This is an HTML version of an attachment to the Freedom of Information request 'Evidence based protocols'.

Medical Services 
 
                              
 
 
 
 
 
 

Heart Failure 
 
Version 2 Final 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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Document control 
 
Version history 
Version Date 
Comments 

Final 
25/03/08 
Signed off by Medical Services Contract 
Management Team 
2f 
3/03/08 
QA comments form customer incorporated 
2e 18/02/08 
Formatting 
2d 
04/02/08 
External reviewer comments by Dr J Munro 
2c 
11/10/07 
Internal QA comments (Dr G Buchanan) 
2b 
28/08/07 
Reformatting and initial review 
2a  
Initial 
Draft 
 
 
 
Changes since last version 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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1. Introduction 
Definition 
 

Heart failure is a clinical condition which occurs when an abnormality 
of cardiac function causes failure of the heart to pump blood at a rate 
sufficient for metabolic requirements under normal filling pressure[1] 
 In practical terms the definition is restricted to those patients whose 
condition is sufficiently severe to cause signs or symptoms. 
Classification 
 
Clinically heart failure may be in one of three categories:- 
 
LEFT sided failure 
RIGHT sided failure 
BIVENTRICULAR (or congestive cardiac) failure 
 
The consequences of heart failure can be divided into those arising 
from inadequate cardiac output (forward failure) and those arising 
from increased filling pressure with fluid retention causing either 
pulmonary or systemic venous congestion (backward failure). 
 
Description 
 
Heart failure manifests itself clinically with breathlessness, effort 
intolerance, fluid retention, malaise and poor survival. [1] 
 
Heart failure may arise as a consequence of a myocardial, valvular, 
pericardial, endocardial or a conduction problem (or some 
combination of these).  
 
In contrast with chronic heart failure, the term acute heart failure is 
often used to mean acute (cardiogenic) dyspnoea characterised by 
signs of pulmonary congestion including pulmonary oedema. 
 
Associated physiological changes in many organ systems occur and 
cause biochemical, metabolic and functional impairments. 
 
 
 
 
 

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Aetiology 
 

The underlying diagnosis and aetiology must be sought in patients 
presenting with heart failure syndrome.  
 
A syndrome is a constellation of symptoms and signs and is not a 
single disease. This is the only way in which optimum treatment can 
be provided i.e. the treatment varies depending on whether the 
underlying cause is myocardial dysfunction, valve disease or some 
other aetiology. 
 
The commonest cause of heart failure is myocardial dysfunction 
which is commonly systolic, i.e. there is reduced left ventricular 
contraction. Around two thirds of these cases result from coronary 
heart disease (CHD) and there is often a past history of myocardial 
infarction (MI).  
 
The remainder have a non-ischaemic cardiomyopathy, which may 
have an identifiable cause (e.g. hypertension, thyroid disease, 
valvular disease, alcohol excess, or myocarditis) or may have no 
known cause (e.g. idiopathic dilated cardiomyopathy). [2] 
 
Prevalence 
 
Both the incidence and prevalence of heart failure increase with age. 
Studies of heart failure in the USA and Europe have found that under 
65 years of age, the annual incidence is 1:1000 for men and 0.4:1000 
for women.  
 
Over 65 years of age, the annual incidence is 11:1000 for men and 
5:1000 for women.  
 
Under 65 years of age, the prevalence of heart failure is 1:1000 for 
men and 1:1000 for women and over age 65 years the prevalence is 
40:1000 for men and 30:1000 for women.  
 
The prevalence of asymptomatic left ventricular systolic dysfunction 
(LVSD) is 3% in the general population.  The mean age of people with 
asymptomatic LVSD is lower than that for symptomatic individuals. 
Both heart failure and asymptomatic LVSD are more common in men. 
  
Systolic heart failure is caused when the heart does not pump out 
enough blood. 
The prevalence of diastolic heart failure (caused when the heart does 
not fully relax, so it does not fill properly with blood) in the community 
is unknown.  
 
 
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The prevalence of heart failure with preserved systolic function in 
people in hospital with clinical heart failure varies from 13 – 74%.  
Fewer than 15% of people with heart failure under 65 years of age 
have normal systolic function, whereas in people over 65 years of age 
normal function is maintained in about 40%  
    
The ageing of the population in Western society has meant that heart 
failure is becoming increasingly common. 
 
Recent improvements in the management of myocardial infarction 
and coronary artery disease, with an increased survival rate, have led 
to the development of more heart failure in later life. [1] 
  
 
 
 
 
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2.  Diagnosis 
 
The presentation of heart failure is variable.  It depends on the 
severity of the disease and the associated clinical disorders. 
 
Diagnosis may be difficult in the early stages when symptoms are 
non-specific. 
 
The important points in the diagnosis are: 
 
  High index of suspicion 
  Thorough history taking 
  Directed clinical examination. 
History and Symptoms 
 
The main presenting symptoms are: 
 
  Reduced exercise capacity 
  Dyspnoea (wheeze,  orthopnoea, paroxysmal nocturnal dyspnoea 
(PND) 
 Reduced 
appetite 
 Weight 
loss. 
 
The clinical symptoms occur as a result of the effects of the impaired 
ventricular function on the various organs.  There is an increase in 
pulmonary pressure with an accumulation of fluid leading to an 
increase in the work of breathing. 
 
The oedematous swelling may also cause a non-asthmatic bronchial 
constriction mimicking asthma. 
 
Increasing pulmonary hypertension may eventually cause gross 
dyspnoea, lung crackles and pink frothy sputum in acute failure. 
 
In chronic failure, the patient remains dyspnoeic but with less well 
marked lung changes. 
 
Heart failure can cause expiratory airflow reduction, especially at 
night.  This may cause confusion in differentiating heart failure from 
asthma. 
 
  
 
 
 

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Informal Observations 
 

In chronic heart failure the patient will tend to walk slowly, with signs 
of breathlessness and fatigue.  The observed tachypnoea with the 
use of accessory muscles of respiration and gasping gives an 
indication of the severity of heart failure and disability. 
 
These observations will be noticeable on climbing on and off the 
examination couch, dressing and undressing, and walking up stairs.  
At more severe degrees of disablement they will be apparent on 
walking on the flat and ultimately even at rest. 
Clinical Signs 
 

The important signs on examination are: 
 
  Abnormal blood pressure 
  Forceful apex beat 
 Abnormal 
pulse 
 Respiratory 
crackles 
 Oedema 
  Abnormal heart sounds 
 Raised 
JVP 
 Hepatomegaly/ascites 
 Pleural 
effusion 
 Parasternal 
heave. 
 
A similar picture can develop in conditions with volume or pressure 
overload such as: 
 
 Severe 
anaemia 
 Overtransfusion 
 Arteriovenous 
malformation 
 Shunts 
  Prosthetic valve dysfunction 
Investigations 
 

Basic early investigations are necessary to differentiate heart failure 
from other conditions and to provide prognostic information. 
Urinalysis, serum urea and creatinine tests may help to determine if 
there is kidney failure since symptoms of kidney failure are similar to 
those of CHF (chronic heart failure). 
 
 
 
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Chest X-ray may indicate signs of CHF such as cardiomegaly, 
pulmonary congestion or pleural effusion and also non-cardiac 
indications such as lung tumours which account for breathlessness. 
Other basic investigations should include:- 
Full blood count 
Fasting blood glucose 
Serum urea and electrolytes 
Thyroid function. 
Further Investigations 
 

Following clinical examination and basic investigation a decision 
should be made as to whether the patient should undergo 
echocardiogram. To help make this decision the patient should 
undergo either:- 
Electrocardiogram (ECG) 
or 
Brain natriuretic peptide (BNP) test 
or both. 
ECG 
 

The ECG is used firstly as a screening test to assess the likelihood of 
CHF and the need for subsequent echocardiography to confirm or 
refute a diagnosis  
It is unusual for a patient with Chronic Heart Disease to have a normal 
ECG. The ECG changes reported in CHD are non-specific and 
common in elderly patients.  CHD is a disease of the heart caused by 
decreased blood flow to the heart muscle which may result in 
myocardial infarction, or in angina but not necessarily with failure.  
 
Electrocardiograph abnormalities seen in CHD may include:- 
Pathological Q waves 
Left bundle branch block 
Left ventricular hypertrophy (LVH) 
Atrial fibrillation 
Non-specific ST and/or T wave changes 
 
In CHF there has been described association of peripheral (o)edema 
(PERED), sometimes even imperceptible on physical examination, of 
patients with CHF, and attenuation (ATTEN) of the amplitude of P-
waves, QRS-complexes, and T-waves. 
Electrocardiography is also useful once the diagnosis of CHF has 
been confirmed as it may help to determine the cause (e.g. Q waves 
indicate previous MI, LVH is seen in hypertension and aortic valve 
disease) and it is important to exclude atrial fibrillation. 
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B-Type Natriuretic Peptide 
 

Brain natriuretic peptide and N terminal-pro-BNP (NT-proBNP) are 
peptide hormones produced in the heart by breakdown of a precursor 
protein (pro-BNP). BNP promotes natriuresis (the process of excretion 
of  sodium in the urine via action of the kidneys), diuresis, 
vasodilatation and muscle relaxation. NT-proBNPis inactive. 
 
 
Plasma BNP and NT-proBNP tend to rise in patients with heart failure 
and the concentrations tend to rise with New York Heart Association 
(NYHA) classification. (see Appendix C) 
Echocardiography 
 

Echocardiography is a safe and relatively inexpensive investigation 
which is very helpful in diagnosing heart failure and determining the 
cause.  
It may reveal previously undiagnosed valve disease. 
It provides a semi-quantitative assessment of left ventricular systolic 
and diastolic function, valve disorders can usually be accurately 
delineated, and pulmonary artery systolic pressure can be estimated. 
As it may not be feasible or cost effective to refer all patients with 
suspected heart failure for echocardiography, screening with either 
ECG and/or BNP is desirable. Brain natriuretic peptide testing has the 
practical advantage of being a simple blood test. 
 
See diagram below. [2] 
Chest X-ray 
 
This is still considered important in the assessment of left heart 
failure.  The rise in pulmonary venous pressure first shows as a 
distension of the upper pulmonary lobe veins. 
 
Subsequent changes include the development of Kerley B lines. 
 
 
 
 
 
 
 
 
 
 
 
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Diagnostic algorithm for patients with suspected 
chronic heart failure 
Symptoms or signs  
suggestive of CHF  
 
 
 
 
Clinical examination  
(full blood count, fasting blood glucose, serum urea and electrolytes,  
urinalysis, thyroid function and chest x-ray)  
 
 
 
 
 
 
 
B N P
 
(or NT pro-BNP)  
 
and / or ECG  
 
 
 
 
 
 
 
 
Low BNP (or NT pro-BNP) 
Raised BNP (or NT pro-BNP) 
and normal ECG 
or abnormal ECG  
CHF excluded  
C H F possible 
Consider alternative cause for  
Refer for echocardiography  
symptoms  
E C G 
(If not already done, to  
determine cause of CHF)  
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3.  Management 
Lifestyle Changes 
 
The mainstays of treatment are listed in Appendix B and include: 
 
  General life style advice 
 Treatment 
of 
any 
underlying cause(s) 
 Drug 
therapy. 
General Measures 
 
Advice should be given as to: 
 
  Influenza and pneumococcal immunisation, 
  Abstinence from smoking, 
  Moderation of alcohol intake, 
 Avoidance 
of 
harmful 
drugs. 
  Restriction of salt intake may be useful in some patients 
 
Adequate patient education is important, and the patient should be 
made aware of the necessity of any required lifestyle modifications 
and of the need for any regular medication. 
Exercise training 
 
This can improve functional capacity by 15 - 20% and reduce cardiac 
events.  It is advised in those with stabilised mild to moderate heart 
failure. [4] [7] 
 
 
Concurrent Illness 
 
Any associated disease (e.g. hypertension, hypothyroidism, coronary 
artery disease, and cardiomyopathy) which may be contributing to the 
heart failure should be treated.  
(see Appendix A) 
 
 
Mood Disorders 
 

Depression is common in patients with chronic heart failure and is 
associated with an increased risk of mortality in some but not all 
studies and may be related to morbidity and rehospitalisation. 
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Screening in heart failure may help to identify patients who are at 
poorer prognostic risk. If antidepressant medication is to be used then 
a tricyclic antidepressant should not be used in patients with chronic 
heart failure. 
Drug Therapy 
 
Drug therapy, and in particular balanced vasodilatation, leads to the 
greatest clinical benefit. 
Angiotensin Converting Enzyme Inhibitors 
 
ACE inhibitors (such as enalapril or ramipril): These improve 
function and reduce mortality by 23% and hospital admissions by 
35%. [2]  They are used as first line treatment in patients with a 
reduced left ventricular (LV) ejection fraction.  If used in asymptomatic 
LV dysfunction, fewer develop heart failure. [4] [11]  Side effects of 
cough, the development of allergy, renal impairment or hyperkalaemia 
may limit their use. 
Beta Blockers 
 

-blockers: Combining -Blockers with ACE inhibitors can reduce 
hospital admissions and mortality.  Careful titration of the dose is 
needed to avoid bradycardia and hypotension.   
Bisoprolol and Carvedilol have been shown to reduce mortality.  
Treatment should be initiated under specialist supervision 
There is consistent evidence for positive benefits from beta blockers 
in patients with heart failure, with a risk of mortality from 
cardiovascular causes reduced by 29%, mortality due to pump failure 
reduced by 36% and all cause mortality reduced by 23%. [2] 
Angiotensin Receptor Blockers 
 

Angiotensin II type1 receptor blockers (ARBs) block the biological 
effect of angiotensin II, mimicking the effect of ACE inhibitors. 
Unlike ACE inhibitors they do not produce cough as a side effect and 
should be used in patients who cannot tolerate an ACE inhibitor. 
Candesartan is the drug of choice. 
 
Aldosterone Antagonists 
 

Aldosterone produces many adverse extra-renal effects, for example 
on vascular function and myocardial fibrosis.  
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The RALES trial demonstrated that adding the aldosterone antagonist 
Spironolactone to an ACE inhibitor reduced all cause mortality by 
30% and cardiac mortality by 31%. The frequency of hospitalisation 
for worsening heart failure was 35% lower in patients receiving 
Spironolactone 
 
Diuretics/ Loop Diuretics/ Metolazone 
 

Diuretics: These are essential for the treatment of fluid overload and 
can cause a rapid improvement in symptoms and exercise tolerance.  
Both thiazides (such as bendroflumethiazide) and loop diuretics (such 
as furosemide) are used, often with an ACE inhibitor. Side effects 
such as gout or urinary retention in subacute prostatism may become 
a problem. 
 
Digoxin 
 

A Cochrane review has shown a 64% improvement in symptoms and 
a 23% reduction in hospitalisation for patients receiving Digoxin. 
Digoxin did not improve survival.  
 
Evidence of benefit must be weighed against the possibility of an 
increase in sudden death due to toxicity associated with Digoxin. 
 
In patients with heart failure and atrial fibrillation a beta-blocker is 
preferred for control of ventricular rate, though digoxin may be used 
initially while the beta-blocker is being introduced.  
 
If excessive bradycardia occurs with both drugs then digoxin should 
be withdrawn. [2] 
 
Summary of the use of major drug classes in the treatment of 
Heart Failure [2] 
 
Class Prescribe 
NYHA I 

ACE inhibitor 
Beta blocker 

NYHAII-III ACE 
inhibitor 
Beta blocker 
Candesartan (initiation requires specialist advice) 

NYHA III-IV  ACE inhibitor 
Beta blocker 
Spironolactone (initiation requires specialist advice) 

 
 
 
 

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Other Measures 
 

Bed rest for a short period is a common treatment for acute failure.  
However it is preferable that the patient be treated in the sitting 
position rather than lying prone. 
 
In cases of severe, intractable failure, surgical intervention such as 
cardiomyoplasty or cardiac transplantation may be considered.  [9] 
Prognosis 
 

The prognosis of heart failure is poor, with 5 year mortality ranging 
from 26% – 75%.  Up to 16% of people are readmitted with heart 
failure within 6 months of first admission.  
 
In the USA, heart failure is the leading cause of hospital admission 
among people over 65 years of age.   
 
In people with heart failure, a new myocardial infarction increases the 
risk of death by nearly eight fold. 
 
(Relative risk 7.8; [95% Confidence interval 6.9 to 8.8]).  
About a third of all deaths in people with heart failure are preceded by 
a major ischaemic event.  Sudden death, mainly caused by ventricular 
arrhythmia, is responsible for 25 – 50% of all deaths, and is the most 
common cause of death in people with heart failure.   
 
This is being constantly improved with increasing use of implanted 
intracardiac defibrillators (AICDs). 
 
The presence of asymptomatic LVSD increases an individual's risk of 
having a cardiovascular event.  
 
One large prevention trial found that the risk of heart failure, 
admission for heart failure, and death, increased linearly as the 
ejection fraction fell.   
Relative risk for heart failure was 1.20 (95% confidence interval 1.13 
to 1.26).  
 
Relative risk for hospital admission was 1.28 (95% confidence interval 
1.18 to 1.38).  
 
For each 5% reduction in ejection fraction the relative risk for mortality 
was1.20 (95% confidence interval of 1.13 to 1.29).  
 
The annual mortality for people with diastolic heart failure varies in 
observational studies (1.3% – 17.5%).  
 
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The reasons for this variation appear to include age, the presence of 
coronary artery disease, and variation in the partition value used to 
define abnormal ventricular systolic function.  
 
The annual mortality for left ventricular diastolic dysfunction is lower 
than that found in people with systolic dysfunction. [1] 
 
 
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4.  Main Disabling Effects 
General Considerations 
 

The actual disability due to chronic heart failure is very variable, and 
each patient must be assessed individually. 
 
In the early stages, there is very little impairment of daily function. The 
decrease in exercise tolerance in severe heart failure can be very 
limiting.   
 
Functional capacity can be improved by alteration in general and 
lifestyle factors and most notably by drug treatment. 
 
One of the most marked changes in the skeletal system is a 
substantial reduction in total skeletal muscle bulk, and subtle changes 
may be functionally important in heart failure. 
 
Patients frequently complain that muscle fatigue is a major limitation 
to their daily performance.  Some patients with chronic failure may 
benefit from exercise training.  In a patient with stable chronic heart 
failure and no evidence of exercise induced ventricular arrhythmia, 
regular exercise should be encouraged. [5] 
 
For those in employment, heavy industry where the employee is 
required to climb stairs or carry heavy weights (e.g. 20 kg) may be 
impossible, but lighter or sedentary work may be well within their 
capabilities (see Appendix D). 
 
An ability to reach Stage 4 of the Bruce Protocol (see Appendix E) is 
judged to place an individual at low risk of sudden cardiac events.  
This is reflected in the DVLA guidelines which allow vocational driving 
at this stage.  These guidelines are now being applied more widely to 
other occupations where there may be a significant risk attached to a 
sudden cardiovascular collapse. 
Assessing the Claimant 
 
Clinical examination findings in mild to moderate heart failure do not 
correlate well with functional ability and the assessment is best made 
from the evidence of: 
 
1.  The History of Activities of Daily Living  (Typical  Day)  taking           
  variation into account. 
 
2.  Informal Observation of the claimant’s activities at examination. 
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3.  Medication taken (see Appendix B.) and attendance at Cardiac 
Clinic. 
 
Claimants with well treated mild and moderate failure are likely to 
retain the ability to self care, and although exercise tolerance may be 
reduced should be able to walk to local shops or round a 
supermarket. 
 
Severe heart failure can cause appreciable functional impairment.  It 
is likely that in these cases the claimant would be under active 
specialist care and be on maximum doses of medication.  Significant 
abnormalities would be present on clinical examination. 
 
The drugs used in the treatment of heart failure usually have few side 
effects, but can occasionally have a functional effect e.g. causing 
postural hypotension or polyuria with diuretics. 
 
Psychological factors may sometimes be very important in the 
disability due to heart failure.  An individual may have only mild 
physical symptoms, but be significantly restricted due to depression or 
fear of an untoward event.  Similarly, the family may try to protect the 
patient and erroneously discourage any physical activity.  [10] 
 
In the IB-PCA, the functional areas first affected are Walking Up and 
Down Stairs, and then Walking. 
 
Later the effort of mild exertion limits activities, such as dressing and 
undressing, washing, rising from sitting and walking even a few steps. 
  
 
Eventually even minimal effort is not tolerated and there will be 
breathlessness at rest.   
 
Exemption from the assessment should be considered if the limitation 
of effort tolerance is severe and progressive, causing significant 
limitation of normal daily activities such as self care tasks.   
 
 
 
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Appendix A  -  Causes of Heart Failure 
 
Most Common Cause: 
 
  Ischaemic Heart Disease 
 
 
Other Causes: 
 
 Hypertension  
 
 Cardiomyopathy (familial, infective, toxic) 
  Rheumatic heart disease. 
 Valvular disorders 
 Arrhythmias 
 Endocarditis 
 Endocrine disorders. 
 
 
Rare Causes: 
 
  Nutritional deficiencies (e.g. thiamine, iron) 
  Infiltrative conditions (e.g. sarcoid, neoplasms) 
 Myocardial fibrosis 
 
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Appendix B - Treatment of Chronic Heart Failure 
 
General Measures. 
 
 Achieve optimal weight 
 No smoking 
 Encourage exercise 
  Discourage added salt 
  Treat hypertension if appropriate 
  Discourage excess alcohol  
  Detect and treat associated risk factors (e.g. diabetes, 
myxoedema, hyperlipidaemia) 
 
 
Mild Failure 
 
  Thiazide loop diuretic 
 ACE inhibitor 
  Beta blocker for atrial fibrillation 
 
 
Moderate Failure: 
 
  Loop diuretic or combination of diuretics 
 ACE inhibitor 
 Beta blocker 
 
 
Severe Failure: 
 
 ACE inhibitor 
 Beta blocker 
 Spironolactone 
 Digoxin  
 Cardiomyoplasty 
 Transplant 
 
 
 
 
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Appendix C - Functional Classification of 
Cardiac Diseases 

 
New York Heart Association Functional Classification 
of Cardiac Disease 
 
Grade 1 Ordinary 
activity 
does not cause symptoms of 
undue fatigue, palpitations, dyspnoea, or anginal pain. 
 
Grade 2  Greater than ordinary physical activity results in 
symptoms.  (Relevant for PCA) 
 
Grade 3  Ordinary physical activity results in symptoms.  
(May be exemptible for PCA) 
 
Grade 4  Symptoms at rest, and worse with any physical 
activity.  (Exemptible for PCA.  May be relevant for DLA/AA) 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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Appendix D  -  Haskell Work Classification 
 
 
Type of Work 
Activity 
Very Heavy 
Climb stairs 
Medium 
Carry 50 lbs.  (22.5 kg) 
Light 
Carry 20 lbs.  (9 kg) 
Sedentary 
Sit/carry 10 lbs.  (4.5 kg) 
 
This is a standard grading of work effort requirement. 
 
The critique that it does not take into account the occasional 
increased episodic requirements for normal jobs is entirely 
reasonable.  [13] 
 
The classification can be linked to graded exercise tests 
(see Appendix E) 
 
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Appendix E- Bruce Protocols 
 
Full (Standard) Bruce Protocol 
 
Stage  Speed  Gradient Duration Cumulative time  METS 
(mph)  (%) 
(min.) 
(mins 
I 1.7 
10  3  3 

II 2.5 
12  3  6 

III 3.4 14  3 

10 
IV 4.2 16  3 
12 
13 
V 5.0 
18  3 
15 
16 
VI 5.5 20  3 
18 
19 
VII 6.0 22 

21 
22 
 
This is a standard graded exercise test, and is a good 
measure of exercise tolerance in cardiac disease.   
 
It may be too strenuous for the deconditioned subject, in 
which case the modified Bruce protocol can be used.   
 
The energy used to accomplish a particular task can be 
calculated in METS (a measure of energy expenditure as a 
multiple of resting energy expenditure). 
 
Haskell Work Classification (Appendix D) 
 
Task Grade 
Peak METs 
Activity 
Very Heavy 
>6 
Climb stairs 
Medium 
4-6 
Carry 50 lbs (22.5 kg) 
Light 
2-4 
Carry 20 lbs ( 9 kg) 
Sedentary 
<2 
Sit.  Carry 10 lbs (4.5 kg) 
 
 
 
 
 
 
 
 
 
 
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Medical Services 
 
Modified Bruce Protocol 
 
 

Stage Speed Gradient Duration Cumulative  METS 
(mph)  (%) 
(mins.) 
time(mins.) 

1.7 
  0 

  3 

II 
1.7 
  5 

  6 

III 
1.7 
10 

  9 

IV 2.5 
12 

12 

V 3.4 
14 

15 
10 
VI 4.2 
16 

18 
13 
VII 5.0 
18 

21 
16 
 
 

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Medical Services 
 
 
References 
 
1. BMJ Clinical Evidence 2006 
 
2. Management of Chronic Heart Failure. Scottish Intercollegiate                      
    Guidelines Feb 2007 
 
3 The Framingham Disability Study: relationship of various coronary heart       
   disease manifestations to disability in older persons living in the community. 
   Am J Pub Health 1990 Nov 80; 11: 1363-7 
 
4. Remme WJ, Swedberg K. (Task Force Chairmen, European Society of       
    Cardiology) Task Force Report.  Guidelines for the Diagnosis and                
    Treatment of Chronic Heart Failure.   
    European Heart Journal  2001; 22: 1527-1560 
 
5. Aronow WS, Tresch D.  Epidemiology, pathophysiology and etiology of       
    congestive heart failure in older adults.   
    J Am Geriatr Soc  1997; 45: 968-974 
 
6 .Armstrong PW, Moe GW.  Medical Advances in the Treatment of                 
    Congestive Heart Failure.  Circulation 1993;  88 (No.6): 2941-52 
 
7 .Piepoli MF, Scott AC, Capucci A, et al.  Skeletal Muscle Training in Chronic 
    Heart Failure.  Acta Physiol Scand 2001; 171: 295-303 
 
8. Packer M.  β - Adrenergic blockade in chronic heart failure; principles,         
    progress and practice.  Prog Cardiovasc Dis41:  39-52 
 
9. Grady KL, Jalowiec A, White Williams C.  Improvement in quality of life in    
    patients with heart failure who undergo transplantation.   
    J Heart Lung Transplant 1996;15: 749-57. 
 
10. Lipkin DP, Scriven AJ, Crake T et al.  Six minute walking test for                
      assessing exercise capacity in chronic heart failure.   
      Br Med J (Clin Res Ed)1986; 292:  653-5 
 
11. Yusuf S, Sleight P, et al.  Effects of an angiotensin-converting enzyme      
       inhibitor, ramipril, on cardiovascular events in high risk patients.   
       New England Journal of Medicine 2000; 342(3): 145-153 
 
12. Cay EL, Walker DD.  Psychological factors and return to work.  European 
      Heart Journal
 1988; (Suppl L):74-81 
 
13. Ainsworth BE. (2002, January) The Compendium of Physical Activities      
      Tracking Guide. Prevention Research Center, Norman J. Arnold School of 
      Public Health, University of South Carolina. 
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