Heart failure 1: pathogenesis, presentation and diagnosis

Copyright EMAP Publishing 2017

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Nursing Practice

Review

Heart failure

Keywords Cardiac dysfunction/

Ejection fraction/NYHA classification

This article has been

double-blind peer reviewed

In this article...

¡ñ P

 athophysiology and aetiology of heart failure

¡ñ Different classifications of heart failure

¡ñ Symptoms, signs and investigations for diagnosing heart failure

Heart failure 1: pathogenesis,

presentation and diagnosis

Key points

Heart failure should

be considered a

syndrome rather

than a disease

The condition means

the heart is unable

to pump enough

blood to meet the

needs of the body

The leading causes

in the developed

world are ischaemic

heart disease and

hypertension

The clinical

diagnosis is based

on clinical

assessment, history

taking, signs and

symptoms,

laboratory and

imaging tests

Authors Selina Jarvis is research nurse and former Mary Seacole development

scholar, King¡¯s Health Partners and Kingston and St George¡¯s University of London;

Selva Saman is consultant, Port Shepstone Regional Hospital, Port Shepstone,

South Africa.

Abstract Heart failure is a common long-term condition with increasing incidence.

More a syndrome than a disease, it can have many causes. The main clinical

symptoms are breathlessness, fatigue and ankle swelling, but these are not specific

to the condition; patients can also present with depression. This article, the first in a

three-part series, describes the pathophysiology, aetiology, clinical presentation and

diagnostic features of this long-term condition. Part two covers management,

treatment options and the crucial role of nurses in supporting and educating patients,

while part three covers the management of heart failure in frail patients.

Citation Jarvis S, Saman S (2017) Heart failure 1: pathogenesis, presentation and

diagnosis. Nursing Times [online]; 113: 9, 49-53.

H

eart failure (HF) is a major

public health problem in the

developed world and one of the

fastest-growing illnesses over

recent decades (World Health Organization, 2011). It is associated with frequent

hospital admissions, high readmission

rates and high morbidity and mortality ¨C

with major costs to the NHS. This first

article in a three-part series explains the

underlying pathophysiology, aetiology,

clinical features and diagnosis of HF.

alamy

Epidemiology and cost

Heart failure is a common long-term condition; it affects 26 million people worldwide (Bui et al, 2011), and in many countries population-based studies have shown

that it affects 1-2% of the general population (Ponikowski et al, 2014). In England,

around 900,000 people have a diagnosis of

HF (NHS England, 2013). Incidence and

prevalence increase with advancing age,

and are likely to rise in the future as the UK

population ages. In terms of prognosis,

Nursing Times [online] September 2017 / Vol 113 Issue 9

50

globally, 17-45% of patients admitted to

hospital die within one year of admission

and the majority die within four to five

years (Ponikowski et al, 2014; L¨®pezSend¨®n, 2011; Hobbs et al, 2007).

Acute HF ¨C whether new-onset in

patients without known cardiac dysfunction or caused by acute decompensation in

those with chronic HF ¨C is a common cause

of hospital admissions and is linked to

high readmission rates in the first six

months after the first admission.

In 2015-16, around 188,000 hospital

inpatient admissions in the UK were

attributed to HF; it remains the leading

cause of hospital admissions in people

aged 65 and over, accounts for 2% of total

NHS expenditure, and the total global cost

of HF has been reported as ?108bn per year

(Cook et al, 2014, Brown and Clarke, 2013).

Understanding heart failure

Definition

There are multiple definitions of HF,

which indicates that it should be



Copyright EMAP Publishing 2017

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Nursing Practice

Review

Fig 1. Pathophysiology of heart failure

Reduced cardiac output from heart failure

Carotid baroreceptor response

Kidney: activation of RAA system

due to low renal perfusion

Increased activity of sympathetic

nervous system

Renin release

Angiotensinogen

Angiotension I

Angiotensinconverting enzyme

Heart rate increased and

positive effects on myocardial

contraction (inotropy)

Angiotension II

Vasoconstriction and

increased BP (increased

afterload for the heart)

Adrenal gland

secretes aldosterone

Pituitary gland secretes

antidiuretic hormone

Sodium and fluid retention,

myocardial fibrosis

Fluid retention

Negative remodelling of the heart and worsening left ventricular function

Sympathetic compensatory mechanism

RAA compensatory mechanism

BP = blood pressure; RAA system = renin-angiotensin-aldosterone system

considered a syndrome rather than a disease (Pearse and Cowie, 2014). The 2016

European Society of Cardiology guidelines

define HF as:

¡°[A] clinical syndrome

characterized by typical symptoms

(e.g. breathlessness, ankle swelling and

fatigue) that may be accompanied by

signs (e.g. elevated jugular venous

pressure, pulmonary crackles and

peripheral oedema) caused by a

structural and/or functional cardiac

abnormality, resulting in a reduced

cardiac output and/or elevated

intracardiac pressures at rest or

during stress¡± (Ponikowski et al, 2016).

Pathophysiology

The heart acts as the pump that, through

coordinated muscle activity, supplies the

organs and tissues of the body with oxygenated blood. To function properly, it

must undergo proper relaxation to aid

appropriate filling of blood during diastole, and have coordinated contraction

dependent on a functional heart muscle

(or myocardium) during systole. In HF, the

heart is unable to pump enough blood to

meet the body¡¯s needs; this may be due ¨C

among other causes ¨C to abnormalities of

the heart muscle after a myocardial infarction, or problems with heart valves or

heart rhythm. HF can affect the left or the

Nursing Times [online] September 2017 / Vol 113 Issue 9

51

right ventricle, and is consequently

referred to as left or right HF.

In patients with HF, cardiac output

(stroke volume multiplied by the heart

rate) is reduced. As a result, two tightly

regulated compensatory mechanisms are

activated (Fig 1):

l S

 ympathetic compensatory

mechanism ¨C the baroreceptors sense

a decrease in blood pressure (BP),

leading to the release of catecholamine

(noradrenaline), which stimulates

beta-1 adrenoceptor cells in the heart.

This culminates in an increased heart

rate, contraction and stroke volume,

which will increase the cardiac output.



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Although it can be helpful in the short

term to maintain cardiac output, in the

long term the mechanism can be

damaging and actually exacerbate HF;

l R

 enin-angiotensin-aldosterone (RAA)

compensatory mechanism ¨C the

underperfusion due to reduced BP is

detected by the kidneys. This activates

the RAA pathway, which controls

BP and electrolyte balance.

Vasoconstriction, salt and fluid

retention are some of the

consequences. In the short term,

this maintains organ perfusion, but

in the long term, it exacerbates cardiac

dysfunction and remodelling.

Some of the pharmacological treatments discussed in part two of this article

target these sympathetic and RAA compensatory responses.

Aetiology

The aetiology of HF is diverse and there is

geographical variation, so the underlying

cause of the cardiac dysfunction should

always be determined in patients presenting with suspected HF. In the developed world, ischaemic heart disease and

hypertension are the leading causes, while

rheumatic heart disease leading to valvular

dysfunction is more likely in developing

countries (Pearse and Cowie, 2014). The

main causes of HF are shown in Table 1.

Classifying heart failure

According to severity of symptoms

HF can be classified according to the

symptoms and degree of limitation of

physical activity. One classification system

is that of the New York Heart Association

(NYHA), which encompasses four main

classes (NYHA, 1994) (Table 2). The use of

the NYHA classification has been questioned in recent years, but it is still the

most widely used, both in clinical practice

and when deciding which treatment

options are best for a particular patient.

Many clinical trials recruit and report on

patient outcomes according to NYHA

class. The American College of Cardiology/

American Heart Association has produced

a staging tool for HF, which is sometimes

used (Hunt et al, 2001) (Table 2).

Cardiac function or structure

Regardless of aetiology, the consequence

of HF is a decline in the pump function of

the heart. This may lead to the patient

experiencing progressive episodes of acute

decompensation, further reducing the

ability of the heart to fill with or eject blood

(Abraham et al, 2017). Ejection fraction

Table 1. Aetiology of heart failure

Cause

Diseased myocardium

Ischaemic heart disease

Toxic

Immune mediated

Infiltrative

Metabolic/nutritional

Genetic abnormalities

Abnormal loading

Hypertension

Valve problems

Pericardial

Volume overload

High output state

Arrhythmias

Tachyarrhythmias

Bradyarrhythmias

Examples

Myocardial scar, coronary artery disease

Alcoholic cardiomyopathy, cocaine, anabolic steroids,

drugs, copper, iron

Infections, autoimmune diseases

Amyloidosis, sarcoidosis, haemochromatosis, metastases

Thyroid storm, phaeochromocytoma, diabetes, thiamine

deficiency

Muscular dystrophies, hypertrophic cardiomyopathy,

arrhythmogenic right ventricular cardiomyopathy

Essential and secondary hypertension

Acquired and congenital valvular abnormalities

Constrictive pericarditis, pericardial effusions

Renal failure, iatrogenic fluids

Severe anaemia, sepsis, thyrotoxicosis

Atrial and ventricular tachycardias

Sinus node or conduction disorders

Source: Adapted from Ponikowski et al (2016)

(the percentage of blood ejected from the

left ventricle per beat) can vary between

patients, but ultimately the process culminates in similar symptoms and signs.

There are different categorisations of HF

based on left ventricular ejection fraction

(LVEF) (Ponikowski et al, 2016) (Table 3):

l I n HF with reduced ejection fraction

(HFrEF), the condition affects the

contraction of the heart muscle and the

systolic function of the heart is

affected; in this case the LVEF is 18/min)

l Oxygen saturation 400 pg/ml (116pmol/L) or NTproBNP level >2,000pg/ml (236pmol/L)

should be referred for urgent transthoracic

Doppler 2D echocardiography and see a

specialist within two weeks (NICE, 2017).

Transthoracic Doppler 2D echocardiography is the most widely used imaging

technique as it can add structural information about the heart, help exclude cardiac

valvular disease and quantify ejection fraction. It can be used diagnostically and is

performed in the vast majority of patients

presenting with an acute exacerbation of

HF (National Institute for Cardiovascular

Outcomes Research, 2015).

Conclusion

Once a diagnosis of HF has been made,

patients should be seen by the HF specialist team. How the disease is managed

will depend on the underlying aetiology,



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Table 2. Classification of heart failure

NYHA classification according to severity of symptoms

Class I: Patient is comfortable with ordinary physical activity, but elevated activity causes symptoms such as fatigue and

shortness of breath

Class II: Patient is comfortable at rest, but ordinary physical activity causes symptoms

Class III: Even light activity causes patient fatigue, heart palpitation or shortness of breath

Class IV: Patient shows symptoms at rest and any physical activity only increases the discomfort

ACC/AHA staging tool

Stage A: Patient at high risk of developing heart failure with no structural disorder of the heart

Stage B: Patient with structural disorder of the heart without symptoms of heart failure

Stage C: Patient with past or current symptoms of heart failure associated with underlying structural heart disease

Stage D: Patient with end-stage disease who requires specialised treatment strategies

Key: ACC = American College of Cardiology; AHA = American Heart Association; NYHA = New York Heart Association.

Source: Adapted from Hunt et al (2001) and New York Heart Association (1994)

Table 3. Criteria for diagnosing heart failure according to left ventricular impairment

HFrEF

HFmrEF

HFpEF

Symptoms

and signs

Breathlessness, ankle swelling,

fatigue, elevated jugular

venous pressure, pulmonary

crackles, peripheral oedema

Breathlessness, ankle swelling,

fatigue, elevated jugular venous

pressure, pulmonary crackles,

peripheral oedema

Breathlessness, persistent coughing,

wheeze, ankle swelling, lack of

appetite or nausea, elevated jugular

venous pressure, pulmonary crackles,

peripheral oedema

LVEF

35pg/ml) and/or

NT-proBNP (>125pg/ml)

2. Plus either:

a. Diastolic dysfunction

b. Relevant structural heart disease

1. Elevated BNP (>35pg/ml) and/or

elevated NT-proBNP (>125pg/ml)

2. Plus either:

a. Diastolic dysfunction

b. Relevant structural heart disease

Key: BNP = brain natriuretic peptide; HFmrEF = heart failure with mid-range ejection fraction; HFpEF = heart failure with preserved ejection fraction;

HFrEF = heart failure with reduced ejection fraction; LVEF = left ventricular ejection fraction; NT-proBNP = N-terminal pro-B-type natriuretic peptide.

Source: Adapted from Ponikowski et al (2016)

precipitating factors, type of cardiac dysfunction and NYHA status (NICE, 2017).

Nurses have a vital role in caring for

patients with HF and helping them understand their condition. NT

¡ñ Part two of this series (page 54) covers

pharmacological and non-pharmacological

treatment options, self-care and the role

of nurses. Part three, to be published in

October, covers the management of

heart failure in frail patients.

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Cook C et al (2014) The annual global economic

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Hobbs FD et al (2007) Prognosis of all-cause heart

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For more on this topic go online...

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care in acute coronary syndrome

Bit.ly/NT_ACS



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