1. HEART FAILURE Jamil Mayet Consultant Cardiologist

2. 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

6. Heart failure - diagnosis

7. 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

8. Heart failure - diagnosis

9. ECG - normal If ECG normal very unlikely to be systolic dysfunction

10. ECG - abnormal Previous MI, LBBB, Non-specific ST/T abnormalities

11. CXR – pulmonary oedema

12. CXR – septal lines

13. 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

14. 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

15. Chronic heart failure - Mortality

16. 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

17. 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

21. 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

23. Treatment – beta blockers

24. Similar degree to ACEI and additive Possibly via reduction in sympathetic activation May precipitate pulmonary oedema –Start low doses and slowly titrate up

25. Treatment – spironolactone

26. Treatment - spironolactone Probably via blockage of aldosterone May precipitate hyperkalaemia and renal failure

28. Diagnosing ischaemic heart disease 75% of white males in SOLVD were related to ischaemic heart disease75% of white males in SOLVD were related to ischaemic heart disease 50% of patients in Framingham had an ischaemic aetiology to their heart failure50% of patients in Framingham had an ischaemic aetiology to their heart failure Identification of patients who will benefit from revascularisationIdentification of patients who will benefit from revascularisation

29. Hibernating myocardium Chronic LV dysfunction does not necessarily imply dead myocardiumChronic LV dysfunction does not necessarily imply dead myocardium “Hibernating myocardium” termed by Rahimtoola in 1989“Hibernating myocardium” termed by Rahimtoola in 1989 LV systolic function improved following coronary revascularisationLV systolic function improved following coronary revascularisation Rahimtoola. Am Heart J 1989;117:211-21

30. Hibernating myocardium

31. Pacing for heart failure

32. Defibrillators for heart failure

33. 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

34. 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