Acute coronary syndrome
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This document discusses acute coronary syndrome (ACS), including unstable angina and myocardial infarction (MI). It defines the conditions and describes the pathophysiology. For diagnosis of MI, there must be a rise in cardiac biomarkers along with symptoms. Investigations include ECG, biomarkers like troponin, and echocardiography. Management of NSTEMI involves bed rest, oxygen, anti-ischemic and anti-thrombotic drugs. For STEMI, reperfusion therapy like primary PCI or fibrinolytic therapy is used within 2 hours of diagnosis. Complications can include arrhythmias, further ischemia, and embolism.
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Acute Coronary Syndrome
This document provides an overview of acute coronary syndrome (ACS). It begins with a review of coronary artery anatomy and variations. It then discusses the presentations of ACS, including ischemic chest pain and equivalents. The main types of ACS - unstable angina, NSTEMI, and STEMI - are defined based on symptoms, electrocardiogram findings, and cardiac biomarker levels. Diagnosis and management strategies are outlined, including reperfusion therapies and drug treatments. Follow-up care after ACS and indications for procedures like cardiac catheterization and ICD placement are also summarized.
coronary microvascular dysfunction
This document discusses coronary microvascular dysfunction (CMVD), which can cause angina despite normal coronary arteries. It defines CMVD and classifies it into 4 types based on underlying causes. The pathophysiology involves endothelial dysfunction, smooth muscle cell abnormalities, and remodeling. Patients present with stable or unstable angina and show evidence of ischemia on stress tests. Assessment includes measuring coronary flow reserve. Guidelines recommend aspirin, statins, beta-blockers as first-line treatment, and calcium channel blockers if needed. Additional therapies like nicorandil or spinal cord stimulation may help refractory cases. Overall, CMVD has heterogeneous causes, symptoms often recur despite management, and current practice focuses on reassurance rather than addressing underlying path
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1. The document discusses the classification, diagnosis, and treatment of acute coronary syndromes including unstable angina and myocardial infarction.
2. Key points include definitions of unstable angina, NSTEMI, and STEMI; causes of acute coronary syndromes including plaque rupture and vasospasm; the importance of history, ECG, biomarkers in diagnosis; and the use of antiplatelet agents, beta blockers, nitroglycerin, and anticoagulants in treatment.
3. Primary percutaneous coronary intervention is recommended over thrombolysis when certain criteria are met for STEMI patients.
Acute Coronary Syndrome, Myocardial Infarction.
The document discusses acute coronary syndrome (ACS), which includes unstable angina, ST elevation myocardial infarction (STEMI), and non-ST elevation myocardial infarction (NSTEMI). ACS is characterized by new or worsening chest pain or discomfort due to reduced blood flow in the coronary arteries. The main causes are atherosclerotic plaque rupture and thrombosis formation, which can completely or partially block blood flow. Investigation and management involves ECG, cardiac biomarkers, risk stratification scores, antiplatelet and anticoagulant therapy, and often coronary angiography.
Medical Management of Acute Coronary Syndromes
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Constrictive pericarditis
The document discusses constrictive pericarditis, providing details on:
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2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
Stemi by dr.mehelina
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.
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Acute Coronary Syndrome
This document provides an overview of acute coronary syndrome (ACS). It begins with a review of coronary artery anatomy and variations. It then discusses the presentations of ACS, including ischemic chest pain and equivalents. The main types of ACS - unstable angina, NSTEMI, and STEMI - are defined based on symptoms, electrocardiogram findings, and cardiac biomarker levels. Diagnosis and management strategies are outlined, including reperfusion therapies and drug treatments. Follow-up care after ACS and indications for procedures like cardiac catheterization and ICD placement are also summarized.
coronary microvascular dysfunction
This document discusses coronary microvascular dysfunction (CMVD), which can cause angina despite normal coronary arteries. It defines CMVD and classifies it into 4 types based on underlying causes. The pathophysiology involves endothelial dysfunction, smooth muscle cell abnormalities, and remodeling. Patients present with stable or unstable angina and show evidence of ischemia on stress tests. Assessment includes measuring coronary flow reserve. Guidelines recommend aspirin, statins, beta-blockers as first-line treatment, and calcium channel blockers if needed. Additional therapies like nicorandil or spinal cord stimulation may help refractory cases. Overall, CMVD has heterogeneous causes, symptoms often recur despite management, and current practice focuses on reassurance rather than addressing underlying path
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1. The document discusses the classification, diagnosis, and treatment of acute coronary syndromes including unstable angina and myocardial infarction.
2. Key points include definitions of unstable angina, NSTEMI, and STEMI; causes of acute coronary syndromes including plaque rupture and vasospasm; the importance of history, ECG, biomarkers in diagnosis; and the use of antiplatelet agents, beta blockers, nitroglycerin, and anticoagulants in treatment.
3. Primary percutaneous coronary intervention is recommended over thrombolysis when certain criteria are met for STEMI patients.
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The document discusses acute coronary syndrome (ACS), which includes unstable angina, ST elevation myocardial infarction (STEMI), and non-ST elevation myocardial infarction (NSTEMI). ACS is characterized by new or worsening chest pain or discomfort due to reduced blood flow in the coronary arteries. The main causes are atherosclerotic plaque rupture and thrombosis formation, which can completely or partially block blood flow. Investigation and management involves ECG, cardiac biomarkers, risk stratification scores, antiplatelet and anticoagulant therapy, and often coronary angiography.
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The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
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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.
Acute coronary syndrome
This document provides an overview of acute coronary syndrome (ACS). It defines ACS and describes the epidemiology in Malaysia. The pathophysiology, classification, clinical presentation and investigations are discussed for unstable angina/NSTEMI and STEMI. Management is outlined for both conditions, including medications, fibrinolytic therapy, percutaneous coronary intervention and complications. A clinical case of STEMI is then presented demonstrating diagnosis and management. The document concludes with references to Malaysian clinical practice guidelines for ACS.
Supra ventricular tachyarrhythmia
1. Rate control has equivalent efficacy to rhythm control for managing atrial fibrillation and has less drug-related side effects.
2. Drugs like digoxin, beta blockers, and calcium channel blockers can be used for rate control, while antiarrhythmics like amiodarone, dofetilide and sotalol are used for rhythm control.
3. Electrical cardioversion can be used to restore sinus rhythm but has a risk of recurrence, so anticoagulation is recommended afterwards to prevent stroke from clots that may form during the arrhythmia.
Acute Coronary Syndrome
The document discusses acute coronary syndrome (ACS), including the clinical presentation, risk factors, diagnostic testing such as electrocardiograms and cardiac enzymes, and treatment approaches for ACS depending on whether it presents with ST-elevation myocardial infarction (STEMI) or non-ST-elevation ACS such as unstable angina or non-STEMI. For STEMI patients, reperfusion therapy through either fibrinolysis or primary percutaneous coronary intervention is recommended to open the blocked vessel within specific time goals in order to reduce mortality.
Ischemic Heart Disease
1. Ischaemic heart disease is caused by an imbalance between myocardial oxygen supply and demand, usually due to atherosclerosis limiting blood flow in the coronary arteries.
2. The main types of ischaemic heart disease are stable angina, unstable angina, myocardial infarction (STEMI and NSTEMI), and sudden cardiac death. Clinical presentation and ECG/biomarker findings are used to distinguish these conditions.
3. Treatment involves lifestyle modifications and medications like nitrates, beta-blockers, and calcium channel blockers to reduce oxygen demand and increase supply. Revascularization procedures like PCI or CABG may also be used in certain patients.
Noncompaction cardiomyopathy
This document discusses left ventricular noncompaction cardiomyopathy (LVNC), a rare genetic heart condition where the heart muscle does not compact properly during fetal development. It begins by defining LVNC and describing its increasing recognition due to advances in diagnostic imaging. The document then discusses the embryological development of the heart and how a disruption in the normal compaction process can lead to LVNC. It outlines the characteristic features of LVNC seen on imaging studies and potential genetic associations. The document concludes by discussing the challenges in diagnosing and managing LVNC.
Ventricular arrhythmias
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
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1. The document summarizes a clinical trial that evaluated the safety and efficacy of intravenous omecamtiv mecarbil (OM) in patients hospitalized for acute heart failure. 2. The trial found no significant difference between OM and placebo in the primary outcome of dyspnea response. 3. Exploratory analyses identified modest relationships between higher OM doses/concentrations and increased dyspnea response and reductions in heart rate and systolic blood pressure.
Updates in management of Acute coronary syndrome
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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.
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The document discusses carotid artery disease and treatment options such as carotid angioplasty and stenting. It notes that stroke is a major cause of death and disability in the US. Carotid artery stenosis over 75% poses a high risk of stroke without treatment. Newer techniques like carotid stenting aim to achieve low stroke/death rates of less than 6% for symptomatic patients and 3% for asymptomatic patients. Success requires choosing the right tools, techniques, and protection devices tailored to each patient's anatomy and plaque characteristics. Ongoing studies evaluate newer neuroprotection systems to further reduce embolic risks of carotid stenting.
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This document discusses acute coronary syndrome (ACS) and non-ST-segment elevation acute coronary syndrome (NSTE-ACS). It defines unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI) and covers their clinical presentation, diagnostic criteria, laboratory investigation, and management. The key goals of diagnosis and treatment for NSTE-ACS patients are to recognize or exclude myocardial infarction, detect resting ischemia, and identify coronary artery obstruction. Treatment involves anti-ischemic, antithrombotic medications and consideration of coronary revascularization.
Acute coronary syndrome
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
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This document defines and discusses the management of supraventricular tachyarrhythmias. It begins by defining terms like tachyarrhythmia, tachycardia, and supraventricular tachyarrhythmia. It then discusses various types of supraventricular tachycardias that arise from different areas of the heart including the sinoatrial node, atrioventricular node, atria, and accessory pathways. The document provides guidance on clinical evaluation, ECG patterns, mechanisms, and treatment approaches for common supraventricular tachycardias such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial fibrillation, atrial flutter, and atrial
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This document discusses the classification, presentation, diagnosis, and treatment of acute coronary syndrome (ACS). ACS results from an imbalance between myocardial oxygen supply and demand due to a thrombotic coronary artery. It is classified as ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), or unstable angina (UA) based on electrocardiogram findings and cardiac biomarker levels. Initial treatment involves oxygen, nitroglycerin, aspirin, a P2Y12 inhibitor, and anticoagulation. STEMI patients should receive reperfusion via primary percutaneous coronary intervention or fibrinolysis if primary PCI cannot be performed in a timely manner.
Stent thrombosis
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This document summarizes a review on ivabradine, a drug that lowers heart rate by selectively inhibiting funny (If) channels in the sinoatrial node. It discusses the pathophysiology of elevated heart rate and heart rate control. Ivabradine is a selective If current inhibitor that reduces heart rate without affecting contractility or blood pressure. Clinical trials such as BEAUTIFUL showed ivabradine reduced rates of hospitalization for heart failure and myocardial infarction in patients with coronary artery disease and heart rates over 70 beats per minute. Ivabradine may provide benefit as an add-on to standard heart failure therapy in select patient groups.
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This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
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Heart is a muscular organ. Pathology of heart indicates any disorder of heart, a properly functioning heart is important to sustain a live because it pumps blood out to whole body providing oxygen and nutrients. Here I've discussed on two common cardiovascular pathological condition.
Ami
AMI is caused by formation of an occlusive thrombus at the site of a ruptured or eroded atherosclerotic plaque. It presents with chest pain and symptoms of ischemia. Investigations show changes on ECG, elevated cardiac enzymes, and echocardiogram may show regional wall motion abnormalities. Treatment involves oxygen, aspirin, anticoagulants, reperfusion with thrombolysis or PCI, and adjunctive therapies like beta blockers. Goals are to limit damage and prevent complications through risk factor modification and medical management.
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Acute coronary syndrome
This document provides an overview of acute coronary syndrome (ACS). It defines ACS and describes the epidemiology in Malaysia. The pathophysiology, classification, clinical presentation and investigations are discussed for unstable angina/NSTEMI and STEMI. Management is outlined for both conditions, including medications, fibrinolytic therapy, percutaneous coronary intervention and complications. A clinical case of STEMI is then presented demonstrating diagnosis and management. The document concludes with references to Malaysian clinical practice guidelines for ACS.
Supra ventricular tachyarrhythmia
1. Rate control has equivalent efficacy to rhythm control for managing atrial fibrillation and has less drug-related side effects.
2. Drugs like digoxin, beta blockers, and calcium channel blockers can be used for rate control, while antiarrhythmics like amiodarone, dofetilide and sotalol are used for rhythm control.
3. Electrical cardioversion can be used to restore sinus rhythm but has a risk of recurrence, so anticoagulation is recommended afterwards to prevent stroke from clots that may form during the arrhythmia.
Acute Coronary Syndrome
The document discusses acute coronary syndrome (ACS), including the clinical presentation, risk factors, diagnostic testing such as electrocardiograms and cardiac enzymes, and treatment approaches for ACS depending on whether it presents with ST-elevation myocardial infarction (STEMI) or non-ST-elevation ACS such as unstable angina or non-STEMI. For STEMI patients, reperfusion therapy through either fibrinolysis or primary percutaneous coronary intervention is recommended to open the blocked vessel within specific time goals in order to reduce mortality.
Ischemic Heart Disease
1. Ischaemic heart disease is caused by an imbalance between myocardial oxygen supply and demand, usually due to atherosclerosis limiting blood flow in the coronary arteries.
2. The main types of ischaemic heart disease are stable angina, unstable angina, myocardial infarction (STEMI and NSTEMI), and sudden cardiac death. Clinical presentation and ECG/biomarker findings are used to distinguish these conditions.
3. Treatment involves lifestyle modifications and medications like nitrates, beta-blockers, and calcium channel blockers to reduce oxygen demand and increase supply. Revascularization procedures like PCI or CABG may also be used in certain patients.
Noncompaction cardiomyopathy
This document discusses left ventricular noncompaction cardiomyopathy (LVNC), a rare genetic heart condition where the heart muscle does not compact properly during fetal development. It begins by defining LVNC and describing its increasing recognition due to advances in diagnostic imaging. The document then discusses the embryological development of the heart and how a disruption in the normal compaction process can lead to LVNC. It outlines the characteristic features of LVNC seen on imaging studies and potential genetic associations. The document concludes by discussing the challenges in diagnosing and managing LVNC.
Ventricular arrhythmias
Ventricular arrhythmias originate in the ventricles and include premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Ventricular tachycardia is defined as three or more consecutive ventricular beats at a rate over 100 beats per minute and can be caused by mechanisms like reentry, automaticity, and triggered activity. Polymorphic ventricular tachycardia includes conditions like torsades de pointes and Brugada syndrome. Acute management of sustained ventricular tachycardia includes termination attempts using antiarrhythmic drugs or cardioversion, while long term prevention focuses on drugs, ablation, or implantable cardioverter defibrillators depending on symptoms and left ventricular function.
Cardiac myosin activators
1. The document summarizes a clinical trial that evaluated the safety and efficacy of intravenous omecamtiv mecarbil (OM) in patients hospitalized for acute heart failure. 2. The trial found no significant difference between OM and placebo in the primary outcome of dyspnea response. 3. Exploratory analyses identified modest relationships between higher OM doses/concentrations and increased dyspnea response and reductions in heart rate and systolic blood pressure.
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Early and effective treatment of patients with acute coronary syndrome saves lives. Lot of progress has been made in last few years in understanding patho-physiology and management of these patients.
Chronic stable angina
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.
Carotid angioplasty
The document discusses carotid artery disease and treatment options such as carotid angioplasty and stenting. It notes that stroke is a major cause of death and disability in the US. Carotid artery stenosis over 75% poses a high risk of stroke without treatment. Newer techniques like carotid stenting aim to achieve low stroke/death rates of less than 6% for symptomatic patients and 3% for asymptomatic patients. Success requires choosing the right tools, techniques, and protection devices tailored to each patient's anatomy and plaque characteristics. Ongoing studies evaluate newer neuroprotection systems to further reduce embolic risks of carotid stenting.
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This document discusses acute coronary syndrome (ACS) and non-ST-segment elevation acute coronary syndrome (NSTE-ACS). It defines unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI) and covers their clinical presentation, diagnostic criteria, laboratory investigation, and management. The key goals of diagnosis and treatment for NSTE-ACS patients are to recognize or exclude myocardial infarction, detect resting ischemia, and identify coronary artery obstruction. Treatment involves anti-ischemic, antithrombotic medications and consideration of coronary revascularization.
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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
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Acute coronary syndrome (ACS) refers to conditions caused by reduced blood flow to the heart. It includes unstable angina, non-ST elevation myocardial infarction, and ST elevation myocardial infarction. Symptoms include chest pain, shortness of breath, nausea, and fatigue. Diagnosis involves ECG changes such as ST elevation or T wave changes and elevated cardiac biomarkers. Treatment focuses on reperfusion with medications or procedures like PCI, along with anticoagulants, antiplatelets, and lifestyle modifications. Complications can be mechanical, arrhythmic, embolic or inflammatory.
Managing supraventricular tachyarrythmias
This document defines and discusses the management of supraventricular tachyarrhythmias. It begins by defining terms like tachyarrhythmia, tachycardia, and supraventricular tachyarrhythmia. It then discusses various types of supraventricular tachycardias that arise from different areas of the heart including the sinoatrial node, atrioventricular node, atria, and accessory pathways. The document provides guidance on clinical evaluation, ECG patterns, mechanisms, and treatment approaches for common supraventricular tachycardias such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial fibrillation, atrial flutter, and atrial
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This document discusses the classification, presentation, diagnosis, and treatment of acute coronary syndrome (ACS). ACS results from an imbalance between myocardial oxygen supply and demand due to a thrombotic coronary artery. It is classified as ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), or unstable angina (UA) based on electrocardiogram findings and cardiac biomarker levels. Initial treatment involves oxygen, nitroglycerin, aspirin, a P2Y12 inhibitor, and anticoagulation. STEMI patients should receive reperfusion via primary percutaneous coronary intervention or fibrinolysis if primary PCI cannot be performed in a timely manner.
Stent thrombosis
Stent thrombosis is a rare but devastating complication occurring in less than 1% of patients within 30 days of stenting and 0.2-6% annually afterwards. It is associated with higher thrombus burden and less procedural success, resulting in higher rates of death, recurrent heart attack, and recurrent stent thrombosis. Risk factors include stent-related issues like early versus late thrombosis, procedure-related issues like incomplete apposition or expansion, vessel-related issues like long lesions or small vessel size, and patient-related issues like diabetes, impaired heart function, renal disease, or non-compliance with dual anti-platelet therapy. Management depends on thrombus burden grade, with direct angioplasty and stenting for small burdens and
Ivabradine review
This document summarizes a review on ivabradine, a drug that lowers heart rate by selectively inhibiting funny (If) channels in the sinoatrial node. It discusses the pathophysiology of elevated heart rate and heart rate control. Ivabradine is a selective If current inhibitor that reduces heart rate without affecting contractility or blood pressure. Clinical trials such as BEAUTIFUL showed ivabradine reduced rates of hospitalization for heart failure and myocardial infarction in patients with coronary artery disease and heart rates over 70 beats per minute. Ivabradine may provide benefit as an add-on to standard heart failure therapy in select patient groups.
No reflow and slow flow phenomenon during pci
This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
Acute Coronary Syndrome: MI
The document discusses myocardial infarction and acute coronary syndrome, providing definitions, causes, risk factors, types, pathophysiology, clinical manifestations, diagnostic measures, management, and nursing management of MI. It covers topics such as the epidemiology of MI/ACS, diagnostic criteria and biomarkers for diagnosis, treatments including percutaneous coronary intervention and fibrinolytic therapy, and complications of MI.
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This presentation is made to help students prepare for EDIC exam. this is board review for any exam for critical care examining acute MI, myocardial infarction, acute coronary syndrome.
Acute coronary syndrome (acs)
Acute coronary syndrome (ACS) refers to a spectrum of conditions caused by reduced blood flow in the coronary arteries. This includes unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). STEMI is diagnosed based on specific ECG findings and requires urgent reperfusion therapy. Initial management involves pain control, antithrombotic therapy, and reperfusion with either primary PCI or thrombolysis to limit infarct size.
Myocardial infarction
Acute myocardial infarction, or heart attack, occurs when blood supply to the heart is diminished leading to cell damage and death. It is usually caused by a blockage in the coronary arteries from atherosclerotic plaque or a blood clot. Diagnosis involves EKGs, blood tests of cardiac enzymes, and imaging tests. Treatment depends on the type and severity of MI but may include medications to break up clots, angioplasty and stenting, or coronary bypass surgery. Complications can affect the heart muscles and blood vessels if not properly treated.
3. Acute coronary syndrome.pptx
Acute coronary syndrome is caused by decreased blood flow to the heart and includes unstable angina and myocardial infarction. It is usually due to atherosclerosis and plaque rupture in the coronary arteries. Risk factors include smoking, obesity, diabetes, hypertension, and family history. Symptoms include chest pain and shortness of breath. Diagnosis involves ECG, cardiac enzymes, and coronary angiography. Treatment focuses on pain relief, improving blood flow, and restoring heart function through medications, percutaneous coronary intervention, or coronary artery bypass grafting. Nursing care emphasizes reducing pain and anxiety, improving cardiac output, preventing complications, and increasing activity tolerance.
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Acute coronary syndrome
Acute Coronary Syndrome (ACS) refers to a spectrum of clinical presentations caused by acute coronary athero-thrombosis that obstruct myocardial blood flow. This includes ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. NSTEMI is diagnosed with elevated cardiac biomarkers and detected ischemia on electrocardiograms or stress tests. Treatment involves antithrombotic and anti-ischemic drugs to reduce ischemia and prevent clots. In some cases, coronary angiography and revascularization by percutaneous coronary intervention may be recommended.
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Acute coronary syndrome
- 1. Acute coronary syndrome HS Sithu Bala Medical ward, NYGH
- 2. • Unstable angina • Myocardial infarction(MI)-STEMI – -NSTEMI Definition
- 4. Pathophysiology • Unstable angina - ischemia caused by dynamic obstruction of the coronary artery due to plaque rupture or erosion with superimposed thrombosis • Myocardial infarction - Myocardial necrosis caused by acute occlusion of the coronary artery due to plaque rupture or erosion with the superimposed thrombosis
- 7. Criteria for AMI • Detection of the rise and/or fall of cardiac biomarker values (preferably cardiac troponin) with at least one of the following: 1. Symptoms of ischemia 2. New or presumed new significant ST segment- T wave (ST-T) changes or new LBBB 3. Development of pathological Q waves 4. Identification of the intracoronary thrombus by angiography or post-mortem
- 16. Investigations 1. ECG •. STEMI - Tall T wave, ST elevation, or new LBBB occur within hours. T wave inversion, pathological Q wave follow over hours to days. •. NSTEMI/unstable angina - ST depression, T wave inversion, non-specific changes or normal. •. In 20% of MI, ECG may be normal initially.
- 22. 2. Biomarkers • Unstable angina - no detectable rise in cardiac biomarkers or enzymes • MI- cardiac troponin levels T & I are the most sensitive and specific markers. - Others cardiac enzymes( CK-MB, LDH,AST) are sensitive but less specific. • CK starts to rise at 4-6 hours, peak at about 12 hours and falls to normal within 48-72 hours • Troponin T and I are released within 4-6 hours and remains elevated for up to 2 weeks
- 25. 3. Blood tests • ESR - increased • CRP - increased • Leucocytosis is usual, reaching a peak on first day
- 26. 4. Chest X Ray • Heart size - often normal but there may be cardiomegaly due to preexisting myocardial damage • Pulmonary edema may be detected. 5. Echocardiography • To assess ventricular function • To detect complications such as mural (LV) thrombus, cardiac rupture, ventricular septal defect(VSD), mitral regurgitation(MR) and pericardial effusion
- 37. Management of NSTEMI Bed Rest for the first 12 hours with continuous ECG monitoring for ST deviation and cardiac arrhythmias Supplemental Oxygen – if arterial oxygen saturation less than 90% or respiratory distress Anti-Ischaemic treatment Ant-Thrombotic therapy
- 38. Anti-Ischaemic treatment • Nitrates • Beta-Blockers • Calcium channel blockers • Statins • Morphine
- 39. Anti Thrombotic Therapy • Anti Platelet Drugs - Aspirin - Clopidogrel • Low – molecular weight heparin - Enoxaparin
- 52. Management of STEMI • Reperfusion Therapy • Primary PCI • Fibrinolytic Therapy • CABG
- 55. Primary percutaneous coronary intervention(PCI) • Treatment of choice for STEMI • It is used in combination with glycoprotein IIb/IIIa receptor antagonists and coronary stent in implantation. • Associated with greater reduction in the risk of death, recurrent MI or stroke than thrombolytic therapy. • Primary PCI should be achieved within 2 hours of diagnosis.
- 60. Thrombolysis • Alteplase (human tissue plasminogen activator or tPA) 15mg bolus dose, followed by 0.75mg/kg but not exceeding 50mg over 30mins, and then 0.5mg/kg but not exceeding 35mg over 60mins. • Other thrombolytic agents; streptokinase, tenecteplase and reteplase(analogues of tPA) • The major hazard of thrombolytic therapy is intracerebral bleeding so the treatment should be withheld if there is a significant risk of serious bleeding.
- 63. low molecular weight heparin enoxaprin
- 72. Complications of ACS • Arrhythmia - VF, AF, Bradycardia • Ischemia • Acute circulatory failure • Pericarditis • Embolism
- 76. Thank you for your attention.