Continuing professional development

Chronic heart failure: pathophysiology,

diagnosis and treatment
NOP584 Nicholson C (2014) Chronic heart failure: pathophysiology,
diagnosis and treatment. Nursing Older People. 26, 7, 29-38.
Date of submission: March 18 2014. Date of acceptance: May 23 2014.

Abstract
Heart failure has significant prevalence in older people: the mean average age of patients with the condition is
77. It has serious prognostic and quality of life implications for patients, as well as health service costs. Diagnosis
requires confirmatory investigations and consideration of causative processes. First-line treatment involves
education, lifestyle modification, symptom-controlling and disease-modifying medication. Further treatment may
include additional medications, cardiac devices and surgery. End of life planning is part of the care pathway.

Aims and intended learning outcomes

This article aims to provide an overview of heart failure
for nurses who are not specialists in the condition. It
focuses on chronic, rather than acute, disease. After
reading this article and completing the time out activities
you should be able to:
Summarise the significance of heart failure for older
people in terms of prevalence and clinical outcomes.
Define the key terms used to describe heart failure.
Describe the diagnostic pathway.
Summarise standard treatments.
Detail the lifestyle changes that are prompted
by diagnosis.

cardioprotective effect of female hormones, have a role

(Bhupathy et al 2010).
Heart failure is caused by a number of pathological
conditions (Box 1). Some causes are reversible, but
others are not. Around two thirds of patients with
heart failure in the UK have a history of ischaemic
heart disease (NICE 2010). Other common causes
include hypertension and arrhythmias but the list
of potential causes is extensive (American College
of Cardiology Foundation (ACCF)/American Heart
Association (AHA) 2013).
Patients can have acute heart failure without
underlying chronic heart failure but more commonly

Introduction

Box 1 Causes of heart failure*

Heart failure is a complex syndrome characterised by

reduced heart efficiency and resultant haemodynamic
and neurohormonal responses (Poole-Wilson 1985).
It is common, affecting around one million people in the
UK (National Institute for Health and Care Excellence
(NICE) 2010). Incidence and prevalence are rising as
the population ages and survives more primary cardiac
events (Mosterd and Hoes 2007).
In the UK the average age of patients with the
disease is 77 (Mosterd and Hoes 2007), rising to
80 in hospitalised patients (National Heart Failure
Audit (NHFA) 2013). Gender balance in heart failure
is weighted towards younger men and older women
(NHFA 2013): part of this effect is because women
live longer than men but other factors, such as the

Ischaemic heart disease.

Hypertension.
Arrhythmias.
Valve disorders.
Myocarditis.
Alcohol-induced cardiomyopathy.
Chemotherapy-induced cardiomyopathy.
Genetic cardiomyopathies.
Amyloidosis.
Sarcoidosis.
Metabolic disorders.

NURSING OLDER PEOPLE

Christopher Nicholson is lead

clinician, Cardiac and Respiratory
Service, Minerva Centre,
Lancashire Care NHS Foundation
Trust, Preston
Correspondence
christopher.nicholson@
lancashirecare.nhs.uk
Conflict of interest
None declared
Keywords
Cardiology, cardiovascular
disease, chronic heart failure
This article has been
subject to double-blind review
and checked using antiplagiarism
software. For related articles visit
our online archive and search
using the keywords
Author guidelines
rcnpublishing.com/r/nop-authorguidelines

*This is a shortened list see American College of Cardiology

Foundation/American Heart Association (2013) or McMurray et al
(2012) guidelines for fuller lists

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Continuing professional development

acute presentations are due to destabilisation of
chronic disease. Acute heart failure accounts for 5% of
emergency hospital admissions and 2% of bed days in
the UK on average each year (NICE 2010). The average
length of stay in hospital is 12 days (NHFA 2013). In
the community, heart failure is a frequent reason for GP
appointments and has high medication costs. Managing
patients with the disease is a significant NHS cost.
Patients who are well managed can have a good
quality of life and extend their prognosis, but heart
failure is unpredictable and difficult to prognosticate
for individual patients. Current in-hospital heart failure
mortality is 9%, with 25% of hospitalised patients dying
within one year of admission (NHFA 2013). Patients
who avoid hospitalisation have better outcomes but all
will eventually reach end of life.
Now do time out 1.

Time out

Causes
How many of your caseload of patients, or
the patients you have seen this week, have a
heart failure diagnosis? Using Box 1 (page 29)
list the causes, where known.

Definitions
The terminology used to describe heart failure can be
confusing and jargon is best avoided during patient
communication.
Heart muscle abnormalities are known as
cardiomyopathy and classified as dilated, hypertrophic,
restrictive, or mixed patterns. Dilated cardiomyopathy is
the most common pattern. An enlarged heart is known
as cardiomegaly.
Ventricles are the hearts main pumping chambers
and dysfunction is seen in either or both left
ventricular dysfunction or left ventricular failure and right
ventricular dysfunction or right ventricular failure. Where
both ventricles are impaired, the terms biventricular
dysfunction or biventricular failure are used. The
phrase congestive cardiac failure is sometimes used as
a synonym for biventricular failure but a patient may
have biventricular failure without overt pulmonary or
peripheral congestion. The upper chambers of the heart,
the atria, may also be impaired and/or dilated.
Specific areas of the heart muscle, the myocardium,
may be shown not to move (akinesia) on scanning, may
not move powerfully (hypokinesia) or may not move in
co-ordination with the rest of the myocardium (dyskinesia).
Heart failure can also be defined in terms of where
the impairment is in the phases of the cardiac cycle
during contraction (systole) or relaxation (diastole).
30 September 2014 | Volume 26 | Number 7

The terms are left ventricular systolic dysfunction or left

ventricular diastolic dysfunction.
Pumping efficiency of the heart can be implied from
left ventricular ejection fraction (LVEF) and this important
measure is often used to categorise the severity of heart
failure. The calculation is made by dividing the amount
of blood that leaves the left ventricle on each contraction,
the stroke volume (SV), by the amount of blood in the
left ventricle before contraction, the left ventricular end
diastolic volume (LVEDV). For example, if SV 70ml and
LVEDV 120ml then LVEF 0.58. It is usual to express
LVEF as a percentage and normal range is 50-60%.
The preferred basic description of heart failure is
either heart failure with reduced ejection fraction or heart
failure with preserved ejection fraction (HF-PEF). The
HF-PEF syndrome is linked to diastolic dysfunction and
often seen in older female patients.

Diagnosis
Heart failure should be diagnosed using the pathway
in the European Society of Cardiology (ESC) guidelines
(McMurray et al 2012), as follows.
Clinical presentation (Table 1, pages 32-33) may
raise suspicion but is not sufficient to confirm diagnosis
because these symptoms and signs occur in other
conditions. Once diagnosis is confirmed the severity of
symptoms can be expressed using the New York Heart
Association (NYHA) classification (Box 2) (Criteria
Committee of the NYHA 1994). The NYHA classification
can also be used to monitor progress. Absence of
symptoms and signs does not exclude the heart being
dysfunctional or having structural abnormalities (ACCF/
AHA 2013). Many of the disease processes that occur
with heart failure are on a continuum and will start
before the patient has symptoms. For example, some
patients are at risk of heart failure because they are
genetically predisposed to hypertension, but for diagnosis
investigations should confirm abnormality of cardiac
structure or function.
Box 2 New York Heart Association (NYHA)
classification of heart failure
Class I No limitations to ordinary physical activity.
Class II Slight limitations to ordinary physical
activity with undue breathlessness, fatigue
or palpitations.
Class III Marked limitations to less than ordinary
physical activity with undue breathlessness,
fatigue or palpitations.
Class IV Symptoms may be present at rest and
discomfort made worse with any physical
activity.
(Criteria Committee of the NYHA 1994)

NURSING OLDER PEOPLE

Time out

Diagnosis
Mr Smith is a new nursing home resident. His
only medical history is short-term memory
loss and high blood pressure. He has become
breathless on exertion over the past month
and his ankles have started to swell. What
is the next diagnostic step? Compare what
you have written with the answer given on
page 37.

Comorbidity
Patients with heart failure have more comorbidities
than age-matched controls, and comorbidities have
a significant effect on symptoms, hospitalisations
and prognosis (van Deursen et al 2014). Cardiac
comorbidities may cause heart failure, or sometimes
co-exist with and influence the condition, and prevalence
of cardiac comorbidities increases with age. For example,
the prevalence of atrial fibrillation doubles with each
decade of life (Cleland et al 2002). Hypertension affects
myocardium by ventricular hypertrophy and diastolic
dysfunction, which can present as heart failure with
preserved ejection fraction. Chronic valve dysfunction
NURSING OLDER PEOPLE

progresses with age. Non-cardiac comorbidities can

affect heart failure directly, usually via metabolic effects,
or indirectly through limiting treatment.

Management
Education and self-management Patients and carers
require education about heart failure to develop the staffpatient relationship and improve treatment concordance,
especially in older patients (Anderson et al 2005).
Specific education should address individual adaptation
to the condition, warning signs and what to do in acute
situations. Education empowers patients and increases
successful self-management. For example, some patients
may be given discretion over the dose of their diuretic or
be given monitoring parameters for rapid weight gain.
Lifestyle modification Certain behaviours help the heart
to function either efficiently or inefficiently. For example,
excess alcohol depresses myocardial cell function
and causes dilated cardiomyopathy and arrhythmias.
In smokers, as well as endothelial wall effects, the
immediate release of nicotine contracts arteries,
increasing the risk of ischaemia (Lanza et al 2011).
Obesity and being sedentary adversely affect resting
heart rate and increase cardiac demands. Anaemia
increases cardiac workload (Levick 2009).
Conversely, exercise has significantly positive effects
on symptoms and left ventricular function (Piepoli et al
2004). Good control of comorbid conditions such as
diabetes, hypercholesterolaemia and kidney disease
improves cardiac outcomes. Patients with heart failure
who are hospitalised for another condition have longer
stays and worse outcomes than matched populations
without heart failure (Ahluwalia et al 2012).
How patients can be supported to achieve these
outcomes is outside the scope of this article but is
covered comprehensively in nursing texts, for example,
Nicholson (2007).
Now do time out 3.

3
Time out

Patients with a history of myocardial infarction

(MI) are likely to have heart failure if they present with
potential signs and symptoms. They should have an
urgent, that is, within two weeks, echocardiogram
(NICE 2010). If the patient has no history of MI he or
she should be screened by a 12-lead electrocardiogram
(ECG) and/or a brain natriuretic peptide blood test. Both
have a high negative predictive value if normal the
patient is unlikely to have heart failure. Normal levels of
brain natriuretic peptide are low: they rise slightly with
age and a range of other conditions but are markedly
higher if the heart is under strain. Brain natriuretic
peptide may also be useful in monitoring treatment
response and as a prognostic marker (Januzzi 2012,
van Veldhuisen et al 2013, Troughton et al 2014). If
ECG or brain natriuretic peptide tests are abnormal an
echocardiogram is indicated. Echocardiograms provide
information about heart structure and function. Further
investigations, such as nuclear scans, cardiac magnetic
resonance imaging (MRI) and coronary angiography, may
also be needed.
Once heart failure is confirmed it is important to
consider causes. Some are reversible, such as thyroid
imbalance, whereas others are not. Some require
different prioritisation of treatment: for example, patients
with alcoholic dilated cardiomyopathy must stop
drinking to excess if they do not then prognosis is poor
(Adam et al 2008).
Now do time out 2.

Medications
List the first-line medications used to
treat heart failure. Reflect on how you
would explain to patients how these drugs
work. Remember that some patients will
need a simpler and some a more detailed
explanation.

Medication The mainstay of heart failure treatment

(Table 2, page 34), medication can relieve
symptoms, reduce hospitalisations, shorten length
of stay and improve quality of life and prognosis
(McMurray et al 2012). There are strong evidence bases
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Table 1

Clinical presentation of heart failure

Symptoms
Breathlessness

Acute and/or chronic. Grade using

New York Heart Association (NYHA)
classification look for class changes
(Criteria Committee of the NYHA 1994).
Breathlessness at rest is either acute
decompensation, end-stage condition or
other cause. Confounding comorbidities
like respiratory disease or anaemia.

Peripheral oedema

Oedema settles by gravity so usual

pattern of progression through feet,
ankles, legs, genitalia/sacrum and
abdomen. Oedema due to heart failure
soft, pitting and bilateral. Persistent
oedema can compromise tissue and
secondary cellulitis. Consider alternative
systemic and local causes.

Orthopnoea (shortness of
breath on lying flat)

Soon after lying flat. Relieved by sitting

up. Symptom of acute or advanced
disease. Patients with severe chronic
obstructive pulmonary disease (COPD)
and arthritis may sleep upright.

Loss of appetite

Associated acutely with abdominal

fluid retention and chronically with the
metabolic changes in end-stage disease.

Bloated feeling

Associated acutely with fluid retention

in the abdomen and chronically with
hepatomegaly.

Confusion

Association between heart failure and

progressive cognitive impairment.
Acute confusion with acute metabolic
derangement secondary to heart failure
and/or its treatment.

Palpitations

May be a symptom of sinus tachycardia,

atrial or ventricular arrhythmia, or
ectopic (early or missed heart beats)
all of which are common in heart
failure patients.

Angina (chest pain of

cardiac origin)

May indicate the underlying cause

of heart failure or may be secondary
consequence of poor myocardial
perfusion when cardiac output low.

Syncope (transient loss of

consciousness)

May occur with arrhythmias,

hypotension and valve disorders.

Depression and anxiety

Common symptoms that affect morbidity

and quality of life.

Paroxysmal nocturnal
dyspnoea (PND) (sudden
difficulty breathing at
night)

Soon after going to sleep. Symptom

of acute or advanced disease.
Sometimes with copious, frothy,
even blood-speckled, sputum. Patients
may also wake acutely breathless; as
can patients having panic attacks.

Nocturnal cough

With or without PND.

Sleep disorders

Sleep apnoea and left ventricular

dysfunction associated. Cortisol release
changes sleep patterns in heart failure.

Fatigue

Common symptom but non-specific.

Fatigue patterns and changes over time.
Rule out other causes like anaemia,
nutrition and exercise levels.

Reduced exercise
capacity

Common symptom. Rule out other

causes.

for most treatments but in some areas the evidence is

weaker or lacking (McMurray et al 2012).
The evidence base is from trials of heart failure
with reduced ejection fraction: treatment of heart
failure with preserved ejection fraction does not
have a substantial evidence base at present. Some
treatments, notably diuretics, predate the clinical
trial era and are mainly evidenced by registry
observational level data. Other common drugs,
such as digoxin, have not been specifically trialled in
older adults.
A criticism of many research designs is that they do
not match clinical populations, with lower average ages
32 September 2014 | Volume 26 | Number 7

and fewer comorbidities in trial populations. The mean

average age of UK heart failure patients is 77 years but
in most heart failure randomised controlled trials it is
around 60 years (Witte and Clark 2008).
Trials do usually contain patients aged in their
seventies but people in their eighties are underrepresented so results cannot be unquestionably
applied to all older patients.
Older heart failure patients are often undertreated
or dosed (Witte and Clark 2008). Some older patients
tolerate higher doses of medication less well than
younger patients (Krum et al 2000). Age-related bias
may be a factor in dosing and treatment decisions should
NURSING OLDER PEOPLE

Signs
Tachypnoea

High resting respiratory rate could be

sign of acute heart failure.

Tachycardia

High resting heart rate always

significant and could be haemodynamic
compensatory response. Acute
tachyarrhythmia can provoke heart
failure in a patient with a normal heart
and is likely to make patients with an
abnormal heart unwell.

Abnormal pulse

Displaced apex beat

An irregular pulse could be atrial

fibrillation. A pattern of a regular strong
then weak pulse may be pulse alternans
a sign of advanced heart failure.
The apex beat the point of maximal
impulse on precordium can be
displaced down and left laterally when
the heart is dilated.

Third heart sound/gallop

rhythm

With sinus tachycardia.

Raised jugular venous

pressure

Raised right atrial pressure, usually due

to volume overload.

Heart murmurs

Commonly noted murmurs in

patients with heart failure are mitral
regurgitation, tricuspid regurgitation and
aortic stenosis.

Wheezing

New acute wheezing can be sign

of acute lung congestion. Rule out
alternative respiratory causes like acute
asthma and COPD exacerbation.

Lung crepitation

Sign of possible fluid in lungs secondary

to acute left ventricular failure. Also
occurs in smokers and patients with
respiratory disease.

Weight changes

Rapid weight gain >2-3kg a week may

be fluid retention. Rapid weight loss
may be over-diuresis. Slower weight
gain may be reduced exercise capacity.
Slower weight loss can occur in
end-stage disease.

Basal pleural effusions

Reduced basal air entry can suggest

pleural effusions with/after acute
pulmonary oedema. Pleural effusions
can persist for months.

Hepatomegaly

Enlarged liver can occur with right

heart failure. Consider alternative
causes of hepatomegaly.

Tissue wasting

Patients at end-stage disease with

poor cardiac output can show signs
of cachexia-like muscle wasting the
deltoid and intercostal muscles are
useful sites to check.

Note: Clinical presentation will depend on the patients acuteness, severity of heart failure
and particular pattern of disease. Patients can therefore have some, or even none, of the
above signs and symptoms.

be made after individualised assessment and risk-benefit

analysis, not assumed because of a patients age.
Concern over polypharmacy in older adults is
another factor affecting prescribing practice. Heart
failure patients typically have several medications
prescribed. As treatment has significant positive
effects on mortality, morbidity, hospitalisations and
symptoms, it is arguably not constructive to think of
polypharmacy negatively.
Treatments only work if the clinician and patient
agree about the treatment and then carry it out.
Non-concordance is a significant reason for deterioration
and hospitalisation (van der Wal et al 2005). It is
NURSING OLDER PEOPLE

important to know if patients are not following treatment

plans, which requires open and honest communication,
and then to understand why not. It may be that they
have misunderstood plans or disagree with them, or they
are finding a drug intolerable. There may be age-related
problems that require a specific solution, for example,
incontinence for people with mobility problems on
high-dose diuretics or forgetting to take medicines if
short-term memory loss is present.
Diuretics Diuretics are water tablets: they reduce
sodium and water reabsorption. Patients can retain
fluid due to neurohormonal over-activation. Typically
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Table 2

Medications for heart failure in the UK

Disease-modifying drugs

Initial dose

Full dose

Indication

Bisoprolol

1.25mg once daily (OD)

5mg BD or 10mg OD

Carvedilol

3.125mg twice daily (BD)

25mg or 50mg BD
depending on weight

All patients with left ventricular ejection fraction (LVEF)

<40%. Use with ACE inhibitor.

Nebivolol

1.25mg OD

10mg OD

Beta blockers

Angiotensin-converting enzyme (ACE) inhibitors

Enalapril

2.5mg BD

20mg BD

Lisinopril

2.5mg OD

35mg OD

Ramipril

2.5mg OD

5mg BD

Perindopril

2mg OD

8mg OD

All patients with LVEF <40%. Use with beta blocker.

Angiotensin-receptor blockers (ARBs)

Candesartan

4mg OD

32mg OD

Valsartan

40mg BD

160mg BD

Losartan

50mg OD

150mg OD

All patients with LVEF <40% intolerant of ACE inhibitors

due to cough, or symptomatic patients who are on an ACE
inhibitor but intolerant of MRAs.

Mineralocorticoid-receptor antagonists (MRAs)

Spironolactone

25mg OD

50mg OD

Eplerenone

25mg OD

50mg OD

All symptomatic patients with LVEF <35% despite being

prescribed beta blocker and ACE inhibitor.

Other drugs to assist with symptoms

Loop diuretics
Furosemide

20-40mg

Up to 240mg

Symptomatic patients and those with evidence of pulmonary

or peripheral oedema.

Bumetanide

0.5-1mg

Up to 5mg

Bendroflumethiazide

2.5mg

10mg

Metolazone*

2.5mg

10mg

Indapamide

2.5mg

5mg

Ivabradine

2.5mg

10mg

Symptomatic patients in sinus rhythm with a heart rate >70

despite a beta blocker or if intolerant of a beta blocker.

Digoxin

62.5mcg OD

250mcg OD

Symptomatic patients with persistent symptoms despite a

beta blocker or if intolerant of a beta blocker.

Thiazide diuretics
As either a milder alterative to a loop diuretic or an addition
to a loop diuretic to produce synergistic action.

Heart rate control

Hydralazine and
isosorbide dinitrate

As an alternative in symptomatic patients intolerant to an ACE

inhibitor or ARB. Trial evidence from African-American cohort.

*Note: Metolazone is no longer manufactured in the UK but supplies are still being used up at the time of writing.

34 September 2014 | Volume 26 | Number 7

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patients are on a small maintenance dose of a loop

diuretic such as furosemide or bumetanide which
is increased in dose or supplemented with synergistic
thiazide diuretic if fluid builds. Even without overt
peripheral oedema diuretics can improve breathlessness
by reducing cardiac preload, the amount of fluid
returning to the heart, which affects intracardiac
pressures and vascular congestion.
Diuretics can affect the renal system, fluid and
electrolyte balance, and blood pressure, especially at
higher doses and if more than one type of diuretic is
combined. Patients most vulnerable are those at risk of
dehydration, including some older adults. In patients
with declining renal function diuretic resistance may
necessitate higher doses to achieve the same beneficial
effects but with additional adverse risks of hypotension,
dehydration and acute kidney failure.
Beta blockers Adrenergic neurohormones, part of the
fight or flight autonomic sympathetic nervous system,
stimulate the heart. Blocking adrenoreceptors has
therapeutic benefits including reducing afterload, slowing
heart rate, increasing myocardial perfusion, suppressing
arrhythmias, vasodilation, reducing renin excretion and
improving cardiac remodelling. These physiological
effects improve clinical outcomes.
The Cardiac Insufficiency Bisoprolol Study II
(CIBIS II) found that for every 23 patients with mild
to moderate heart failure treated with the beta blocker
bisoprolol, one life was saved a year, and for every 14
patients with severe heart failure treated with bisoprolol,
one life was saved a year (CIBIS-II Investigators and
Committees 1999).
Beta blockers should be used with care. They
should be introduced when the patient is stable, at
low dose and gradually titrated to the maximum dose
tolerated (optimal dose). Beta blockers should not be
increased if the patient has symptomatic hypotension
or bradycardia. Other potential side effects are postural
hypotension, lethargy, sleep disturbances, worsening
peripheral circulation and diabetic glycaemic control.
Beta blockers are not contraindicated in patients with
chronic obstructive pulmonary disease but patients
with a history of asthmatic bronchospasm
are considered too high risk for beta blockers
(McMurray et al 2012).
The benefits of beta blockers are similar in older
and younger people. All three UK approved beta
blockers for heart failure bisoprolol, carvedilol and
nebivolol have data showing benefits in older patients
(Dulin et al 2005). The Study of the Effects of Nebivolol
Intervention on Outcomes and Rehospitalisation in
Seniors (SENIORS) with heart failure compared patients
older than 85 with those aged 75-85 and found similar
benefits (Flather et al 2005).
NURSING OLDER PEOPLE

Angiotensin-converting enzyme inhibitors and

angiotensin-receptor blockers The renin-angiotensinaldosterone system (RAAS) regulates blood pressure,
plasma volume and electrolyte balance in response
to renal perfusion. In heart failure the system can
be maladaptive, leading to pulmonary oedema as
intracardiac pressures increase as well as volume
expansion, increasing venous return and shifting fluid
into interstitial spaces as peripheral oedema.
Medications mediating the RAAS reduce symptoms,
slow left ventricular dysfunction, prevent hospitalisations,
shorten length of stay and improve morbidity and
prognosis. Mortality was halved in patients with severe
heart failure taking the angiotensin-converting enzyme
(ACE) inhibitor enalapril in the Co-operative North
Scandinavian Enalapril Survival Study (CONSENSUS)
(Swedberg and Kjekshus 1988).
The mortality benefits of enalapril included
asymptomatic patients with left ventricular dysfunction
in the Studies of Left Ventricular Dysfunction-Prevention
(SOLVD-Prevention) (Konstam 1995). The Assessment
of Treatment with Lisinopril and Survival (ATLAS) study
showed better outcomes at higher treatment doses
(Packer et al 1999). Where ACE inhibitors are not
tolerated, usually due to persistent cough, angiotensinreceptor blockers (ARBs) can be substituted.
Studies show that ACE inhibitors are effective in older
adults: the Perindopril in Elderly People with Chronic
Heart Failure (PEP-CHF) study showed that the benefits of
perindopril in patients aged 70 and older were equivalent
to those under the age of 70 (Cleland et al 2006). The
Candesartan in Heart Failure Assessment of Reduction
in Mortality and Morbidity (CHARM) Preserved study
randomised 929 patients aged over 75 and found the
greatest benefits in those aged over 65 compared with
those aged under 65 (Yusuf et al 2003).
Use of ACE inhibitors in older adults has been a
concern because of renal dysfunction and hypotension
risks. Although worsening renal function is associated
with poor prognosis, analysis of the SOLVD-Prevention
found that after ACE inhibitor initiation, worsening renal
function in patients with heart failure did not have a
negative effect on prognosis and the survival benefit from
ACE inhibitors remained (Testani et al 2011).
Chronic kidney disease (CKD) is common and often
more severe with older age. CKD is not a contraindication
to heart failure treatment but care is needed with
diuretics, RAAS drugs and vasodilating drugs due to
hypotension, especially in patients with severe CKD or
renal artery stenosis. Renal physician guidance should be
sought, as per CKD guidelines (NICE 2014).
Mineralocorticoid-receptor antagonists Patients with
left ventricular dysfunction who remain symptomatic
despite beta blockers, ACE inhibitors and ARBs
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Box 3 Device therapy indications*
Device

Criteria

Cardiac resynchronisation therapy

(CRT-P)

Patients in sinus rhythm, left ventricular ejection fraction (LVEF) <35%,

New York Heart Association (NYHA) class III or IV (Criteria Committee
of the NYHA 1994), despite optimised medical therapy, a QRS duration
of >120mS in left bundle branch block, or a QRS>150mS regardless of
QRS morphology, who are expected to survive for more than a year with
good functional status.

CRT-D

Patients with CRT-P indication who also meet the ICD criteria or who
have LVEF <30%.

Implantable cardioverter defibrillator

(ICD)

Primary prevention
Symptomatic heart failure with an LVEF <35% despite three months of
optimised medical therapy and the patient is expected to survive for more
than a year with good functional status.
Secondary prevention
Evidence of ventricular arrhythmia leading to haemodynamic instability
and the patient is expected to survive for more than a year with good
functional status.

*Device therapy indications are based on the evidence from trial populations but there are areas which are uncertain or where trial data are
lacking or limited, such as in patients with atrial fibrillation, right bundle branch block and those with a conventional pacemaker indication who
also have reduced LV function. Therefore, precise practice may vary between clinicians.

Other therapeutic drugs There is not scope in this

article to discuss in detail second-line drugs, such as
nitrates, hydralazine, ivabradine and digoxin. For further
information see Table 2 (page 34) or refer to the ESC
guidelines (McMurray et al 2012).
Drugs to avoid Glitazones, to control diabetes, can
worsen heart failure and increase hospitalisations.
Calcium-channel blockers reduce inotropy, the contractile
force, and can worsen heart failure and increase fluid
retention, although amlodipine and felodipine have
fewer reported incidences of such side effects.
Steroids, non-steroidal anti-inflammatory drugs and
cyclooxygenase-2 inhibitors worsen sodium and water
retention and chronic use should be avoided in patients
with heart failure (McMurray et al 2012).
Now do time out 4.
36 September 2014 | Volume 26 | Number 7

4
Time out

should be considered for mineralocorticoid-receptor

antagonists (MRAs). By blocking aldosterone these
drugs reduce fluid retention and cardiac preload. In
the Randomized Aldactone Evaluation Study (RALES)
involving spironolactone, and Eplerenone Post-AMI
Heart Failure Efficacy and Survival Trial (EPHESEUS),
additional mortality relative risk reductions of 30% and
24% respectively were seen (McMurray et al 2012).
Triple therapy of an ACE inhibitor, ARB and MRA is not
recommended because it significantly increases risk of
acute renal dysfunction.

Optimising treatment
Referring to the patients you noted for time
out 1, add the heart failure drugs they are
prescribed to the list. Are they all on optimal
treatment? If not, is there a documented
reason why not in their records?

Advanced treatments
Cardiac devices Symptomatic patients on optimised
medication might benefit from biventricular pacing, also
known as cardiac resynchronisation therapy (CRT-P).
Criteria for CRT-P are listed in Box 3. A third wire paces
the left ventricle and the device co-ordinates electrical
stimulation of the heart and can improve symptoms and
quality of life significantly. However, around one quarter
of patients who seem suitable for CRT-P do not respond
(Fox et al 2005).
Half of heart failure patients die of arrhythmia.
Ventricular arrhythmia survival is improved with
an implantable cardioverter defibrillator (ICD).
The device can be a stand-alone ICD or with CRT
pacemaker functions (CRT-D). Criteria for ICDs are
listed in Box 3.
Devices are inserted under local anaesthetic
and there are no age restrictions. In patients with
terminal diagnosis, unlikely to survive a year, it is
NURSING OLDER PEOPLE

 Poor left ventricular function and large heart size.

Severity of New York Heart Association (NYHA)
class/symptoms (Criteria Committee of the
NYHA 1994).
High levels of brain natriuretic peptide.
Frequent decompensations/hospitalisations.
Worsening organ failure.
usually inappropriate to implant a device. Patients
require periodic functionality and battery checks.
Devices preclude patients from MRI but not computed
tomography scans, although some patients with devices
have had MRI safely and MRI-safe devices are under
development (Roguin et al 2008).
Cardiac surgery Most patients do not require cardiac
surgery except under specific circumstances. Older age
does not preclude cardiac surgery but is a risk factor for
its safety and success.
If heart failure is secondary to cardiac ischaemia then
revascularisation by percutaneous coronary intervention
or coronary artery bypass grafting is considered. If heart
failure is caused by cardiac valve problems then repair
or replacement is considered. Heart valves are stretched
by a dilated heart and regurgitate, particularly if the
heart is overloaded or in arrhythmia, in which case the
valve problem is secondary and valve surgery is unlikely
to help. If heart failure is due to an aneurysm in the left
ventricle then reconstruction such as the Dor procedure
aneurysmectomy is considered.
Replacing the heart cardiac transplantation is
not common. In the financial year 2013/14 there were
197 UK cardiac transplants (NHS Blood and Transplant
2014). Availability of donor hearts limits this option
and older patients will not usually meet transplant
suitability criteria. Left ventricular assist devices (LVADS)
are implantable mechanical heart pumps. These are
sometimes used to stabilise patients and bridge to
transplant. LVADs are not used as destination therapy at
present in the UK.

End of life
Heart failure causes death through either terminal
pump failure or arrhythmia. Some people die within
months of diagnosis and others survive years, but there
comes a phase when every patient is at the end of life
(Box 4). Recognising end of life is important to plan
changing care needs. Palliative care planning should take
place as for any dying patient, with emphasis on symptom
control. Non-essential medication can be discontinued,
although neurohormonal drugs and diuretics may be
controlling symptoms and stopping them could make some
patients feel worse.
NURSING OLDER PEOPLE

It is difficult to be sure when patients are reaching

end of life. Prognosis is variable because of different
underlying disease pathologies and because patients
respond differently.
Heart failure is characterised by episodes of
decompensation, where the patient seems close to
death but may rally and survive. Treatable causes
of cardiac decompensation for example, chest
infections should always be addressed. Registries
show age is a marker of potential poor prognosis
but that requires qualification: older patients have
more comorbidities and social issues but are not a
homogeneous population.
An additional specific end of life issue is around
cardiac devices. If the patient has an ICD it will
probably detect ventricular arrhythmias as the patient
is dying and defibrillate. This would put the patient and
family through unnecessary distress and the decision is
usually made to deactivate the ICD.
A cardiac technician can do this wirelessly and it is
best planned in advance. Switching off does not hasten
death, it simply allows patients to die without risk of
unwanted defibrillation. Patients with CRT-D devices can
have ICD function switched off and pacemaker function
left on: the pacemaker is probably helping symptom
control. After death, cardiac devices must be removed
before final disposal of the body.
Now do time out 5.

5
Time out

Box 4 Markers of poor prognosis in heart failure

Best practice
Reflect on one patient with heart failure who
you have cared for. Did his or her diagnosis,
treatment and progression fit with best
practice guidelines? What systems were in
place to ensure the patient received optimal
care? If you are unsure, consult the ESC
guidelines (McMurray et al 2012).

Conclusion
Understanding and being able to manage heart failure
is important for patients quantity and quality of life,
regardless of age. It is also important for health service
costs. Heart failure is most common in older adults and
it is expected that the average age of patients will rise.
Nurses have a crucial role in the care of patients but
a multidisciplinary approach is mandatory, including
partnership with older adult services.
Suggested answer to time out 2
A screening test such as brain natriuretic peptide blood
test or ECG. It is possible he has heart failure with the
September 2014 | Volume 26 | Number 7 37

Continuing professional development

6
Time out

history of hypertension and the clinical presentation

so investigations are warranted. As he has not had a
myocardial infarction, an urgent echocardiogram is not
required but, if the screening test is positive, he will
require echocardiogram within six weeks to confirm
diagnosis. If the screening test is negative alternative
causes of his signs and symptoms should
be investigated.

Reflective account
Now that you have completed reading the
article you might like to write a reflective
account. Guidelines to help you are on
page 39.

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