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Similar to b-blockers.pptx is a presentation about beta blockers
b-blockers.pptx is a presentation about beta blockers
- 1.
- 2. Beta blockers •Drugs whichinhibit adrenergic response mediated by beta receptors
- 3. BETA RECEPTORS Receptors Sitesactions β1 Heart JG cells-kidney Posterior pituitary Adipose tissue stimulatory Renin release ADH release lipolysis β2 Bronchi Blood vessels of skeletal muscle Smooth muscle (Uterus ,intestine , detrusor) Liver, Muscle Adipose tissue Eye Bronchodilation Vasodilatation Relaxation Glycogenolysis Lipolysis Enhanced aqueous secretion β3 Adipose tissue Lipolysis
- 4. Mechanism of action •Via GPCR Antagonist binding to receptor No stimulation of G protein No change in cAMP conc. No EFFECT
- 5. Properties • Receptor Blockade –Nonselective β blockade – Selective β1 blockade – Β+α blockade • Intrinsic sympathomimetic property-ISA (partial agonistic action) • Membrane stabilising action-MSA (Local anaesthetic action-Na channel block)
- 6. CLASSIFICATION Beta blockers 1st generation Classical Non selective 2nd generation Classical Beta 1 selective 3rdgeneration Newer Non selective & beta1 selective + Add. properties
- 7. 1st generation –Non selective • Without ISA &MSA Timolol Nadolol Sotalol • With ISA only Penbutolol • With MSA only Propranolol • With ISA & MSA Pindolol
- 8. 2nd generation –Selective β1 agents • Without ISA &MSA Atenolol Bisoprolol Esmolol • With MSA only Metoprolol • With ISA & MSA Acebutolol
- 9. 3rd generation Non selectiveSelective With ISA Carteolol With ISA Celiprolol With MSA Betaxolol With MSA Carvedilol With MSA & ISA Labetalol
- 10. β blockers With ISA Penbutolol Carteolol Celiprolol Both Pindolol Acebutolol Labetalol WithMSA Propranolol Metoprolol Betaxolol Carvedilol Without ISA & MSA Timolol, Sotalol, Nadolol Atenolol, Bisoprolol, Esmolol
- 11. Properties of beta1selectivity • Less broncho constriction • Less interference with CHO metabolism less hypoglycemia preferred in diabetics • Less chances of Raynaud's phenomenon • Less deleterious effect on blood lipid profile • Less impairment of exercise capacity • Less effect on tremor
- 12. Properties of ISA •Less bradycardia • Less rebound effect on withdrawal • Less deleterious effect on blood lipid profile • Not effective in migraine prophylaxis • Not suitable for secondary prophylaxis of MI
- 13. Actions • On CVS –Heart •Negative –Ionotropy –Chronotropy –Dromotropy –Bathmotropy
- 14. Actions…. • On CVS –Bloodvessel •Vasoconstriction in prone individuals Direct •Vasodilatation due to additional properties Precipitates Reynaud's disease •α1 blockade •β2 agonism •Ca ++ channel block •K+ channel opening •NO production
- 15. Actions…. • On CVS –Antihypertensiveaction • Decreased CO • Decreased renin release • Decreased TPR on long term administration • Central action – reduction of sympathetic outflow
- 16. Betablockers with vasodilatorproperty Alpha blockade Labetalol Carvedilol Bucindolol Bevantolol Nipradilol Beta2 agonism Celiprolol Carteolol Bopindolol CCB action Betaxolol Bevantolol Carvedilol Pot. Channel opening Tilisolol NO production Celiprolol Carteolol Bopindolol Nipradilol Nebivolol Anti oxidant Carvedilol
- 17. Actions -CNS • Antianxiety • Behaviour changes • Forgetfulness • Night mares • Increased dreaming Nonselective lipid soluble
- 18. Actions -Metabolic • CHOmetabolism – Hypoglycemia • Inhibits muscle glycogenolysis – Hypoglycemic unawareness • Lipid – Increases VLDL(TG) levels – Alters HDL/LDL ratio Less with β 1 selective agents
- 19. Actions - Eye •Decrease secretion of aqueous • Decrease IOT • No effect on pupil size or accommodation Ciliary body
- 20. Actions- Bronchus Increases airway resistance Lesswith beta 1 selective agents
- 21. SKELETAL muscles •Decrease exercisecapacity –By decreasing blood flow –Inhibit glycogenolysis and lipolysis.
- 22. MISCELLANEOUS • Antagonise catecholamineinduced –Tremor –Inhibition of mast cell degranulation • Prevent platelet aggregation and promote fibrinolysis
- 23. Adverse effects -CVS • Bradycardia • Exacerbation of angina • Precipitation of CHF
- 24. Adverse reactions • Increasedair way resistance worsening of bronchial asthma
- 25. Adverse reactions • Impairmentof carbohydrate tolerance • Alteration of lipid profile • Increased risk of CAD • Rebound hypertension on withdrawal • Cold hands and feet, worsening of PVD
- 26. Adverse effects… Nightmares Decreased exercisecapacity Tiredness Lack of drive
- 27. Drug interactions Pharmacokinetic Al salts,Cholestyramine Decrease absorption Enzyme inducers Decrease plasma conc. Cimitidine, Hydralazine Increase BA They impair clearance of lidocaine Pharmaco dynamic • Digoxin • CCB (Verapamil) • CCB (DHP) • NSAIDs • Adrenaline & other α agonists
- 28. Uses Cardiovascular • Hypertension • Angina •Myocardial infarction • Arrhythmia • Cardiomyopathy • CCF • Dissecting aneurysm of aorta Non cardiovascular • Thyrotoxicosis • Pheochromocytoma • Migraine prophylaxis • Essential tremor • Glaucoma • Anxiety • Portal hypertension • Anti psychotic induced akathesia
- 29. Hypertension • Cardioselective betablockers • Rationale –Decrease in HR,CO ,myocardial contractility. –Decrease renin release –Decrease central sympathetic out flow
- 30. Angina • Metoprolol • Atenolol •Bisoprolol Prophylaxis Treatment Contraindication •Variant angina
- 31. Angina - Rationale DecreaseHR & contractility Decrease myocardial oxygen demand Antianginal action
- 32. MI Prophylaxis Treatment Anti anginal action Reduceinfarct size Prevents arrhythmia Prevents reinfarction Prevents arrhythmia Metoprolol Esmolol Timolol
- 33. Arrythmias • Propranolol • Esmolol •Acebutolol • Sotalol Decreases AV conduction Inhibits impulses from atria to ventricle controls ventricular rate Mainly effective in Arrhythmias precipitated by catecholamines Sotalol K+ channel block class3 anti arrhythmic Esmolol ultra short acting supraventricular tachycardia
- 34. ARRHYTHMIA • Control ventricularrate in atrial flutter and fibrillation. • Suppress extrasystole and tachycardia especially mediated adrenergically .
- 35. HOCM • ↓ contractility •↓ LV outflow obstruction • Improve cardiac output in exercise
- 36. CHF ONLY in compensatedCHF • Antagonise sympathetic overactivity on myocardium • Prevents myocyte apoptosis • ↓ cardiac remodelling • Retard progression of CHF Metoprolol Bisoprolol Carvedilol
- 37. Dissecting aortic aneurysm •↓ cardiac contractility, and aortic pulsation.
- 38. Non cardiac uses •Pheochromocytoma – Used after an α blocker – To control tachycardia and arrhythmia – Suppress cardiomyopathy due to excess catecholamines • Thyrotoxicosis – Control sympathetic symptoms – Inhibit peripheral conversion of T4 to T3 – Preoperative use
- 39. Migraine prophylaxis • Propranolol •Nadolol • Metoprolol
- 40. Portal hypertension • ToDecrease Portal Vein Pressure in Patients with Cirrhosis • Decrease variceal bleeding Propranolol
- 41. Glaucoma • Decrease aqueous humoursecretion • Attenuating neuronal Ca and Na influx Protection to retinal neurons • Inhibit ganglion cell death Timolol Carteolol Betaxolol Levobetaxolol Levobunolol Metipranolol
- 42. CNS • Anxiety • Essentialtremor • Akathisia induced by antipsychotics • Alchohol withdrawal
- 43. 3rd generation agents DrugMSA ISA Beta blockade Other properties Labetalol + + Non selective α1 blockade Carvedilol + Non selective α1 blockade,CCB Antioxidant Bucindolol + Non selective α1 blockade,β2,β3 agonism Increases HDL cholesterol Celiprolol + β1 selective β2 agonism NO release Nebivolol β1 selective •NO release •Inhibits platelet aggregation Bevantolol Nonselective α1 blockade CCB
- 44. CONTRAINDICATIONS Absolute 1. Severe Bradycardia 2.Pre-existing High Grade Heart Block 3. Overt Untreated Heart Failure 4. Cardiogenic Shock 5. Severe Bronchospasm 6. Severe Depression 7. Active Raynaud’s Phenomenon
- 45. CONTRAINDICATIONS Relative 1. Prinzmetals Angina 2.Concomitant Use Of :Verapamil/ Diltiazam/Digoxin 3. Mild Asthma 4. Insulin Requiring DM
- 46. OVERDOSAGE Manifestations extensionof pharmacological properties Hypotension Bradycardia Prolonged Conduction Times Widened QRS Complexes
- 47. SIGNS AND SYMPTOMS •Seizures • Depression • Hypoglycemia • Bronchospasm
- 48. Treatment • Atropine Initially •Cardiac Pacemakers Required • Large amt of Isoproterenol / Agonist • Glucagon
- 49. α + βADRENERGIC BLOCKERS • Labetalol β1 + β2 + α1 blocking as well as weak β2 agonistic activity β blocking potency is about 1/3 that of propranolol α blocking potency is about 1/10 of phentolamine
- 50. • Fall inBP (both systolic and diastolic) is due to α1 and β1 blockade as well as β2 agonism (vasodilatation) • moderately potent antihypertensive USES • pheochromocytoma, clonidine withdrawal, pregnancy induced hypertension (preeclampsia) and hypertensive emergencies, as well as in essential hypertension. • A/E- postural hypotension, Failure of ejaculation
- 51. Carvedilol • β1 +β2 + α1 adrenoceptor blocker which produces vasodilatation due to α1 blockade as well as calcium channel blockade • Antioxidant property has also been demonstrated • β blocker especially employed as cardioprotective in CHF
- 52. DRUGS FOR GLAUCOMA •Open angle (wide angle, chronic simple) glaucoma β blockers do not affect pupil size, tone of ciliary muscle or outflow facility, but lower i.o.t. by reducing aqueous formation. Timolol- nonselective (β1 + β2 ) has no local anaesthetic or intrinsic sympathomimetic activity
- 53. • Betaxolol -β1 selective blocker • Advantage of less bronchopulmonary and probably less cardiac, central and metabolic side effects.