Chapter 88: Chronic heart failure

Heart failure occurs when the heart is unable to maintain sufficient cardiac output to meet the demands of the body for blood supply during rest and activity.

Chronic heart failure (CHF) remains a very serious problem with a poor prognosis. It has a 50% mortality within 3 years of the first hospital admission.¹ Australian and overseas data indicate that 1.5% of the adult population have heart failure. The prevalence of CHF has been shown to increase from approximately 1% in those aged 50–59 years to over 5% in those 65 and older, to over 50% in those 85 years and older.² Australian research suggests that under-treatment with the all-important ACE inhibitors continues to be a problem. ACE inhibitors (or ARBs) and beta blockers are the gold standard for treating systolic heart failure, with aldosterone antagonists providing added benefit if symptoms persist.³ The clinical diagnosis is based on a careful history and examination. A major goal of management of CHF is the identification and reversal where possible of underlying causes and/or precipitating factors. CHF is characterised by two pathophysiological factors: fluid retention and reduction in cardiac output.

The clinical diagnosis is based on a careful history and examination. The classic symptom of CHF is dyspnoea on exertion but symptoms may be reported relatively late, particularly with a sedentary lifestyle. Dyspnoea can progress as follows: exertional dyspnoea → dyspnoea at rest → orthopnoea → paroxysmal nocturnal dyspnoea.

Symptoms in summary

Fluid accumulation:

• Dyspnoea and orthopnoea (as above)

• Dry irritating cough (especially at night)

• Lethargy/fatigue

• Weight change: gain (mainly) or loss

• Ankle oedema

• Abdominal discomfort: hepatic congestion

Poor cardiac output:

• Dizzy spells/syncope

• Weakness

• Fatigue

Note: The irritating cough due to left ventricular failure can be mistaken for asthma, bronchitis or ACE-inhibitor-induced cough. Poor cardiac output causes fatigue and weakness.

The physical examination is very important for the initial diagnosis and evaluation of progress. The signs are as follows.

Signs

There may be no abnormal signs initially. It is helpful clinically to differentiate between the signs of right and left heart failure:

Left heart failure

• Tachycardia

• Low volume pulse (pulse pressure <25 mm Hg)

• Tachypnoea

• Laterally displaced apex beat

• Bilateral basal crackles

• Gallop rhythm (3rd heart sound)

• Pleural effusion

• Poor peripheral perfusion—cool, pale extremities

Right heart failure

• Elevated jugular venous pressure

• Right ventricular heave

• Peripheral/ankle oedema

• Hepatomegaly

• Ascites

Auscultation is important to identify adventitious sounds, a third heart sound and possible underlying valvular disease.

Systolic versus diastolic heart failure

The classic heart failure is systolic failure due to an inadequate pumping action of the heart. The ventricle is dilated and contracting poorly (left ventricular ejection fraction <40%).⁴

Diastolic heart failure is due to impairment of left ventricular filling with preserved systolic function. A substantial proportion of heart failure presentations are due to diastolic heart failure (impaired ventricular relaxation).² It should be suspected in the elderly with hypertension and a normal heart size on chest X-ray who present with dyspnoea or pulmonary oedema.³ It is particularly common in elderly females.

Note: Patients can have simultaneous systolic and diastolic failure.

The oedema of heart failure

Peripheral oedema appears initially on the lower legs as ‘pitting’. To assess the presence of pitting, which is usually graded on a four-point scale, press firmly yet gently with the thumb for 5–10 seconds over the dorsum of the feet, behind each medial malleolus and over the shins. With increasing severity of failure the oedema extends proximally to involve the abdomen. In the recumbent position it may be apparent over the sacrum.⁵

Determining severity of heart failure

The severity of heart failure can be considered from three different perspectives: the severity of the symptoms, the degree of impairment of cardiac function and the severity of the congestive state. The severity of the symptoms or the degree of functional disability is usually described according to the New York Heart Association criteria (see TABLE 88.1).⁶ The left ventricular ejection fraction provides an indication of cardiac function.

Causes of CHF can be classified under systolic heart failure (impaired ventricular contraction) and diastolic heart failure (impaired ventricular relaxation and filling despite normal contractions). Diagnosis is based on echocardiography.

Systolic heart failure

Ischaemic heart disease, including previous myocardial infarction, is the most common cause, accounting for approximately two-thirds. There is often a history of at least one myocardial infarction.² Essential hypertension is the other common cause.

Other causes:

• valvular heart disease, mainly aortic and mitral incompetence

• high output states (e.g. anaemia, hyperthyroidism, Paget disease)

• non-ischaemic idiopathic dilated cardiomyopathy

• viral cardiomyopathy

• alcoholic cardiomyopathy

• other cardiomyopathies—diabetic, familial

• persistent arrhythmias, especially atrial fibrillation

• other systemic illness (e.g. sarcoidosis, SLE, scleroderma, myxoedema)

• chemotherapy

• peripartum

Diastolic heart failure

• Obesity, hypertension and diabetes significant risk factors

• Familial: more common in women and the elderly

• Common causes include ischaemic heart disease, systemic hypertension, aortic stenosis, atrial fibrillation (inadequate filling), hypertrophic cardiomyopathy, pericardial disease

• Significant morbidity and difficult to diagnose

The following should be considered:

• Echocardiography²—the transthoracic echocardiogram is the investigation of choice to measure ventricular function. It can differentiate between systolic dysfunction and those with normal systolic function but abnormal diastolic filling. It gives information about left and right ventricular systolic and diastolic function, left and right ventricular size, volumes, thickness, structure and function. It also provides information about cardiac valves, congenital heart defects and pericardial disease.

• Electrocardiogram—a key investigation to look for evidence of ischaemia, conduction abnormalities, arrhythmias and LV hypertrophy

• Chest X-ray to look for:

  • – cardiomegaly and interstitial oedema

  • – upper lobe blood diversion

  • – fluid in fissures

  • – oedema in perihilar area with prominent vascular markings

  • – small basal pleural effusions

  • – Kerley B lines = raised pulmonary venous pressure

  • – frank pulmonary oedema

    Note: a normal CXR does not exclude CHF.

• Spirometry/respiratory function testing—to detect associated airways dysfunction

• B-type natriuretic peptide—a hormone secreted from the ventricular myocardium is an indicator of severity of CHF and prognosis

Peripheral markers

• FBE and ESR: anaemia can occur with CHF; severe anaemia may cause CHF

• Serum electrolytes: usually normal in CHF, important to monitor management

• Kidney function tests: for monitoring drug therapy

• Liver function tests: congestive hepatomegaly gives abnormal LFTs

• Urinalysis

• Thyroid function tests, especially if atrial fibrillation

• Viral studies: for suspected viral myocarditis

Specialised cardiac investigation (specialist directive)

• Coronary angiography—for suspected and known ischaemia. CT angiography and cardiovascular MRI preferred

• Haemodynamic testing

• Endomyocardial biopsy

• Nuclear cardiology

The treatment of heart failure includes determination and treatment of the cause, removal of any precipitating factors, appropriate patient education, general non-pharmaceutical measures and drug treatment. Studies have shown the benefit of an integrated, multidisciplinary approach to management.

Prevention of heart failure

The emphasis on prevention is very important since the onset of heart failure is generally associated with a poor prognosis. Approximately 50% of patients with heart failure die within 5 years of diagnosis.⁷

The scope for prevention includes the following measures:⁸

• dietary advice (e.g. achievement of ideal weight, optimal nutrition)

• emphasising the dangers of smoking and excessive alcohol

• control of hypertension

• control of other risk factors (e.g. hypercholesterolaemia)

• early detection and control of diabetes mellitus

• early intervention during myocardial infarction to preserve myocardial function (e.g. thrombolytic therapy)

• secondary prevention after the occurrence of myocardial infarction (e.g. beta blockers, ACE inhibitors and aspirin)

• appropriate timing of surgery or angioplasty for ischaemic or valvular heart disease

Treatment of causes and precipitating factors

Any underlying cause should be identified and treated, if possible. Precipitating factors that should be treated include:

• arrhythmias (e.g. atrial fibrillation)

• electrolyte imbalance, especially hypokalaemia

• anaemia

• myocardial ischaemia, especially myocardial infarction

• dietary factors (e.g. malnutrition, excessive salt or alcohol intake)

• adverse drug reactions (e.g. fluid retention with NSAIDs and COX-2 agents) (see TABLE 88.2)⁹

• infection (e.g. bronchopneumonia, endocarditis)

• hyper- and hypothyroidism

• lack of compliance with therapy

• fluid overload

Note: Be mindful of complementary medications.

General non-pharmacological management

• Education and support

• Smoking: encourage no smoking

• Refer for a rehabilitation program with interdisciplinary care

• Encourage physical activity especially when symptoms absent or mild

• Rest while symptoms are severe

• Weight reduction, if patient obese

• Advice on food supplementation—dietitian

• Salt restriction: advise no-added-salt diet (<2 g or 60–100 mmol/day)

• Water restriction: water intake should be limited to 1.5–2 L/day or less in patients with advanced heart failure, especially when the serum sodium level falls below 130 mmol/L⁷

• Limit caffeine to 1–2 cups coffee/tea a day

• Limit alcohol to 1 standard drink a day

• Fluid aspiration—if pleural or pericardial effusion present

• Daily weighing—check significant weight gain or loss

Other general measures¹

• Optimise cardiovascular risk factors (e.g. BP, lipids, HbA_1C)

• Monitor emotional factors including depression

• Regular review

• Vaccination: annual influenza, 5-yearly pneumococcus

• 2-yearly echocardiography (or more) as indicated

• Pleurocentesis or pericardiocentesis (if applicable)

• Treat co-existing obstructive sleep apnoea

Drug therapy of heart failure due to left ventricular systolic dysfunction

Any identified underlying factor should be treated.

Evidence from RCTs shows the beneficial results from ACE inhibitors^2,9 (or angiotensin II blockers), digoxin (improves outcome in people already receiving diuretics and ACE inhibitors), beta blockers and spironolactone (in severe heart failure).

Atrial fibrillation should be treated with digoxin. Vasodilators are widely used for heart failure and angiotensin converting enzyme inhibitors (ACEI) are currently the most favoured vasodilator.

Note: Monitor and maintain normal potassium level in all patients.

ACE inhibitors improve prognosis in all grades of heart failure and should be employed as the initial therapy in all patients, except where contraindicated (e.g. kidney artery stenosis, angioedema).

Diuretics have an important place in patients with fluid overload. As a rule they should be added to an ACEI to achieve euvolaemia. Diuretics should be used in moderation and excessive doses of a single drug avoided. In patients with systolic LV dysfunction they should not be used as monotherapy.⁸ Close monitoring of weight, kidney function and electrolytes is required. Loop diuretics such as frusemide, bumetanide or ethacrynic acid are commonly used, especially for heart failure of moderate severity.⁸ Thiazide and related diuretics produce a gradual diuresis and are recommended for mild heart failure. Examples include hydrochlorothiazide, bendrofluazide, chlorthalidone or indapamide.

Initial therapy of heart failure^7,10

1. ACE inhibitor (start low, aim high)

   Dosage of ACE inhibitor: commence with ¼ to ½ lowest recommended therapeutic dose and then adjust it for the individual patient by gradually increasing it to the maintenance or maximum dose (see TABLE 88.3). Once-daily agents are preferred. Use an ARB if cough is problematic.

ACE inhibitors

• ACE inhibitors are regarded as the agents of first choice because they correct neuroendocrine abnormalities and reduce cardiac load by their vasodilator action.

• Every effort should be made to up-titrate to the highest tolerated dose.

• Consider giving the first dose at bedtime if there is a risk of orthostatic hypotension.

• If the ACEI is not tolerated (e.g. due to cough) consider an angiotensin II receptor blocker (ARB) as they have proven benefit in CHF.¹¹

• In practice the usual initial treatment of heart failure is an ACE inhibitor plus diuretic. This combination optimises response and improves diuretic safety.

• Consider stopping any diuretic for 24 hours before starting treatment with an ACEI.

• Potassium-sparing diuretics or supplements should not be given with ACEI (or should at least be used with caution) because of the danger of hyperkalaemia.

• Kidney function and potassium levels should be monitored in all patients.

• 2 Add a diuretic (if congestion):

  • loop diuretic (preferred)

  • frusemide 20–40 mg (o) once or twice daily

  • or

  • ethacrynic acid 50 mg (o) daily

  • or

  • (thiazide-type diuretic)

  • hydrochlorothiazide 25–50 mg (o) daily (or other thiazide)

  • or

  • indapamide 1.5–2.5 mg (o) daily

• 3 Add an aldosterone antagonist diuretic (if fluid overload not controlled):

  • spironolactone 12.5–50 mg (o) daily

  • or

  • eplerenone 25–50 mg (o) daily

Some authorities are concerned about the over-reliance on diuretics and also about compliance as well as side effects. Once the diuretic effect has been achieved, diuretics may be withdrawn and fluid restriction advised. The ACEI is then used alone or with a beta blocker.

Beta blockers

Selective beta blockers have been shown to prolong survival of patients with mild to moderate CHF taking ACE inhibitors who are stabilised. Start with extremely low doses (see TABLE 88.4). Commence when patient stable and euvolaemic.

Digoxin

Digoxin was the mainstay of treatment of heart failure for decades prior to the use of ACE inhibitors. It was an effective agent but limited. The two indications for its current use are in patients with atrial fibrillation to control rapid ventricular rate and in patients with sinus rhythm not adequately controlled by the other agents above it in FIGURE 88.1. Most patients are started on a low dose digoxin:

62.5–250 mcg (o) daily

New agents⁷

Ivabradine is a direct sinus node inhibitor which can be added to a beta blocker in patients with continuing symptoms of moderate to severe failure, or where beta blockers are contraindicated or not tolerated. Other new agents to consider for optimal treatment include sacubitril/valsartan (Entresto)—an angiotension/neprilysin inhibitor.

Heart failure (unresponsive to first-line therapy)—stepwise strategy^2,7

• ACE inhibitor

• plus

• frusemide 40–80 mg (o) bd

• plus

• spironolactone 12.5 (starting)—25 mg (o) daily (monitor potassium and RFTs), if still congestion

• plus

• a selective beta blocker (if patient euvolaemic)

• plus

• digoxin (if not already taking it):⁷ loading dose:

  • – 0.5–0.75 mg (o) statim (depending on kidney function)

  • – then 0.5 mg (o) 4 hours later

  • – then 0.5 mg the following day

  • – then individualise maintenance

Severe heart failure^7,10

Seek specialist advice.

• Hospital with bed rest.

• ACE inhibitor to maximum tolerated dose

• plus

• frusemide to max. 500 mg/day

• plus

• spironolactone (low dose) 25 mg/day

If poorly controlled, consider adding:

• thiazide diuretic

• spironolactone—doses up to 100–200 mg daily

• a beta blocker

• digoxin

• heparin (if confined to bed)

Vasodilators

If still uncontrolled consider vasodilators other than ACEIs or ARBs:

• isosorbide dinitrate 20–40 mg (o) 6 hourly

• plus

• hydralazine 50–100 mg (o) 6 hourly

A glyceryl nitrate patch can be used for the relief of symptoms, especially nocturnal dyspnoea.

Consider cardiac transplantation for appropriate patients with end-stage heart failure (e.g. patients under 50 with no other major disease). Other surgical options include heart valvular surgery, coronary artery bypass surgery and surgical ventricular restoration (surgical reduction of an enlarged left ventricle).

A flow chart for the basic management of heart failure is presented in FIGURE 88.1.

Diastolic heart failure^2,8

Management is based on treating the cause such as hypertension, ischaemia and diabetes. The basic treatment is with inotropic agents such as calcium channel blockers (verapamil or diltiazem) and beta blockers. If possible avoid diuretics (except for congestion), digoxin, nitrates/vasodilators and nifedipine. Excessive diuresis from overzealous diuretic therapy can cause severe consequences for cardiac output. ACE inhibitors can be used with caution.

Pitfalls in management

• The most common treatment error—excessive use of diuretics³

• Giving an excessive loading dose of ACE inhibitor

• Failure to correct remedial causes or precipitating factors

• Failure to measure left ventricular function

• Failure to monitor electrolytes and kidney function

Acute severe heart failure

For the treatment of acute pulmonary oedema refer to CHAPTER 128.

Device-based heart failure treatments¹

The use of mechanical devices to treat patients with severe failure is gaining momentum. Devices include:

• implantable cardiac defibrillators

• biventricular pacemakers

• left ventricular assist devices (definitive VentrAssist)

The evidence for the efficacy of these devices is good, but limitations include cost and infection. Biventricular pacing or cardiac resynchronisation therapy resynchronises cardiac contraction in patients with systolic CHF and left branch bundle block. VentrAssist is based on a continuous flow rotary blood pump that is surgically implanted in the abdominal wall and attached to the apex of the ventricle.

• Age <65 years

• Uncertainty of diagnosis, especially diastolic heart failure

• Complex management issues (especially with beta blockers, digoxin)

• Familial screening (where appropriate)

• Acute decompensation

• Refractory symptoms

• Device implantation or cardiac transplantation

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Heart failure