Transcript Heart Failure

Susie Bowell
BA (Hons) RGN
Heart Failure Specialist Nurse
RGN BA (Hons)
The very essence of cardiovascular practice is the early
detection of heart failure’
Sir Thomas Lewis, 1933
Heart failure (HF) is a complex clinical syndrome of symptoms and
signs that suggest impairment of the heart as a pump
supporting physiological circulation.
It is caused by structural or functional abnormalities of the heart.
The demonstration of objective evidence of these cardiac
abnormalities is necessary for the diagnosis of heart failure to
be made.
NICE GUIDELINES, 2010
30-40% of newly diagnosed will die within one year
After the first year there is a less than
10% per year mortality rate
NICE 2010
Incidence and hospital admissions are predicated to
rise by 50% over the next 25 years due to ageing
demographics and the success in treating Ischaemic
Heart Disease.
Mean age of HF patient 74years
Prevalence approx. 8‐10% in over 75s have
heart failure
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The diagnosis of HF-REF (systolic) requires
three conditions to be satisfied:
1. Symptoms typical of HF
2. Signs typical of HF
3. Reduced LVEF
The diagnosis of HF-PEF (Diastolic)
requires four conditions to be satisfied:
1. Symptoms typical of HF
2. Signs typical of HF
3. Normal or only mildly reduced LVEF
and LV not dilated
4. Relevant structural heart disease (LV
hypertrophy/LA
enlargement) and/or diastolic dysfunction
ESC Guidelines 2012
NEW YORK HEART ASSOCIATION CLASSIFICATION OF
HEART FAILURE (NYHA)
CLASS I
Impaired Left Ventricular but no
symptoms
CLASS II
Breathless on moderate exertion e.g. 2
flights of stairs, walking briskly, walking
uphill
CLASS III
Breathless during everyday activities,
e.g. walking around the house
CLASS IV
Symptoms at rest, e.g. unable to eat a
meal comfortably without dyspnoea
Over the last 10 years it has become evident that almost half the
patients with heart failure syndrome do not have Left Ventricular
Systolic Dysfunction (LVSD) and have a preserved ejection fraction (EF).
There is a lack of universal agreement on the threshold of
ejection fraction (EF) at which LVSD and HF with preserved
ejection fraction (HFPEF) are defined.
Some experts maintain that there is impaired
contraction of the long axis of the left ventricle
in HFPEF.
Others that HFPEF is synonymous with diastolic heart failure.
A drop in cardiac output is immediately sensed in baro-receptors in
the aortic arch and carotid sinus.
This results in stimulation of the sympathetic nervous system and
adrenal medulla.
Adrenaline is released from the adrenal medulla into the circulation.
Nor-adrenaline is released at nerve endings.
This results in the stimulation of cardiac and vascular alpha (α) and
beta (β) receptors
Stimulation of α receptors results in ↑ vasoconstriction of both arterial
and venous system
Stimulation of β receptors results in ↑ contractility of the myocardium
↑ increased heart rate
Immediate
α effects:
↑ arterial BP
 Protection of blood supply to vital vascular beds (cerebral and
coronary)
 Long term effects - ↑ afterload and vascular resistance causes ↑myocardial
oxygen demand (and potentially ischaemia) and ↓ perfusion of non essential
vascular beds.
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Immediate
β effects:
↑ inotropy (myocardial contractility)
↑ chronotropy (increased heart rate)
↑ lusitropy (diastolic relaxation)
Stimulates renin release in kidneys
Long term effects – ↑ cardiac rhythm disturbances, premature apoptosis,
↓ chronic down regulation of the system
As heart failure has a poor prognosis, early pharmacological
treatment is important and can have a great affect on future
prognosis. The improved prognosis of heart failure patients with
left ventricular systolic dysfunction in the last decade is likely to be
related to the greater use of and earlier intervention with,
pharmacological treatment.
Mortality within the first month of diagnosis remains
high at 6%.
Diagnosis and Treatment
Studies show diagnosis incorrect
in approx 40‐50% of cases
based on signs and symptoms.
An echocardiogram is essential
for diagnostic purposes4
Chest crepitations, oedema,
tachycardia –not specific
S3, ↑JVP, displaced apex –
insensitive, poor inter‐observer
agreement
Many patients have symptoms
only –dyspnoea, fatigue are
non specific
1.
Refer patients with suspected heart failure and previous myocardial
infarction (MI) urgently, to have echocardiography and specialist
assessment within 2 weeks.
2.
Measure serum natriuretic peptides BNP or NTproBNP in patients with
suspected heart failure without previous MI.
3.
Because very high levels of serum natriuretic peptides carry a poor
prognosis, refer patients with suspected heart failure and a BNP level above
400 pg/ml (116 pmol/litre) or an NTproBNP level above 2000 pg/ml (236
pmol/litre) urgently, to have transthoracic Doppler 2D echocardiography
and specialist assessment within 2 weeks.
NICE HF GUIDELINES 2010
Perform an ECG and consider the following tests to evaluate possible
aggravating factors and/or alternative diagnoses:
chest X-ray
blood tests:
electrolytes, urea and creatinine, eGFR (estimated glomerular filtration rate)
Thyroid function tests
Liver function tests
Fasting lipids
Fasting glucose
Full blood count
Urinalysis
Peak flow or spirometry.
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Natriuretic Peptides
Vasodilatory neurohormones
Released from the ventricles
in respond to wall
stress/strain
Effects are:
Natriuresis and diuresis
Suppression of the RAAS and
sympathetic tone
NTproBNP more stable than
BNP.
Raised in LVSD and HFPEF
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Cut off levels in European
Society of Cardiology
guidelines lower than NICE.
Be aware that affected by
ACE, BB’s and diuretics
especially.
If entirely normal, HF can be
ruled out.
If used in conjunction with an
ECG – guide to patient
needing an echo.
Currently being funded by
CCG for central patients.
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There are several conditions that may affect the serum NP levels
beyond heart failure – for example
Left Ventricular Hypertrophy,
Ischaemia,
Tachycardia,
Right Ventricular overload,
Hypoxaemia (including pulmonary embolism),
Renal dysfunction,
Sepsis,
Advanced age and
Cirrhosis of the liver.
Levels may be lower in obesity and in females
Results should be interpreted in the context of current
pharmacological treatment
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A high natriuretic peptide level is not only of diagnostic significance, but also of
prognostic significance.
Thresholds:
BNP>400 pg/ml (>116 pmol/l) or NT-proBNP>2000 pg/ml (>236 pmol/l): Need an
echocardiogram and specialist clinical assessment no longer than 2 weeks from the
time of presentation.
BNP 100-400 pg/ml (29-116 pmol/l) or NT-proBNP 400-2000 pg/ml (47-236 pmol/l):
Need an echocardiogram and clinical assessment by the Specialist within 6 weeks
from the time of presentation.
BNP <100 pg/ml (<29 pmol/l) or NT-proBNP <400 pg/ml (<47 pmol/l), in the absence
of heart failure therapy: Heart Failure is an unlikely cause for the presentation
HFREF
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Ejection fraction (EF)
Valves –
stenosis/regurgitation
Wall motility/evidence of
ischaemia
Congenital abnormalities
Signs of infection
Signs of clot formation
Normal blood flow
Pulmonary Artery Pressure
HFPEF
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Wall size
EF >50%
LV End diastolic dimensions
Mitral valve velocities
Left atrial pressures and
dimensions
+ measurements as left
Prevention, delay or regression of cardiac remodelling
Prevention of sudden arrhythmic death
Improved quality and increased quantity of life
Reduced morbidity
Prevention/reduction of end organ damage
Prevention of remodelling of the myocardium
Achieved by interference with neuroendocrine systems known to
promote cardiac remodelling and myocyte apoptosis –
Causes of Death
NYHA II
NYHA III
CHF
12%
CHF
Other
26%
59%
Sudden
Death
24%
64%
15%
n = 103
Other
Sudden
Death
n = 103
NYHA IV
33%
11%
CHF
Other
56%
Sudden
Death
n = 27
MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized
intervention trial in congestive heart failure (MERIT-HF). LANCET. 1999;353:2001-07.
ACE inhibitors – Titrate to maximum tolerated dose
ARBs: if ACE I intolerant. candesartan/valsartan
Betablockers -bisoprolol or carvedilol - maximum tolerated dose; Nebivolol for>70yrs
Aldosterone receptor antagonists: spironolactone, eplerenone
Stop agents that exacerbate HF: NSAIDs, verapamil, diltiazem doxazosin,
dronedarone, class I Anti Arrhythmic Drugs, glitizones
Loop diuretics: as low a dose as possible to achieve euvolaemia
Consider –
Ivabradine: for some patients in SR if HR>70 despite max
tolerated BB
Hydralazine/ ISDN if ACEI/ARB intolerant
Digoxin: sometimes AF, occasionally in SR
ACE Inhibitor/ARB (all NYHA)
ACE first. ARB’s if ACE not tolerated – titrate to maximum tolerated dose.
Contra-indications:
Renal Artery stenosis – if suspected – US scan prior to use.
Previous angioedema associated with ACE inhibitor therapy (rare <1% more
frequently in African Americans) – ARB’s may be better tolerated
Caution in patients with:
Impaired renal function (follow guidelines for use)
Aortic valve stenosis or cardiac outflow obstruction
Hypovolaemia or dehydration
HF patients can often tolerate a low blood pressure – continue if patient is
asymptomatic and U+E’s satisfactory.
It is better to reduce than stop ACE/ARB
In most cases ACE/ARBs can be continued if the decline in eGFR is<30% over
4 months from baseline.
An ACE licensed for heart failure should always be used prior to an ARB.
Ramipril may have a less hypotensive affect than Lisinopril
Some ACE/ARB is better than none, however, always titrate to maximum
evidenced for optimal prevention of remodelling, blocking of the RAAS and
reduction in hospitalisations.
Consider an ARB licensed for heart failure as an alternative to an ACE
inhibitor for patients with heart failure due to left ventricular systolic
dysfunction who have intolerable side effects with ACE inhibitors. ARB’s are
less likely to cause angioedema, however it can occur.
Monitor serum urea, electrolytes, creatinine and eGFR for signs of renal
impairment or hyperkalaemia.
β-blocker (all NYHA)
Reduce absolute annual mortality by 6-8%
Contra-indications – true brittle asthma
COPD with reversibility
Any greater than 1st degree heart block
To reduce cardiac oxygen and energy demand, remodelling and premature apoptosis,
titrate to maximum tolerated recommended dose.
Remember some beta-blocker is better than no beta-blocker – if necessary, take
titration very slowly and monitor HR, BP and clinical response.
HR TARGET APPROX 60-70 BPM
There is no evidence that selective betablockers will worsen these patients‟
pulmonary function. (Salpeter 2005).
Beta-blockers are often avoided in patients with peripheral vascular disease for
fear of exacerbating intermittent claudication, but this concern is
unfounded (Radack 1991).
Switch stable patients who are already taking a beta-blocker for a co-morbidity
(for example, angina or hypertension), and who develop heart failure due
to left ventricular systolic dysfunction, to a beta-blocker licensed for heart
failure. [new to NICE GUIDELINES 2010
Clinical tips:
Transient pulmonary congestion could occur at times during uptitration of beta-blockers. If clinically indicated, diuretics can
ameliorate symptoms during introduction and titration of
betablockers and the use (or increase if necessary) of diuretics
should be considered at this stage to aid titration.
In order to promote adherence the patient should be informed that
they may feel worse/more fatigued before they feel better due to
the blunting of the beta-adrenergic response.
Try to titrate to trail evidence to maximise betablockade which in
turn helps reduce stimulation of the RAAS.
Patients may not feel a real benefit for up to three months post
maximal titration – they should be informed of the mortality
benefits and and the importance to their heart of persistence with
betablockade. Titration can be taken as slow as necessary.
Bisoprolol is generally better tolerated in patients, however
Carvedilol may be more useful in patients with PVD due to its
alpha blocking qualities
Spironolactone in NYHA III‐IV
RALES: All‐Cause Mortality
Risk reduction 30%
Aldosterone receptor antagonist + ACE inhibitor + loop diuretic
± digitalis placebo
Eplerenone in post MI NYHA II heart failure –
EMPHASIS-HF
Trial stopped early because of significant benefit
37% reduction in primary end point
24% reduction in cardiovascular death
42% reduction in hospitalisation for HF
Recommended for additional treatment once beta-blockers and ACE Inhibitors
have been titrated for further symptomatic control.
Provide additional blocking of the Renin Angiotensin system
The general side effects of this class of drug are hyperkalaemia and renal
impairment and gynaecomastia with Spironolactone.
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The current Chronic heart failure evidence reviewed suggests that
Spironolactone should be used in severe chronic heart failure (NYHA Class
III-IV) when ACE/ARB and betablocker titrated. Eplerenone should be used
in the patients with heart failure following myocardial infarction and should
ideally be introduced within the first two weeks post MI.
Enhances inotropy of cardiac muscle
Reduces activation of SNS and RAAS
Fourth line treatment for symptomatic patients.
Not always only in patients in AF
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Reduces symptoms
Decreases risk of HF progression
Reduces hospitalisation rates for
decompensated HF
Does not improve survival
Trial data shows deterioration in symptoms if
stopped
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Works on the sino atrial node on the If channel
Only to be used in sinus rhythm – not suitable for patients
in atrial fibrillation
Slows heart rate without reducing blood pressure
Can be used to help titrate beta blockers. If beta blockers
can only be titrated slowly, a low dose of Ivabradine can be
used to slow the heart rate in the mean time, beta blockade
can be increased slowly dependent upon heart rate, patient
tolerance and blood pressure and then the Ivabradine can
be discontinued or maintained if additional HR control is
required to maintain target dose.
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Loop diuretics:
Furosemide and Bumetanide
(40mg Furosemide = 1mg Bumetanide)
Bumetanide has better bioavailability
Strong thiazide diuretics like Metolazone should only be used with
caution and very temporarily as they can reduce renal function
quickly. U+Es should be monitored after approximately 3 days use
and their effects monitored closely
Diuretics do not treat HF, they only treat the symptoms and
unnecessary use can deteriorate renal function and result in
increased dosage requirement in decompensation
May have more of a place in HFPEF than LVSD, however HFPEF
patients are less tolerant of a greatly reduced preload
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Diuretics should always be considered for titration down as well as up during a
patient review. However, the patient needs to be educated on the signs of
decompensation if they are to be down titrated.
Increased blockade of the RAAS can result in the reduction of the need for
diuretic therapy in LVSD, however, they may be necessary during titration of
betablockade. Always assess patient stability prior to alteration and encourage a
balance of potassium/sodium intake which may require a reduction in salt for
the patient as frequently patients are taking far more than the recommended
daily allowance.
To reduce requirement for diuretics, a stable intake of fluids of approximately 2
litres/day is recommended for heart failure patients.
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Explain to the patient the importance of performing a daily weight, 1 st thing in
the morning before drinking or eating and after using the toilet. This should,
ideally, be recorded by the patient. An increase of 2-3kg (2-3 litres) over approx
2-3 days could indicate early decompensation and the patient needs to inform
you for adjustment of their diuretic therapy to avoid hospital admissions, the
need for IV diuretics and further decompensation.
There is an increasing incidence of cardio-renal syndrome. At end stage HF
decompensation is a lot harder to manage if the renal function is reduced
and the response to diuretics is poor.
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NSAIDS
Diltiazem and Verapamil – associated with a worse prognosis
Amlodipine is the only calcium channel blocker recommended for
additional bp control in systolic heart failure. No recommendations
yet for HFPEF
Nicorandil – review necessity as Nicorandil is not recommended for
LVSD if the patient has low filling pressures
Doxazosin not recommended – Doxazosin arm of ALLHAT trial
stopped early due to markedly increased incidence of heart failure
in patients
Review long term use of Amiodarone regularly (NICE guidelines)
Class 1c anti-arrhythmic therapy is not recommended in HF and
associated with a worse prognosis
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Consider referral for consideration of CRT-P device therapy if your patient is titrated to
their maximal therapy tolerated and they fulfil the following criteria:
CRT-P if:
Patient is currently experiencing or have recently experienced NYHA class III-IV symptoms.
They have:
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An EF of 35% or less
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In sinus rhythm either with a QRS duration of 150ms or longer (ECG)
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Or with a QRS of 120-149ms (ECG) and de-synchrony on echo
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Also known as a bi-ventricular pacemaker
For Implantable cardioverter defibrillator (ICD) the criteria are:
Primary and secondary prevention of sudden cardiac death.
LVEF of 30% (no worse than class III NYHA)
And a QRS duration of equal to or more than 120 ms
Combined Therapy
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If fulfilling criteria for both devices
Primary prevention
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History of MI (> 4 weeks) +
LVEF <35% (no worse than
class III NYHA) and
Non sustained VT on 24hr
monitoring +
Inducible VT on
electrophysiology testing
Or
EF < 30% (no worse than class
III NYHA) +
QRS equal to or > 120
Also famillial conditions – see
guidelines
Secondary Prevention
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Post MI due to either VT or VF
Spontaneous sustained VT
causing syncope or significant
haemodynamic compromise
Sustained VT without syncope
or cardiac arrest and who have
an associated reduction in EF
(<35%)
The prevailing paradigm of hypertensive heart disease is that
it first leads to concentric ventricular hypertrophy,
followed by the development of ventricular dilation and
contractile impairment with systolic dysfunction and a
reduced left ventricular ejection fraction
Effective treatment of hypertension leads to regression of
LVH and a few studies have demonstrated decreases in LV
mass
Berenji et al (2013)
Variability of the left ventricular ejection fraction measured by
different imaging modalities, and the lack of universal agreement
on the threshold of ejection fraction at which LVSD and preserved
ejection fraction are defined.
Some assert that even in patients with HFPEF, there is an impairment
of the contraction of the long axis of the left ventricle
Characterised by increased wall volume, elevated filling pressures and
abnormal LV filling.
Tolerate tachycardia poorly
Abrupt increases in blood pressure can precipitate decompensation
As yet there are no conclusive treatment options and current advice
suggests treatment according to guidelines of underlying diseases
ie diabetes, hypertension, IHD.
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The hormone aldosterone promotes fibrosis in the heart and
contributes to diastolic stiffness
Most patients with HFPEF complain of symptoms predominantly
during exercise and have a reduced response to increased demand
Enhancement of contractility during exercise in HFPEF may be
related to subtle resting contractile dysfunction, abnormal calcium
handling, passive stiffening, ischemia, oxidative stress, or
abnormal myocardial energy utilisation.
LVDD is considered by some to lie on a continuum to LVSD and the
reduction/prevention of cardiac remodelling could be considered a
target
However...........
The term diastolic dysfunction is not synonymous with HFPEF
In one trial ACE, compared with placebo, significantly reduced HF
hospitalisation up to 12 months
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No significant difference for
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All cause mortality or unplanned hospitalisations (12 months)
All cause mortality 6-12months and 12-54 months
HF hospitalisations 12-54 months
Quality of life up to 6 months
NYHA class up to 6 months
Clinical evidence showed that ACEI therapy did not improve mortality but it
significantly reduced hospital admissions in patients with heart failure and
preserved LVEF. Given that ACEI treatment is relatively cheap; the use of
this therapy in patients with HFPEF is likely to be cost-effective, however it
was decided that the evidence was inadequate to support the use of ACEI in
HFPEF.
NICE GUIDELINES 2010
One third of the population recruited into the SENIORS study of Nebivolol in
heart failure in older adults were patients with an EF>40%
The effect in this sub group was insignificant therefore NICE guidelines felt
unable to currently recommend use of betablockers in HFPEF until further
research has been performed.
Patients with HFPEF are intolerant of tachycardia, especially in AF (which
has been found to be increased in elderly female patients with diastolic
dysfunction). However, there is no current HR target in HFPEF treatment
modalities.
If patients can be considered to be on a continuum from Diastolic
remodelling to LVSD then there may be a place for betablocker therapy in
long term prevention.
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May be more of a requirement in HFPEF for diuretics.
Patients are more friable and likely to decompensate and develop
pulmonary oedema easily with increases in HR and blood pressure.
Note however that they are less able to cope with a greatly reduced
preload.
Some evidence for use of thiazide diuretics – however, this may be related
purely to their blood pressure reducing function.
Encourage patient to monitor their weight everyday and educate them on
the signs and symptoms of early decompensation and what action to take
with an increase in weight of 2-3kg.
Encourage the patient to balance their potassium and sodium intake (which
may require a reduction in salt intake to current UK guidelines). An
imbalance in intake of sodium contributes to hypertension and can cause
fluid retention.
Emerging evidence/current trials:
Statins
Calcium Channel blockers
Novel treatments to reduce oxidative stress
Aldosterone Antagonists to help prevent fibrotic changes
More research is being carried out into ACE/ARB’s and BB’s
Current advice is to use underlying disease processes guidance to
treat patients – ie hypertension, diabetes guidelines as there is
currently no concrete evidence.
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Patient Education is essential to the prognosis and
treatment aims of both types of heart failure and may be
particularly important in management of heart failure with
preserved ejection fraction.
Weight monitoring
Fluid intake – including alcohol
Diet & Nutrition and reduction of salt intake to current
guidelines and balancing with potassium intake
Smoking cessation
Immunisation
Rest/activity & Exercise
Sexual activity and erectile dysfunction
Travel/flying/driving
Follow up and contact details
Criteria
Impaired LV systolic function
NYHA III / IV symptoms
Receiving optimal medical
treatment (beta blockers,
ACE inhibitors/ angiotensin
receptor blocker and
aldosterone antagonists)
Resynchronisation and/or
defibrillator implanted (if
indicated)
Poor prognosis
Elevated natriuretic peptide
levels despite full medical
treatment
A poor prognosis indicated by
the Heart Failure Survival
Score or Seattle Heart Failure
Model
On the decline in the UK
Have to be well enough/sick
enough
Gold standard
May have a left ventricular assist
device as a bridge to
transplant
131 transplants nationwide in
2010/11
Difficult to predict in HF
Uncertainty creates barriers & problems in advance planning.
Patients either die very suddenly –Sudden Cardiac Death
Or they deteriorate slowly- become more fatigued, weak, sleepy,
cachexic.
GSF, 2005
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Difficult to address end of life with heart failure patients due to
uncertain trajectory and changing prognosis of heart failure
patients
Consideration should be made for placing the patient on the GSF
so that appropriate conversations can take place
Discussions around de-activation of ICD’s should take place early
so as not to cause anxiety and difficulties at the end of life.
A patient with an ICD should be made aware that de-activation of
the defibrillation action of his/her device does not de activate the
pacemaker facility and their heart will not just ‘stop’.
If the patient’s preferred place to die is at home, help should if
possible be made available to support this within the home
environment. Difficulties around decompensation and diuretic
management and increasing breathlessness often end with a
relative admitting the patient to hospital due to increase anxiety
with home management.
Oxygen for dyspnoea
Stimulants for fatigue
Benzodiazepines/counselling for anxiety
Exercise limbs to help relieve fatigue and dyspnoea
CPAP/02 for sleep disordered breathing
Treat depression -investigation and intervention
People often die because of multi-organ failure which
may trigger inappropriate investigations and
admissions
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It is important to address deactivation of a patient’s ICD. This
should ideally be done prior to
implantation and also when it is
recognised that a patient may be in
their last year of life/on the Gold
Standards framework. This prevents
problems at the last minute.
De-activation of the shock mode of an
ICD does not deactivate the
pacemaker function and in itself does
not end a patient’s life, but will allow
for a natural death without the risk of
unpleasant and unnecessary shocks.
Who can request de-activation?
The decision can be made in
conjunction with the patient,
carers and family by any of the
following:
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Consultant Cardiologist or SpR
GP
Palliative Care Practitioners (in
consultation with
Consultant/GP
Specialist Nurse or experienced
Community Nurse in
consultation with Consultant or
GP
Other hospital
Consultant/senior Doctor
Indications for De-activation
Following discussion between
the medical team, patient and
carers, a decision has been
made that continued use of an
ICD is inconsistent with
patients goals of care.
The patient is considered to be
imminently dying and eligible
to be started on the Care of the
Dying Pathway
The patient has end stage
terminal disease or palliative
care requirements and has
requested that their device be
deactivated.
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After discussions have taken place, a de-activation form (which is attached
to the guideline) should be completed by the physician and patient (if
possible). Verbal consent may be appropriate provided it documented in
the patient’s records.
A strong magnet placed over the device on the patients chest, can be used
temporarily to de-activate the shocking therapy of the ICD device. These
are located at your local centres.
The appropriate local centre should then be contacted to discuss with the
Cardiac Physiologist and the consent to de-activate form should then be
faxed to them.
Hospital Name
Contact 9 - 5
Contact outside 9-5
Manchester Heart Centre
CMFT
Pacing/ICD Physiologist
0161 901 7537
On call registrar
0161 276 1234 Bleep 4004
ICD Specialist Nurses
0161 276 4657
Coronary Care Unit
0161 276 4200
Pacing/ICD Physiologist
0161 291 4615
On call registrar
0161 998 7070
Wythenshawe Hospital UHSM
ICD Specialist Nurses
0161 291 5076
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The new de-activation policy can be found on the Greater
Manchester and Cheshire Cardiovascular Network website.
Follow clinical working groups – heart rhythm management and
look under documents:
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http://www.gmccsn.nhs.uk/cardiac/clinical-working-groups/heart-rhythmmanagement-group/
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The consent form that is attached to the document has not yet been confirmed for
use.
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It is important to always record a blood pressure and manual pulse
taking note of rhythm as well as rate every time the patient comes
in to surgery. This needs coding on the EMIS system
HF patients should be reviewed at least every 6 months when
stabilised and their medications titrated.
It is very important that every patient has education and
assessment for referral to an exercise program. They need an
understanding of the need for compliance with medications, signs
and symptoms of decompensation, what individual medications do
and the importance of lifestyle to help delay the progression of the
disease due to the poor prognosis.
Consider referral to ACM for unstable patients with multiple comorbidities – new heart failure pathway being developed to help
care for patients in the community to prevent hospitalisation
It is essential that every patient is coded correctly – ensuring that either
OR
585f –
585g -
left ventricular systolic dysfunction (on echo)
left ventricular diastolic dysfunction codes are used
correctly (on echo)
If an echo is abnormal with no evidence of heart failure the code 58531 can be used as a standalone code
Patients need the correct code for LVSD/LVDD or abnormal echo and a heart failure diagnosis on the
system.
QOF CODING
HF001
- The contractor establishes and maintains a register of patients with heart failure
HF002 - The percentage of patients with a diagnosis of heart failure (diagnosed on or after 1 April 2006)
which has been confirmed by an echocardiogram or by specialist assessment 3 months before or 12
months after entering on to the register
HF003. In those patients with a current diagnosis of heart failure due to left ventricular systolic
dysfunction, the percentage of patients who are currently treated with an ACE-I or ARB
HF004. In those patients with a current diagnosis of heart failure due to left ventricular systolic
dysfunction who are currently treated with an ACE-I or ARB, the percentage of patients who are
additionally currently treated with a beta-blocker licensed for heart failure