Heart failure pathophysiology and treatment .pptx

The pathophysiology of heart failure and it's effects

1. INVESTIGATION MODALITIES : ECG – normal of high NPV Chest X ray r/o DD Dyspnoea 2D Echocardiography LV dysfunction systolic/ diastolic Aetiology Biochemistry and haematology Natriuretic peptides; NT- BNP Others: Stress testing; Holter , Catheterisation, RNA, MRI

2. Management Aims Prevention Prevention and/ or controlling of diseases leading to cardiac dysfunction and heart failure Prevention of progression to heart failure once cardiac dysfunction is established Morbidity: Maintenance or improvement in quality of life Mortality: increased longevity Management Strategies Non pharmacological intervention and lifestyle modification Symptomatic therapy Disease modifying therapy Other pharmacological agents Device therapy Surgical options

3. Non- Pharma and Lifestyle Modifications Physical activity Beneficial effects of exercise, skeletal muscle, autonomic endothelial ad neurohormonal function, insulin sensitivity, but no positive effects on survival Walking and cycling Daily measurement of weight diuretic optimisation Dietary Modification Moderate dietary sodium restriction Reduce/ stop alcohol consumption Weight reduction and monitoring Vaccination- influenza, pneumococcal Education and counselling of pt and family or caretakers on the condition

4. Symptomatic Therapy Diuretic <<Signs and symptoms of HF No mortality benefit Mega- doses = poorer outcome Fluid restriction Loop diuretic  sequential nephron blockade with a thiazide better than higher doses of loop alone With RAAS blocker Monitor renal function, correct <<K+

5. Digoxin Role – less clear absence AF (NSR): Useful in rate control in AF Indicated in: Symptomatic pts after maximal doses medical Rx and frequent hospitalizations Rate control in AF Large RCTs – no mortality benefit DIG trial DIG trial No mortality benefit (digoxin) Improves symptoms, exercise tolerance Reduced morbidity – worsening HF & hospitalization Indication: symptomatic after maximal EBM Low dose Avoid hyperkalemia

6. DISEASE MODIFYING THERAPY : Neurohormonal Interventions ACE Inhibitors Beta- adrenoceptor antagonists Aldosterone antagonists AT- II Receptor antagonists Hydralazine/ Nitrates

7. ACE-I 1 st line agents Indicated in all with LVSD  symptomatic with diuretic in decompensated states Unequivocally shown to reduce M & M Mean RR reduction 25% in large trials Contraindications Significant renal disease Angio-edema Persistent cough   AT – II Receptor Antagonists Effective alternative to truly ACE- I intolerant pts

8.   Beta blockers Provide significant mortality and long- term symptomatic benefits in All grades of HF Post MI- LVSD Evidence based: Nebivolol , Metoprolol, Bisoprolol , Carvedilol Start only in pts free of decompensation, then “start slow- go slow” Beta blockers… not indicated with Unstable HF Systolic pressure < 90mmHg Severe fluid overload Intravenous inotropic agent Sinus bradycardia, atrioventricular block Bronchospastic disorder   Aldosterone Antagonists

9. Aldosterone antagonists: Spironolactone/ Eplerenone Reduced morbidity and mortality in pts with moderate- severe HF (NYHA III/ IV) combined with standard ACE-I + BB therapy Caution: hyperkalaemia   Hydralazine/ Nitrates Considered In pts intolerable to ACE-I and ARBs African- American descent

10. Drugs to avoid The following may exacerbate HF NSAIDS Rate limiting CCBS- Diltiazem/ Verapamil Class I antiarrhythmics Steroids TCAs