Continuing professional development Chronic heart failure: pathophysiology, diagnosis and treatment NOP584 Nicholson C (2014) Chronic heart failure: pathophysiology, diagnosis and treatment. Nursing Older People. 26, 7, 29-38. Date of submission: March 18 2014. Date of acceptance: May 23 2014. Abstract Heart failure has significant prevalence in older people: the mean average age of patients with the condition is 77. It has serious prognostic and quality of life implications for patients, as well as health service costs. Diagnosis requires confirmatory investigations and consideration of causative processes. First-line treatment involves education, lifestyle modification, symptom-controlling and disease-modifying medication. Further treatment may include additional medications, cardiac devices and surgery. End of life planning is part of the care pathway. Aims and intended learning outcomes This article aims to provide an overview of heart failure for nurses who are not specialists in the condition. It focuses on chronic, rather than acute, disease. After reading this article and completing the time out activities you should be able to: ■■ Summarise the significance of heart failure for older people in terms of prevalence and clinical outcomes. ■■ Define the key terms used to describe heart failure. ■■ Describe the diagnostic pathway. ■■ Summarise standard treatments. ■■ Detail the lifestyle changes that are prompted by diagnosis. cardioprotective effect of female hormones, have a role (Bhupathy et al 2010). Heart failure is caused by a number of pathological conditions (Box 1). Some causes are reversible, but others are not. Around two thirds of patients with heart failure in the UK have a history of ischaemic heart disease (NICE 2010). Other common causes include hypertension and arrhythmias but the list of potential causes is extensive (American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) 2013). Patients can have acute heart failure without underlying chronic heart failure but more commonly Introduction Box 1 Causes of heart failure* Heart failure is a complex syndrome characterised by reduced heart efficiency and resultant haemodynamic and neurohormonal responses (Poole-Wilson 1985). It is common, affecting around one million people in the UK (National Institute for Health and Care Excellence (NICE) 2010). Incidence and prevalence are rising as the population ages and survives more primary cardiac events (Mosterd and Hoes 2007). In the UK the average age of patients with the disease is 77 (Mosterd and Hoes 2007), rising to 80 in hospitalised patients (National Heart Failure Audit (NHFA) 2013). Gender balance in heart failure is weighted towards younger men and older women (NHFA 2013): part of this effect is because women live longer than men but other factors, such as the ■■ Ischaemic heart disease. ■■ Hypertension. ■■ Arrhythmias. ■■ Valve disorders. ■■ Myocarditis. ■■ Alcohol-induced cardiomyopathy. ■■ Chemotherapy-induced cardiomyopathy. ■■ Genetic cardiomyopathies. ■■ Amyloidosis. ■■ Sarcoidosis. ■■ Metabolic disorders. NURSING OLDER PEOPLE Christopher Nicholson is lead clinician, Cardiac and Respiratory Service, Minerva Centre, Lancashire Care NHS Foundation Trust, Preston Correspondence christopher.nicholson@ lancashirecare.nhs.uk Conflict of interest None declared Keywords Cardiology, cardiovascular disease, chronic heart failure This article has been subject to double-blind review and checked using antiplagiarism software. For related articles visit our online archive and search using the keywords Author guidelines rcnpublishing.com/r/nop-authorguidelines *This is a shortened list – see American College of Cardiology Foundation/American Heart Association (2013) or McMurray et al (2012) guidelines for fuller lists September 2014 | Volume 26 | Number 7 29 Continuing professional development acute presentations are due to destabilisation of chronic disease. Acute heart failure accounts for 5% of emergency hospital admissions and 2% of bed days in the UK on average each year (NICE 2010). The average length of stay in hospital is 12 days (NHFA 2013). In the community, heart failure is a frequent reason for GP appointments and has high medication costs. Managing patients with the disease is a significant NHS cost. Patients who are well managed can have a good quality of life and extend their prognosis, but heart failure is unpredictable and difficult to prognosticate for individual patients. Current in-hospital heart failure mortality is 9%, with 25% of hospitalised patients dying within one year of admission (NHFA 2013). Patients who avoid hospitalisation have better outcomes but all will eventually reach end of life. Now do time out 1. Time out 1 Causes How many of your caseload of patients, or the patients you have seen this week, have a heart failure diagnosis? Using Box 1 (page 29) list the causes, where known. Definitions The terminology used to describe heart failure can be confusing and jargon is best avoided during patient communication. Heart muscle abnormalities are known as cardiomyopathy and classified as dilated, hypertrophic, restrictive, or mixed patterns. Dilated cardiomyopathy is the most common pattern. An enlarged heart is known as cardiomegaly. Ventricles are the heart’s main pumping chambers and dysfunction is seen in either or both – left ventricular dysfunction or left ventricular failure and right ventricular dysfunction or right ventricular failure. Where both ventricles are impaired, the terms biventricular dysfunction or biventricular failure are used. The phrase congestive cardiac failure is sometimes used as a synonym for biventricular failure but a patient may have biventricular failure without overt pulmonary or peripheral congestion. The upper chambers of the heart, the atria, may also be impaired and/or dilated. Specific areas of the heart muscle, the myocardium, may be shown not to move (akinesia) on scanning, may not move powerfully (hypokinesia) or may not move in co-ordination with the rest of the myocardium (dyskinesia). Heart failure can also be defined in terms of where the impairment is in the phases of the cardiac cycle – during contraction (systole) or relaxation (diastole). 30 September 2014 | Volume 26 | Number 7 The terms are left ventricular systolic dysfunction or left ventricular diastolic dysfunction. Pumping efficiency of the heart can be implied from left ventricular ejection fraction (LVEF) and this important measure is often used to categorise the severity of heart failure. The calculation is made by dividing the amount of blood that leaves the left ventricle on each contraction, the stroke volume (SV), by the amount of blood in the left ventricle before contraction, the left ventricular end diastolic volume (LVEDV). For example, if SV 70ml and LVEDV 120ml then LVEF 0.58. It is usual to express LVEF as a percentage and normal range is 50-60%. The preferred basic description of heart failure is either heart failure with reduced ejection fraction or heart failure with preserved ejection fraction (HF-PEF). The HF-PEF syndrome is linked to diastolic dysfunction and often seen in older female patients. Diagnosis Heart failure should be diagnosed using the pathway in the European Society of Cardiology (ESC) guidelines (McMurray et al 2012), as follows. Clinical presentation (Table 1, pages 32-33) may raise suspicion but is not sufficient to confirm diagnosis because these symptoms and signs occur in other conditions. Once diagnosis is confirmed the severity of symptoms can be expressed using the New York Heart Association (NYHA) classification (Box 2) (Criteria Committee of the NYHA 1994). The NYHA classification can also be used to monitor progress. Absence of symptoms and signs does not exclude the heart being dysfunctional or having structural abnormalities (ACCF/ AHA 2013). Many of the disease processes that occur with heart failure are on a continuum and will start before the patient has symptoms. For example, some patients are at risk of heart failure because they are genetically predisposed to hypertension, but for diagnosis investigations should confirm abnormality of cardiac structure or function. Box 2 New York Heart Association (NYHA) classification of heart failure Class I No limitations to ordinary physical activity. Class II Slight limitations to ordinary physical activity with undue breathlessness, fatigue or palpitations. Class III Marked limitations to less than ordinary physical activity with undue breathlessness, fatigue or palpitations. Class IV Symptoms may be present at rest and discomfort made worse with any physical activity. (Criteria Committee of the NYHA 1994) NURSING OLDER PEOPLE Time out 2 Diagnosis Mr Smith is a new nursing home resident. His only medical history is short-term memory loss and high blood pressure. He has become breathless on exertion over the past month and his ankles have started to swell. What is the next diagnostic step? Compare what you have written with the answer given on page 37. Comorbidity Patients with heart failure have more comorbidities than age-matched controls, and comorbidities have a significant effect on symptoms, hospitalisations and prognosis (van Deursen et al 2014). Cardiac comorbidities may cause heart failure, or sometimes co-exist with and influence the condition, and prevalence of cardiac comorbidities increases with age. For example, the prevalence of atrial fibrillation doubles with each decade of life (Cleland et al 2002). Hypertension affects myocardium by ventricular hypertrophy and diastolic dysfunction, which can present as heart failure with preserved ejection fraction. Chronic valve dysfunction NURSING OLDER PEOPLE progresses with age. Non-cardiac comorbidities can affect heart failure directly, usually via metabolic effects, or indirectly through limiting treatment. Management Education and self-management Patients and carers require education about heart failure to develop the staffpatient relationship and improve treatment concordance, especially in older patients (Anderson et al 2005). Specific education should address individual adaptation to the condition, warning signs and what to do in acute situations. Education empowers patients and increases successful self-management. For example, some patients may be given discretion over the dose of their diuretic or be given monitoring parameters for rapid weight gain. Lifestyle modification Certain behaviours help the heart to function either efficiently or inefficiently. For example, excess alcohol depresses myocardial cell function and causes dilated cardiomyopathy and arrhythmias. In smokers, as well as endothelial wall effects, the immediate release of nicotine contracts arteries, increasing the risk of ischaemia (Lanza et al 2011). Obesity and being sedentary adversely affect resting heart rate and increase cardiac demands. Anaemia increases cardiac workload (Levick 2009). Conversely, exercise has significantly positive effects on symptoms and left ventricular function (Piepoli et al 2004). Good control of comorbid conditions such as diabetes, hypercholesterolaemia and kidney disease improves cardiac outcomes. Patients with heart failure who are hospitalised for another condition have longer stays and worse outcomes than matched populations without heart failure (Ahluwalia et al 2012). How patients can be supported to achieve these outcomes is outside the scope of this article but is covered comprehensively in nursing texts, for example, Nicholson (2007). Now do time out 3. 3 Time out Patients with a history of myocardial infarction (MI) are likely to have heart failure if they present with potential signs and symptoms. They should have an urgent, that is, within two weeks, echocardiogram (NICE 2010). If the patient has no history of MI he or she should be screened by a 12-lead electrocardiogram (ECG) and/or a brain natriuretic peptide blood test. Both have a high negative predictive value – if normal the patient is unlikely to have heart failure. Normal levels of brain natriuretic peptide are low: they rise slightly with age and a range of other conditions but are markedly higher if the heart is under strain. Brain natriuretic peptide may also be useful in monitoring treatment response and as a prognostic marker (Januzzi 2012, van Veldhuisen et al 2013, Troughton et al 2014). If ECG or brain natriuretic peptide tests are abnormal an echocardiogram is indicated. Echocardiograms provide information about heart structure and function. Further investigations, such as nuclear scans, cardiac magnetic resonance imaging (MRI) and coronary angiography, may also be needed. Once heart failure is confirmed it is important to consider causes. Some are reversible, such as thyroid imbalance, whereas others are not. Some require different prioritisation of treatment: for example, patients with alcoholic dilated cardiomyopathy must stop drinking to excess – if they do not then prognosis is poor (Adam et al 2008). Now do time out 2. Medications List the first-line medications used to treat heart failure. Reflect on how you would explain to patients how these drugs work. Remember that some patients will need a simpler and some a more detailed explanation. Medication The mainstay of heart failure treatment (Table 2, page 34), medication can relieve symptoms, reduce hospitalisations, shorten length of stay and improve quality of life and prognosis (McMurray et al 2012). There are strong evidence bases September 2014 | Volume 26 | Number 7 31 Continuing professional development Table 1 Clinical presentation of heart failure Symptoms Breathlessness Acute and/or chronic. Grade using New York Heart Association (NYHA) classification – look for class changes (Criteria Committee of the NYHA 1994). Breathlessness at rest is either acute decompensation, end-stage condition or other cause. Confounding comorbidities like respiratory disease or anaemia. Peripheral oedema Oedema settles by gravity so usual pattern of progression through feet, ankles, legs, genitalia/sacrum and abdomen. Oedema due to heart failure soft, pitting and bilateral. Persistent oedema can compromise tissue and secondary cellulitis. Consider alternative systemic and local causes. Orthopnoea (shortness of breath on lying flat) Soon after lying flat. Relieved by sitting up. Symptom of acute or advanced disease. Patients with severe chronic obstructive pulmonary disease (COPD) and arthritis may sleep upright. Loss of appetite Associated acutely with abdominal fluid retention and chronically with the metabolic changes in end-stage disease. Bloated feeling Associated acutely with fluid retention in the abdomen and chronically with hepatomegaly. Confusion Association between heart failure and progressive cognitive impairment. Acute confusion with acute metabolic derangement secondary to heart failure and/or its treatment. Palpitations May be a symptom of sinus tachycardia, atrial or ventricular arrhythmia, or ectopic (early or missed heart beats) – all of which are common in heart failure patients. Angina (chest pain of cardiac origin) May indicate the underlying cause of heart failure or may be secondary consequence of poor myocardial perfusion when cardiac output low. Syncope (transient loss of consciousness) May occur with arrhythmias, hypotension and valve disorders. Depression and anxiety Common symptoms that affect morbidity and quality of life. Paroxysmal nocturnal dyspnoea (PND) (sudden difficulty breathing at night) Soon after going to sleep. Symptom of acute or advanced disease. Sometimes with copious, frothy, even blood-speckled, sputum. Patients may also wake acutely breathless; as can patients having panic attacks. Nocturnal cough With or without PND. Sleep disorders Sleep apnoea and left ventricular dysfunction associated. Cortisol release changes sleep patterns in heart failure. Fatigue Common symptom but non-specific. Fatigue patterns and changes over time. Rule out other causes like anaemia, nutrition and exercise levels. Reduced exercise capacity Common symptom. Rule out other causes. for most treatments but in some areas the evidence is weaker or lacking (McMurray et al 2012). The evidence base is from trials of heart failure with reduced ejection fraction: treatment of heart failure with preserved ejection fraction does not have a substantial evidence base at present. Some treatments, notably diuretics, predate the clinical trial era and are mainly evidenced by registry observational level data. Other common drugs, such as digoxin, have not been specifically trialled in older adults. A criticism of many research designs is that they do not match clinical populations, with lower average ages 32 September 2014 | Volume 26 | Number 7 and fewer comorbidities in trial populations. The mean average age of UK heart failure patients is 77 years but in most heart failure randomised controlled trials it is around 60 years (Witte and Clark 2008). Trials do usually contain patients aged in their seventies but people in their eighties are underrepresented so results cannot be unquestionably applied to all older patients. Older heart failure patients are often undertreated or dosed (Witte and Clark 2008). Some older patients tolerate higher doses of medication less well than younger patients (Krum et al 2000). Age-related bias may be a factor in dosing and treatment decisions should NURSING OLDER PEOPLE Signs Tachypnoea High resting respiratory rate could be sign of acute heart failure. Tachycardia High resting heart rate always significant and could be haemodynamic compensatory response. Acute tachyarrhythmia can provoke heart failure in a patient with a normal heart and is likely to make patients with an abnormal heart unwell. Abnormal pulse Displaced apex beat An irregular pulse could be atrial fibrillation. A pattern of a regular strong then weak pulse may be pulse alternans – a sign of advanced heart failure. The apex beat – the point of maximal impulse on precordium – can be displaced down and left laterally when the heart is dilated. Third heart sound/gallop rhythm With sinus tachycardia. Raised jugular venous pressure Raised right atrial pressure, usually due to volume overload. Heart murmurs Commonly noted murmurs in patients with heart failure are mitral regurgitation, tricuspid regurgitation and aortic stenosis. Wheezing New acute wheezing can be sign of acute lung congestion. Rule out alternative respiratory causes like acute asthma and COPD exacerbation. Lung crepitation Sign of possible fluid in lungs secondary to acute left ventricular failure. Also occurs in smokers and patients with respiratory disease. Weight changes Rapid weight gain >2-3kg a week may be fluid retention. Rapid weight loss may be over-diuresis. Slower weight gain may be reduced exercise capacity. Slower weight loss can occur in end-stage disease. Basal pleural effusions Reduced basal air entry can suggest pleural effusions with/after acute pulmonary oedema. Pleural effusions can persist for months. Hepatomegaly Enlarged liver can occur with right heart failure. Consider alternative causes of hepatomegaly. Tissue wasting Patients at end-stage disease with poor cardiac output can show signs of cachexia-like muscle wasting – the deltoid and intercostal muscles are useful sites to check. Note: Clinical presentation will depend on the patient’s acuteness, severity of heart failure and particular pattern of disease. Patients can therefore have some, or even none, of the above signs and symptoms. be made after individualised assessment and risk-benefit analysis, not assumed because of a patient’s age. Concern over polypharmacy in older adults is another factor affecting prescribing practice. Heart failure patients typically have several medications prescribed. As treatment has significant positive effects on mortality, morbidity, hospitalisations and symptoms, it is arguably not constructive to think of polypharmacy negatively. Treatments only work if the clinician and patient agree about the treatment and then carry it out. Non-concordance is a significant reason for deterioration and hospitalisation (van der Wal et al 2005). It is NURSING OLDER PEOPLE important to know if patients are not following treatment plans, which requires open and honest communication, and then to understand why not. It may be that they have misunderstood plans or disagree with them, or they are finding a drug intolerable. There may be age-related problems that require a specific solution, for example, incontinence for people with mobility problems on high-dose diuretics or forgetting to take medicines if short-term memory loss is present. Diuretics Diuretics are ‘water tablets’: they reduce sodium and water reabsorption. Patients can retain fluid due to neurohormonal over-activation. Typically September 2014 | Volume 26 | Number 7 33 Continuing professional development Table 2 Medications for heart failure in the UK Disease-modifying drugs Initial dose Full dose Indication Bisoprolol 1.25mg once daily (OD) 5mg BD or 10mg OD Carvedilol 3.125mg twice daily (BD) 25mg or 50mg BD depending on weight All patients with left ventricular ejection fraction (LVEF) <40%. Use with ACE inhibitor. Nebivolol 1.25mg OD 10mg OD Beta blockers Angiotensin-converting enzyme (ACE) inhibitors Enalapril 2.5mg BD 20mg BD Lisinopril 2.5mg OD 35mg OD Ramipril 2.5mg OD 5mg BD Perindopril 2mg OD 8mg OD All patients with LVEF <40%. Use with beta blocker. Angiotensin-receptor blockers (ARBs) Candesartan 4mg OD 32mg OD Valsartan 40mg BD 160mg BD Losartan 50mg OD 150mg OD All patients with LVEF <40% intolerant of ACE inhibitors due to cough, or symptomatic patients who are on an ACE inhibitor but intolerant of MRAs. Mineralocorticoid-receptor antagonists (MRAs) Spironolactone 25mg OD 50mg OD Eplerenone 25mg OD 50mg OD All symptomatic patients with LVEF <35% despite being prescribed beta blocker and ACE inhibitor. Other drugs to assist with symptoms Loop diuretics Furosemide 20-40mg Up to 240mg Symptomatic patients and those with evidence of pulmonary or peripheral oedema. Bumetanide 0.5-1mg Up to 5mg Bendroflumethiazide 2.5mg 10mg Metolazone* 2.5mg 10mg Indapamide 2.5mg 5mg Ivabradine 2.5mg 10mg Symptomatic patients in sinus rhythm with a heart rate >70 despite a beta blocker or if intolerant of a beta blocker. Digoxin 62.5mcg OD 250mcg OD Symptomatic patients with persistent symptoms despite a beta blocker or if intolerant of a beta blocker. Thiazide diuretics As either a milder alterative to a loop diuretic or an addition to a loop diuretic to produce synergistic action. Heart rate control Hydralazine and isosorbide dinitrate As an alternative in symptomatic patients intolerant to an ACE inhibitor or ARB. Trial evidence from African-American cohort. *Note: Metolazone is no longer manufactured in the UK but supplies are still being used up at the time of writing. 34 September 2014 | Volume 26 | Number 7 NURSING OLDER PEOPLE patients are on a small maintenance dose of a loop diuretic – such as furosemide or bumetanide – which is increased in dose or supplemented with synergistic thiazide diuretic if fluid builds. Even without overt peripheral oedema diuretics can improve breathlessness by reducing cardiac preload, the amount of fluid returning to the heart, which affects intracardiac pressures and vascular congestion. Diuretics can affect the renal system, fluid and electrolyte balance, and blood pressure, especially at higher doses and if more than one type of diuretic is combined. Patients most vulnerable are those at risk of dehydration, including some older adults. In patients with declining renal function diuretic resistance may necessitate higher doses to achieve the same beneficial effects but with additional adverse risks of hypotension, dehydration and acute kidney failure. Beta blockers Adrenergic neurohormones, part of the ‘fight or flight’ autonomic sympathetic nervous system, stimulate the heart. Blocking adrenoreceptors has therapeutic benefits including reducing afterload, slowing heart rate, increasing myocardial perfusion, suppressing arrhythmias, vasodilation, reducing renin excretion and improving cardiac remodelling. These physiological effects improve clinical outcomes. The Cardiac Insufficiency Bisoprolol Study II (CIBIS II) found that for every 23 patients with mild to moderate heart failure treated with the beta blocker bisoprolol, one life was saved a year, and for every 14 patients with severe heart failure treated with bisoprolol, one life was saved a year (CIBIS-II Investigators and Committees 1999). Beta blockers should be used with care. They should be introduced when the patient is stable, at low dose and gradually titrated to the maximum dose tolerated (‘optimal’ dose). Beta blockers should not be increased if the patient has symptomatic hypotension or bradycardia. Other potential side effects are postural hypotension, lethargy, sleep disturbances, worsening peripheral circulation and diabetic glycaemic control. Beta blockers are not contraindicated in patients with chronic obstructive pulmonary disease but patients with a history of asthmatic bronchospasm are considered too high risk for beta blockers (McMurray et al 2012). The benefits of beta blockers are similar in older and younger people. All three UK approved beta blockers for heart failure – bisoprolol, carvedilol and nebivolol – have data showing benefits in older patients (Dulin et al 2005). The Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors (SENIORS) with heart failure compared patients older than 85 with those aged 75-85 and found similar benefits (Flather et al 2005). NURSING OLDER PEOPLE Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers The renin-angiotensinaldosterone system (RAAS) regulates blood pressure, plasma volume and electrolyte balance in response to renal perfusion. In heart failure the system can be maladaptive, leading to pulmonary oedema as intracardiac pressures increase as well as volume expansion, increasing venous return and shifting fluid into interstitial spaces as peripheral oedema. Medications mediating the RAAS reduce symptoms, slow left ventricular dysfunction, prevent hospitalisations, shorten length of stay and improve morbidity and prognosis. Mortality was halved in patients with severe heart failure taking the angiotensin-converting enzyme (ACE) inhibitor enalapril in the Co-operative North Scandinavian Enalapril Survival Study (CONSENSUS) (Swedberg and Kjekshus 1988). The mortality benefits of enalapril included asymptomatic patients with left ventricular dysfunction in the Studies of Left Ventricular Dysfunction-Prevention (SOLVD-Prevention) (Konstam 1995). The Assessment of Treatment with Lisinopril and Survival (ATLAS) study showed better outcomes at higher treatment doses (Packer et al 1999). Where ACE inhibitors are not tolerated, usually due to persistent cough, angiotensinreceptor blockers (ARBs) can be substituted. Studies show that ACE inhibitors are effective in older adults: the Perindopril in Elderly People with Chronic Heart Failure (PEP-CHF) study showed that the benefits of perindopril in patients aged 70 and older were equivalent to those under the age of 70 (Cleland et al 2006). The Candesartan in Heart Failure – Assessment of Reduction in Mortality and Morbidity (CHARM) Preserved study randomised 929 patients aged over 75 and found the greatest benefits in those aged over 65 compared with those aged under 65 (Yusuf et al 2003). Use of ACE inhibitors in older adults has been a concern because of renal dysfunction and hypotension risks. Although worsening renal function is associated with poor prognosis, analysis of the SOLVD-Prevention found that after ACE inhibitor initiation, worsening renal function in patients with heart failure did not have a negative effect on prognosis and the survival benefit from ACE inhibitors remained (Testani et al 2011). Chronic kidney disease (CKD) is common and often more severe with older age. CKD is not a contraindication to heart failure treatment but care is needed with diuretics, RAAS drugs and vasodilating drugs due to hypotension, especially in patients with severe CKD or renal artery stenosis. Renal physician guidance should be sought, as per CKD guidelines (NICE 2014). Mineralocorticoid-receptor antagonists Patients with left ventricular dysfunction who remain symptomatic despite beta blockers, ACE inhibitors and ARBs September 2014 | Volume 26 | Number 7 35 Continuing professional development Box 3 Device therapy indications* Device Criteria Cardiac resynchronisation therapy (CRT-P) Patients in sinus rhythm, left ventricular ejection fraction (LVEF) <35%, New York Heart Association (NYHA) class III or IV (Criteria Committee of the NYHA 1994), despite optimised medical therapy, a QRS duration of >120mS in left bundle branch block, or a QRS>150mS regardless of QRS morphology, who are expected to survive for more than a year with good functional status. CRT-D Patients with CRT-P indication who also meet the ICD criteria or who have LVEF <30%. Implantable cardioverter defibrillator (ICD) Primary prevention Symptomatic heart failure with an LVEF <35% despite three months of optimised medical therapy and the patient is expected to survive for more than a year with good functional status. Secondary prevention Evidence of ventricular arrhythmia leading to haemodynamic instability and the patient is expected to survive for more than a year with good functional status. *Device therapy indications are based on the evidence from trial populations but there are areas which are uncertain or where trial data are lacking or limited, such as in patients with atrial fibrillation, right bundle branch block and those with a conventional pacemaker indication who also have reduced LV function. Therefore, precise practice may vary between clinicians. Other therapeutic drugs There is not scope in this article to discuss in detail second-line drugs, such as nitrates, hydralazine, ivabradine and digoxin. For further information see Table 2 (page 34) or refer to the ESC guidelines (McMurray et al 2012). Drugs to avoid Glitazones, to control diabetes, can worsen heart failure and increase hospitalisations. Calcium-channel blockers reduce inotropy, the contractile force, and can worsen heart failure and increase fluid retention, although amlodipine and felodipine have fewer reported incidences of such side effects. Steroids, non-steroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors worsen sodium and water retention and chronic use should be avoided in patients with heart failure (McMurray et al 2012). Now do time out 4. 36 September 2014 | Volume 26 | Number 7 4 Time out should be considered for mineralocorticoid-receptor antagonists (MRAs). By blocking aldosterone these drugs reduce fluid retention and cardiac preload. In the Randomized Aldactone Evaluation Study (RALES) involving spironolactone, and Eplerenone Post-AMI Heart Failure Efficacy and Survival Trial (EPHESEUS), additional mortality relative risk reductions of 30% and 24% respectively were seen (McMurray et al 2012). ‘Triple therapy’ of an ACE inhibitor, ARB and MRA is not recommended because it significantly increases risk of acute renal dysfunction. Optimising treatment Referring to the patients you noted for time out 1, add the heart failure drugs they are prescribed to the list. Are they all on optimal treatment? If not, is there a documented reason why not in their records? Advanced treatments Cardiac devices Symptomatic patients on optimised medication might benefit from biventricular pacing, also known as cardiac resynchronisation therapy (CRT-P). Criteria for CRT-P are listed in Box 3. A third wire paces the left ventricle and the device co-ordinates electrical stimulation of the heart and can improve symptoms and quality of life significantly. However, around one quarter of patients who seem suitable for CRT-P do not respond (Fox et al 2005). Half of heart failure patients die of arrhythmia. Ventricular arrhythmia survival is improved with an implantable cardioverter defibrillator (ICD). The device can be a stand-alone ICD or with CRT pacemaker functions (CRT-D). Criteria for ICDs are listed in Box 3. Devices are inserted under local anaesthetic and there are no age restrictions. In patients with terminal diagnosis, unlikely to survive a year, it is NURSING OLDER PEOPLE ■■ Poor left ventricular function and large heart size. ■■ Severity of New York Heart Association (NYHA) class/symptoms (Criteria Committee of the NYHA 1994). ■■ High levels of brain natriuretic peptide. ■■ Frequent decompensations/hospitalisations. ■■ Worsening organ failure. usually inappropriate to implant a device. Patients require periodic functionality and battery checks. Devices preclude patients from MRI but not computed tomography scans, although some patients with devices have had MRI safely and MRI-safe devices are under development (Roguin et al 2008). Cardiac surgery Most patients do not require cardiac surgery except under specific circumstances. Older age does not preclude cardiac surgery but is a risk factor for its safety and success. If heart failure is secondary to cardiac ischaemia then revascularisation by percutaneous coronary intervention or coronary artery bypass grafting is considered. If heart failure is caused by cardiac valve problems then repair or replacement is considered. Heart valves are stretched by a dilated heart and regurgitate, particularly if the heart is overloaded or in arrhythmia, in which case the valve problem is secondary and valve surgery is unlikely to help. If heart failure is due to an aneurysm in the left ventricle then reconstruction – such as the Dor procedure aneurysmectomy – is considered. Replacing the heart – cardiac transplantation – is not common. In the financial year 2013/14 there were 197 UK cardiac transplants (NHS Blood and Transplant 2014). Availability of donor hearts limits this option and older patients will not usually meet transplant suitability criteria. Left ventricular assist devices (LVADS) are implantable mechanical heart pumps. These are sometimes used to stabilise patients and ‘bridge’ to transplant. LVADs are not used as destination therapy at present in the UK. End of life Heart failure causes death through either terminal pump failure or arrhythmia. Some people die within months of diagnosis and others survive years, but there comes a phase when every patient is at the end of life (Box 4). Recognising end of life is important to plan changing care needs. Palliative care planning should take place as for any dying patient, with emphasis on symptom control. Non-essential medication can be discontinued, although neurohormonal drugs and diuretics may be controlling symptoms and stopping them could make some patients feel worse. NURSING OLDER PEOPLE It is difficult to be sure when patients are reaching end of life. Prognosis is variable because of different underlying disease pathologies and because patients respond differently. Heart failure is characterised by episodes of decompensation, where the patient seems close to death but may rally and survive. Treatable causes of cardiac decompensation – for example, chest infections –should always be addressed. Registries show age is a marker of potential poor prognosis but that requires qualification: older patients have more comorbidities and social issues but are not a homogeneous population. An additional specific end of life issue is around cardiac devices. If the patient has an ICD it will probably detect ventricular arrhythmias as the patient is dying and defibrillate. This would put the patient and family through unnecessary distress and the decision is usually made to deactivate the ICD. A cardiac technician can do this wirelessly and it is best planned in advance. Switching off does not hasten death, it simply allows patients to die without risk of unwanted defibrillation. Patients with CRT-D devices can have ICD function switched off and pacemaker function left on: the pacemaker is probably helping symptom control. After death, cardiac devices must be removed before final disposal of the body. Now do time out 5. 5 Time out Box 4 Markers of poor prognosis in heart failure Best practice Reflect on one patient with heart failure who you have cared for. Did his or her diagnosis, treatment and progression fit with best practice guidelines? What systems were in place to ensure the patient received optimal care? If you are unsure, consult the ESC guidelines (McMurray et al 2012). Conclusion Understanding and being able to manage heart failure is important for patients’ quantity and quality of life, regardless of age. It is also important for health service costs. Heart failure is most common in older adults and it is expected that the average age of patients will rise. Nurses have a crucial role in the care of patients but a multidisciplinary approach is mandatory, including partnership with older adult services. Suggested answer to time out 2 A screening test such as brain natriuretic peptide blood test or ECG. It is possible he has heart failure with the September 2014 | Volume 26 | Number 7 37 Continuing professional development 6 Time out history of hypertension and the clinical presentation so investigations are warranted. As he has not had a myocardial infarction, an urgent echocardiogram is not required but, if the screening test is positive, he will require echocardiogram within six weeks to confirm diagnosis. If the screening test is negative alternative causes of his signs and symptoms should be investigated. Reflective account Now that you have completed reading the article you might like to write a reflective account. Guidelines to help you are on page 39. References Adam A, Nicholson C, Owens L (2008) Alcoholic dilated cardiomyopathy. Nursing Standard. 22, 38, 42-47. Ahluwalia S, Gross C, Chaudhry S et al (2012) Impact of comorbidity on mortality among older persons with advanced heart failure. Journal of General Internal Medicine. 27, 5, 513-519. American College of Cardiology Foundation/ American Heart Association (2013) Guideline for the management of heart failure. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. https://circ.ahajournals.org/content/128/16/ e240.extract (Last accessed: August 8 2014.) Anderson C, Deepak B, Amoateng-Adjepong Y et al (2005) Benefits of comprehensive inpatient education and discharge planning combined with outpatient support in elderly patients with congestive heart failure. Congestive Heart Failure. 11, 6, 315-321. Dulin B, Haas S, Abraham W et al (2005) Do elderly systolic heart failure patients benefit from beta blockers to the same extent as the non-elderly? 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