Transcript Document
HEART FAILURE Jamil Mayet Consultant 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 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