Definition - 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
Risk Factors - Strong
- MI
- diabetes mellitus
- dyslipidaemia
- old age
- male
- hypertension
- left ventricular dysfunction
- cocaine abuse
- exposure to cardiotoxic agents
- history of left ventricular hypertrophy
- renal insufficiency
- valvular heart disease
- sleep apnoea
- elevated homocysteine
- 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
- Weak
- low socio-economic status
- tobacco consumption
- excess alcohol consumption
- excess sodium intake
- excess coffee consumption
- obesity
- tachycardia
- depression/stress
- microalbuminuria
Differential diagnosis Epidemiology - 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. [3]
- 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. [4]
- 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. [1]
Aetiology - There are numerous and varied causes of heart failure:
- Other cardiovascular disease:
- coronary artery disease
- cardiomyopathies
- hypertension
- myocarditis
- valvular heart disease
- congenital heart diseases
- Pericardial disease
- Toxin-induced
- heroin
- alcohol
- cocaine
- amfetamines
- lead
- arsenic
- cobalt
- phosphorus
- Infection
- bacterial
- fungal
- viral (HIV)
- Borrelia burgdorferi (Lyme disease)
- Infiltrative diseases
- amyloidosis
- haemochromatosis
- sarcoid
- Electrolyte imbalance
- hypocalcaemia
- hypophosphataemia
- hypokalaemia
- hyponatraemia
- Endocrine disorders
- diabetes mellitus
- thyroid disease
- hypoparathyroidism with hypocalcaemia
- phaeochromocytoma
- acromegaly
- Systemic collagen vascular diseases
- lupus
- rheumatoid arthritis
- systemic sclerosis
- polyarteritis nodosa
- hypersensitivity vasculitis
- Takayasu syndrome
- polymyositis
- Reiter's syndrome
- Drug-induced
- adriamycin
- cyclophosphamide
- sulphonamides
- some antiviral agents
- Nutritional deficiencies
- thiamine
- protein
- selenium
- L-carnitine
- Pregnancy
- peripartum cardiomyopathy.
- 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
Clinical features - Key diagnostic factors
- presence of risk factors (common)
- dyspnoea (common)
- neck vein distension (common)
- S3 gallop (common)
- cardiomegaly (common)
- hepatojugular reflux (common)
- rales (common)
- orthopnoea and paroxysmal nocturnal dyspnoea (uncommon)
- nocturia (uncommon)
- Other diagnostic factors
- tachycardia (HR >120 bpm) (common)
- chest discomfort (common)
- hepatomegaly (common)
- ankle oedema (common)
- night cough (common)
- pleural effusion (common)
- fatigue, muscle weakness or tiredness (common)
- palpitations, pre-syncope, or syncope (uncommon)
- lethargy/confusion (uncommon)
Pathophysiology - 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
Investigations- transthoracic echocardiogram
- 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
- ECG
- evidence of underlying CAD, LVH, or atrial enlargement
- may be conduction abnormalities and abnormal QRS duration
- CXR
- FBC
- 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)
- altered potassium
- Important to record baseline values
- serum creatinine, blood urea nitrogen
- Reflects tissue perfusion, fluid status, rules out renal disease
- normal to elevated
- blood glucose
- LFT
- TFTs (especially TSH)
- hypothyroidism: elevated TSH, decreased FT3, decreased FT4
- hyperthyroidism: decreased TSH, elevated FT3, elevated FT4
- blood lipids
- 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
- endomyocardial biopsy
- rarely necessary to establish the aetiology of heart failure
- provides definitive pathological evidence of cardiac and systemic disease
Managementa) conservative- 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.
- Fluid restriction
- 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. [131]
- Exercise training
- Has also been shown to be beneficial. [86] [87]
b) medical - ACE inhibitors
- Shown to decrease the morbidity and mortality associated with heart failure, [1] [88] [89] [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.
- Beta-blockers
- All patients with chronic heart failure receive a beta-blocker once established on an ACE inhibitor
- Unless there is a contra-indication
- Carvedilol seems superior to metoprolol, [132] although there is no evidence of superiority to other beta-blockers.
- Aldosterone antagonists
- 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). [1]
- 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), [1]
- Has demonstrated benefit in black patients with heart failure. [99] [100]
- 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. [133] [134]
- Development of nitrate tolerance seems to be minimised by prescription of a nitrate-free interval of at least 10 hours. [1]
- Carvedilol use has been shown to prevent nitrate tolerance in patients with CHF. [135] [136]
- Diuretics
- 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. [139]
- Diuretics alone are unable to maintain the clinical stability of patients with heart failure for long periods of time, [139]
- Risk of clinical decompensation can be reduced when they are combined with an ACE inhibitor and a beta-blocker. [140]
- Digoxin
- 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.
c) surgicalPrognosis- 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. [187]
- 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. [181]
- 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. [1]
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