Treating heart failure

1. Treating heart failure First talk in series of 3

2. Common causes of chronic heart failure • Myocardial dysfunction: • Hypertension • Ischaemic heart disease. • The cardiomyopathies (e.g. alcohol). • Valvular heart disease • Stenosis • Incompetence. • High output states

3. Common causes of acute heart failure • Acute myocardial dysfunction: • Cardiogenic shock after MI. • Myocarditis. • Acute valve defects • Rupture in infective endocarditis • Altered rhythm • Fast – poor filling = low CO = shock • Slow – low rate = low CO = shock • Massive pulmonary embolism

4. Left, right or both? • We distinguish left and right sided failure. • Biventricular failure and left heart failure are common. • Isolated right heart failure (“cor pulmonale”) is less common.

5. Prevention is better than cure • Detect and effectively manage HBP. • Smoking, diabetes mellitus and other vascular risk factors. • Alcohol.

6. Symptoms of left heart failure • Chronic: • Dyspnoea, orthopnoea and PND. • Cough and wheeze. • Malaise • Acute: • Same plus… • Symptoms of low blood pressure • Cough – frothy pink sputum

7. Signs of left heart failure • Fine basal crackles. • Third or fourth heart sound (or both – “Gallop rhythm”). • Central cyanosis. • Low BP, if the problem is acute.

8. Symptoms of right heart failure • Chronic (usually in presence of LHF) • Peripheral swelling (dependent parts) • Acute (e.g. after massive PE) • Hepatic pain

9. Signs of right heart failure • Pitting oedema of legs and sacrum • Raised JVP • Hepatomegaly. • Ascites.

10. Prognosis, and aims of treatment • 5-year survival with LVF is as bad as many cancers • Save life in the acute circumstance. • Relieve symptoms. • Prolong life (spironolactone and -blockers).

11. Differential diagnoses • Left heart failure: • Asthma • Pneumonia • Right heart failure: • Nephrotic syndrome. • Chronic liver disease

12. Initial investigation • Biochemistry and haematology • Renal impairment, albumin, thyroid function and haemoglobin • Chest X-ray: • cardiac size, presence of pulmonary oedema or effusions. • ECG: • cardiac size and evidence of muscle disease • Echocardiography: • Dimensions, valve function

13. Drugs for heart failure • Diuretics • Thiazides • Loop • Potassium sparing • Vasodilators • ACE-inhibitors • A2 receptor antagonists • Nitrates • Inotropic agents • (Beta blockers)

14. Thiazides • Mainly used for hypertension. • Not potent naturesis, so less useful for heart failure. • Example: bendrofluazide. • Adverse effects: • Hypokalaemia • Hyperuricaemia and gout • Hypercalcaemia • Reduced glucose tolerance. • Impotence

15. The loop diuretics: mode of use • Potent naturesis and diuresis. • Steep dose-response curve. • Given i.v. for acute pulmonary oedema. Symptoms may be ameliorated within 30 min. • Given orally (often twice daily) in the ‘maintenance’ treatment of CCF. • Examples: frusemide (furosemide) and bumetanide.

16. The loop diuretics: mechanism of action • Filtered by the glomerulus. • Action is from the LUMINAL side of the tubular cells (so action correlates inversely with renal function). • Inhibition of Na Cl absorption in the ascending loop of Henle • At high concentration frusemide is a vasodilator.

17. Loop diuretics: adverse effects • Severe dehydration – even shock. • Hypokalaemic metabolic alkalosis. • Hypomagnesaemia. • Ototoxicity: especially with i.v. use. • Hyperuricaemia and gout • Calcium excretion. • Reduced glucose tolerance.

18. Potassium-sparing diuretics: e.g. spironolactone. • Antagonists of aldosterone. • Not usually potent enough alone. • Usually + loop diuretic. • Reduce mortality (+ACE-i and loop diuretic) • Adverse effects: • Hyperkalaemia (especially with ACE-i) • Gynaecomastia

19. Vasodilators: ACE-inhibitors. • ACE converts A1 to A2. • A2 is an arteriolar constrictor. • A2 increases adrenalin release from adrenal medulla. • A2 causes aldosterone release (hence salt retention). These actions increase heart work by raising the peripheral resistance (afterload). This action increases heart work by raising the venous return (pre-load).

20. Vasodilators: ACE-inhibitors. • ACE-i lower preload and afterload by blocking the synthesis of A2. • Example: enalapril. • No parenteral formulation: ACE-i are used orally in chronic left, or biventricular, heart failure.

21. Vasodilators: ACE-inhibitors. • Adverse effects include: • Renal failure (especially in Renal Artery Stenosis). • Chronic cough. • Hypotension (especially with the first dose).

22. Vasodilators: ACE-inhibitors. • Contraindications and cautions: • Renal artery stenosis. • Aortic stenosis. • Previous angioedema • Pregnancy

23. Vasodilators: A2 receptor antagonists • Competitive antagonism of A2 at its receptors. • Example: losartan. • Used for hypertension. • More recently, also licensed for heart failure. • Unlike ACE-i, A2 antagonists do not cause cough

24. Vasodilators: nitrates • Examples: GTN (brief action) isosorbide (longer action). • All cause release of NO in smooth muscle  relaxation (mainly veins). • Reduced venous return. • GTN: first pass metabolism. • Isosorbide metabolised to active form. Available for i.v. use. Angina Angina and CCF (the intravenous form is used in acute CCF.

25. Vasodilators: nitrates • Adverse effects during intravenous use: • Dose-related hypotension. • Adverse effects during oral use: • Headache.

26. Inotropic drugs • Most commonly needed after large MI, with ‘cardiogenic shock’. • Low BP, poor renal/splanchnic perfusion. Acute renal failure. • High mortality rate.

27. Inotropic drugs • Example: dobutamine. • Given i.v. and very short half-life. So, infusion rate determines plasma concentration. • Lower infusion rates:  contractility and CO. • Higher infusion rates: arterial constriction (and tendency to reduced splanchnic perfusion).

28. Oral inotropes • Digoxin: mainly used to control ventricular rate in atrial fibrillation. • Digoxin does have some + inotropic action. • And is used in advanced CCF in the hope of benefit.

29. -Blockers. • -Blockers are negatively inotropic, and make CCF worse if used incautiously. • But they have other actions too (inc. anti-arrhythmic). • And reduce mortality in patients on treatment with diuretic and ACE-i. • Example: carvedilol.

30. Emergency management of LVF causing pulmonary oedema • High flow oxygen. • Sit upright. • Intravenous loop diuretic. • Cautious use of diamorphine (beware BP; beware type-2 resp failure). • IV infusion of nitrate (by pump). • Inotropic support if BP low.