Download Hibernating myocardium

HEART FAILURE
Jamil Mayet
Consultant Cardiologist
Heart failure
• Cardiac output that is insufficient to meet the
needs of the body
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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
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SOBE
Orthopnoea, PND
Ankle swelling
Anorexia, weight loss
Cold peripheries
Tiredness
Heart failure signs
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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
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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
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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
disease
• 75% of white males in SOLVD were related
to ischaemic heart disease
• 50% of patients in Framingham had an
ischaemic aetiology to their heart failure
• Identification of patients who will benefit
from revascularisation
Hibernating myocardium
• Chronic LV dysfunction does not
necessarily imply dead myocardium
• “Hibernating myocardium” termed by
Rahimtoola in 1989
• LV systolic function improved following
coronary revascularisation
Rahimtoola. Am Heart J 1989;117:211-21
Hibernating myocardium
Pacing for heart failure
Defibrillators 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 inadequate
therapy
CCF appropriate
therapy