Management of heart failure

Dr Ambakederemo TE
Consultant physician/cardiologist
NDUTH
 outline
• Definition
• Epidemiology
• Aetiology & precipitants
• Pathophysiology
• Clinical features
• Investigations
• Treatment
• Prognosis
 definition
• Heart failure (HF) is a complex clinical
syndrome that can result from any structural
or functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject
blood
 epidemiology
• Over 23 million individuals worldwide have HF.

• Lifetime risk for developing HF at age 40 years is

21% for men and 20% for women

• Incidence of HF approaches 10 per 1000 population

after age 65 and approximately 80% of patients
hospitalized with HF are more than 65 years old

• The overall prevalence of HF in the adult population

in developed countries is 2%
 Epidemiology continued
• The overall prevalence of heart failure is thought to
be increasing in the developed world

• In Africa, at least 3-7% of all hospital admissions are

caused by heart failure

• Little is known with respect to the prevalence or

risk of developing heart failure in the developing
world because of a paucity of population–based
studies
 Classification of heart failure

• HF with a depressed ejection fraction (commonly

referred to as systolic failure) or HF with a preserved EF
(commonly referred to as diastolic failure).

• High output heart failure and low output heart failure

• Acute heart failure and chronic heart failure

• Biventricular heart failure, right and left heart failure

 aetiology
 Any condition that leads to an alteration in LV
structure or function
They include :
 Main causes
 Hypertension
 Cardiomyopathy (mostly dilated)
 Rheumatic heart disease
 Ischaemic heart disease/CAD
 Other causes
 Atrial and ventricular septal defects
 Chronic bradyarrhythmias and chronic
tachyarrhythmias(atrial fibrillation, complete heart
block, the sick sinus syndrome)
• Cardiomyopathy (undilated):
hypertrophic/obstructive, restrictive (EMF,
amyloidosis, sarcoidosis)
• Alcohol and drugs (e.g. chemotherapy)
• Hyperdynamic circulation (anaemia, thyrotoxicosis,
arteriovenous fistula, wet beri-beri, Paget's disease)
• Right heart failure (RV infarct, pulmonary
hypertension, pulmonary embolism, cor pulmonale
(COPD)
• Pericardial disease (constrictive pericarditis,
pericardial effusion)
• Viral infections (infective myocarditis)
• Rheumatic heart disease remains a major cause of HF
in Africa and Asia.

• In industrialized countries CAD is a predominant cause

and is responsible for 60–75% of cases of HF.

• Hypertension contributes to the development of HF in

75% of patients, including most patients with CAD.

• Although the contribution of DM to HF is not well

understood, DM accelerates atherosclerosis and often
is associated with hypertension.
 Factors aggravating or precipitating heart
failure
• Any factor that increases myocardial work may
aggravate existing heart failure or initiate failure.

• The most common are arrhythmias, anaemia,

thyrotoxicosis, pregnancy, infective endocarditis,
pulmonary infection, change of heart failure
therapy including poor compliance.

• Readmission rates range from 29% and 47% within

3-6 months of hospital discharge
 prognosis
• 30–40% of patients die within 1 year of diagnosis and
60–70% die within 5 years, mainly from worsening HF
or as a sudden event (probably because of a ventricular
arrhythmia).

• Patients with symptoms at rest [New York Heart

Association (NYHA) class IV] have a 30–70% annual
mortality rate, whereas patients with symptoms with
moderate activity (NYHA class II) have an annual
mortality rate of 5–10%.

• functional status is an important predictor of patient

outcome
 New York Heart Association Classification
• CLASS I: Patients with cardiac disease but without
resulting limitation of physical activity. Ordinary
physical activity does not cause undue fatigue,
palpitations, dyspnoea, or anginal pain. (dyspnoea
on severe exertion)

• CLASS II: Patients with cardiac disease resulting in

slight limitation of physical activity. They are
comfortable at rest. Ordinary physical activity
results in fatigue, palpitation, dyspnoea, or anginal
pain. (dyspnoea on moderate exertion)
• CLASS III: Patients with cardiac disease resulting in
marked limitation of physical activity. They are
comfortable at rest. Less than ordinary activity
causes fatigue, palpitation, dyspnoea, or anginal
pain. (dyspnoea on mild exertion)

• CLASS IV: Patients with cardiac disease resulting in

inability to carry on any physical activity without
discomfort. Symptoms of heart failure or the
anginal syndrome may be present even at rest. If
any physical activity is undertaken, discomfort is
increased. (dyspnoea at rest)
 Pathophysiology
• HF may be viewed as a progressive disorder that is
initiated after an index event either damages the
heart muscle or disrupts the ability of the
myocardium to generate force, thereby preventing
the heart from contracting normally.

• This index event may be abrupt, e.g myocardial

infarction (MI); or may be gradual or insidious, as
e.g hemodynamic pressure (e.g. HPT, AS) or
volume overloading (e.g. AR,MR);
• or it may be hereditary, as in the case of many of
the genetic cardiomyopathies.

• Regardless of the nature of the inciting event, the

feature that is common to each of these index
events is that they all in some manner produce a
decline in the pumping capacity of the heart.

• a number of compensatory mechanisms become

activated in the presence of cardiac injury and/or
LV dysfunction allowing patients to sustain LV
function for a period of months to years.
• The compensatory mechanisms include activation
of the adrenergic nervous system, the renin-
angiotensin-aldosterone system and the cytokine
system.

• These systems maintain cardiac output through

increased retention of salt and water and
increased myocardial contractility

• Activation of adrenergic nervous system results in

tachycardia, this restores cardiac output as cardiac
output= stroke volume X heart rate
• Chronic adrenergic nervous system /sympathetic
activation, however, has deleterious effects as it
has a direct toxic effect on myocardial cells

• reduced cardiac output also leads to diminished

renal perfusion, activating the renin-angiotensin
system and enhancing salt and water retention

• this increases venous pressure and leads to

accumulation of fluid in the interstitium, producing
many of the physical signs of heart failure such as
dyspnoea, orthopnoea, PND, dependent oedema,
ascites, tender hepatomegaly
• Prolonged RAAS activation also has a direct toxic
effect on the heart further worsening heart failure

• A reduced cardiac output results in an increased

end diastolic volume, and the Frank Starling’s law
is thus set in motion, this law states that the initial
length of a muscle fibre determines the force of
contraction.

• An increased end diastolic volume(preload) results

in stretch of the cardiac muscles and initial
improvement in cardiac output but eventually this
declines as heart failure progresses
• An increased afterload (the load or resistance
against which the ventricle contracts) is formed by
pulmonary and systemic resistance, physical
characteristics of the vessel walls.

• There is wide spread peripheral vasoconstriction in

heart failure. This increases the afterload and
hence decreases the cardiac output.
• Other mechanisms in HF include abnormal calcium
homeostasis (causing prolonged contraction and
relaxation), changes in cardiac contractile protein gene
expression to fetal and neonatal isoforms.

• Hormones such as atrial and brain natriuretic peptide

prostaglandins (PGE2 & PGI2), and nitric oxide (NO),
induce vasodilation and natriuresis in an attempt to
counteract the actions of RAAS and the adrenergic
nervous system(ANS) but their effect is overwhelmed
by the actions of RAAS and ANS.

• Endothelin (vasoconstrictor), and ADH (causing

reabsorption of water) levels also increase in HF
• Left ventricular remodelling
• is a process of progressive alteration of ventricular size,
shape, and function due to influence of mechanical,
neurohormonal, and genetic factors in conditions such
as myocardial infarction, cardiomyopathy,
hypertension, and valvular heart disease.

• Its hallmarks include hypertrophy, loss of myocytes, and

increased interstitial fibrosis

• Left ventricular remodelling in heart failure causes

further impairment of overall function of the heart as a
pump .
 CLINICAL FEATURES
• LEFT HEART FAILURE

• CAUSES include:

• ischaemic heart disease

• systemic hypertension

• mitral and aortic valve disease

•
• cardiomyopathies
• Symptoms are predominantly fatigue, exertional
dyspnoea, orthopnoea and paroxysmal nocturnal
dyspnoea.

• Physical signs include cardiomegaly , S3, S4

• A PSM may be present due to dilatation of the

mitral annulus which results in functional mitral
regurgitation.

• Crackles are heard at the lung bases.

• RIGHT HEART FAILURE : This syndrome occurs in
association with:
• left heart failure
• chronic lung disease (cor pulmonale)
• pulmonary embolism or pulmonary hypertension
• tricuspid valve disease
• pulmonary valve disease
• left-to-right shunts (e.g. atrial or ventricular septal
defects)
• isolated right ventricular cardiomyopathy
• mitral valve disease with pulmonary hypertension.
• Symptoms include fatigue, anorexia and nausea, leg
and abdominal swelling

• Physical signs are usually more prominent than the

symptoms, with:
• jugular venous distension (± v waves of tricuspid
regurgitation)
• tender smooth hepatic enlargement
• dependent pitting oedema
• development of free abdominal fluid (ascites)
• pleural effusion (commonly right-sided).
• Tachycardia and a right ventricular third heart sound
are usual.
 Cardiac cachexia
• The term cardiac cachexia describes the loss of lean
(non-oedematous) body mass that occurs in some
patients with moderate or severe heart failure.

• Most patients with cachexia are over 40 years of

age, have had heart failure for at least 5 years and
are in NYHA functional class 3/4.

• Its presence is associated with increased morbidity

and mortality.
 Mechanisms for cardiac cachexia
• Malabsorption &anorexia caused by intestinal
oedema and drugs

• loss of nutrients through the gastrointestinal tracts.

• increased metabolic rate secondary to increased

sympathetic activity

• Tumour necrosis factor alpha (TNF-α) is increased in

patients with cardiac cachexia and contributes to
the phenomenon.
 Framingham’s criteria for Diagnosis of
heart failure
• Major criteria:
• Paroxysmal nocturnal dyspnoea.
• Neck vein distention.
• Rales.
• Cardiomegaly (radiographic).
• Acute pulmonary oedema.
• S3 gallop.
• Increased venous pressure (>16cm H2O).
• Positive hepatojugular reflux
 Framingham’s criteria for Diagnosis of
heart failure contd
• Minor criteria:
• Extremity oedema (ankle oedema)
• Night cough
• Dyspnoea on exertion
• Hepatomegaly
• Pleural effusion
• Tachycardia (> 120bpm)
• The above criteria will be used in the diagnosis of heart
failure when there is simultaneous presence of at least
two major criteria or one major criterion in conjunction
with two minor criteria
 investigations
• Echocardiography. Two-dimensional and Doppler
echocardiography establish the presence of systolic
and/or diastolic impairment of the left or right
ventricle.

• They may also reveal the aetiology (valve disease,

regional wall motion abnormalities in ischaemic heart
disease, cardiomyopathy, amyloid), and may detect
intracardiac thrombus.

• An ejection fraction of < 0.45 is generally accepted as

evidence for systolic dysfunction.
• Chest X-ray - cardiac size and evidence of pulmonary
congestion, upper lobe diversion, fluid in fissures and
Kerley B lines (ABCDE)

• Electrocardiogram - evidence of ischaemia,

hypertension or arrhythmia.

• Blood tests - full blood count, liver biochemistry, Cr,

urea and electrolytes, cardiac enzymes in acute heart
failure to diagnose myocardial infarction, thyroid
function.

• Natriuretic peptide-A normal plasma level of BNP

excludes heart failure
 NON ROUTINE INVESTIGATIONS FOR
HEART FAILURE

• Stress echocardiography
• Nuclear cardiology.
• Cardiac MRI.
• Positron emission tomography (PET).
• Cardiac catheterization
• Cardiac biopsy
• Cardiopulmonary exercise testing. Peak oxygen
consumption (VO2) is a strong independent
predictor of hospital admission and death in
patients with heart failure but is not widely
available. A 6-minute exercise walk may be used
instead.

• Ambulatory (24-48 hours) ECG monitoring - if

arrhythmia is suspected.

• Resting and stress radionuclide angiography

(MUGA) - for estimation of ejection fraction,
regional wall motion abnormality.
 TREATMENT OF HEART FAILURE
• AIMS
• relieve symptoms,
• Identify and treat cause and precipitating factors of
heart failure
• retarding disease progression and improve quality
and length of life.
 Drug management
• 1. Diuretics : act by promoting renal excretion of
salt and water by blocking tubular reabsorption of
sodium and chloride.

• The resulting loss of fluid reduces ventricular filling

pressures (preload), and rapidly improves dyspnoea
and peripheral oedema.

• The intravenous administration of loop diuretics

such as furosemide also causes arteriolar
vasodilatation, hence reducing afterload, an action
that is independent of its diuretic effect
• Loop diuretics eg furosemide, ethacrynic acid
bumetanide: S/E= hypokalaemia, hypercalcaemia,
hypomagnesaemia, dyslipidaemia, hyperuricaemia

• Thiazide diuretics e.g bendroflumethiazide,

hydrochlorothiazide, chlorthalidone. S/E=
hypokalaemia

• Thiazide diuretics in combination with loop diuretics

have a synergistic action and greater diuretic effect.
Associated metabolic abnormalities are more likely
and close supervision is needed.
• Metolazone is a powerful thiazide, producing
profound diuresis acting synergistically with loop
diuretics.

• This combination is only used for the treatment of

severe and resistant heart failure.

• NO SURVIVAL BENEFIT OF DIURETICS

• Depletion of potassium and magnesium may

predispose to the development of lethal ventricular
arrhythmias
• Potassium-sparing diuretics: aldosterone
antagonists: Spironolactone, eplerenone

• Randomized Aldactone Evaluation Study (RALES)

showed a 30% reduction in all-cause mortality
when spironolactone (up to 25 mg) was added to
conventional treatment in patients with moderate
to severe heart failure.

• These results have now been confirmed with

another aldosterone antagonist - eplerenone - that
has less hormonal side-effects.
• 2.Angiotensin-converting enzyme inhibitors ACEI

• CONSENSUS and SOLVD trials showed symptom

improvement and improved prognosis

• SAVE study showed reduced development of overt

heart failure in asymptomatic patients.

• ACEI lower systemic vascular resistance and venous

pressure, and reduce levels of circulating
catecholamines, thus improving myocardial
performance.
• S/E: first-dose hypotension, hyperkalaemia, cough
(inhibition of bradykinin metabolism)
• E.g. Captopril, enalapril, lisinopril, ramipril

• 3. Angiotensin II receptor antagonists (ARA) (e.g.

losartan, ibersartan, candesartan and valsartan)
have similar haemodynamic effects to ACEI, but as
they do not affect bradykinin metabolism, they do
not produce a cough.

• Also reduce death and hospital admission.

• 4. Venodilators . Short- and long-acting nitrates (e.g.
glyceryl trinitrate and isosorbide mononitrate) act by
reducing preload and lowering venous pressure, with
resulting reduction in pulmonary and dependent
oedema.

• With chronic use, tolerance develops with loss of

efficacy and consequent worsening of heart failure.

• Only combination therapy of nitrate with hydralazine

(Veterans Heart Failure Trials, VHeFT) has been shown
to improve mortality and exercise performance, and
may be useful when ACEI are contraindicated. The
benefit of vasodilators is not as great as with ACEI
(VHeFT 2).
• 5. β-Adrenoceptor blocking agents
• MERIT and CIBIS 2 trials using the beta-blockers
metoprolol and bisoprolol respectively have shown
improved symptomatic class, exercise tolerance,
left ventricular function and mortality in patients
with heart failure of any cause.

• The US Carvedilol Studies using carvedilol, a non-

selective vasodilator beta-blocker with additional
vasodilator and antioxidant properties, has also
demonstrated a significant improvement in
mortality.
• The current guidelines recommend that beta-
blockers bisoprolol and carvedilol should be
initiated in patients with confirmed heart failure

• initial doses should be low, e.g. carvedilol 3.125 mg

twice daily and should be titrated slowly over a
period of months rather than days.

• Patients who are in heart failure and already on

treatment with a beta-blocker for a coexisting
condition, such as coronary artery disease or
hypertension, should continue with their current
beta-blocker initially.
• 6. Digitalis glycosides : Digitalis
\ glycosides have
been used for many years in patients with heart
failure and atrial fibrillation.

• A large prospective trial (Digoxin Investigation

Group (DIG) trial) showed digoxin does not improve
mortality but reduces hospital stay in patients in
heart failure

• patients who are hospitalized or present with

severe heart failure in spite of therapy with
vasodilators, beta-blockers, diuretics should have
digoxin added to their therapeutic regimen.
• 90% is excreted unchanged in urine, accumulation
can occur in renal failure.

• Digoxin acts as a positive inotrope by competitive

inhibition of Na+/K+-ATPase, producing high levels of
intracellular Na+. This is then exchanged for
extracellular Ca2+.

• High levels of intracellular Ca2+ result in enhanced

actin-myosin interaction & increased contractility
• Digoxin is administered orally (1 mg loading and
0.125-0.25 mg daily according to body mass and
renal function).

• Trough serum levels should be monitored (1.3-2.6

nmol/L) and hypokalaemia should be avoided.

• The elderly and patients with hyperthyroidism are

more prone to digoxin toxicity.

• In patients with fluctuating renal function, digitoxin,

which is metabolized by the liver, is preferable
• The most common features of digoxin toxicity:
anorexia, nausea, altered vision , arrhythmia (e.g.
ventricular premature beats especially bigeminy,
ventricular tachycardia and AV block) occur at
digoxin levels > 2.5 nmol/L.

• Digoxin toxicity is treated by stopping the drug,

restoration of serum potassium and management
of arrhythmias.

• Digoxin antibody (FAB fragments) is a specific

antidote that is useful for life-threatening toxicity
• 7. IV inotropes E.g. Epinephrine (adrenaline),
dobutamine, dopexamine and dopamine are
intravenous adrenergic agonists.

• Used in severe heart failure especially in

cardiogenic shock

• E.g dobutamine, epinephrine

• Dobutamine predominantly acts on the β1-
adrenoceptor, increasing intracellular cyclic AMP,
which in turn increases calcium availability for
myocardial contraction.

• Dobutamine also causes peripheral vasodilatation

by an anti-α-adrenergic effect.

• Dopexamine is a selective β2 agonist with an

additional action on peripheral dopamine receptors
that theoretically results in improved renal
perfusion.
• Dopamine is a less selective inotrope that is often
used in a low dose to improve renal perfusion (via
dopaminergic receptors)

• Intermittent intravenous infusions of dobutamine

may produce long-lasting improvements in
symptoms and exercise performance at the cost of
increased mortality.
• 8.Anticoagulants and antiplatelets: Heart failure is
associated with a fourfold increase in the risk of a
stroke.

• Oral anticoagulants e.g warfarin, dabigatran are

recommended in patients with atrial fibrillation and
are also recommended in sinus rhythm with a
history of thromboembolism, endocardial thrombus
or LV aneurysm.

• Aspirin (75mg or 81mg) is recommended in HF

patients with ischemic heart disease for the
prevention of MI and death
• 9. Antiarrhythmic agents : Precipitating factors
should be treated, in particular electrolyte
disturbance.
• Atrial fibrillation (AF) is common in HF and leads to a
deterioration in symptoms. Amiodarone is
commonly used in treatment of AF.

• Restoration of sinus rhythm, either by electrical

cardioversion or drugs, is desirable but less
successful in the presence of structural heart
disease and decompensated HF.

• Rate control with digoxin is often preferred in AF.

• Arrhythmias are frequent in HF and are implicated
in sudden death.

• Patients with sustained episodes of ventricular

tachycardia should receive an implantable
cardioverter-defibrillator (ICD).

• The ICD is likely to improve the survival prospects of

patients who have not yet developed serious
ventricular arrhythmias and when a life-threatening
arrhythmia has already been suffered, an ICD is the
best therapy to prevent mortality due to ventricular
arrhythmias.
• Beta-blockers, ACEI, ARBs and spironolactone
reduce sudden cardiac death in patients with heart
failure.

• It should be noted that ACEI probably exert an

indirect antiarrhythmic effect by reducing high
circulating levels of norepinephrine (noradrenaline)
and improving cardiac function.

• Patients with diastolic heart failure have similar

prognostic implications to those with systolic heart
failure and should be treated in a similar way.
• Drugs such as α-adrenergic blockers (e.g. prazosin)
and direct smooth-muscle relaxants (e.g.
hydralazine) are potent arteriolar vasodilators but
are not very effective in heart failure.

• Calcium-channel blockers also reduce afterload, but

first-generation calcium antagonists (diltiazem,
nifedipine) may have a detrimental effect on left
ventricular function in patients with heart failure.

• The PRAISE 2 trial showed that the second-

generation calcium antagonist amlodipine showed
no prognostic benefit in patients with heart failure.
 Non-pharmacological treatment of heart
failure

• 1. Revascularization:
• Factors that must be considered before
recommending surgery include age, symptoms and
evidence for reversible myocardial ischaemia.

• Techniques to try to identify reversible myocardial

include stress echocardiography, nuclear imaging
techniques and positron emission tomography.
• 2. Biventricular pacemaker or implantable
cardioverter-defibrillator

• Pacemakers are indicated in patients with sinoatrial

disease and atrioventricular conduction block.

• Pacemakers are also valuable in patients with

prolonged PR intervals and left bundle branch block

• In patients with NYHA 3 heart failure and left

bundle branch block (MUSTIC study) biventricular
pacing results in an improvement in symptoms and
exercise tolerance.
• Biventricular pacing should also be considered in
patients not responding to therapy in the following
situations:
• systolic heart failure
• non-reversible cause
• highly symptomatic (New York Heart Association
grade 3/4)
• optimal medical therapy
• ventricular dys -synchrony: left bundle branch block
QRS > 120 ms
• Atrio -biventricular pacing has been shown to
improve symptoms and reduce admission to hospital
in patients with left bundle branch block and heart
failure with poor LV function.

• One large trial (COMPANION) shows 21% reduction in

all-cause mortality and all-cause admissions to
hospital in the groups receiving biventricular pacing.

• ICD therapy in patients with NYHA (Grade 1 and 2)

has shown a reduction in mortality compared with
placebo and amiodarone.
• 3. Cardiac transplantation: Cardiac transplantation
has become the treatment of choice for younger
patients with severe intractable heart failure,
whose life expectancy is less than 6 months.

• With careful recipient selection, the expected 1-

year survival for patients following transplantation
is over 90%, and is 75% at 5 years.

• Irrespective of survival, quality of life is dramatically

improved for the majority of patients. The
availability of heart transplantation is limited.
• Several alternatives to transplantation are available:

• cardiomyoplasty (augmentation of left ventricular

contraction by wrapping a latissimus dorsi muscle
flap around the ventricle),

• and the Batista procedure (surgical ventricular size

reduction and remodelling the geometry of the left
ventricle).

• Both procedures have a high mortality and limited

evidence of substantial benefit in the medium term.
• LVAD (left ventricular assist device) and artificial
heart :

• Artificial hearts and left ventricular assist devices

are used as bridges to transplantation or corrective
surgery.

• The available ventricular assist devices include

extracorporeal membrane oxygenation,
univentricular and biventricular extracorporeal non-
pulsatile devices, extracorporeal and implantable
pulsatile devices, and the total artificial heart.
 Monitoring of heart failure patients
• The clinical condition of a person with heart failure may
fluctuate, and repeated admission to hospital is
common.

• Monitoring of clinical status is necessary

• Essential monitoring includes assessment of:
• a. functional capacity (e.g. VO2 max, exercise tolerance
tests, echocardiography)
• b. fluid status (body weight)
• c. cardiac rhythm (ECG, 24-hour tape)
• Renal status (EUCr), Others: FBC, urinalysis
 Multidisciplinary team approach
• Heart failure care should be delivered by a
multidisciplinary team

• The multidisciplinary team should involve specialist

healthcare professionals: heart failure nurse,
dietician, pharmacist, occupational therapist,
physiotherapist, palliative care adviser.

• Good communication is essential for best clinical

management, which should include advice on
anxiety, depression and 'end of life' issues
 Measures to prevent heart failure
• effective treatment of hypertension, diabetes and
hypercholesterolaemia,

• pharmacological therapy following myocardial

infarction.

• cessation of smoking, alcohol and illicit drugs,

 General lifestyle advice
• Education

• Obesity control

• Dietary modification

• Salt restriction is necessary

• In severe heart failure fluid restriction is necessary.

• Alcohol has a negative inotropic effect and heart

failure patients should avoid consumption.

• Smoking should be stopped, with help from anti-

smoking clinics if necessary.

• Physical activity, exercise training and rehabilitation

: For patients with exacerbations of congestive
cardiac failure, bed rest reduces the demands on
the heart and is useful for a few days.
• Migration of fluid from the interstitium promotes a
diuresis, reducing heart failure.

• However, prolonged bed rest may lead to development

of deep vein thrombosis; this can be avoided by daily
leg exercises, low-dose subcutaneous heparin and
elastic support stockings.

• Low-level endurance exercise (e.g. 20-30 minutes

walking three or five times per week, or 20 minutes
cycling at 70-80% of peak heart rate five times per
week) is encouraged in patients with compensated HF.
Strenuous isometric activity should be avoided.
• Vaccination: While prospective clinical trials are
lacking, it is recommended that patients with heart
failure be vaccinated against pneumococcal disease
and influenza.

• Air travel : This is possible for most patients, subject

to clinical circumstances. Check with the airline -
most have guidelines on who should travel.

• Sexual activity: Tell patients on nitrates not to take

phosphodiesterase type 5 inhibitors (e.g. sildenafil)
as it may induce profound hypotension.
• Driving guidance : Driving motor cars and
motorcycles may continue provided there are no
symptoms that distract the driver's attention.

• Symptomatic heart failure disqualifies patients from

driving large lorries and buses.
 Poor prognostic factors in heart failure
• NYHA class 3 or 4
• Cheyne stokes respiration
• Cardiac cachexia
• Low ejection fraction on echocardiogram (<35%)
• Hyponatraemia
• High levels of endothelin
• High levels of Brain natriuretic peptide
• High levels of ADH