Pharmacology of Heart failure

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Presentation transcript:

Pharmacology of Heart failure By Rutendo Ganyani and Sarah Folkerts

What are the signs & symptoms of heart failure?

Signs and Symptoms of heart failure Dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Fatigue Cough (pink, frothy sputum) Nocturia Signs: Resting tachycardia JVP elevation Lung crackles Wheezing 3rd heart sound Peripheral oedema Ascites

What are the NICE guidelines for treatment of LV heart failure?

NICE Guidelines Diuretic for symptom relief…..then ACEi + Beta blockers Consider ARB if patient can’t tolerate ACEi Consider adding an Aldosterone antagonist or an ARB or hydralazine + nitrate Consider hydralazine + nitrate if patient can’t tolerate ACEi and ARBs Digoxin ACEi, beta-blockers, ARB & Spironolactone have mortality benefit in addition to relieving symptoms; Diuretics and digoxin -> symptomatic relief; Hydralazines & Nitrates beneficial to Afro-Caribbean patients Implantable devices When other heart pathologies or risk factors are present, consider treatment for these. e.g. aspirin, Ca-channel blockers Transplantation

Describe the mechanism of action of ACE inhibitors! Side effects? Example?

ACEi pharmacology stop the conversion of angiotensin I to angiotensin II thus stopping all the downstream effects. (vasodilation) Side effects: Dry cough Hyperkalaemia Other side effects include: Teratogenic Hypotension Renal impairment (do not use w/ renal artery stenosis!) Examples: Ramipril Dry cough due to the fact that ACE also converts bradykinin to inactive metabolites -> ACEi cause increased concentration of bradykinin and bradykinin causes cough (prob through bronchoconstriction)

Describe the mechanism of action of ARBs! Side effects? Example?

Angiotensin receptor blocker (ARB) pharmacology Inhibit action of Angiotensin II Reduce vascular resistance Restore tissue perfusion Reduce afterload Reduce aldosterone production Reduced sodium reabsorption Water loss Side effects: Hypotension Renal impairment Hyperkalaemia Examples: Losartan

Control of renin release and formation and action of angiotensin II (RAAS system) Angiotensinogen is produced by the liver. ACE is produced by cells of the pulmonary and renal endothelium.

Describe the mechanism of action of beta blockers! Side effects? Example?

Beta blocker pharmacology block beta-1 adrenergic receptors (Gs coupled receptors which cause an increase in cAMP -> increase in PK-A -> increase of intracellular Ca in cardiac myocytes) in the heart. Reduced heart rate Decrease cardiac contractility Reduce arterial pressure Attenuate ventricular remodelling: fibrosis, apoptosis and arrythmogenesis Side effects: Bronchoconstriction Cardiac depression Bradycardia Hypoglycaemia Fatigue Cold extremities Examples: Bisoprolol, metoprolol Blood pressure lowering effect of beta-blockers: patients with hypertension (although not normotensive subjects) show a gradual fall in arterial pressure that takes several days to develop fully. The mechanism is complex and involves the following: Reduction in cardiac output Reduction of renin release from the juxtaglomerular cells in the kidney a central action, reducing sympathetic activity

Describe the mechanism of action of Aldosterone antagonists! Side effects? Example?

Aldosterone receptor blocker pharmacology Blocks action of aldosterone at DCT (block mineralocorticoid receptors) Reduced expression of ENac Reduced Na+ reabsorption Increased water excretion K+-sparing Side effects: Hyperkalaemia, Hypotension Mainly w/ spironolactone Gynaecomastia, Impotence Examples: Eplerenone, spironolactone Gynaecomastia -> spironolactone also acts as an antagonists on androgen receptors and inhibits androgen production; Epleronone is more selective to the mineralocorticoid receptors and thus has less side effects related to the androgenic receptors

Describe the mechanism of action of Nitrates! Side effects? Example?

Pharmacology of nitrates Metabolised to NO  activate guanylate cyclase  increase in cGMP  activates protein kinase G  vascular relaxation Side effect Headache (due to dilatation of intracranial arteries) Postural hypotension Dizziness Also problem with quickly developing tolerance that can lead to abnormal constriction of coronary arteries following withdrawal

………….and the others Digoxin Digoxin (in particular for heart failure w/ established atrial fibrillation or if symptomatic despite diuretics and ACEi) -> increases inotropy (=pos. inotrope) Hydralazine - Unknown mechanism of action, however it dilates arteries & arterioles -> reducing the afterload. (= vasodilator) Side effects: Tachycardia Headache We will not be looking at transplantation or implantable devices….. Don’t worry about this at this stage. Just know the options exist. Digoxin = cardiac glycoside -> works by inhibiting the Na+/K+ pump in cardiac myocytes; -> more Na+ inside the cell -> Na+/Ca+ exchanger pumps Na+ out of cell in exchange for Ca+ -> Ca+ inside cell accumulates -> force of contraction increases (main effect); additional effects: increase in ectopic pacemaker activity, impairment of AV conduction, increased vagal activity -> bradycardia (Don’t worry about this too much at this stage.)

Summary of site of action of different drugs used to treat heart failure

Any Questions?