Chronic Heart Failure (CHF)

• Establish breathlessness, orthopnoea (ask how many pillows) and paroxysmal nocturnal dyspnoea (waking gasping for breath)?

• Check for ischaemic heart disease, hypertension, atrial fibrillation, diabetes or known valve disease?

• Ask about fatigue or reduced exercise tolerance compared with the patient's baseline?

• Ask about previous myocardial infarction or cardiotoxic chemotherapy (anthracyclines, trastuzumab)?

• Confirm ankle or leg swelling – and whether it resolves overnight?

• Identify drugs that cause or worsen heart failure – NSAIDs, verapamil/diltiazem, pioglitazone?

• Ask about abdominal bloating, early satiety or anorexia (ascites or hepatic congestion)?

• Explore alcohol intake (alcoholic cardiomyopathy) and any recreational drug use?

• Ask about palpitations, nocturnal cough or syncope?

• Ask about family history of cardiomyopathy or sudden cardiac death?

• In known heart failure, confirm any rapid weight gain or step-change in symptoms (decompensation)?

• Ask about recent viral illness (myocarditis) or symptoms of thyroid disease?

➤ "Explore the patient's understanding of the heart failure diagnosis and any concerns about prognosis or the future?"

➤ "Ask how symptoms limit daily activities, and what impact they have on mood and quality of life?"

➤ Severe breathlessness at rest → suspected acute pulmonary oedema → 999 / emergency admission

➤ Hypoxia or respiratory distress (for example SpO₂ < 94% on air) → emergency admission

➤ Haemodynamic instability (systolic BP < 90 mmHg, signs of shock, new confusion) → 999

➤ Sudden, significant deterioration in symptoms over a short period → urgent same-day assessment

➤ Exertional or unexplained syncope → possible arrhythmia or outflow obstruction → urgent assessment

➤ Known heart failure with rapid weight gain and worsening congestion → impending decompensation → urgent review

• Elevated jugular venous pressure (JVP) or a positive hepatojugular reflux – the most useful bedside sign of congestion.

• Bilateral basal crackles on auscultation (pulmonary oedema), sometimes with a wheeze ("cardiac asthma").

• Displaced apex beat (laterally), indicating cardiomegaly.

• Third heart sound (S3) gallop, or murmurs suggesting valvular disease.

• Pitting peripheral or sacral oedema, hepatomegaly and ascites.

• Pulse, blood pressure and weight – note tachycardia, an irregular pulse (AF) and resting tachypnoea.

Heart failure means your heart isn't pumping as well as it should, which can leave you breathless and cause fluid to build up.
We can't cure it, but modern treatment is very effective – we use a combination of medicines proven to help people feel better and live longer.
The plan is to get you on the right medicines and support you with lifestyle changes to keep you well.

🧠 Clinical pearl

A "normal" NT-proBNP does not always exclude heart failure. Levels are pushed down by obesity, by African or African–Caribbean family background, and by the very drugs used to treat heart failure (diuretics, ACE inhibitors, ARBs, ARNIs, beta-blockers and MRAs). If clinical suspicion is high despite a level below 400 ng/L – particularly in an obese or already-treated patient – discuss with the heart failure team rather than stopping there.

• Confirm the diagnosis and ejection fraction type via NT-proBNP-led referral and echocardiography.

• Red flags of decompensation (hypoxia, hypotension, pulmonary oedema) → immediate admission.

• Treat by phenotype: HFrEF → the four pillars; HFmrEF → consider the four pillars; HFpEF → SGLT2 inhibitor + MRA + comorbidity control.

• Persistent symptoms despite optimal four-pillar therapy → urgent specialist review.

• Use a loop diuretic to relieve congestion, titrated to symptoms and daily weight (symptom relief only).

• IV diuretics and respiratory support are managed in secondary care.

• Identify and treat reversible factors and comorbidities – AF, iron deficiency/anaemia, hypertension, thyroid disease, depression.

• Discuss palliative care and advance care planning as the illness advances.

• Offer annual influenza and one-off pneumococcal vaccination; refer to cardiac rehabilitation; review in primary care at least 6-monthly.

🔑 Key principle – treat for prognosis, not just symptoms

In HFrEF, the four pillars – an ACE inhibitor (or ARNI), a beta-blocker, an MRA and an SGLT2 inhibitor – each independently reduce mortality. They should be started early and titrated to the maximum tolerated evidence-based dose, not simply started and left. Do not withhold a beta-blocker on the grounds of age, COPD, peripheral vascular disease, erectile dysfunction or diabetes. By contrast, loop diuretics relieve symptoms but do not prolong life.

➤ For symptom relief (fluid overload) – all phenotypes

→ Loop diuretic – furosemide or bumetanide; titrate to symptoms and weight to the lowest effective dose. Relieves congestion but does not improve survival.

➤ HFrEF (LVEF ≤ 40%) – the "four pillars" (each is prognostic; start early, titrate to maximum tolerated dose)

→ ACE inhibitor – e.g. ramipril, lisinopril or enalapril; up-titrate roughly every 2–4 weeks towards target (e.g. ramipril 10 mg daily); monitor renal function and potassium.

→ Beta-blocker licensed for heart failure – bisoprolol, carvedilol or nebivolol. Avoid in second- or third-degree heart block without a pacemaker, or if heart rate < 50 bpm.

→ MRA – spironolactone or eplerenone; monitor potassium and renal function closely (hyperkalaemia risk, especially combined with an ACE inhibitor/ARB).

→ SGLT2 inhibitor – dapagliflozin (Forxiga) or empagliflozin (Jardiance); may be initiated in primary or specialist care depending on the local pathway.

→ If ACE inhibitor not tolerated (non-angioedema) → use an ARNI in its place; if angioedema → beta-blocker + MRA + SGLT2 inhibitor, and consider an ARB.

➤ Persistent symptoms on maximal four pillars – specialist-led

→ Switch the ACE inhibitor to an ARNI – sacubitril/valsartan (Entresto). Stop the ACE inhibitor at least 36 hours beforehand to reduce the risk of angioedema; do not co-prescribe with an ACE inhibitor or ARB.

→ Consider ivabradine (sinus rhythm, heart rate ≥ 75 bpm), digoxin (worsening HFrEF, or for rate control in AF), or hydralazine with a nitrate (particularly in patients of African or Caribbean family origin) – all specialist decisions.

➤ HFmrEF (41–49%) and HFpEF (≥ 50%)

→ HFmrEF → consider the same four pillars as HFrEF. HFpEF → an SGLT2 inhibitor and finerenone (a non-steroidal MRA, detailed below), a loop diuretic for congestion, and treatment of hypertension, AF, obesity and diabetes.

➤ Finerenone in HFpEF and HFmrEF (NICE TA1182, 2026)

→ Finerenone is a non-steroidal MRA recommended by NICE (TA1182) for symptomatic heart failure with a preserved or mildly reduced ejection fraction (LVEF ≥ 40%); only the second disease-modifying option here after SGLT2 inhibitors (FINEARTS-HF trial). Specialist-initiated (cardiology), with primary care monitoring under shared care. Start 20 mg once daily (10 mg if eGFR is 25 to 59), titrating towards a 40 mg maintenance dose as potassium and renal function allow. Do not start if serum potassium is above 5.0 mmol/L or eGFR is below 25. Check potassium and eGFR at baseline, about 4 weeks after starting or any dose increase, then periodically; the main risk is hyperkalaemia. As a non-steroidal MRA it is used instead of a steroidal MRA (spironolactone, eplerenone), not alongside one.

➤ Key safety warning – SGLT2 inhibitors

→ Rare but serious risk of diabetic ketoacidosis, including euglycaemic DKA (normal or near-normal glucose). Counsel on "sick-day" rules – pause during acute serious illness – and test for ketones if symptoms suggest ketoacidosis even when glucose is normal.

➤ Drugs to avoid in HFrEF

→ Avoid verapamil, diltiazem and short-acting dihydropyridines; avoid NSAIDs and pioglitazone, which worsen fluid retention.

⚠️ Common pitfall

Treating the symptoms and forgetting the prognosis. It is easy to keep increasing the furosemide when a patient with HFrEF feels breathless and stop there – but the loop diuretic does nothing for survival. The mortality benefit comes from establishing and up-titrating all four pillars. A patient parked on a large dose of diuretic with sub-target doses of disease-modifying therapy is under-treated, not optimised.

📌 DVLA – fitness to drive (heart failure, including ischaemic and dilated cardiomyopathy)

• Asymptomatic (NYHA I): Group 1 – may drive and need not notify DVLA. Group 2 – may drive if LV ejection fraction is at least 40% but must notify DVLA.

• NYHA II: Group 1 – may drive if symptoms are stable and not likely to distract the driver or otherwise affect safe driving; need not notify DVLA. Group 2 – may drive if LVEF is at least 40% and symptoms are stable, but must notify DVLA.

• NYHA III: Group 1 – may drive if symptoms are stable and not likely to distract the driver or otherwise affect safe driving; need not notify DVLA. Group 2 – must not drive and must notify DVLA; licence refused or revoked, with relicensing only if symptoms are controlled and in NYHA I or II and LVEF is at least 40%.

• NYHA IV: Group 1 – must not drive and must notify DVLA; licence refused or revoked, with relicensing only if symptoms are controlled and in NYHA I, II or III. Group 2 – must not drive and must notify DVLA; relicensing only if symptoms are controlled and in NYHA I or II and LVEF is at least 40%.

• Left ventricular assist device: both groups must not drive and must notify DVLA; Group 1 may be reassessed under individual assessment only after 3 months, Group 2 is barred permanently.

• Red flags of acute decompensation (hypoxia, hypotension, pulmonary oedema) → emergency admission

• NT-proBNP > 2,000 ng/L → specialist assessment and echocardiography within 2 weeks

• NT-proBNP 400–2,000 ng/L → specialist assessment and echocardiography within 6 weeks

• Exertional or unexplained syncope → urgent assessment

• Persistent symptoms despite optimal four-pillar therapy → urgent specialist review

• Stable established heart failure → structured primary-care review at least 6-monthly, plus cardiac rehabilitation

🧭 AKT – high-yield facts

• NT-proBNP thresholds: < 400 ng/L heart failure unlikely (untreated) · 400–2,000 ng/L echo within 6 weeks · > 2,000 ng/L echo within 2 weeks.

• NT-proBNP is lowered by obesity, African/African–Caribbean background and HF drugs (diuretic, ACEi/ARNI/ARB, beta-blocker, MRA); raised by age, CKD, AF, sepsis and COPD.

• HFrEF (LVEF ≤ 40%) four pillars: ACE inhibitor + beta-blocker + MRA + SGLT2 inhibitor; switch the ACE inhibitor to an ARNI if still symptomatic on maximum tolerated doses.

• Loop diuretics relieve symptoms but do not reduce mortality – a classic exam point.

• Beta-blockers licensed for heart failure: bisoprolol, carvedilol, nebivolol; don't withhold for age or COPD; avoid in second/third-degree block without a pacemaker or if HR < 50. Avoid verapamil and diltiazem in HFrEF.

• Consider IV iron if haemoglobin < 150 g/L with ferritin < 100 ng/mL or transferrin saturation < 20%. SGLT2 inhibitors carry a risk of euglycaemic DKA.

• DVLA: Group 1 NYHA IV must stop and notify; Group 2 must notify, needs LVEF ≥ 40%, and is barred in NYHA III–IV until controlled to NYHA I–II.

🎯 SCA

A 78-year-old man with HFrEF (LVEF 30%) attends with his daughter after his third hospital admission this year. Despite optimal four-pillar therapy, he is now breathless at rest (NYHA IV) and asks, "Am I going to get better?" The challenge is genuine: the honest answer is that his prognosis is poor and uncertain, with a real risk of sudden cardiac death, yet his daughter wants "everything done" and he is understandably frightened – so the consultation must deliver unwelcome news and open advance care planning without removing hope.

A strong consultation explores his and his daughter's ideas, concerns and expectations (ICE); discusses prognosis sensitively and in small chunks, acknowledging uncertainty while being frank about the risk of sudden death; agrees a shared plan covering symptom control, what matters most to him, a ceiling of care and any advance care plan or device considerations, with specialist and palliative input as needed; and provides clear safety-netting about who to contact if he deteriorates – all while showing empathy and respecting his autonomy.