Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Diagnose heart failure promptly, phenotype it by LVEF, relieve congestion and deliver current NICE disease-modifying therapy with safe titration, specialist escalation and device referral.
Heart failure is a clinical syndrome caused by structural or functional cardiac abnormality. Symptoms alone are non-specific; natriuretic peptide triage and echocardiography establish likelihood, phenotype and cause.
HFrEF is LVEF 40% or lower, HFmrEF 41–49%, and HFpEF 50% or higher in contemporary use. Treatment evidence and NICE strength differ between phenotypes.
Optimisation means reaching maximum tolerated evidence-based therapy, not necessarily target doses in every patient. Introduce therapies promptly but tailor order, interval and dose to congestion, BP, pulse, renal function, frailty and preference.
Every diagnosis should trigger aetiology work-up: ischaemia, hypertension, valve disease, arrhythmia, toxins, cardiomyopathy, endocrine disease, infiltrative disease and congenital causes may require specific treatment.
Prior infarction, repeated ischaemia or hibernating myocardium can reduce contractile mass and promote scar-based remodelling. Coronary disease may also cause acute decompensation through infarction or ischaemic valve dysfunction.
Longstanding hypertension, stenotic valves, regurgitant valves and congenital shunts impose chronic mechanical load. Compensatory hypertrophy or dilatation eventually becomes maladaptive, raising filling pressure and reducing reserve.
Inherited cardiomyopathy, myocarditis, toxins and infiltrative disorders directly impair myocytes or ventricular compliance. The resulting phenotype may be reduced, mildly reduced or preserved ejection fraction.
Persistent tachyarrhythmia, bradycardia, endocrine disease, severe anaemia and renal disease can cause or amplify heart failure. Identifying these contributors is important because some are reversible.
Structural or functional disease impairs ventricular contraction, relaxation or both. Stroke volume falls, filling pressure rises, or these changes become apparent only when circulatory demand increases.
Reduced effective perfusion activates sympathetic, renin–angiotensin–aldosterone and vasopressin pathways. Faster heart rate, vasoconstriction and fluid retention initially defend blood pressure and organ flow.
Continued sodium retention increases preload, while vasoconstriction increases afterload. These responses raise myocardial oxygen demand and filling pressures, turning short-term compensation into progressive congestion and dysfunction.
Chronic wall stress drives hypertrophy, chamber dilatation, fibrosis and functional valve regurgitation. Geometry and electrical conduction deteriorate, further reducing mechanical efficiency and creating arrhythmic substrate.
Left-sided pressure produces pulmonary congestion, while right-sided pressure causes peripheral and abdominal fluid accumulation. Advanced low output compromises renal, cerebral, hepatic and coronary perfusion.
Exertional breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, ankle swelling, abdominal distension and reduced exercise tolerance.
Raised JVP, pulmonary crackles, peripheral oedema, displaced apex, S3, tachycardia, cool peripheries, hepatomegaly or a causative murmur.
Severe breathlessness at rest, hypoxia, widespread crackles, pink frothy sputum or inability to lie flat requires emergency treatment.
Hypotension, confusion, cold/clammy skin, oliguria, rising lactate or narrow pulse pressure suggests cardiogenic shock and needs critical-care/shock-team escalation.
ACS, rapid AF or ventricular arrhythmia, infection, hypertensive emergency, pulmonary embolism, acute severe valve disease, renal failure or medication toxicity can destabilise heart failure.
COPD, asthma or interstitial lung disease can cause exertional breathlessness and low oxygen saturation. Wheeze, pulmonary-function abnormalities and lung-imaging findings may predominate, but pulmonary disease and heart failure commonly coexist.
Acute dyspnoea, chest pain, hypoxaemia and raised natriuretic peptide may resemble decompensated heart failure. Sudden onset, venous thromboembolic risk and right-heart strain direct pulmonary vascular imaging.
Kidney failure, cirrhosis and chronic venous insufficiency can each cause peripheral swelling. Urine, renal and liver findings or local venous changes may support an alternative or additional cause; coexisting cardiac congestion still needs assessment.
Reduced oxygen-carrying capacity, frailty and inactivity commonly cause fatigue and exertional breathlessness. Blood count and functional assessment may support these explanations, although any can coexist with heart failure.
Obesity, reduced fitness and sleep apnoea cause breathlessness, oedema and fatigue while potentially suppressing natriuretic peptide concentrations. Sleep history and objective cardiac evidence help avoid misclassification.
A rapid rise in left-sided filling pressure drives fluid into alveoli, causing severe hypoxaemia and respiratory distress. It requires emergency treatment and investigation of an acute precipitant.
Severe pump failure can no longer sustain organ perfusion, producing hypotension, cold peripheries, confusion, oliguria and rising lactate. Without rapid escalation, multiorgan failure may follow.
Low forward flow and venous congestion reduce kidney filtration and congest the liver. Organ dysfunction then restricts treatment tolerance, promotes fluid retention and worsens prognosis.
Chamber stretch, fibrosis, ischaemia and electrolyte disturbance promote atrial fibrillation and ventricular arrhythmia. These may worsen output, cause thromboembolism or lead to sudden cardiac death.
Persistent congestion and low output drive exercise intolerance, muscle wasting, falls and loss of independence. Repeated decompensation often marks advanced disease and a need to revisit goals and specialist options.
NT-proBNP determines urgency but cannot distinguish HFrEF from HFpEF and can be raised by age, renal dysfunction and AF.
NICE explicitly asks clinicians to tailor order, timing and dose to the individual; clinically useful doses across classes are preferable to a prolonged one-drug-at-a-time delay.
A patient can be oedematous yet intravascularly vulnerable. Reassess JVP, weight, BP, renal function and symptoms rather than chasing ankle oedema alone.
Relapse after withdrawing HFrEF treatment is common in recovered dilated cardiomyopathy; continued therapy is usually appropriate unless a specialist-led reason exists.
NICE eligibility uses TSAT/ferritin plus Hb and does not require microcytosis. Oral iron is not an equivalent evidence-based substitute for the IV-HF pathway.
LVEF 35% or lower opens assessment, but QRS width/morphology, NYHA class, ischaemic risk and pacing needs decide ICD versus CRT-P/CRT-D.
Diagnosing or excluding HF from NT-proBNP alone without echocardiography and aetiology review.
Waiting to maximise one drug before introducing every other foundational HFrEF class.
Starting a beta-blocker during unstable, congested decompensation or stopping it abruptly without assessment.
Combining an ACE inhibitor with sacubitril/valsartan or omitting the 36-hour washout.
Treating oedema with escalating loop diuretic while overlooking disease-modifying therapy, renal injury or a precipitant.
Applying a fixed IV-iron dose without the selected product's weight/Hb calculation and safety monitoring.
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A treatment-naive 74-year-old has progressive exertional dyspnoea and an NT-proBNP of 2460 ng/L. They are stable at rest. What is the NICE-recommended next step?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 25 Aug 2026; clinical approval remains outstanding.
Check BP, creatinine/eGFR and potassium before and 1–2 weeks after every start/increment. Avoid in pregnancy, previous ACE-inhibitor angioedema, bilateral renal artery stenosis and with sacubitril/valsartan; cough and hyperkalaemia may limit use.
Pretreatment ECG. Do not use with heart rate below 50 beats/min or unpaced second/third-degree AV block. Monitor pulse, BP, congestion and bronchospasm; slow or pause titration if decompensation occurs and never stop abruptly without a clinical reason.
Avoid significant hyperkalaemia, Addison disease and combination with another potassium-sparing diuretic. Monitor potassium/renal function closely; gynaecomastia can occur. Specialist/renal input is needed with advanced CKD.
Assess volume status and renal function; counsel genital infection and euglycaemic DKA symptoms. Interrupt during hospitalisation for major surgery or acute serious illness, monitor blood ketones and restart only once ketones are normal and the patient is stable.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Stop ACEi for at least 36 hours first; never combine with ACEi or another ARB. Do not initiate if systolic BP is below 100 mmHg or potassium above 5.4 mmol/L. Contraindicated with prior ACEi/ARB angioedema, pregnancy and severe hepatic impairment; monitor BP, renal function and potassium.
Monitor weight, BP, renal function, sodium, potassium and magnesium; avoid over-diuresis, hypotension and gout exacerbation. Acute pulmonary oedema requires hospital treatment rather than unsupervised oral escalation.
Use a setting able to manage hypersensitivity; monitor during administration and for at least 30 minutes afterwards. Ferric carboxymaltose can cause hypophosphataemia; repeat phosphate in at-risk or repeated high-dose patients.