icc cronica fisiopatologia 2014
TRANSCRIPT
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URSING OLDER PEOPLE September 2014 | Volume 26 | Number 7 29
Continuing professional development
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-author-
guidelines
Chronic heart failure: pathophysiology,diagnosis and treatment
OP584 Nicholson C (2014) Chronic heart failure: pathophysiology,
iagnosis and treatment. Nursing Older People. 26, 7, 29-38.
ate 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
equires confirmatory investigations and consideration of causative processes. First-line treatment involves
education, lifestyle modification, symptom-controlling and disease-modifying medication. Further treatment may
nclude additional medications, cardiac devices and surgery. End of life planning is part of the care pathway.
Box 1 Causes of heart failure*
■ Ischaemic heart disease.
■ Hypertension.■ Arrhythmias.
■ Valve disorders.
■ Myocarditis.
■ Alcohol-induced cardiomyopathy.
■ Chemotherapy-induced cardiomyopathy.
■ Genetic cardiomyopathies.
■ Amyloidosis.
■ Sarcoidosis.
■ Metabolic disorders.
*This is a shortened list – see American College of Cardiology
Foundation/American Heart Association (2013) or McMurray et al
(2012) guidelines for fuller lists
ims and intended learning outcomes
is article aims to provide an overview of heart failure
nurses who are not specialists in the condition. It
cuses on chronic, rather than acute, disease. After
ading this article and completing the time out activities
u 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.
troduction
eart failure is a complex syndrome characterised by
duced heart efficiency and resultant haemodynamic
d neurohormonal responses (Poole-Wilson 1985).
s common, affecting around one million people in the
K (National Institute for Health and Care Excellence
ICE) 2010). Incidence and prevalence are rising as
e population ages and survives more primary cardiac
ents (Mosterd and Hoes 2007).
In the UK the average age of patients with the
sease is 77 (Mosterd and Hoes 2007), rising to
0 in hospitalised patients (National Heart Failure
dit (NHFA) 2013). Gender balance in heart failure
weighted towards younger men and older women
HFA 2013): part of this effect is because women
e longer than men but other factors, such as the
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
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1 Causes
T i m e o u t 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.
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 averagelength 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.
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 heart’s 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).
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 importantmeasure 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)
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Patients with a history of myocardial infarction
I) are likely to have heart failure if they present with
tential signs and symptoms. They should have an
gent, that is, within two weeks, echocardiogramICE 2010). If the patient has no history of MI he or
e should be screened by a 12-lead electrocardiogram
CG) and/or a brain natriuretic peptide blood test. Both
ve a high negative predictive value – if normal the
tient is unlikely to have heart failure. Normal levels of
ain natriuretic peptide are low: they rise slightly with
e and a range of other conditions but are markedly
gher if the heart is under strain. Brain natriuretic
ptide may also be useful in monitoring treatment
sponse and as a prognostic marker (Januzzi 2012,
n Veldhuisen et al 2013, Troughton et al 2014). If
CG or brain natriuretic peptide tests are abnormal an
hocardiogram is indicated. Echocardiograms provideormation about heart structure and function. Further
vestigations, such as nuclear scans, cardiac magnetic
sonance imaging (MRI) and coronary angiography, may
so be needed.
Once heart failure is confirmed it is important to
nsider causes. Some are reversible, such as thyroid
balance, whereas others are not. Some require
ferent prioritisation of treatment: for example, patients
th alcoholic dilated cardiomyopathy must stop
nking to excess – if they do not then prognosis is poor
dam et al 2008).
Now do time out 2.
omorbidity
tients with heart failure have more comorbidities
an age-matched controls, and comorbidities have
significant effect on symptoms, hospitalisations
d prognosis (van Deursen et al 2014). Cardiac
morbidities may cause heart failure, or sometimes
-exist with and influence the condition, and prevalence
cardiac comorbidities increases with age. For example,
e prevalence of atrial fibrillation doubles with each
cade of life (Cleland et al 2002). Hypertension affects
yocardium by ventricular hypertrophy and diastolic
sfunction, which can present as heart failure with
eserved ejection fraction. Chronic valve dysfunction
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 staff-
patient 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 heartto 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.
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
2 Diagnosis
T i m e o u t 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.
3 Medications
T i m e o u t
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.
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able 1 Clinical presentation of heart failure
Symptoms
Breathlessness Acute and/or chronic. Grade usingNew 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.
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.
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.
Peripheral oedema Oedema settles by gravity so usualpattern 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.
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 retentionin 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.
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
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 under-
represented 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
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gns
chypnoea High resting respiratory rate could be
sign of acute heart failure.
chycardia 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.
normal pulse 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.
splaced apex beat The apex beat – the point of maximal
impulse on precordium – can be
displaced down and left laterally when
the heart is dilated.
ird heart sound/gallop
ythm
With sinus tachycardia.
ised jugular venous
essure
Raised right atrial pressure, usually due
to volume overload.
eart murmurs Commonly noted murmurs in
patients with heart failure are mitral
regurgitation, tricuspid regurgitation and
aortic stenosis.
heezing 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 acutepulmonary 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 patient’s acuteness, severity of heart failure
and particular pattern of disease. Patients can therefore have some, or even none, of the
above signs and symptoms.
made after individualised assessment and risk-benefit
alysis, not assumed because of a patient’s age.
Concern over polypharmacy in older adults is
other factor affecting prescribing practice. Heart
lure patients typically have several medications
escribed. As treatment has significant positive
ects on mortality, morbidity, hospitalisations and
mptoms, it is arguably not constructive to think of
lypharmacy negatively.
Treatments only work if the clinician and patient
ree about the treatment and then carry it out.
on-concordance is a significant reason for deterioration
d hospitalisation (van der Wal et al 2005). It is
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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able 2 Medications for heart failure in the UK
isease-modifying drugs Initial dose Full dose Indication
eta blockers
isoprolol 1.25mg once daily (OD) 5mg BD or 10mg OD All patients with left ventricular ejection fraction (LVEF)
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tients are on a small maintenance dose of a loop
uretic – such as furosemide or bumetanide – which
increased in dose or supplemented with synergistic
azide diuretic if fluid builds. Even without overtripheral oedema diuretics can improve breathlessness
reducing cardiac preload, the amount of fluid
urning to the heart, which affects intracardiac
essures and vascular congestion.
Diuretics can affect the renal system, fluid and
ectrolyte balance, and blood pressure, especially at
gher doses and if more than one type of diuretic is
mbined. Patients most vulnerable are those at risk of
hydration, including some older adults. In patients
th declining renal function diuretic resistance may
cessitate higher doses to achieve the same beneficial
ects but with additional adverse risks of hypotension,
hydration and acute kidney failure.
ta blockers Adrenergic neurohormones, part of the
ght or flight’ autonomic sympathetic nervous system,
mulate the heart. Blocking adrenoreceptors has
erapeutic benefits including reducing afterload, slowing
art rate, increasing myocardial perfusion, suppressing
rhythmias, vasodilation, reducing renin excretion and
proving cardiac remodelling. These physiological
ects improve clinical outcomes.
The Cardiac Insufficiency Bisoprolol Study II
BIS II) found that for every 23 patients with mild
moderate heart failure treated with the beta blocker
soprolol, one life was saved a year, and for every 14
tients with severe heart failure treated with bisoprolol,
e life was saved a year (CIBIS-II Investigators and
mmittees 1999).
Beta blockers should be used with care. They
ould be introduced when the patient is stable, at
w dose and gradually titrated to the maximum dose
erated (‘optimal’ dose). Beta blockers should not be
creased if the patient has symptomatic hypotension
bradycardia. Other potential side effects are postural
potension, lethargy, sleep disturbances, worsening
ripheral circulation and diabetic glycaemic control.
ta blockers are not contraindicated in patients with
ronic obstructive pulmonary disease but patients
th a history of asthmatic bronchospasm
e considered too high risk for beta blockers
cMurray et al 2012).
The benefits of beta blockers are similar in older
d younger people. All three UK approved beta
ockers for heart failure – bisoprolol, carvedilol and
bivolol – have data showing benefits in older patients
ulin et al 2005). The Study of the Effects of Nebivolol
ervention on Outcomes and Rehospitalisation in
niors (SENIORS) with heart failure compared patients
der than 85 with those aged 75-85 and found similar
nefits (Flather et al 2005).
Angiotensin-converting enzyme inhibitors and
angiotensin-receptor blockers The renin-angiotensin-
aldosterone system (RAAS) regulates blood pressure,
plasma volume and electrolyte balance in responseto 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, angiotensin-
receptor 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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4 Optimising treatment
T i m e o u t Referring to the patients you noted for time
out 1, add the heart failure drugs they areprescribed to the list. Are they all on optimal
treatment? If not, is there a documented
reason why not in their records?
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.
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.
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
Box 3 Device therapy indications*
Device Criteria
Cardiac resynchronisation therapy(CRT-P)
Patients in sinus rhythm, left ventricular ejection fraction (LVEF) 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
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ually inappropriate to implant a device. Patients
quire periodic functionality and battery checks.
vices preclude patients from MRI but not computed
mography scans, although some patients with devices
ve had MRI safely and MRI-safe devices are under
velopment (Roguin et al 2008).
rdiac surgery Most patients do not require cardiac
rgery except under specific circumstances. Older age
es not preclude cardiac surgery but is a risk factor for
safety and success.
If heart failure is secondary to cardiac ischaemia then
vascularisation by percutaneous coronary intervention
coronary artery bypass grafting is considered. If heart
lure is caused by cardiac valve problems then repair
replacement is considered. Heart valves are stretched
a dilated heart and regurgitate, particularly if the
art is overloaded or in arrhythmia, in which case the
ve problem is secondary and valve surgery is unlikely
help. If heart failure is due to an aneurysm in the left
ntricle then reconstruction – such as the Dor procedure
eurysmectomy – is considered.
Replacing the heart – cardiac transplantation – is
t common. In the financial year 2013/14 there were
97 UK cardiac transplants (NHS Blood and Transplant
014). Availability of donor hearts limits this option
d older patients will not usually meet transplant
itability criteria. Left ventricular assist devices (LVADS)
e implantable mechanical heart pumps. These are
metimes used to stabilise patients and ‘bridge’ to
nsplant. LVADs are not used as destination therapy at
esent in the UK.
nd of life
eart failure causes death through either terminal
mp failure or arrhythmia. Some people die within
onths of diagnosis and others survive years, but there
mes a phase when every patient is at the end of life
ox 4). Recognising end of life is important to plan
anging care needs. Palliative care planning should take
ace as for any dying patient, with emphasis on symptom
ntrol. Non-essential medication can be discontinued,
hough neurohormonal drugs and diuretics may be
ntrolling symptoms and stopping them could make some
tients feel worse.
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 andfamily 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.
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
5 Best practice
T i m e o u t 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).
ox 4 Markers of poor prognosis in heart failure
■ Poor left ventricular function and large heart size.
■ Severity of New York Heart Association (NYHA)
class/symptoms (Criteria Committee of theNYHA 1994).
■ High levels of brain natriuretic peptide.
■ Frequent decompensations/hospitalisations.
■ Worsening organ failure.
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September 2014 | Volume 26 | Number 7 NURSING OLDER PEOPLE
ontinuing professional development
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 willrequire echocardiogram within six weeks to confirm
diagnosis. If the screening test is negative alternative
causes of his signs and symptoms should
be investigated.
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eferences
6 Reflective account
T i m e o
u t Now that you have completed reading the
article you might like to write a reflectiveaccount. Guidelines to help you are on
page 39.
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C o p y r i g h t o f N u r s i n g O l d e r P e o p l e i s t h e p r o p e r t y o f R C N P u b l i s h i n g C o m p a n y a n d i t s
c o n t e n t m a y n o t b e c o p i e d o r e m a i l e d t o m u l t i p l e s i t e s o r p o s t e d t o a l i s t s e r v w i t h o u t t h e
c o p y r i g h t h o l d e r ' s e x p r e s s w r i t t e n p e r m i s s i o n . H o w e v e r , u s e r s m a y p r i n t , d o w n l o a d , o r e m a i l
a r t i c l e s f o r i n d i v i d u a l u s e .