Chronic heart failure

• Prevalence is 1-2% of all adults. If aged > 85 it’s 15%.
• HF-related admissions account for 2% of all NHS beds.
• Significantly under-diagnosed
• 50% 5-year survival
• About half have HFrEF, and half have HFpEF

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Definitions

• HF with preserved EF (EF ≥50%, previously diastolic HF)
• HF with mildly reduced EF (EF 41-49%)
• HF with reduced EF (EF ≤40%, previously systolic HF)
• HF due to valve disease
• HF due to RV dysfunction – may be due to pulmonary HTN (especially), valve disease, MI, ARVC 

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Causes of chronic HF

• Cardiovascular (common)
  • • Hypertensive HD
    • IHD (more common in HFrEF than HFpEF)
    • Valvular disease
    • Sustained arrhythmias
    • Congenital HD
    • Cardiomyopathies
    • Myocarditis
    • Infiltrative (eg amyloid, sarcoid, haemochromatosis)
• Increased metabolic demand – Pregnancy, Pagets, hyperthyroidism, anaemia, obesity
• Drugs – Chemotherapy, immunotherapy, steroids, NSAIDs, ETOH, cocaine and amphetamines, glitazones, CCBs
• Pulmonary – PE, ILD
• Rare – Storage disorders, carcinoid, endomyocardial fibrosis, neuromuscular disease

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History and exam

• Ask about
  • • Orthopnoea, PND, bendopnoea, cough
    • Reduced exercise tolerance
    • Weight loss or weight gain
    • Dizziness, falls, fatigue, fluid intake
    • Number of pillows used at night, known dry weight
    • Symptoms that suggest recent precipitants – chest pain (ischaemia), palpitations or syncope (arrhythmia), non-compliance with medications or fluid restriction, fevers (infection, myocarditis)
    • Family hx (cardiomyopathies)
• Examine for
  • • Leg oedema, sacral oedema, ascites, JVP
    • Murmurs, 3rd and 4th heart sounds
• Not all pedal/pretibial oedema is heart failure. Can be dependent oedema (chair sleeping), amlodipine, hypoalbuminemia or CKD for example. See Oedema
• Try to quantify symptoms / clinical severity
  • • Often classed by NYHA class 1-4. Symptoms are prognostic.
      • • Class I – No limitation of physical activity
        • Class II – Comfortable at rest, but ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
        • Class III – Comfortable at rest, but less than ordinary activity results undue breathlessness, fatigue, or palpitations.
        • Class IV – Unable to carry on any physical activity without discomfort. Symptoms at rest can be present

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Investigations

• Echo
  • • In HF with reduced EF
      • • Tends to be thin-walled heart, may be dilated
        • Diastolic function is implicit with reduced EF
    • In HF preserved EF
      • • At least mild LVH, normal or small chamber size.
        • Mild diastolic dysfunction is common/expected in older patients.
        • Moderate to severe can be significant (but easy to over-interpret the echo)
        • Check E/E’ (E to E prime)
    • In HF due to RV dysfunction – check fractional area change (FAC), tricuspid annular plane systolic excursion (TAPSE) and Doppler tissue imaging-derived systolic S′ velocity of the tricuspid annulus
    • May identify valve disease, which can be causative
    • Dilated LA – a degree of diastolic dysfunction increases the risk of AF
• ECG
  • • Look for AF / arrythmias, ischaemia, Q waves, QRS width (can be an indication for CRT)
    • HF unlikely with a normal ECG
    • AI can ‘diagnose’ reduced LV function based on the ECG – sensitivity is about 85% when LV EF <35%, and around 70% for LV EF <50%. The Negative predictive value is very high (98%), the positive prediction value is not very high. Single lead hand-held ECGs still perform pretty well.
    • Risk of LBBB in a patient with HFrEF is around 10% per year – so ensure ECGs repeated regularly
• CxR – can be normal, or show cardiomegaly and fluid overload
• Bloods – Hb, iron status (benefit from replacement even if not anaemic), BNP, troponin, HbA1C, CRP, U&Es (capacity for diuresis), LFTs (albumin), TFTs (high output failure)
• Troponin – often fixed moderate elevation. It is a prognostic marker. A dynamic elevation suggests ischaemia
• Consider secondary HTN screen if warranted
• Urine PCR (nephrotic syndrome in differential of oedema)
• NT-Pro BNP
  • • High negative predictive value – good rule out
    • Positive predictive value 70%
    • Compare to baseline (taken when well) – can help judge degree of progression
    • BNP should also improve during admission once HF treated
    • If NTproBNP is >400 ng/l, the patient should be referred for echo and HF specialist assessment.
      • • 2-week wait if NTproBNP >2,000 ng/l
        • 6-week wait if NTproBNP 400–2,000 ng/l
    • However, fewer than 10% get assessment in this time period
    • Marked NT-proBNP elevation is related to poorer prognosis and HF assessment is urgent for these patients
    • It is also elevated in
      • • AF (sometimes to > 3000), HTN, CVA, CKD, CLD with ascites, sepsis (can be markedly elevated), COPD, burns, anaemia, DKA, pulmonary HTN and a host of cardiac conditions
        • Anything that puts a load on the heart
        • BNP climbs with age
• Angiogram or CTCA if suspected ischaemic aetiology
• Cardiac MRI
  • • Can help distinguish aetiology ie. ischaemic, DCM, HCM (vs HTN), infiltrative (amyloid, sarcoid)
    • Useful if patient habitus makes echo difficult
    • Can help to quantify regurgitation
    • Good for picking up congenital defects (esp ASDs, VSDs)
    • Important in patients with a suspected cardiomyopathy or related condition
• Right heart catheterisation
  • • If HF is suspected to be due to constrictive pericarditis, restrictive cardiomyopathy, congenital HD or high output states
    • Sometimes done in HFpEF to confirm diagnosis
    • Advised in advanced HF if being worked up for transplant
    • Consider in cases of probable pulmonary HTN
• Holter if suspected arrythmias or lots of ectopics
• Cardiomyopathy work up if one suspected (which may include genetic testing) if indicated
• Consider investigating for underlying cardiac amyloid – it’s underdiagnosed
  • • Due to AL cardiac amyloid (light chain) or transthyretin (ATTR)
    • Suspect in patents > 65 who were previously hypertensive, and are now hypotensive or normotensive
    • Can be macroglossia, peripheral neuropathy, CKD, carpal tunnel, dysautonomia, deafness, severe aortic stenosis
    • BNP can be disproportionately high
    • Echo may show granular sparkling myocardium, AS, pericardial effusion, reduced longitudinal strain with apical sparing, LV wall thickness >12mm
    • Do myeloma screen and advanced imaging. Confirm with histology. More here

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General management of chronic HF

• Lifestyle advice – smoking, diet, alcohol, exercise
• Treat risk factors – HTN (but avoid diltiazem and monoxidine), hyperlipidaemia, obesity, DM, CAD
• Goal Directed Medical Therapy if reduced EF (‘the four pillars’, more below)
• Document dry weight (and monitor early morning weights, after voiding) and review if weight gain >1.5mg in 2 days or symptoms worse. Consider fluid restriction.
• Stop aggravating drugs – eg doxazosin, NSAIDs, glitazones, diltiazem, steroids, TCAs, verapamil
• Cardiac rehab
• Consider driving, mood, sleep, sex, care needs
• Self-care monitoring – electronic scales, BP machine, apple watch, sats monitor etc
• Vaccinations – pneumococcal, flu
• F/U in heart failure clinic
• Involve palliative care in advanced HF cases

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 Drug Treatment for HF with reduced EF

• There are currently four cardinal pharmacological treatments for HFrEF: together they compromise the so-called GDMT (goal directed medical therapy)
  • • Renin–angiotensin–aldosterone system inhibitors (RAASi), which include ACE-inhibitors (ACE-I), angiotensin receptor blockers (ARB) and angiotensin receptor/neprilysin inhibitors (ARNI)
    • Beta blockers
    • Mineralocorticoid receptor antagonists (MRAs)
    • Sodium glucose cotransporter-2 inhibitors (SGLT2i)
• Decongestion
  • • Not compulsory – and if not needed, can be easier to uptitrate the four pillars. Only give if signs/symptoms, however most patients with HF at diagnosis are wet
    • Can be transformative
    • If insufficient response – consider splitting doses, reducing fluid intake, measure urinary Na, switching to bumetanide, sequential nephron blockade (add a thiazide, a loop and an MCA in that order)
• Goal Directed Medical Therapy (GDMT) in stats
  • • Can reduce annual mortality in HF from around 60% to <10% with medications
    • Overall a beta blocker and a CRT device have the greatest impact on mortality in HF
    • Being on the 4 prognostic meds achieves relative risk reduction of 72%, and an absolute risk reduction of 25%. Probably best to get on all the drugs, then uptitrate doses, and can usually uptitrate quickly. Give > 8 years free from CV death or hospital admission
    • If someone in their 60s is on a betablocker and an ACEi for HF, and you take 3 interventions – add MRA, add SGLT2i, convert ACE-I to ARNI – you can add over 5 years to their lifespan
• How to sequence HF treatments
  • • Lots of opinions on this! Best to use an individualised approach and react to events. Currently ESC guidelines advise a rapid uptitration over 6 weeks.
    • Moving quickly with drug treatment may reduce risk of death/hospitalisation (verses small additional risks of hypotension and renal dysfunction)
    • Can base initiation on renal function (uptitrate over 4-6 weeks). For example:
      • • If eGFR < 15 – start low dose betablocker
        • If eGFR 15-30 – start triple therapy, with low dose betablocker, SGLT2-i (if eGFR >20) and low dose ACE-i
        • If eGFR 30-60 start triple therapy with betablocker (low dose), SGLT2-i, ARNI (low dose)
        • If eGFR >60 initiate quadruple therapy with betablocker (low dose), SGLT2-i, ARNI (low dose) and MRA
        • Then – at 7-14 days, in all groups, if systolic BP > 100 and eGFR >30 – start MRA
        • Then – at 14-21 days, start dose titration
        • Titrate ARNI or ACE-I to max dose providing creatinine rises <50% from baseline, K+<5.5 and no symptomatic hypotension
        • Titrate betablocker to max dose providing HR >60 and no symptomatic hypotension
• Issues
  • • Hypotension – stop other (non-prognostic) antihypertensives, assess volume status, consider low volume state / cardiomyopathy. If the drugs cause hypotension, generally only stop is symptomatic. Can also think about changing times for medications so not all given at once.
    • Falling eGFR – stop nephrotoxics, consider renal work up including US doppler for renal artery stenosis
    • Hyperkalaemia – treat as per protocol, consider binder. Stop MRA
    • Bradycardia ie HR <50 – ECG, treat AV block, hold betablocker

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Notes on GDMT

• RAAS blockade
  • • An ACE-inhibitor should not be initiated in a person with a clinical suspicion of haemodynamically significant valve disease, until the valve disease has been assessed by a specialist.
    • Avoid if systolic BP <90
    • Accept small changes in renal function
    • Often an ARNI used instead of an ACE-I (eg Entresto – combination of sacubitril and valsartan).
      • • Neprilysin inhibitor
        • Dose of Entresto is 97/103mg BD (but start at 49/51mg BD)
        • However, this will drop BP by more than an ACEI, so maybe avoid if BP borderline (and ACEI more titratable)
        • Often best in ambulatory patients with HFrEF who remain symptomatic despite optimal treatment on 4 pillars (but ensure 36 hour washout period after ACEi stopped as risk of angioedema)
        • Avoid if eGFR <30
    • If the person is unable to tolerate an ACE-I (usually due to persistent troublesome cough), prescribe can stop ACE-I and check if cough goes away – if it does, avoid ACE-I in future.
    • Aim to uptitrate to 10mg of Ramipril (often given as 5mg BD), starting at 2.5mg OD as long as renal function and BP ok.
    • ACE-i therapy leads to a 35% reduction in all-cause mortality
    • Can continue if 15-30% rise in creatinine from baseline (this does not imply they are ACE-I intolerant), but repeat U&Es weekly. Stop other nephrotoxics, and stop diuretics if no oedema / overdiuresed.
    • Get specialist advice if creat >200 or K+>5
    • Accept K+ up to 5.5. If >5.5 – ensure any nephrotoxics stopped, reduce diuretics if possible, consider low K+ diet. If 6-6.5, consider K+ binders, and consider stopping ACE-I and reintroducing at lower dose once K+ better.
    • Contraindicated in bilateral RAS, angioedema. Generally not given in aortic or mitral valve stenosis or HOCM.
    • Alternatives
      • • Lisinopril 35mg OD (starting 2.5-5mg OD)
        • Enalapril 20mg BD (starting at 2.5mg BD)
        • Captopril 50mg TDS (starting at 6.25mg TDS)
    • Candesartan
      • • Use if ACE-I cause side effects
        • Target dose is 32 mg daily, start at 4mg OD, same limitations as for ACEi

• Betablockers
  • • Betablocker has 31% reduction in all-cause mortality (so try not to stop them!)
    • Can start Bisoprolol at 1.25mg OD and aim for 10mg OD, uptitrating every 2-3 days.
    • If reintroducing, best not to start at high dose again, uptitrate.
    • Cautions
      • • Monitor ECG – stop if 2nd degree or complete heart block. They should be started in all patients with heart rates >50bpm (and stopped if HR <50). Use with caution in first degree block / SAN disease
        • Significant bronchial asthma
        • COPD without significant obstruction and peripheral vascular disease are not contraindications.
        • Don’t start in acute HF (but can continue in decompensated chronic HF)
        • Can cause worsening congestion in first few weeks – may need to up diuretics, or halve betablocker dose if occurs. Often best to diurese before commencing if overloaded
        • Hypotension
        • Can mask hypoglycaemic symptoms, so be careful in DM
    • Side effects
      • • Hypotension, fatigue, night terrors, erectile dysfunction
        • Stopping suddenly can cause rebound effects
    • Alternatives to bisoprolol
      • • Carvedilol is a good alternative depending on side effect profile (target dose 25 mg bd, or 50mg BD if weight >85kg. Strat at 3.125mg BD)
        • Nebivolol is an alternative in hypertensive patients as it has effect on endothelial NO mechanism as well. Start at 1.25mg OD, with a target of 10mg OD

• Aldosterone antagonist
  • • Can use these in HFpEF or HFrEF
    • Spironolactone or eplerenone
    • 20% reduction in all-cause mortality
    • Caution if creatinine >200 or K+>5
    • Avoid starting if eGFR <30
    • Monitor for hyperkalaemia, and consider Lokelma
    • Can be useful if patients suffer from hypokalaemia due to diuretics
    • Spironolactone
      • • Use for NYHA class III-IV HF with no recent history of myocardial infarction.
        • Target dose is 25-50mg OD (start 25mg OD)
    • Eplerenone
      • • NYHA class II with left ventricular systolic dysfunction (LVEF ≤30%) or in stable patients with left ventricular dysfunction (LVEF ≤ 40 %) and clinical evidence of heart failure after recent myocardial infarction.
        • Should also be used if hormonal side effects from spironolactone (gynaecomastia, reduced libido, erectile dysfunction). If switching, the gynaecomastia can take months to improve (explain this)
        • Target dose is 25-50mg OD (start 25mg OD)
    • Finerenone – may be approved for HF in the future

• SGLT2 inhibitor
  • • Indicated in HFrEF or HFpEF
    • Not just good for glycaemic control but cause osmotic diuresis and can be used if CKD present eg. Sotagliflozin, dapagliflozin (10mg OD if eGFR >15), empagliflozin (10mg OD if eGFR >20)
    • No dose titration once initiated and well tolerated
    • Can initially cause decline in renal function – expected, as with ACE-I.
    • Reduces risk of CV death
    • Omission of SGLT2 inhibitors in the setting of an intercurrent illness causing reduced oral intake is advised to reduce risk of ketoacidosis
    • Avoid in T1DM, previous DKA, recurrent UTIs/genital infections, eGFR <20 or <15
    • Caution in acute severe illness, GU or yeast infections (glycosuric), with other hypoglycaemic agents (often reduce dose of others), hypovolaemia
    • Can cause normoglycaemic DKA

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Other medications used in chronic heart failure

• Statin and antiplatelet in all patients
• Antihypertensives and anti-anginals can be used eg amlodipine (but avoid verapamil and diltiazem)
• Potassium binders – if hyperkalaemic from the MRA
• Intravenous iron
  • • Good evidence for iron infusions if iron deplete.
    • A ferritin of < 100 in pt with heart failure indicates deficiency, and if 100-300 and reduced transferrin saturations (<20%), probably also iron deficient
    • No indication for EPO
• Hydralazine in combination with a nitrate (especially if the person is of Afro-Caribbean origin)
  • • Alternative to ACE-I/ARB in renal failure or hyperkalaemia.
    • Can be used in addition to ACE-I/ARB in African / Caribbean patients that remain symptomatic, blood pressure permitting.
    • Reduce dose of hydralazine in severe renal dysfunction (eGFR <30ml/min).
• Digoxin
  • • No mortality benefit, useful in NYHA 2 or 3
• Ivabradine
  • • Slows the heart rate in sinus rhythm
    • Might be useful in NYHA 2 or more
    • In patients with LVEF <35% and resting heart rates ≥ 75 bpm in sinus rhythm despite maximal tolerated beta blocker dose. Can also be used if betablocker not tolerated/contraindicated
    • Target dose is 5 mg BD or 7.5 mg BD for rate control.
• Anticoagulation
  • • May be indicated for people with heart failure who are in sinus rhythm and have a history of thromboembolism, left ventricular aneurysm, AF or intracardiac thrombus
• Tafamidis
  • • For patients with genetically proven hTTR-cardiac amyloid, and NYHA I or II symptoms
    • Extremely expensive but strong evidence of benefit

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Other management strategies

• Coronary revascularization can be considered depending on aetiology of HF, imaging and symptoms
• Fluids
  • • Advise the person to monitor their weight at home to detect fluid retention of worsening heart failure, if practical. Also reduce their dietary salt
    • People with severe symptomatic heart failure should restrict fluid intake (for example to less than 1.5–2 L a day to relieve symptoms)
• CRT/ICD
  • • Consider for those:
      • • Expected to live more than 1 year
        • Who have received > 3 months of optimised GDMT
        • And have a persisting LVEF of ≤35%
    • ICD – If EF<35% and QRS < 130ms.
      • • Does not improve EF, but prevents dangerous arrhythmias.
        • ICDs are indicated as secondary prophylaxis in patients with pulseless VT/VF, or for primary prophylaxis in patients with LVEF ≤ 35%.
    • Biventricular Pacing (Cardiac Resynchronisation Therapy, or CRT) with or without an ICD, is indicated if:
      • • Symptomatic on maximum achievable medical therapy
        • and a LVEF ≤ 35%
        • and LBBB on ECG (QRS > 130msec or RBBB with QRS > 150msec) or chronically RV paced if LVEF < 50%.
    • Comprises three leads – RA, LV and RV generator lead. This resynchronises and improves EF. Can pace and defibrillate
• Heart failure MDT as effective as commonly used drugs and reduces mortality, as does heart failure clinic follow up
• Heart Transplant
  • • May be indicated in advanced heart failure without any other therapeutic options (except an LV assist device)
    • Generally candidates are aged <65, with BNP climbing, and single organ dysfunction
    • Contraindicated if active infection, severe PAD or cerebrovascular disease, irreversible pulmonary hypertension, malignancy, irreversible cirrhosis or eGFR <30 (unless kidneys transplanted as well), BMI >35, alcohol/drug use, psychological instability, insufficient social support
    • Post transplant one year survival is >90%. Median survival 12.5 years

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HF with preserved EF (HFpEF)

• A description (raised filling pressures), not a diagnosis
• The term ‘diastolic HF’ has been superseded by HFpEF as it’s a complex, multisystem syndrome rather than an isolated issue
• Common (around 50% of HF), underrecognized and heterogenous
• Symptoms and signs of HF, with normal or borderline EF (and no previous hx of HErEF)
• Due to fibrosis and impaired filling, stiff LVs
• It’s defining haemodynamic feature is elevated LV filling pressures at rest or during exertion
• Patients more often older and female
• Slightly lower mortality than HFrEF but outcomes are fairly similar
• Prevalence is increasing
• Risk factors include DM, CKD, obesity and OSA, HTN
• Symptoms
  • • Unexplained SOB (often in a patient with CV risk factors)
    • Fatigue, reduced ET
    • Orthopnoea is specific but insensitive
    • Can be congestion / oedema (but can be absent, and especially if already on diuretics)
• Phenotypes
  • • Hypertensive (classic HFpEF, older patient)
    • Cardiometabolic (obese, DM, multimorbid, younger)
    • Ischaemic
    • AF with prominent LA myopathy
    • Pulmonary vascular disease / RV dysfunction
    • Exercise limited phenotype (with normal resting haemodynamics)
• Investigations
  • • Raised BNP supports the diagnosis (although falsely high in CKD and AF, and falsely low in obesity, diuretic treatment and LVH). If normal, HFpEF is not excluded (especially if patient obese or well diuresed)
    • Echo
      • • Not diagnostic in isolation. Most echo features of HFpEF lack specificity.
        • Can be useful to exclude other causes
        • May show (and the more present, the more likely the diagnosis)
          • • EF >50% and non-dilated LV
            • Increased LV wall thickness
            • Increased LA volume / LA enlargement
            • Elevated E/e’ ratio at rest (>15, with 9-14 being indeterminate)
            • PA systolic pressure >35
            • TR velocity at rest >2.8m/s
        • Thresholds may need adjusting in AF
        • LA strain and GLS also have a role
        • If EF previously <50% but now normal – usually best to treat as HFrEF (unless clear reason for a transient decrease)
    • Can do exercise testing if echo equivocal
    • Cardiac MRI useful to explore mimics and causes
    • Test of other conditions eg sleep studies etc if required
    • If diagnostic uncertainty (eg echo indeterminate, BNP raised but no clear cause) consider exercise echo (look for E/e’ at peak stress>15), CMR, PET, CTCA, invasive haemodynamic assessment
• Scoring systems
  • • Not diagnostic but can be supportive
    • Many about but the H₂FPEF Score is probably best for rapid, bedside clinical estimation of HFpEF probability using routine variables
    • Need to know age, BMI, E/e’ ratio, PASP, AF
    • Gives a % probability of diagnosis
• Ensure you rule out differentials / mimics / comorbidities before diagnosis (often misdiagnosed)
  • • Cardiac amyloid (easily missed, present in 6% of HFpEF)
    • HOCM (often accompanies HFpEF)
    • Pericardial diseases (incl constrictive pericarditis)
    • Respiratory disease / cor pulmonale
    • Valvular HD
    • IHD
    • Hypertensive HD
    • Cardiac sarcoid
    • Congenital HD
    • High output syndromes (anaemia, thyroid disease, AV shunt)
    • Infiltrative and storage disorders (eg Fabrys)
    • Inflammatory disorders
    • Pulmonary hypertension
    • Pulmonary vein stensosis
    • Isolated right heart failure (RV infaction, carcinoid)
    • Cardiac tumours
    • Deconditioning / severe frailty
• Complications
  • • Propensity for AF
    • Commonly decompensate with HTN and arrhythmias – they tolerate tachycardia badly as they need filling time
    • Worse prognosis if cardiac amyloid
• Management
  • • If acute deterioration – decongestion, treat precipitants (eg AF, infection, ischaemia, uncontrolled HTN)
    • SGLT2i approved for treatment (1a recommendation). Caution in IDDM
    • MRA is advised if no contraindications
    • Give loop diuretic for symptoms (at lowest possible dose) this should reduce pulmonary arterial pressure
    • Consider GLP1 if obesity or DM – some evidence they help in HFpEF
    • ARNI/ARB sometimes given as with HFpEF, but data less strong. ARNI best if EF lower end of normal and co-existent HTN.
    • Betablocker not routine unless other indication (and avoid if chronotropic incompetence which is common in HFpEF)
    • Remove precipitants (alpha-blockers, NSAIDs, CCB)
    • Avoid long-acting nitrates
    • Managing comorbidities and risk factors is key – AF (common), HTN (common, treat aggressively), CKD, DM, obesity, CAD, lung disease, OSA
    • Advise exercise and consider cardiac rehab

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Special situations

• HF and co-existing angina
  • • CABG best revascularisation strategy if fit for surgery (but especially if DM or multivessel disease)
    • Avoid CABG if they have a LV assist device
• Hx of syncope or presyncope – if not clearly due to postural hypotension, refer to a cardiologist as this may be due to ventricular tachycardia
• HF with AF
  • • Risk factors for HF and AF are closely aligned, and AF is both a cause and a consequence of HF. Acute AF commonly precipitates acute HF
    • All of the 4 pillars (prognostic meds) reduce risk of AF in HF
    • Avoid CCB for rate control, and be cautious with betablockers. Digoxin ok but takes time to work
    • Ablation can improve outcomes
• HF and postural hypotension
  • • Some patients run a low BP – they don’t need fluid challenges
    • High BP doesn’t always need treating
    • If significant postural drop with symptoms and reduced EF – try to keep the bisoprolol, rest could be ditched if needed
    • If preserved EF – just stop antihypertensives and don’t worry much about the supine BP
    • Do not give fludrocortisone, midodrine or pyridostigmine
• HF and severe AS, MR or TR – increasingly using percutaneous intervention in HF. TAVI most often done in AS, and edge to edge repair in MR
• End stage HF
  • • Signs include NT-Pro BNP>5000 or uptrending, deranged LFTs and renal function, EF <20%, hx of shocks, lots of hospitalisations, low BP, escalating diuretics, inability to uptitrate prognostic meds
    • Cardiology review of all treatments including possible planned deactivation (or re-programming) of implantable cardioverter-defibrillators
    • Consider heart transplant in select cases
    • Consider palliative care
    • Consider turning the defib off (do not use magnet as this will switch pacing off too and shorten patient’s life. Instead d/w cardiac physiology.
    • If DNA-CPR – consider discussing whether the ICD function of a device needs switching off
• HF with mildly reduced EF
  • • Currently good evidence for diuretics and SGLT2i
    • Some evidence (but weaker) for ACEi/ARNI/ARB, MRA and betablockers

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Prognosis in HF

• EF does not affect prognosis much in HF patients, unless very low (generally patients with preserved EF HF do about the same)
• Age and renal impairment have a clear relationship with prognosis. CKD is a strong predictor of outcome for a variety of reasons
• Sometimes I NEED HELP acronym used to identify those with poor prognosis (if more than one, consider referral for transplant assessment if considered eligible)
  • • Inotropes/IABP
    • NT-ProBNP elevated/rising (or NYHA 3-4)
    • End organ dysfunction (eg kidneys)
    • EF <20%
    • Defibrillator shocks (especially high hazard ratio of >5)
    • Hospitalisation
    • Escalating diuretic dose
    • Low BP
    • Prognostic meds not tolerated
• Up to 30% of patients will recover heart function, especially favourable prognosis if non-ischaemic aetiology, short duration of HF, women, LBBB and CRT, lower EF, higher LVIDd (measure of LV size), absent LGE, lower BNP
• MAGGIC heart failure score helpful to assess risk/prognosis