fist clenching leading to haemolysis) or delayed processing.
- Repeat bloods and consider a low-potassium diet before stopping therapy.
Useful resources to refer to when reviewing blood test results:
Always counsel on adequate hydration (1.5-2L/day) and sick day rules to avoid AKI:
Also, don’t panic if systolic BP is <110mmHg. If the patient is asymptomatic and not exhibiting postural hypotension, continue to titrate towards target doses, not target blood pressures. Explain this to patients and colleagues to avoid premature de-escalation.
The risk of postural hypotension increases with age, frailty and polypharmacy. It’s important to review all medications that may contribute – not just HF drugs. This includes antihypertensives, opioids, antiepileptics, antidepressants and antipsychotics. Where appropriate, consider adjusting the timing or splitting doses of HF medications that may be worsening symptoms. Don’t forget to assess fluid intake and check for any signs of dehydration, which can further exacerbate hypotension.
8. Mind the iron gap: don’t overlook anaemia in HFrEF
Iron deficiency is quite common in HFrEF and contributes to worsening fatigue and breathlessness and reduced quality of life. Yet we may overlook this if focusing on renal function.
In symptomatic patients, make sure to periodically request:
- FBC
- Ferritin
- Transferrin saturation (TSAT)
A ferritin level <100ng/mL or 100–299ng/mL with TSAT <20% confirms iron deficiency in HF.6
Iron replacement can improve symptoms and exercise tolerance, therefore consider seeking advice and guidance from your secondary care colleagues whether an IV iron referral is indicated. IV iron is recommended in these cases over oral iron supplementation in HF, due to upregulation of hepcidin (hormone that regulates iron levels) which results in impaired absorption of oral iron.13 Oral iron may still be considered as a treatment option temporarily – however, be mindful it may not be as effective.
Please ensure alternative causes for iron deficiency anaemia have been considered and investigated.
Final thoughts
Heart failure reviews are more than a checklist – they’re an opportunity to transform outcomes. With the right approach, practice pharmacists are ideally placed to lead on optimisation, safety monitoring and patient-centred care.
That said, it’s important to make sure you are documenting QOF requirements on HF (if they apply to your practice). See box 1 above outlining QOF HF indicators.
Use these tips to structure your reviews, advocate for timely therapy changes and empower both patients and the wider MDT. A well-informed heart failure medication review can be the difference between deterioration and stability for your HF patients minimising clinical inertia.
Robin Mullen is an independent prescriber specialising in heart failure and delivering heart failure clinics across her practices at ASPIRE PCN, Nottingham City GP Alliance (NCGPA), where she is Senior PCN Clinical Pharmacist and PCN Pharmacy Team Manager
References
- NHS England. Quality and Outcomes Framework guidance for 2025/26
- NICE. Chronic heart failure in adults: diagnosis and management. [NG106] Draft update for consultation. June 2025
- Packer M and McMurray J. Rapid evidence-based sequencing of foundational drugs for heart failure and a reduced ejection fraction.Eur J Heart Fail 2021; 23(6):882-894
- NICE. Dapagliflozin for treating chronic heart failure with preserved or mildly reduced ejection fraction. [TA902]
- NICE. Empagliflozin for treating chronic heart failure with preserved or mildly reduced ejection fraction. [TA929]
- McDonagh T et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) With the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 2021; 42:3599-3726
- Heidenreich P et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.Circulation 2022;145(18):e895-e1032
- NICE. CKS. LUTS in men. Prescribing information: Antimuscarinics. Last revised June 2025
- NHS Specialist Pharmacy Service. Choosing an antidepressant for people with coronary heart disease. Last updated April 2025
- The Renal Association/Think Kidneys/British Society for Heart Failure. Changes in kidney function and serum potassium during ACEI/ARB/diuretic treatment in primary care: A position statement from Think Kidneys, the Renal Association, and the British Society for Heart Failure. 2017
- National Kidney Foundation. Your guide to a low potassium diet.
- Pumping Marvellous. Sick Day Rules.
- Alnuwaysir R et al. Iron deficiency in heart failure: mechanisms and pathophysiology. J Clin Med 2021;11(1):125
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