Condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure
It can result from any cardiac disease that compromises ventricular systolic or diastolic function or both
The term "congestive heart failure" is reserved for patients with breathlessness and abnormal sodium and water retention resulting in oedema
left ventricular dysfunction
exposure to cardiotoxic agents
history of left ventricular hypertrophy
valvular heart disease
elevated tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)
elevated C-reactive protein (CRP)
decreased insulin-like growth factor-1 (IGF-1)
elevated natriuretic peptides
dilation of the left ventricle
increased left ventricular mass
abnormal left ventricular diastolic filling
family history of heart failure
low socio-economic status
excess alcohol consumption
excess sodium intake
excess coffee consumption
Post-partum cardiomyopathy (PPCM)
The prevalence of CHF in the western world has been estimated at 1% to 2%
The incidence is thought to approach 5 to 10 per 1000 people per year. 
In the UK, CHF is thought to account for a total of 1 million inpatient bed days and 5% of all emergency admissions
These figures are projected to rise by as much as 50% in the next 25 years. 
The number of deaths is increasing steadily despite advances in treatment
in part because of increasing numbers of patients with heart failure
due to better treatment and reduced mortality of patients with acute MIs earlier in life.
The incidence of heart failure approaches 10 per 1000 population after age 65 years
Approximately 80% of patients hospitalised are more than 65 years old. 
There are numerous and varied causes of heart failure:
Other cardiovascular disease:
coronary artery disease
valvular heart disease
congenital heart diseases
Borrelia burgdorferi (Lyme disease)
hypoparathyroidism with hypocalcaemia
Systemic collagen vascular diseases
some antiviral agents
These conditions tend to increase metabolic demand
May or may not be matched by a sufficient increase in cardiac output by the failing heart
Tachyarrhythmias also decrease the diastolic ventricular filling time and increase myocardial oxygen demand
Uncontrolled hypertension depresses systolic function
Increases the afterload against which the failing ventricle must pump blood
May be the first clinical manifestation.
Many of these causes may be completely reversible given appropriate and timely treatment/intervention
Some causes, such as scarred myocardium or dilated cardiomyopathy, are currently considered irreversible
Key diagnostic factors
presence of risk factors (common)
neck vein distension (common)
S3 gallop (common)
hepatojugular reflux (common)
orthopnoea and paroxysmal nocturnal dyspnoea (uncommon)
Other diagnostic factors
tachycardia (HR >120 bpm) (common)
chest discomfort (common)
ankle oedema (common)
night cough (common)
pleural effusion (common)
fatigue, muscle weakness or tiredness (common)
palpitations, pre-syncope, or syncope (uncommon)
Heart failure represents a complex syndrome
An initial myocardial insult results in the over-expression of multiple peptides
With different short- and long-term effects on the cardiovascular system
Neurohormonal activation is recognised to play a pivotal role in the development as well as the progression of heart failure
In the acute phase, neurohormonal activation seems to be beneficial
Maintains adequate cardiac output and peripheral perfusion
Sustained neurohormonal activation, however, is deleterious
Results in increased wall stress, dilation, and ventricular remodelling
Contribute to disease progression in the failing myocardium
Eventually leads to further neurohormonal activation.
Remodelling occurs in several clinical conditions, including MI, cardiomyopathy, hypertension, and valvular heart disease
Hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis.
One potential deleterious outcome of remodelling is the development of mitral regurgitation
As the left ventricle dilates and the heart assumes a more globular shape
Mitral regurgitation results in an increasing volume overload on the overburdened left ventricle
Further contributes to remodelling and progression of disease and symptoms
systolic heart failure
depressed and dilated left and/or right ventricle with low ejection fraction
diastolic heart failure
left ventricular ejection fraction (LVEF) normal
but left ventricular hypertrophy (LVH) and abnormal diastolic filling patterns
evidence of underlying CAD, LVH, or atrial enlargement
may be conduction abnormalities and abnormal QRS duration
Anaemia and high lymphocyte percentage are strong risk factors and prognostic markers of poor survival
laboratory testing may reveal important heart failure aetiologies
presence of disorders or conditions that can lead to or exacerbate heart failure
laboratory testing could also reveal important modulators of therapy
serum electrolytes (including calcium and magnesium)
decreased sodium (usually <135 millimols/L)
Important to record baseline values
serum creatinine, blood urea nitrogen
Reflects tissue perfusion, fluid status, rules out renal disease
normal to elevated
elevated in diabetes
normal to elevated
TFTs (especially TSH)
hypothyroidism: elevated TSH, decreased FT3, decreased FT4
hyperthyroidism: decreased TSH, elevated FT3, elevated FT4
elevated in dyslipidaemia
decreased in end-stage heart failure, especially in the presence of cardiac cachexia
B-type natriuretic peptide (BNP)/N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels
standard exercise stress testing (bicycle or treadmill)
reduced exercise capacity in idiopathic dilated cardiomyopathy
reduced exercise capacity and signs of impaired myocardial perfusion in ischaemic cardiomyopathy
cardiopulmonary exercise testing (CPX) with VO2max
6-minute walking test exercise
as an alternative to CPX it may provide an objective assessment of the patient's functional status
right heart catheterisation
provides objective haemodynamic assessment of left ventricular filling pressure
gives direct measures of cardiac output and pulmonary and systemic resistance
rarely necessary to establish the aetiology of heart failure
provides definitive pathological evidence of cardiac and systemic disease
Dietary sodium intake
Easily modifiable factor that complements pharmacological therapy for heart failure.
Patient and family are advised to follow a daily dietary sodium intake between 2 and 3 g.
Further restriction to 1 to 2 g/day may be necessary for patients with advanced symptoms refractory to therapy.
Mostly used as an in-hospital complimentary measure in cases of acute exacerbations
In addition, fluid restriction may be warranted in cases of severe hyponatraemia.
However, it would be of importance to advise the patient to keep a daily intake/output balance at home.
Patients are advised to monitor their weight daily
Heart failure patients need continuous and close monitoring of their health
A variety of programmes have been shown to decrease morbidity and rehospitalisation in this context
Home nursing, telephone advice/triage, telemedicine services, and specialised heart failure clinic-based care. 
Shown to decrease the morbidity and mortality associated with heart failure,    [A Evidence]
Should be given to all patients with left venticular (LV) dysfunction, symptomatic or otherwise
Unless there is a contra-indication or prior intolerance to therapy.
Should be used with caution in patients in cardiogenic shock, with marginal renal output or hyperkalaemia.
If patients have an idiosyncratic reaction, with angio-oedema, ACE inhibitors should not be rechallenged.
All patients with chronic heart failure receive a beta-blocker once established on an ACE inhibitor
Unless there is a contra-indication
Bradycardia, reactive airway disease, and unstable or low-output heart failure.    [A Evidence]
Carvedilol seems superior to metoprolol,  although there is no evidence of superiority to other beta-blockers.
Decrease the morbidity and mortality associated with symptomatic chronic heart failure
Should be used in early post-MI patients with LV dysfunction and/or moderate-to-severe heart failure (NYHA III or IV). 
Should be initiated after titration of standard medical therapy.
Spironolactone[B Evidence] and eplerenone[A Evidence] can both cause hyperkalaemia
Precautions should be taken to minimise the risk.
These agents should be used with caution in patients with renal dysfunction and hyperkalaemia.
Hydralazine + isosorbide dinitrate
Reasonable for patients with reduced left ventricular ejection fraction (LVEF) who are already taking an ACE inhibitor and beta-blocker for symptomatic heart failure and who have persistent symptoms (class IIa), 
Has demonstrated benefit in black patients with heart failure.  
May decrease symptoms of dyspnoea at night and during exercise
May improve exercise tolerance in patients who have persistent limitations despite optimisation of other therapies.  
Development of nitrate tolerance seems to be minimised by prescription of a nitrate-free interval of at least 10 hours. 
Carvedilol use has been shown to prevent nitrate tolerance in patients with CHF.  
Produce symptomatic benefits more rapidly than any other drug for heart failure.
Can relieve pulmonary and peripheral oedema within hours or days.
Few patients with heart failure and fluid retention can maintain sodium balance without the use of diuretic drugs. 
Diuretics alone are unable to maintain the clinical stability of patients with heart failure for long periods of time, 
Risk of clinical decompensation can be reduced when they are combined with an ACE inhibitor and a beta-blocker. 
Can be beneficial in patients with current or prior symptoms of heart failure or reduced left ventricular ejection fraction (LVEF)
Especially those with atrial fibrillation.
All existing models to predict the risk of death or need for urgent transplantation have features that may limit their applicability.
Haemoglobin A1c was also found to be an independent progressive risk factor for cardiovascular death, hospitalisation, and mortality, even in non-diabetic patients. 
The most comprehensive prognostic model is the Seattle Heart Failure Model. [The Seattle Heart Failure Model] (external link)
Has been implemented as an interactive programme that employs the Seattle Heart Failure Score to estimate mean, 1-, 2-, and 5-year survival and the benefit of adding medicines and/or devices for an individual patient. 
Despite standard medical therapy, a patient with persistent NYHA class IV symptoms still has an annual mortality risk of 40% to 60%, compared with 5% to 10% for NYHA I or II patients.