Heart Failure with Reduced Ejection Fraction (HFrEF)
Written 27th February 2020 - Last Update 27th August 2026
Heart Failure with Reduced Ejection Fraction (HFrEF)
Heart failure occurs when the heart can no longer maintain a blood supply sufficient for the body’s metabolic needs, or can only do so at the cost of raised filling pressures. It affects around 318,000 Australians, with over 60,000 newly diagnosed each year — roughly eight patients under care and two new diagnoses per GP per year. Prognosis remains poor: about 50% die within five years of their first heart failure admission.
This page covers HFrEF, where the pump is weak. For a preserved ejection fraction, see Heart Failure with Preserved Ejection Fraction.
Classification
| HFrEF | HFpEF | |
|---|---|---|
| Symptoms ± signs of heart failure | Required | Required |
| LVEF | <50% | ≥50% |
| Additional criteria | Required if LVEF 41–49% — signs of heart failure, or objective evidence of high filling pressure | Structural heart disease (LV hypertrophy, left atrial enlargement) and/or diastolic dysfunction with high filling pressure |
The Australian guideline uses LVEF <50% for HFrEF, not the <40% cut-off used by ESC and US guidelines and by most of the landmark trials. Expect three different numbers in play at once:
- <50% — the Australian diagnostic threshold for HFrEF.
- ≤40% — the entry criterion for most pillar trials, and what PBS restrictions and device criteria generally use.
- 41–49% — the “mildly reduced” band, discussed below.
Recovered HFrEF — an LVEF that has improved to >50% on treatment — is still treated as HFrEF. The pathophysiology is not thought to have changed, and therapy should not be withdrawn on the strength of a better echo.
Asymptomatic LV dysfunction (LVEF <50%, no current or prior clinical heart failure) is not heart failure, but is a strong risk factor for it.
Causes worth actively looking for
Several causes are treatable, and finding one changes management rather than just labelling it:
- Ischaemic heart disease — the commonest cause; consider revascularisation assessment.
- Hypertension — see Hypertension.
- Atrial fibrillation or frequent ventricular ectopy — tachycardia-mediated cardiomyopathy can reverse with rate or rhythm control; see Atrial Fibrillation.
- Alcohol — may partially respond to abstinence ± thiamine.
- Stimulants — cocaine, methamphetamine.
- Valvular disease — especially aortic stenosis and mitral regurgitation.
- Thyroid disease — particularly with AF.
- Cardiomyopathies — familial/dilated, peripartum, chemotherapy-related (anthracyclines, trastuzumab), haemochromatosis, infiltrative disease. See Cardiomyopathies.
- Diabetes — largely indirectly, via ischaemia, hypertension and LVH.
Non-cardiac mimics of the syndrome include renal failure, liver disease, chronic lung disease with cor pulmonale, pulmonary embolism and pericardial disease.
History and examination
The classic symptom is exertional dyspnoea, with orthopnoea and paroxysmal nocturnal dyspnoea being the more specific ones. Also: fatigue, dry cough, ankle oedema, right upper quadrant discomfort from hepatic congestion (later), and dizziness or syncope.
Examination remains genuinely useful here — displaced apex beat, elevated JVP, bibasal crackles, pleural effusion, peripheral oedema, hepatomegaly and hepatojugular reflux. A third heart sound is specific but frequently missed.
Grade functional severity with the NYHA class, since it drives both treatment escalation and PBS criteria:
| Class | Description |
|---|---|
| I | No limitation of ordinary physical activity |
| II | Slight limitation of ordinary activity; no symptoms at rest |
| III | Marked limitation of ordinary activity; no symptoms at rest |
| IV | Symptoms on any physical activity, or at rest |
Investigations
Echocardiography — it gives the LVEF that determines the diagnostic category and therefore the entire treatment pathway. An LVEF <50% with symptoms establishes HFrEF. If the LVEF is ≥50%, the patient either has HFpEF, a non-myocardial cause (valvular disease, pericardial constriction or effusion), or does not have heart failure at all.
BNP / NT-proBNP is most useful for ruling out heart failure when the diagnosis is uncertain — a normal level in an untreated, symptomatic patient makes it unlikely.
| BNP (ng/L) | NT-proBNP (ng/L) | |
|---|---|---|
| Rule out | <100 | <300 |
| Rule in | >400 | Age <50: >450 · Age 50–75: >900 · Age >75: >1800 |
Levels rise with age, renal impairment and AF, and are lowered by obesity — interpret in context. Not universally rebated; costs the patient roughly $40–70 if not covered.
Also:
- FBC (anaemia)
- U&E/eGFR (baseline before starting therapy, then monitoring)
- iron studies including transferrin saturation
- TFTs (especially with AF)
- LFTs
- HbA1c/lipids
- ECG (a completely normal ECG makes HFrEF unlikely; look for prior infarction, LBBB, AF, LVH)
- CXR
Management: the four pillars
Four drug classes each independently reduce mortality and hospitalisation, and their benefits are additive. Together they are estimated to cut three-year mortality substantially, with benefit apparent within 30 days of starting.
| Pillar | Agents | Practical target |
|---|---|---|
| RAS inhibitor — ARNI preferred | Sacubitril/valsartan; or an ACEI; ARB only if neither tolerated | Sacubitril/valsartan 97/103mg BD |
| HF-specific beta blocker | Bisoprolol, carvedilol, metoprolol succinate, nebivolol | Maximum tolerated; resting HR ~55–60 in sinus rhythm |
| MRA | Spironolactone, eplerenone | 25–50mg daily |
| SGLT2 inhibitor | Dapagliflozin 10mg daily, empagliflozin 10mg daily | Fixed dose — no titration needed |
Start all four unless contraindicated, and start early. The old model of maximising one drug before adding the next is obsolete — delaying initiation and up-titration costs lives and admissions. Current Australian practice is to start two, then add the other two, and titrate afterwards:
- If congested: RAS inhibitor + SGLT2 inhibitor → add MRA → add the beta blocker once euvolaemic.
- If euvolaemic: RAS inhibitor + beta blocker → add MRA and SGLT2 inhibitor.
Then up-titrate to maximum tolerated doses, generally favouring the beta blocker first unless the patient is congested or the heart rate is <50. A dose lower than target still confers benefit — do not abandon a pillar because target dose is unreachable.
RAS inhibitor
ARNI (sacubitril/valsartan) is more effective than an ACEI at reducing death and heart failure hospitalisation, and is now preferred first-line rather than reserved for treatment failure. An ACEI may still be preferred where blood pressure is marginal, since ARNI causes more symptomatic hypotension. An ARB is a fallback only.
| Current ACEI/ARB dose | Starting sacubitril/valsartan | Titration |
|---|---|---|
| Full dose | 49/51mg BD | Increase after 2–4 weeks to 97/103mg BD or maximum tolerated |
| Low dose | 24/26mg BD | Double every 4 weeks to 97/103mg BD or maximum tolerated |
- Allow 36 hours between the last ACEI dose and the first ARNI dose to avoid angioedema. No washout is needed switching from an ARB.
- Never combine an ARNI with an ACEI or ARB.
- Reduce the loop diuretic by 25–50% when starting or up-titrating an ARNI.
- Start at the lower dose if age >75, eGFR <60, moderate hepatic impairment, or transaminases more than twice the upper limit of normal. If systolic BP is <100mmHg the hypotension risk may outweigh benefit.
- Note the PBS criteria require the patient to be stabilised on an ACEI or ARB at initiation unless contraindicated or not tolerated.
Beta blocker
Only the four HF-specific agents have outcome evidence — switch patients taking a different beta blocker for angina or hypertension across to one of them. Treat groups in whom beta blockers are traditionally avoided, including older patients and those with COPD without reversibility.
Start low, double every 2–4 weeks. Do not start during decompensation or while congested. Warn patients that symptoms may transiently worsen. If a dose increase is not tolerated (e.g. HR <50), drop back and retry in a few weeks.
MRA
Spironolactone or eplerenone both improve survival. The limiting issue is hyperkalaemia, particularly with renal impairment, older age and concurrent RAS inhibition.
- Monitor potassium and eGFR 1–2 weeks after starting or increasing, then 4-weekly for 12 weeks, at 6 months, then 6-monthly.
- K⁺ 5.5–5.9: halve the dose. K⁺ >6.0: stop immediately, restart at a lower dose once K⁺ <5.0.
- Generally avoid if K⁺ >5.0 at baseline or creatinine clearance is low; avoid in CKD stages 4–5 and involve a nephrologist. See Chronic Kidney Disease.
- Eplerenone causes less gynaecomastia than spironolactone.
- Eplerenone’s PBS listing was broadened from 1 April 2026 to NYHA class II–IV with LVEF ≤40%, without requiring a prior MI — it can now be initiated in general practice. Check the current PBS restriction before prescribing.
SGLT2 inhibitor
Dapagliflozin or empagliflozin, 10mg daily, with or without diabetes. No titration, minimal blood pressure effect, and benefit within weeks. Do not withhold for mild-to-moderate CKD — they are used down to an eGFR of roughly 20–30 mL/min/1.73m² depending on the agent.
- Expect a small early dip in eGFR; this is haemodynamic and not a reason to stop.
- Reduce the loop diuretic by 25–50% at initiation in euvolaemic, normotensive patients.
- Euglycaemic ketoacidosis is the serious risk. Give a sick-day plan: withhold when unwell, fasting, dehydrated, or having bowel prep; cease three days before surgery; restart when eating and drinking normally.
- If on insulin or a sulfonylurea, reduce insulin by about 20% and cease sulfonylureas or glitazones at initiation. See Type 2 Diabetes — Management.
- Counsel about genitourinary infections.
Monitoring and troubleshooting
Check BP, postural symptoms, heart rate, renal function and electrolytes 1–2 weeks after each change, then 6-monthly long term. On initiation, expect and tolerate a fall in BP, a creatinine rise of up to 30%, and a potassium rise within the normal range — these are usually transient and do not require stopping treatment.
- Symptomatic hypotension: reassess volume status and down-titrate or stop the diuretic first; split dose timing across morning and night; consider a Home Medicines Review.
- Deteriorating renal function: reassess volume status; withhold or reduce the loop diuretic if not congested; stop NSAIDs; then consider reducing the RAS inhibitor or MRA; exclude obstruction.
- Hyperkalaemia: stop potassium supplements, review diet, then reduce the RAS inhibitor or MRA as above. Potassium binders are increasingly used to allow pillar therapy to continue rather than be sacrificed.
Beyond the four pillars
- Loop diuretics — for congestion only. They improve symptoms but not survival, and should be down-titrated once euvolaemic. Give a diuretic action plan for self-managed dose increases with weight gain.
- Intravenous iron — ferric carboxymaltose or ferric derisomaltose in iron deficiency with or without anaemia improves symptoms, exercise capacity and quality of life, and on current evidence also reduces heart failure hospitalisation and cardiovascular death. Iron deficiency can be defined as Ferritin < 100 or transferrin saturation <20%. For Ferinject, calculate the dose of IV Iron using the simplifed formula. See Anaemia.
- Vericiguat — a soluble guanylate cyclase stimulator, suggested after a recent worsening episode despite optimised therapy, particularly if NT-proBNP is below 5000 pg/mL.
- Ivabradine — if in sinus rhythm with a heart rate persistently ≥70–77 despite maximum tolerated beta blockade.
- Digoxin — for persisting symptoms, and useful for rate control in coexisting AF. No mortality benefit.
- Hydralazine + nitrate — if an ACEI/ARB/ARNI is contraindicated or not tolerated, or as add-on for refractory symptoms.
Drugs to avoid or use with care: NSAIDs, non-dihydropyridine calcium channel blockers (verapamil, diltiazem) in HFrEF, thiazolidinediones, and nasal decongestants.
Non-drug management
- Education on the diagnosis, the medicines, and what each is for.
- Heart failure action plan, daily weights, and early reporting of weight gain or worsening dyspnoea.
- Modest fluid restriction, individualised to congestion status — commonly quoted as 1.5–2L/day, though “modest fluid intake restriction (2–3 L per day) and regular monitoring of patient weight at home” is the figure a 2022 AJGP review gives — and salt restriction.
- Regular physical activity; refer for cardiac rehabilitation or to an exercise physiologist — exercise training has good evidence in HFrEF.
- Vaccination — influenza, pneumococcal, COVID-19.
- Screen for depression, which is common and under-treated in heart failure.
- Weight management and smoking cessation; treat sleep apnoea where present.
- Review within 7 days of hospital discharge — the highest-risk window for readmission.
- A Home Medicines Review has been associated with around a 45% reduction in hospitalisation and a GP Chronic Condition Management Plan with around 17%; consider referral to a heart failure nurse service.
- Discuss prognosis and advance care planning early — see Terminal Care.
Device and advanced therapies
- ICD — for sudden cardiac death prevention where LVEF remains ≤35% despite ≥3 months of optimised therapy, with reasonable life expectancy.
- CRT (biventricular pacing) — for a broad QRS, particularly LBBB, with persisting symptoms and low LVEF. See Cardiac Implantable Electronic Devices.
- Cardiac contractility modulation — an emerging option for LVEF 25–45% with persisting symptoms in patients unsuitable for CRT.
- LVAD and transplantation — for advanced disease; refer early rather than late.
LVEF 41–49% — the Heart Failure with “mildly reduced” Ejection Fraction
This is the group where guidelines disagree, and it is a common finding in general practice.
The Australian position (NHFA/CSANZ 2018, reaffirmed by the 2025 iCARDIO Alliance guideline): there is no separate HFmrEF category. An LVEF <50% is HFrEF. The committee’s stated reasoning was that no distinct clinical syndrome has been defined for the mid-range group; that a 10-percentage-point band is too narrow to assign reliably given the reproducibility of echocardiographic LVEF measurement; and that it was unclear how a separate category would change management — post-hoc trial analyses suggested these patients derive similar benefit from RAS blockade, beta blockers and MRAs to those with an LVEF <40%.
Internationally, ESC and AHA/ACC/HFSA guidelines do define HFmrEF as LVEF 41–49%, and you will see the term constantly in the literature and in specialist correspondence.
What this means in practice:
- The Australian guideline requires additional criteria to diagnose heart failure in this band — signs of heart failure, or objective evidence of high filling pressure by echocardiography, natriuretic peptides or invasive measurement. A borderline LVEF alone is not enough.
- Once heart failure is diagnosed, treat as HFrEF: the four pillars are the reasonable default, with the honest caveat that the evidence in this band is largely post-hoc rather than from dedicated trials.
- SGLT2 inhibitors are the exception with direct evidence — EMPEROR-Preserved and DELIVER both enrolled patients with an LVEF >40%, so this band was studied prospectively. Empagliflozin has been PBS-listed since November 2023 for chronic heart failure with an LVEF >40%, which covers exactly these patients.
- Finerenone also has direct evidence here — FINEARTS-HF enrolled patients with an LVEF ≥40%. See the HFpEF page for detail.
- Device therapy criteria (ICD, CRT) generally require an LVEF ≤35% and are not met by this group.
- Repeat the echo. A mildly reduced LVEF may be improving recovered HFrEF, deteriorating early HFrEF, or measurement noise — the trajectory is more informative than any single number.
Referral
Refer for cardiology assessment:
- At diagnosis — all new heart failure warrants at least one specialist review to establish aetiology.
- Persisting NYHA II–IV symptoms despite optimised therapy.
- Device consideration when LVEF remains ≤35%.
- Suspected ischaemic or infiltrative aetiology.
- Consideration of advanced therapies.
Ongoing titration and monitoring is shared care, well suited to general practice.