icc cronica fisiopatologia 2014

8/15/2019 ICC Cronica Fisiopatologia 2014

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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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September 2014 | Volume 26 | Number 7 NURSING OLDER PEOPLE

ontinuing professional development

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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31URSING OLDER PEOPLE September 2014 | Volume 26 | Number 7

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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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.

am A, Nicholson C, Owens L (2008)

oholic dilated cardiomyopathy. Nursing

ndard . 22, 38, 42-47.

uwalia S, Gross C, Chaudhry S et al

12) Impact of comorbidity on mortality

ong older persons with advanced heart

ure. Journal of General Internal Medicine.

5, 513-519.

erican College of Cardiology Foundation/

erican Heart Association (2013) Guideline

the management of heart failure. A

ort of the American College of Cardiology

ndation/American Heart Association Task

ce on practice guidelines. Circulation.

ps://circ.ahajournals.org/content/128/16/

0.extract (Last accessed: August 8 2014.)

derson C, Deepak B, Amoateng-Adjepong Y

al (2005) Benefits of comprehensive inpatient

cation and discharge planning combined

h outpatient support in elderly patients

h congestive heart failure. Congestive Heart

ure. 11, 6, 315-321.

upathy P, Haines C, Leinwand L (2010)

uence of sex hormones and phytoestrogens

heart disease in men and women. Women’s

alth. 6, 1, 77-95.

IS-II Investigators and Committees

99) The Cardiac Insufficiency Bisoprolol

dy II (CIBIS-II): a randomised trial. The

ncet . 353, 9146, 9-13.

land J, Chattopadhyay S, Khand A et al

02) Prevalence and incidence of arrhythmias

sudden death in heart failure. Heart Failure

views. 7, 3, 229-242.

land J, Tendera M, Adamus J et al (2006)

perindopril in elderly people with chronic

rt failure (PEP-CHF) study. European Heart

rnal. 27, 19, 2338-2345.

eria Committee of the New York Heart

ociation (1994) Nomenclature and Criteria

Diagnosis of Diseases of the Heart and

at Vessels. Ninth edition. Little, Brown & Co,

ton MA.

Dulin B, Haas S, Abraham W et al (2005) Do

elderly systolic heart failure patients benefit

from beta blockers to the same extent as the

non-elderly? Meta-analysis of >12,000 patients

in large-scale clinical trials. American Journal of

Cardiology . 95, 7, 896-898.

Flather M, Shibata M, Coats A et al (2005)

Randomized trial to determine the effect of

nebivolol on mortality and cardiovascularhospital admission in elderly patients with

heart failure (SENIORS). European Heart

Journal . 26, 3, 215-225.

Fox D, Fitzpatrick A, Davidson N (2005)

Optimisation of cardiac resynchronisation

therapy: addressing the problem of ‘non-

responders’. Heart . 91, 8, 1000-1002.

Januzzi J Jr (2012) The role of natriuretic

peptide testing in guiding chronic heart

failure management: review of available data

and recommendations for use. Archives of

Cardiovascular Diseases. 105, 1, 40-50.

Konstam M (1995) Angiotensin converting

enzyme inhibition in asymptomatic left

ventricular systolic dysfunction and early

heart failure. European Heart Journal . 16,

Suppl N, 59-64.

Krum H, Ninio D, MacDonald P (2000) Baseline

predictors of tolerability to carvedilol in

patients with chronic heart failure. Heart .

84, 6, 615-619.

Lanza G, Careri G, Crea F (2011) Mechanisms

of coronary artery spasm. Circulation.

124, 16, 1774-1782.

Levick J (2009) An Introduction to

Cardiovascular Physiology . Fifth edition.

Butterworth Heinemann, Oxford.

McMurray J, Adamopoulos S, Anker S et al

(2012) ESC Guidelines for the diagnosis

and treatment of acute and chronic heart

failure 2012. European Heart Journal.

33, 14, 1787-1847.

Mosterd A, Hoes A (2007) Clinical

epidemiology of heart failure. Heart .

93, 9, 1137-1146.

NHS Blood and Transplant (2014) Organ

Donation and Transplantation – Activity

Figures for the UK as at 11 April 2014. www.

organdonation.nhs.uk/statistics/downloads/

annual_stats.pdf (Last accessed: July 25 2014.)

National Heart Failure Audit (2013) National

Heart Failure Audit April 2012-March 2013 .

www.ucl.ac.uk/nicor/audits/heartfailure/

documents/annualreports/hfannual12-13.pdf

(Last accessed: August 8 2014.)

National Institute for Health and Care

Excellence (2010) Chronic Heart Failure:

Management of Chronic Heart Failure in

Adults in Primary and Secondary Care. Clinical

guideline 108. NICE, London.

National Institute for Health and Care

Excellence (2014) Chronic Kidney Disease:

Early Identification and Management of Chronic

Kidney Disease in Adults in Primary and

Secondary Care. Clinical guideline 182 . NICE,

London.

Nicholson C (2007) Heart Failure: A Clinical

Nursing Handbook . John Wiley and Sons,Chichester.

Packer M, Poole-Wilson P, Armstrong P et al

(1999) Comparative effects of low and high

doses of the angiotensin-converting enzyme

inhibitor, lisinopril, on morbidity and mortality

in chronic heart failure. ATLAS Study Group.

Circulation. 100, 23, 2312-2318.

Piepoli M, Davos C, Francis D et al

(2004) Exercise training meta-analysis of

trials in patients with chronic heart failure

(ExTraMATCH). BMJ . 328, 7433, 189-196.

Poole-Wilson P (1985) Heart failure. Medicine

International . 2, 7, 866-871.

Roguin A, Schwitter J, Vahlhaus C et al (2008)

Magnetic resonance imaging in individuals with

cardiovascular implantable electronic devices.

Europace. 10, 3, 336-346.

Swedberg K, Kjekshus J (1988) Effects of

enalapril on mortality in severe congestive

heart failure: results of the Cooperative

North Scandinavian Enalapril Survival Study

(CONSENSUS). American Journal of Cardiology .

62, 2, 60A-66A.

Testani J, Kimmel S, Dries D et al (2011)

Prognostic importance of early worsening

renal function after initiation of angiotensin-converting enzyme inhibitor therapy in patients

with cardiac dysfunction. Circulation. Heart

Failure. 4, 6, 685-691.

Troughton R, Michael Felker G, Januzzi J

Jr (2014) Natriuretic peptide-guided heart

failure management. European Heart Journal.

35, 1, 16-24.

van Deursen V, Damman K, van der Meer P

et al (2014) Co-morbidities in heart failure.

Heart Failure Reviews . 19, 2, 163-172.

van der Wal M, Jaarsma T, van Veldhuisen D

(2005) Non-compliance in patients with heart

failure; how can we manage it? European

Journal of Heart Failure. 7, 1, 5-17.

van Veldhuisen D, Linssen G, Jaarsma T et al

(2013) B-type natriuretic peptide and prognosis

in heart failure patients with preservedand reduced ejection fraction. Journal

of the American College of Cardiology .

61, 14, 1498-1506.

Witte K, Clark A (2008) Carvedilol in the

treatment of elderly patients with chronic

heart failure. Clinical Interventions in Aging.

3, 1, 55-70.

Yusuf S, Pfeffer M, Swedberg K et al (2003)

Effects of candesartan in patients with chronic

heart failure and preserved left-ventricular

ejection fraction: the CHARM-Preserved Trial.

The Lancet . 362, 9386, 777-781.

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 .

icc cronica fisiopatologia 2014

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