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Transcript
Heart Failure
Definition:
Clinical syndrome resulting from inability to maintain adequate cardiac output.
Incidence:
1-2%>/=65 years, 10%>/=75 years
Pathophysiology:
Inadequate cardiac output stimulates compensatory mechanisms which are initially
beneficial but then become maladaptive…
Neurohormonal activation - increase vasoconstrictors- provoke salt + water retention
– increase cardiac afterload – decrease LV emptying and depress CO further –
greater neuroendocrine activation etc
Ventricular dilatation – impaired systolic function + fluid retention increases
ventricular volume – mechanically inefficient, if energy supply limited e.g coronary
disease – further contractile failure and neuroendocrine activation
Left Heart Failure:
 Breathlessness- worse when lying down (orthopnoea), especially in middle of
night (paroxysmal nocturnal dyspnoea)
 Tacchypnoea, tachycardia, 3rd heart sound (gallop rhythm)
 Bibasilar inspiratory pulmonary crepitations- if severe cyanosis, pink frothy
sputum, extensive crepitations
Right heart failure:
 Fluid retention in legs and in severe cases ascites
 Increased JVP + peripheral oedema
Chronic heart failure:
 Cardiomegaly and secondary mitral/tricuspid regurg
 Skeletal muscle loss (cardiac cachexia)
Classification:
Acute heart failure- largely synonymous with LH failure, results from sudden failure
to maintain CO, insufficient time for compensatory mechanisms to develop and
pulmonary oedema predominates.
Chronic heart failure- CO declines gradually, features relating to compensatory
mechanisms dominate, CHF results in secondary pulmonary hypertension + RH
failure = congestive cardiac failure
Aetiology:
LH failure
 inadequate LV filling (mitral stenosis, LVH, pericardial constriction)
 pressure overload (aortic stenosis, hypertension)
 volume overload (aortic/mitral regurg)
 high output (beri beri, thyrotoxicosis)
 LV muscle disease (MI, cardiomyopathy, myocarditis)
RH failure
 Any cause of LH failure
 Pulmonary hypertension (PE, lung disease)
 ASD
Provoking/exacerbating factors- arrhythmias, drug issues (non compliance or fluid
retaining eg NSAIDs), anaemia, infection
Investigations:
Bedside tests- ECG (old MI, LVH, arrhythmias)
Blood tests - BNP
 Electrolytes, renal function, FBC for anaemia, TFTs
Imaging
- CXR= Alveolar oedema, kerley B lines, Cardiomegaly, Diversion to
upper lobes, pleural Effusion
 Echo (transthoracic or transoesophageal)– LV function, ejection
fraction, regional wall abnormalities, valvular disease
Special tests – nuclear isotope scanning, cardiac catheterisation
Management:
Conservative
 Smoking cessation
 Alcohol cessation
 Weight loss/ diet and exercise
 Cardiac rehabilitation
Medical
 Acute- sit up, high flow oxygen, ABC, furosemide, GTN infusion
 Chronic – ACEi/ARB, beta blockers, aldosterone antagonist, digoxin
See NICE guidelines algorithms on page 4 and 6
http://www.nice.org.uk/nicemedia/live/13099/50526/50526.pdf
Surgical
 Cardiac resynchronisation therapy (CRT)
 ICD
 Transplant
Complications:
Thromboembolism- DVT/PE esp in severe CHF, risk reduced by warfarin
AF- complicates CHF, deteriorates, rate control + warfarin
Progressive pump failure- may respond to increasing doses of diuretics, heart
transplant may be an option in some patients
Ventricular arrhythmias- common and may cause syncope or sudden death (25-50%
of deaths in CHF), Tx amiodarone, implantable defibrillators