Post on 21-Jan-2016
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HEART FAILURE
Jamil MayetConsultant Cardiologist
Heart failure
• Cardiac output that is insufficient to meet the needs of the body
– Myocardial dysfunction eg IHD, CM– Volume overload eg AR, MR– Obstruction eg AS, HCM– Diastolic dysfunction eg Constriction– Mechanical problems eg LV aneurysm– Rhythm disturbance eg A fib– High output eg anaemia, shunts, thyrotox
Heart failure - diagnosis
Heart failure symptoms• SOBE
• Orthopnoea, PND
• Ankle swelling
• Anorexia, weight loss
• Cold peripheries
• Tiredness
Heart failure signs• Tachycardia, hypotension
• Raised JVP, S3
• May be PSM of MR (or TR)
• Basal crepitations
• Ankle oedema
Not useful to divide into right and left heart failure
Heart failure - diagnosis
ECG - normal
If ECG normal very unlikely to be systolic dysfunction
ECG - abnormal
Previous MI, LBBB, Non-specific ST/T abnormalities
CXR – pulmonary oedema
CXR – septal lines
Echocardiography
• Confirms / refutes diagnosis of systolic dysfunction
• Can exclude significant valvular disease• Can suggest ischaemic aetiology if regional
wall motion abnormality• Can assess diastolic dysfunction
Treatment – Acute heart failure• Sit up
• High dose oxygen
• Intravenous loop diuretic
• Venodilation eg intravenous GTN
• Possibly intravenous diamorphine
• (Venesection, dialysis)
• Intubation and ventilation
Cardiogenic shock•Severe hypotension
•Poor tissue perfusion - Oliguria, Confusion
•Mortality 80%+
•Inotropes eg Dopamine, Dobutamine
•IABP +/- angioplasty if cardiac ischaemia
Chronic heart failure - Mortality
Heart failure - treatment
• Salt restriction
• Fluid restriction
• Diuretics– Usually loop diuretics– Occasionally add thiazides
• May lead to excessive diuresis, electrolyte imbalance
• Amiloride, triamtarene may prevent low K
Treatment – vasodilators
• Reduce preload / afterload– ACEI
• Reduce morbidity and mortality• Interact with RAAS• Prevent adverse remodelling post MI• May precipitate renal failure• Cough in 10-15% (consider AII blockers)
– Nitrates and hydralazine• Reduce morbidity / mortality but less than ACEI
Treatment - inotropes
• Digoxin – Reduces hospital admissions– No reduction in mortality– Stopping may precipitate deterioration
• All other oral positive inotropes to date have caused an increased mortality
Treatment – beta blockers
Treatment – beta blockers
• Similar degree to ACEI and additive
• Possibly via reduction in sympathetic activation
• May precipitate pulmonary oedema– Start low doses and slowly titrate up
Treatment – spironolactone
Treatment - spironolactone
• Probably via blockage of aldosterone
• May precipitate hyperkalaemia and renal failure
Diagnosing ischaemic heart Diagnosing ischaemic heart diseasedisease
• 75% of white males in SOLVD were related 75% of white males in SOLVD were related to ischaemic heart diseaseto ischaemic heart disease
• 50% of patients in Framingham had an 50% of patients in Framingham had an ischaemic aetiology to their heart failureischaemic aetiology to their heart failure
• Identification of patients who will benefit Identification of patients who will benefit from revascularisationfrom revascularisation
Hibernating myocardiumHibernating myocardium
• Chronic LV dysfunction does not Chronic LV dysfunction does not necessarily imply dead myocardiumnecessarily imply dead myocardium
• ““Hibernating myocardium” termed by Hibernating myocardium” termed by Rahimtoola in 1989Rahimtoola in 1989
• LV systolic function improved following LV systolic function improved following coronary revascularisationcoronary revascularisation
Rahimtoola. Am Heart J 1989;117:211-Rahimtoola. Am Heart J 1989;117:211-2121
Hibernating myocardiumHibernating myocardium
Pacing for heart failurePacing for heart failure
Defibrillators for heart failureDefibrillators for heart failure
Diastolic heart failure
• Up to a third of patients have clinical heart failure with normal LV systolic function
• Underlying pathophysiology relates to diastolic dysfunction
• Commonest underlying pathologies – Normal ageing– Hypertension– Myocardial ischaemia
Mechanisms of diastolic dysfunction
• Impaired ventricular relaxation– Energy dependent process– Susceptible to myocardial ischaemia
• Decreased myocardial compliance– Altered compliance mediated by collagen– Fibrosis related to activation of RAAS
Heart failure therapy - rule of halves
Treatment - no CCF
CCF - inadequatetherapy
CCF -appropriatetherapy