Heart failure 1: pathogenesis, presentation and diagnosis
嚜澧opyright EMAP Publishing 2017
This article is not for distribution
Nursing Practice
Review
Heart failure
Keywords Cardiac dysfunction/
Ejection fraction/NYHA classification
This article has been
double-blind peer reviewed
In this article...
♂ P
athophysiology and aetiology of heart failure
♂ Different classifications of heart failure
♂ 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 每
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車pezSend車n, 2011; Hobbs et al, 2007).
Acute HF 每 whether new-onset in
patients without known cardiac dysfunction or caused by acute decompensation in
those with chronic HF 每 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 每
among other causes 每 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 每 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 每 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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Nursing Practice
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cardiology
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
♂ 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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Brown R, Clarke AL (2012) Reducing the cost of
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Bui AL et al (2011) Epidemiology and risk profile of
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Cook C et al (2014) The annual global economic
burden of heart failure. Int J Cardiol 15: 368-76
Hobbs FD et al (2007) Prognosis of all-cause heart
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Hunt SA et al (2001) ACC/AHA guidelines for the
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Bit.ly/NICEHFPathway
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and Great Vessels, 9th edn. Boston, MA: Lippincott
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For more on this topic go online...
l Diagnosis, management and nursing
care in acute coronary syndrome
Bit.ly/NT_ACS
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