The document provides guidelines for the diagnosis and management of chronic stable angina, defining it as chest discomfort caused by myocardial ischemia that is typically triggered by exertion or stress. It discusses the pathophysiology, risk factors, diagnostic testing options including ECG, stress testing, and imaging, and recommendations for invasive coronary angiography. The guidelines are intended to help clinicians properly evaluate and treat patients experiencing chronic stable angina.
This document discusses the assessment, investigation, and treatment of chronic stable angina. It defines chronic stable angina as chest pain or discomfort that is reproducibly associated with exertion or stress and relieved by rest. The document outlines how to evaluate patients presenting with chest pain through history, physical exam, risk factor assessment, and probability estimation models. It recommends initial tests like ECG, cardiac biomarkers, and stress testing. Treatment focuses on lifestyle changes, medications like aspirin, beta-blockers, calcium channel blockers, and revascularization if needed. Regular patient follow up and education are also emphasized.
Mitral stenosis is characterized by obstruction of blood flow from the left atrium to the left ventricle due to thickening and immobility of the mitral valve leaflets. The most common cause is rheumatic heart disease. As the stenosis progresses, the left atrial pressure rises, leading to pulmonary congestion and right-sided heart failure over time. On examination, findings may include an accentuated S1, opening snap, and mid-diastolic murmur with presystolic accentuation. Chest x-ray may show an enlarged left atrium and signs of pulmonary congestion. Treatment involves rate control for atrial fibrillation, diuretics, and potentially balloon valvuloplasty or
Mitral stenosis is commonly caused by rheumatic heart disease which leads to inflammation and fusion of the mitral valve leaflets, reducing the mitral valve orifice area. Severe mitral stenosis, defined as a mitral valve area less than 1.0 cm2, can cause pulmonary hypertension, pulmonary edema, atrial fibrillation, and right heart failure as the heart tries to maintain sufficient cardiac output against the back pressure. Physical exam may reveal signs of pulmonary hypertension like a loud pulmonary component to S2, as well as a tapping apex, opening snap, and mid-diastolic rumble on cardiac auscultation. Echocardiography can determine the severity of mitral stenosis and assess
Unstable angina is a form of ischemic heart disease where a person experiences chest pain or discomfort that occurs at rest or with minimal exertion. It is caused by decreased blood supply to the heart muscle due to partial blockage of the coronary arteries. Diagnosis involves taking a medical history, electrocardiogram, cardiac enzyme tests, and stress testing. Treatment consists of blood thinners, nitroglycerin, blood pressure medications, and cholesterol-lowering drugs medically or early cardiac catheterization and angioplasty or bypass surgery if high risk.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
This document discusses aortic regurgitation (AR), which occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion of the aorta. Common causes include rheumatic heart disease, bicuspid aortic valves, hypertension, and Marfan syndrome. Over time, the left ventricle must work harder to compensate for the backflow of blood, which can lead to enlarged and weakened heart muscles. Symptoms may include palpitations, chest pain, and shortness of breath. Diagnosis involves listening for an early diastolic murmur and confirming the diagnosis with echocardiogram
Definition of heart failure - causes and types of heart failure - pathophysiology and risky factors for heart failure - Diagnosis clinical manifestations and investigations and classification of heart failure- treatment of chronic heart failure
Also Acute heart failure causes - clinical picture and treatment
This document discusses the assessment, investigation, and treatment of chronic stable angina. It defines chronic stable angina as chest pain or discomfort that is reproducibly associated with exertion or stress and relieved by rest. The document outlines how to evaluate patients presenting with chest pain through history, physical exam, risk factor assessment, and probability estimation models. It recommends initial tests like ECG, cardiac biomarkers, and stress testing. Treatment focuses on lifestyle changes, medications like aspirin, beta-blockers, calcium channel blockers, and revascularization if needed. Regular patient follow up and education are also emphasized.
Mitral stenosis is characterized by obstruction of blood flow from the left atrium to the left ventricle due to thickening and immobility of the mitral valve leaflets. The most common cause is rheumatic heart disease. As the stenosis progresses, the left atrial pressure rises, leading to pulmonary congestion and right-sided heart failure over time. On examination, findings may include an accentuated S1, opening snap, and mid-diastolic murmur with presystolic accentuation. Chest x-ray may show an enlarged left atrium and signs of pulmonary congestion. Treatment involves rate control for atrial fibrillation, diuretics, and potentially balloon valvuloplasty or
Mitral stenosis is commonly caused by rheumatic heart disease which leads to inflammation and fusion of the mitral valve leaflets, reducing the mitral valve orifice area. Severe mitral stenosis, defined as a mitral valve area less than 1.0 cm2, can cause pulmonary hypertension, pulmonary edema, atrial fibrillation, and right heart failure as the heart tries to maintain sufficient cardiac output against the back pressure. Physical exam may reveal signs of pulmonary hypertension like a loud pulmonary component to S2, as well as a tapping apex, opening snap, and mid-diastolic rumble on cardiac auscultation. Echocardiography can determine the severity of mitral stenosis and assess
Unstable angina is a form of ischemic heart disease where a person experiences chest pain or discomfort that occurs at rest or with minimal exertion. It is caused by decreased blood supply to the heart muscle due to partial blockage of the coronary arteries. Diagnosis involves taking a medical history, electrocardiogram, cardiac enzyme tests, and stress testing. Treatment consists of blood thinners, nitroglycerin, blood pressure medications, and cholesterol-lowering drugs medically or early cardiac catheterization and angioplasty or bypass surgery if high risk.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
1) Atrial fibrillation is the most common cardiac arrhythmia characterized by disorganized atrial activity without effective contractions. It increases risk of stroke and prevalence rises with age.
2) Management involves restoring sinus rhythm through drugs, cardioversion, or ablation or controlling heart rate and preventing clots with anticoagulants. Rate control uses beta blockers, calcium channel blockers, or digoxin while restoring rhythm uses antiarrhythmics, cardioversion, or ablation.
3) Treatment depends on whether AF is paroxysmal, persistent or permanent and involves restoring rhythm if possible or controlling rate and preventing complications if not.
This document discusses aortic regurgitation (AR), which occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion of the aorta. Common causes include rheumatic heart disease, bicuspid aortic valves, hypertension, and Marfan syndrome. Over time, the left ventricle must work harder to compensate for the backflow of blood, which can lead to enlarged and weakened heart muscles. Symptoms may include palpitations, chest pain, and shortness of breath. Diagnosis involves listening for an early diastolic murmur and confirming the diagnosis with echocardiogram
Definition of heart failure - causes and types of heart failure - pathophysiology and risky factors for heart failure - Diagnosis clinical manifestations and investigations and classification of heart failure- treatment of chronic heart failure
Also Acute heart failure causes - clinical picture and treatment
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
Dilated cardiomyopathy is characterized by an enlarged and poorly contracting left ventricle. The main causes include inflammatory, toxic, metabolic, inherited, idiopathic and miscellaneous factors. On evaluation, patients typically present with decreased cardiac output, tachycardia and signs of congestion. Tests include echocardiogram, which shows increased left ventricular size and reduced ejection fraction, and ECG, which may show conduction delays. Treatment focuses on managing symptoms with diuretics and blocking neurohormonal activation to prevent worsening, while devices like ICDs are used in eligible patients.
1) Acute coronary syndromes (ACS) describe conditions caused by coronary plaque rupture and include ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina.
2) Plaque rupture triggers blood clot formation, which can partially or completely block blood flow to the heart. STEMI involves complete blockage, while NSTEMI and unstable angina involve partial blockages.
3) Diagnosis involves ECG, cardiac enzyme tests, and angiography. Treatment depends on diagnosis but commonly includes aspirin, blood thinners, beta-blockers, and procedures like thrombolysis or angioplasty to restore blood flow.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of acute myocardial infarction (MI), also known as a heart attack. It discusses the definition, causes, risk factors, pathogenesis, classification, diagnosis and management of MI. The diagnosis involves taking a patient history, examining signs and symptoms, electrocardiography, serum analysis and echocardiography. Management is staged and involves pre-hospital, emergency department and post-discharge care, with a focus on reperfusing the blocked artery as quickly as possible, such as through percutaneous coronary intervention or thrombolytic therapy. The goal is to correctly identify the type of MI, treat the patient according to guidelines and manage any complications.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
This document provides an overview of infective endocarditis, including its definition, pathogenesis, epidemiology, clinical presentation, diagnosis, and treatment. It defines infective endocarditis as a microbial infection of the heart valves or endocardium. It discusses the typical pathogens involved and describes the formation of vegetations on heart valves. It also outlines the diagnostic criteria, including blood cultures and echocardiography. Treatment involves prolonged antibiotic therapy tailored to the causative organism, and may require surgery in cases of heart failure or uncontrolled infection.
1. Pericarditis is inflammation of the pericardium and is usually caused by viral or bacterial infections. It can occur acutely or become chronic.
2. The main symptoms are sudden onset of sharp chest pain that worsens with breathing or coughing. A pericardial friction rub may also be heard on examination.
3. Treatment focuses on relieving pain and inflammation, usually with NSAIDs. Corticosteroids may be used for refractory cases or certain causes like connective tissue diseases.
This document discusses STEMI (ST-elevation myocardial infarction). It defines STEMI and provides the universal definition involving cardiac biomarkers and ECG changes. It describes the five types of MI and lists the signs, symptoms, risk factors, diagnostic criteria involving ECG and cardiac enzymes. Treatment options including fibrinolytic therapy, PCI and medical therapies are summarized. Complications of STEMI both early and late are outlined.
Coronary artery disease (CAD) is a major cause of death in India. Atherosclerosis underlies most CAD cases. Unstable angina and NSTEMI are types of acute coronary syndrome (ACS) caused by a reduction in oxygen supply to the heart. The clinical presentation of ACS can include chest pain and other symptoms. Diagnosis involves ECG, cardiac biomarkers, and risk stratification. Treatment focuses on anticoagulation, antiplatelet therapy, and revascularization. Myocardial infarction (MI or heart attack) occurs when an atherosclerotic plaque ruptures completely blocking a coronary artery. This leads to necrosis of heart muscle cells. Diagnosis of MI requires specific ECG changes and elevated cardiac
This document provides information about infective endocarditis:
- Infective endocarditis is a microbial infection of the heart valves, heart lining, or blood vessels that is usually caused by bacteria.
- It can affect both native and prosthetic heart valves. Staphylococcus aureus is now the most common cause.
- Diagnosis is based on modified Duke criteria using clinical findings, blood cultures, and echocardiography findings. Treatment involves prolonged antibiotic therapy and may require surgery to remove infected tissues.
- Complications can include heart valve damage, embolic events, heart failure, and extension of the infection. Proper antibiotic prophylaxis is important for those at high risk
Chest pain can be cardiac or non-cardiac in origin. Cardiac causes include angina, myocardial infarction, and pericarditis while non-cardiac causes include pulmonary embolism, pneumonia, gallbladder disease, and musculoskeletal disorders. Characteristics of ischemic cardiac chest pain include a central, pressing or squeezing quality that radiates to the jaw/arm and is provoked by exertion. Differential diagnosis of chest pain requires evaluating characteristics like location, quality, duration and associated features to determine cardiac vs. non-cardiac etiology.
This document defines and describes acute coronary syndrome, which includes unstable angina and myocardial infarction. It discusses the etiology, pathogenesis, clinical features, investigations, management, and prognosis of acute coronary syndrome. The key points are that acute coronary syndrome is caused by atherosclerosis and involves plaque disruption and thrombosis in the coronary arteries, leading to symptoms such as chest pain. Diagnosis involves electrocardiography, cardiac biomarker tests, and imaging. Treatment focuses on analgesia, antithrombotics, reperfusion therapy, and long-term secondary prevention. Prognosis depends on factors like the infarct location and timeliness of treatment.
Cor pulmonale, or right heart failure, is caused by high blood pressure in the pulmonary artery and right ventricle due to conditions that restrict pulmonary blood flow such as chronic lung diseases. It develops when pulmonary hypertension leads to enlargement and failure of the right ventricle. Symptoms include shortness of breath, leg swelling, and fatigue. Diagnosis involves physical exam, imaging like echocardiogram and chest x-ray, and assessing pulmonary pressures. Treatment focuses on managing the underlying lung condition, giving diuretics and vasodilators, and may involve oxygen therapy or lung transplantation in severe cases.
Atrial fibrillation and atrial flutter are types of arrhythmia where the heart beats irregularly. Atrial fibrillation occurs when rapid, irregular electrical signals cause the heart's upper chambers (atria) to beat very fast and irregularly. Atrial flutter is similar but the heart beats fast in a regular pattern. These conditions are diagnosed through electrocardiograms which detect abnormal heart rhythms. Holter monitors and event recorders can also detect arrhythmias over longer periods of time when symptoms occur. Complications include stroke and heart failure, so treatment focuses on rate or rhythm control and preventing clots.
An abdominal aortic aneurysm (AAA) is an abnormal dilatation of the abdominal aorta due to weakness in the vessel wall. AAAs are usually asymptomatic but can cause back pain. Risk factors include age, hypertension, smoking and family history. Large AAAs (>5.5cm diameter) have a high risk of rupture and require surgical repair via open surgery or endovascular aneurysm repair (EVAR) to exclude the aneurysm and prevent rupture. Ruptured AAAs have a mortality rate over 80% and are a major cause of death in older men.
This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
Angina pectoris is a recurrent chest pain or discomfort caused by myocardial ischemia. The document defines angina and provides historical context, summarizes the pathophysiology involving an imbalance between myocardial oxygen supply and demand, and lists various clinical presentations and classifications of angina. It also discusses investigations like exercise stress testing and identifies high-risk features, and outlines management approaches.
Myocarditis is an inflammatory disease of the heart muscle that can be caused by infectious or non-infectious triggers. It has a variable clinical presentation ranging from mild symptoms to life-threatening conditions. The diagnosis is challenging due to the heterogeneity of symptoms but can involve electrocardiogram, cardiac biomarkers, echocardiogram, cardiac MRI and endomyocardial biopsy. About half of acute cases resolve in 2-4 weeks but some develop heart failure or arrhythmias. Treatment focuses on supporting heart function and managing symptoms while the disease runs its course.
Dilated cardiomyopathy is characterized by an enlarged and poorly contracting left ventricle. The main causes include inflammatory, toxic, metabolic, inherited, idiopathic and miscellaneous factors. On evaluation, patients typically present with decreased cardiac output, tachycardia and signs of congestion. Tests include echocardiogram, which shows increased left ventricular size and reduced ejection fraction, and ECG, which may show conduction delays. Treatment focuses on managing symptoms with diuretics and blocking neurohormonal activation to prevent worsening, while devices like ICDs are used in eligible patients.
1) Acute coronary syndromes (ACS) describe conditions caused by coronary plaque rupture and include ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina.
2) Plaque rupture triggers blood clot formation, which can partially or completely block blood flow to the heart. STEMI involves complete blockage, while NSTEMI and unstable angina involve partial blockages.
3) Diagnosis involves ECG, cardiac enzyme tests, and angiography. Treatment depends on diagnosis but commonly includes aspirin, blood thinners, beta-blockers, and procedures like thrombolysis or angioplasty to restore blood flow.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
The document discusses various pericardial diseases including acute pericarditis, constrictive pericarditis, pericardial effusion, and cardiac tamponade. It provides details on the anatomy and functions of the pericardium, pathophysiology, clinical features, diagnostic tests, and management of these conditions. Key points include that pericardial diseases can present with non-specific symptoms, clinical suspicion is important for diagnosis, and treatment depends on underlying etiology and presence of hemodynamic compromise. Differentiating constrictive pericarditis from restrictive cardiomyopathy is important as treatment approaches differ significantly.
This document provides an overview of acute myocardial infarction (MI), also known as a heart attack. It discusses the definition, causes, risk factors, pathogenesis, classification, diagnosis and management of MI. The diagnosis involves taking a patient history, examining signs and symptoms, electrocardiography, serum analysis and echocardiography. Management is staged and involves pre-hospital, emergency department and post-discharge care, with a focus on reperfusing the blocked artery as quickly as possible, such as through percutaneous coronary intervention or thrombolytic therapy. The goal is to correctly identify the type of MI, treat the patient according to guidelines and manage any complications.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
This document provides an overview of infective endocarditis, including its definition, pathogenesis, epidemiology, clinical presentation, diagnosis, and treatment. It defines infective endocarditis as a microbial infection of the heart valves or endocardium. It discusses the typical pathogens involved and describes the formation of vegetations on heart valves. It also outlines the diagnostic criteria, including blood cultures and echocardiography. Treatment involves prolonged antibiotic therapy tailored to the causative organism, and may require surgery in cases of heart failure or uncontrolled infection.
1. Pericarditis is inflammation of the pericardium and is usually caused by viral or bacterial infections. It can occur acutely or become chronic.
2. The main symptoms are sudden onset of sharp chest pain that worsens with breathing or coughing. A pericardial friction rub may also be heard on examination.
3. Treatment focuses on relieving pain and inflammation, usually with NSAIDs. Corticosteroids may be used for refractory cases or certain causes like connective tissue diseases.
This document discusses STEMI (ST-elevation myocardial infarction). It defines STEMI and provides the universal definition involving cardiac biomarkers and ECG changes. It describes the five types of MI and lists the signs, symptoms, risk factors, diagnostic criteria involving ECG and cardiac enzymes. Treatment options including fibrinolytic therapy, PCI and medical therapies are summarized. Complications of STEMI both early and late are outlined.
Coronary artery disease (CAD) is a major cause of death in India. Atherosclerosis underlies most CAD cases. Unstable angina and NSTEMI are types of acute coronary syndrome (ACS) caused by a reduction in oxygen supply to the heart. The clinical presentation of ACS can include chest pain and other symptoms. Diagnosis involves ECG, cardiac biomarkers, and risk stratification. Treatment focuses on anticoagulation, antiplatelet therapy, and revascularization. Myocardial infarction (MI or heart attack) occurs when an atherosclerotic plaque ruptures completely blocking a coronary artery. This leads to necrosis of heart muscle cells. Diagnosis of MI requires specific ECG changes and elevated cardiac
This document provides information about infective endocarditis:
- Infective endocarditis is a microbial infection of the heart valves, heart lining, or blood vessels that is usually caused by bacteria.
- It can affect both native and prosthetic heart valves. Staphylococcus aureus is now the most common cause.
- Diagnosis is based on modified Duke criteria using clinical findings, blood cultures, and echocardiography findings. Treatment involves prolonged antibiotic therapy and may require surgery to remove infected tissues.
- Complications can include heart valve damage, embolic events, heart failure, and extension of the infection. Proper antibiotic prophylaxis is important for those at high risk
Chest pain can be cardiac or non-cardiac in origin. Cardiac causes include angina, myocardial infarction, and pericarditis while non-cardiac causes include pulmonary embolism, pneumonia, gallbladder disease, and musculoskeletal disorders. Characteristics of ischemic cardiac chest pain include a central, pressing or squeezing quality that radiates to the jaw/arm and is provoked by exertion. Differential diagnosis of chest pain requires evaluating characteristics like location, quality, duration and associated features to determine cardiac vs. non-cardiac etiology.
This document defines and describes acute coronary syndrome, which includes unstable angina and myocardial infarction. It discusses the etiology, pathogenesis, clinical features, investigations, management, and prognosis of acute coronary syndrome. The key points are that acute coronary syndrome is caused by atherosclerosis and involves plaque disruption and thrombosis in the coronary arteries, leading to symptoms such as chest pain. Diagnosis involves electrocardiography, cardiac biomarker tests, and imaging. Treatment focuses on analgesia, antithrombotics, reperfusion therapy, and long-term secondary prevention. Prognosis depends on factors like the infarct location and timeliness of treatment.
Cor pulmonale, or right heart failure, is caused by high blood pressure in the pulmonary artery and right ventricle due to conditions that restrict pulmonary blood flow such as chronic lung diseases. It develops when pulmonary hypertension leads to enlargement and failure of the right ventricle. Symptoms include shortness of breath, leg swelling, and fatigue. Diagnosis involves physical exam, imaging like echocardiogram and chest x-ray, and assessing pulmonary pressures. Treatment focuses on managing the underlying lung condition, giving diuretics and vasodilators, and may involve oxygen therapy or lung transplantation in severe cases.
Atrial fibrillation and atrial flutter are types of arrhythmia where the heart beats irregularly. Atrial fibrillation occurs when rapid, irregular electrical signals cause the heart's upper chambers (atria) to beat very fast and irregularly. Atrial flutter is similar but the heart beats fast in a regular pattern. These conditions are diagnosed through electrocardiograms which detect abnormal heart rhythms. Holter monitors and event recorders can also detect arrhythmias over longer periods of time when symptoms occur. Complications include stroke and heart failure, so treatment focuses on rate or rhythm control and preventing clots.
An abdominal aortic aneurysm (AAA) is an abnormal dilatation of the abdominal aorta due to weakness in the vessel wall. AAAs are usually asymptomatic but can cause back pain. Risk factors include age, hypertension, smoking and family history. Large AAAs (>5.5cm diameter) have a high risk of rupture and require surgical repair via open surgery or endovascular aneurysm repair (EVAR) to exclude the aneurysm and prevent rupture. Ruptured AAAs have a mortality rate over 80% and are a major cause of death in older men.
This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
Angina pectoris is a recurrent chest pain or discomfort caused by myocardial ischemia. The document defines angina and provides historical context, summarizes the pathophysiology involving an imbalance between myocardial oxygen supply and demand, and lists various clinical presentations and classifications of angina. It also discusses investigations like exercise stress testing and identifies high-risk features, and outlines management approaches.
This document discusses the clinical assessment of patients presenting with chest pain, including recommendations for history, physical exam, initial tests, stress testing, and risk stratification. It provides details on evaluating pretest likelihood of coronary artery disease, diagnostic testing options, and prognostic markers from exercise stress testing. Key recommendations include obtaining an ECG, labs, and chest x-ray, as well as using stress echocardiography or nuclear imaging for intermediate-high risk patients and exercise ECG as initial testing for lower risk patients.
This document provides a summary of angina pectoris (chest pain). It begins with an example case history and treatment. It then defines angina and describes the main types (stable and unstable). It discusses the pathophysiology and clinical presentation. It outlines the diagnostic tests and procedures used to diagnose angina. The goals and approaches to treatment are summarized, including drug therapies like nitrates, beta blockers, and calcium channel blockers. Other measures for managing coronary artery disease are mentioned like lifestyle changes and procedures.
The document discusses the management of chronic stable angina. It defines angina and stability, and outlines the typical treatment approach which includes patient education, risk factor modification through lifestyle changes and medical therapy, and consideration of revascularization. The mainstay of treatment is optimal medical therapy focusing on symptom control through anti-anginal medications like beta-blockers, calcium channel blockers, and nitrates, as well as prevention of adverse outcomes with aspirin and other drugs.
Chronic stable angina is a chronic condition where episodes of chest pain occur periodically due to temporary deficiencies in the heart's blood supply. The document outlines the objectives, definition, epidemiology, pathophysiology, differences between chronic stable angina and acute coronary syndrome, pharmacological treatments including beta blockers, calcium channel blockers, nitrates, antiplatelet agents, ACE inhibitors, and ranolazine. It discusses patient education on drug effects, potential adverse effects and interactions, and monitoring requirements. Lifestyle recommendations including diet, exercise, smoking cessation, and weight loss are also provided.
This document discusses angina pectoris, or chest pain caused by reduced blood flow to the heart. It defines three main types of angina - stable, unstable, and variant (Prinzmetal's angina). Stable angina occurs with exertion and is relieved by rest, while unstable angina happens more frequently and is less responsive to treatment. Variant angina involves coronary artery spasms, often occurring at certain times. The document outlines symptoms, risk factors, initiating factors, and common drug treatments for angina, including nitrates like nitroglycerin and calcium channel blockers.
This document discusses ischaemic heart disease and angina pectoris. It defines IHD as a condition where there is inadequate blood supply and oxygen to the myocardium. Angina pectoris is defined as a clinical syndrome characterized by precordial discomfort due to myocardial ischemia, typically brought on by exertion and relieved by rest. The document covers the epidemiology, risk factors, pathophysiology, clinical manifestations, diagnosis and treatment of these conditions. It emphasizes that risk factor identification and modification are important for managing patients with known or suspected IHD.
The document discusses two severity scores - CURB-65 and CRB-65 - that are used to evaluate the severity of community-acquired pneumonia. CURB-65 assesses confusion, blood urea nitrogen level, respiratory rate, low blood pressure, and age 65 and older, while CRB-65 excludes blood urea nitrogen. Both have been validated for predicting prognosis in community-acquired pneumonia patients based on studies comparing them to other prediction rules.
Mr. I, a 64-year-old male, presented to the hospital with chest pain. He reported feeling pressure and tightness in his chest for the past 5 months that had worsened. Examinations found elevated blood pressure, tachycardia, and signs of cardiomegaly on chest x-ray. ECG showed sinus rhythm with poor R wave progression. Echocardiogram indicated left ventricular dysfunction. The working diagnosis was unstable angina pectoris and hypertension. Management included medications to reduce blood pressure and prevent clots, with monitoring through daily ECGs.
This document provides information about angina pectoris (angina), including its causes, types, diagnosis, and treatment. It begins by defining angina as a heart condition marked by chest pain due to reduced oxygen to the heart. It then discusses the different types of angina (stable, unstable, variant), symptoms, diagnostic tests, and pharmacological treatments which work to improve the oxygen demand/supply ratio to the heart through vasodilation and other mechanisms. The main drug classes used to treat angina are discussed in detail: nitrates, calcium channel blockers, beta-blockers, and antiplatelets.
The document summarizes cardiac conduction and the action potential in heart cells. It discusses:
- Two types of heart cells: electrical pacemaker cells and contractile myocardial cells
- The cardiac action potential involves depolarization and repolarization through ion channel openings and closings in four phases: upstroke, plateau, repolarization, and rest.
- The cardiac conduction system generates and conducts electrical impulses, starting from the sinoatrial node and traveling through specialized conduction pathways to the atria and ventricles.
- Abnormalities in rate or rhythm can occur if the sinoatrial node or other conduction tissues assume control of pacing.
A 65-year-old male presented to the emergency department with severe chest pain and sweating. He has a history of smoking and nausea/vomiting. Examination and ECG were performed. The differential diagnoses included stable angina, unstable angina, and subendocardial MI. The plan was for an ECG, and possible PCI. Stable angina occurs with exertion and is relieved by rest, while unstable angina occurs at rest and is not relieved by rest, and may indicate an impending heart attack. The document discusses the pathophysiology, clinical features, investigation, and management of stable and unstable angina.
Treatment Options For The Chronic Stable AnginaRodolfo Rafael
This document discusses treatment options for chronic stable angina, including the metabolic agent trimetazidine. It provides an overview of angina and its epidemiology. Trimetazidine improves energy metabolism in ischemic heart tissue by inhibiting fatty acid oxidation and stimulating glucose utilization. Clinical trials show trimetazidine reduces angina symptoms and improves exercise tolerance. It may benefit patients with heart failure or diabetes by optimizing energy production and preserving heart cell function.
EECP therapy provides an alternative treatment for refractory angina by increasing coronary perfusion pressure and reducing cardiac workload through the sequential inflation and deflation of compressive cuffs on the lower limbs. It has been shown to significantly reduce angina symptoms and improve quality of life. EECP therapy involves 35 hours of treatment over 7 weeks, with daily 1-2 hour sessions separated by rest periods. It appears to be a safe and effective option for refractory angina patients who are not candidates for revascularization.
Nitrates work by relaxing smooth muscle in blood vessels via the production of nitric oxide. This leads to vasodilation and reduced preload and afterload, lowering oxygen demand on the heart. Common side effects include headaches and hypotension. Tolerance develops with chronic use and can be prevented through intermittent dosing schedules and adjunctive treatments that replenish nitric oxide stores. Nitrates are available in various oral, topical, and intravenous formulations for use in angina and heart failure.
Ranolazine is a new antianginal drug that represents a new class of drugs. It partially inhibits fatty acid oxidation and shifts energy production to a more efficient carbohydrate oxidation during ischemia. It also inhibits late inward sodium currents, reducing calcium overload and improving diastolic function and myocardial perfusion. Ranolazine has been shown to reduce angina frequency and improve exercise ability with no effects on blood pressure or heart rate. Its benefits and mechanisms of action were discussed along with its indications, studies, and potential role in other conditions such as diabetes and cardioplegia.
This document discusses Team Based Learning (TBL), including its benefits and process. TBL involves students working in assigned groups, completing individual and group readiness assurance tests (iRAT and tRAT), and receiving feedback. It can be used in face-to-face, blended, or online courses. Supportive technologies include classroom response systems, learning management system tools, and web conferencing. The workshop modeled TBL and encouraged participants to apply it to their own courses.
The document discusses unstable angina and non-ST-elevation myocardial infarction (UA/NSTEMI). It describes the pathophysiology, clinical presentation, diagnosis, and risk stratification of patients presenting with suspected UA/NSTEMI. The diagnostic evaluation involves assessing the likelihood of coronary artery disease, monitoring the patient for recurrent symptoms and checking cardiac biomarkers and electrocardiograms, and may include stress testing to evaluate for significant CAD if the initial workup is inconclusive. Early risk assessment using markers like troponin levels, ST changes, and risk scores can help guide treatment and identify patients most likely to benefit from a more aggressive strategy.
It contains meaning, pathophysiology, types, risk factors, lab and diagnostic procedures and tests, Rx goals, appropriate medications for ANGINA PECTORIS ..... Enjoy and Learn from it!!!!
Angina pectoris is chest pain or discomfort that occurs when the heart muscle does not get enough oxygen. It is usually caused by narrowed coronary arteries that cannot supply enough blood and oxygen to meet increased demands. The symptoms include chest pain or pressure that can radiate to the arms, neck or jaw, brought on by activity or stress, and relieved by rest. Diagnosis involves evaluating symptoms, risk factors, and electrocardiogram changes during episodes to confirm ischemia as the cause of symptoms.
Ischaemic heart disease is caused by an imbalance between the heart's supply and demand for oxygenated blood, usually due to atherosclerosis narrowing the coronary arteries. The main symptoms are chest pain or discomfort known as angina. There are different types of angina that vary based on their triggers and patterns. Diagnosis involves tests like ECG, echocardiogram, stress tests and angiography. Treatment options include medications to reduce demands on the heart like nitrates, beta-blockers, and calcium channel blockers, as well as interventions like angioplasty, stents and bypass surgery.
This document discusses chronic coronary syndrome, also known as stable angina. It describes the pathophysiology as fixed atherosclerotic lesions causing an imbalance between myocardial oxygen supply and demand, leading to demand-induced ischemia. The key clinical features are chest pain or discomfort that is precipitated by exertion or stress and relieved by rest. Investigations include electrocardiograms, stress tests, echocardiography, myocardial perfusion scans, CT coronary angiography, and invasive coronary angiography to diagnose coronary artery disease and determine management.
This document discusses ischemic heart disease and acute coronary syndrome. It covers the anatomy of the heart, pathophysiology of coronary artery disease, management of stable angina, and prognosis. Key topics include diagnosis of ischemic heart disease, treatment of risk factors, drug therapy for angina, stress testing, revascularization options, and the differences between NSTEMI and STEMI.
Related with cardio vascular system. Angina is Retrosternal chest pain which if left untreated can cause the higher complications with respect to cardiac health of human body. May be this is simple chest pain but if exceeds can cause major damage # prevention is better than cure :-)
Chest pain can be caused by many serious cardiac and pulmonary conditions. It is considered a medical emergency and requires prompt evaluation and treatment. Common causes of chest pain include acute coronary syndrome, aortic dissection, pulmonary embolism, pericarditis, gastroesophageal reflux disease, and psychological factors like panic attacks and anxiety. A careful history, physical exam, electrocardiogram, cardiac enzyme tests, imaging studies, and other diagnostics are used to determine the underlying cause and guide management.
[Int. med] chest pain 3rd year class from SIMS LahoreMuhammad Ahmad
Chest pain can be caused by many serious cardiac and pulmonary conditions. It is considered a medical emergency and requires prompt evaluation and treatment. Common causes of chest pain include acute coronary syndrome, aortic dissection, pulmonary embolism, pericarditis, gastroesophageal reflux disease, and psychological factors like panic attacks and anxiety. A careful history, physical exam, electrocardiogram, cardiac enzyme tests, imaging studies, and other diagnostics are used to determine the underlying cause and guide management.
The document discusses acute coronary syndrome (ACS), which refers to a clinical syndrome indicating acute myocardial ischemia and includes ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (UA). The pathogenesis is generally due to atherosclerosis of the coronary arteries leading to rupture of atherosclerotic plaques and formation of thrombi that obstruct coronary blood flow. Risk factors include those that are uncontrollable like age, sex, and heredity as well as controllable factors like hypertension, high cholesterol, smoking, lack of physical activity, obesity, diabetes, and stress.
This document discusses ischemic heart disease and angina. It defines ischemic heart disease as a condition where there is inadequate blood supply and oxygen to the heart muscle. Angina is described as chest pain or discomfort caused by an imbalance between the heart's oxygen supply and demand. The document outlines the causes, types, risk factors, diagnosis, and management of angina through lifestyle modifications and medications like aspirin to control symptoms and reduce health risks.
This document discusses ischaemic heart disease (IHD), which is caused by an imbalance between the myocardial supply and demand for oxygenated blood. The most common cause is coronary atherosclerosis, which affects the coronary arteries and reduces blood flow to the heart muscle. Symptoms include stable or unstable angina, myocardial infarction (MI), and sudden cardiac death. Diagnosis involves assessing risk factors, symptoms, electrocardiograms, cardiac enzymes and biomarkers, imaging tests, and occasionally coronary angiography. Management focuses on controlling symptoms, treating risk factors, and revascularization when needed to improve outcomes.
1) Coronary artery disease and myocardial infarction are caused by atherosclerosis and plaque buildup in the arteries leading to ischemia. Unstable angina is a change in a previously stable pattern of chest pain and is part of the acute coronary syndrome continuum.
2) Myocardial infarction is caused by a blockage of blood flow to the heart muscle leading to cell death. It is diagnosed through electrocardiogram changes and cardiac biomarker levels. Complications include arrhythmias and heart failure.
3) Heart failure occurs when the heart can no longer pump sufficiently to meet the body's needs. It can be caused by conditions like coronary artery disease damaging the heart muscle. Types include left or right ventricular failure and
Acute chest pain is one of the most common reason for seeking care in the emergency department (10% of all visits)
Only 10-15% of patients with chest pain actually have ACS.
CORONARY ARTERY DISEASE in medicine and nurses.pptxfmwansagalizye
This document discusses coronary artery disease (CAD) and angina pectoris. It defines CAD and describes the different types of angina. Risk factors for angina include atherosclerosis, smoking, diabetes, hypertension, high cholesterol, obesity, and sedentary lifestyle. Signs and symptoms include chest pain and shortness of breath. Diagnosis involves ECG, echocardiogram, angiogram, and stress testing. Nursing management focuses on reducing anxiety, preventing pain by balancing activity and rest, and teaching self-care and management of modifiable risk factors.
MUCLecture_2022_12319533. Medical surgical nursing pptxssuser47b89a
1. The document discusses hypertension and coronary artery diseases. It defines hypertension and describes its pathophysiology, causes, signs and symptoms, assessment, and treatment including lifestyle changes and medications.
2. Coronary artery disease and angina pectoris are explained. Angina is caused by reduced blood flow to the heart. Its clinical manifestations and treatment including medications are outlined.
3. Myocardial infarction is summarized including its causes, clinical manifestations involving different body systems, diagnostic tests such as ECG and cardiac biomarkers, and treatment with thrombolytics, analgesics, and invasive procedures.
Angina pectoris is a clinical syndrome characterized by chest pain or pressure due to insufficient blood flow to the heart muscle. It is usually caused by an imbalance between myocardial oxygen supply and demand. There are different types of angina including stable, unstable, and variant angina. Risk factors include family history, diabetes, hypertension, smoking, and high cholesterol. Diagnosis involves ECG, stress test, and angiography. Treatment focuses on decreasing oxygen demand on the heart and increasing supply by using nitrates, beta blockers, calcium channel blockers, antiplatelet drugs, and statins. Emergency treatment for unstable angina may include thrombolytics. Lifestyle changes and medication aim to prevent future cardiac events associated with untreated
This document provides an overview of acute myocardial infarction (MI or heart attack). It defines MI as diminished blood supply to the heart muscle leading to cell damage and death. Risk factors include age, family history, smoking, diabetes, hypertension, hyperlipidemia, obesity, and physical inactivity. Symptoms may include chest pain, nausea, sweating, and changes in vital signs. Diagnosis involves electrocardiograms and cardiac enzyme levels. Treatment aims to restore blood flow and includes medications, fibrinolytic therapy, angioplasty, and bypass surgery. Nursing focuses on monitoring for ischemia, controlling chest pain, educating patients, and modifying risk factors.
Angina pectoris is the medical term for chest pain or discomfort due to coronary heart disease. It occurs when the heart muscle doesn't get as much blood as it needs. This usually happens because one or more of the heart's arteries is narrowed or blocked, also called ischemia.
2- nursing care for Myocardial Infarction.pptxZakTal
This document provides an overview of coronary artery disease (CAD), angina pectoris, and myocardial infarction (MI). It describes the etiology, pathophysiology, clinical manifestations, diagnosis, and treatment of these conditions. For CAD and angina, it discusses risk factors, types of angina, goals of medical management, and nursing priorities like pain management, coronary precautions, and patient education. For MI, it addresses classification, complications, goals of reperfusion therapy, and nursing focus areas like monitoring for dysrhythmias and complications, balancing oxygen supply and demand, and preventing issues like atelectasis.
Angina pectoris is chest pain caused by an imbalance between oxygen supply and demand in the heart muscle. It is a common symptom of coronary artery disease. There are different classifications of angina including stable, unstable, and variant forms. Angina is caused by conditions that narrow the coronary arteries like atherosclerosis. Symptoms include chest pain that can radiate to the arm or jaw, brought on by exertion and relieved by rest. Diagnosis involves tests like ECG, stress testing, and angiography. Treatment focuses on lifestyle changes, medications like nitrates and beta blockers, and procedures like angioplasty if medications do not control symptoms. Unstable angina specifically involves worsening chest pain at rest and is
This document provides a 10 step checklist for male catheterization. The steps include taking consent, preparing equipment, anesthetizing the urethra with lidocaine, cleaning and lubricating the penis, slowly inserting the catheter into the urethra while monitoring for urine return, inflating the balloon, and securing the catheter. The objective is to properly insert a urinary catheter while reassuring the patient and following aseptic technique.
This document outlines 6 clinical themes that will be covered in a 4-week kidney module, including patients presenting with painful hematuria, generalized edema, difficulty passing urine, oliguria, rising serum creatinine, and renal transplant. Each theme includes an associated clinical case, objectives, and critical thinking questions to guide student learning through interactive sessions, group discussions, and practical skills.
This document discusses risk factors, prevalence, symptoms, and management of chronic obstructive pulmonary disease (COPD) and asthma. It provides statistics on the increasing mortality rates of COPD compared to declines in other causes of death. Studies from Pakistan show the frequency of asthma, allergic rhinitis, and their relationship to socioeconomic status. The document examines the pathology and inflammatory processes of COPD compared to asthma and how these differences impact clinical presentation and therapy.
Tuberculosis is a global health problem, infecting one third of the world's population and causing millions of deaths annually. It is the 6th highest cause of disease in Pakistan, where the incidence of active TB cases is over 80 per 100,000 people each year. TB is caused by the bacterium Mycobacterium tuberculosis, which is transmitted through the air when people with active TB cough or sneeze. It most often affects the lungs but can damage other organs. While the immune system usually keeps the infection under control, active disease can develop if the bacteria overpowers immunity.
A previously healthy 32-year-old male presented with a 2-day history of fever, chills, productive cough, dyspnea, and chest pain. On examination, he had tachycardia, tachypnea, and reduced breath sounds with crackles on the left side of his chest. He likely has pneumonia based on his symptoms and physical exam findings of reduced breath sounds and crackles.
This case study describes a 64-year-old male patient with heart failure who was prescribed digoxin therapy. He experienced side effects from antibiotics prescribed for a lung infection. His digoxin dose was later increased when he reported new symptoms. After being diagnosed with chronic renal failure years later, his digoxin levels became toxic as his kidneys could no longer clear the drug appropriately. His digoxin dose was adjusted and monitored based on his kidney function to safely control his heart condition.
The document classifies antiarrhythmic drugs into four categories based on their mechanism of action:
Class I drugs block sodium channels, Class II drugs block beta receptors, Class III drugs block potassium channels, and Class IV drugs block calcium channels. It describes the conduction pathways in the heart from the sinoatrial node through the atrioventricular node and Purkinje fibers to the ventricles, noting the atrioventricular node has a slower conduction velocity than other tissues. The document also provides a table summarizing the classification of antiarrhythmic drugs and an illustration of ion movement across cell membranes.
Hypertension is defined as a sustained blood pressure greater than 140/90 mm Hg. It is a major risk factor for atherosclerosis and cardiovascular disease. The pathogenesis of essential hypertension involves genetic and environmental factors that alter cardiac output and peripheral resistance. Primary defects include renal sodium retention and vasoconstriction/hypertrophy. Secondary causes include endocrine, renal, and neurological conditions.
This case study describes a 64-year-old male patient with heart failure who was prescribed digoxin therapy. He experienced side effects from antibiotics prescribed for a lung infection. His digoxin dose was later increased when he reported new symptoms. After being diagnosed with chronic renal failure years later, his digoxin levels became toxic, requiring his dose to be adjusted. The case study poses questions about the patient's treatment and digoxin pharmacokinetics related to his comorbidities and changing renal function over time.
2003 cvs shifa permeation through biological membranesMuhammad Saim
This document describes a case study of a 64-year-old male patient with heart failure who was prescribed digoxin. After initial improvement, he later developed side effects from high digoxin levels due to renal failure. His digoxin dose was adjusted and he stabilized. The document also covers key concepts about drug transport across membranes, ionization, and using the Henderson-Hasselbalch equation to understand how drug properties impact absorption and excretion.
The document discusses three main topics:
1. Theories of drug distribution and elimination including single compartment, two compartment, and multiple compartment theories.
2. Bioavailability and factors affecting it including extent of absorption, rate of absorption, and first pass elimination through the liver.
3. Drug clearance and factors related to it including first order and capacity limited elimination, flow dependence, and plasma protein binding. Clearance is a measure of how quickly a drug is removed from the body.
This document discusses cardiac arrhythmias and their treatment. It defines normal cardiac rhythm and atrial arrhythmias. It describes the cardiac action potential and ECG waves. It explains the differences between pacemaker and non-pacemaker cell action potentials. The document discusses mechanisms of arrhythmias including disorders of impulse formation and conduction. It provides an overview of antiarrhythmic drug classes and mechanisms of action including sodium channel blockade, beta-blockade, and calcium channel blockade.
1) The document discusses the renin-angiotensin-aldosterone system and its role in regulating blood pressure.
2) Angiotensin-converting enzyme inhibitors (ACEIs) work by preventing the conversion of angiotensin I to angiotensin II, thereby lowering blood pressure.
3) ACEIs, beta blockers, and aldosterone antagonists have been shown to reduce mortality in patients with heart failure by 23%, 35%, and 30% respectively over 2 years.
The retina contains photoreceptors that detect light and send signals through bipolar and amacrine cells to retinal ganglion cells. Ganglion cell axons form the optic nerve and cross at the optic chiasm, with nasal fibers crossing to the opposite side. The optic tract carries signals to the lateral geniculate nucleus and superior colliculus. The LGN projects to primary visual cortex, which separates visual properties and sends them to different visual association areas for further analysis of color, shape, motion, and location.
The orbital contents include the eyeball, extraocular muscles, blood vessels, and nerves. The orbital fascia is a thin layer of connective tissue that lines the bony orbit and separates the orbital contents from surrounding structures. It helps support and position the eyeball and extraocular muscles within the orbit.
The lacrimation reflex is stimulated by irritation of the eye's conjunctiva and cornea, which increases tear volume. Afferent nerves in the ophthalmic and infraorbital nerves carry impulses to the brainstem and spinal cord. Efferent parasympathetic nerves from the pterygopalatine ganglion and sympathetic nerves from the upper thoracic spinal cord then activate the lacrimal and accessory glands to secrete the aqueous layer of tears, while tarsal and goblet cells produce the lipid and mucus layers.
The document discusses the anatomy and function of cranial nerves III, IV, and VI. It describes how CN III contains motor neurons that innervate most of the extraocular muscles and parasympathetic fibers. CN IV is the only crossed cranial nerve, originating from the contralateral side and innervating the superior oblique muscle. CN VI innervates the lateral rectus muscle and has a long intracranial course, making it susceptible to compression or damage. Clinical presentations of lesions or palsies of each of these nerves are also outlined.
The document summarizes the layers of the eyeball. It describes the three coats that make up the eye: the fibrous coat containing the sclera and cornea, the vascular/uveal coat containing the choroid, ciliary body and iris, and the nervous coat containing the retina. It then provides details on the structures and layers within each of these coats, including their anatomical features, components, blood supply and functions.
Hyperopia, also known as hypermetropia, is a refractive error where light focuses behind the retina rather than on it when the eye is at rest and not accommodating. This results in a blurred image. The eye will unconsciously accommodate to try and bring the image into focus. Hyperopia can be corrected using a convex lens, which helps bring the light rays back to focus on the retina. It is often not noticed until later in life when the eye loses its ability to accommodate as strongly.
The limbic system is a ring of structures located deep within the brain that is involved in emotion, motivation, learning, and memory. It includes the hippocampus, amygdala, hypothalamus, and other structures. The limbic system regulates behaviors related to survival like eating, drinking, and reproduction through reward and punishment centers. It also plays a role in emotions, memory formation, and decision making. Damage to limbic structures can impact behaviors, with lesions to areas like the hippocampus causing anterograde amnesia and lesions to the amygdala producing symptoms like the Kluver-Bucy syndrome.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
2. DEFINITION
• STABLE ANGINA:
It is a clinical syndrome characterized by:
Discomfort in the: chest, jaw, shoulder, back, or
arms, typically elicited by exertion or emotional
stress and relieved by rest or nitroglycerin.
Less typically in epigastric region.
William Heberden first introduced the term ‘angina pectoris’ in
1772 to characterize a syndrome in which there was ‘a sense
of strangling and anxiety’ in the chest, especially associated
with exercise
2
5. PATHOPHYSIOLOGY
This clinical syndrome is attributable to myocardial ISCHEMIA.
• Myocardial ischaemia is caused by an imbalance between
myocardial oxygen supply and consumption and coronary flow,
which is dependent on the luminal crossectional area of the
coronary artery and coronary arteriolar tone.
• Both cross-sectional area and arteriolar tone may be dramatically
altered by the presence of atherosclerotic plaque within the vessel
wall.
• Ischaemia-induced sympathetic activation can further increase the
severity of ischaemia through a variety of mechanisms including a
further increase of myocardial oxygen consumption and coronary
5
vasoconstriction.
6. PATHOPHYSIOLOGY (CONTD.)
• The ischaemic cascade is characterized by a sequence of
events, resulting in :
– metabolic abnormalities,
– perfusion mismatch,
– regional and then global diastolic and systolic dysfunction,
– electrocardiographic (ECG) changes, and angina.
Adenosine released by ischaemic myocardium appears to
be the main mediator of angina (chest pain) through stimulation
of A1 receptors located on cardiac nerve endings.
• Ischaemia is followed by reversible contractile dysfunction
known as ‘stunning’
• Recurrent episodes of ischemia and stunning may lead to a chronic but
still reversible form of dysfunction known as ‘hibernation’.
6
7. • In the majority of patients, the pathological substrate of stable angina
is atheromatous, narrowing of the coronary arteries.
• Which leads to coronary obstruction.
• At Luminal obstruction of 40% Maximal flow during exercise can
usually be maintained.
• At luminal obstruction of >50% Coronary ischemia occurs
• At Luminal obstruction of >80% Coronary vascular resistance
increases 3 times
Ischemic threshold is influenced by other factors
including :
– The degree of development of collateral circulation
– The degree of transmural distribution of myocardial
perfusion from the more vulnerable subendocardium to the
subepicardium.
– coronary vascular tone
– platelet aggregation
7
8. Silent angina
Myocardial ischaemia may also be silent:
Lack of pain may be due to:
– Ischaemia of insufficient duration and/or severity,
– To damage of afferent cardiac nerves, or to
– Inhibition of ischemic cardiac pain at spinal or supraspinal
level.
In patients who exhibit painless ischaemia,
shortness of breath, and palpitation may
represent anginal equivalents.
Breathlessness may be due to ischaemic left ventricular
systolic or diastolic dysfunction or to transient ischamic
mitral regurgitation.
8
9. EPIDEMIOLOGY
• The prevalence of angina in community studies
increases sharply with age in both sexes
0.1–1% in women aged 45–54
10–15% in women aged 65–74
2–5% in men aged 45–54
10–20% in men aged 65
According to an estimate 20 000 – 40 000
individuals in most European countries, of the
population per million suffer from angina. 9
10. PROGNOSTIC INDICATORS
In general, the outcome is worse in patients with:
• reduced LV function
• a greater number of diseased vessels
• more proximal locations of coronary stenosis
• greater severity of lesions
• more severe angina
• more extensive ischaemia
• greater age
10
12. Exertional or classical
• It occurs due to increase myocardial oxygen
demand during exertion or emotion in a
patient of narrow coronary arteries. It relieved
by rest and nitroglycerine.
• Coronary artery obstructions are not sufficient
to result in resting myocardial ischemia.
However, when myocardial demand increases,
ischemia results.
13. Variant or Prinzmetal’s Angina
• Transient impairment of coronary blood
supply by vasospasm or platelet aggregation
• Majority of patients have an atherosclerotic
plaque
• Generalized arterial hypersensitivity
• Long term prognosis very good
14. Prinzmetal’s Angina
• Spasm of a large coronary artery
• Transmural ischemia
• ST-Segment elevation at rest or with exercise
• More prolonged than in classical angina.
• It occurs more in women under age 50.
15. Anginal Equivalent Syndrome
• Patient’s with exertional dyspnea rather than
exertional chest pain
• Caused by exercise induced left ventricular
dysfunction
16. Syndrome X
• Typical, exertional angina with positive
exercise stress test
• Anatomically normal coronary arteries
• Reduced capacity of vasodilation in
microvasculature
• Long term prognosis very good
• Calcium channel blockers and beta blockers
effective
17. Silent Ischemia
• Very common
• More episodes of silent than painful ischemia
in the same patient
• Difficult to diagnose
• Holter monitor
• Exercise testing
19. SYMPTOMS
Clinical classification of chest pain
Typical angina (definite) Meets three of the following
characteristics:
• Substernal chest discomfort of
characteristic quality
and duration
• Provoked by exertion or
emotional stress
• Relieved by rest and/or GTN
Atypical angina (probable) Meets two of these characteristics
Non-cardiac chest pain Meets one or none of
the characteristics
19
20. Classification of angina severity according to the
Canadian Cardiovascular Society
Class Level of symptoms
Class- I ‘Ordinary activity does not cause angina’
Angina with strenuous or rapid
or prolonged exertion only
Class - II ‘Slight limitation of ordinary activity’
Angina on walking or climbing stairs rapidly,
walking uphill or exertion after meals, in
cold weather, when under emotional stress,
or only during the first few hours after awakening
Class - III ‘Marked limitation of ordinary physical activity’
Angina on walking one or two blocks on the level
or one flight of stairs at a normal pace under
normal condition
Class - IV ‘Inability to carry out any physical activity
without discomfort’ or ‘angina at rest’
20
21. PHYSICAL EXAMINATION
Physical examination of a patient with (suspected) angina pectoris is important
to assess the presence of :
• Hypertension
• Valvular heart disease
• Hypertrophic obstructive cardiomyopathy.
Physical examination should include:
• Assessment of body-mass index (BMI)
• Waist circumference to assist evaluation of the metabolic syndrome
• Evidence of non-coronary vascular disease which may be asymptomatic
• Other signs of comorbid conditions.
However, there are no specific signs in angina pectoris.
During or immediately after an episode of myocardial ischaemia:
• a third or fourth heart sound may be heard and
• mitral insufficiency may also be apparent during ischaemia.
Such signs are, however, elusive and non-specific.
21
23. Recommendations for laboratory investigation in initial
assessment of stable angina
CLASS – I: (In all patients)
• Fasting lipid profile, including TC, LDL, HDL, and
triglycerides (level of evidence B)
• Fasting glucose (level of evidence B)
• Full blood count including Hb and white cell count (level
of evidence B)
• Creatinine (level of evidence C)
CLASS – I: (if specifically indicated on the basis
of clinical evaluation)
• Markers of myocardial damage if evaluation suggests
clinical instability or ACS (level of evidence A)
• Thyroid function if clinically indicated (level of evidence
C)
23
24. LAB TESTS (Contd...)
CLASS – IIa:
• Oral glucose tolerance test (level of evidence B)
CLASS – IIb:
• Hs-C-reactive protein (level of evidence B)
• Lipoprotein a, ApoA, and ApoB (level of
evidence B)
• Homocysteine (level of evidence B)
• HbA1c (level of evidence B)
• BNP (level of evidence B)
24
25. Recommendations for blood tests for routine
reassessment in patients with chronic stable
angina
CLASS IIa:
• Fasting lipid profile
• Fasting glucose
On an annual basis (level of evidence C)
25
26. CHEST X- RAY
CLASS – I:
• CXR in patients with suspected heart failure (level of
evidence C)
• CXR in patients with clinical evidence of significant
pulmonary disease (level of evidence B)
The presence of :
• Cardiomegaly
• Pulmonary congestion
• Atrial enlargement
• Cardiac calcifications
– has been related to impaired prognosis
26
28. ECG
Recommendations for resting ECG for initial
diagnostic assessment of angina:
CLASS – I:
• Resting ECG while pain free (level of evidence C)
• Resting ECG during episode of pain (if possible)
(level of evidence B)
Recommendations for resting ECG for routine
reassessment in patients with chronic stable
angina:
CLASS –IIb:
• Routine periodic ECG in the absence of clinical
change (level of evidence C)
28
29. ECG
• ST segment depression with or without T
wave inversion that reverse after ischemia
disappears.
N.A.N 2009
30. AMBULATORY ECG
RECOMMENDATIONS:
CLASS – I:
• Angina with suspected arrhythmia (level of
evidence B)
CLASS – IIa:
• Suspected vasospastic angina (level of
evidence C)
30
32. ECG STRESS TESTING
• SENSITIVITY = 68%
• SPECIFICITY = 77%
• Has no diagnostic value in the presence of:
o LBBB
o PACED RHYTHM
o WPW- SYNDROME
• FALSE POSITIVE results are seen in:
o LVH
o ELECTROLYTE IMBALANCE
o INTERVENTRICULAR CONDUCTION ABNORMALITY
o DIGITALIS USE
o ALSO LESS SENSITIVE & SPECIFIC IN WOMEN
32
33. Interpretation of ETT
TEST WOULD BE POSITIVE IF:
– Horizontal or down sloping ST – Depression of =/> 1mm
(0.1mV)
– Chest pain
– Occur at low work load or in early stages exercise
– Persist for >3 mins in recovery period
– Impaired LV function with increased probability of CAD:
• Fall in systolic blood pressure
• Lack of increase in BP with exercise
• Appearance of a systolic murmur of MR
• Ventricular Arrhythmias
33
34. REASON TO TERMINATE ETT
• Symptom limitation, e.g. pain, fatigue, dyspnoea, and claudication
• Combination of symptoms such as pain with significant ST-changes
Safety reasons such as the following:
• Marked ST-depression (>2 mm ST-depression can be taken as a
relative indication for termination and 4 mm as an absolute
indication to stop the test)
• ST-elevation 1 mm
• Significant arrhythmia
• Sustained fall in systolic blood pressure >10 mmHg
• Marked hypertension (>250 mmHg systolic or >115 mmHg diastolic)
• Achievement of maximum predicted heart rate may also be a reason
to terminate the test in patients with excellent exercise tolerance
who are not tired and at the discretion of the supervising physician.
34
35. Stable Angina
Exercise Testing
• The goal of exercise testing is to induce a
controlled, temporary ischemic state during
clinical and ECG observation
37. ECHOCARDIOGRAPHY
RECOMMECDATIONS:
CLASS – I:
1. Patients with abnormal auscultation suggesting
valvular heart disease or hypertrophic
cardiomyopathy (level of evidence B)
2. Patients with suspected heart failure (level of
evidence B)
3. Patients with prior MI (level of evidence B)
4. Patients with LBBB, Q-waves, or other significant
pathological changes on ECG, including ECG LVH (level
of evidence C)
37
38. Stable Angina
Stress Echo
• Ischemia may cause wall motion abnormalities, no rise
of fall in LVEF ( left ventricular ejection fraction )
• This formula gives one a fraction, e.g., 0.60. Multiply this fraction by 100 gives a % figure, e.g., 60%
• Sensitivity/specificity same as nuclear testing
40. CT - SCAN
• Detects calcium in coronaries.
• Quantifies the extent of calcification.
The Agatston score the most commonly used score, is based
on the area and density of calcified plaques.
SENSITIVITY: 95%
SPECIFICITY: 98%
NEGATIVE PREDICTIVE VALUE: 93 – 99%
RECOMMENDATIONS:
CLASS – IIb:
Patients with a low pre-test probability of disease, with
a non-conclusive exercise ECG or stress imaging test
(level of evidence C)
40
41. INVASIVE CORONARY ANGIOGRAPHY
CLASS – I:
• Severe stable angina (Class 3 or greater CCS, with a high
pre-test probability of disease, particularly if the symptoms
are inadequately responding to medical treatment
(level of evidence B)
• Survivors of cardiac arrest (level of evidence B)
• Patients with serious ventricular arrhythmias (level of evidence C)
• Patients previously treated by myocardial revascularization (PCI,
CABG) who develop early recurrence of moderate or severe angina
pectoris (level of evidence C)
CLASS – IIb:
• Patients with an inconclusive diagnosis on non-invasive testing, or
conflicting results from different noninvasive modalities at
intermediate to high risk of coronary disease (level of evidence C)
• Patients with a high risk of restenosis after PCI if PCI has been
performed in a prognostically important site (level of evidence C)
41
42. Cardiac Catheterization
Indications
• Suspicion of multi-vessel CAD
• Determine if CABG/PTCA feasible
• Rule out CAD in patients with
persistent/disabling chest pain and
equivocal/normal noninvasive testing
• percutaneous transluminal coronary angioplasty
• coronary artery bypass grafting
44. ANGINA WITH NORMAL CORONARIES:
Features of chest pain may suggest:
• Non- cardiac chest pain
• Atypical angina including vasospastic angina
• Cardiac syndrome X
Important to differentiate non-cardiac chest pain from
other 2 conditions:
If angiographic appearances are suggestive of non-
obstructing lesions & stress imaging techniques identify an
extensive area of ischemia then :
Intravascular USG or assessment of coronary flow reserve or
fractional flow reserve may be considered to exclude missed
obstructive lesions.
Intra coronary ACETYLCHOLINE or ERGONOVINE may be
administered during coronary arteriography
44
45. VASOSPASTIC / VARIANT ANGINA
• Characterized by typically located pain.
• Usually occurs at rest (occasionally with exertion)
• Relieved within minutes with Nitrates
• Pain is associted with ST elevation
• May coexist with typical exertional angina due to fixed coronary
lesions.
• Vasospasm may occur in response to:
– Smoking
– Electrolyte disturbance
– Cocaine use
– Cold stimulation
– Autoimmune disease
– Hyperventilation
– Insulin resistance
• Prognosis depends on underlying coronary artery disease.
• Ambulatory ST segment monitoring may be helpful.
• TREATMENT FOCUSES ON REMOVING THE STIMULUS, Ca CHANNEL
BLOCKERS AND Nitrates. 45
46. Syndrome X
It requires the presence of:
– Typical exercise induced angina
– Positive ETT or STRESS IMAGING
– Normal coronary arteries
Resting ECHO LVH & Diastolic dysfunction (CLASS-I ,
LOE-C)
Intracoronary acetylcholine & intracoronary USG , flow
reserve or FFR (CLASS- IIb, LOE-C)
Survival prognosis is favourable, morbidity is high
Treatment should focus on symptom relief
Other risk factors of endothelial dysfunction like HTN,
Dyslipedemias should be treated appropriately.
46
49. AIMS OF TREATMENT
1. To improve prognosis by preventing
myocardial infarction & death
o Reduce plaque progression
o Stabilize plaque
o Prevent thrombosis if endothelial dysfunction or
plaque rupture occur
2. To minimize or abolish symptoms
49
50. GENERAL MANAGEMENT
• Patients & their close associates should be informed of the nature of
angina & the implications of the diagnosis & treatment should be
recommended.
• Advice should be given for the management of an acute attack i-e to
rest briefly at least, from the activity that provoked the angina and
the use of sublingual nitrates.
• Patient should be informed of the potential S.E of NITRATES & its
appropriate use.
• Patient should be informed of the need to seek medical advice if
angina symptoms persist for > 20 mins after rest & is not relieved
after taking Nitrates.
• Cigarette smoking should be STRONGLY discouraged.
• Patient should be advised to take MEDITERRANEAN diet with
vegetables, fruits, fish & poultry being the mainstay.
• Alcohol in moderation may be beneficial but excessive consumption
is harmful.
50
51. General management (Cont..)
• Fish oils rich in OMEGA-3 are recommended atleast
once weekly.
• Physical activity within the patient’s limitations should
be encouraged.
• Concomitant disorders like HTN & D.M should be
managed appropriately:
– Pts with DM & or Renal disease should be treated with a
BP goal of < 130/80 mm of Hg
– Multifactorial intervention in diabetic patient may reduce
both cardiovascular & diabetic complications.
• Anemia & hyperthyroidism, if present, should be
corrected.
51
53. RECOMMENDATIONS
ANTITHROMBOTIC DRUGS:
– Low dose Asprin (75mg/Day) in all patients
without contraindications:
• Active GI bleeding
• Asprin allergy
• Intolerance (CLASS- I, LOE-A )
– Clopidogrel in pts who can not take asprin.
(CLASS- IIa, LOE- B)
53
54. LIPID LOWERING DRUGS:
• STATIN therapy for all patients with CAD.
(CLASS – I,LOE-A)
• High dose statin therapy in high risk pts with
proven CAD. ( CLASS – IIa, LOE- B)
• Fibrate therapy in pts with low HDL & high TGs
who have DM or METABOLIC syndrome (CLASS–
IIb, LOE-B)
• Fibrates or Nicotinic Acid as adjunctive therapy to
statins in pts with low HDL & high TGs at HIGH
RISK. (CLASS – IIb, LOE-C)
54
55. ACE - INHIBITORS:
• Patients with co-incident indications for ACE
Inhibition e.g HTN ,HF
(CLASS-I, LOE-A)
• All patients with Angina & proven CAD.
(CLASS-IIa, LOE-B)
BETA – BLOCKERS:
• Patient post MI or with HF (CLASS–I, LOE-A)
55
56. PHARMACOLOGICAL AGENTS
DRUGS ACTION COMMENTS RECOMMENDA
TIONS
SHORT ACTING Venodilation, dec. •Sublingual adm. IC
NITRATES Diastolic filling, •Situational prophylaxis
reduced intra -
cardiac pressure,
LONG ACTING •Oral/transdermal prep. IC
dec. subendocardial
NITRATES • Care to maintain a
perfusion.
nitrate free interval
BETA - BLOCKERS Dec oxygen demand •Less SE with B1 selective IA
by dec HR, dec agents
contractility, dec BP. •Titrate dose
•Proven to red.
ferquency of symptoms
& improves exercise
tolerance.
56
57. DRUGS ACTION COMMENTS REOMMENDATION
PHARMACOLOGICAL AGENTS (cont...) S
CALCIUM channel •Systemic & •Proven to reduce IA
BLOCKERS Coronary frequency of
vasodilatation by symptoms &
inhibition of L-type improve exercise
channels tol.
•Verapamil & •Efficacy
diltiazem red. comparable with
myocardial Beta blockers
contractility, HR & •Particularly
AV cond effective in
•Dihydropyridines vasospastic angina
are more
vasoselective
K-CHANNEL •Activates K- Nicorandil has IC
OPENER channels shown to dec.
•Nitrate like vaso death, MI &
dilator effect hopitalizations in
one RCT.
57
58. SINUS NODE Reduces HR directly As effective as Beta IIa B
INHIBITORS blockers in reducing
symptoms
METABOLIC Increases glucose Limited IIb B
AGENTS metabolism haemodynamic
effects,
Trimetazidine not
available in all
countries,
Ranolazine not yet
licensed in Eourope
58
59. GENERAL RECOMMENDATIONS FOR
PHARMACOLOGICAL THERAPY
• Anti anginal treatment should be tailored according to the
needs of individual patients & should be monitored
individually.
• Short acting nitrate therapy for immediate relief of acute
symptoms.
• Different drugs may have additive anti anginal effects
• Dosing of 1 drug should be optimized before adding
another.
• Advisable to switch drug combinations before attempting 3
drugs regimen.
• Poor compliance should be considered when drug therapy
is unsuccessful.
• Patients with symptoms who are poorly controlled on
double therapy should be assessed for suitability for
revascularization if not already considered.
59
61. CABG
• Main indications: prognostic & symptomatic
• Prognostic benefit mainly due to reduction in
cardiac mortality.
• Anatomical groups shown to have better outcome:
– Significant stenosis of left main stem.
– Significant proximal stenosis of 3 major coronary
arteries.
– Significant stenosis of 2 major coronary arteries
including high grade stenosis of LAD artery.
– 3 vessel disease with impaired LV function.
• Reduces symptoms of angina & ischemia in pts
with CAD.
• OVERALL OPERATIVE MORTALITY OF 1 – 4%
61
62. PERCUTANEOUS CORONARY
INTERVENTION (PCI)
• Single or multivessel PCI can be performed
with high likelihood of success using BMS &
DES + adjuvent medical therapy.
– Risk of death = 0.3 -1 %
• Compared with medical therapy:
– PCI does not provide survival benefit in stable
angina.
– PCI is more effective at reducing events that
impair quality of life.
62
63. Revascularization Vs Medical therapy
• Initial pharmacological approach to symptom
control may be taken in patients NOT at high risk.
• Revascularization may be recommended for
patients with suitable anatomy who do not
respond adequately to medical therapy OR for
patients who wish to remain physically active.
• Optimal secondary preventive therapy (e.g
Antiplatelets & Statins) should be continued in
patients after revascularization IRRESPECTIVE of
the need of anti-anginal therapy.
63
64. SELECTION OF PATIENTS FOR
REVASCULARIZATION
It should be based on:
• Risk of peri-procedural morbidity & mortality
• Likelihood of success ( technical suitability)
• Risk of restenosis or graft occlusion
• Completeness of revascularization
• Diabetic status
• Local hospital experience in Cardiac surgery & PCI
• Patient’s preference
64