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.
- Pulmonary embolism (PE) is a blockage in the lung's arteries caused by blood clots that travel from deep veins, most often in the legs.
- Risk factors include recent surgery or trauma, cancer, older age, and genetic predispositions. Symptoms can range from mild to life-threatening depending on the size and location of the clots.
- Diagnosis involves blood tests, imaging like CT scans, ventilation-perfusion scans, or angiography. Treatment focuses on anticoagulation with blood thinners to prevent further clotting as well as supporting heart and lung function. For some patients, more aggressive options like thrombolysis or surgery may be considered.
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 summarizes pulmonary embolism (PE), including its causes, symptoms, diagnosis, and treatment. PE occurs when blood clots or other substances block arteries in the lungs, and is usually caused by deep vein thrombosis. Common symptoms include chest pain, difficulty breathing, and cough. Diagnosis involves tests like plasma D-dimer levels, ECGs, lung scans, and pulmonary angiography. Treatment focuses on anticoagulation therapy, and sometimes thrombolytic therapy or inferior vena cava filters for severe cases. Prognosis is generally good with proper diagnosis and treatment.
This document provides information on pulmonary embolism (PE). It defines PE as thrombosis originating in the venous system and embolizing to the pulmonary arterial circulation. PE contributes to 5-10% of hospital deaths. Risk factors include prolonged immobility, recent surgery or trauma, and inherited or acquired thrombophilias. Symptoms include dyspnea, chest pain, coughing up blood. Diagnostic tests include D-dimer, CT pulmonary angiogram, ventilation-perfusion scan, echocardiogram. Treatment involves anticoagulation with heparin or novel oral anticoagulants to prevent early death and recurrence, as well as thrombolysis for massive PE to restore pulmonary blood flow.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Pulmonary embolism (PE) occurs when a blood clot forms in the veins (usually in the legs) and travels to the lungs. It can be life-threatening and is a major cause of hospital deaths. Risk factors include prolonged bed rest, recent surgery, cancer, and certain genetic conditions. Symptoms may include sudden shortness of breath, chest pain, and coughing up blood. Diagnosis involves blood tests, imaging like CT scans, and assessment of clinical probability based on risk factors and symptoms. Treatment depends on severity but typically involves blood thinners, oxygen supplementation, and in some cases thrombolysis or surgery to break up clots. Preventing recurrence requires identifying risk factors and continuing anticoag
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.
- Pulmonary embolism (PE) is a blockage in the lung's arteries caused by blood clots that travel from deep veins, most often in the legs.
- Risk factors include recent surgery or trauma, cancer, older age, and genetic predispositions. Symptoms can range from mild to life-threatening depending on the size and location of the clots.
- Diagnosis involves blood tests, imaging like CT scans, ventilation-perfusion scans, or angiography. Treatment focuses on anticoagulation with blood thinners to prevent further clotting as well as supporting heart and lung function. For some patients, more aggressive options like thrombolysis or surgery may be considered.
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 summarizes pulmonary embolism (PE), including its causes, symptoms, diagnosis, and treatment. PE occurs when blood clots or other substances block arteries in the lungs, and is usually caused by deep vein thrombosis. Common symptoms include chest pain, difficulty breathing, and cough. Diagnosis involves tests like plasma D-dimer levels, ECGs, lung scans, and pulmonary angiography. Treatment focuses on anticoagulation therapy, and sometimes thrombolytic therapy or inferior vena cava filters for severe cases. Prognosis is generally good with proper diagnosis and treatment.
This document provides information on pulmonary embolism (PE). It defines PE as thrombosis originating in the venous system and embolizing to the pulmonary arterial circulation. PE contributes to 5-10% of hospital deaths. Risk factors include prolonged immobility, recent surgery or trauma, and inherited or acquired thrombophilias. Symptoms include dyspnea, chest pain, coughing up blood. Diagnostic tests include D-dimer, CT pulmonary angiogram, ventilation-perfusion scan, echocardiogram. Treatment involves anticoagulation with heparin or novel oral anticoagulants to prevent early death and recurrence, as well as thrombolysis for massive PE to restore pulmonary blood flow.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Pulmonary embolism (PE) occurs when a blood clot forms in the veins (usually in the legs) and travels to the lungs. It can be life-threatening and is a major cause of hospital deaths. Risk factors include prolonged bed rest, recent surgery, cancer, and certain genetic conditions. Symptoms may include sudden shortness of breath, chest pain, and coughing up blood. Diagnosis involves blood tests, imaging like CT scans, and assessment of clinical probability based on risk factors and symptoms. Treatment depends on severity but typically involves blood thinners, oxygen supplementation, and in some cases thrombolysis or surgery to break up clots. Preventing recurrence requires identifying risk factors and continuing anticoag
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.
Pulmonary hypertension (PH) is a disease involving remodeling of the pulmonary vasculature that increases pulmonary artery pressure and resistance. The main causes are left heart or lung disease, or it can occur as a complication of pulmonary embolism. Pulmonary arterial hypertension (PAH) is a distinct PH subtype characterized by vascular cell abnormalities and symptoms of dyspnea and chest pain. Untreated PH has a high mortality due to right heart failure. Diagnosis involves evaluating signs/symptoms, imaging, and right heart catheterization to measure pressures.
Computed Tomography Angiography in Chronic Pulmonary ThromboembolismApollo Hospitals
Chronic thromboembolic pulmonary hypertension is clearly more common than previously was thought, and misdiagnosis is common because patients often present with nonspecific symptoms related to pulmonary hypertension. Computed tomography (CT) is a useful alternative to conventional angiography not only for diagnosing chronic pulmonary thromboembolism but also for determining which cases are treatable with surgery and confirming technical success postoperatively. Early recognition of chronic pulmonary thromboembolism may help improve the outcome, since the condition is potentially curable with pulmonary thromboendarterectomy.
The document discusses pulmonary hypertension and the pulmonary circulation. It covers:
1) The anatomy of the pulmonary circulation including the pulmonary arterial and bronchial circulations.
2) The physiology of the low pressure pulmonary system and how blood flow is regulated.
3) The classifications, causes, signs and symptoms, and imaging manifestations of various types of pulmonary hypertension including pulmonary arterial hypertension, pulmonary hypertension due to lung/hypoxic diseases, chronic thromboembolic pulmonary hypertension, and pulmonary hypertension related to left heart disease.
4) The pathophysiology and histopathological changes seen in different forms of pulmonary hypertension.
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
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 pulmonary embolism (PE), including:
- PE occurs when blood clots (thrombi) block pulmonary arteries, ranging from acute massive PE to chronic PE.
- Deep vein thrombosis is the main cause of PE. Risk factors include recent surgery, oral contraceptive use, and malignancy.
- Symptoms can range from asymptomatic to sudden death. Common symptoms include dyspnea and chest pain.
- Diagnostic tests include CT pulmonary angiography, ventilation-perfusion scanning, echocardiography, and D-dimer levels. CT pulmonary angiography has high sensitivity and specificity for PE diagnosis.
This document discusses pulmonary embolism (PE), including its risk factors, pathophysiology, diagnosis, and management. It notes that PE is a leading cause of cardiovascular death and hospital mortality. Rudolf Virchow identified three main factors that contribute to venous thrombosis and PE: venous stasis, hypercoagulability of blood, and endothelial injury. The pathophysiology of PE involves increased pulmonary vascular resistance and right heart strain or failure. Diagnosis involves assessing clinical risk factors, biomarkers like troponin and BNP, imaging tests like CTPA, and echocardiography. PE is classified as massive, submassive, or low-risk depending on the presence of hypotension and right heart dysfunction. Management involves he
The document discusses pulmonary hypertension and the pulmonary circulation. It provides details on:
1) The anatomy and physiology of the pulmonary circulation and how it differs from the systemic circulation with lower pressures and resistance.
2) The pathophysiology of pulmonary hypertension including abnormalities in the endothelium, smooth muscle cells, and vascular remodeling in different types.
3) Clinical definitions of pulmonary hypertension, pulmonary arterial hypertension, and evaluation tools like echocardiogram, CT, right heart catheterization.
4) Treatment involves vasodilators, diuretics, calcium channel blockers and general measures depending on the severity and type of pulmonary hypertension.
The document provides information on pulmonary hypertension and pulmonary circulation. It discusses:
1) The pulmonary circulation begins at the right ventricle and ends at the left atrium, transporting the entire cardiac output to the lungs. It has low resistance and high compliance.
2) Pulmonary artery pressures are normally lower than systemic pressures, with mean pulmonary artery pressure around 10-12 mmHg.
3) Pulmonary vascular resistance is low due to a balance of vasodilator and vasoconstrictor prostaglandins. Resistance primarily occurs in small arteries and arterioles.
4) Pulmonary hypertension is defined as a mean pulmonary artery pressure over 25 mmHg at rest. Its causes
This document summarizes pulmonary embolism (PE), including its epidemiology, risk factors, pathophysiology, clinical features, diagnostic testing, and treatment. PE is the second most common cause of unexpected death, with risk factors including recent surgery, trauma, cancer, and inherited or acquired thrombophilias. Diagnosis involves assessing clinical probability then confirming with D-dimer, imaging like CT pulmonary angiogram, or lung scintigraphy. For acute PE, initial treatment is heparin or fondaparinux followed by long-term oral anticoagulation to prevent recurrence. New oral anticoagulants targeting factor Xa provide alternatives to warfarin.
Pulmonary embolism is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs or pelvis. It can be life-threatening and is responsible for around 100,000-200,000 deaths in the US each year. Risk factors include inherited or acquired hypercoagulability, venous stasis, or vessel wall injury. Diagnosis involves assessment of likelihood using scoring systems, blood tests like D-dimer, and imaging tests like CT pulmonary angiogram. Treatment depends on stability but generally involves anticoagulants like heparin or newer oral medications to prevent further clots. Prevention focuses on early mobilization, stockings, and blood thinners for
Tricuspid atresia is a congenital heart defect where the tricuspid valve is absent, preventing blood flow from the right atrium to the right ventricle. It occurs in approximately 1-2.4% of congenital heart defects. Survival depends on the presence of an atrial septal defect to allow blood to bypass the right ventricle. Treatment involves multiple staged surgeries culminating in the Fontan procedure to reroute systemic venous return directly to the pulmonary arteries. Complications can include arrhythmias, ventricular dysfunction, protein-losing enteropathy, and thromboembolic events.
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
This document discusses venous thrombosis and pulmonary embolism. It covers risk factors, pathophysiology, diagnostic evaluation, and treatment options. The main points are:
1. Venous thrombosis and pulmonary embolism are concerns in postoperative and ICU patients. Thrombi often form silently in leg veins and can break off and travel to the lungs.
2. Diagnostic evaluations include D-dimer, ventilation-perfusion scans, echocardiograms, angiograms. Imaging shows defects from clots blocking blood flow.
3. Treatment involves anticoagulation initially with heparin or low molecular weight heparin. Warfarin is used long-term. Thrombolytics or inferior v
- Pulmonary embolism affects approximately 500,000 individuals per year in the US, with around 50,000 deaths annually.
- Deep vein thrombosis accounts for over 95% of pulmonary emboli. Risk factors for DVT and thus PE include surgery, trauma, cancer, prolonged immobility, and genetic or acquired hypercoagulable states.
- Diagnosis is suggested by symptoms like dyspnea and chest pain but requires imaging tests like CT pulmonary angiogram, ventilation-perfusion scanning, or echocardiogram to confirm the presence of emboli. Treatment involves anticoagulation with heparin or warfarin.
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 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 embolism (PE), which occurs when a blood clot forms in the lungs. It defines PE, lists risk factors like immobilization and oral contraceptive use, and describes the two main types - thrombotic and non-thrombotic. Signs and symptoms include dyspnea, tachypnea, and hypoxemia. Diagnostic tests include D-dimer, CT scans, ventilation-perfusion scans, and angiograms. Treatment involves anticoagulants like heparin and warfarin to prevent further clotting. Nursing care focuses on monitoring for complications, managing pain and anxiety, and educating patients about anticoagulant therapy and risk reduction.
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.
Pulmonary hypertension (PH) is a disease involving remodeling of the pulmonary vasculature that increases pulmonary artery pressure and resistance. The main causes are left heart or lung disease, or it can occur as a complication of pulmonary embolism. Pulmonary arterial hypertension (PAH) is a distinct PH subtype characterized by vascular cell abnormalities and symptoms of dyspnea and chest pain. Untreated PH has a high mortality due to right heart failure. Diagnosis involves evaluating signs/symptoms, imaging, and right heart catheterization to measure pressures.
Computed Tomography Angiography in Chronic Pulmonary ThromboembolismApollo Hospitals
Chronic thromboembolic pulmonary hypertension is clearly more common than previously was thought, and misdiagnosis is common because patients often present with nonspecific symptoms related to pulmonary hypertension. Computed tomography (CT) is a useful alternative to conventional angiography not only for diagnosing chronic pulmonary thromboembolism but also for determining which cases are treatable with surgery and confirming technical success postoperatively. Early recognition of chronic pulmonary thromboembolism may help improve the outcome, since the condition is potentially curable with pulmonary thromboendarterectomy.
The document discusses pulmonary hypertension and the pulmonary circulation. It covers:
1) The anatomy of the pulmonary circulation including the pulmonary arterial and bronchial circulations.
2) The physiology of the low pressure pulmonary system and how blood flow is regulated.
3) The classifications, causes, signs and symptoms, and imaging manifestations of various types of pulmonary hypertension including pulmonary arterial hypertension, pulmonary hypertension due to lung/hypoxic diseases, chronic thromboembolic pulmonary hypertension, and pulmonary hypertension related to left heart disease.
4) The pathophysiology and histopathological changes seen in different forms of pulmonary hypertension.
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
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 pulmonary embolism (PE), including:
- PE occurs when blood clots (thrombi) block pulmonary arteries, ranging from acute massive PE to chronic PE.
- Deep vein thrombosis is the main cause of PE. Risk factors include recent surgery, oral contraceptive use, and malignancy.
- Symptoms can range from asymptomatic to sudden death. Common symptoms include dyspnea and chest pain.
- Diagnostic tests include CT pulmonary angiography, ventilation-perfusion scanning, echocardiography, and D-dimer levels. CT pulmonary angiography has high sensitivity and specificity for PE diagnosis.
This document discusses pulmonary embolism (PE), including its risk factors, pathophysiology, diagnosis, and management. It notes that PE is a leading cause of cardiovascular death and hospital mortality. Rudolf Virchow identified three main factors that contribute to venous thrombosis and PE: venous stasis, hypercoagulability of blood, and endothelial injury. The pathophysiology of PE involves increased pulmonary vascular resistance and right heart strain or failure. Diagnosis involves assessing clinical risk factors, biomarkers like troponin and BNP, imaging tests like CTPA, and echocardiography. PE is classified as massive, submassive, or low-risk depending on the presence of hypotension and right heart dysfunction. Management involves he
The document discusses pulmonary hypertension and the pulmonary circulation. It provides details on:
1) The anatomy and physiology of the pulmonary circulation and how it differs from the systemic circulation with lower pressures and resistance.
2) The pathophysiology of pulmonary hypertension including abnormalities in the endothelium, smooth muscle cells, and vascular remodeling in different types.
3) Clinical definitions of pulmonary hypertension, pulmonary arterial hypertension, and evaluation tools like echocardiogram, CT, right heart catheterization.
4) Treatment involves vasodilators, diuretics, calcium channel blockers and general measures depending on the severity and type of pulmonary hypertension.
The document provides information on pulmonary hypertension and pulmonary circulation. It discusses:
1) The pulmonary circulation begins at the right ventricle and ends at the left atrium, transporting the entire cardiac output to the lungs. It has low resistance and high compliance.
2) Pulmonary artery pressures are normally lower than systemic pressures, with mean pulmonary artery pressure around 10-12 mmHg.
3) Pulmonary vascular resistance is low due to a balance of vasodilator and vasoconstrictor prostaglandins. Resistance primarily occurs in small arteries and arterioles.
4) Pulmonary hypertension is defined as a mean pulmonary artery pressure over 25 mmHg at rest. Its causes
This document summarizes pulmonary embolism (PE), including its epidemiology, risk factors, pathophysiology, clinical features, diagnostic testing, and treatment. PE is the second most common cause of unexpected death, with risk factors including recent surgery, trauma, cancer, and inherited or acquired thrombophilias. Diagnosis involves assessing clinical probability then confirming with D-dimer, imaging like CT pulmonary angiogram, or lung scintigraphy. For acute PE, initial treatment is heparin or fondaparinux followed by long-term oral anticoagulation to prevent recurrence. New oral anticoagulants targeting factor Xa provide alternatives to warfarin.
Pulmonary embolism is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs or pelvis. It can be life-threatening and is responsible for around 100,000-200,000 deaths in the US each year. Risk factors include inherited or acquired hypercoagulability, venous stasis, or vessel wall injury. Diagnosis involves assessment of likelihood using scoring systems, blood tests like D-dimer, and imaging tests like CT pulmonary angiogram. Treatment depends on stability but generally involves anticoagulants like heparin or newer oral medications to prevent further clots. Prevention focuses on early mobilization, stockings, and blood thinners for
Tricuspid atresia is a congenital heart defect where the tricuspid valve is absent, preventing blood flow from the right atrium to the right ventricle. It occurs in approximately 1-2.4% of congenital heart defects. Survival depends on the presence of an atrial septal defect to allow blood to bypass the right ventricle. Treatment involves multiple staged surgeries culminating in the Fontan procedure to reroute systemic venous return directly to the pulmonary arteries. Complications can include arrhythmias, ventricular dysfunction, protein-losing enteropathy, and thromboembolic events.
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
This document discusses venous thrombosis and pulmonary embolism. It covers risk factors, pathophysiology, diagnostic evaluation, and treatment options. The main points are:
1. Venous thrombosis and pulmonary embolism are concerns in postoperative and ICU patients. Thrombi often form silently in leg veins and can break off and travel to the lungs.
2. Diagnostic evaluations include D-dimer, ventilation-perfusion scans, echocardiograms, angiograms. Imaging shows defects from clots blocking blood flow.
3. Treatment involves anticoagulation initially with heparin or low molecular weight heparin. Warfarin is used long-term. Thrombolytics or inferior v
- Pulmonary embolism affects approximately 500,000 individuals per year in the US, with around 50,000 deaths annually.
- Deep vein thrombosis accounts for over 95% of pulmonary emboli. Risk factors for DVT and thus PE include surgery, trauma, cancer, prolonged immobility, and genetic or acquired hypercoagulable states.
- Diagnosis is suggested by symptoms like dyspnea and chest pain but requires imaging tests like CT pulmonary angiogram, ventilation-perfusion scanning, or echocardiogram to confirm the presence of emboli. Treatment involves anticoagulation with heparin or warfarin.
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 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 embolism (PE), which occurs when a blood clot forms in the lungs. It defines PE, lists risk factors like immobilization and oral contraceptive use, and describes the two main types - thrombotic and non-thrombotic. Signs and symptoms include dyspnea, tachypnea, and hypoxemia. Diagnostic tests include D-dimer, CT scans, ventilation-perfusion scans, and angiograms. Treatment involves anticoagulants like heparin and warfarin to prevent further clotting. Nursing care focuses on monitoring for complications, managing pain and anxiety, and educating patients about anticoagulant therapy and risk reduction.
Similar to Chronic Thrombo Embolic Pulmonary Hypertension.pptx (20)
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- Thyroid imaging with ultrasound and radioactive iodine uptake scans can identify high-risk features that increase the likelihood of malignancy, such as hypoechogenicity, microcalcifications, irregular shape, and lack of iodine uptake in the nodule.
- Cytology results are categorized using the Bethesda or THY classification systems. Suspicious or malignant results
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
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Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
Pictorial and detailed description of patellar instability with sign and symptoms and how to diagnose , what investigations you should go with and how to approach with treatment options . I have presented this slide in my 2nd year junior residency in orthopedics at LLRM medical college Meerut and got good reviews for it
After getting it read you will definitely understand the topic.
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
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The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Know the difference between Endodontics and Orthodontics.Gokuldas Hospital
Your smile is beautiful.
Let’s be honest. Maintaining that beautiful smile is not an easy task. It is more than brushing and flossing. Sometimes, you might encounter dental issues that need special dental care. These issues can range anywhere from misalignment of the jaw to pain in the root of teeth.
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
2. DEFINITION
CTEPH is defined as pre-capillary Pulmonary Hypertension as assessed by right heart catheterization
(mean PAP ≥25 mmHg, PAWP ≤15 mmHg) in the presence of multiple chronic/organized occlusive
thrombi/emboli in the elastic pulmonary arteries (main, lobar, segmental, subsegmental) after at least
three months of effective anticoagulation.
3. CTEPH is defined as pre-capillary Pulmonary Hypertension as assessed by right heart catheterization
(mean PAP ≥25 mmHg, PCWP ≤15 mmHg) in the presence of multiple chronic/organized occlusive
thrombi/emboli in the elastic pulmonary arteries (main, lobar, segmental, subsegmental) after at least three
months of effective anticoagulation.
4. CTEPH is defined as pre-capillary Pulmonary Hypertension as assessed by right heart catheterization
(mean PAP ≥25 mmHg, PCWP ≤15 mmHg) in the presence of multiple chronic/organized occlusive
thrombi/emboli in the elastic pulmonary arteries (main, lobar, segmental, subsegmental) after at least three
7. NATURAL HISTORY OF CTEPH
• Honeymoon period after acute PE
• Usually present in their 40s
• Later presents with dyspnea, hypoxemia & RV dysfunction
• Death usually due to RV failure
11. CHRONIC PULMONARY THROMBOEMBOLISM
PATHOPHYSIOLOGY
CTEPH can develop several months or years after an acute PE (which
may be silent), despite continuing anticoagulation, and in the absence of
new symptoms or any new acute event.
12. THROMBUS NONRESOLUTION IN CTEPH
• In acute PE, the fresh clots are red, easily detached from the pulmonary artery wall and consist
mainly of red cells and platelets in a fibrin mesh.
• In CTEPH, the chronic clots are yellow, highly adherent to the pulmonary vascular wall, and
contain collagen, elastin, inflammatory cells, re-canalised vessels and more rarely, calcification.
• Organisation and fibrosis of this residual thrombotic material impairs blood flow, and ultimately
leads to the development of CTEPH.
14. CANCER
Various Mechanisms cause increased risk of thromboembolic events resulting from
activation of the fibrinolytic and coagulation systems acute-phase reactions,
inflammation and cytokine production.
15. INFLAMMATION AND INFECTION
Patients with chronic thromboembolic pulmonary hypertension (CTEPH) have
elevated levels of C-reactive protein (CRP) and tumor necrosis factor-α, which are
reduced after pulmonary endarterectomy (PEA), and chronic infection with
Staphylococcus aureus is common in CTEPH patients.
16. BIOLOGICAL AND GENETIC RISK FACTORS FOR
THROMBUS NONRESOLUTION
• Patients with thrombus nonresolution could have a hypercoagulability state.
• There is no evidence to suggest that deficiencies in Protein C, Protein S,
Antithrombin, or mutations of Factor V and II are more prevalent in patients with
Chronic Thromboembolic Pulmonary Hypertension (CTEPH) compared to healthy
control populations.
17. BIOLOGICAL AND GENETIC RISK FACTORS FOR
THROMBUS NONRESOLUTION – ADAMTS 13
• ADAMTS13 A Disintegrin And Metalloproteinase With Thrombospondin Type 1
Motif, Member 13,
• von Willebrand factor-cleaving protease.
• Regulates the size of von Willebrand factor and plays a fundamental role in
haemostasis.
• Severe deficiency of ADAMTS13 causes thrombotic thrombocytopenic purpura.
• Patients with DVT showed relatively lower plasma levels of ADAMTS13 activity.
18. BLOOD GROUPS
• The ABO locus is a susceptibility locus for VTE and non-O carriers have
a higher risk for VTE than O carriers
19. FIBRINOGEN AND FIBRINOLYTIC ABNORMALITIES
IN CTEPH
• Patients with CTEPH appear to have a high prevalence of abnormal
fibrinogen molecules in the blood such as fibrinogen Aα-Thr312Ala .
• This mutation leads to a modified fibrin structure in clots, including
increased cross-linking of α-chains
• The common feature are that they are able to resist physiological
thrombolysis, and thus affect thrombus resolution
20. PLATELET FUNCTION IN CTEPH
• Conditions such as thyroid hormone replacement therapy and
splenectomy are risk factors for CTEPH.
• Patients with CTEPH have a higher mean platelet volume, increased
spontaneous platelet aggregation and decreased platelet aggregation
in response to agonists.
21. SMALL-VESSEL DISEASE IN CTEPH
• There is evidence that in addition to mechanical obstruction of
proximal arteries, some patients develop severe pulmonary
microvasculopathy (small-vessel disease), first described by Moser
and Bloor.
Moser KM, Bloor CM. Pulmonary vascular lesions occurring in patients with chronic major vessel thromboembolic
pulmonary hypertension. Chest. 1993 Mar;103(3):685-92. doi: 10.1378/chest.103.3.685. PMID: 8449052.
22. • This vascular remodelling affects the wall of distal muscular pulmonary
arteries (0.1−0.5 mm in diameter), and may even reach arterioles and
venules of <0.1 mm in diameter.
• Redistribution of the pulmonary flow in nonoccluded pulmonary arteries
are exposed to high pressure and shear stress, leading to endothelial
dysfunction, a progressive increase in PVR and ultimately to symptomatic
CTEPH.
23.
24. RV DYSFUNCTION AND FAILURE IN CTEPH
• Chronic increase in RV afterload and wall stress
• RV is not capable of sustaining long-term pressure overload, which
increases further during physical activity.
• Continuously increasing burden on the RV, leads to its maladaptive
remodelling.
• Eccentric hypertrophy, RV dilatation, reduced RV contractile force,
diastolic dysfunction and myocardial fibrosis.
28. CLINICAL PRESENTATION.
• Cardinal Symptom : Dyspnea on progressively minor exertion.
• Mainly linked to right ventricle (RV) dysfunction.
• A patient may carry on relatively normal activities following a pulmonary embolic
event, whether clinically apparent or occult, even when extensive pulmonary
vascular occlusion has occurred (asymptomatic – honeymoon period)
29.
30. • Central, peripheral, or mixed cyanosis
• Accentuated pulmonary component of second heart sound
• RV third heart sound
• Systolic murmur of tricuspid regurgitation
• Diastolic murmur of pulmonary regurgitation
SIGNS OF PULMONARY HYPERTENSION
33. INVESTIGATIONS : CHEST RADIOGRAPHY
• Enlargement of main pulmonary arteries or asymmetry in the size of
the central pulmonary arteries
• Areas of hypoperfusion or hyperperfusion.
• Evidence of old pleural disease, unilaterally or bilaterally
• Right atrial or right ventricular enlargement, based on the outline of
the right cardiac border.
• Cardiomegally.
34. ELECTROCARDIOGRAPHY (ECG)
• Right axis deviation
• Right ventricular hypertrophy
• Right atrial enlargement
• Right bundle – branch block
• ST segment displacement
• T- wave inversions in anterior precordial and inferior limb leads.
• ECG = Predictive Value. Normal ECG + Normal Biomarkers = Low
Likelihood for PH.
35. • Useful for excluding coexisting parenchymal lung disease or airflow
obstruction
• A mild obstructive defect may be present as a result of mucosal hyperemia,
which is related to development of a large bronchial arterial collateral
circulation.
• Resting arterial PO2 may be within normal limits.
• Hypoxemia at rest implies very severe right ventricular dysfunction or the
presence of a right -to- left shunt.
• Majority of patients have a decline in the arterial PO2 with exercise.
PULMONARY FUNCTION TESTS AND ARTERIAL BLOOD
GASES
36. • PH leads to RV pressure overload and dysfunction, which can be
detected by echocardiography.
• Enlargement and reduced systolic function of the right ventricle are
usually apparent
• ECHO is useful for excluding;
1. Left ventricular dysfunction
2. Valvular disease
3. Cardiac malformations
ECHOCARDIOGRAPHY
37.
38.
39. • A ventilation/perfusion (V/Q) lung scan (planar or SPECT) is recommended
in the diagnostic work-up of patients with suspected or newly diagnosed
PH, to rule out or detect signs of CTEPH.
• In the absence of parenchymal lung disease, a normal perfusion scan
excludes CTEPH with a negative predicted value of 98%.
• Non-matched perfusion defects similar to those seen in CTEPH may be
present in 7–10% of patients with PAH.
VENTILATION/PERFUSION LUNG SCAN
43. 54 YEAR OLD FEMALE WITH DYSPNEA AND DEC.
O2 SATURATION.
44.
45. COMPUTED TOMOGAPHY (CT)
• Right atrial and ventricular enlargement
• Chronic thromboembolic material within dilated central pulmonary arteries
• Central pulmonary artery enlargement (PA-to-aorta ratio >0.9)
• Variations in the size of lobar and segmental level vessels
• Presence of mediastinal collateral vessels arising from the systemic arterial
circulation.
• Combination of three parameters (PA diameter ≥30 mm, RVOT wall thickness ≥6
mm, and septal deviation ≥140° [or RV:LV ratio ≥1]) is highly predictive of PH.
46. COMPUTED TOMOGRAPHY PULMONARY
ANGIOGRAPHY
• Direct or indirect signs of CTEPH, such as filling defects (including
thrombus adhering to the vascular wall), webs or bands in the PAs, PA
retraction/dilatation, mosaic perfusion, and enlarged bronchial
arteries.
• To detect other cardiovascular abnormalities, including intracardiac
shunts, abnormal pulmonary venous return, patent ductus arteriosus,
and PAVMs.
48. DIGITAL SUBTRACTION ANGIOGRAPHY
• Pulmonary artery webs or bands
• Intimal irregularities
• Abrupt narrowing of the major pulmonary arteries
• Obstruction of lobar or segmental vessels at their
point of origin, with complete absence of blood flow
to pulmonary segments normally perfused by those
vessels.
• Measuring pulmonary arterial haemodynamics
during right heart catheterisation.
49. CARDIAC CATHETERIZATION
• Right heart catheterization is the gold standard for diagnosing and classifying PH.
• The guidelines recommend a complete haemodynamic evaluation by right heart
catheterisation including cardiac output because PVR is important to assess
prognosis and the risks associated with PEA.
• In addition to diagnosing and classifying PH, clinical indications include
haemodynamic assessment of heart or Lung Transplant candidates.
57. SURGICAL PULMONARY ENDARTERECTOMY.
• Type I disease (15%)
• Refers to the situation in which major
vessel clot is present and readily
visible on the opening of the
pulmonary arteries.
• All central thrombotic material has to
be completely removed before the
endarterectomy.
58. In Type II disease (approximately 50% of
cases no major vessel thrombus can be
appreciated.
In these cases only thickened intima can be
seen, occasionally with webs, and the
endarterectomy plane is raised in the main,
lobar, or segmental vessels.
SURGICAL PULMONARY ENDARTERECTOMY.
59. Type III disease (approximately 30% of cases)
presents the most challenging surgical situation.
The disease is very distal and confined to the
segmental and subsegmental branches.
No occlusion of vessels can be seen initially. The
endarterectomy plane must be carefully raised
in each segmental and subsegmental branch.
SURGICAL PULMONARY ENDARTERECTOMY.
60. Type IV disease does not represent primary
thromboembolic pulmonary hypertension
and is inoperable.
In this entity there is intrinsic small vessel
disease, although secondary thrombus may
occur as a result of stasis.
SURGICAL PULMONARY ENDARTERECTOMY.
61. • Riociguat – for inoperable CTEPH / recurrent PH after PEA. After 16 weeks of therapy, improved 6MWD and reduced PVR by 31%
compared with placebo, and is approved for this indication.
• Treprostinil s.c. showed improved 6MWD at week 24 in patients with inoperable CTEPH or those with persistent/recurrent PH
after PEA and is approved for this indication.
• Macitentan 10 mg improved PVR and 6MWD vs. placebo at 16 and 24 weeks, respectively.
• Other medical therapies—PDE5is (e.g. sildenafil) and ERAs (e.g. bosentan)—have been used off-label, as their efficacy in
inoperable CTEPH has not been proven by RCTs or registry data.
• However, oral combination therapy, including PDE5is and ERAs, is common practice in patients with CTEPH with severe
haemodynamic compromise.
MEDICAL THERAPY
Ghofrani HA, D'Armini AM, Grimminger F, Hoeper MM, Jansa P, Kim NH, Mayer E, Simonneau G, Wilkins MR, Fritsch A, Neuser D. Riociguat for the treatment of chronic thromboembolic
pulmonary hypertension. New England Journal of Medicine. 2013 Jul 25;369(4):319-29.
Sadushi-Kolici R, Jansa P, Kopec G, Torbicki A, Skoro-Sajer N, Campean IA, Halank M, Simkova I, Karlocai K, Steringer-Mascherbauer R, Samarzija M. Subcutaneous treprostinil for the
treatment of severe non-operable chronic thromboembolic pulmonary hypertension (CTREPH): a double-blind, phase 3, randomised controlled trial. The lancet respiratory medicine. 2019 Mar
1;7(3):239-48.
Ghofrani HA, Simonneau G, D'Armini AM, Fedullo P, Howard LS, Jaïs X, Jenkins DP, Jing ZC, Madani MM, Martin N, Mayer E. Macitentan for the treatment of inoperable chronic
thromboembolic pulmonary hypertension (MERIT-1): results from the multicentre, phase 2, randomised, double-blind, placebo-controlled study. The Lancet Respiratory Medicine. 2017 Oct
1;5(10):785-94.
62. Balloon pulmonary angioplasty is an established treatment for selected patients with
inoperable CTEPH or persistent/ recurrent PH after PEA, improving haemodynamics
(PVR decrease 49–66%), right heart function, and exercise capacity.
A staged interventional procedure with a limited number of dilated PA segments per
session is preferred.
Procedural and post-interventional complications include vascular injury due to wire
perforation, and lung injury with haemoptysis and/or hypoxia.
INTERVENTIONAL TREATMENT
63.
64. • Patients should be regularly followed-up, including invasive assessment with RHC 3–6 months
after intervention, allowing for consideration of a multimodal treatment approach.
• After successful treatment, yearly non-invasive followup, including echocardiography and an
evaluation of exercise capacity, is indicated because recurrent PH has been described
• Most experts accept achieving a good functional class (WHO-FC I–II) and/or normalization or near
normalization of haemodynamics at rest, obtained at RHC 3–6months post-procedure (PEA or last
BPA), and improvement in quality of life.
FOLLOWUP
CTEPH is defined as pre-capillary Pulmonary Hypertension as assessed by right heart catheterization (mean PAP ≥25 mmHg, PAWP ≤15 mmHg) in the presence of multiple chronic/organized occlusive thrombi/emboli in the elastic pulmonary arteries (main, lobar, segmental, subsegmental) after at least three months of effective anticoagulation.
Pulmonary Circulation is divided into 3 parts, the precapillary part, capillary part and the post capillary part.
Pathologies like chronic lung diseases affect the capillary parts where as for precapillary, there is PAH and for post capillary, there is PVH.
Right heart catheterization is the modality used to determine PA pressues where a catheter is passed through the femoral vein into the RA then to RV and eventually into the PA where pressures are measured.
There is presence of multiple chronic or organized occlusive thrombus / embolus in the elastic Pulmonary Arteries which can be in the
Main Pulmonary Artery
Lobar
Segmental
or
Subsegmental PA.
According to the 2022 European Society of Cardiology guidelines for the diagnosis and treatment of pulmonary HTN, Pulmonary Hypertension associated with Pulmonary Artery Obstruction is classified under Group 4.
This chart is a brief summary of the disease where we see that Pulmonary Hypertension associated with Pulmonary Artery Obstruction is a rather rare entity among patients with PAH and various modalities of treatment are listed as
Pulmonary Endarterectomy, Balloon Pulmonary Angioplasty and Medical Management.
The Natural History of CTEPH is dismal and nearly all patients eventually die of progressive right heart failure.
It has an insidious onset.
There is a Honeymoon period after acute PE
And diagnosis is often made later in the progression of the disease and patients present with dyspnea, hypoxemia & RV dysfunction
Severity of pulmonary hypertension correlates inversely with duration of survival.
Now, An Acute Pulmonary Embolism which may be Silent, can lead to incomplete resolution and organization of the thrombus which eventually leads to Vascular stenosis and occlusion, causing shear stress and Progressive increase in PVR, ultimately leading to CTEPH.
Vascular stenosis also can cause distal thrombosis of pulmonary arteries causing increased pulmonary vascular resistance.
And shear stress can cause small vessel disease causing increased PVR.
All ultimately leading to Symptomatic CTEPH.
Incidence is 0.5-3.8 % of patients with Acute PE end up with CTEPH
and it is more common in patients with Recurrent PE - upto 10%
CTEPH can develop several months or years after an acute PE (which may be silent), despite continuing anticoagulation, and in the absence of new symptoms or any new acute event.
Events such as Inflammation, Infection or THrombosis cause CTEPH which leads to chronic obstruction, small vessel disease and eventually right heart failure.
THROMBUS NONRESOLUTION IN CTEPH
In acute PE, the fresh clots are red, easily detached from the pulmonary artery wall and consist mainly of red cells and platelets in a fibrin mesh.
In CTEPH, the chronic clots are yellow, highly adherent to the pulmonary vascular wall, and contain collagen, elastin, inflammatory cells, re-canalised vessels and more rarely, calcification.
Organisation and fibrosis of this residual thrombotic material impairs blood flow, and ultimately leads to the development of CTEPH.
CLINICAL CONDITIONS PREDISPOSING TO CTEPH
VTE (Large pulmonary emboli = higher risk of CTEPH)
Recurrent Pulmonary Emboli.
Insufficient Anticoagulation.
Autoimmune and Haematological Disorders.
Hypercoagulability
Malignancy
Nonmalignant thrombophilia
Pregnancy Postpartum status.
Long-distance travel.
Recent surgery
Recent trauma (especially the lower extremities and pelvis)
Patients with cancer have an increased risk of thromboembolic events, resulting from various mechanisms including activation of the fibrinolytic and coagulation systems, acute-phase reactions, inflammation and
cytokine production
There are higher levels of C-reactive protein (CRP) seen in patients compared with healthy controls, as well as a significant reduction in CRP is seen after pulmonary endarterectomy (PEA).
Tumour necrosis factor-α: levels are elevated in patients with CTEPH compared with controls, and are reduced after PEA
The presence of chronic infection (e.g. Staphylococcus aureus) has been identified in patients with CTEPH
Patients with thrombus nonresolution could have a hypercoagulability state.
There is no evidence to suggest that deficiencies in Protein C, Protein S, Antithrombin, or mutations of Factor V and II are more prevalent in patients with (CTEPH) compared to healthy control populations.
ADAMTS13
is a von Willebrand factor-cleaving protease.
Regulates the size of von Willebrand factor and plays a fundamental role in haemostasis.
Severe deficiency of ADAMTS13 causes thrombotic thrombocytopenic purpura.
Patients with DVT showed relatively lower plasma levels of ADAMTS13 activity.
The ABO locus is a susceptibility locus for VTE and non-O carriers have a higher risk for VTE than O carriers
Patients with CTEPH appear to have a high prevalence of abnormal fibrinogen molecules in the blood.
This mutation leads to a modified fibrin structure in clots, including increased cross-linking of α-chains
The common feature are that they are able to resist physiological thrombolysis, and thus affect thrombus resolution
Platelet-activating conditions such as thyroid hormone replacement therapy and splenectomy are risk factors for CTEPH suggests a role for platelets in its genesis.
Patients with CTEPH have a higher mean platelet volume, increased spontaneous platelet aggregation and decreased platelet aggregation in response to agonists.
SMALL VESSEL DISEASE IN CTEPH
There is evidence that in addition to mechanical obstruction of proximal arteries, some patients develop severe pulmonary microvasculopathy (small-vessel disease), first described by Moser and Bloor.
This vascular remodelling affects the wall of distal muscular pulmonary arteries (0.1−0.5 mm in diameter), and may even reach arterioles and venules of <0.1 mm in diameter.
Redistribution of the pulmonary flow in nonoccluded pulmonary arteries are exposed to high pressure and shear stress, leading to endothelial dysfunction, a progressive increase in PVR and ultimately to symptomatic CTEPH.
This image is a Schematic representation of anastomosis between systemic and pulmonary circulation through hypertrophic bronchial arteries and vasa vasorum.
There exists large anastomoses between the systemic circulation and pulmonary arterial circulation (via hypertrophic bronchial arteries and vasa vasorum) in patients with CTEPH.
Pre-existing anastomoses are opened by the pressure gradient between bronchial arteries and postobstruction pulmonary arteries.
CTEPH is characterized by a chronic increase in RV afterload and wall stress.
RV is not capable of sustaining long-term pressure overload, which increases further during physical activity.
Moreover, progressive remodelling of the initially patent pulmonary arteriolar bed imposes a continuously increasing burden on the RV, leading to its maladaptive remodelling.
This is characterised by eccentric hypertrophy RV dilatation, reduced RV contractile force, diastolic dysfunction and myocardial fibrosis.
As the pulmonary artery narrows, there is increased load on the right ventricle.
As the load on the right ventricle keeps on increasing, the RV compensates by increasing its muscle contractility and wall thickness – a phenomenon known as COUPLING.
Further progression causes RV dilatation which results in increased wall stress and o2 consumption.
In the final stage, ”UNCOUPLING” occurs, where the RV cannot keep up with the increased PA pressures and ultimately leads to a reduced output and eventually RV failure.
The diagnostic approach to CTEPH is mainly focused on two tasks.
The primary goal is to raise early suspicion of PH and ensure fast-track referral to PH centres in patients with a high likelihood of PAH, CTEPH, or other forms of severe PH.
The second objective is to identify underlying diseases and to rule out, LHD (group 2 PH) and lung disease (group 3 PH), as well as comorbidities, to ensure proper classification, risk assessment, and treatment.
Symptoms of PH are mainly linked to right ventricle (RV) dysfunction, and typically associated with exercise in the earlier course of the disease.
The cardinal symptom is dyspnoea on progressively minor exertion. Other common symptoms are related to the stages and severity of the disease, Importantly, the physical examination may also be the key to identifying the underlying cause of PH.
Early symptoms include
Dyspnoea on exertion (WHO-FC)
Fatigue and rapid exhaustion
Dyspnoea when bending forward (bendopnoea)
Palpitations
Haemoptysis
Exercise-induced abdominal distension and nausea
Weight gain due to fluid retention
Syncope (during or shortly after physical exertion)
Rare symptoms due to pulmonary artery dilation
Exertional chest pain: dynamic compression of the left main coronary artery
Hoarseness (dysphonia): compression of the left recurrent laryngeal nerve (cardiovocal or Ortner´s syndrome)
Shortness of breath, wheezing, cough, lower respiratory tract infection, atelectasis: compression of the bronchi.
Thoracic compression syndromes are found in a minority of patients with PAH with pronounced dilation of the pulmonary artery, and may occur at any disease stage and even in patients with otherwise mild functional impairment.
Signs of pulmonary hypertension
Central, peripheral, or mixed cyanosis
Accentuated pulmonary component of second heart sound
RV third heart sound
Systolic murmur of tricuspid regurgitation
Diastolic murmur of pulmonary regurgitation
Signs of RV backward failure include
Distended and pulsating jugular veins
Abdominal distension
Hepatomegaly
Ascites
Peripheral oedema
Signs of RV forward failure consists of
Peripheral cyanosis (blue lips and tips)
Dizziness
Pallor
Cool extremities
Prolonged capillary refill
Radiographic signs of PH include RA/RV and PA enlargement, with pruning of the peripheral vessels.
Areas of hypoperfusion or hyperperfusion.
Evidence of old pleural disease, unilaterally or bilaterally
Right atrial or right ventricular enlargement, based on the outline of the right cardiac border.
Cardiomegally.
Electrocardiogram (ECG) abnormalities may raise suspicion of PH, deliver prognostic information, and detect arrhythmias. In adults with clinical suspicion of PH (e.g. unexplained dyspnoea on exertion), right axis deviation has a high predictive value for PH.
A normal ECG does not exclude the presence of PH, but a normal ECG in combination with normal biomarkers (BNP/ NT-proBNP) is associated with a low likelihood of PH in patients referred for suspected PH or at risk of PH (i.e. after acute PE).
Other Findings include
Right axis deviation
Right ventricular hypertrophy
Right atrial enlargement
Right bundle – branch block
ST segment displacement
T- wave inversions in anterior precordial and inferior limb leads.
Pulmonary function tests (PFTs) and analysis of arterial blood gas (ABG) are used to
assess comorbidities and the need for supplementary oxygen, and determine disease severity.
Useful for excluding coexisting parenchymal lung disease or airflow obstruction
A mild obstructive defect may be present as a result of mucosal hyperemia, which is related to development of a large bronchial arterial collateral circulation.
Resting arterial PO2 may be within normal limits.
Hypoxemia at rest implies very severe right ventricular dysfunction or the presence of a right -to- left shunt.
Majority of patients have a decline in the arterial PO2 with exercise.
PH leads to RV pressure overload and dysfunction, which can be detected by echocardiography.
Enlargement and reduced systolic function of the right ventricle are usually apparent
ECHO is useful for excluding;
Left ventricular dysfunction
Valvular disease
Cardiac malformations
In the Parasternal Long Axis View, We can see that the RV is enlarged.
In the Apical 4 chamber view, We can measure the Dilated RV along with Basal RV/LV ratio >1.0
Parasternal Short Axis View shows a flattened IVS Leading to a D shaped LV.
And the Subcostal view shows a distended IVC with reduced inspiratory collapsibility.
Also we can see in 4 chamber view, in systole and diastole, there is reduced RV fractional area change. (<35%) and there is enlarged right atrial area.
There is Decreased Tricuspid Annular Plane Systolic Excursion in M Mode (<18mm)
In Doppler, we can see decreased peak systolic velocity of tricuspid annulus and increased systolic peak tricuspid regurgitant velocity. Along with that, PA pressures can also be measured.
And presence of pericardial effusion can be seen in 4 chamber view or subcostal view.
A ventilation/perfusion (V/Q) lung scan (planar or single-photon emission computed tomography [SPECT]) is recommended in the diagnostic work-up of patients with suspected or newly diagnosed PH, to rule out or detect signs of CTEPH.
V/Q SPECT is superior to planar imaging.
In the absence of parenchymal lung disease, a normal perfusion scan excludes CTEPH with a negative predicted value of 98%.
Non-matched perfusion defects similar to those seen in CTEPH may be present in 7–10% of patients with PAH.
Lobar mismatch. PE.
CT Scan Shows
Right atrial and ventricular enlargement
Chronic thromboembolic material within dilated central pulmonary arteries
Central pulmonary artery enlargement (PA-to-aorta ratio >0.9)
Variations in the size of lobar and segmental level vessels
Presence of mediastinal collateral vessels arising from the systemic arterial circulation.
Combination of three parameters (PA diameter ≥30 mm, RVOT wall thickness ≥6 mm, and septal deviation ≥140° [or RV:LV ratio ≥1]) is highly predictive of PH.
CT Pulmonary Angiography is useful to
To detect direct or indirect signs of CTEPH, such as filling defects (including thrombus adhering to the vascular wall), webs or bands in the PAs, PA retraction/dilatation, mosaic perfusion, and enlarged bronchial arteries.
Computed tomography pulmonary angiography may also be used to detect other cardiovascular abnormalities, including intracardiac shunts, abnormal pulmonary venous return, patent ductus arteriosus, and PAVMs.
MR Angio has
Limited sensitivity
No extra advantage over CTA
Catheter pulmonary angiography is done for the assessment of pulmonary vasculature
It can detect Pulmonary artery webs or bands
Intimal irregularities
Abrupt narrowing of the major pulmonary arteries
Obstruction of lobar or segmental vessels at their point of origin, with complete absence of blood flow to pulmonary segments normally perfused by those vessels.
DSA has the advantage of measuring pulmonary arterial haemodynamics during right heart catheterisation.
Right heart catheterization is the gold standard for diagnosing and classifying PH.
The guidelines recommend a complete haemodynamic evaluation by right heart catheterisation including cardiac output because PVR is important to assess prognosis and the risks associated with PEA.
In addition to diagnosing and classifying PH, clinical indications include haemodynamic assessment of heart or LTx candidates.
A patient with Exertional Dyspnoea and or suspected PH, when meeting with the GP for the first time, Undergoes a complete history and a thorough physical exam.
Warning signs include rapid progression of symptoms, severely reduced exercise capacity, pre-syncope or syncope on mild exertion, signs of right heart failure
Upon arrival at the Pulmonary Hypertension Centre, THorough Evaluation of PH is done and risk factors for CTEPH are assessed.
Patient undergoes VQ scan and ECHO which if shows high probability of CTEPH,
further testing in the form of CTPA/DSA and RHC is done which confirms the diagnosis of CTEPH.
Treatment is always done by a Multidisciplinary Team at a CTEPH Centre.
Patients with confirmed CTEPH are offered Lifelong Anticoagulation which is a CLASS 1 indication.
And is assessed for operability by a MDT.
If operable, Pulmonary Endarterectomy is offerd to the patient as a treatment of choice.
and is followed up at the CTEPH center lifelong.
This chart describes the treatment modality based on the levels of disease.
Proximal PA fibrotic obstructions (vessel diameter 10–40 mm).
Distal segmental and subsegmental PA fibrotic obstruction potentially suitable for both PEA and BPA interventions (vessel diameter 2–10 mm).
Distal subsegmental PA fibrotic obstructions form a web-lesion in a subsegmental branch of the PA suitable for BPA interventions (vessel diameter 0.5–5 mm).
Distal subsegmental PA fibrotic obstructions, which might be accompanied by microvasculopathy (vessel diameter ,0.5 mm).
Microvasculopathy (vessel diameter ,0.05 mm) treated with medical therapy.
Also, there are 4 broad types of pulmonary occlusive disease related to the thrombus that can be appreciated.
Type I disease (15%)
Refers to the situation in which major vessel clot is present and readily visible on the opening of the pulmonary arteries.
All central thrombotic material has to be completely removed before the endarterectomy.
Surgical specimen removed from a patient showing evidence of some fresh and some old thrombus in the main and both right and left pulmonary arteries.
Simple removal of the gross disease initially encountered on pulmonary arteriotomy will not be therapeutic, and any meaningful outcome involves a full endarterectomy into all the distal segments.
In Type II disease (approximately 50% of cases no major vessel thrombus can be appreciated.
In these cases only thickened intima can be seen, occasionally with webs, and the endarterectomy plane is raised in the main, lobar, or segmental vessels.
Specimen removed in a patient with type II disease. Both pulmonary arteries have evidence of chronic thromboembolic material.
Note the distal tails of the specimen in each branch. Full resolution of pulmonary hypertension is dependent on complete removal of all the distal tails.
Type III disease (approximately 30% of cases) presents the most challenging surgical situation.
The disease is very distal and confined to the segmental and subsegmental branches.
No occlusion of vessels can be seen initially. The endarterectomy plane must be carefully raised in each segmental and subsegmental branch.
Specimen removed from a patient with type III disease.
the disease is distal, and the plane was raised at each segmental level.
Type IV disease does not represent primary thromboembolic pulmonary hypertension and is inoperable.
In this entity there is intrinsic small vessel disease, although secondary thrombus may occur as a result of stasis.
the absence of distal “tails” in this specimen removed from a patient with surgical classification type IV. All “tails” are replaced by “trousers.” No clinical benefit was obtained from this procedure and the patient’s postoperative hemodynamics was not improved.
The patient had primary pulmonary hypertension.
Medical Therapy
Riociguat – for inoperable CTEPH / recurrent PH after PEA. After 16 weeks of therapy, improved 6 MWD and reduced PVR by 31% compared with placebo, and is approved for this indication.
Treprostinil s.c. showed improved 6MWD at week 24 in patients with inoperable CTEPH or those with persistent/recurrent PH after PEA and is approved for this indication.
Macitentan 10 mg improved PVR and 6MWD vs. placebo at 16 and 24 weeks, respectively.
oral combination therapy, including SIldenafil and Bosentan, is common practice in patients with CTEPH with severe haemodynamic compromise.
Balloon pulmonary angioplasty is an established treatment for selected patients with inoperable CTEPH or persistent/ recurrent PH after PEA, improving haemodynamics (PVR decrease 49–66%), right heart function, and exercise capacity.
A staged interventional procedure with a limited number of dilated PA segments per session is preferred.
Procedural and post-interventional complications include vascular injury due to wire perforation, and lung injury with haemoptysis and/or hypoxia.
The procedure of BPA shows
(A) the obstruction (arrow) in the pulmonary artery depicted in pulmonary angiography and
(B) after BPA procedure the obstruction (arrow) is cleared and blood flow appears until peripheral artery.
Patients should be regularly followed-up, including invasive assessment with RHC 3–6 months after intervention, allowing for consideration of a multimodal treatment approach.
After successful treatment, yearly non-invasive followup, including echocardiography and an evaluation of exercise capacity, is indicated because recurrent PH has been described
Most experts accept achieving a good functional class (WHO-FC I–II) and/or normalization or near normalization of haemodynamics at rest, obtained at RHC 3–6months post-procedure (PEA or last BPA), and improvement in quality of life.
