Heart Failure

Introduction

Definition

Heart failure is a complex clinical syndrome in which the heart fails to meet the metabolic demands of the body. It can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. A diagnosis of heart failure is based on the presence of a triad of typical symptoms (shortness of breath on exertion and at rest, fatigue), signs (tachycardia, tachypnoea, raised jugular venous pressure, peripheral oedema, and pulmonary congestion), and objective evidence of a structural or functional cardiac abnormality (cardiomegaly, abnormal echocardiogram, raised natriuretic peptide concentration). A clinical response to treatment directed at heart failure alone (e.g. diuretic use) may be a useful adjunct but is not sufficient to establish the diagnosis.

Epidemiology and prognosis

Heart failure is the fastest-growing cardiovascular disease, affecting 2-3% of the overall population. The prevalence rises with age, affecting between 10% and 20% of the population aged over 70 years. Although recent epidemiological studies indicate improved survival, the overall prognosis remains poor, with mortality exceeding 50% at 5 years. The primary causes of death are either progressive pump failure or sudden cardiac death secondary to ventricular arrhythmia. Morbidity also remains poor, with a high rate of rehospitalization (up to 50% in a year), placing a significant burden on national healthcare systems.

Pathophysiology

The origin of symptoms in heart failure is poorly understood. An initial event (infarction, inflammation, pressure/volume overload) causes myocardial damage, resulting in an increase in myocardial wall stress. This is followed by the activation of multiple neuroendocrine systems including the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the release of cytokines such as tumour necrosis factor (TNF). Neuroendocrine activation is also accompanied by structural and metabolic changes in the peripheral skeletal muscle and by abnormalities in cardiopulmonary reflex function such as the baroreflex and chemoreflex. These produce further wall stress, perpetuating this vicious cycle (see Fig. 7.1).

Fig. 7.1 Pathophysiology of heart failure. LV = left ventricle; LVEF = left ventricular ejection fraction.

Forms of heart failure

Acute vs. chronic heart failure

The clinical manifestations depend on the speed with which the syndrome develops. Acute heart failure is often used to describe the patient with acute-onset dyspnoea and pulmonary oedema, but can also apply to cardiogenic shock where the patient is hypotensive and oliguric. Compensatory mechanisms have not yet become operative. Acute deterioration may be a consequence of myocardial infarction (MI), arrhythmia, or acute valve dysfunction (e.g. endocarditis). See

Acute pulmonary oedema: assessment, p. 724.

Systolic vs. diastolic heart failure

Most patients with heart failure have evidence of both systolic (failure of the ventricle to eject blood) and diastolic (failure of the ventricle to relax and fill with blood) dysfunction. Patients with diastolic heart failure have symptoms and signs of heart failure with a preserved LVEF. Current studies indicate that more than 50% of heart failure patients have a normal or near-normal ejection fraction (EF), and their prognosis appears to be similar to that of those with systolic heart failure. The terms diastolic heart failure, heart failure with normal ejection fraction (HFNEF), and heart failure with preserved ejection fraction are used interchangeably.

Right vs. left heart failure

Right and left heart failure refers to whether the patient has either predominantly systemic venous congestion (swollen ankles, hepatomegaly) or pulmonary venous congestion (pulmonary oedema). These terms do not necessarily indicate which ventricle is most seriously affected.

Fluid retention in heart failure is due to a combination of factors: reduced glomerular filtration rate (GFR), and activation of the renin-angiotensin-aldosterone system, and sympathetic system. However, remember there are causes for swollen ankles other than heart failure (gravitational disorder, e.g. immobility, venous thrombosis or obstruction, varicose veins, hypoproteinaemia, e.g. nephrotic syndrome or liver disease, lymphatic obstruction).

High-output vs. low-output heart failure

A variety of high-output states may lead to heart failure, e.g. thyrotoxicosis, Paget’s disease, beri-beri, and anaemia. This is characterized by warm extremities and normal or widened pulse pressure. The arterial-mixed venous oxygen saturation (a marker of the ability of the heart to deliver oxygen to the metabolizing tissues) is typically normal or even low in highoutput heart failure. In contrast, low-output states are characterized by cool pale extremities, cyanosis due to systemic vasoconstriction, and low pulse volume. The arterial-mixed venous oxygen saturation is typically abnormally high in low-output states.

Causes and precipitants

In all patients with heart failure, it is important to carefully consider the underlying aetiology, as there may be specific exacerbating factors or other diseases that influence the patients’ management. A non-exhaustive list is given below.

Aetiology of heart failure

Ischaemic heart disease (accounting for 70% of patients with heart failure in the developed world)
Idiopathic dilated cardiomyopathy (unknown aetiology, up to 50% may be familial)
Valve disease (accounting for 10% of patients with heart failure)
Hypertension (the primary cause of heart failure in patients of African-Caribbean descent)

Alcoholic cardiomyopathy
Post viral
Peripartum cardiomyopathy
Infiltrative disease (amyloidosis, sarcoidosis)
Connective tissue disease
Iatrogenic (chemotherapy, radiotherapy)
Infections (Chagas’ disease, human immunodeficiency virus (HIV))
Thyroid disease (severe hypo- or hyperthyroidism)
Haemochromatosis
Nutritional (beri-beri)

Patients with compensated heart failure have a high rate of readmission to hospital with acute exacerbations. A number of studies have demonstrated that a precipitating cause for emergency admission to hospital with heart failure can be identified in up to two-thirds of patients.

Inappropriate reduction in therapy: self-discontinuation or iatrogenic withdrawal of diuretics, angiotensin-converting enzyme inhibitor (ACE-I), digoxin, as well as dietary excess of salt are recognized precipitants. Education of the patient/family is important.
Cardiac arrhythmias: most commonly atrial fibrillation (AF), but any tachyarrhythmia will further reduce LV filling and stroke volume, and may exacerbate ischaemia. Marked bradycardia reduces cardiac output, especially if stroke volume cannot increase any further.
Myocardial ischaemia or infarction: exacerbates LV dysfunction, and may worsen mitral regurgitation (MR) due to ischaemia of papillary muscles.
Infection: respiratory infections are more common, but any systemic sepsis can precipitate heart failure due to a combination of factors such as direct myocardial depression from inflammatory cytokines, sinus tachycardia, fever, etc.
Anaemia: this causes a high-output state that may precipitate acute heart failure, and may exacerbate underlying ischaemia.
Concomitant drug therapy: drugs that directly depress myocardial function (e.g. calcium antagonists—verapamil, diltiazem; many antiarrhythmics, anaesthetics, over-enthusiastic initiation of β-blockers, etc.), as well as drugs causing salt and water retention (e.g. non-steroidal antiinflammatory drugs (NSAIDs), oestrogens, steroids, COX-2 antagonists) may precipitate heart failure.
Alcohol: this is directly toxic and, in excess, can depress myocardial function as well as predispose to arrhythmias.
Pulmonary embolism: the risk increases in the immobile patient with low-output state and AF.

It is very important to look for precipitating causes in all patients with heart failure. Once the precipitant has been identified and treated, appropriate measures (patient and family/education, adjustment of therapy, etc) should be put into place to prevent recurrence. See Table 7.1.

Table 7.1 Population-attributable risk of heart failure related to various risk factors^a

Risk factor	Attributable risk (%)
Coronary disease	61.6
Cigarette smoking	17.1
Hypertension	10.1
Physical inactivity	9.2
Male sex	8.9
<High school education	8.9
Overweight	80
Diabetes	3.1
Valvular heart disease	2.2
^aHe, J, Ogden LG, Bazzano LA, et al (2001). Risk factors for congestive heart failure in US men and women: NHANES 1 Epidemiologic follow-up study. Arch Intern Med 161: 996.

Conditions mimicking heart failure

Obesity
Chest disease—including lung, diaphragm, or chest wall
Venous insufficiency in lower limbs.
Drug-induced ankle swelling (e.g. dihydropyridine calcium blockers)
Drug-induced fluid retention (e.g. NSAIDs)
Hypoalbuminaemia

Intrinsic renal disease
Intrinsic hepatic disease
Pulmonary embolic disease
Depression and/or anxiety disorders
Severe anaemia
Thyroid disease
Bilateral renal artery stenosis

Signs and symptoms

The evaluation of a heart failure patient should start with a comprehensive history and clinical examination. Primary symptoms can be attributed to either reduced cardiac output or fluid accumulation, and include:

fatigue
dyspnoea (on exertion or at rest)
orthopnoea
paroxysmal noctural dyspnoea
peripheral oedema
chest pain

palpitations (tachycardia)
hypotension
raised jugular venous pressure (JVP)
displaced apex beat
gallop rhythm (3rd heart sound)
cahexia.

It is important to remember that heart failure is a multisystem disorder affecting every single aspect of a patient’s body. It is not unusual for patients to present with:

gastrointestinal symptoms secondary to congestive hepatomegaly, ascites, reduced bowel perfusion, and oedema (abdominal distension and pain, anorexia, bloating, nausea, constipation, jaundice)
genitourinary symptoms secondary to impaired renal perfusion (oliguria/anuria, urinary frequency, nocturia)
cerebrovascular symptoms secondary to cerebral hypoperfusion and associated electrolyte abnormalities (confusion, memory impairment, anxiety, headaches, insomnia, bad dreams or nightmares, psychosis with disorientation, delirium, or hallucinations)
musculoskeletal symptoms (gout, carpal tunnel syndrome, muscle cramps).

Many of these signs can be difficult to elicit particularly in a noisy emergency or outpatient clinic. Even in study conditions, the reproducibility and inter-observer agreement of the presence of signs is low. Despite this, a clinical diagnosis of heart failure can be made with some certainty when multiple signs are present in the same patient (see Table 7.2).

Symptoms alone can be used to classify the severity of congestive heart failure (CHF) and to monitor the effect of treatment, although the link between symptoms and degree of LV dysfunction is weak. The New York Heart Association classification (NYHA) is widely used.

NYHA classification of heart failure

Class I	No limitation of physical activity.
Class II	Slight limitation of physical activity—symptoms with ordinary levels of exertion (e.g. walking up stairs).
Class III	Marked limitation of physical activity—symptoms with minimal levels of exertion (e.g. dressing).
Class IV	Symptoms at rest.

An alternative classification system of heart failure is the ‘Stages of Heart Failure’ proposed by the American College of Cardiology (ACC) and the American Heart Association (AHA). This classification system places particular emphasis on the progressive nature of the heart failure, and defines the appropriate therapeutic approach for each stage (see Table 7.2). Unlike the NYHA classification, this system is unidirectional and therefore cannot be used as a means of assessing the patient’s response to treatment. See also Fig. 7.2.

Table 7.2 ACC/AHA stages of heart failure

Stage A	Stage B	Stage C	Stage D
At high risk for developing heart failure (HF) but without identified structural or functional heart disease, symptoms or signs of HF	Structural or functional heart disease but without symptoms or signs of HF	Structural or functional heart disease with current or prior symptoms or signs of HF	Refractory HF symptoms despite maximal medical therapy
e.g. patients with: hypertension, atherosclerosis, diabetes, obesity, metabolic syndrome	e.g. previous MI, left ventricular hypertrophy, reduced EF, valvular lesions	e.g. known structural heart disease with associated dyspnoea, fatigue, oedema	e.g. marked symptoms on minimal exertion or at rest, hospitalized patients

Fig. 7.2 Algorithm summarizing recommendations for the diagnosis of heart failure.

*Alternative methods of imaging the heart should be considered when a poor image is produced by transthoracic Doppler 2D-echocardiography—alternatives include transoesophageal echocardiography (TOE), radionuclide imaging, or cardiac magnetic resonance imaging (MRI).

BNP = B-type natriuretic peptide; ECG = electrocardiogram; FBC = full blood count; LFTs = liver function tests; NTproBNP = N-terminal pro-B-type natriuretic peptide; TFTs = thyroid function tests; U&Es = urea and electrolytes.

Investigations

Investigations for all patients with heart failure

ECG: although there are no specific changes in heart failure, a normal ECG is observed in only 2% of cases and should encourage the clinician to consider an alternative diagnosis in the absence of firm clinical signs. Common findings include: sinus tachycardia/bradycardia, arrhythmias, voltage criteria for left ventricular hypertrophy (LVH), evidence of current or past ischaemia/infarction, and conduction system defects.
Chest X-ray (CXR): permits assessment of pulmonary congestion and may demonstrate other non-cardiac causes of dyspnoea. Common findings include: cardiomegaly, pulmonary congestion with alveolar oedema, prominent upper lobe vessels, ‘bat’s wings’ and Kerley B lines and pleural effusions (see Fig. 7.3).
Echocardiography (ECHO): this is the key investigation in patients with HF and is mandatory for confirming the diagnosis. Apart from documenting systolic and diastolic left ventricular function, the scan is useful in the identification of various causes or complications of heart failure (see Table 7.3). If an echocardiogram does not confirm a diagnosis of HF despite suggestive clinical symptoms and signs, consider an alternative diagnosis or a referral for a specialist review.
Natriuretic peptides: evidence exists supporting the use of plasma concentrations of natriuretic peptides for diagnosing, staging, or even identifying patients at risk for clinical events. A normal plasma concentration in an untreated patient has a high negative predictive value, making HF an unlikely cause of symptoms.
Blood tests: FBC, U&Es, LFTs, TFTs, glucose, uric acid.

Investigations to consider for selected patients with heart failure

Blood tests: troponin I or T, iron studies, folate, vitamin B₁₂, autoimmune screen, immunoglobulins and protein electrophresis, serum ACE
Viral titres
Urine sample: albumin/creatinine ratio, 24-hour urine collection for protein, catecholamines, Bence-Jones protein
Arterial blood gases
Pulmonary function tests
Exercise testing
Ambulatory ECG monitoring (QT dispersion, heart-rate variability)
Stress imaging
Radionucleotide ventriculography
Cardiac magnetic resonance
Coronary angiography (computed tomography (CT) or conventional)
Myocardial biopsy
Right-heart catheterization.

Table 7.3 Conditions predisposing to or complicating heart failure that may be identified by echocardiography

Echocardiographic findings	Examples of possible aetiology
Identification of anatomical defects	Atrial septal defect (ASD), ventricular septal defect (VSD)
Valvular pathology	Aortic valve or mitral valve stenosis or insufficiency
Pericardial disease	Acute or chronic pericarditis Constrictive pericarditis Pericardial effusion
Identification of regional ventricular wall motion abnormalities	Ischaemic heart disease
Altered myocardial architecture	Hypertrophic cardiomyopathy Infiltrative diseases (amyloidosis)
Estimation of pulmonary artery pressure	Pulmonary hypertension (cor pulmonale as a result of primary pulmonary hypertension or secondary to lung disease)
Identifying complications of reduced ventricular function	Intramural thrombus secondary to ventricular dilatation, reduced contraction, or aneurysm

Fig. 7.3 CXR findings in heart failure. (a) There is cardiomegaly with prominent upper lobe vessels and alveolar oedema (‘Bat’s wing shadowing’); (b) magnification of the right costophrenic angle showing septal lines (Kerley B lines) due to interstitial oedema.

Management of heart failure

Management outline in chronic heart failure

Establish a firm diagnosis of HF
Attempt to determine the aetiology and ascertain the severity of HF
Correct precipitating or exacerbating factors
Multidisciplinary approach to treatment (HF is a complex syndrome necessitating the involvement of a number of healthcare professionals in the community and secondary care including: general practiitoner (GP), cardiologist, electrophysiologist, cardiac surgeon, heart failure nurse, cardiac rehabilitation team, dietician, psychologist, expert in sexual dysfunction)
Education of the patient and relatives (see Table 7.4)
Monitor progress and manage accordingly.

Objectives of treatment

Reduce mortality
Reduce morbidity (to improve quality of life by relieving symptoms, increasing exercise capacity, reducing the need for hospitalization and providing end-of-life care)
Prevention (can be divided into two separate entities: (1) prevention of cardiovascular risk factors that may lead or contribute to the development of heart failure, i.e. hypertension, diabetes, obesity, and (2) prevention of progression of myocardial damage, remodelling, and reoccurrence of symptoms once HF is established).

Fig 7.4 summarizes a treatment algorithm for patients with symptomatic HF and reduced systolic function.

Table 7.4 Essential topics in patient education with associated skills and appropriate self-care behaviours

Educational topics	Skills and self-care behaviours
Definition and aetiology of heart failure	Understand the cause of heart failure and why symptoms occur
Symptoms and signs of heart failure	Monitor and recognize signs and symptoms Record daily weight and recognize rapid weight gain Know how and when to notify healthcare provider Use flexible diuretic therapy if appropriate
Pharmacological treatment	Understand indications, dosing, and effects of drugs Recognize the common side-effects of each drug
Risk-factor modification	Understand the importance of smoking cessation Monitor blood pressure if hypertensive Maintain good glucose control if patient has diabetes Avoid obesity
Diet recommendation	Sodium restriction if prescribed Avoid excessive fluid intake Modest intake of alcohol Monitor and prevent malnutrition
Exercise recommendation	Be reassured, comfortable about physical activity Understand the benefits of exercise Perform exercise training regularly
Sexual activity	Discuss problems with healthcare professionals Be reassured about engaging in sexual intercourse and understand specific sexual problems and various coping strategies
Immunization	Receive immunization against infections such as influenza and pneumococcal disease
Sleep and breathing disorders	Recognize preventive behaviour such as reducing weight in obese, smoking cessation, abstinence from alcohol Learn about treatment options if appropriate
Adherence	Understand the importance of following treatment recommendations Maintain motivation to follow treatment plan
Psychosocial aspects	Understand that depressive symptoms and cognitive dysfunction are common in patients with HF, and the importance of social support Learn about treatment options if appropriate
Prognosis	Understand important prognostic factors and make realistic decisions Seek psychosocial support if appropriate
ESC guidelines for the diagnosis and treatment of acute and chronic heart failure (2008). Eur Heart J 29: 2388-2442.

Fig. 7.4 Treatment algorithm for patients with symptomatic heart failure and reduced systolic function. Adapted from ESC (2008). Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 29: 2388-2442 and NICE guidelines

www.nice.org. ARB = angiotensin receptor blocker; LVAD = left ventricular assist device.

Diuretics in heart failure

Diuretics provide symptomatic relief from pulmonary and systemic congestion by reducing fluid overload.
With the exception of aldosterone antagonists (spironalactone and eplerenone), diuretics do not offer any significant prognostic benefit.
Loop diuretics cause more pronounced diuresis (and natriuresis), and are the option of choice in patients with moderate to severe heart failure.
A thiazide may be used in combination with loop diuretics for resistant oedema. Regular monitoring is required to avoid dehydration, hyponatraemia, hypokalaemia, and hypomagnesimia.
Diuretics cause activation of the renin-angiotensin-aldosterone system and should be used in combination with an ACE-I/ARB when possible.
Start with a low dose (especially in diuretic-naive patients and the elderly) and increase the dose until clinical improvement occurs.
Once fluid overload resolves, readjust the diuretic dose to avoid dehydration. Aim to maintain ‘dry weight’ with the lowest dose possible.
Self-adjustment of the diuretic dose based on daily weight measurements and other clinical signs of fluid retention should be part of the patient education.
It is essential to monitor potassium, sodium, and creatinine levels during diuretic therapy.

Practical considerations in the treatment of heart failure with loop diuretics

See Table 7.5.

Table 7.5 Considerations in the treatment of heart failure with loop diuretics

Problems	Suggested action
Hypokalaemia/hypomagnesaemia	Increase ACE-I/ARB dosage Add aldosterone antagonist Potassium supplements Magnesium supplements
Hyponatraemia	Fluid restriction Stop thiazide diuretic or switch to loop diuretic Reduce dose/stop loop diuretics if possible Consider arginine vasopressin (AVP) antagonist if available Intravenous (IV) inotropic support Consider ultrafiltration
Hyperuricaemia/Gout	Consider allopurinol For symptomatic gout use colchicine for pain relief Avoid NSAIDs
Hypovolaemia/dehydration	Assess volume status Consider reduction of diuretic dosage
Insufficient response or diuretic resistance	Check compliance, fluid and salt intake Review other drugs (NSAIDs, steroids) Increase dose of diuretic Consider switching from furosemide to bumetanide or torasemide Add aldosterone antagonist Combine loop diuretic and thiazide/metolazone Administer loop diuretic twice daily or on empty stomach Consider short-term IV infusion of loop diuretic Consider low-dose dopamine infusion
Renal failure (excessive rise in urea and/or creatinine)	Check for hypovolaemia/dehydration Exclude use of other nephrotoxic agents, e.g. NSAIDs, trimethoprim Withhold aldosterone antagonist If using concomitant loop and thiazide diuretic stop thiazide diuretic Consider reducing dose of ACE-I/ARB Consider ultrafiltration
Adapted from ESC (2008). Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 29: 2388-2442.

Diuretic doses used in patients with heart failure

See Table 7.6.

Table 7.6 Diuretic doses used in patients with heart failure

Diuretics	Initial dose (mg)	Usual daily dose (mg)
Loop diuretics^a
Furosemide	20-40	40-240
Bumetanide	0.5-1.0	1-5
Torasemide	5-10	10-20
Thiazides^b
Bendroflumethiazide	2.5	2.5-10
Hydrochlorothiazide	25	25-100
Metolazone	2.5	2.5-10
Indapamide	2.5	2.5-5
Potassium-sparing diuretics^c
Spironolactone/eplerenone	12.5-25	50
Amiloride	2.5	5-20
Triamterene	25	50
Adapted from ESC (2008). Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 29: 2388-442.
^aHigher doses may be required in individuals with renal impairment; excessive doses however may cause renal impairment and ototoxicity. ^bDo not use thiazides if estimated GFR (eGFR)<30 mL/min, except when prescribed synergistically with loop diuretics. ^cAldosterone antagonists should always be preferred to other potassium-sparing diuretics.

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Tags: Oxford Handbook of Cardiology

Jul 22, 2016 | Posted by drzezo in CARDIOLOGY | Comments Off

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