Class antianginal
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This document discusses the patterns of angina pectoris and their characteristics. It describes stable angina, which produces reproducible chest pain relieved by rest. Unstable angina occurs with less exertion or at rest and is less responsive to nitroglycerin. Prinzmetal angina is an uncommon variant occurring at rest, often in young individuals, triggered by substances like alcohol. The document also outlines various drug classes used to treat angina, including nitrates, calcium channel blockers, beta blockers, and other adjunctive therapies. It provides details on the mechanisms and side effects of these drug classes.
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Class antianginal
- 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC. 1
- 2. 2
- 3. Angina occurs in three overlapping patterns: Stable angina Unstable angina Prinzmetal (variant) angina 3
- 4. “Stable” indicates the reproducible nature of the angina; the same activity at the same intensity faithfully produces symptoms. Typically this type of angina is relieved by rest or acute use of nitroglycerin. 4
- 5. Unstable angina occurs when anginal symptoms occur with less cardiac demand; previously tolerated activities elicit symptoms, of great concern is angina at rest. These episodes are less or un-responsive to nitroglycerine or rest. Crescendo angina describes a rapid progression of myocardial ischemia often heralding infarction. 5
- 6. 1. uncommon pattern of myocardial ischemia usually occurring at rest and often in young individuals (particularly women) lacking classic risk factors or significant demonstrable coronary disease. 2. The anginal attacks in PVA tend to have a circadian rhythm and generally occur in the early morning hours. 3. These attacks can be triggered by alcohol, rapid eye movement sleep, atrial pacing, cocaine, nicotine, acetylcholine, and hyperventilation. 4. It is induced by coronary artery vasospasm it generally responds promptly to vasodilators. PVA has been associated with other vasospastic disorders such as migraine headaches and Raynaud’s phenomena. 6
- 7. I ORGANIC NITRATES a) Rapid onset slow acting-AMYL NITRATE, NITROGLYCERINE b) Slow onset, long acting- ISOSORBIDE DINITRATE, ISOSORBIDE MONONITRATE, ERYTHRITYL TETRANITRATE, PENTAERYTHRITOL TETRANITRATE II. CALCIUM CHANNEL BLOCKERS VERAPAMIL, DILTIAZEM, NIFEDIPINE, NICARDIPINE, NITRENDIPINE, ISARDIPINE, AMLODIPINE, BENIDIPINE 7
- 8. III BETA BLOCKERS PROPRANOLOL, ATENOLOL, METAPROLOL, NADOLOL, BISOPROLOL AND CELIPROLOL MISCELLANEOUS 1. Potassium Channel Openers: NICORANDIL 2. Cytoprotective Drugs: TRIMETAZIDINE, RANOLAZINE 3. Antiplatelet Drugs: ASPIRIN, TICLOPIDINE, CLOPIDOGREL, DIPYRIDAMOLE, CILASTAZOL 4. Bradycardic Drugs: IVABRADINE 5. HMG-Co A Reductase Inhibitors: STATINS 6. PVD: NAFTIDOFURYL AND PENTOXIPHYLLINE 8
- 9. ORGANIC NITRATES a) Rapid onset slow acting-AMYL NITRATE, NITROGLYCERINE(GTN)-t1/2-2min b) Slow onset, long acting- ISOSORBIDE DINITRATE-s/l and oral, t1/2- 40min, , ISOSORBIDE MONONITRATE t1/2-4-6hrs, ERYTHRITYL TETRANITRATE, PENTAERYTHRITOL TETRANITRATE--chronic prophylaxis 9
- 10. 10
- 11. 11
- 12. The difference between nitrate preparations is mainly in time of onset of action. 1. Nitroglycerin suffers marked 1st pass metabolism so administration is sublingual (rapid absorption and onset (<1 minute), t1/2 ~10 minutes. As nitroglycerin is metabolized anginal symptoms will return. Transdermal administration either as patch or paste provides a depot of agent for a steady availability. 2. Isosorbide mononitrate & isosorbide dinitrate are long acting nitrates that are relatively resistant to hepatic catabolism t1/2 ~ 1 hour. 12
- 13. Angina pectoris Acute coronary symptoms Biliary colic Cyanide poisoning CHF and acute LVF Myocardial infarction(MI) Esophagial spasm 13
- 14. Orthostatic hypotension Tachycardia Severe throbing headache Flushing syncope 14
- 15. decrease in the effect of drug when administered in long acting form. develops with all nitrates is dose dependent disappears in 24hrs after stopping the drug Tolerance can be avoided -Using the least effective dose -Creating discontinuous plasma levels D/I: Sildenafil 15
- 16. Previous hypersensitivity Hypotension ( < 80 mmHg) AMI with low ventricular filling pressure 1st trimester of pregnancy Constrictive pericarditis Intracranial hypertension Hypertrophic cardiomyopathy 16
- 17. PROPRANOLOL, ATENOLOL, METAPROLOL, NADOLOL, BISOPROLOL AND CELIPROLOL 17
- 18. 18
- 19. Hypotension: bp < 100 mmhg Bradycardia: hr < 50 bpm Chronic bronchitis, asthma Severe chronic renal insufficiency 19
- 20. Dihydropyridines: NIFEDIPINE, NICARDIPINE, NITRENDIPINE, ISARDIPINE, AMLODIPINE, BENIDIPINE Non-Dihydropyridines: VERAPAMIL, DILTIAZEM, 20
- 21. 21
- 22. Immediate release capsules- headache, ankle oedema Headache Tachycardia and gingival hyperplasia Negetive ionotropic effect C/I- unstable angina, LV failure, aortic stenosis, obstuctive cardiomyopathy D/I-enzyme inhibitors 22
- 23. Beta Blockers prevent reflex tachycardia and contractility produced by nitrate-induced hypotension. Nitrates prevent any coronary vasospasm produced by Beta Blockers. Nitrates prevent increases in left ventricular filling pressure or preload resulting from the negative inotropic effects produced by Beta Blockers. Nitrates and Beta Blockers both reduce myocardial oxygen consumption by different mechanisms. Nitrates and Beta Blockers both increase subendocardial blood flow by different mechanisms 23
- 24. Preload----------------- After load-------------- Myocardial wall size-- Coronary blood flow--------- Collateral blood flow--------- Blood flow to ischemic area- 24
- 25. 25
- 26. POTASSIUM CHANNEL OPENERS-Nicorandil Dual mechanism antianginal drug activates ATP sensitive K+ channels membrane hyperpolarisation Also act as NO donors- relaxes blood vessels by increasing cGMP arterial dilatation is coupled with venodilatation fall in BP Cardioprotective action stimulating ischaemic preconditioning activation of mitochondrial KATP channels ADR-flushing, palpitation, headache, dizziness 26
- 27. TRIMETAZIDINE-non-haemodynamic mechanism Cytoprotective effect on myocardial o2 demand Inhibits (LC3-KAT)-3 Ketoacyl-CoA-thiolase- a key enzyme in fatty acid oxidation shifts heart from utilizing fatty acid to glucose decreases myocardial oxygen demand Inhibits superoxide cytotoxicity maintains LV function Stable angina Frequency of angina is decreased S/E-fatigue, muscle cramps, gastritis 27
- 28. PFOI-partial fatty Acid Oxidation Inhibitor Inhibits inward sodium current (INa+) during ischemia facilitates calcium entry Na+/Ca+ exchanger reduction in ca overload cardioprotective effect Prolongs exercise tolerance to angina but has no action on HR and BP 500mg BD orally Safe in combination with Ca channel blockers, Beta-blockers and nitrates S/E –QT prolongation, constipation, postural hypotension D/I-class I and III antiarrhythmic drugs 28
- 29. Blockade of cardiac pacemaker(sino-atrial)cell f channels active in phase 4 depolarisation Decreases the myocardial oxygen demand No effect negetive ionotropic effect, negetive lucitropic, electrophysiological Heart rate reduction decreases oxygen demand and prolongation of diastole Prolongs exercise tolerance to angina 29
- 30. Aspirin, Ticlopidine and Clopidogrel Inhibits binding of ADP to its receptors Reduce platelet aggregation Cilastozole Phosphodiesterase III inhibitor Vasodilatation and inhibits platelet aggregation Metabolised by cyp3A4 100mg bd 30
- 31. Powerful coronary dialator Inhibits adenosine deaminase adenosinelocal mediator in autoregulation of coronary flow inhibits phosphodiesterase potentiates PGI2 Inhibit platelet aggregation For prophylaxis of coronary and cerebral thrombosis S/E- exacerbation of anginacoronary steal phenomenon, GIT distress 31
- 33. Statins They regression of atheromatous plaque Improvement of endothelial function 33
- 34. Pentoxiphylline (oxypentifylline) Is a theobromine analogue and inhibits phosphodiesterase enzyme Reduces blood viscosity Improves the blood flow in ischemic area No coronary steal phenomenon Used in non-haemorrhagic stroke, chronic cerebrovascular insufficiency 400mg bd 34
- 35. CILOSTOZOL-antiplatelet drug-PDE3 inhibitor NAFTIDOFURYL(-5HT2A) receptor antagonist-drug for PVD LEVOCARNITINE-improves the metabolic status of skeletal muscle CYCLANDELATE –cerebrovascular and peripheral vascular disorders 400mg TDS 35
- 36. 1. Pain and anxiety-- -GTN, morphine 2. Opioid analgesics and Antianxiety agents 3. Pethidine, Diazepam, alprazolam 4. General measures-O2 therapy, dopamine, 5. atropine, diltiazem, 6. Maintainance of blood volume-Saline , dextran 7. Correction of acidosis- sod. Bicarbonate infusion 8. Prevention of treatment of arrhythmias 9. -beta blocker 36
- 37. 7. Pump failure-furosemide, vasodilators, ionotropic drugs 8. Prevention of thrombus extension, venous thrombosis- aspirin, heparin, anticoagulants- dalteparin, Enoxaparin 9. Thrombolysis and reperfusion-fibrinolytic agents- streptokinase, urokinase 10. Prevention of remodeling and CHF-ACE inhibitors, ARBs- lisinopril, ramipril 11. Prevention of future attacks-platelet inhibitors- clopidogrel, β blockers, statins 37
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