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Heart failure means the heart is not pumping as well as it should, so the body does not get enough blood and fluid builds up. The main symptoms are breathlessness, tiredness and swelling of the legs or abdomen. It does not mean the heart is about to stop — many people live well with it using medicines, fluid and salt awareness, daily weight checks and supervised exercise. Treating the underlying cause and catching flare-ups early are key. This page explains heart failure and how it is managed.
Definition
Heart failure is a clinical syndrome characterised by symptoms (breathlessness, ankle swelling, fatigue) that may be accompanied by signs (elevated jugular venous pressure, pulmonary crackles, peripheral oedema), caused by a structural and/or functional cardiac abnormality, resulting in reduced cardiac output and/or elevated intracardiac pressures.
Pathophysiology
Heart failure is classified by left ventricular ejection fraction (LVEF):
- HFrEF (reduced EF) — LVEF ≤40%.
- HFmrEF (mildly reduced EF) — LVEF 41–49%.
- HFpEF (preserved EF) — LVEF ≥50% with evidence of cardiac structural/functional abnormality and elevated natriuretic peptides.
Classification is moving away from fixed cut-offs. The 2026 Second Universal Definition of Heart Failure — issued jointly by the American Heart Association (AHA), American College of Cardiology (ACC), European Society of Cardiology (ESC) and World Heart Federation (WHF) — groups heart failure as reduced, preserved or improved ejection fraction (an ejection fraction that was reduced and has since recovered) rather than by fixed percentage thresholds, and keeps the four stages — at risk, pre-heart-failure, heart failure and advanced heart failure — with stage B (pre-heart-failure) highlighted as the point at which early treatment changes the course.1 These are guidelines, not rules — a clinician should still apply clinical judgement to the individual patient.
Pathophysiological mechanisms include impaired contractility, abnormal relaxation and filling, increased ventricular stiffness, neurohormonal activation (sympathetic, renin-angiotensin-aldosterone, natriuretic peptide systems), pro-inflammatory and pro-fibrotic remodelling, and contributions from co-morbidities.
Co-morbidities
Co-morbidities are frequent and contribute substantially to symptoms and outcomes. Key co-morbidities include atrial fibrillation, chronic kidney disease, anaemia, iron deficiency, sleep-disordered breathing (particularly central sleep apnoea in HFrEF), diabetes, depression, frailty, sarcopenia and cachexia, and COPD.
Prevalence
Heart failure affects approximately 480,000 Australians and is a leading cause of hospital admission, particularly in those over 65 years. Hospitalisation rates and readmission within 30 days are high, making heart failure a priority condition for integrated chronic disease management.
Causes
The leading causes are ischaemic heart disease, hypertension, valvular heart disease, and cardiomyopathies (dilated, hypertrophic, restrictive, peripartum, takotsubo, alcoholic, infiltrative such as amyloidosis). Other contributors include tachyarrhythmias, congenital heart disease, drug-induced cardiomyopathy (chemotherapy, alcohol, cocaine), thyroid disease, and high-output states.
Symptoms
Functional classification
Symptoms include exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, exercise intolerance, ankle swelling, and reduced appetite. The NYHA functional classification (I–IV) describes symptom severity and is used for clinical decisions and as an entry criterion for many therapies.
Acute decompensated heart failure
Acute decompensation presents with worsening dyspnoea, orthopnoea, peripheral oedema, weight gain, and reduced exercise tolerance. Severe presentations may include pulmonary oedema, cardiogenic shock, or end-organ hypoperfusion. Each hospitalisation increases the risk of death and represents an opportunity to optimise long-term therapy.
Diagnosis
Importance of a diagnosis
Confirmed diagnosis enables initiation of evidence-based foundational therapy — which substantially improves symptoms, hospitalisation rates, and survival — alongside accurate prognostication, identification of treatable causes, and integration into multidisciplinary management programmes.2,3
How is it diagnosed?
Diagnosis is based on: symptoms and/or signs of heart failure, plus objective evidence of cardiac dysfunction (typically by echocardiography), with natriuretic peptide testing used as a rule-out tool in primary care. A specific underlying cause should be sought in all patients.
ECG
A normal ECG makes heart failure less likely. ECG may reveal evidence of previous infarction, left ventricular hypertrophy, atrial fibrillation, bundle branch block (particularly LBBB, relevant for resynchronisation therapy), or other arrhythmias contributing to or resulting from heart failure.
Echocardiography and cardiac imaging
Transthoracic echocardiography is the key investigation. It quantifies LVEF, characterises chamber size and wall thickness, assesses diastolic function, identifies valvular pathology, estimates pulmonary artery pressure, and detects pericardial disease. Cardiac MRI is used to characterise myocardial tissue (e.g. fibrosis, infiltrative disease) and may identify a specific aetiology.
Cardiac biomarkers
Natriuretic peptides (BNP, NT-proBNP) support diagnosis (particularly as a rule-out in primary care: low values make heart failure unlikely) and provide prognostic information. Troponin may be elevated in heart failure and informs prognosis. Other biomarkers (ferritin, transferrin saturation for iron deficiency; thyroid function; renal function) are part of the standard work-up.
Investigations for cause
All patients warrant investigation for ischaemic aetiology (coronary angiography, CT coronary angiography, or non-invasive ischaemia imaging). Additional investigations are tailored to suspected aetiology: cardiac MRI for cardiomyopathy characterisation, genetic testing for inherited cardiomyopathies, screening for amyloidosis (cardiac scintigraphy, free light chains, immunofixation), and screening for sleep-disordered breathing.
Management
Management and goals
Goals are to: reduce symptoms, prevent hospitalisation, slow disease progression, reduce mortality, and improve quality of life. Patient education and self-management are integral.
Treatment options
In HFrEF, foundational therapy (the “four pillars”) should be initiated and titrated early:4,5,6
- ARNI (sacubitril/valsartan) — preferred over an ACE inhibitor or ARB in most patients.
- Beta-blocker (bisoprolol, carvedilol, metoprolol succinate, or nebivolol).
- Mineralocorticoid receptor antagonist (spironolactone or eplerenone).
- SGLT2 inhibitor (dapagliflozin or empagliflozin).
- Loop diuretic for fluid management — symptomatic, not prognostic.
- Device therapy where indicated — ICD (primary prevention in selected patients with LVEF ≤35%), CRT (LBBB and QRS ≥130 ms in selected patients).
- Treatment of iron deficiency (IV iron in symptomatic patients with HFrEF/HFmrEF and iron deficiency).
- Vericiguat in selected patients.
- Advanced therapies in end-stage disease (mechanical circulatory support, transplant).
- Cardiac rehabilitation and structured exercise — strong evidence in HFrEF; emerging evidence in HFpEF.
In HFpEF, SGLT2 inhibitors have demonstrated benefit. Management focuses on aggressive treatment of co-morbidities (hypertension, atrial fibrillation, obesity, OSA, diabetes), volume management with diuretics, and exercise.
Identifying decompensation
Patients should be educated to monitor and recognise warning signs:
- Weight gain of >2 kg in 2–3 days (suggests fluid retention).
- Increasing breathlessness, particularly at rest or lying flat.
- New or worsening leg swelling.
- New cough, particularly at night.
- Reduced exercise tolerance.
- Need for additional pillows to sleep.
- New palpitations or rapid pulse.
Action plan
A written heart failure action plan defines: usual symptoms and weight (“green zone”), early warning signs requiring extra diuretic and clinician contact (“yellow zone”), and severe symptoms requiring urgent medical review or ambulance (“red zone”). Daily weighing, fluid management, and clear escalation pathways are central. Self-management and a heart failure nurse contact point are associated with reduced readmission.
Medications
Medications for heart failure
See the four foundational classes above for HFrEF. In addition:
- Loop diuretics (furosemide, bumetanide) — used for symptom and volume management, titrated to weight and symptoms.
- Digoxin — selected patients with HFrEF and persistent symptoms, or for rate control in AF.
- Ivabradine — selected patients with sinus rhythm, LVEF ≤35%, and heart rate ≥70 bpm despite a beta-blocker.
- Anticoagulation when AF or another indication is present.
- Statins are not recommended solely for heart failure but continue for usual cardiovascular indications.
- Avoid or minimise NSAIDs, non-DHP calcium channel blockers (verapamil, diltiazem) in HFrEF, and most antiarrhythmics other than amiodarone.
Correct use of medications
Patients should understand the rationale for each medication, the importance of not stopping medications during periods of feeling well, how to manage missed doses, and which over-the-counter and prescription medications to avoid. Medication reconciliation at each clinical encounter is critical, particularly post-discharge.
Order and timing of medications
Most heart failure medications are taken once daily, simplifying adherence. Particular considerations:
- Diuretics: take in the morning (or split morning and early-afternoon dose) to limit night-time micturition.
- Beta-blockers: introduce at low dose and titrate every 1–2 weeks.
- ARNI and ACE inhibitors: monitor blood pressure, renal function and potassium during initiation and up-titration.
- SGLT2 inhibitors: do not require titration; pause during acute illness with risk of euglycaemic ketoacidosis.
- MRAs: monitor potassium and renal function.
Multi-system manifestations
Renal dysfunction (cardio-renal syndrome)
Renal function frequently declines in heart failure and is exacerbated by diuresis and RAAS blockade. SGLT2 inhibitors have shown renal benefits. Coordinated cardio-renal management — sometimes requiring acceptance of modest creatinine rises during initiation of disease-modifying therapy — is the standard.
Atrial fibrillation
AF is common in heart failure and is bidirectionally related to it. Management involves anticoagulation (when indicated), rate or rhythm control, and consideration of catheter ablation, which has demonstrated outcomes benefits in patients with HFrEF.
Iron deficiency and anaemia
Iron deficiency (with or without anaemia) is highly prevalent in heart failure and worsens symptoms and prognosis. Iron studies should be measured in all patients and IV iron offered to symptomatic patients with HFrEF/HFmrEF and iron deficiency.
Sleep-disordered breathing
OSA and central sleep apnoea are prevalent and contribute to symptoms, arrhythmias and outcomes. Screening and sleep study referral are indicated. CPAP may be considered for OSA; treatment of central sleep apnoea requires specialist input.
Frailty, sarcopenia and cachexia
Loss of muscle mass and function is common and contributes substantially to symptoms and prognosis. Comprehensive geriatric assessment, nutritional support, and resistance training are essential. Cardiac cachexia carries a particularly poor prognosis.7,8
Depression and anxiety
Depression affects up to one in three people with heart failure and worsens adherence, symptoms, and survival. Routine screening and access to psychological treatment are core elements of care.
Living with heart failure
Nutrition
Dietary recommendations are individualised. Moderate sodium restriction (commonly <2–3 g/day in symptomatic patients) and avoidance of excess fluid intake are widely used, though strict fluid restriction is reserved for advanced disease or persistent congestion. Adequate protein and energy intake to prevent cachexia are critical. Dietitian input is recommended.
Sleep
Orthopnoea, paroxysmal nocturnal dyspnoea, nocturia from diuretics, and sleep-disordered breathing all disrupt sleep. Symptom management and screening for sleep apnoea are essential. Elevating the head of the bed may be useful symptomatically.
Travel
Most stable patients can travel. Considerations include: a recent clinician review, carrying medications and a current medication list, awareness of healthcare options at destination, avoidance of prolonged immobility (deep vein thrombosis risk), and assessment for in-flight oxygen and altitude tolerance in advanced disease.
Prognosis
Prognosis varies widely and depends on LVEF, NYHA class, biomarkers (BNP, troponin), co-morbidities, hospitalisation history, and adherence to evidence-based therapy. Validated prognostic models include the Seattle Heart Failure Model and MAGGIC risk score. Modern foundational therapy has substantially improved outcomes.
Anxiety, depression and advance care planning
Heart failure is a serious, often progressive condition. Advance care planning should be a routine and unhurried conversation across the disease course, addressing patient values, treatment preferences, and goals of care. Palliative care integration alongside active treatment improves symptoms and quality of life.
Role of the physiotherapist
Supervised exercise training is a core, evidence-based part of heart-failure care. The physiotherapist delivers cardiac rehabilitation (with strong evidence in HFrEF and emerging evidence in HFpEF), teaches pacing and energy conservation, supports daily weight and symptom self-monitoring, and educates on recognising and acting on decompensation.9,10,11
Warning signs
Part 1 · References
- Walsh MN, Kober L, Sliwa K, et al. AHA/ACC/ESC/WHF expert consensus document: second universal definition of heart failure (2026). Circulation 2026. doi:10.1161/CIR.0000000000001455
- McDonagh TA, Metra M, Adamo M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42(36):3599–3726.
- Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: guidelines for the prevention, detection, and management of heart failure in Australia 2018. Heart Lung Circ 2018;27(10):1123–1208.
- O'Connor CM, Whellan DJ, Lee KL, et al. Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial. JAMA 2009;301(14):1439–1450.
- Taylor RS, Walker S, Smart NA, et al. Impact of exercise rehabilitation on exercise capacity and quality-of-life in heart failure: individual participant meta-analysis. J Am Coll Cardiol 2019;73(12):1430–1443.
- Long L, Mordi IR, Bridges C, et al. Exercise-based cardiac rehabilitation for adults with heart failure. Cochrane Database Syst Rev 2019;(1):CD003331.
- Kitzman DW, Whellan DJ, Duncan P, et al. Physical rehabilitation for older patients hospitalized for heart failure (REHAB-HF). N Engl J Med 2021;385(3):203–216.
- Kitzman DW, Brubaker P, Morgan T, et al. Effect of caloric restriction or aerobic exercise training on peak oxygen consumption and quality of life in obese older patients with heart failure with preserved ejection fraction: a randomized clinical trial. JAMA 2016;315(1):36–46.
- Ellingsen Ø, Halle M, Conraads V, et al. High-intensity interval training in patients with heart failure with reduced ejection fraction (SMARTEX-HF). Circulation 2017;135(9):839–849.
- Edelmann F, Gelbrich G, Düngen HD, et al. Exercise training improves exercise capacity and diastolic function in patients with heart failure with preserved ejection fraction (Ex-DHF pilot). J Am Coll Cardiol 2011;58(17):1780–1791.
- Dall'Ago P, Chiappa GRS, Guths H, Stein R, Ribeiro JP. Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial. J Am Coll Cardiol 2006;47(4):757–763.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Supervised exercise, breathing technique and self-management education are the mainstay of cardiorespiratory physiotherapy for this condition.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. The 2026 Second Universal Definition of Heart Failure — issued jointly by the American Heart Association (AHA), American College of Cardiology (ACC), European Society of Cardiology (ESC) and World Heart Federation (WHF) — groups heart failure as reduced (HFrEF), preserved (HFpEF) or improved (HFimpEF) ejection fraction rather than by fixed left ventricular ejection fraction (LVEF) thresholds, retains the four-stage continuum and centres stage B, pre-heart failure, as the detection window.1 That matters to physiotherapy: a stage-B patient already on a rehabilitation or musculoskeletal caseload is a prevention opportunity rather than a contraindication. These are guidelines, not rules — a clinician should still apply clinical judgement to the individual patient. Both the ESC guideline and its Australian counterpart give exercise-based rehabilitation a class I recommendation alongside pharmacological therapy.2,3 Physiotherapy is therefore not an adjunct here — it is guideline-mandated treatment, with a randomised evidence base that now extends to acutely decompensated older inpatients.
Exercise training
- HF-ACTION found training safe, with a modest reduction in the adjusted composite of all-cause mortality and hospitalisation and consistent improvement in health status; adherence, not safety, was the limiting factor.4
- Individual-participant meta-analysis (ExTraMATCH II) confirmed improvements in exercise capacity and quality of life across HFrEF trials, with benefit independent of age, sex, ejection fraction and baseline capacity.5
- The Cochrane review reports reduced heart-failure-specific hospitalisation and clinically important quality-of-life gains, with uncertain effect on mortality in the short term.6
- High-intensity interval training is not superior to moderate continuous training for left ventricular remodelling or peak VO2 in HFrEF (SMARTEX-HF), so intensity should be chosen on tolerance and adherence rather than on presumed superiority.7
- In HFpEF, exercise training improves exercise capacity and quality of life (Ex-DHF), and combining caloric restriction with exercise produced the largest gains in peak VO2 in obese HFpEF.8,9
- REHAB-HF showed that an early, tailored, multi-domain rehabilitation programme (strength, balance, mobility, endurance) started during hospitalisation for acute decompensated heart failure improved physical function in older patients — evidence for rehabilitating the frail inpatient rather than waiting for stability.10
- Inspiratory muscle training improves inspiratory strength and functional capacity in patients with inspiratory muscle weakness, a useful entry point when whole-body training is not initially tolerated.11
Physiotherapy implications
- Prescribe by symptoms, not by heart rate, in patients on beta blockade, with atrial fibrillation or with a device: use Borg 11–14, the talk test and a workload target, and reassess as medication is titrated.
- Combine aerobic and progressive resistance work and add balance and functional training in the frail — the REHAB-HF model, not aerobic training alone, is what improved function in older inpatients.10
- Teach daily self-monitoring: morning weight, ankle and abdominal swelling, orthopnoea and exercise tolerance, with an action plan for a gain of 2 kg over two days.2
- Know the device parameters: defibrillator therapy zone (train roughly 20 bpm below it), pacing mode and any rate-response settings, plus post-implant shoulder restrictions.
- Withhold or modify training during decompensation: rest breathlessness, new or worsening orthopnoea, rapid weight gain, symptomatic hypotension, uncontrolled arrhythmia, or fever — then resume progressively rather than restarting from zero.
- Anticipate medication effects in the session: diuretic timing and urgency, postural hypotension with sacubitril–valsartan and beta blockade, dehydration and dizziness with SGLT2 inhibitors.2
- Screen for the drivers of readmission: sleep-disordered breathing, iron deficiency, depression, frailty and sarcopenia, poor health literacy around fluid and salt.
Clinical reasoning
- Distinguish congestion (weight gain, orthopnoea, oedema — a medical problem) from deconditioning (exertional fatigue with stable weight — a training problem). Treating the wrong one is the commonest error.
- Peripheral limitation is often the dominant constraint in chronic heart failure; leg strength and skeletal-muscle function respond even when cardiac output does not.5
- Breathlessness disproportionate to examination and stable weight should prompt consideration of anaemia, arrhythmia, pulmonary disease, pulmonary hypertension or breathing pattern disorder.
- Frailty is not a reason to withhold rehabilitation — it is the indication for a multi-domain version of it.10
Evidence gaps
- Optimal intensity, modality and long-term maintenance model remain unresolved, and benefits attenuate once supervision ends.6,7
- Rehabilitation evidence in HFpEF is smaller and more heterogeneous than in HFrEF, despite HFpEF now representing about half of cases.8
- Interaction between contemporary quadruple therapy and exercise response has not been studied.
- Cost-effective delivery models for frail, rural and multimorbid patients — the majority of the real caseload — are still being defined.
References for the clinical evidence summary
- Walsh MN, Kober L, Sliwa K, et al. AHA/ACC/ESC/WHF expert consensus document: second universal definition of heart failure (2026). Circulation 2026. doi:10.1161/CIR.0000000000001455
- McDonagh TA, Metra M, Adamo M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42(36):3599–3726.
- Atherton JJ, Sindone A, De Pasquale CG, et al. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: guidelines for the prevention, detection, and management of heart failure in Australia 2018. Heart Lung Circ 2018;27(10):1123–1208.
- O'Connor CM, Whellan DJ, Lee KL, et al. Efficacy and safety of exercise training in patients with chronic heart failure: HF-ACTION randomized controlled trial. JAMA 2009;301(14):1439–1450.
- Taylor RS, Walker S, Smart NA, et al. Impact of exercise rehabilitation on exercise capacity and quality-of-life in heart failure: individual participant meta-analysis. J Am Coll Cardiol 2019;73(12):1430–1443.
- Long L, Mordi IR, Bridges C, et al. Exercise-based cardiac rehabilitation for adults with heart failure. Cochrane Database Syst Rev 2019;(1):CD003331.
- Ellingsen Ø, Halle M, Conraads V, et al. High-intensity interval training in patients with heart failure with reduced ejection fraction (SMARTEX-HF). Circulation 2017;135(9):839–849.
- Edelmann F, Gelbrich G, Düngen HD, et al. Exercise training improves exercise capacity and diastolic function in patients with heart failure with preserved ejection fraction (Ex-DHF pilot). J Am Coll Cardiol 2011;58(17):1780–1791.
- Kitzman DW, Brubaker P, Morgan T, et al. Effect of caloric restriction or aerobic exercise training on peak oxygen consumption and quality of life in obese older patients with heart failure with preserved ejection fraction: a randomized clinical trial. JAMA 2016;315(1):36–46.
- Kitzman DW, Whellan DJ, Duncan P, et al. Physical rehabilitation for older patients hospitalized for heart failure (REHAB-HF). N Engl J Med 2021;385(3):203–216.
- Dall'Ago P, Chiappa GRS, Guths H, Stein R, Ribeiro JP. Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial. J Am Coll Cardiol 2006;47(4):757–763.
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