This document discusses drugs used for the treatment of ischemic heart disease (IHD). IHD is caused by a lack of oxygenated blood flow to the heart muscle and includes stable angina and acute coronary syndromes. Nitrates, beta blockers, and calcium channel blockers are first-line treatments for stable angina by reducing oxygen demand on the heart and dilating blood vessels. Nitrates work primarily by venous dilation to reduce preload, while beta blockers lower heart rate and contractility. Calcium channel blockers inhibit calcium influx. For unstable angina/acute coronary syndromes, antiplatelet agents like aspirin are also used to prevent clots.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Angina is caused by an imbalance in myocardial oxygen supply and demand. It is usually due to coronary artery disease which decreases oxygen supply. Antianginal drugs work to improve this balance by either dilating coronary arteries to increase supply or reducing demands on the heart to decrease oxygen needs. The main drug classes used are nitrates, beta blockers, and calcium channel blockers. Combination therapy with two or more classes is often used if single drug therapy is insufficient. Other treatment options include percutaneous coronary intervention to open blocked arteries or coronary artery bypass graft surgery to create new routes for blood flow around blockages.
This document discusses angina pectoris, its types and treatment. It defines angina as chest pain due to insufficient blood supply to the heart. There are three main types - stable angina, unstable angina and vasospastic angina. Treatment focuses on reducing oxygen demand on the heart and increasing oxygen supply. The main drug classes used are organic nitrates, beta blockers, and calcium channel blockers. Nitrates provide quick relief of chest pain while beta blockers and calcium channel blockers are used long-term to prevent angina episodes.
PH1.28 Describe the mechanisms of action, types, doses, side effects, indicat...Dr Pankaj Kumar Gupta
PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
This document discusses antianginal drugs used to treat angina pectoris and coronary artery disease. It describes the types and causes of angina, the classes of antianginal drugs including their mechanisms of action, effects, examples, and uses. The main classes discussed are nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Adverse effects and pharmacokinetics are also summarized for several drug classes and examples.
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Angina is caused by an imbalance in myocardial oxygen supply and demand. It is usually due to coronary artery disease which decreases oxygen supply. Antianginal drugs work to improve this balance by either dilating coronary arteries to increase supply or reducing demands on the heart to decrease oxygen needs. The main drug classes used are nitrates, beta blockers, and calcium channel blockers. Combination therapy with two or more classes is often used if single drug therapy is insufficient. Other treatment options include percutaneous coronary intervention to open blocked arteries or coronary artery bypass graft surgery to create new routes for blood flow around blockages.
This document discusses angina pectoris, its types and treatment. It defines angina as chest pain due to insufficient blood supply to the heart. There are three main types - stable angina, unstable angina and vasospastic angina. Treatment focuses on reducing oxygen demand on the heart and increasing oxygen supply. The main drug classes used are organic nitrates, beta blockers, and calcium channel blockers. Nitrates provide quick relief of chest pain while beta blockers and calcium channel blockers are used long-term to prevent angina episodes.
PH1.28 Describe the mechanisms of action, types, doses, side effects, indicat...Dr Pankaj Kumar Gupta
PH1.28 Describe the mechanisms of action, types, doses, side effects, indications and contraindications of the drugs used in ischemic heart disease (stable, unstable angina and myocardial infarction), peripheral vascular disease
This document discusses antianginal drugs used to treat angina pectoris and coronary artery disease. It describes the types and causes of angina, the classes of antianginal drugs including their mechanisms of action, effects, examples, and uses. The main classes discussed are nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Adverse effects and pharmacokinetics are also summarized for several drug classes and examples.
Angina pectoris is chest pain due to ischemia of the heart muscle. It is usually felt as a tightness or pressure in the middle of the chest that may spread to the neck, jaw, or arm. There are three main types - stable angina brought on by exertion, unstable angina that occurs at rest, and Prinzmetal or variant angina caused by coronary artery spasm. Treatment involves medications to relieve symptoms like nitrates, beta blockers, calcium channel blockers, and newer drugs that open potassium channels or have a cytoprotective effect. Combination therapy with two or more classes is often used for better management of angina.
This document discusses different types of angina and treatments. It describes 3 main types of angina: atherosclerotic angina which is caused by partially blocked arteries and accounts for 90% of cases; vasospastic angina which involves coronary artery spasms and can occur at rest; and unstable angina which is a medical emergency and precursor to heart attack. The major treatment strategies aim to increase oxygen delivery to the heart and reduce oxygen demand. Traditional pharmacological therapies discussed include nitrates, calcium channel blockers, and beta blockers which all work to relax blood vessels or reduce heart rate to improve oxygen supply. Newer drugs like ranolazine and ivabradine are also mentioned.
This document discusses the classification, treatment, and management of angina pectoris. Angina is chest pain caused by an imbalance between myocardial oxygen supply and demand. It classifies angina into exertional, variant, and unstable types based on symptoms and etiology. Treatment involves short-acting nitrates for acute episodes and long-acting nitrates, calcium channel blockers, beta-blockers, or potassium channel openers for prophylaxis. Combination drug therapy and surgical options like balloon angioplasty or bypass surgery may also be used in severe cases.
This document discusses angina pectoris (chest pain), including its causes, types, risk factors, and treatment. It begins by defining angina as chest pain due to temporary heart muscle ischemia, usually due to coronary artery obstruction. It describes the three main types of angina - stable, unstable, and mixed forms. The major risk factors for angina are then listed. The document focuses on drug therapies for angina, explaining the mechanisms and effects of the three main classes: organic nitrates, beta-blockers, and calcium channel blockers. Specific drugs like nitroglycerin and nifedipine are discussed in terms of their pharmacokinetics, mechanisms of action, and adverse effects in treating an
This document discusses stable and acute ischemic heart disease. It begins by defining coronary heart disease and coronary artery disease. It then discusses the etiology, pathophysiology, risk factors, classification, clinical presentation, and desired outcomes of stable ischemic heart disease. It covers the general treatment approach including risk factor modification, drug therapy using antiplatelet agents, ACE inhibitors, statins, beta-blockers, calcium channel blockers, and nitrates. It then discusses acute coronary syndromes including unstable angina, non-ST-elevation myocardial infarction, and ST-elevation myocardial infarction. It covers risk stratification, general treatment approach, and early pharmacotherapy for ST-elevation myocardial infarction.
Anti Anginal Drugs and its side affect and useswajidullah9551
This document discusses anti-anginal drugs used to treat angina pectoris. There are three main classes of drugs: nitrates, beta blockers, and calcium channel blockers. Nitrates work by reducing preload and afterload, increasing coronary blood flow and oxygen supply. Beta blockers decrease oxygen demand by lowering heart rate and contractility. Calcium channel blockers increase oxygen supply by dilating coronary arteries and reduce afterload by decreasing peripheral resistance. The document provides details on the mechanisms, effects, and examples of drugs in each class.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
This document discusses the pharmacology of antianginal drugs. It begins by defining angina pectoris and the two principal forms - classical angina and variant/Prinzmetal angina. It then covers the mechanisms of action and classifications of major classes of antianginal drugs, including nitrates, beta blockers, calcium channel blockers, potassium channel openers, and others like dipyridamole and trimetazidine. Specific drugs within each class are discussed in terms of their mechanisms, effects, uses, and adverse effects. The history and mechanisms of calcium channel blockers and their subclasses are described in detail.
The document discusses the use of organic nitrates and calcium antagonists to treat angina. It provides details on their mechanisms of action, pharmacological effects, and clinical uses. Specifically, it explains that organic nitrates act by relaxing smooth muscle and increasing cGMP, while calcium antagonists prevent the opening of voltage-gated calcium channels. Both drug classes are used to reduce cardiac oxygen demand and redistribute blood flow for the treatment of stable and unstable angina.
The document discusses various drugs used to treat angina pectoris and myocardial infarction. It describes the classes of drugs which include nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, ACE inhibitors, and captopril. It explains the mechanisms of action, pharmacokinetics, indications, contraindications and side effects of these drug classes and examples like nitroglycerin, atenolol, nifedipine, verapamil, aspirin, and captopril.
The document discusses drugs used for the treatment of angina pectoris. It details the pharmacology of various antianginal drugs including nitrates, calcium channel blockers, beta blockers, and potassium channel openers. The mechanisms of action, indications, and side effects of these drug classes are explained in relation to managing the imbalance between myocardial oxygen supply and demand in angina.
This document provides information on the treatment of angina pectoris, including the types of angina and agents used. It discusses the main strategies for treating angina as reducing oxygen demand and increasing oxygen delivery. The key agents discussed are nitrates, calcium channel blockers, and beta blockers. Nitrates act by releasing nitric oxide to cause vasodilation and reduce preload and afterload. Calcium channel blockers block calcium channels to reduce contraction. Beta blockers reduce cardiac work and oxygen demand by lowering heart rate and contractility. All three are effective prophylactically for different types of angina.
Antianginal Drugs Pharmacology 5th sem B.Pharm.pptxMrSALAJKHARE
This document provides information on angina pectoris and antianginal drugs. It defines angina pectoris as recurring chest pain due to decreased blood supply to the heart muscle. It describes the three main types of angina and the mechanisms of classical and variant angina. It then discusses several classes of antianginal drugs in detail, including their mechanisms of action, effects, uses, and adverse effects. The major drug classes covered are nitrates, calcium channel blockers, beta blockers, and potassium channel openers.
This document provides learning objectives and content on the management of ischemic heart disease. It defines stable and unstable angina, describing their underlying pathologies. It classifies drugs used to treat angina, describing the mechanisms of action, uses, and side effects of nitrates, calcium channel blockers, beta blockers, nicorandil, and ivabradine. The management of myocardial infarction is also covered, outlining treatment strategies for pain, oxygenation, hemodynamics, arrhythmias, and use of antiplatelet/anticoagulant drugs and thrombolysis.
anti anginal drugs and side affect and Symptomswajidullah9551
This document discusses different types of angina pectoris and antianginal drugs. It describes typical angina, variant angina, and unstable angina. The main classes of antianginal drugs covered are nitrates, beta-blockers, calcium channel blockers, and potassium channel openers. Nitrates work by vasodilation to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium influx to relax smooth muscle. Potassium channel openers like nicorandil dilate blood vessels.
This document summarizes different types of angina pectoris and treatments for it. It describes:
- The main causes of angina pectoris including atherosclerosis and coronary vasospasm.
- Classes of drugs used to treat angina including nitrates, beta blockers, calcium channel blockers, and others.
- The mechanisms of these drugs in reducing oxygen demand on the heart and increasing oxygen supply such as dilating blood vessels and reducing heart rate/contractility.
- Guidelines for use of different drug classes for stable angina, unstable angina, and variant angina. Potential side effects and cautions for combinations are also outlined.
Angina pectoris refers to chest pain caused by myocardial ischemia. There are different types of angina including stable angina characterized by pain during physical activity, Prinzmetal's variant angina caused by coronary vasospasm, and unstable angina which can lead to myocardial infarction. Current therapies include nitrates, calcium channel blockers, beta blockers, and antiplatelet drugs, but newer treatments are being studied such as nicorandil, ranolazine, trimetazidine, fasudil, ivabradine, and allopurinol which may help address unmet needs and limitations of existing therapies. Gene and angiogenesis therapies are also under investigation as alternative methods for treating chronic ischemic heart disease.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
This document provides an overview of respiratory system disorders for nursing students. It begins with the objectives and anatomy and physiology of the respiratory system. It then discusses various upper and lower respiratory tract disorders like pharyngitis, tonsillitis, adenoiditis, peritonsillar abscess, laryngitis and their associated nursing assessments, signs and symptoms, diagnoses and management. Surgical procedures like tonsillectomy are also outlined.
This document provides standard treatment guidelines for general hospitals in Ethiopia. It is published by the Drug Administration and Control Authority of Ethiopia and covers guidelines for infectious diseases, non-infectious diseases, pediatric diseases, and dermatological disorders. For each condition, it provides recommendations on diagnosis, treatment, and management. The guidelines are intended to help standardize care across hospitals in Ethiopia.
This document discusses different types of angina and treatments. It describes 3 main types of angina: atherosclerotic angina which is caused by partially blocked arteries and accounts for 90% of cases; vasospastic angina which involves coronary artery spasms and can occur at rest; and unstable angina which is a medical emergency and precursor to heart attack. The major treatment strategies aim to increase oxygen delivery to the heart and reduce oxygen demand. Traditional pharmacological therapies discussed include nitrates, calcium channel blockers, and beta blockers which all work to relax blood vessels or reduce heart rate to improve oxygen supply. Newer drugs like ranolazine and ivabradine are also mentioned.
This document discusses the classification, treatment, and management of angina pectoris. Angina is chest pain caused by an imbalance between myocardial oxygen supply and demand. It classifies angina into exertional, variant, and unstable types based on symptoms and etiology. Treatment involves short-acting nitrates for acute episodes and long-acting nitrates, calcium channel blockers, beta-blockers, or potassium channel openers for prophylaxis. Combination drug therapy and surgical options like balloon angioplasty or bypass surgery may also be used in severe cases.
This document discusses angina pectoris (chest pain), including its causes, types, risk factors, and treatment. It begins by defining angina as chest pain due to temporary heart muscle ischemia, usually due to coronary artery obstruction. It describes the three main types of angina - stable, unstable, and mixed forms. The major risk factors for angina are then listed. The document focuses on drug therapies for angina, explaining the mechanisms and effects of the three main classes: organic nitrates, beta-blockers, and calcium channel blockers. Specific drugs like nitroglycerin and nifedipine are discussed in terms of their pharmacokinetics, mechanisms of action, and adverse effects in treating an
This document discusses stable and acute ischemic heart disease. It begins by defining coronary heart disease and coronary artery disease. It then discusses the etiology, pathophysiology, risk factors, classification, clinical presentation, and desired outcomes of stable ischemic heart disease. It covers the general treatment approach including risk factor modification, drug therapy using antiplatelet agents, ACE inhibitors, statins, beta-blockers, calcium channel blockers, and nitrates. It then discusses acute coronary syndromes including unstable angina, non-ST-elevation myocardial infarction, and ST-elevation myocardial infarction. It covers risk stratification, general treatment approach, and early pharmacotherapy for ST-elevation myocardial infarction.
Anti Anginal Drugs and its side affect and useswajidullah9551
This document discusses anti-anginal drugs used to treat angina pectoris. There are three main classes of drugs: nitrates, beta blockers, and calcium channel blockers. Nitrates work by reducing preload and afterload, increasing coronary blood flow and oxygen supply. Beta blockers decrease oxygen demand by lowering heart rate and contractility. Calcium channel blockers increase oxygen supply by dilating coronary arteries and reduce afterload by decreasing peripheral resistance. The document provides details on the mechanisms, effects, and examples of drugs in each class.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
This document discusses the pharmacology of antianginal drugs. It begins by defining angina pectoris and the two principal forms - classical angina and variant/Prinzmetal angina. It then covers the mechanisms of action and classifications of major classes of antianginal drugs, including nitrates, beta blockers, calcium channel blockers, potassium channel openers, and others like dipyridamole and trimetazidine. Specific drugs within each class are discussed in terms of their mechanisms, effects, uses, and adverse effects. The history and mechanisms of calcium channel blockers and their subclasses are described in detail.
The document discusses the use of organic nitrates and calcium antagonists to treat angina. It provides details on their mechanisms of action, pharmacological effects, and clinical uses. Specifically, it explains that organic nitrates act by relaxing smooth muscle and increasing cGMP, while calcium antagonists prevent the opening of voltage-gated calcium channels. Both drug classes are used to reduce cardiac oxygen demand and redistribute blood flow for the treatment of stable and unstable angina.
The document discusses various drugs used to treat angina pectoris and myocardial infarction. It describes the classes of drugs which include nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, ACE inhibitors, and captopril. It explains the mechanisms of action, pharmacokinetics, indications, contraindications and side effects of these drug classes and examples like nitroglycerin, atenolol, nifedipine, verapamil, aspirin, and captopril.
The document discusses drugs used for the treatment of angina pectoris. It details the pharmacology of various antianginal drugs including nitrates, calcium channel blockers, beta blockers, and potassium channel openers. The mechanisms of action, indications, and side effects of these drug classes are explained in relation to managing the imbalance between myocardial oxygen supply and demand in angina.
This document provides information on the treatment of angina pectoris, including the types of angina and agents used. It discusses the main strategies for treating angina as reducing oxygen demand and increasing oxygen delivery. The key agents discussed are nitrates, calcium channel blockers, and beta blockers. Nitrates act by releasing nitric oxide to cause vasodilation and reduce preload and afterload. Calcium channel blockers block calcium channels to reduce contraction. Beta blockers reduce cardiac work and oxygen demand by lowering heart rate and contractility. All three are effective prophylactically for different types of angina.
Antianginal Drugs Pharmacology 5th sem B.Pharm.pptxMrSALAJKHARE
This document provides information on angina pectoris and antianginal drugs. It defines angina pectoris as recurring chest pain due to decreased blood supply to the heart muscle. It describes the three main types of angina and the mechanisms of classical and variant angina. It then discusses several classes of antianginal drugs in detail, including their mechanisms of action, effects, uses, and adverse effects. The major drug classes covered are nitrates, calcium channel blockers, beta blockers, and potassium channel openers.
This document provides learning objectives and content on the management of ischemic heart disease. It defines stable and unstable angina, describing their underlying pathologies. It classifies drugs used to treat angina, describing the mechanisms of action, uses, and side effects of nitrates, calcium channel blockers, beta blockers, nicorandil, and ivabradine. The management of myocardial infarction is also covered, outlining treatment strategies for pain, oxygenation, hemodynamics, arrhythmias, and use of antiplatelet/anticoagulant drugs and thrombolysis.
anti anginal drugs and side affect and Symptomswajidullah9551
This document discusses different types of angina pectoris and antianginal drugs. It describes typical angina, variant angina, and unstable angina. The main classes of antianginal drugs covered are nitrates, beta-blockers, calcium channel blockers, and potassium channel openers. Nitrates work by vasodilation to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium influx to relax smooth muscle. Potassium channel openers like nicorandil dilate blood vessels.
This document summarizes different types of angina pectoris and treatments for it. It describes:
- The main causes of angina pectoris including atherosclerosis and coronary vasospasm.
- Classes of drugs used to treat angina including nitrates, beta blockers, calcium channel blockers, and others.
- The mechanisms of these drugs in reducing oxygen demand on the heart and increasing oxygen supply such as dilating blood vessels and reducing heart rate/contractility.
- Guidelines for use of different drug classes for stable angina, unstable angina, and variant angina. Potential side effects and cautions for combinations are also outlined.
Angina pectoris refers to chest pain caused by myocardial ischemia. There are different types of angina including stable angina characterized by pain during physical activity, Prinzmetal's variant angina caused by coronary vasospasm, and unstable angina which can lead to myocardial infarction. Current therapies include nitrates, calcium channel blockers, beta blockers, and antiplatelet drugs, but newer treatments are being studied such as nicorandil, ranolazine, trimetazidine, fasudil, ivabradine, and allopurinol which may help address unmet needs and limitations of existing therapies. Gene and angiogenesis therapies are also under investigation as alternative methods for treating chronic ischemic heart disease.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload. Calcium channel blockers and beta blockers are also outlined as treatments that reduce oxygen demand. Combination therapies are noted to provide additive effects.
The document discusses different types of angina pectoris and treatments for angina. It defines typical angina, variant angina, and unstable angina. It then explains drugs that can be used to treat angina by decreasing oxygen demand and/or increasing oxygen supply, including nitrates, calcium channel blockers, and beta blockers. Nitrates are described as being effective for treating acute angina by dilating blood vessels and reducing workload on the heart. Calcium channel blockers and beta blockers are also outlined as treatments that decrease oxygen demand. Combination therapies are noted to provide additive effects in managing angina.
This document provides an overview of respiratory system disorders for nursing students. It begins with the objectives and anatomy and physiology of the respiratory system. It then discusses various upper and lower respiratory tract disorders like pharyngitis, tonsillitis, adenoiditis, peritonsillar abscess, laryngitis and their associated nursing assessments, signs and symptoms, diagnoses and management. Surgical procedures like tonsillectomy are also outlined.
This document provides standard treatment guidelines for general hospitals in Ethiopia. It is published by the Drug Administration and Control Authority of Ethiopia and covers guidelines for infectious diseases, non-infectious diseases, pediatric diseases, and dermatological disorders. For each condition, it provides recommendations on diagnosis, treatment, and management. The guidelines are intended to help standardize care across hospitals in Ethiopia.
This document provides an overview of a curriculum on advanced nursing education and curriculum development. It discusses objectives of acquiring practical and theoretical knowledge, demonstrating teaching skills, developing lesson plans, and creating applicable curriculums. It also covers the purpose of nursing education in developing the nursing profession and delivering healthcare. Different types of discussion tasks are outlined, including guided, inquiry-based, reflective, and exploratory discussions. Criteria for effective learning through discussion include defining terms, identifying themes, allocating time, and applying material. References on student engagement techniques and the learning through discussion approach are also provided.
Acid base titration III [Compatibility Mode].pdfSani191640
I. Percentage content of Furosemide in the sample
= (Amount of furosemide found/Amount of furosemide claimed) x 100
Amount of furosemide found
= (Volume of NaOH used for sample - Volume of NaOH used for blank) x Normality of NaOH x Equivalent weight of furosemide
= (9.6 - 2) ml x 0.1 N x 33.07 mg/ml
= 319.92 mg
Amount of furosemide claimed
= Total furosemide in 20 tablets / Number of tablets
= 20 x 40 mg / 20 tablets
= 40 mg
Percentage content = (319
The document provides an overview of the neurological examination. It describes the key structures and functions of the nervous system. It then outlines the objectives and components of a complete neurological exam, including assessing mental status, cranial nerves, motor function, coordination, and gait. The document provides detailed instructions on techniques for testing each cranial nerve and evaluating muscle tone, strength, and coordination.
This document defines pediatric seizures and epilepsy, describes the different types of seizures including partial, generalized, absence, myoclonic, atonic, and tonic-clonic seizures. It discusses the epidemiology, pathophysiology, classification, and etiologies of seizures in children. Seizures are common in children, especially those under 3 years old, and have different characteristics compared to seizures in adults due to the immature nervous system in children. Febrile seizures occur in 3% of children. Genetic factors account for 20% of childhood epilepsy cases.
This document summarizes chronic complications of diabetes mellitus, including macrovascular complications like coronary heart disease, stroke, and peripheral arterial disease, as well as microvascular complications like diabetic neuropathy, retinopathy, and nephropathy. It provides details on the pathogenesis, clinical presentation, diagnosis and management of peripheral diabetic neuropathy, noting that tight glycemic control through intensive insulin therapy can help prevent or delay the risk of developing diabetic complications.
Anemias are diseases characterized by decreased hemoglobin and red blood cells, resulting in reduced oxygen-carrying capacity of blood. Anemias can be classified based on red blood cell morphology, etiology, or pathophysiology. Treatment depends on the underlying cause but may involve oral or parenteral iron for iron deficiency, oral vitamin B12 and folic acid for deficiencies of those vitamins, and addressing the underlying chronic disease for anemia of chronic disease. The goals of treatment are to alleviate symptoms, correct the underlying cause, and prevent recurrence of anemia.
A 6-year-old female child presented with general body swelling, fever, loss of appetite, and dermatitis around the lower extremities for one month. She was diagnosed with severe acute malnutrition (SAM) with kwashiorkor. Her treatment plan included nutritional therapy with F-75 and F-100, antibiotics including amoxicillin, ampicillin, gentamicin, and cloxacillin to treat potential infections, and vitamin A supplementation. Her drug therapy was changed from amoxicillin to cloxacillin due to ineffective treatment with amoxicillin. Her condition improved with the treatment plan.
This document provides an introduction to medical and surgical nursing. It discusses key topics like the differences between medical and surgical nursing, Maslow's hierarchy of needs, stress responses, and stages of the stress response. The roles of nurses in medical-surgical settings are outlined. Concepts like health, illness, disease, and wellness are defined. Factors that influence psychological responses to illness like crisis and coping are also explained.
Atherosclerosis develops as a chronic inflammatory response to endothelial injury. Lesions progress through interactions between modified lipoproteins, immune cells, and arterial wall cells. Atherosclerosis is characterized by atheromatous plaques that protrude into and obstruct arteries. Major complications include myocardial infarction, stroke, aneurysms, and peripheral vascular disease. Coronary artery disease occurs when plaques accumulate in the coronary arteries, restricting blood flow and oxygen supply to heart muscle. Left untreated, coronary artery disease can progress to myocardial infarction.
Unit II. Respiratory system disorders.pptxSani191640
This document provides information on disorders of the respiratory system. It begins by describing the anatomy and functions of the respiratory system, including the conducting airways. It then discusses various upper and lower respiratory tract disorders like tonsillitis, pharyngitis, laryngitis, sinusitis, acute tracheo-bronchitis, and chronic bronchitis. For each disorder, it provides information on definition, causes, signs and symptoms, management, and nursing interventions. The document concludes with describing assessment techniques for respiratory disorders.
This document provides an overview of musculoskeletal disorders, including soft tissue injuries like sprains and strains, their signs and symptoms, and general management using RICE (rest, ice, compression, and elevation). Joint disorders like dislocations, osteoarthritis, and rheumatoid arthritis are also discussed. Osteomyelitis, a bone infection, is described in terms of causes, symptoms, diagnosis, and nursing interventions. The document aims to educate nurses on caring for patients with various musculoskeletal conditions.
This document discusses antidiabetic drugs used to treat diabetes mellitus. It describes the two main types of diabetes and then focuses on insulin and oral hypoglycemic agents. Insulin is described in detail including its mechanism of action, types, administration, and potential complications. Oral hypoglycemic agents discussed include sulfonylureas, which stimulate insulin release, and biguanides like metformin, which lower hepatic glucose production and increase insulin sensitivity. The document provides information on the mechanisms, pharmacokinetics, uses, and adverse effects of these important antidiabetic medications.
This document discusses pediatric nutrition and malnutrition. It begins by outlining the changing nutritional needs of children based on their age and development. It then discusses the global burden of child malnutrition. The document covers nutritional recommendations for infants from birth to 1 year old, including the benefits of breastfeeding. It also discusses protein-energy malnutrition, providing classifications and clinical manifestations such as marasmus and kwashiorkor. The principles of management are outlined, including resolving life-threatening conditions, restoring nutritional status through feeding phases, and ensuring rehabilitation.
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2. Ischemic heart disease (IHD)
• IHD is an umbrella term that encompasses a spectrum
of cardiac disorders caused by myocardial ischemia.
• IHD is defined as lack of oxygen and decreased or no
blood flow to the myocardium resulting from coronary
artery narrowing or obstruction.
• Myocardial ischemia is a state of decreased perfusion
during which the oxygen supply to the myocardium is
insufficient to meet its metabolic demands.
2
3. Conventional classification of IHD
SIHD is also frequently known as stable coronary artery disease
(SCAD)
Stable angina is the chief manifestation of SIHD or SCAD
Stable & vasospastic
angina
Symptomatic ischemic
cardiomyopathy
Microvascular angina
3
5. Pathophysiology
Atherosclerosis
is the fundamental pathophysiological basis of IHD
results in the buildup of plaque in the coronary
arteries
subsequently lead to stable angina and ACS.
Stable angina is caused by narrowing of the
coronary artery and limitation of the blood supply to
part of myocardium.
On the other hand, the sudden rupture of a plaque
and the subsequent thrombosis are responsible for
5
6. Angina
Angina, formally known as angina pectoris, is a
term used to describe chest pain.
The angina pain may be felt in the jaw, arm, neck,
back, or shoulder as well.
Angina, caused by a reduced amount of oxygen
flowing to the heart, is the primary symptom of IHD
and is not a medical condition itself.
Angina signifies that the affected individual is at a
greater risk of suffering from a heart attack or
cardiac arrest.
6
7. Angina…
The imbalance may be caused by
• By an increase in myocardial oxygen demand
(which is determined by heart rate, ventricular
contractility, and ventricular wall tension) or
• By a decrease in myocardial oxygen supply
(primarily determined by coronary blood flow &
diastolic filling time).
7
10. Organic Nitrates
• Glyceryl trinitrate (nitroglycerine)
• Isosorbide dinitrate (IDN)
• Isosorbide mononitrate (IMN)
• Erythrityl trinitrate
• Pentaerythritol tetranitrate
• Amyl nitrite
Nitrates release nitric oxide (NO) within smooth muscle
cells, probably through the action of the mitochondrial
enzyme aldehyde dehydrogenase-2 (ALDH2).
10
11. Nitrates…
Nitrates cause vasodilating effects on both peripheral
veins and arteries but with more prominent effects on
the veins.
The enzyme responsible for releasing NO from the
nitrates is present mainly in the veins (therefore
selective venodilator action).
Nitrates primarily reduce cardiac oxygen demand by
decreasing preload (left ventricular end‐diastolic
pressure).
They may modestly reduce afterload, dilate coronary
12
12. ADME
Drugs Preparation Onset of
action
Duration of action
Nitroglycerin
Sublingual tablet or
spray
1-3 min 25min
Oral, sustained release 35 min 4-8hr
Trans-dermal 30 min 10-12 hr
Isosorbide
dinitrate
Sublingual 5 min 1 hr
Oral, slow release 30 min 8 hr
Isosorbide
mononitrate
Oral, extended release 30 min >12-24 hr
13
13. ADME…
Drugs Oral
BA(%)
Elimination half‐life Metabolism and excretion
Nitroglycerin 40 1–3 min Hepatic denitration to dinitrates
and mononitrates; renal
excretion
Isosorbide
dinitrate
25 45min; 5h for the
activemetabolite,5‐
mononitrate
Hepatic denitration followed by
glucuronidation; renal excretion
Isosorbide
mononitrate
~100 5h No significant first‐pass effects;
hepatic denitration and renal
excretion
14
14. Mechanisms of Antianginal
Efficacy
The major antianginal effect for classic angina is
mediated by preload reduction rather than coronary
artery dilation.
NO-mediated vasodilation of large (venous, arterial)
> small (resistance) vessels ⇒ preferential preload
reduction without steal effect.
Coronary vasodilatory action is mainly responsible
for the therapeutic benefit of nitrates in variant/
prinzmetal angina.
15
15. Nitrate tolerance
• Tolerance has been a major problem with the use of
nitrates as chronic antianginal therapy.
• Proposed mechanisms
I. impaired nitroglycerin bioconversion to 1,2‐glyceryl
dinitrate with decreased formation of nitric oxide
II. reduced bioactivity of nitric oxide
III. activation of the RAAS and sympathetic nervous
system in response to nitrate‐induced vasodilation.
16
16. Ways to manage tolerance?
Nitrate free interval (Need 6-8 hr nitrate free time) to
restart activity
Exertional angina is prominent during day time: nitrate
free interval during night
Prinzimetal’s angina is precipitated at morning
(circadian catecholamine surges, adrenergic supply
from adrenaline is more): nitrate free evening
Alternatives (BBs or CCBs)
Partially prevented or reversed with a sulfhydryl-
regenerating. 17
17. Clinical use of nitrates
Stable Angina Pectoris
Short-acting nitrates for standby therapy
• Sublingual GTN is the most commonly used for acute
relief
• Sublingual ISDN, but not ISMN, is an alternative to
GTN
Longer-acting nitrates for the prophylaxis of angina
• Sustained-release oral preparations (ISDN, ISMN &
GTN)
• chronic treatment with nitrates is not associated with a
18
18. Clinical use of nitrates…
Variant (Prinzmetal) Angina
long-acting nitrates alone are occasionally efficacious in
abolishing episodes of variant angina.
additional therapy with Ca2+ channel blockers usually is
required.
Ca2+ channel blockers, but not nitrates, have been shown
to influence mortality and the incidence of MI favorably in
variant angina.
• they should generally be included in therapy.
• But not beta blockers!
19
19. Clinical use of nitrates…
Unstable Angina Pectoris (ACSs)
Resistance to nitrates classifies angina symptoms as
“unstable” and is a characteristic feature of ACSs,
typically caused by transient or permanent
thrombotic occlusion of coronary vessels.
Nitrates do not modify this process specifically and
are second-line drugs.
20
20. Adverse effects of organic nitrates
Mainly due to excessive vasodilatation
Severe headache (throbbing headache), dizziness,
flushing
Orthostatic hypotension, reflex tachycardia
Syncope (fainting)….cerebral cortex hypo
perfusion….loss of consciousness
A friend of nitrates is BBs ….reduce reflex
tachycardia
Serious drug interaction with PDE5 inhibiters
Sildenafil (exaggerated response to nitrates, more
21
21. β Blockers
Only antianginal drug class with proven prognostic
benefits in CAD (post MI).
They are therefore recommended as first line
treatment of patients with stable CAD and unstable
angina/ACS.
β Blockers are not useful for vasospastic angina
and, if used in isolation, may worsen that condition.
Standard compounds for the treatment of angina
are β1-selective and without intrinsic
sympathomimetic activity (e.g., atenolol, bisoprolol,
22
22. β Blockers…
• The beneficial effects of β-blocking agents are related
to their hemodynamic effects— decreased heart rate,
blood pressure, and contractility—which decrease
myocardial oxygen requirements at rest and during
exercise.
• Lower heart rate is also associated with an increase in
diastolic perfusion time that may increase coronary
perfusion.
myocardial O2 consumption at rest and during
23
23. β Blockers…
Moreover, BBs can increase blood flow toward
ischemic regions (preventing blood from being
shunted away from the ischemic myocardium):
“reverse steal or Robin Hood phenomenon”.
Undesirable effects: in end-diastolic volume and an
in ejection time ( myocardial oxygen requirement)
• Combination (nitrate + BBs)
• EDV (caused by BB) & reflex tachycardia (caused
by nitrates) can be prevented.
24
24. β Blockers…
Note:
• It is important not to discontinue β-
blocker therapy abruptly.
• The dose should be gradually tapered off
over 2 to 3 weeks to avoid rebound angina,
MI, and hypertension.
25
25. Ca2+ Channel Blockers
Calcium influx is increased in ischemia because of
the membrane depolarization that hypoxia produces.
In turn, this promotes the activity of several ATP-
consuming enzymes, thereby depleting energy stores
and worsening the ischemia.
The Ca++ channel blockers protect the tissue by
inhibiting the entrance of Ca++ into cardiac and
smooth muscle cells of the coronary and systemic
arterial beds.
26
26. Ca2+ Channel Blockers…
Dihydropyridines: (amlodipine, nifedipine extended R)
Their effect for classic angina is mainly by peripheral
arterial vasodilation and afterload reduction.
Their efficacy in vasospastic angina is due to
relaxation of the coronary arteries.
Short-acting dihydropyridines should be avoided in
CAD because of evidence of increased mortality
after an MI.
27
27. Nodihydropyridine Ca2+ Channel
Blockers
Verapamil:
more direct negative inotropic and chronotropic
effects
Cause a reduction in myocardial O2 demand
contraindicated in patients with preexisting depressed
cardiac function or AV conduction abnormalities.
Diltiazem
Diltiazem can relieve coronary artery spasm and is
particularly useful in patients with variant angina.
28
28. Ca2+ Channel Blockers…
Variant Angina
Ca2+ channel blockers are effective in about 90% of
patients.
These agents are considered first-line treatment and may
be combined with nitro-vasodilators.
Exertional Angina
also are effective in the treatment of exertional angina
considered the drugs of choice if β blockers do not
achieve sufficient symptomatic benefit or are not tolerated
• evidence for life-prolonging efficacy is lacking
29
29. Ca2+ Channel Blockers…
Unstable Angina (ACS)
Verapamil and diltiazem are recommended only---
for patients who continue to show signs of ischemia,
do not tolerate β blockers, have no clinically
significant left ventricular dysfunction, and show no
signs of disturbed AV conduction.
not to use dihydropyridines without concurrent
therapy with β blockers.
30
30. Antiplatelet Agents
Antiplatelet agents represent the cornerstone of
therapy for ACS
Aspirin (low dose 75-125 mg), P2Y12 receptor
antagonists [clopidogrel, prasugrel, ticagrelor,
cangrelor (IV)]
↓ Platelet aggregation by inhibiting COX-1
mediated TxA2 production (aspirin) or ADP
receptors (P2Y12 receptor antagonists)
31
31. Antiplatelet Agents…
Newer thienopyridines (prasugrel, ticagrelor,
cangrelor)
All three appear superior to clopidogrel in treating
patients with ACS; contributing factors likely include
faster onset of action and less-variable
pharmacokinetics.
The hepatic activation of prasugrel is more stable
and faster than that of clopidogrel
Ticagrelor and prasugrel as the primary choice in
patients with ACS and clopidogrel as an alternative
32
32. Antithrombotic Agents
Heparin, in its unfractionated form and as low-
molecular-weight heparin (e.g., enoxaparin), also
reduces symptoms and prevents infarction in
unstable angina.
Fondaparinux, a heparinoid pentasaccharide,
antithrombin III-dependent Factor Xa inhibitor has
the best efficacy-safety profile of all anticoagulants
and is therefore currently first choice.
Statins can be added to reduce associated
dyslipidemia. 33
33. Myocardial Infarction
For the treatment of acute ST elevation MI, thrombolytic
therapy (streptokinase, urokinase, anistreplase,
alteplase, reteplase, tenecteplase etc.) should be
instituted as early as possible, preferably within first 3
hours.
10% reduction in mortality can still be attained even if
these are administered after 12 hours.
Morphine like opioid is administered i.v. to decrease pain
and increased sympathetic activity (pain in MI results in
the increased sympathetic outflow).
34
Indeed, the main symptomatic clinical presentations of SIHD include
classical chronic stable angina caused by epicardial stenosis;
angina caused by microvascular dysfunction (also known as microvascular angina)
angina caused by vasospasm (vasospastic angina), and
Symptomatic ischemic cardiomyopathy.
Acute coronary syndrome (ACS) is an umbrella term inclusive of unstable angina (UA) or acute myocardial infarction (MI) consisting of ST segment elevation MI (STEMI) or non–ST segment MI (NSTEMI).
The difference between UA and myocardial infarction is whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of cardiac troponins. Significant myocardial damage occurs in NSTEMI and STEMI, but not in UA.
ST-elevation myocardial infarction
is generally due to a complete obstruction of a large coronary artery.
The mainstay in these patients is immediate reperfusion by primary angioplasty and stenting or, in the absence of invasive options, fibrinolytic therapy
Non–ST-elevation myocardial infarction
Due to transient obstruction of larger coronary arteries or occlusion of small branches, leading to disseminated myocardial necrosis.
Primary angioplasty is also indicated in these patients.
Unstable angina is differentiated from NSTEMI by the absence of increased plasma troponin concentrations.
The term atherosclerosis comes from the Greek words athero (meaning gruel or paste) and sclerosis (hardness).
It refers to the process of fatty substances, cholesterol, cellular waste products, calcium, and fibrin (a clotting material in the blood) building up in the inner lining of an artery. The resulting buildup is called plaque
In some patients, anginal symptoms may occur without any increase in myocardial O2 demand, but rather as a consequence of an abrupt reduction in blood flow, as might result from coronary thrombosis (unstable angina or ACS) or localized vasospasm (variant or Prinzmetal angina).
Stable angina -common
In vascular smooth muscle cells, nitric oxide activates guanylate cyclase, which increases cGMP leading to dephosphorylation of myosin light chain and thereby smooth muscle relaxation.
Nitric oxide may also activate calcium‐dependent potassium channels, leading to membrane hyperpolarization and thereby smooth muscle cell relaxation
For use in rectal fissures, intra‐anal administration of nitrates results in decreased sphincter tone and intra‐anal pressure.
Nitrates have significant antiplatelet and antithrombotic properties; however, the clinical importance of these potentially beneficial effects is unclear.
High dose, This can happen to such an extent that coronary flow is compromised, and the sympathetic increase in myocardial O2 demand overrides the beneficial action of the nitrovasodilators, leading to ischemia.
Glyceryl dinitrate metabolites of nitroglycerin, which have about one-tenth the vasodilator potency, appear to have half lives of about 40 min.
The partially denitrated metabolites have much longer half-lives (up to 3 hours).
Nitroglycerin metabolites (two dinitroglycerins and two mononitro forms)
-The 1,2-dinitro derivative has significant vasodilator efficacy, provides most of the therapeutic effect of orally administered nitroglycerin.
Oral isosorbide dinitrate →denitration to two mononitrates (active)
Isosorbide mononitrate has improved bioavailability and long duration of action to its stability against hepatic breakdown
Ellimination: glutathione-organic nitrate reductase
Reduction in liver to denitrated organic compounds glucuronide conjugation and excretion in kidney
blood flow to ischemic sub-endocardial myocardium may contribute to relief of pain in a typical anginal attack
Nonselective vasodilators such as adenosine or dipyridamole can worsen the perfusion of ischemic areas by dilating the relatively constricted arterioles of the healthy myocardium, leading to redistribution of blood flow away from the ischemic myocardium (“steal phenomenon”).
Nitrovasodilators, in contrast, do not have a major effect on the smaller resistance arteries (and therefore do not cause steal phenomena).
Molsidomine is an emerging agent in this category to which tolerance does not develop.
Patients should be instructed to seek medical attention immediately if three tablets of GTN taken over a 15-min period do not relieve a sustained attack because this situation may be indicative of MI, unstable angina, or another cause of the pain.
Sustained-release ISDN and ISMN are typically given in two doses administered 6–7 h apart, followed by a nitrate-free interval of at least 8 h.
Nitroglycerin is indicated for either the acute relief of an attack or prophylaxis of angina pectoris due to coronary artery disease
Isosorbide dinitrate and isosorbide mononitrate are indicated only for the prevention of angina pectoris due to coronary artery disease.
This is because the onset of action of isosorbide dinitrate or isosorbide mononitrate is not sufficiently rapid for them to be useful in aborting an acute anginal episode.
This is also true for the extended release formulations of nitroglycerin, which are only indicated for prophylaxis of angina pectoris.
A friend of nitrates is BBs ….reduce reflex tachycardia
Palpitation….unpleasant awareness of cardiac activity
These drugs do not dilate coronary vessels; rather vasoconstriction may occur (unopposed α mediated vasoconstriction due to blockade of β2 mediated vasodilation). These drugs are therefore, contra-indicated in variant angina
Reversed Robin Hood Syndrome (RRHS) was first described in 2007 as a cause of worsening neurological deficit in the setting of an acute ischemic event. RRHS is the shunting of cerebral blood flow to nonstenotic vascular territories due to impaired vasodilation bought on by hypercapnia.
Concurrent therapy of a dihydropyridine with a β blocker has proven more effective than either agent given alone in exertional angina, presumably because the β blocker suppresses reflex tachycardia.
In contrast, the concurrent administration of verapamil or diltiazem with a β blocker is contraindicated for the potential for AV block, severe bradycardia, and decreased left ventricular function.
Regular daily use of aspirin
In acute MI: reduce mortality by 23% and in combination with streptokinase reduce mortality by 42% and reinfarction by 52%
In unstable angina reduce MI and death by 50%
In secondary prevention
reduce reinfarction by 32% and combined vascular events by 25%
Clopidogrel: A 9% reduction in adverse cardiovascular events
Initiate a loading dose of 300 mg and then 75 mg once daily
In unstable angina combined with aspirin reduces mortality
Avoid within first few days of an MI and first 7 days of an ischemic stroke (no clear benefit)
Same incidence of bleeding as aspirin but possibly lower GI bleeding
Thrombin inhibitors, such as hirudin or bivalirudin, directly inhibit even clot-bound thrombin, are not affected by circulating inhibitors, and function independently of antithrombin III.
Bivalirudin provides no benefit over heparin in ACS (Valgimigli et al., 2015). Thrombolytic agents such as rTPA are of no benefit in unstable angina. The new oral anticoagulants (factor IIa inhibitor dabigatran and factor Xa inhibitors rivaroxaban, apixaban, and edoxaban) have no established place in the treatment of CAD.
Pentazocine and pethidine should not be used for this indication since these agents cause tachycardia and can worsen the symptoms.