Heart Failure Management

See related article Heart Failure Diagnosis and Investigation.

• Further/worsening ischaemia
• Myocardial infarction
• Additional valvular or diastolic dysfunction
• Infections
• Arrhythmias (commonly AF)
• Electrolyte imbalance
• Worsening co-morbidities - e.g. anaemia, thyroid dysfunction, pulmonary disease, renal dysfunction, diabetes
• New medications

Patient education and self-care

Patient and family education and training in self-care is effective at improving adherence, symptom control, functional capacity and well-being. Topics should include:

• Nature and cause of symptoms
• Available treatments, likely side-effects and responses
• Recognition and reaction to symptoms (e.g. flexible dosing of diuretics which can be titrated to symptoms with advice as to when to contact the healthcare team)
• Risk factor modification
• Dietary and exercise advice
• Psychosocial aspects to the disease
• Prognosis

Specialist heart failure nurses²

Community-based heart failure nurses provide an important adjunct to self-care, as well as a bridge to secondary care. Referral of those with moderate to severe heart failure to such a service improves symptom management, reduces hospital admissions and also assists in the transition to a palliative care approach when appropriate.

Lifestyle modification

Smoking

Encourage to stop smoking and provide support with smoking cessation.

Diet and fluid intake

• Advise regarding good nutrition and provide help for obese patients to reduce their weight. Cachexic patients (weight loss over 6 months >6% of previous, stable body weight) should be assessed by a dietician.
• Suggest patients avoid foods with a high-salt content and do not add salt to their food. Salt intake should not exceed 2-3 g per day. Consider moderate sodium restriction in severe CCF; take care that 'low-salt' alternatives are not over-used as they can be very rich in potassium which may be a problem for patients on ACE inhibitors or spironolactone.
• Advise patients with severe CCF, particularly in conjunction with hyponatraemia, to restrict their fluid intake sensibly. Take care to avoid excessive dehydration – particularly in elderly patients on high-dose diuretics.
• Patients can contribute to monitoring their fluid retention by regularly weighing themselves. Where a sudden, unexpected weight gain of >2 kg in 3 days, advice should be sought. Some patients may benefit from being able to vary their diuretic dose on the basis of regular weights. Self-weighing complements ongoing monitoring of weight in the GP surgery, hospital outpatient and inpatient wards.

Alcohol

Alcohol can act as a negative inotrope, increase blood pressure and the risk of arrhythmias. Restrict alcohol intake to 10-20 g/day (equivalent to 1-2 glasses of wine) or advise abstention if alcohol-induced cardiomyopathy.

Exercise

Encourage aerobic exercise, preferably as part of a supervised cardiac rehabilitation programme, for patients with heart failure up to and including NYHA grade III which has proven beneficial effect.³

Travel

Air travel is not restricted in stable patients (and may be preferable to other means of transportation for long journeys); however, long-haul flights increase the risk of peripheral oedema and DVT. High altitudes and travel to very hot and humid areas should be discouraged in symptomatic patients who may not adapt easily.

Sex and reproductive health

• There are no specific restrictions for sexual activity, although there is a slight risk of decompensation in those with NHYA class III-IV.
• Advise patients that symptoms such as dyspnoea, palpitations, angina are unlikely to occur related to sex unless similar symptoms are experienced with moderate exercise (e.g. climbing two flights of stairs reasonably quickly). Sexual activity is least likely to cause symptoms if engaged in following sleep, with the least affected partner doing most of the physical work. The most provocative occasions will be sex with a new partner, after a hot bath or on a full stomach.
• Sexual problems are common in patients with heart failure related to concurrent cardiovascular disease, side-effects of treatment (e.g. beta blockers) and psychological factors.
  • Sublingual glycerol trinitrate may be used prophylactically against dyspnoea and chest pain during sex but nitrates must never be combined with phosphodiesterase inhibitors such as sildenafil.
  • Phosphodiesterase inhibitors are not currently recommended for use in those with advanced heart failure.
• Pregnancy risks worsening of heart failure due to increased blood volume and cardiac output and many relevant medications are contra-indicated in pregnancy. Potentially fertile women with heart failure should receive prenatal counselling to enable informed reproductive choice.

Mental health and well-being

Depression is very common in heart failure, occurring in at least 1 in 5 patients and at much higher levels in those with advanced disease. Screening and appropriate treatment should be considered in those with symptoms.

Immunisation

Offer:

• Annual influenza vaccination
• A single pneumococcal vaccination

See Acute Pulmonary Oedema Management article.

• Treat the co-morbidities aggressively.
• Best evidence is for the use of angiotensin receptor agonists (more limited for ACEI).
• Use diuretics if pulmonary or systemic congestion but avoid over-diuresis.
• Consider the use of beta blockers.
• Refer to cardiologist for full assessment and review of treatment.

ACE Inhibitors¹

• All patients with a left ventricular ejection fraction (LVEF) of 40% or less, regardless of symptom severity, should receive an ACE inhibitor unless contraindicated or not tolerated.⁷
• This is because ACE inhibitors have been shown to improve ventricular function and patient well-being, to reduce mortality and hospital admissions in many large clinical trials and are indicated in all stages of left ventricular systolic dysfunction (LVSD).
• Contra-indications include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/l), severe renal impairment (serum creatinine >220 μmol/l) and severe aortic stenosis.
• Check U&Es and renal function prior to starting treatment and then after 1-2 weeks of treatment or dose adjustment.
• Titrate dose up after 2-4 weeks, provided there is no worsening of renal function or hyperkalaemia, aiming for the evidence-based target dose or maximum tolerated dose.
• Recheck U&Es at 1, 3 and 6 months after achieving maintenance dose and twice-yearly thereafter.
• If renal function worsens, check and eliminate other nephrotoxic drugs such as NSAIDs. An increase of up to 50% from baseline or to an absolute creatinine concentration of 265 μmol/l is deemed acceptable, but above this reduce the ACEI dose. Stop the ACEI where the creatinine concentration is ≥310 μmol/l.
• Warn patient regarding initial symptoms of dizziness, where this does not improve with time or causes risk of falling, reduce dose or stop other hypotensive medications. Switch to an angiotensin receptor blocker if chronic cough develops.

Diuretics¹

• Symptomatic failure usually requires loop diuretics such as furosemide (formerly frusemide). Diuretics give symptom relief but do not alter prognosis. They should usually be used in combination with an ACE inhibitor.
• Give initial doses intravenously in cases of severe failure as their onset of action is faster (5 minutes compared to 1–2 hours p.o.) and oral absorption may be reduced by intestinal mucosal oedema (bumetanide has slightly better bioavailability in the oedematous gut).
• Beware of both over- and under-treatment with diuretics (start with low dose and increase depending on response), and review clinical condition and electrolytes regularly – watch for hypokalaemia, hypovolaemia leading to circulatory collapse and uraemia, particularly in the older patient. Note that creatinine is not a reliable indicator of overall renal function and that GFR may be reduced by up to 75% before it begins to rise, particularly in patients with a low muscle mass.
• Weight monitoring is invaluable in assessing the degree of fluid retention and optimal diuretic strategy. Aim to maintain 'dry weight' with the lowest achievable dose of diuretic.
• Where diuretic response is insufficient:
  • Check compliance and fluid intake.
  • Increase dose of diuretic.
  • Consider switch from furosemide to bumetanide or torasemide.
  • Add an aldosterone antagonist.
  • Combine a loop diuretic with a thiazide (e.g. metolazone)
  • Give the loop diuretic b.d. or on an empty stomach.
  • Consider short-term use of IV infusion of loop diuretic.
• Excessive diuresis increases the risk of hypotension and renal dysfunction associated with ACE inhibitor therapy. Where ACE inhibitors or aldosterone antagonists are used with a diuretic, potassium replacement is not usually required.

Beta blockers^1,8

• Current guidance suggests that beta blockers should be used in all patients with symptomatic heart failure and an LVEF ≤40%, where tolerated and not contra-indicated. Trial evidence shows beta blockers increase ejection fraction, exercise tolerance, reduce morbidity, mortality and hospital admissions additional to that produced by co-prescription of ACE inhibitors.
• They should be initiated in stabilised patients already on diuretics and ACE inhibitors, regardless of whether or not symptoms persist (NICE guidance).⁷
• Evidence for the benefit of beta blockade in heart failure is limited to bisoprolol, carvedilol, metoprolol and nebivolol. We cannot assume that it is a class effect despite NICE guidance that if patients were already taking a non-recommended beta blocker such as atenolol, they should continue with this. Updated QOF targets for 2009/10 will look at the percentage of patients with heart failure on beta blockers licensed for that indication, i.e. bisoprolol, carvedilol and nebrivolol.
• A study looking at beta blocker prescribing in British General Practice between 2000-2005 showed that only about a fifth of patients with heart failure received beta blockers.⁹ A major barrier to this practice is the prior, longstanding contra-indication of beta blockers in heart failure and concerns about the difficulty of initiating beta blockers in such patients.¹⁰ This was based on the belief that sudden loss of sympathetic drive to the failing myocardium would precipitate worse failure. This has been demonstrated not to be the case and low-dose treatment with cardio-selective beta blockers can be safely initiated/titrated in the community in elderly patients and others with relative contra-indications (e.g. diabetes, mild hypotension, fixed airways obstruction).
• Asthma, second- or third-degree heart block, sick sinus syndrome (without pacemaker) and sinus bradycardia (<50 beats per minute) remain contra-indications to beta blocker use.
• Initiate at low dose, with increases every 2-3 weeks until the target evidence-based dose or maximum tolerated dose are reached.
• Monitor blood pressure and heart rate with each increase in dose. If hypotensive, discontinue other vasodilator drugs (e.g. nitrates, calcium channel blockers) where possible. Where bradycardia (<60 beats per min) develops, stop other contributory medications (e.g. digoxin, amiodarone).
• Do not abruptly stop beta blockers as this risks an MI or arrhythmia.

Angiotensin II receptor antagonists¹

• Angiotensin II receptor antagonists can be used in patients intolerant of standard ACE inhibitors. Candesartan and valsartan are now licensed for this indication. They do not cause the chronic cough side-effect associated with ACE inhibitors.
• They are also recommended in combination with an ACEI and a beta blocker in patients with heart failure and an LVEF ≤40% who nonetheless remain symptomatic.
• They must only be used in patients with adequate renal function and a normal serum potassium. Serial monitoring of renal function and U&Es is vital, particularly when used in combination with an ACE inhibitor.

Aldosterone antagonists¹

• A low-dose aldosterone antagonist should be considered in all patients with an LVEF ≤35% and severe symptoms (NHYA class III or IV), unless contra-indicated or not tolerated and in the absence of hyperkalaemia and significant renal dysfunction.
• The RALES study suggested that, in moderate or severe heart failure, the combination of ACE inhibitor, loop diuretic and spironolactone reduces deterioration and mortality.¹¹
• Hyperkalaemia was unlikely under trial conditions where low doses of spironolactone were used (<25 mg/day)¹² but is more common in clinical practice, particularly in elderly patients or those with poor renal function. The combination of an ACE inhibitor and aldosterone antagonist increases the risk of severe hyperkalaemia and careful monitoring is required.
• Measure renal function and U&Es at 1 week and 4 weeks after starting/increasing dose. This should be repeated monthly for the first 3 months and then at least twice a year on maintenance treatment.
• Where breast tenderness or enlargement occurs, switch from spironlactone to eplerenone.

Digoxin¹

• In atrial fibrillation, digoxin is very useful in controlling heart rate, and as a positive inotrope where there is concomitant heart failure. It is often used to gain initial rate control and to treat decompensated heart failure prior to the initiation of a beta blocker. In the longer term, a beta blocker, either alone or in combination with digoxin, is preferred for rate control in patients with an LVEF ≤40%.
• It also improves symptoms in those patients with moderate and severe failure who are in sinus rhythm, and hence should be considered if symptoms of failure continue in spite of optimal treatment with diuretics and ACE inhibitors.
• Digoxin is of use in severe LVSD and, whilst it does not appear to alter mortality rates, did appear to help prevent recurrent admissions to hospital.^13,14
• A single daily maintenance dose of 0.25 mg is suggested in adults with normal renal function (reduced to 0.125 or 0.0625 mg in the elderly or those with renal impairment).
• In patients on digoxin, monitor U+E and maintain potassium at 4–5 mmol/l.
• Digoxin levels may also need monitoring – 6 hrs post dose, to ensure therapeutic (but not toxic) levels. Therapeutic range occurs between 0.6-1.2 ng/ml.
• For use of other inotropes (e.g. dobutamine) click here to see article on Acute Pulmonary Oedema Management.

Vasodilators¹

• Long-acting nitrates work in a complex manner by reducing venous filling pressure (preload), reducing output impedance and improving coronary filling.
• They are particularly appropriate if the patient has episodes of angina.
• H-ISDN does reduce mortality (although inferior to ACE inhibitors) in symptomatic patients with LVEF ≤40% and such a combination may be considered in patients intolerant of ACE inhibitors or those still symptomatic despite maximal first and second line therapy. Evidence is strongest in patients of an African-American descent.
• Alpha-blockers should be avoided, as the ALLHAT hypertensive study suggests they cause significantly more congestive cardiac failure and cardiac events than a simple diuretic.¹⁵
• Calcium channel blockers should also be avoided, as they are generally negatively inotropic and also increase morbidity and mortality. However, amlodipine is recommended by NICE to treat concomitant angina/hypertension as it appears to have no net effect.¹⁶

Opiates or opioids (morphine or diamorphine)

• They may relieve anxiety, distress and pain and are important in the management of severe acute heart failure, or in terminal disease (particularly if difficulty sleeping).
• They also produce transient venodilation, thus reducing cardiac filling pressures, preload and pulmonary congestion.

Drugs to treat cardiovascular co-morbidity¹

Anticoagulants and antiplatelet agents

• Patients with severe heart failure have a greater incidence of strokes and emboli.
• Warfarin is recommended in patients with heart failure and permanent, persistent or paroxysmal AF without contra-indication to anticoagulation. It is also recommended for those with intracardiac thrombus or with evidence of systemic embolism.
• Aspirin is less effective than warfarin in preventing thromboembolism in patients with AF. There is no evidence that antiplatelet agents reduce atherosclerotic risk in patients with heart failure but they are widely used in all patients with ischaemic heart disease without contraindications.
• There has been a long-running controversy about a potential, negative interaction between aspirin and ACE inhibitors which now seems to have been largely discounted.

Statins

In elderly patients with symptomatic chronic heart failure caused by coronary artery disease, secondary prevention with statins may reduce hospitalisations.

• Where heart failure is caused or exacerbated by surgically correctable conditions, these should be detected and treated appropriately by:
  • Revascularisation - surgical (coronary artery bypass grafting) or radiological (percutaneous coronary intervention) techniques should be considered in selected heart failure patients with coronary artery disease.
  • Valvular disease - decisions regarding surgery should be individualised. Medical management of heart failure and co-morbidities should be optimised prior to surgery.
• Cardiomyoplasty and partial left ventriculectomy (Batista's operation) are not recommended as a treatment of heart failure or alternative to heart transplantation.¹⁹
• Cardiac resynchronisation therapy (CRT), also known as biventricular pacing, is recommended to reduce mortality and morbidity in patients with moderate-to-severe heart failure who remain symptomatic despite optimal medical therapy, have a reduced LVEF ≤35% and QRS prolongation (≥120 ms).²⁰ Pacing improves the coordination of ventricular contraction with subsequent gains in cardiac output.
• Implantable cardioverter defibrillator (ICD) is recommended:
  • For secondary prevention in survivors of ventricular fibrillation and for those who have experienced haemodynamically unstable VT or VT with syncope, in those with LVEF ≤40%, on optimal medical treatment and with an expectation of survival with good functional status of over a year.
  • For primary prevention in those with LV dysfunction due a previous MI or non-ischaemic cardiomyopathy, with an LVEF ≤35%, in NHYA functional class II or III, receiving optimal medical treatment and have a reasonable expectation of survival with good functional status of over a year.
• CRS can be combined with ICD function but its survival benefit has yet to be determined.
• Heart transplantation may be considered in selected patients when end-stage heart failure is reached without other treatment options. Constraints include lack of donor hearts and problems of rejection/long-term immunosuppression.
• Left ventricular assist devices (LVADs) and artificial hearts are used currently for bridging to transplantation and managing patients with acute, severe myocarditis.

See article Palliative Care of Heart Failure

There are considerable similarities between dying from cancer and dying from heart failure, with anxiety, severe dyspnoea and pain being prominent in both cases. Dissimilarities include the more uncertain trajectory compared to cancer - with periods of relative stability interspersed at increasing frequency by crises and the threat of sudden cardiac death.
The end-of-life care approach that evolved from the care of those with cancer is today being adapted for use with those with end-stage heart failure involving multi-disciplinary team working between palliative, cardiac and community health care teams. Generic palliative care needs exist and include the management of refractory symptoms, communication, advance planning and decision making issues, as well as the need for family support.

Prognosis is poor with around 80% of patients dying within 6 years of diagnosis. Optimal and early therapy with ACE inhibitors, beta blockers and appropriate non-pharmacological care can improve this outlook and it is hoped that the prognosis of the general heart failure population will improve as diagnoses are made earlier and optimal treatment strategies are followed.

The use of plasma BNP concentration monitoring to guide treatment may improve prognosis:²¹ patients with heart failure appear to do better where doctors try to achieve low level targets (<100 pg/ml) by applying more aggressive therapy,²² although no benefit over symptom-guided treatment has been found in other studies.²³