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Heart Failure

Heart Failure. Susie Bowell BA (Hons) RGN Heart Failure Specialist Nurse RGN BA (Hons). The very essence of cardiovascular practice is the early detection of heart failure ’ Sir Thomas Lewis, 1933. Heart Failure Definition.

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Heart Failure

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  1. Heart Failure Susie Bowell BA (Hons) RGN Heart Failure Specialist Nurse RGN BA (Hons)

  2. The very essence of cardiovascular practice is the early detection of heart failure’ Sir Thomas Lewis, 1933

  3. Heart Failure Definition Heart failure (HF) is a complex clinical syndrome of symptoms and signs that suggest impairment of the heart as a pump supporting physiological circulation. It is caused by structural or functional abnormalities of the heart. The demonstration of objective evidence of these cardiac abnormalities is necessary for the diagnosis of heart failure to be made. NICE GUIDELINES, 2010

  4. Heart Failure 30-40% of newly diagnosed will die within one year After the first year there is a less than 10% per year mortality rate NICE 2010 Incidence and hospital admissions are predicated to rise by 50% over the next 25 years due to ageing demographics and the success in treating Ischaemic Heart Disease. Mean age of HF patient 74years Prevalence approx. 8‐10% in over 75s have heart failure

  5. ESC GUIDELINES The diagnosis of HF-REF (systolic) requires three conditions to be satisfied: 1. Symptoms typical of HF 2. Signs typical of HF 3. Reduced LVEF The diagnosis of HF-PEF (Diastolic) requires four conditions to be satisfied: 1. Symptoms typical of HF 2. Signs typical of HF 3. Normal or only mildly reduced LVEF and LV not dilated 4. Relevant structural heart disease (LV hypertrophy/LA enlargement) and/or diastolic dysfunction ESC Guidelines 2012 .

  6. NYHA CLASSIFICATIONS

  7. LVSD/HFPEF Over the last 10 years it has become evident that almost half the patients with heart failure syndrome do not have Left Ventricular Systolic Dysfunction (LVSD) and have a preserved ejection fraction (EF). There is a lack of universal agreement on the threshold of ejection fraction (EF) at which LVSD and HF with preserved ejection fraction (HFPEF) are defined. Some experts maintain that there is impaired contraction of the long axis of the left ventricle in HFPEF. Others that HFPEF is synonymous with diastolic heart failure.

  8. Immediate and Long Term Maintenance Mechanisms A drop in cardiac output is immediately sensed in baro-receptors in the aortic arch and carotid sinus. This results in stimulation of the sympathetic nervous system and adrenal medulla. Adrenaline is released from the adrenal medulla into the circulation. Nor-adrenaline is released at nerve endings. This results in the stimulation of cardiac and vascular alpha (α)and beta (β) receptors Stimulation of α receptors results in ↑ vasoconstriction of both arterial and venous system Stimulation of β receptors results in ↑ contractility of the myocardium ↑increased heart rate

  9. α and β EFFECTS Immediate α effects: • ↑ arterial BP • Protection of blood supply to vital vascular beds (cerebral and coronary) • Long term effects - ↑afterload and vascular resistance causes ↑myocardial oxygen demand (and potentially ischaemia) and ↓ perfusion of non essential vascular beds. Immediate β effects: ↑ inotropy (myocardial contractility) ↑ chronotropy (increased heart rate) ↑ lusitropy (diastolic relaxation) Stimulates renin release in kidneys Long term effects – ↑ cardiac rhythm disturbances, premature apoptosis, ↓ chronic down regulation of the system

  10. Heart failure with reduced ejection fraction (HFREF)versusheart failure with preserved ejection fraction (HFPEF)

  11. As heart failure has a poor prognosis, early pharmacological treatment is important and can have a great affect on future prognosis. The improved prognosis of heart failure patients with left ventricular systolic dysfunction in the last decade is likely to be related to the greater use of and earlier intervention with, pharmacological treatment. Mortality within the first month of diagnosis remains high at 6%.

  12. hfref Diagnosis and Treatment

  13. Diagnosis Studies show diagnosis incorrect in approx 40‐50% of cases based on signs and symptoms. An echocardiogram is essential for diagnostic purposes4 Chest crepitations, oedema, tachycardia –not specific S3, ↑JVP, displaced apex –insensitive, poor inter‐observer agreement Many patients have symptoms only –dyspnoea, fatigue are non specific

  14. Diagnosis • Refer patients with suspected heart failure and previous myocardial infarction (MI) urgently, to have echocardiography and specialist assessment within 2 weeks. 2. Measure serum natriuretic peptides BNP or NTproBNP in patients with suspected heart failure without previous MI. 3. Because very high levels of serum natriuretic peptides carry a poor prognosis, refer patients with suspected heart failure and a BNP level above 400 pg/ml (116 pmol/litre) or an NTproBNP level above 2000 pg/ml (236 pmol/litre) urgently, to have transthoracic Doppler 2D echocardiography and specialist assessment within 2 weeks. NICE HF GUIDELINES 2010

  15. NICE GUIDELINES Perform an ECG and consider the following tests to evaluate possible aggravating factors and/or alternative diagnoses: chest X-ray blood tests: electrolytes, urea and creatinine, eGFR (estimated glomerular filtration rate) Thyroid function tests Liver function tests Fasting lipids Fasting glucose Full blood count Urinalysis Peak flow or spirometry.

  16. NTproBNP • Natriuretic Peptides • Vasodilatory neurohormones • Released from the ventricles in respond to wall stress/strain • Effects are: • Natriuresis and diuresis • Suppression of the RAAS and sympathetic tone • NTproBNP more stable than BNP. • Raised in LVSD and HFPEF • Cut off levels in European Society of Cardiology guidelines lower than NICE. • Be aware that affected by ACE, BB’s and diuretics especially. • If entirely normal, HF can be ruled out. • If used in conjunction with an ECG – guide to patient needing an echo. • Currently being funded by CCG for central patients.

  17. NTproBNP • There are several conditions that may affect the serum NP levels beyond heart failure – for example • Left Ventricular Hypertrophy, • Ischaemia, • Tachycardia, • Right Ventricular overload, • Hypoxaemia (including pulmonary embolism), • Renal dysfunction, • Sepsis, • Advanced age and • Cirrhosis of the liver. • Levels may be lower in obesity and in females • Results should be interpreted in the context of current pharmacological treatment

  18. NTproBNP • A high natriuretic peptide level is not only of diagnostic significance, but also of prognostic significance. Thresholds: BNP>400 pg/ml (>116 pmol/l) or NT-proBNP>2000 pg/ml (>236 pmol/l): Need an echocardiogram and specialist clinical assessment no longer than 2 weeks from the time of presentation. BNP 100-400 pg/ml (29-116 pmol/l) or NT-proBNP 400-2000 pg/ml (47-236 pmol/l): Need an echocardiogram and clinical assessment by the Specialist within 6 weeks from the time of presentation. BNP <100 pg/ml (<29 pmol/l) or NT-proBNP <400 pg/ml (<47 pmol/l), in the absence of heart failure therapy: Heart Failure is an unlikely cause for the presentation

  19. Echocardiogram HFREF • Ejection fraction (EF) • Valves – stenosis/regurgitation • Wall motility/evidence of ischaemia • Congenital abnormalities • Signs of infection • Signs of clot formation • Normal blood flow • Pulmonary Artery Pressure HFPEF • Wall size • EF >50% • LV End diastolic dimensions • Mitral valve velocities • Left atrial pressures and dimensions • + measurements as left

  20. Treatment Aims Prevention, delay or regression of cardiac remodelling Prevention of sudden arrhythmic death Improved quality and increased quantity of life Reduced morbidity Prevention/reduction of end organ damage

  21. Targets for Treatment Prevention of remodelling of the myocardium Achieved by interference with neuroendocrine systems known to promote cardiac remodelling and myocyte apoptosis –

  22. Pathophysiology

  23. Causes of Death NYHA III NYHA II CHF CHF 12% Other 26% Other 59% Sudden 24% Sudden Death 64% 15% Death n = 103 n = 103 NYHAIV CHF Other 33% 56% Sudden Death 11% n = 27 MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized intervention trial in congestive heart failure (MERIT-HF). LANCET. 1999;353:2001-07.

  24. HFREFPharmacological Treatment ACE inhibitors – Titrate to maximum tolerated dose ARBs: if ACE I intolerant. candesartan/valsartan Betablockers -bisoprolol or carvedilol - maximum tolerated dose; Nebivolol for>70yrs Aldosterone receptor antagonists: spironolactone, eplerenone Stop agents that exacerbate HF: NSAIDs, verapamil, diltiazemdoxazosin, dronedarone, class I Anti Arrhythmic Drugs, glitizones Loop diuretics: as low a dose as possible to achieve euvolaemia Consider – Ivabradine: for some patients in SR if HR>70 despite max tolerated BB Hydralazine/ ISDN if ACEI/ARB intolerant Digoxin: sometimes AF, occasionally in SR

  25. ACE/ARB’s ACE Inhibitor/ARB (all NYHA) ACE first. ARB’s if ACE not tolerated – titrate to maximum tolerated dose. Contra-indications: Renal Artery stenosis – if suspected – US scan prior to use. Previous angioedema associated with ACE inhibitor therapy (rare <1% more frequently in African Americans) – ARB’s may be better tolerated Caution in patients with: Impaired renal function (follow guidelines for use) Aortic valve stenosis or cardiac outflow obstruction Hypovolaemia or dehydration HF patients can often tolerate a low blood pressure – continue if patient is asymptomatic and U+E’s satisfactory. It is better to reduce than stop ACE/ARB In most cases ACE/ARBs can be continued if the decline in eGFR is<30% over 4 months from baseline.

  26. ACE/ARB’s An ACE licensed for heart failure should always be used prior to an ARB. Ramipril may have a less hypotensive affect than Lisinopril Some ACE/ARB is better than none, however, always titrate to maximum evidenced for optimal prevention of remodelling, blocking of the RAAS and reduction in hospitalisations. Consider an ARB licensed for heart failure as an alternative to an ACE inhibitor for patients with heart failure due to left ventricular systolic dysfunction who have intolerable side effects with ACE inhibitors. ARB’s are less likely to cause angioedema, however it can occur. Monitor serum urea, electrolytes, creatinine and eGFR for signs of renal impairment or hyperkalaemia.

  27. ß-blockers β-blocker (all NYHA) Reduce absolute annual mortality by 6-8% Contra-indications – true brittle asthma COPD with reversibility Any greater than 1st degree heart block To reduce cardiac oxygen and energy demand, remodelling and premature apoptosis, titrate to maximum tolerated recommended dose. Remember some beta-blocker is better than no beta-blocker – if necessary, take titration very slowly and monitor HR, BP and clinical response. HR TARGET APPROX 60-70 BPM

  28. Betablockers There is no evidence that selective betablockers will worsen these patients‟ pulmonary function. (Salpeter 2005). Beta-blockers are often avoided in patients with peripheral vascular disease for fear of exacerbating intermittent claudication, but this concern is unfounded (Radack 1991). Switch stable patients who are already taking a beta-blocker for a co-morbidity (for example, angina or hypertension), and who develop heart failure due to left ventricular systolic dysfunction, to a beta-blocker licensed for heart failure. [new to NICE GUIDELINES 2010

  29. Betablocker Clinical Tips Clinical tips: Transient pulmonary congestion could occur at times during up-titration of beta-blockers. If clinically indicated, diuretics can ameliorate symptoms during introduction and titration of betablockers and the use (or increase if necessary) of diuretics should be considered at this stage to aid titration. In order to promote adherence the patient should be informed that they may feel worse/more fatigued before they feel better due to the blunting of the beta-adrenergic response. Try to titrate to trail evidence to maximise betablockade which in turn helps reduce stimulation of the RAAS. Patients may not feel a real benefit for up to three months post maximal titration – they should be informed of the mortality benefits and and the importance to their heart of persistence with betablockade. Titration can be taken as slow as necessary. Bisoprolol is generally better tolerated in patients, however Carvedilol may be more useful in patients with PVD due to its alpha blocking qualities

  30. Aldosterone Antagonists Spironolactone in NYHA III‐IV RALES: All‐Cause Mortality Risk reduction 30% Aldosterone receptor antagonist + ACE inhibitor + loop diuretic ± digitalis placebo Eplerenone in post MI NYHA II heart failure – EMPHASIS-HF Trial stopped early because of significant benefit 37% reduction in primary end point 24% reduction in cardiovascular death 42% reduction in hospitalisation for HF

  31. Aldosterone Antagonists Recommended for additional treatment once beta-blockers and ACE Inhibitors have been titrated for further symptomatic control. Provide additional blocking of the Renin Angiotensin system The general side effects of this class of drug are hyperkalaemia and renal impairment and gynaecomastia with Spironolactone. • The current Chronic heart failure evidence reviewed suggests that Spironolactone should be used in severe chronic heart failure (NYHA Class III-IV) when ACE/ARB and betablocker titrated. Eplerenone should be used in the patients with heart failure following myocardial infarction and should ideally be introduced within the first two weeks post MI.

  32. DIGOXIN Enhances inotropy of cardiac muscle Reduces activation of SNS and RAAS Fourth line treatment for symptomatic patients. Not always only in patients in AF • Reduces symptoms • Decreases risk of HF progression • Reduces hospitalisation rates for decompensated HF • Does not improve survival • Trial data shows deterioration in symptoms if stopped

  33. Ivabradine • Works on the sino atrial node on the If channel • Only to be used in sinus rhythm – not suitable for patients in atrial fibrillation • Slows heart rate without reducing blood pressure • Can be used to help titrate beta blockers. If beta blockers can only be titrated slowly, a low dose of Ivabradine can be used to slow the heart rate in the mean time, beta blockade can be increased slowly dependent upon heart rate, patient tolerance and blood pressure and then the Ivabradine can be discontinued or maintained if additional HR control is required to maintain target dose.

  34. Diuretics • Loop diuretics: • Furosemide and Bumetanide • (40mg Furosemide = 1mg Bumetanide) • Bumetanide has better bioavailability • Strong thiazide diuretics like Metolazone should only be used with caution and very temporarily as they can reduce renal function quickly. U+Es should be monitored after approximately 3 days use and their effects monitored closely • Diuretics do not treat HF, they only treat the symptoms and unnecessary use can deteriorate renal function and result in increased dosage requirement in decompensation • May have more of a place in HFPEF than LVSD, however HFPEF patients are less tolerant of a greatly reduced preload

  35. Diuretics • Diuretics should always be considered for titration down as well as up during a patient review. However, the patient needs to be educated on the signs of decompensation if they are to be down titrated. • Increased blockade of the RAAS can result in the reduction of the need for diuretic therapy in LVSD, however, they may be necessary during titration of betablockade. Always assess patient stability prior to alteration and encourage a balance of potassium/sodium intake which may require a reduction in salt for the patient as frequently patients are taking far more than the recommended daily allowance. To reduce requirement for diuretics, a stable intake of fluids of approximately 2 litres/day is recommended for heart failure patients. • Explain to the patient the importance of performing a daily weight, 1st thing in the morning before drinking or eating and after using the toilet. This should, ideally, be recorded by the patient. An increase of 2-3kg (2-3 litres) over approx 2-3 days could indicate early decompensation and the patient needs to inform you for adjustment of their diuretic therapy to avoid hospital admissions, the need for IV diuretics and further decompensation. • There is an increasing incidence of cardio-renal syndrome. At end stage HF decompensation is a lot harder to manage if the renal function is reduced and the response to diuretics is poor.

  36. MEDICATIONS TO STOP/REVIEW • NSAIDS • Diltiazem and Verapamil – associated with a worse prognosis • Amlodipine is the only calcium channel blocker recommended for additional bp control in systolic heart failure. No recommendations yet for HFPEF • Nicorandil – review necessity as Nicorandil is not recommended for LVSD if the patient has low filling pressures • Doxazosin not recommended – Doxazosin arm of ALLHAT trial stopped early due to markedly increased incidence of heart failure in patients • Review long term use of Amiodarone regularly (NICE guidelines) • Class 1c anti-arrhythmic therapy is not recommended in HF and associated with a worse prognosis

  37. Cardiac Resynchronisation Therapy (CRT) • Consider referral for consideration of CRT-P device therapy if your patient is titrated to their maximal therapy tolerated and they fulfil the following criteria: CRT-P if: Patient is currently experiencing or have recently experienced NYHA class III-IV symptoms. They have: • An EF of 35% or less • In sinus rhythm either with a QRS duration of 150ms or longer (ECG) • Or with a QRS of 120-149ms (ECG) and de-synchrony on echo • Also known as a bi-ventricular pacemaker For Implantable cardioverter defibrillator (ICD) the criteria are: Primary and secondary prevention of sudden cardiac death. • LVEF of 30% (no worse than class III NYHA) • And a QRS duration of equal to or more than 120 ms Combined Therapy - If fulfilling criteria for both devices

  38. CRT with Internal Cardiovertor Defibrillator • Primary prevention • History of MI (> 4 weeks) + • LVEF <35% (no worse than class III NYHA) and • Non sustained VT on 24hr monitoring + • Inducible VT on electrophysiology testing • Or • EF < 30% (no worse than class III NYHA) + • QRS equal to or > 120 • Also famillial conditions – see guidelines • Secondary Prevention • Post MI due to either VT or VF • Spontaneous sustained VT causing syncope or significant haemodynamic compromise • Sustained VT without syncope or cardiac arrest and who have an associated reduction in EF (<35%)

  39. HFPEF

  40. LVDD TO LVSDA CONTINUUM The prevailing paradigm of hypertensive heart disease is that it first leads to concentric ventricular hypertrophy, followed by the development of ventricular dilation and contractile impairment with systolic dysfunction and a reduced left ventricular ejection fraction Effective treatment of hypertension leads to regression of LVH and a few studies have demonstrated decreases in LV mass Berenji et al (2013)

  41. HFPEF Variability of the left ventricular ejection fraction measured by different imaging modalities, and the lack of universal agreement on the threshold of ejection fraction at which LVSD and preserved ejection fraction are defined. Some assert that even in patients with HFPEF, there is an impairment of the contraction of the long axis of the left ventricle Characterised by increased wall volume, elevated filling pressures and abnormal LV filling. Tolerate tachycardia poorly Abrupt increases in blood pressure can precipitate decompensation As yet there are no conclusive treatment options and current advice suggests treatment according to guidelines of underlying diseases ie diabetes, hypertension, IHD.

  42. Pathophysiology of HFPEF • The hormone aldosterone promotes fibrosis in the heart and contributes to diastolic stiffness • Most patients with HFPEF complain of symptoms predominantly during exercise and have a reduced response to increased demand • Enhancement of contractility during exercise in HFPEF may be related to subtle resting contractile dysfunction, abnormal calcium handling, passive stiffening, ischemia, oxidative stress, or abnormal myocardial energy utilisation. • LVDD is considered by some to lie on a continuum to LVSD and the reduction/prevention of cardiac remodelling could be considered a target However........... • The term diastolic dysfunction is not synonymous with HFPEF

  43. ACE IN HFPEF In one trial ACE, compared with placebo, significantly reduced HF hospitalisation up to 12 months • No significant difference for • All cause mortality or unplanned hospitalisations (12 months) • All cause mortality 6-12months and 12-54 months • HF hospitalisations 12-54 months • Quality of life up to 6 months • NYHA class up to 6 months Clinical evidence showed that ACEI therapy did not improve mortality but it significantly reduced hospital admissions in patients with heart failure and preserved LVEF. Given that ACEI treatment is relatively cheap; the use of this therapy in patients with HFPEF is likely to be cost-effective, however it was decided that the evidence was inadequate to support the use of ACEI in HFPEF. NICE GUIDELINES 2010

  44. Betablockers in HFPEF One third of the population recruited into the SENIORS study of Nebivolol in heart failure in older adults were patients with an EF>40% The effect in this sub group was insignificant therefore NICE guidelines felt unable to currently recommend use of betablockers in HFPEF until further research has been performed. Patients with HFPEF are intolerant of tachycardia, especially in AF (which has been found to be increased in elderly female patients with diastolic dysfunction). However, there is no current HR target in HFPEF treatment modalities. If patients can be considered to be on a continuum from Diastolic remodelling to LVSD then there may be a place for betablocker therapy in long term prevention.

  45. Diuretic therapy in HFPEF • May be more of a requirement in HFPEF for diuretics. • Patients are more friable and likely to decompensate and develop pulmonary oedema easily with increases in HR and blood pressure. • Note however that they are less able to cope with a greatly reduced preload. • Some evidence for use of thiazide diuretics – however, this may be related purely to their blood pressure reducing function. • Encourage patient to monitor their weight everyday and educate them on the signs and symptoms of early decompensation and what action to take with an increase in weight of 2-3kg. • Encourage the patient to balance their potassium and sodium intake (which may require a reduction in salt intake to current UK guidelines). An imbalance in intake of sodium contributes to hypertension and can cause fluid retention.

  46. HFPEF Emerging evidence/current trials: Statins Calcium Channel blockers Novel treatments to reduce oxidative stress Aldosterone Antagonists to help prevent fibrotic changes More research is being carried out into ACE/ARB’s and BB’s Current advice is to use underlying disease processes guidance to treat patients – ie hypertension, diabetes guidelines as there is currently no concrete evidence.

  47. Patient Education • Patient Education is essential to the prognosis and treatment aims of both types of heart failure and may be particularly important in management of heart failure with preserved ejection fraction. • Weight monitoring • Fluid intake – including alcohol • Diet & Nutrition and reduction of salt intake to current guidelines and balancing with potassium intake • Smoking cessation • Immunisation • Rest/activity & Exercise • Sexual activity and erectile dysfunction • Travel/flying/driving • Follow up and contact details

  48. Prognosis

  49. Heart Transplant Criteria Impaired LV systolic function NYHA III / IV symptoms Receiving optimal medical treatment (beta blockers, ACE inhibitors/ angiotensin receptor blocker and aldosterone antagonists) Resynchronisation and/or defibrillator implanted  (if indicated) Poor prognosis Elevated natriuretic peptide levels despite full medical treatment A poor prognosis indicated by the Heart Failure Survival Score or Seattle Heart Failure Model On the decline in the UK Have to be well enough/sick enough Gold standard May have a left ventricular assist device as a bridge to transplant 131 transplants nationwide in 2010/11

  50. End of Life Difficult to predict in HF Uncertainty creates barriers & problems in advance planning. Patients either die very suddenly –Sudden Cardiac Death Or they deteriorate slowly- become more fatigued, weak, sleepy, cachexic. GSF, 2005

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