Pulmonary embolism - Notes are made from textbook of Internal medicine to assist medical students and residents to grasp subject in totality. Resources: Harrison's 20thEd, ESC 2019 guidelines on PE
Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, usually originating from deep vein thrombosis. Symptoms range from sudden shortness of breath to chest pain. Diagnosis involves tests like CT scans, V/Q scans, echocardiograms and blood tests. Treatment consists of oxygen, anticoagulant drugs, and sometimes fibrinolytics for massive clots. Long term prevention focuses on continued anticoagulation and devices like IVC filters for recurrent embolisms despite treatment.
This document discusses pneumothorax, which is an abnormal collection of air in the pleural space. A pneumothorax can occur when the negative pressure that normally exists in the pleural space is lost, allowing the lung to collapse. Symptoms include chest pain and dyspnea. Different types of pneumothorax are discussed, as well as causes, diagnostic tools, and treatment approaches which may include observation, needle aspiration, chest tube placement, or surgery depending on the size and severity in each case. Recurrent pneumothorax may warrant surgical pleurectomy or chemical pleurodesis to prevent future occurrences.
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
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.
This document discusses hypertrophic cardiomyopathy (HCM), including its definition, causes, variants, pathophysiology, clinical presentation, diagnostic workup, and management. Key points include:
- HCM is defined by left and/or right ventricular hypertrophy, usually involving the septum with a thickness over 15mm. It is commonly caused by genetic mutations affecting cardiac proteins.
- Presentation can range from being asymptomatic to symptoms of heart failure, angina, or syncope. Exams may reveal murmurs and EKGs often show abnormal patterns. Echocardiograms and cardiac catheterization are used for diagnosis and assessment.
- Management involves medications like beta-blockers to reduce
Pulmonary embolism occurs when a blood clot blocks an artery in the lungs, usually originating from deep vein thrombosis. Symptoms range from sudden shortness of breath to chest pain. Diagnosis involves tests like CT scans, V/Q scans, echocardiograms and blood tests. Treatment consists of oxygen, anticoagulant drugs, and sometimes fibrinolytics for massive clots. Long term prevention focuses on continued anticoagulation and devices like IVC filters for recurrent embolisms despite treatment.
This document discusses pneumothorax, which is an abnormal collection of air in the pleural space. A pneumothorax can occur when the negative pressure that normally exists in the pleural space is lost, allowing the lung to collapse. Symptoms include chest pain and dyspnea. Different types of pneumothorax are discussed, as well as causes, diagnostic tools, and treatment approaches which may include observation, needle aspiration, chest tube placement, or surgery depending on the size and severity in each case. Recurrent pneumothorax may warrant surgical pleurectomy or chemical pleurodesis to prevent future occurrences.
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
This document discusses pulmonary thromboembolism (PE), which refers to blood clots (thrombi) traveling from deep veins to the lungs. Most clots originate in the lower extremities. Risk factors include inherited conditions, surgery, trauma, immobilization, cancer and pregnancy. PE can cause hypoxemia and pulmonary hypertension. Diagnosis involves clinical assessment, D-dimer testing, chest imaging like CT pulmonary angiogram (gold standard), ventilation-perfusion scanning and echocardiogram. Treatment aims to relieve symptoms and prevent complications like right heart strain.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
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.
This document discusses hypertrophic cardiomyopathy (HCM), including its definition, causes, variants, pathophysiology, clinical presentation, diagnostic workup, and management. Key points include:
- HCM is defined by left and/or right ventricular hypertrophy, usually involving the septum with a thickness over 15mm. It is commonly caused by genetic mutations affecting cardiac proteins.
- Presentation can range from being asymptomatic to symptoms of heart failure, angina, or syncope. Exams may reveal murmurs and EKGs often show abnormal patterns. Echocardiograms and cardiac catheterization are used for diagnosis and assessment.
- Management involves medications like beta-blockers to reduce
A pulmonary embolism occurs when a blood clot or other material occludes the pulmonary artery or its branches. This most commonly results from a deep vein thrombosis in the lower leg that embolizes to the lung. When a PE occurs, it causes ventilation-perfusion mismatching in the lungs. Diagnosis is difficult due to nonspecific symptoms but evaluation involves a Wells criteria assessment, D-dimer testing, echocardiogram, and CT pulmonary angiogram. Treatment consists of anticoagulation with low molecular weight heparin or novel oral anticoagulants. Fibrinolytic therapy may be used in massive PEs. Prevention focuses on prophylaxis in high risk hospitalized patients.
Pulmonary embolism is a potentially deadly condition caused by blood clots in the lungs. It is difficult to diagnose due to non-specific symptoms. Imaging tests like CT scans and ventilation-perfusion scans are used to identify clots in the lungs. Prompt diagnosis and treatment are important to reduce the high mortality rate associated with untreated pulmonary embolism.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
Left ventricular hypertrophy is an increase in the mass of the left ventricle that can be caused by hypertension, hypertrophic cardiomyopathy, aortic stenosis, or athletic training. It is defined on an ECG as increased voltages in certain leads. Risk factors include age, gender, high blood pressure, obesity, and genetic factors. If left untreated, LVH can lead to heart failure, arrhythmias, heart attack, or sudden cardiac death. Right ventricular hypertrophy is the enlargement of the right ventricle and can be caused by pulmonary hypertension, congenital heart defects, or lung diseases. Both LVH and RVH are diagnosed using ECG criteria and can cause chest pain, palpitations
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
This document discusses pulmonary embolism (PE). Some key points:
- PE causes 50,000-200,000 deaths annually in the US, with an incidence of 500,000 cases.
- Risk factors include stasis, injury to veins, and coagulation issues.
- PE occurs when clots, usually from deep leg veins, travel to the lungs and block vessels. This can strain the right ventricle.
- Symptoms include sudden dyspnea, tachycardia, chest pain, hemoptysis. No single symptom confirms PE.
- Diagnosis involves CXR, blood tests, V/Q scan, CT, and angiogram. ECG may show right
1) Pulmonary embolism (PE) was first described in the 18th century and risk factors include both modifiable factors like obesity and smoking as well as non-modifiable factors like age, family history, and cancer.
2) PE is classified by size from massive to small, with massive PE affecting half the pulmonary arteries and causing shock while small PE causes few symptoms.
3) Diagnosis involves assessment of clinical probability with tools like Wells Criteria followed by tests like CT, ventilation-perfusion scan, or ultrasound depending on the patient's situation.
4) Treatment involves anticoagulation with drugs like heparin or novel oral anticoagulants, with duration depending on prov
This document discusses the case of a 62-year-old man presenting with acute dyspnea. On examination, the patient is pale, sweaty, coughing pink sputum, and in respiratory distress. His pulse is 140 BPM, respiratory rate is 30, and oxygen saturation is 85%. The document outlines potential causes of acute dyspnea including pulmonary edema and provides guidance on evaluating, diagnosing, and initially managing such a patient. Key factors to consider include the patient's medical history, signs of heart failure on examination, and portable chest x-ray findings suggestive of pulmonary edema. The goals of treatment are to place the patient in a sitting position, provide high-flow oxygen, administer diuretics and opioids,
1) Respiratory failure is a condition where the lungs cannot properly oxygenate the blood and remove carbon dioxide, classified as Type I (hypoxemic) or Type II (hypercapnic).
2) It can result from problems affecting gas exchange in the lungs, respiratory control centers in the brain, or the chest wall muscles.
3) Common causes of Type I respiratory failure include pneumonia, ARDS, and severe asthma, while Type II is often due to conditions that decrease breathing, such as COPD.
This document provides an overview of pulmonary hypertension (PH), including its definition, classification, mechanisms, pathology, clinical presentation, diagnosis, treatment, and prognosis. PH is defined as a mean pulmonary arterial pressure greater than 25 mm Hg at rest. It is classified into 5 groups based on etiology. Common mechanisms include vasoconstriction, vascular obstruction, increased blood flow, and loss of pulmonary vascular bed. Pathology often involves remodeling of small pulmonary arteries and arterioles. Presentation is usually nonspecific symptoms like dyspnea. Diagnosis involves echocardiogram, cardiac catheterization, and ruling out other causes. Treatment includes vasodilators, anticoagulation, diuretics, oxygen supplementation and sometimes
Venous thromboembolism refers to blood clots forming in the veins, which can break off and travel to the lungs (pulmonary embolism). Deep vein thrombosis is a blood clot that forms deep in the leg veins and can progress upwards. Superficial vein thrombosis involves shallow leg veins near the skin surface. Risk factors include surgery, trauma, cancer, genetic conditions. Symptoms include leg pain/swelling. Diagnosis involves D-dimer testing and ultrasound imaging of leg veins. Treatment is blood thinners to prevent clot growth and embolism.
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Pulmonary hypertension (2014) dr.tinku josephDr.Tinku Joseph
This document provides information on pulmonary hypertension (PH), including its definition, classification, pathogenesis, diagnosis, and treatment. It begins with defining PH as a mean pulmonary arterial pressure greater than 25 mmHg at rest based on right heart catheterization. PH is classified into 5 groups. The pathogenesis and pathology of each group is described. Diagnostic workup includes labs, imaging like CXR, echocardiogram and right heart catheterization. Treatment involves general measures, diuretics, anticoagulants, oxygen, and PAH-specific therapies like endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and calcium channel blockers in some cases. Prognostic factors and goals of treatment are also discussed.
Pulmonary edema is a condition where fluid builds up in the lungs, making breathing difficult. It is usually caused by issues with the heart like a heart attack or valve problems that back fluid up into the lungs. Symptoms include extreme shortness of breath, anxiety, coughing, and pale skin. Diagnosis involves listening to the chest, chest x-rays, and echocardiograms. Treatment requires immediate hospitalization for oxygen, diuretics to remove fluid, heart medications, and treating the underlying heart condition. Pulmonary edema can be life-threatening but is often curable with prompt treatment and managing the long-term heart disorder.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
Pulmonary embolism occurs when a blood clot forms in the veins (usually in the legs) and travels to the lungs, blocking blood flow. Risk factors include prolonged immobility, recent surgery or trauma, older age, and certain medical conditions. Symptoms can range from mild chest pain to life-threatening issues like respiratory failure. Diagnosis involves tests like chest x-rays, CT scans, and blood tests. Treatment may include blood thinners, clot-busting drugs, or occasionally surgery to remove large clots. Nursing care focuses on preventing further clots, reducing pain and anxiety, and monitoring for complications of treatment.
Acute pulmonary embolism is a form of venous thromboembolism that occurs when a blood clot breaks off and lodges in the pulmonary arteries of the lungs. The clinical presentation of PE can be variable and non-specific, making diagnosis challenging. It is important to efficiently evaluate patients suspected of having a PE to diagnose and treat it quickly in order to reduce morbidity and mortality. Treatment involves hemodynamic and respiratory support, initial anticoagulation with drugs like heparin, and potentially reperfusion therapies for more severe cases including thrombolysis or embolectomy.
The document discusses the circulation in the lungs and pulmonary hypertension. It describes the double blood supply and drainage of the lungs from the pulmonary and bronchial arteries and veins. It discusses the types of pulmonary arteries and how they change in size and composition from the main pulmonary artery towards the capillaries. It also summarizes pulmonary hypertension, its genetics, pathobiology involving endothelial dysfunction, smooth muscle proliferation, remodeling, inflammation and thrombosis.
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
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
This document discusses hemostasis, thrombosis, pulmonary embolism, risk factors, diagnosis, and treatment of venous thromboembolism. It defines key terms like thrombus, embolus, and saddle pulmonary embolism. Diagnostic tests covered include D-dimer, ventilation-perfusion scan, and CTA. Treatment involves anticoagulants like heparin, LMWH, factor Xa inhibitors, and thrombolytic therapy. Long-term management uses warfarin or novel oral anticoagulants. Prophylaxis is also discussed.
CYANOTIC CONGENITAL HEART DISEASES WITH DECREASED BLOOD FLOWbadrik19
This document discusses cyanosis and its causes in neonates. It begins by defining cyanosis as a bluish tinge of the skin and mucous membranes, detectable when hemoglobin is reduced by more than 5g% or oxygen saturation is below 85%. It then lists various pulmonary, cardiac, central nervous system, metabolic, hematologic, and infectious conditions that can cause cyanosis in newborns. The majority of the document focuses on describing tetralogy of Fallot, including its characteristic features, pathophysiology, clinical presentation, diagnosis, and management. It provides details on the anatomy, causes, hypoxic spells, and treatment approaches for tetralogy of Fallot.
A pulmonary embolism occurs when a blood clot or other material occludes the pulmonary artery or its branches. This most commonly results from a deep vein thrombosis in the lower leg that embolizes to the lung. When a PE occurs, it causes ventilation-perfusion mismatching in the lungs. Diagnosis is difficult due to nonspecific symptoms but evaluation involves a Wells criteria assessment, D-dimer testing, echocardiogram, and CT pulmonary angiogram. Treatment consists of anticoagulation with low molecular weight heparin or novel oral anticoagulants. Fibrinolytic therapy may be used in massive PEs. Prevention focuses on prophylaxis in high risk hospitalized patients.
Pulmonary embolism is a potentially deadly condition caused by blood clots in the lungs. It is difficult to diagnose due to non-specific symptoms. Imaging tests like CT scans and ventilation-perfusion scans are used to identify clots in the lungs. Prompt diagnosis and treatment are important to reduce the high mortality rate associated with untreated pulmonary embolism.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
Left ventricular hypertrophy is an increase in the mass of the left ventricle that can be caused by hypertension, hypertrophic cardiomyopathy, aortic stenosis, or athletic training. It is defined on an ECG as increased voltages in certain leads. Risk factors include age, gender, high blood pressure, obesity, and genetic factors. If left untreated, LVH can lead to heart failure, arrhythmias, heart attack, or sudden cardiac death. Right ventricular hypertrophy is the enlargement of the right ventricle and can be caused by pulmonary hypertension, congenital heart defects, or lung diseases. Both LVH and RVH are diagnosed using ECG criteria and can cause chest pain, palpitations
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
This document discusses pulmonary embolism (PE). Some key points:
- PE causes 50,000-200,000 deaths annually in the US, with an incidence of 500,000 cases.
- Risk factors include stasis, injury to veins, and coagulation issues.
- PE occurs when clots, usually from deep leg veins, travel to the lungs and block vessels. This can strain the right ventricle.
- Symptoms include sudden dyspnea, tachycardia, chest pain, hemoptysis. No single symptom confirms PE.
- Diagnosis involves CXR, blood tests, V/Q scan, CT, and angiogram. ECG may show right
1) Pulmonary embolism (PE) was first described in the 18th century and risk factors include both modifiable factors like obesity and smoking as well as non-modifiable factors like age, family history, and cancer.
2) PE is classified by size from massive to small, with massive PE affecting half the pulmonary arteries and causing shock while small PE causes few symptoms.
3) Diagnosis involves assessment of clinical probability with tools like Wells Criteria followed by tests like CT, ventilation-perfusion scan, or ultrasound depending on the patient's situation.
4) Treatment involves anticoagulation with drugs like heparin or novel oral anticoagulants, with duration depending on prov
This document discusses the case of a 62-year-old man presenting with acute dyspnea. On examination, the patient is pale, sweaty, coughing pink sputum, and in respiratory distress. His pulse is 140 BPM, respiratory rate is 30, and oxygen saturation is 85%. The document outlines potential causes of acute dyspnea including pulmonary edema and provides guidance on evaluating, diagnosing, and initially managing such a patient. Key factors to consider include the patient's medical history, signs of heart failure on examination, and portable chest x-ray findings suggestive of pulmonary edema. The goals of treatment are to place the patient in a sitting position, provide high-flow oxygen, administer diuretics and opioids,
1) Respiratory failure is a condition where the lungs cannot properly oxygenate the blood and remove carbon dioxide, classified as Type I (hypoxemic) or Type II (hypercapnic).
2) It can result from problems affecting gas exchange in the lungs, respiratory control centers in the brain, or the chest wall muscles.
3) Common causes of Type I respiratory failure include pneumonia, ARDS, and severe asthma, while Type II is often due to conditions that decrease breathing, such as COPD.
This document provides an overview of pulmonary hypertension (PH), including its definition, classification, mechanisms, pathology, clinical presentation, diagnosis, treatment, and prognosis. PH is defined as a mean pulmonary arterial pressure greater than 25 mm Hg at rest. It is classified into 5 groups based on etiology. Common mechanisms include vasoconstriction, vascular obstruction, increased blood flow, and loss of pulmonary vascular bed. Pathology often involves remodeling of small pulmonary arteries and arterioles. Presentation is usually nonspecific symptoms like dyspnea. Diagnosis involves echocardiogram, cardiac catheterization, and ruling out other causes. Treatment includes vasodilators, anticoagulation, diuretics, oxygen supplementation and sometimes
Venous thromboembolism refers to blood clots forming in the veins, which can break off and travel to the lungs (pulmonary embolism). Deep vein thrombosis is a blood clot that forms deep in the leg veins and can progress upwards. Superficial vein thrombosis involves shallow leg veins near the skin surface. Risk factors include surgery, trauma, cancer, genetic conditions. Symptoms include leg pain/swelling. Diagnosis involves D-dimer testing and ultrasound imaging of leg veins. Treatment is blood thinners to prevent clot growth and embolism.
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Pulmonary hypertension (2014) dr.tinku josephDr.Tinku Joseph
This document provides information on pulmonary hypertension (PH), including its definition, classification, pathogenesis, diagnosis, and treatment. It begins with defining PH as a mean pulmonary arterial pressure greater than 25 mmHg at rest based on right heart catheterization. PH is classified into 5 groups. The pathogenesis and pathology of each group is described. Diagnostic workup includes labs, imaging like CXR, echocardiogram and right heart catheterization. Treatment involves general measures, diuretics, anticoagulants, oxygen, and PAH-specific therapies like endothelin receptor antagonists, phosphodiesterase inhibitors, prostanoids, and calcium channel blockers in some cases. Prognostic factors and goals of treatment are also discussed.
Pulmonary edema is a condition where fluid builds up in the lungs, making breathing difficult. It is usually caused by issues with the heart like a heart attack or valve problems that back fluid up into the lungs. Symptoms include extreme shortness of breath, anxiety, coughing, and pale skin. Diagnosis involves listening to the chest, chest x-rays, and echocardiograms. Treatment requires immediate hospitalization for oxygen, diuretics to remove fluid, heart medications, and treating the underlying heart condition. Pulmonary edema can be life-threatening but is often curable with prompt treatment and managing the long-term heart disorder.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
Pulmonary embolism occurs when a blood clot forms in the veins (usually in the legs) and travels to the lungs, blocking blood flow. Risk factors include prolonged immobility, recent surgery or trauma, older age, and certain medical conditions. Symptoms can range from mild chest pain to life-threatening issues like respiratory failure. Diagnosis involves tests like chest x-rays, CT scans, and blood tests. Treatment may include blood thinners, clot-busting drugs, or occasionally surgery to remove large clots. Nursing care focuses on preventing further clots, reducing pain and anxiety, and monitoring for complications of treatment.
Acute pulmonary embolism is a form of venous thromboembolism that occurs when a blood clot breaks off and lodges in the pulmonary arteries of the lungs. The clinical presentation of PE can be variable and non-specific, making diagnosis challenging. It is important to efficiently evaluate patients suspected of having a PE to diagnose and treat it quickly in order to reduce morbidity and mortality. Treatment involves hemodynamic and respiratory support, initial anticoagulation with drugs like heparin, and potentially reperfusion therapies for more severe cases including thrombolysis or embolectomy.
The document discusses the circulation in the lungs and pulmonary hypertension. It describes the double blood supply and drainage of the lungs from the pulmonary and bronchial arteries and veins. It discusses the types of pulmonary arteries and how they change in size and composition from the main pulmonary artery towards the capillaries. It also summarizes pulmonary hypertension, its genetics, pathobiology involving endothelial dysfunction, smooth muscle proliferation, remodeling, inflammation and thrombosis.
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
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
This document discusses hemostasis, thrombosis, pulmonary embolism, risk factors, diagnosis, and treatment of venous thromboembolism. It defines key terms like thrombus, embolus, and saddle pulmonary embolism. Diagnostic tests covered include D-dimer, ventilation-perfusion scan, and CTA. Treatment involves anticoagulants like heparin, LMWH, factor Xa inhibitors, and thrombolytic therapy. Long-term management uses warfarin or novel oral anticoagulants. Prophylaxis is also discussed.
CYANOTIC CONGENITAL HEART DISEASES WITH DECREASED BLOOD FLOWbadrik19
This document discusses cyanosis and its causes in neonates. It begins by defining cyanosis as a bluish tinge of the skin and mucous membranes, detectable when hemoglobin is reduced by more than 5g% or oxygen saturation is below 85%. It then lists various pulmonary, cardiac, central nervous system, metabolic, hematologic, and infectious conditions that can cause cyanosis in newborns. The majority of the document focuses on describing tetralogy of Fallot, including its characteristic features, pathophysiology, clinical presentation, diagnosis, and management. It provides details on the anatomy, causes, hypoxic spells, and treatment approaches for tetralogy of Fallot.
- Acute pulmonary embolism (PE) is a common cardiovascular condition caused by obstruction of the pulmonary arteries by blood clots.
- Diagnosis can be difficult as symptoms are nonspecific, but includes dyspnea, chest pain, syncope. Imaging tests like CT pulmonary angiography or ventilation-perfusion scanning are used to diagnose PE.
- Treatment involves anticoagulation to prevent further clot growth. For high risk PE with hemodynamic instability, thrombolysis or embolectomy may be used to rapidly restore blood flow. Risk stratification guides duration of anticoagulation which is typically 3-6 months or longer for recurrent PE or persistent risk factors.
This document discusses pulmonary thromboembolism (PE), which occurs when a blood clot blocks the pulmonary artery or its branches in the lungs. PE is usually caused by deep vein thrombosis, where a clot breaks off and travels to the lungs. Symptoms include dyspnea, chest pain, and coughing. Risk factors include prolonged immobilization, recent surgery or trauma, oral contraceptive use, pregnancy, and inherited or acquired hypercoagulable states. Diagnosis involves chest x-ray, ventilation-perfusion scanning, and pulmonary angiography to detect clots in the pulmonary arteries.
Pulmonary embolism is caused by a blockage in the pulmonary artery from substances traveling through the bloodstream, most commonly from deep vein thrombosis. It is a common and potentially lethal condition. Diagnosis is challenging as symptoms are non-specific and it is often overlooked or missed. Imaging tests like CT pulmonary angiography, ventilation-perfusion scans, and pulmonary angiography are used to diagnose pulmonary embolism, while ultrasound of the legs can identify deep vein thrombosis, a major risk factor. Prompt diagnosis and treatment are important to prevent mortality from this potentially serious condition.
This document discusses pulmonary embolism (PE), including its definition, epidemiology, pathophysiology, risk factors, diagnosis, and treatment. PE refers to obstruction of the pulmonary artery or its branches by material originating elsewhere in the body. It affects around 5 million people annually worldwide and can be life-threatening. Diagnosis involves evaluating risk factors, symptoms, imaging tests like CT scans, and blood tests like D-dimer. Timely diagnosis and treatment are important to prevent right heart failure or death from PE.
Venous thromboembolism (VTE) includes deep vein thrombosis (DVT) and pulmonary embolism (PE), which can cause death or disability. PE is a common cause of preventable death in hospitals. Survivors may develop chronic thromboembolic pulmonary hypertension or post-thrombotic syndrome. DVT and PE are diagnosed using blood tests, imaging like ultrasound and CT scans, and treated with anticoagulation medications to prevent clots from growing or splitting off to travel to the lungs. Treatment duration depends on the clot location and underlying cause.
This document summarizes CT findings that are useful for diagnosing chronic pulmonary thromboembolism (CPTE). It describes risk factors, clinical manifestations, and CT features of CPTE including vascular signs like pulmonary artery obstruction and dilation, parenchymal signs like scarring and mosaic perfusion patterns, and signs of pulmonary hypertension. Differential diagnoses including idiopathic pulmonary hypertension and acute PE are also discussed. CT is important for identifying treatable CPTE in patients with unexplained pulmonary hypertension.
PowerPoint presentation about pulmonary embolism -- Teaching at Zagazig university cardiology department ,
Egypt in 2013 by Islam Ghanem , assistant lecturer of cardiology
This document discusses pulmonary embolism (PE), including its epidemiology, disease burden, risk factors, pathophysiology, signs and symptoms, diagnostic evaluation, and treatment approaches. It notes that PE has an annual incidence of 100-200 per 100,000 people. Diagnostic evaluations discussed include assessment of clinical probability, D-dimer testing, CT pulmonary angiography, lung scintigraphy, and echocardiography. Treatment of acute PE involves hemodynamic support, anticoagulation with unfractionated heparin, low molecular weight heparin or fondaparinux, and potentially thrombolysis for high-risk cases.
Atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), and tetralogy of Fallot (TOF) are four common types of congenital heart disease. ASD is a hole in the atrial septum that allows blood to flow from the left to the right atrium. VSD is a hole in the ventricular septum that allows blood to flow between the ventricles. PDA is a persistent opening between the aorta and pulmonary artery that normally closes after birth. TOF involves four abnormalities that reduce pulmonary blood flow.
Pulmonary embolism is a blockage in the pulmonary artery or its branches by material that travels from elsewhere in the body through the bloodstream. It is commonly caused by deep vein thrombosis. Pulmonary embolisms are classified based on size and location as massive, submassive, low-risk, central or peripheral. Diagnosis involves assessing clinical probability, D-dimer testing, imaging like CT pulmonary angiography, ventilation-perfusion scanning, pulmonary angiography, and echocardiography. Treatment of acute pulmonary embolism includes supportive care, anticoagulation, thrombolytic therapy for high-risk cases, and sometimes surgical or catheter-based interventions.
This document discusses pulmonary embolism (PE) and the use of CT angiography (CTA) for diagnosis. It provides information on the epidemiology and risk factors for PE. It describes the signs and symptoms of PE and clinical diagnostic criteria. The document outlines the technique for CTA for PE diagnosis including contrast injection parameters and common pitfalls. It details CT findings of acute, chronic and evolving PE and discusses prognostic factors seen on CTA such as right ventricular enlargement.
Deep vein thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous thromboembolism (VTE), represent a major global health problem. VTE has significant morbidity and mortality but is also potentially treatable. The incidence of VTE is increasing due to factors like population aging and higher rates of comorbidities. Risk factors for VTE include hypercoagulability, stasis, vascular injury, cancer, immobilization, and surgery. Diagnosis involves assessment of clinical probability with tools like the Wells criteria and D-dimer testing. Imaging options include ultrasound, CT, ventilation-perfusion scanning, and pulmonary angiography. Treatment involves anticoagulation with drugs like heparin or
Diagnosis and managment of pulmonary embolismDrYaqoobBahar
A pulmonary embolism is a sudden blockage in a lung artery, usually caused by a blood clot breaking off and traveling to the lungs. PE is a common cause of death in hospitalized patients. Risk factors include genetic mutations, cancer, obesity, smoking, and surgery. Symptoms may include dyspnea, chest pain, and cough. Diagnosis involves assessing risk factors, blood tests, imaging like CT scans, and echocardiograms. Treatment involves immediate anticoagulation with blood thinners, potentially thrombolytic therapy for severe cases, and inferior vena cava filters for high-risk patients. Anticoagulation may continue for several months depending on the underlying cause of clotting.
Pulmonary embolism is a blockage of the pulmonary artery or its branches by material that has traveled from elsewhere in the body through the bloodstream. It is most commonly caused by deep vein thrombosis in the legs. Symptoms include dyspnea, chest pain, and cough. Risk factors include prolonged bed rest, cancer, oral contraceptives, and recent surgery or trauma. Diagnosis involves evaluating clinical probability and testing such as D-dimer, CT pulmonary angiography, ventilation-perfusion scanning, and pulmonary angiography. Treatment focuses on anticoagulation to prevent further clots.
The document summarizes various congenital heart defects that can cause cyanosis in infants, including tetralogy of Fallot, transposition of the great arteries, truncus arteriosus, total anomalous pulmonary venous return, tricuspid atresia, pulmonary atresia, and Ebstein's anomaly. It describes the characteristic features, causes, evaluations, and treatments for each condition. For the scenario presented, the assistant would start prostaglandin E1 treatment and call cardiology to perform an echocardiogram to determine the specific heart defect.
Pulmonary embolism is a blockage in the pulmonary artery or its branches caused by material traveling through the bloodstream, commonly from deep vein thrombosis. It can be classified based on severity from massive to low-risk. Diagnosis involves assessing clinical probability, D-dimer testing, imaging like CT pulmonary angiography, ventilation-perfusion scanning, or pulmonary angiography. Factors like immobilization, cancer, or pregnancy can predispose to PE. Presentation may include chest pain, dyspnea, tachycardia, and signs of right heart strain. Treatment focuses on anticoagulation and managing complications.
Pulmonary and venous thromboembolism.pptxNidhiBhutada5
This document discusses venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). It covers the risk factors, pathophysiology, classification, clinical presentation, diagnostic modalities including imaging and labs, and treatment including anticoagulation options for VTE. The standard treatment is anticoagulant therapy to prevent further clot formation and extension. Parenteral anticoagulants such as heparin are initially used and then transitioned to oral anticoagulants such as warfarin or newer oral agents.
Pulmonary embolism occurs when one or more arteries in the lungs become blocked by blood clots, usually originating from deep veins in the legs. It can cause sudden shortness of breath, chest pain, and coughing up blood. While potentially life-threatening, prompt treatment with anti-clotting medications can greatly reduce the risk of death if pulmonary embolism is diagnosed. A variety of tests are used to diagnose pulmonary embolism including chest x-rays, CT scans, ventilation-perfusion scans, and angiograms.
1. Sepsis is a life-threatening organ dysfunction caused by a dysregulated immune response to infection. It can progress to septic shock, which involves circulatory and metabolic abnormalities increasing the risk of death.
2. Initial management of sepsis involves screening, resuscitation, infection control, hemodynamic support, and empiric antibiotics within 1-3 hours while obtaining cultures. Ongoing care focuses on organ support, source control, and monitoring for complications.
3. Long term goals include preventing disability, addressing psychosocial needs, and smooth transition to post-acute care and follow up. Prompt recognition and treatment can reduce mortality from this medical emergency.
1. The document discusses various cardiac arrhythmias including supraventricular tachycardias, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
2. It provides details on characteristics, causes, diagnosis, and treatment of these arrhythmias based on American and European cardiology guidelines.
3. The treatment discussed includes electrical cardioversion, antiarrhythmic medications, catheter ablation, and implantable cardioverter defibrillators.
This document provides an overview of atrial fibrillation (AF) and paroxysmal supraventricular tachycardia (PSVT). It defines these conditions and describes their typical ECG patterns, mechanisms, clinical presentations, diagnostic evaluations, and treatment approaches including medications, procedures like cardioversion and ablation. Key points include: AF can be paroxysmal, persistent or permanent, and is caused by mechanisms like reentry and ectopic automaticity; evaluation involves assessing thromboembolic risk with scores like CHA2DS2-VASc; treatment focuses on rate or rhythm control with medications or ablation, while preventing thromboembolism with anticoagulation; PSVT often presents with abrupt
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
download notes of the presentation and study with its print out
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
A 24-year-old woman presented with headache and left-sided weakness. Imaging showed cerebral venous thrombosis involving the superior sagittal sinus and draining veins. She was diagnosed with antiphospholipid syndrome based on recurrent pregnancy loss and positive lupus anticoagulant. She was treated with anticoagulation and anticonvulsants and showed gradual improvement over 10 days with residual mild weakness. Her long-term management plan includes lifelong anticoagulation and screening for recurrent thrombosis.
A 68-year-old male farmer presented with post-traumatic T3-T4 compression fracture and paraplegia in January 2022. He developed recurrent UTIs, hemorrhagic pleural effusion, and a retropharyngeal cyst requiring debulking. In early March, he developed cough, dyspnea, stridor and altered sensorium. He was diagnosed with right lower lobe pneumonia, sepsis and respiratory failure. Treatment included antibiotics, ventilation, and supportive care. He later developed bilateral vocal cord palsy and was discharged at family's request before further evaluation.
Chronic myeloid leukemia (CML) is a stem cell disorder caused by the Philadelphia chromosome, which results from the fusion of the BCR gene on chromosome 22 and the ABL gene on chromosome 9. This fusion produces the BCR-ABL protein which exhibits uncontrolled tyrosine kinase activity, driving excessive proliferation of CML cells. CML progresses through chronic, accelerated and blast crisis phases as additional genetic mutations accumulate. Tyrosine kinase inhibitors (TKIs) target the BCR-ABL protein and have significantly improved survival, with a 10-year survival of 85% with TKI therapy. Monitoring response through cytogenetics, FISH and molecular testing guides treatment decisions such as changing or adding other TKIs.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
surviving sepsis guidelines - Notes are made from surviving sepsis guidelines 2016 article to assist medical students and residents to grasp subject in a easy to read format in a step wise manner. Resources: surviving sepsis guidelines 2016 (free access article)
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THE SPECIAL SENCES- Unlocking the Wonders of the Special Senses: Sight, Sound...Nursing Mastery
Title: Unlocking the Wonders of the Special Senses: Sight, Sound, Smell, Taste, and Balance
Introduction:
Welcome to our captivating SlideShare presentation on the Special Senses, where we delve into the extraordinary capabilities that allow us to perceive and interact with the world around us. Join us on a sensory journey as we explore the intricate structures and functions of sight, sound, smell, taste, and balance.
The special senses are our primary means of experiencing and interpreting the environment, each sense providing unique and vital information that shapes our perceptions and responses. These senses are facilitated by highly specialized organs and complex neural pathways, enabling us to see a vibrant sunset, hear a symphony, savor a delicious meal, detect a fragrant flower, and maintain our equilibrium.
In this presentation, we will:
Visual System (Sight): Dive into the anatomy and physiology of the eye, exploring how light is converted into electrical signals and processed by the brain to create the images we see. Understand common vision disorders and the mechanisms behind corrective measures like glasses and contact lenses.
Auditory System (Hearing): Examine the structures of the ear and the process of sound wave transduction, from the outer ear to the cochlea and auditory nerve. Learn about hearing loss, auditory processing, and the advances in hearing aid technology.
Olfactory System (Smell): Discover the olfactory receptors and pathways that enable the detection of thousands of different odors. Explore the connection between smell and memory and the impact of olfactory disorders on quality of life.
Gustatory System (Taste): Uncover the taste buds and the five basic tastes – sweet, salty, sour, bitter, and umami. Delve into the interplay between taste and smell and the factors influencing our food preferences and eating habits.
Vestibular System (Balance): Investigate the inner ear structures responsible for balance and spatial orientation. Understand how the vestibular system helps maintain posture and coordination, and explore common vestibular disorders and their effects.
Through engaging visuals, interactive diagrams, and insightful explanations, we aim to illuminate the complexities of the special senses and their profound impact on our daily lives. Whether you're a student, educator, or simply curious about how we perceive the world, this presentation will provide valuable insights into the remarkable capabilities of the human sensory system.
Join us as we unlock the wonders of the special senses and gain a deeper appreciation for the intricate mechanisms that allow us to experience the richness of our environment.
The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
English Drug and Alcohol Commissioners June 2024.pptxMatSouthwell1
Presentation made by Mat Southwell to the Harm Reduction Working Group of the English Drug and Alcohol Commissioners. Discuss stimulants, OAMT, NSP coverage and community-led approach to DCRs. Focussing on active drug user perspectives and interests
Basics of Electrocardiogram
CONTENTS
●Conduction System of the Heart
●What is ECG or EKG?
●ECG Leads
●Normal waves of ECG.
●Dimensions of ECG.
● Abnormalities of ECG
CONDUCTION SYSTEM OF THE HEART
ECG:
●ECG is a graphic record of the electrical activity of the heart.
●Electrical activity precedes the mechanical activity of the heart.
●Electrical activity has two phases:
Depolarization- contraction of muscle
Repolarization- relaxation of muscle
ECG Leads:
●6 Chest leads
●6 Limb leads
1. Bipolar Limb Leads:
Lead 1- Between right arm(-ve) and left arm(+ve)
Lead 2- Between right arm(-ve) and left leg(+ve)
Lead 3- Between left arm(-ve)
and left leg(+ve)
2. Augmented unipolar Limb Leads:
AvR- Right arm
AvL- Left arm
AvF- Left leg
3.Chest Leads:
V1 : Over 4th intercostal
space near right sternal margin
V2: Over 4th intercostal space near left sternal margin
V3:In between V2 and V4
V4:Over left 5th intercostal space on the mid
clavicular line
V5:Over left 5th intercostal space on the anterior
axillary line
V6:Over left 5th intercostal space on the mid
axillary line.
Normal ECG:
Waves of ECG:
P Wave
•P Wave is a positive wave and the first wave in ECG.
•It is also called as atrial complex.
Cause: Atrial depolarisation
Duration: 0.1 sec
QRS Complex:
•QRS’ complex is also called the initial ventricular complex.
•‘Q’ wave is a small negative wave. It is continued as the tall ‘R’ wave, which is a positive wave.
‘R’ wave is followed by a small negative wave, the ‘S’ wave.
Cause:Ventricular depolarization and atrial repolarization
Duration: 0.08- 0.10 sec
T Wave:
•‘T’ wave is the final ventricular complex and is a positive wave.
Cause:Ventricular repolarization Duration: 0.2 sec
Intervals and Segments of ECG:
P-R Interval:
•‘P-R’ interval is the interval
between the onset of ‘P’wave and onset of ‘Q’ wave.
•‘P-R’ interval cause atrial depolarization and conduction of impulses through AV node.
Duration:0.18 (0.12 to 0.2) sec
Q-T Interval:
•‘Q-T’ interval is the interval between the onset of ‘Q’
wave and the end of ‘T’ wave.
•‘Q-T’ interval indicates the ventricular depolarization
and ventricular repolarization,
i.e. it signifies the
electrical activity in ventricles.
Duration:0.4-0.42sec
S-T Segment:
•‘S-T’ segment is the time interval between the end of ‘S’ wave and the onset of ‘T’ wave.
Duration: 0.08 sec
R-R Interval:
•‘R-R’ interval is the time interval between two consecutive ‘R’ waves.
•It signifies the duration of one cardiac cycle.
Duration: 0.8 sec
Dimension of ECG:
How to find heart rhytm of the heart?
Regular rhytm:
Irregular rhytm:
More than or less than 4
How to find heart rate using ECG?
If heart Rhytm is Regular :
Heart rate =
300/No.of large b/w 2 QRS complex
= 300/4
=75 beats/mins
How to find heart rate using ECG?
If heart Rhytm is irregular:
Heart rate = 10×No.of QRS complex in 6 sec 5large box = 1sec
5×6=30
10×7 = 70 Beats/min
Abnormalities of ECG:
Cardiac Arrythmias:
1.Tachycardia
Heart Rate more than 100 beats/min
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The Importance of Black Women Understanding the Chemicals in Their Personal C...bkling
Certain chemicals, such as phthalates and parabens, can disrupt the body's hormones and have significant effects on health. According to data, hormone-related health issues such as uterine fibroids, infertility, early puberty and more aggressive forms of breast and endometrial cancers disproportionately affect Black women. Our guest speaker, Jasmine A. McDonald, PhD, an Assistant Professor in the Department of Epidemiology at Columbia University in New York City, discusses the scientific reasons why Black women should pay attention to specific chemicals in their personal care products, like hair care, and ways to minimize their exposure.
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Test bank clinical nursing skills a concept based approach 4e pearson education
1. PULMONARY EMBOLISM
Notes: by Col Bharat Malhotra Senior Advisor Medicine (JAN 2021)
DEFINE
Venous thromboembolism (VTE) = Deep Venous Thrombosis (DVT)
& Pulmonary Embolism (PE)
Pulmonary Embolism: Occlusion or partial occlusion of the pulmonary artery or its branches
Common cause:
An embolized clot from deep vein thrombosis (DVT) involving the lower leg.
Less common causes:
a) Tissue fragments b) Fat embolism c) Air embolism d) Amniotic fluid e) Tumor embolism
EPIDEMIOLOGY
PE is the most common preventable cause of death among hospitalized patients
ETIOLOGY
Stasis
Immobilization, Paralytic stroke
Venous obstruction, Venous
insufficiency, CHF
Endothelial injury
Hip/Knee Surgery,
Fracture lower limbs,
Major Trauma
Central venous lines
Chemotherapy
Infections
Prothrombotic States
factor V Leiden
Prothrombin gene mutation
Antithrombin, protein C, and
protein S deficiency
APLA syndrome
Hyperhomocysteinemia
Cancer, Nephrotic syndrome,
IBD, CHF, COPD,
Autoimmune diseases, Blood
transfusions
OCP, Pregnancy, postpartum
Predisposing factors:
Increase age, Obesity,
cigarette smoking, long-haul
air travel
Activated platelets → proinflammatory mediators → platelet aggregation → platelet-dependent
thrombin generation
Venous thrombi form and flourish in an environment of stasis, low oxygen tension, and
upregulation of proinflammatory genes.
2. PATHOPHYSIOLOGY
Embolize
Deep venous thrombi detach from
their site of formation they
embolize to the vena cava, right
atrium, and right ventricle, and
lodge in the pulmonary arterial
circulation, thereby causing acute
PE.
Many patients with PE have no
evidence of DVT because the clot
has already embolized to the
lungs.
Pulmonary Hypertension, Right Ventricular (RV)
Dysfunction, and RV Microinfarction
Pulmonary artery obstruction and neurohumoral mediators
cause a rise in pulmonary artery pressure and in pulmonary
vascular resistance.
RV wall tension rises → RV dilation and dysfunction ensue,
with release of the cardiac biomarker leading to:
• Compresses the right coronary artery → RV ischemia
• Underfilling of the LV → fall in LV cardiac output and BP
PHYSIOLOGICAL CHANGES
• Arterial hypoxemia
• Increased alveolar-arterial O2 tension gradient, which represents the inefficiency of O2 transfer
across the lungs.
o Increased pulmonary vascular resistance
o Impaired gas exchange
o Alveolar hyperventilation, Increased airway resistance
o Decreased pulmonary compliance due to lung edema, lung hemorrhage, or loss of surfactant
.
3. CLASSIFICATION OF PULMONARY EMBOLISM AND DEEP VENOUS THROMBOSIS
Pulmonary Embolism
Massive PE
5-10%
Extensive thrombosis
affecting at least half of
the pulmonary vasculature
Syncope & collapse, Severe Dyspnea, Central
Chest pain, Cyanosis and hypoxemia
Hypotension
Cardiogenic shock
Die from multisystem organ failure
Sub-massive PE
20-25%
Characterized by RV
dysfunction despite
normal systemic arterial
pressure
Worsening dyspnoea, Anginal chest pain,
Syncope, Haemoptysis
Features of RV dysfunction
Low-risk PE
65-75%
No RV dysfunction
No hypotension
Pulmonary infarction usually indicates a small PE.
This condition is exquisitely painful because the
thrombus lodges peripherally, near the innervation
of pleural nerves.
Deep Venous Thrombosis: Lower extremity DVT usually begins in the calf and propagates
proximally to the popliteal vein, femoral vein, and iliac veins.
DIAGNOSIS
Clinical Evaluation
“the Great Masquerader” Diagnosis is difficult because symptoms and signs are
nonspecific
In some cases, PE may be asymptomatic or discovered incidentally
during diagnostic workup for another disease in predisposed individuals.
The most common symptom is unexplained breathlessness. When occult PE occurs concomitantly
with overt congestive heart failure or pneumonia, clinical improvement often fails to ensue despite
standard medical treatment of the concomitant illness. This scenario presents a clinical clue to the
possible coexistence of PE.
Asymptomatic or discovered incidentally
Worsening dyspnea
Cough, Sputum
Hemoptysis
Syncope
Chest pain – Anginal, Pleuritic
Fever, Diaphoresis
Cardiogenic shock → multiorgan dysfunction
Evidence of DVT
Normal Exam with sinus tachycardia
Sinus Tachycardia
Tachypnoea
Loud S2, RV dysfunction
Crackles, Pleural rub
Hypotension, Cardiogenic shock in massive PE
Evidence of DVT
4. WELLS SCORE – CLINICAL DECISION RULES
DVT
Interpretation of score: High probability if 3 points or more, moderate probability if 1 or 2 points, and low probability if 0 points or less
PULMONARY EMBOLISM
Interpretation of total score:
0-1 point: low probability; 2-6 points: moderate probability; 7 or more points: high probability
DIFFERENTIAL DIAGNOSIS
Not all leg pain is due to DVT, and not all dyspnea is due to PE
Deep Venous Thrombosis (DVT)
Ruptured Baker’s cyst, Muscle strain/injury, Cellulitis, Acute post thrombotic syndrome/venous insufficiency
Pulmonary Embolism (PE)
Costochondritis, Musculoskeletal discomfort, Rib fracture
Pleurisy, Pneumothorax, Pneumonia, Severe asthma, chronic obstructive pulmonary disease
Pericarditis, Congestive heart failure, Acute coronary syndrome, Aortic dissection
Anxiety
5. ALGORITHM OF PE DIAGNOSIS - INTEGRATED DIAGNOSTIC APPROACH
DVT PULMONARY EMBOLISM
Wells score for DVT, ECG, CXR Wells score for Pulmonary Embolism, ECG, CXR
The Great Masquerader – suspect and assess for PE
D Dimer D Dimer Normal → No PE
High → Imaging
USS Doppler venous Leg → CT Angio LL ECHO Sub-massive/Massive PE (RV dysfunction)
CECT Chest → CT Venous angiography for PE
Lung Scan (Second line)
Do USS Doppler venous Leg for DVT
ProBNP: for RV dysfunction
Troponin T: for RV microinfarctions
EVALUATION
NONIMAGING DIAGNOSTIC MODALITIES
plasma D-dimer (ELISA) (> 500 ng/ml or 0.5 mcg/ml)
Rises in the presence of DVT or PE because of the breakdown of
fibrin by plasmin due to endogenous although often clinically
ineffective thrombolysis.
A normal D-dimer is a useful “rule out” test. However, the D-
dimer assay is not specific.
Levels increase in patients due to systemic illness.
Serum troponin – due to RV microinfarction
NT-pro-BNP – myocardial stretch leads to release of Pro-brain
natriuretic peptide.
6. ELECTROCARDIOGRAM
Frequent - sinus tachycardia
RV strain – RBBB, T-wave
inversion in leads V1 to V4
S1Q3T3 sign: S wave in lead
I, Q wave in lead III, and an
inverted T wave in lead III
CHEST ROENTGENOGRAPHY
A normal or nearly normal chest x-ray often
occurs in PE.
Pulmonary opacities
Peripheral wedged-shaped density usually
located at the pleural base (Hampton’s hump)
Horizontal linear opacities
Pleural effusion
Focal oligemia (Westermark’s sign)
Enlarged right descending pulmonary artery
(Palla’s sign).
Elevated hemidiapharm
USS LOWER LIMB VENOUS DOPPLER
Relies on loss of vein compressibility
Loss of normal respiratory variation
thrombus is directly visualized
7. ECHOCARDIOGRAPHY
Echocardiography is not a reliable diagnostic imaging tool for acute PE because most patients with PE
have normal echocardiograms. However, echocardiography is a very useful diagnostic tool for detecting
conditions that may mimic PE
Indirect sign of PE: McConnell’s sign: hypokinesis of the RV free wall with normal or hyperkinetic
motion of the RV apex
CHEST CT WITH VENOUS ANGIOGRAPHY
In patients without PE, the lung parenchymal images
may establish alternative diagnoses not apparent on
chest x-ray that explain the presenting symptoms and
signs
CT of the chest with intravenous contrast is the principal
imaging test for the diagnosis of PE. Sixth-order
branches can be visualized.
When imaging is extended distally below the chest to
the knee, pelvic and proximal leg DVT also can be
diagnosed by CT scanning.
Criteria
Arterial occlusion with failure to enhance the entire lumen due to a large filling defect; the
artery may be enlarged compared with adjacent patent vessels
A partial filling defect surrounded by contrast material, producing the “polo mint” sign on
images acquired perpendicular to the long axis of a vessel and the “railway track” sign on
longitudinal images of the vessel
The diagnosis of PE is very unlikely in patients with normal and nearly normal scans and, in contrast, is about 90% certain in patients with
high-probability scans
8. LUNG SCANNING (second line)
Lung scanning has become a second-line diagnostic test for PE, used mostly for patients who cannot
tolerate intravenous contrast.
INVASIVE PULMONARY ANGIOGRAPHY (not done)
Chest CT with contrast has virtually replaced invasive pulmonary angiography
TREATMENT
Deep Venous Thrombosis
PRIMARY THERAPY
Primary therapy Clot dissolution- catheter-directed thrombolysis
Reserved for patients with extensive femoral, iliofemoral, or upper
extremity DVT leading to less long-term damage to venous valves, with
consequent lower rates of post thrombotic syndrome
9. SECONDARY PREVENTION
Anticoagulation Effective anticoagulation is the foundation for successful treatment of
DVT and PE
Inferior vena caval
(IVC) filter
FDA approved a new retrievable IVC filter that is inserted at the
bedside with ultrasound visualization of the femoral or internal jugular
vein (Angel®
Filter) but without the need for any fluoroscopic or other
radiological imaging.
Indications: Contraindication to anticoagulation, Complication of
anticoagulation necessitating cessation, Propagation/progression of
DVT during therapeutic anticoagulation, Iliocaval or large free-floating
proximal DVT, limited cardiopulmonary reserve, Recurrent PE
Below-knee graduated
compression stockings
Swelling of the legs when acute DVT is diagnosed, may be prescribed,
usually with pressure of 30–40 mmHg, to lessen patient discomfort.
They should be replaced every 3 months because they lose their
elasticity.
Pulmonary Embolism
RISK STRATIFICATION
High risk
of an adverse clinical outcome
Hemodynamic instability, RV dysfunction on echocardiography,
RV enlargement on chest CT, or elevation of the troponin level
due to RV microinfarction
Good clinical outcome RV function remains normal
ANTICOAGULATION
Effective anticoagulation is the foundation for successful treatment of DVT and PE.
There are three major strategies:
1 S/C anticoagulation with (UFH), or (LMWH), or fondaparinux “bridged” 5d → to warfarin
2 S/C anticoagulation with (UFH), or (LMWH), or fondaparinux “bridged” 5d → novel oral
anticoagulant such as dabigatran (a direct thrombin inhibitor) or apixaban (an anti-Xa agent)
3 Oral anticoagulation monotherapy with rivaroxaban (3week) or apixaban (1 week) (both
are anti-Xa agents) loading dose, followed by a maintenance dose without parenteral
anticoagulation.
For patients with VTE in the setting of suspected or proven heparin-induced thrombocytopenia,
one can choose between two parenteral direct thrombin inhibitors: argatroban and bivalirudin
10. Mechanism of Action
PARENTRAL ANTICOAGULANTS
Unfractionated Heparin
Action UFH anticoagulates by binding to and accelerating the activity of
antithrombin, thus preventing additional thrombus formation
Aim UFH is dosed to achieve a target activated partial thromboplastin time
(aPTT) of 60–80 s.
Dose an initial bolus of 80 U/kg, followed by an initial infusion rate of 18 U/kg
per h in patients with normal liver function
Benefit short half-life, which is especially useful in patients in whom hour-to-
hour control of the intensity of anticoagulation
Heparin also has pleiotropic effects that may decrease systemic and local
inflammation.
Low-Molecular-Weight Heparins
These fragments of UFH exhibit less binding to plasma proteins and endothelial cells and
consequently have greater bioavailability, a more predictable dose response, and a longer half-life
than does UFH.
No monitoring or dose adjustment is needed unless the patient is markedly obese or has chronic
kidney disease
11. Fondaparinux
Fondaparinux, an anti-Xa Penta saccharide, is administered as a weight-based once-daily
subcutaneous injection in a prefilled syringe.
No laboratory monitoring is required. Fondaparinux is synthesized in a laboratory and, unlike
LMWH or UFH, is not derived from animal products. It does not cause heparin-induced
thrombocytopenia. The dose must be adjusted downward for patients with renal dysfunction.
ORAL ANTICOAGULANTS
Warfarin Anticoagulation
(Unfractionated heparin, LMWH, and fondaparinux are the usual immediately effective “bridging
agents” used when initiating warfarin) Requires 5–10 days of administration to achieve effectiveness
Warfarin
Action This vitamin K antagonist prevents carboxylation activation of coagulation
factors II, VII, IX, and X
Bridge therapy The full effect of warfarin requires at least 5 days, even if the prothrombin time,
used for monitoring, becomes elevated more rapidly
If warfarin is initiated as monotherapy during an acute thrombotic illness, a
paradoxical exacerbation of hypercoagulability increases the likelihood of
thrombosis. Overlapping UFH, LMWH, fondaparinux, or parenteral direct
thrombin inhibitors with warfarin for at least 5 days will nullify the early
procoagulant effect of warfarin
Dose
Monitor
Usual start dose is 5 mg
Titrate to international normalized ratio (INR), target 2.0–3.0
Continue parenteral anticoagulation for a minimum of 5 days and until two
sequential INR values, at least 1 day apart, achieve the target INR range.
Problems
The warfarin dose is usually titrated empirically to achieve the target INR. Proper
dosing is difficult because hundreds of drug-drug and drug-food interactions
affect warfarin metabolism.
Warfarin can cause major hemorrhage, including intracranial hemorrhage, even
when the INR remains within the desired therapeutic range. Warfarin can cause
“off target” side effects such as alopecia or arterial vascular calcification. Some
patients complain that warfarin makes them feel cold or fatigued
CYP2C9 variant alleles impair the hydroxylation of S-warfarin, thereby lowering
the dose requirement
...
12. Novel Oral Anticoagulants
Novel oral anticoagulants (NOACs) are administered in a fixed dose, establish effective
anticoagulation within hours of ingestion, require no laboratory coagulation monitoring, and have
few of the drug-drug or drug-food interactions
Rivaroxaban and apixaban, direct factor Xa inhibitors, are approved as monotherapy for acute
and extended treatment of DVT and PE, without a parenteral “bridging” anticoagulant.
Dabigatran, a direct thrombin inhibitor, and edoxaban, a factor Xa inhibitor, are approved for
treatment of VTE after an initial 5-day course of parenteral anticoagulation.
Betrixaban, a direct factor Xa inhibitor, was approved by the FDA in 2017 for VTE prophylaxis in
acutely ill medical patients during hospitalization and continuing for a total duration of 5 to 6
weeks.
Non-Warfarin Anticoagulation
Unfractionated heparin, bolus and continuous infusion, to achieve activated partial thromboplastin
time (aPTT) 2–3 times the upper limit of the laboratory normal, or
Enoxaparin 1 mg/kg twice daily with normal renal function, or
Dalteparin 200 U/kg once daily or 100 U/kg twice daily, with normal renal function, or
Tinzaparin 175 U/kg once daily with normal renal function, or
Fondaparinux weight-based once daily; adjust for impaired renal function
Direct thrombin inhibitors: argatroban or bivalirudin (with suspected or proven heparin-induced
thrombocytopenia)
Rivaroxaban 15 mg twice daily for 3 weeks, followed by 20 mg once daily with the dinner meal
thereafter
Apixaban 10 mg twice daily for 1 week, followed by 5 mg twice daily thereafter
Dabigatran 5 days of unfractionated heparin, low-molecular-weight heparin (LMWH), or
fondaparinux followed by dabigatran 150 mg twice daily
Edoxaban 5 days of unfractionated heparin, LMWH, or fondaparinux followed by edoxaban 60 mg
once daily with normal renal function, weight >60 kg, in the absence of potent P-glycoprotein
inhibitors
Complications of Anticoagulants The most serious adverse effect of anticoagulation is hemorrhage.
For life-threatening or intracranial hemorrhage following can be administered
Heparin or LMWH → protamine sulphate Dabigatran → Idarucizumab (NA)
Fondaparinux or factor Xa inhibitors → No reversal Universal anti-Xa antidote → Andexanet (NA)
13. Major bleeding from warfarin is best managed with prothrombin complex concentrate.
With less serious bleeding, fresh-frozen plasma or intravenous vitamin K can be used.
Duration of Anticoagulation
INTERMEDIATE RISK (3-8%) HIGH RISK FACTOR (> 8 %)
Major surgery
Lower limb plaster cast > 3 days
Short-term immobilization for >3 days
Hormonal contraception, pregnancy
Acute infectious disease leading to confinement > 3 days
Inflammatory bowel disease
Active autoimmune disease
Active Cancer
Antiphospholipid syndrome
Previous episodes of VTE
Myeloproliferative disorders
Thrombophilia
For DVT isolated to an upper extremity or calf
that has been provoked by surgery, trauma,
estrogen, or an indwelling central venous
catheter or pacemaker, 3 months of
anticoagulation usually suffice
For an initial episode of provoked proximal leg
DVT or PE, 3–6 months of anticoagulation used
to be the classic teaching
For patients with cancer and VTE, prescribe
LMWH as monotherapy without warfarin and
continue anticoagulation indefinitely unless the
patient is rendered cancer-free.
Patients with antiphospholipid antibody
syndrome may warrant indefinite-duration
anticoagulation, even if the initial VTE was
provoked by trauma or surgery.
Among patients with idiopathic, unprovoked
VTE, the recurrence rate is high after cessation
of anticoagulation. VTE that occurs during long-
haul air travel is considered unprovoked.
Unprovoked VTE may be caused by an
exacerbation of an underlying inflammatory state
and can be conceptualized as a chronic illness,
with latent periods between flares of recurrent
episodes.
American College of Chest Physicians (ACCP) guidelines recommend considering anticoagulation
for an indefinite duration with a target INR between 2 and 3 for patients with idiopathic VTE and
a low bleeding risk.
An alternative approach after the first 6 months of anticoagulation is to reduce the intensity of
anticoagulation and to lower the target INR range to between 1.5 and 2.
Another approach for patients at lower risk of recurrence, especially if there is an important reason
to avoid long-term anticoagulation, is to consider low-dose aspirin after completing the initial
period of standard anticoagulation.
14. INFERIOR VENA CAVA FILTERS (Reserve therapy)
The two principal indications for insertion
of an IVC filter are
(1) active bleeding that precludes
anticoagulation and
(2) recurrent venous thrombosis despite
intensive anticoagulation.
Prevention of recurrent PE in patients with
right heart failure who are not candidates for
fibrinolysis and prophylaxis of extremely
high-risk patients are “softer” indications for
filter placement.
Retrievable filters can now be placed for patients with an anticipated temporary bleeding disorder or
for patients at temporary high risk of PE, such as individuals undergoing bariatric surgery who have a
prior history of perioperative PE. The filters can be retrieved for months after insertion, unless thrombus
forms and is trapped within the filter. The retrievable filter becomes permanent if it remains in place or
if, for technical reasons such as rapid endothelialization, it cannot be removed.
The filter itself may fail by permitting the passage of small- to medium-size clots. Large thrombi may
embolize to the pulmonary arteries via collateral veins that develop. Paradoxically, by providing a nidus
for clot formation, filters increase the DVT rate, even though they usually prevent PE. Therefore, a
common complication is recurrent DVT or caval thrombosis with marked leg swelling.
15. MANAGEMENT OF MASSIVE PE
For patients with massive PE and hypotension, replete volume with 500 mL of normal saline.
Additional fluid should be infused with extreme caution because excessive fluid administration
exacerbates RV wall stress, causes more profound RV ischemia, and worsens LV compliance and
filling by causing further interventricular septal shift toward the LV.
Dopamine and dobutamine are first-line inotropic agents for treatment of PE-related shock. Maintain
a low threshold for initiating these pressors. Often, a “trial-and-error” approach works best; other
agents that may be effective include norepinephrine, vasopressin.
FIBRINOLYSIS
The only Food and Drug Administration–approved indication for PE fibrinolysis is massive PE.
For patients with submassive PE, who have preserved systolic blood pressure but moderate or
severe RV dysfunction, use of fibrinolysis remains controversial
Successful fibrinolytic therapy and may result in a lower rate of death and recurrent PE by
.
Rapidly reverses
right heart
failure and lower
rate of death
(1) dissolving much of the anatomically obstructing pulmonary arterial thrombus,
(2) preventing the continued release of serotonin and other neurohumoral factors
that exacerbate pulmonary hypertension, and
(3) lysing much of the source of the thrombus in the pelvic or deep leg veins,
thereby decreasing the likelihood of recurrent PE
Dose 100 mg of recombinant tissue plasminogen activator (tPA) prescribed as a
continuous peripheral intravenous infusion over 2 h
A popular off-label dosing regimen is 50 mg of TPA administered over 2 h. This
lower dose is widely perceived to be associated with fewer bleeding
complications
Contraindication Intracranial disease, recent surgery, and trauma. The overall major bleeding rate
is about 10%, including a 2–3% risk of intracranial hemorrhage
PHARMACOMECHANICAL CATHETER-DIRECTED THERAPY
Many patients have relative contraindications to full-dose thrombolysis. Pharmaco-mechanical
catheter-directed therapy usually combines physical fragmentation or pulverization of thrombus with
catheter-directed low-dose thrombolysis.
16. EMOTIONAL SUPPORT
PREVENTION OF VTE
Prevention of DVT and PE is of paramount importance because VTE is difficult to detect and poses a
profound medical and economic burden.
• High Risk orthopedic surgery
• Major Orthopedic Surgery
• Cancer Surgery
• Medically ill patients during hospitalization
Low-dose UFH or LMWH is the most common form of in-hospital prophylaxis.
S/C ENOXAPARIN 40 MG OD
Extended-duration prophylaxis with the novel anti-Xa agent, BETRIXABAN, appears to be both
effective and safe in medically ill patients during hospitalization, after hospital discharge, and is
undergoing FDA review.
NOTES: BY COL BHARAT MALHOTRA SENIOR ADVISOR MEDICINE (JAN 2021)
REFERENCES:
DAVIDSON’S PRINCIPLES AND PRACTICE OF MEDICINE 23RD
(2018) CHAPTER 17
HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 20TH
(2018) CHAPTER 273
2019 ESC GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF ACUTE
PULMONARY EMBOLISM.