The document discusses pulmonary embolism (PE), which is a blockage of an artery in the lungs by a substance that has traveled from elsewhere in the body, such as a blood clot. Deep vein thrombosis (DVT) in the legs is the most common source of PE. Key signs and symptoms of PE include shortness of breath, chest pain, and tachycardia. Diagnostic tests include chest x-rays, CT scans, ventilation-perfusion scans, echocardiograms, and D-dimer tests. Treatment focuses on anticoagulation medications to prevent further clotting.
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
The document discusses lung collapse (atelectasis) and consolidation. Collapse is a loss of lung volume while consolidation involves fluid filling the alveoli. Collapse can be caused by obstruction of airways or loss of contact between the lungs and chest wall. Consolidation is seen in conditions like pneumonia. Specific patterns of collapse and consolidation are seen on chest x-rays depending on the affected lung lobe. Signs like fissure shifts and volume changes in the unaffected lobes help identify the collapsed lobe.
This document discusses radiology signs of pneumomediastinum. It begins by defining pneumomediastinum and listing potential sources where air can originate from, both intrathoracic and extrathoracic. It then describes several common radiographic signs seen with pneumomediastinum, including the thymic sail sign, ring around the artery sign, and ginkgo leaf sign. Examples of each sign are shown through radiograph and CT images. Other signs like the continuous diaphragm sign, tubular artery sign, and Naclerio's V sign are also defined. The document emphasizes the importance of recognizing these signs on imaging for diagnosing pneumomediastinum.
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
This document describes the various types and radiographic appearances of lobar and segmental lung collapse. It discusses intrinsic and extrinsic causes of collapse and describes the typical findings for each lobe, including displacement of fissures, loss of volume, and compensatory changes. Specific signs are outlined to help identify collapse of the different lung lobes based on chest x-ray and CT imaging. Rarer forms of collapse including complete opacification and shifting atelectasis are also covered.
Congenital heart disease and vascular abnormality(x-ray findings)z2jeetendra
This document provides an overview of various congenital heart diseases and vascular abnormalities, describing their characteristics and classic radiographic signs. It defines common conditions like transposition of the great vessels, total anomalous pulmonary venous return, partial anomalous pulmonary venous return, endocardial cushion defects, tetralogy of Fallot, aortic coarctation, Ebstein's anomaly. For each condition, it explains the anatomical features and identifies signature radiographic patterns seen on chest x-rays, like the "egg on string sign" and "snowman sign".
This document discusses various tachyarrhythmias, including:
- Supraventricular tachycardias like atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia.
- Ventricular arrhythmias including ventricular tachycardia and ventricular flutter.
- Irregular rhythms such as atrial fibrillation.
It provides details on characteristics like rate, morphology, underlying causes, and treatment approaches for each type of tachycardia. Emphasis is placed on distinguishing ventricular tachycardia from supraventricular tachycardia with aberrancy in clinical evaluation.
The heart during systole, becoming smaller, generally withdraws from the chest wall except for the apex for the reasons explained above. The effect of this withdrawal on the chest wall can be observed as an inward movement of the chest wall during systole called "retraction." Although the heart is basically comprised of two separate pumps (right and left ventricles), these two pumps operate normally at two vastly different pressures. Left ventricular systolic pressures being approximately five times higher than that of the right ventricle, its wall tension is much higher, resulting in the increased wall thickness of the left ventricular chamber. The effect of the increased muscle mass on the left side leads to dominance of the left-sided hydrodynamic forces described above. This results in the left ventricular apex as the only area of normal contact during systole. The rest of the heart essentially retracts from the chest wall. In a normal heart, this retraction of the chest wall can be observed to be located medial to the apical impulse and involving part of the left anterior chest wall (20). Even the right ventricle, which is anatomically an anterior structure, is normally pulled away from the chest wall because of its own contraction (becoming smaller) and, more importantly, the septal contraction also pulling the right ventricle posteriorly. This retraction observed in normal patients is located medial to the apical impulse (23,24). It can be best appreciated with patients in the left lateral decu-bitus position with a palpating finger only on the apical impulse with clear view of the rest of the precordium for proper observation of the inward movement of the retraction (opposite in direction to the outward movement of the apical impulse). This "medial retraction" identifies and indicates that the left ventricle forms the apical impulse. The extent of the area of medial retraction may be variable depending on both cardiac and extracardiac factors such as the compliance of the chest wall. It may sometimes be noted only over a small area very close to the apex beat.
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
The document discusses lung collapse (atelectasis) and consolidation. Collapse is a loss of lung volume while consolidation involves fluid filling the alveoli. Collapse can be caused by obstruction of airways or loss of contact between the lungs and chest wall. Consolidation is seen in conditions like pneumonia. Specific patterns of collapse and consolidation are seen on chest x-rays depending on the affected lung lobe. Signs like fissure shifts and volume changes in the unaffected lobes help identify the collapsed lobe.
This document discusses radiology signs of pneumomediastinum. It begins by defining pneumomediastinum and listing potential sources where air can originate from, both intrathoracic and extrathoracic. It then describes several common radiographic signs seen with pneumomediastinum, including the thymic sail sign, ring around the artery sign, and ginkgo leaf sign. Examples of each sign are shown through radiograph and CT images. Other signs like the continuous diaphragm sign, tubular artery sign, and Naclerio's V sign are also defined. The document emphasizes the importance of recognizing these signs on imaging for diagnosing pneumomediastinum.
1. The ECG shows a 45-year-old diabetic man with episodes of palpitations who presents with ventricular trigeminy.
2. Ventricular trigeminy is characterized by ventricular premature beats occurring after every two normal sinus beats with a compensatory pause.
3. Further investigation with Holter monitoring is recommended to better characterize the ventricular arrhythmia and assess for underlying cardiac disease.
This document describes the various types and radiographic appearances of lobar and segmental lung collapse. It discusses intrinsic and extrinsic causes of collapse and describes the typical findings for each lobe, including displacement of fissures, loss of volume, and compensatory changes. Specific signs are outlined to help identify collapse of the different lung lobes based on chest x-ray and CT imaging. Rarer forms of collapse including complete opacification and shifting atelectasis are also covered.
Congenital heart disease and vascular abnormality(x-ray findings)z2jeetendra
This document provides an overview of various congenital heart diseases and vascular abnormalities, describing their characteristics and classic radiographic signs. It defines common conditions like transposition of the great vessels, total anomalous pulmonary venous return, partial anomalous pulmonary venous return, endocardial cushion defects, tetralogy of Fallot, aortic coarctation, Ebstein's anomaly. For each condition, it explains the anatomical features and identifies signature radiographic patterns seen on chest x-rays, like the "egg on string sign" and "snowman sign".
This document discusses various tachyarrhythmias, including:
- Supraventricular tachycardias like atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia.
- Ventricular arrhythmias including ventricular tachycardia and ventricular flutter.
- Irregular rhythms such as atrial fibrillation.
It provides details on characteristics like rate, morphology, underlying causes, and treatment approaches for each type of tachycardia. Emphasis is placed on distinguishing ventricular tachycardia from supraventricular tachycardia with aberrancy in clinical evaluation.
The heart during systole, becoming smaller, generally withdraws from the chest wall except for the apex for the reasons explained above. The effect of this withdrawal on the chest wall can be observed as an inward movement of the chest wall during systole called "retraction." Although the heart is basically comprised of two separate pumps (right and left ventricles), these two pumps operate normally at two vastly different pressures. Left ventricular systolic pressures being approximately five times higher than that of the right ventricle, its wall tension is much higher, resulting in the increased wall thickness of the left ventricular chamber. The effect of the increased muscle mass on the left side leads to dominance of the left-sided hydrodynamic forces described above. This results in the left ventricular apex as the only area of normal contact during systole. The rest of the heart essentially retracts from the chest wall. In a normal heart, this retraction of the chest wall can be observed to be located medial to the apical impulse and involving part of the left anterior chest wall (20). Even the right ventricle, which is anatomically an anterior structure, is normally pulled away from the chest wall because of its own contraction (becoming smaller) and, more importantly, the septal contraction also pulling the right ventricle posteriorly. This retraction observed in normal patients is located medial to the apical impulse (23,24). It can be best appreciated with patients in the left lateral decu-bitus position with a palpating finger only on the apical impulse with clear view of the rest of the precordium for proper observation of the inward movement of the retraction (opposite in direction to the outward movement of the apical impulse). This "medial retraction" identifies and indicates that the left ventricle forms the apical impulse. The extent of the area of medial retraction may be variable depending on both cardiac and extracardiac factors such as the compliance of the chest wall. It may sometimes be noted only over a small area very close to the apex beat.
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.
Pulmonary embolism (PE) can be detected and investigated through several tests:
Pulse oximetry monitors for hypoxemia and oxygen supplementation is initiated, while further tests are done. Electrocardiograms can show changes indicating conditions like pulmonary embolism or right heart strain. Arterial blood gases may demonstrate hypoxemia, hypocapnia, or acidosis in PE. Chest x-rays can reveal signs of PE like enlarged heart size or perfusion deficits on lung scans. D-dimer tests if elevated suggest a thrombus, while normal levels rule out recent clots. CT pulmonary angiograms are best to diagnose or rule out PE due to speed, availability and ability to detect other lung abnormalities
Lec 3 management of acute pulmonary oedema for mohsEhealthMoHS
This document discusses acute pulmonary edema, which is fluid accumulation in the lungs due to increased pressure in the pulmonary capillaries as a result of left ventricular failure. It provides details on the pathophysiology, causes, symptoms, investigations, treatment and management. The treatment goals are to reduce preload and afterload on the heart to decrease pulmonary capillary pressure and increase cardiac output. Initial treatment involves oxygen, diuretics, vasodilators and inotropic drugs. More severe cases require intensive care monitoring and support like ventilation and inotropes administered via Swan-Ganz catheter.
This document discusses the use of echocardiography in critically ill patients. It outlines the key views and assessments that can be done at the bedside, including estimating volume status, diagnosing causes of circulatory failure, assessing left ventricular function, and distinguishing between cardiogenic and non-cardiogenic pulmonary edema. The document provides guidance on obtaining standard echocardiographic views like the parasternal long axis and apical four-chamber views. It also describes how to use echocardiography to evaluate volume status, diagnose tamponade, measure right ventricular systolic pressure, and calculate cardiac output.
This document contains descriptions and images related to various chest radiographic findings. It discusses topics like atelectasis, consolidation, masses, pneumothorax, vascular markings and abnormalities of the heart and lungs. Examples provided include lung cancer, tuberculosis, pneumonectomy and other pathologies. Key radiographic signs are defined to aid in diagnosis, such as the silhouette sign, S-shaped fissure and tracheal shift.
This document provides an overview of lung ultrasound and discusses various lung pathologies that can be identified using ultrasound. It begins with background on lung anatomy and ultrasound principles. Various normal and abnormal findings are then described, including pneumothorax, pulmonary edema, consolidation, pleural effusions, and lung tumors. Case studies are presented to demonstrate ultrasound identification of conditions like emphysema, pneumonia, pulmonary edema, pneumothorax, and lung cancer. The document emphasizes that lung ultrasound allows accurate diagnosis of many lung conditions at the point of care based on visualization of artifacts, B-lines, lung sliding, and consolidations.
Valvular heart disease refers to abnormalities of the heart valves that result in obstruction of blood flow or backflow of blood. Echocardiography plays a key role in evaluating valve function and structure non-invasively. Common valvular abnormalities include aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Treatment depends on severity and symptoms, ranging from medical management to surgical repair or replacement of the affected valve.
The document summarizes key aspects of respiratory system anatomy and physiology, as well as respiratory assessment and management for an EMT. It describes the main components and functions of the respiratory system, signs of respiratory distress, methods for assessing breathing and circulation, and protocols for providing initial management and oxygenation based on a patient's responsiveness and breathing status. Treatment may involve opening the airway, suctioning, assisting ventilation, and administering oxygen and bronchodilators as appropriate.
Radiographic Presentation of Congenital Heart DiseaseTarique Ajij
1. The document discusses the radiographic presentation of various congenital heart diseases including atrial septal defects, ventricular septal defects, patent ductus arteriosus, atrioventricular septal defects, pulmonic stenosis, aortic stenosis, coarctation of the aorta, tetralogy of Fallot, Ebstein's anomaly, transposition of the great arteries, truncus arteriosus, and total anomalous pulmonary venous connection.
2. Key findings on chest x-rays are described such as enlargement of specific heart chambers, changes in pulmonary vascularity, positioning of the great vessels, and rib notching.
3. Diagnosis is made through precordial examination, echocard
The document provides information on electrocardiogram (ECG) findings and their significance in patients presenting with syncope. It discusses diagnostic criteria and risk stratification tools for evaluating causes of syncope, including the CHESS criteria and San Francisco Syncope Rule. Important ECG findings that warrant further investigation or indicate an underlying cardiac condition are highlighted, such as arrhythmias, conduction abnormalities, signs of ischemia, and structural heart disease. Specific arrhythmias and cardiac conditions like long QT syndrome and Brugada syndrome are also reviewed in the context of evaluating syncope.
This document provides an overview of dyspnea, or shortness of breath. It defines dyspnea and outlines its physiological and clinical definitions. Common causes of dyspnea are then discussed, including pulmonary issues like COPD, pneumonia, and pulmonary embolism, as well as cardiac issues like heart failure, coronary syndromes, and dysrhythmias. The pathophysiology of how these conditions can stimulate breathing and cause the sensation of dyspnea is explained. Finally, the document discusses assessing and diagnosing patients presenting with dyspnea through clinical exams, investigations like chest x-rays, and determining if the cause is chronic or acute.
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 paroxysmal supraventricular tachycardia (PSVT), which represents a subset of supraventricular tachycardias (SVTs) characterized by abrupt onset and termination of a regular, rapid tachycardia. The main types of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) involving an accessory pathway. The document provides details on the mechanisms, clinical presentations, evaluations and management of these arrhythmias. Vagal maneuvers and adenosine are first-line treatment options that can terminate the tachycardias by slowing conduction through the at
A 45-year-old man presented with a 2-month history of cough and hemoptysis. Imaging showed a 7x7.5x6 cm lobulated cystic lesion in the left lower lobe with surrounding consolidation. CT findings were suggestive of an infected bronchogenic cyst. Bronchogenic cysts are congenital malformations that result from aberrant embryological budding of the tracheobronchial tree. They typically appear on imaging as well-defined smooth lesions and can become infected, leading to symptoms like cough.
This document discusses the stages of pulmonary edema seen on chest x-rays and associated wedge pressures. Stage I shows early signs like deer antler sign and Kerley B lines with pressures of 12-18 mmHg. Stage II shows interstitial edema on x-ray with pressures of 19-25 mmHg. Stage III is alveolar edema appearing as bat wing shadowing on x-ray associated with pressures over 25 mmHg.
This document presents the case of a 4-year-old boy with tetralogy of Fallot. The key details are:
- He has had cyanosis, breathlessness and fainting episodes since infancy.
- Examination found cyanosis, clubbing and a grade IV/VI systolic murmur. Echocardiogram showed severe pulmonary stenosis, VSD, and RV hypertrophy consistent with tetralogy of Fallot.
- If left untreated, tetralogy of Fallot can cause serious complications like strokes from anoxic spells or cerebral thrombosis. Surgical repair is usually recommended in childhood.
Non-cardiogenic pulmonary edema (NPE) can have many causes that result in increased pulmonary capillary permeability and fluid leakage into the lungs. These include conditions like acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema, renal failure, negative pressure pulmonary edema, high altitude pulmonary edema, drug overdoses, chemotherapy, and more. The pathogenesis usually involves elevated pulmonary vascular pressures or a direct injury to the lung tissues. Radiographically, NPE presents as diffuse bilateral infiltrates that resolve more quickly than cardiogenic pulmonary edema, lacking features like Kerley lines or enlarged heart size.
Ultrasound is a useful screening tool for the lungs but has limitations. An 8-view ultrasound exam of the lungs can detect extravascular lung water seen as B lines originating from the pleural line. While a normal exam has evenly spaced A lines, more than 2 B lines in any view outside the lung bases indicates abnormality. Ultrasound has good sensitivity and specificity for detecting diffuse lung abnormalities compared to chest x-ray, but can miss localized findings and has a 15% error rate in certain conditions like fibrosis or resolving illnesses.
Approach to cyanotic congenital heart diseaseikramdr01
This document provides guidance on diagnosing cyanotic congenital heart disease through a practical clinical approach. It emphasizes the importance of suspecting heart disease in any child who does not clearly fit the initial diagnosis or has significant desaturation. Key signs to look for include cyanosis, differential pulse oximetry readings, and clues from chest X-ray and ECG. The approach involves classifying heart defects based on hemodynamics like pulmonary blood flow and systemic saturation. For neonates, focus is on duct-dependent lesions presenting with cyanosis or shock. Beyond the neonatal period, diagnosis involves assessing cyanosis and pulmonary congestion to identify lesions like left-to-right shunts, tetralogy of Fallot physiology,
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.
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.
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.
Pulmonary embolism (PE) can be detected and investigated through several tests:
Pulse oximetry monitors for hypoxemia and oxygen supplementation is initiated, while further tests are done. Electrocardiograms can show changes indicating conditions like pulmonary embolism or right heart strain. Arterial blood gases may demonstrate hypoxemia, hypocapnia, or acidosis in PE. Chest x-rays can reveal signs of PE like enlarged heart size or perfusion deficits on lung scans. D-dimer tests if elevated suggest a thrombus, while normal levels rule out recent clots. CT pulmonary angiograms are best to diagnose or rule out PE due to speed, availability and ability to detect other lung abnormalities
Lec 3 management of acute pulmonary oedema for mohsEhealthMoHS
This document discusses acute pulmonary edema, which is fluid accumulation in the lungs due to increased pressure in the pulmonary capillaries as a result of left ventricular failure. It provides details on the pathophysiology, causes, symptoms, investigations, treatment and management. The treatment goals are to reduce preload and afterload on the heart to decrease pulmonary capillary pressure and increase cardiac output. Initial treatment involves oxygen, diuretics, vasodilators and inotropic drugs. More severe cases require intensive care monitoring and support like ventilation and inotropes administered via Swan-Ganz catheter.
This document discusses the use of echocardiography in critically ill patients. It outlines the key views and assessments that can be done at the bedside, including estimating volume status, diagnosing causes of circulatory failure, assessing left ventricular function, and distinguishing between cardiogenic and non-cardiogenic pulmonary edema. The document provides guidance on obtaining standard echocardiographic views like the parasternal long axis and apical four-chamber views. It also describes how to use echocardiography to evaluate volume status, diagnose tamponade, measure right ventricular systolic pressure, and calculate cardiac output.
This document contains descriptions and images related to various chest radiographic findings. It discusses topics like atelectasis, consolidation, masses, pneumothorax, vascular markings and abnormalities of the heart and lungs. Examples provided include lung cancer, tuberculosis, pneumonectomy and other pathologies. Key radiographic signs are defined to aid in diagnosis, such as the silhouette sign, S-shaped fissure and tracheal shift.
This document provides an overview of lung ultrasound and discusses various lung pathologies that can be identified using ultrasound. It begins with background on lung anatomy and ultrasound principles. Various normal and abnormal findings are then described, including pneumothorax, pulmonary edema, consolidation, pleural effusions, and lung tumors. Case studies are presented to demonstrate ultrasound identification of conditions like emphysema, pneumonia, pulmonary edema, pneumothorax, and lung cancer. The document emphasizes that lung ultrasound allows accurate diagnosis of many lung conditions at the point of care based on visualization of artifacts, B-lines, lung sliding, and consolidations.
Valvular heart disease refers to abnormalities of the heart valves that result in obstruction of blood flow or backflow of blood. Echocardiography plays a key role in evaluating valve function and structure non-invasively. Common valvular abnormalities include aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Treatment depends on severity and symptoms, ranging from medical management to surgical repair or replacement of the affected valve.
The document summarizes key aspects of respiratory system anatomy and physiology, as well as respiratory assessment and management for an EMT. It describes the main components and functions of the respiratory system, signs of respiratory distress, methods for assessing breathing and circulation, and protocols for providing initial management and oxygenation based on a patient's responsiveness and breathing status. Treatment may involve opening the airway, suctioning, assisting ventilation, and administering oxygen and bronchodilators as appropriate.
Radiographic Presentation of Congenital Heart DiseaseTarique Ajij
1. The document discusses the radiographic presentation of various congenital heart diseases including atrial septal defects, ventricular septal defects, patent ductus arteriosus, atrioventricular septal defects, pulmonic stenosis, aortic stenosis, coarctation of the aorta, tetralogy of Fallot, Ebstein's anomaly, transposition of the great arteries, truncus arteriosus, and total anomalous pulmonary venous connection.
2. Key findings on chest x-rays are described such as enlargement of specific heart chambers, changes in pulmonary vascularity, positioning of the great vessels, and rib notching.
3. Diagnosis is made through precordial examination, echocard
The document provides information on electrocardiogram (ECG) findings and their significance in patients presenting with syncope. It discusses diagnostic criteria and risk stratification tools for evaluating causes of syncope, including the CHESS criteria and San Francisco Syncope Rule. Important ECG findings that warrant further investigation or indicate an underlying cardiac condition are highlighted, such as arrhythmias, conduction abnormalities, signs of ischemia, and structural heart disease. Specific arrhythmias and cardiac conditions like long QT syndrome and Brugada syndrome are also reviewed in the context of evaluating syncope.
This document provides an overview of dyspnea, or shortness of breath. It defines dyspnea and outlines its physiological and clinical definitions. Common causes of dyspnea are then discussed, including pulmonary issues like COPD, pneumonia, and pulmonary embolism, as well as cardiac issues like heart failure, coronary syndromes, and dysrhythmias. The pathophysiology of how these conditions can stimulate breathing and cause the sensation of dyspnea is explained. Finally, the document discusses assessing and diagnosing patients presenting with dyspnea through clinical exams, investigations like chest x-rays, and determining if the cause is chronic or acute.
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 paroxysmal supraventricular tachycardia (PSVT), which represents a subset of supraventricular tachycardias (SVTs) characterized by abrupt onset and termination of a regular, rapid tachycardia. The main types of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) involving an accessory pathway. The document provides details on the mechanisms, clinical presentations, evaluations and management of these arrhythmias. Vagal maneuvers and adenosine are first-line treatment options that can terminate the tachycardias by slowing conduction through the at
A 45-year-old man presented with a 2-month history of cough and hemoptysis. Imaging showed a 7x7.5x6 cm lobulated cystic lesion in the left lower lobe with surrounding consolidation. CT findings were suggestive of an infected bronchogenic cyst. Bronchogenic cysts are congenital malformations that result from aberrant embryological budding of the tracheobronchial tree. They typically appear on imaging as well-defined smooth lesions and can become infected, leading to symptoms like cough.
This document discusses the stages of pulmonary edema seen on chest x-rays and associated wedge pressures. Stage I shows early signs like deer antler sign and Kerley B lines with pressures of 12-18 mmHg. Stage II shows interstitial edema on x-ray with pressures of 19-25 mmHg. Stage III is alveolar edema appearing as bat wing shadowing on x-ray associated with pressures over 25 mmHg.
This document presents the case of a 4-year-old boy with tetralogy of Fallot. The key details are:
- He has had cyanosis, breathlessness and fainting episodes since infancy.
- Examination found cyanosis, clubbing and a grade IV/VI systolic murmur. Echocardiogram showed severe pulmonary stenosis, VSD, and RV hypertrophy consistent with tetralogy of Fallot.
- If left untreated, tetralogy of Fallot can cause serious complications like strokes from anoxic spells or cerebral thrombosis. Surgical repair is usually recommended in childhood.
Non-cardiogenic pulmonary edema (NPE) can have many causes that result in increased pulmonary capillary permeability and fluid leakage into the lungs. These include conditions like acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema, renal failure, negative pressure pulmonary edema, high altitude pulmonary edema, drug overdoses, chemotherapy, and more. The pathogenesis usually involves elevated pulmonary vascular pressures or a direct injury to the lung tissues. Radiographically, NPE presents as diffuse bilateral infiltrates that resolve more quickly than cardiogenic pulmonary edema, lacking features like Kerley lines or enlarged heart size.
Ultrasound is a useful screening tool for the lungs but has limitations. An 8-view ultrasound exam of the lungs can detect extravascular lung water seen as B lines originating from the pleural line. While a normal exam has evenly spaced A lines, more than 2 B lines in any view outside the lung bases indicates abnormality. Ultrasound has good sensitivity and specificity for detecting diffuse lung abnormalities compared to chest x-ray, but can miss localized findings and has a 15% error rate in certain conditions like fibrosis or resolving illnesses.
Approach to cyanotic congenital heart diseaseikramdr01
This document provides guidance on diagnosing cyanotic congenital heart disease through a practical clinical approach. It emphasizes the importance of suspecting heart disease in any child who does not clearly fit the initial diagnosis or has significant desaturation. Key signs to look for include cyanosis, differential pulse oximetry readings, and clues from chest X-ray and ECG. The approach involves classifying heart defects based on hemodynamics like pulmonary blood flow and systemic saturation. For neonates, focus is on duct-dependent lesions presenting with cyanosis or shock. Beyond the neonatal period, diagnosis involves assessing cyanosis and pulmonary congestion to identify lesions like left-to-right shunts, tetralogy of Fallot physiology,
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.
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.
This document discusses venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE). It notes that VTE causes 100,000 to 180,000 deaths annually and is a preventable cause of death in hospitalized patients. Risk factors discussed include conditions like obesity, hypertension, diabetes, smoking, and hypercholesterolemia. The document reviews the anatomy of veins and pulmonary arteries involved in VTE, types of PE, pathogenesis, clinical presentation, diagnostic tests including D-dimer, Wells criteria for assessing pre-test probability, and imaging options like CT pulmonary angiography.
This document summarizes the diagnostic criteria and causes of misdiagnosis for computed tomography angiography (CTA) of pulmonary embolism (PE). It outlines the diagnostic criteria for acute and chronic PE seen on CTA images, including signs such as intraluminal filling defects and vessel occlusion. It then discusses numerous technical, anatomic and pathological factors that can cause misdiagnosis of PE on CTA images, such as respiratory motion artifact, image noise, vascular bifurcations and lymph node enlargement. Patient-related, equipment and interpretation factors are all reviewed in detail to help reduce incorrect diagnosis.
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.
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 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.
A lecture highlighting the role of Echocardiography as a major hemodynamic monitoring tool in the Intensive Care settings and the assessment of loading conditions.
Presentation1.pptx, radiological imaging of pulmonary embolism.Abdellah Nazeer
This document discusses pulmonary embolism (PE), which occurs when a blood clot or other substance blocks a pulmonary artery in the lungs. PE is commonly caused by deep vein thrombosis. The document outlines common symptoms of PE and risk factors. It then describes various radiological imaging techniques used to diagnose PE, including chest X-rays, CT scans, ultrasound, V/Q scans, pulmonary angiograms, and MRI. The document discusses diagnostic criteria for PE on CT imaging and provides examples of images showing acute and chronic PE. It also covers D-dimer testing and describes the appearance of massive, saddle, and bilateral PE on CT scans.
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
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.
Hemodynamic monitoring involves measuring the motion of blood through the body and interpreting how the cardiovascular system is performing. The goal is optimizing oxygen delivery. Key metrics include cardiac output, arterial and venous oxygen levels, and oxygen delivery and consumption. Common monitoring methods are non-invasive blood pressure, arterial catheters, central venous pressure, pulmonary artery catheters, and pulse oximetry. Each method has advantages and limitations for assessing hemodynamics and tissue oxygenation. Careful interpretation of the data is important for clinical decision making.
Cyanotic congenital heart disease is characterized by a right-to-left shunt and decreased pulmonary blood flow, causing hypoxemia and cyanosis. Tetralogy of Fallot is a common cyanotic heart defect where there is a ventricular septal defect, right ventricular outflow tract obstruction, overriding aorta, and right ventricular hypertrophy. Without surgical intervention, most patients would not survive beyond childhood. Complete repair aims to relieve obstruction and close defects, but may require multiple staged procedures. Preoperative evaluation focuses on assessing cyanosis, growth, polycythemia, and identifying other anomalies to optimize timing of repair.
Pulmonary embolism.pptx by mcac rms ct findingsLaithLutfi1
Pulmonary embolism.pptx by mcac rms ct findings
What Is Pulmonary Embolism (Pulmonary Embolus)?
A pulmonary embolism is a sudden blockage in your pulmonary arteries, the blood vessels that send blood to your lungs. It usually happens when a blood clot in the deep veins in your leg breaks off and travels to your lungs.
A blood clot that travels to another part of your body is called an embolus. When an embolus blocks a blood vessel it's called an embolism. When a pulmonary embolus blocks blood flow to your lungs, it's called a pulmonary embolism
The most common cause of a pulmonary embolism is a the breaking off of a blood clot in your leg's deep veins, known as deep vein thrombosis (DVT). Other, rare causes of a pulmonary embolism include:
Air bubbles
DVT in the upper body
Fat embolus, usually from a severely broken bone
Tumors
You are more likely to develop blood clots if you have risk factors such as:
Cancer
Family history of blood clots or clotting disorders
Heart disease
Health history of blood clots or clotting disorders
Long-term use of birth control pills or estrogen therapy
A pulmonary embolism is also more likely to develop after:
Childbirth
Heart attack or stroke
Long plane or car rides
Long-term bedrest
Severe injuries, burns or fractures
Surgery
Pulmonary Embolism Symptoms
You may not have any symptoms of a pulmonary embolism, depending on the size of the clot and your overall health. As blood flow becomes more and more blocked, you may experience symptoms such as:
Coughing, including a cough that produces bloody mucus
Dizziness
Heart palpitations, sensations of your heart racing or pounding
Leg pain or swelling
Sharp and sudden chest pain
Shortness of breath that worsens with exertion
Pulmonary Embolism Complications
A pulmonary embolism can be life-threatening without treatment. It can cause several complications, including:
Cardiac arrest, when your heart suddenly stops beating
Cardiac arrhythmia, an irregular heart rhythm
Pleural effusion, fluid buildup in the membrane around your lungs (pleura
Pulmonary hypertension, high blood pressure in your lungs
Pulmonary infarction, when lung tissue dies
Diagnosing a Pulmonary Embolism
To diagnose a pulmonary embolism, your doctor does a physical exam, asks about your symptoms and orders one or more tests such as:
Blood tests to check if you have an increased risk of blood clotting
Chest X-rays to take pictures of your heart and lungs
CT pulmonary angiography, using X-rays and specialized computers to create cross-sectional, 3D images of your lungs and pulmonary arteries
Doppler ultrasound, using sound waves to look for deep vein thrombosis in your legs
Echocardiogram to view your heart's structures and blood vessels
Lab tests, such as pulse oximetry to measure oxygen levels in your blood or arterial blood gas tests to measure the balance of oxygen and carbon dioxide
Pulmonary angiogram, using a small, hollow tube (catheter) and a contrast dye to see how blood flows through the pulmonary A
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.
Cardiogenicshock by Dr.Afroza Prioty -140123092109-phpapp02Afroza Prioty
1) Cardiogenic shock is a clinical condition caused by the heart's inability to pump an adequate amount of blood to vital organs, resulting in inadequate tissue perfusion.
2) The document discusses the causes, pathophysiology, clinical manifestations, diagnosis, and management of cardiogenic shock, with a focus on cardiogenic shock caused by acute myocardial infarction.
3) Early revascularization through percutaneous coronary intervention or coronary artery bypass grafting is recommended for suitable patients with cardiogenic shock due to acute myocardial infarction, along with supportive therapies like intra-aortic balloon pump counterpulsation or ventricular assist devices.
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.
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
Constrictive pericarditis is caused by scarring and thickening of the pericardium, restricting cardiac filling. It is diagnosed using echocardiography which shows septal bounce, exaggerated mitral inflow, and hepatic vein reversal. While similar to restrictive cardiomyopathy, constrictive pericarditis shows increased ventricular interaction and respiratory effects on cardiac physiology. Surgical pericardiectomy is usually required for treatment but is high risk, with post-op complications common. Long-term survival depends on the underlying cause of constriction.
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.
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.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
2. DVT : Blood clot formation with inDVT : Blood clot formation with in
the large veins usually in the legsthe large veins usually in the legs
PE results from DVTs that havePE results from DVTs that have
broken off and travelled tobroken off and travelled to
pulmonary arterial circulationpulmonary arterial circulation
The majority of pulmonary emboliThe majority of pulmonary emboli
( 80%) arise from the propagation of( 80%) arise from the propagation of
lower limb DVTlower limb DVT
Other causes : Air, AmnioticOther causes : Air, Amniotic
Fluid, Fat EmbolismFluid, Fat Embolism
Venous thromboembolism
DVT
Pulmonary
Embolism
4. Why it is important?Why it is important?
PE is the most common preventable cause ofPE is the most common preventable cause of
death in hospitalized patientsdeath in hospitalized patients
Majority of patient die because of failure ofMajority of patient die because of failure of
diagnosis rather than inadequate therapy.diagnosis rather than inadequate therapy.
80% of pulmonary emboli occur without prior80% of pulmonary emboli occur without prior
warning signs or symptomswarning signs or symptoms
Mortality rate without treatment is 30%,Mortality rate without treatment is 30%,
whereas with adequate treatment is only 2-8%whereas with adequate treatment is only 2-8%
Early treatment is highly effectiveEarly treatment is highly effective
9. Hypercoagulability
Hereditary Deficiencies:
Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden
Prothrombin gene
mutation
Dysfibrinogenemia
Acquired:
Cancer
Pregnancy & postpartum
period
Oral contraceptives
Hormone replacement
therapy
Polycythemia rubravera
Smoking
Anti phospholipid syndrome
Chemotherapy
Stasis
Immobility/cast/travel
Advanced age
Acute medical illness
Major surgery
Spinal cord injury
Obesity
Endothelial Damage
Major surgery
Trauma
Central venous
catheterization
Risk for thromboembolism approximately doubles for each decade beyond
age 60 years
Risk factors
10. Major Risk (RR 5-20)Major Risk (RR 5-20)
•Major and abdominal surgeryMajor and abdominal surgery
•Lower Limb OrthopedicLower Limb Orthopedic SurgerySurgery
•Obstetric – Late preganancy,Obstetric – Late preganancy,
LSCS, Pre eclampsiaLSCS, Pre eclampsia
•Maliganancy- Pelvic ,Maliganancy- Pelvic ,
abdominal or metastaticabdominal or metastatic
•Lower Leg # , varicose veinsLower Leg # , varicose veins
•History of proven VTEHistory of proven VTE
Minor Risk Factors ( RR
CVS : HF, HTN, Congenital
Heart Disease, Central lines
Estrogen : OCP, HRT
Others : Occult malignancy,
COPD
Neurological disability, obesity,
thrombotic mayeloproliferative
disease, nephrotic syndrome
Inflammatory bowel disease
Risk factors
18. Contd…Contd…
ECGECG
Sinus tachycardia –Sinus tachycardia – m/c abnormality m/c abnormality
Complete or incomplete RBBB –Complete or incomplete RBBB – a/w ↑ mortality a/w ↑ mortality
RV strain pattern –RV strain pattern – T wave ↓ in the right precordial leads T wave ↓ in the right precordial leads
(V1-4) ± the inferior leads(V1-4) ± the inferior leads
Right axis deviationRight axis deviation
S1, Q3, T3 patternS1, Q3, T3 pattern
Right atrial enlargement (P pulmonale) –Right atrial enlargement (P pulmonale) – peaked Ppeaked P
wave in lead II > 2.5 mm in heightwave in lead II > 2.5 mm in height
Atrial Tachyarrhythmias –Atrial Tachyarrhythmias – AF, Flutter AF, Flutter
Non specific ST-segment & T wave changesNon specific ST-segment & T wave changes
23. Chest X-rayChest X-ray
Chest X ray – most common finding with aChest X ray – most common finding with a
PE is a normal x-rayPE is a normal x-ray
But they are useful as X-rays help to ruleBut they are useful as X-rays help to rule
out pneumonia and pneumothorax asout pneumonia and pneumothorax as
causes of dyspnoea etccauses of dyspnoea etc
A normal CXR in the presence ofA normal CXR in the presence of
significant dyspnoea and hypoxemia insignificant dyspnoea and hypoxemia in
absence of bronchospasm and anatomicabsence of bronchospasm and anatomic
cardiac shunt is highly suggestive of PEcardiac shunt is highly suggestive of PE
24. Chest XrayChest Xray
Chest radiograph findings in patient withChest radiograph findings in patient with
pulmonary embolismpulmonary embolism
ResultResult PercentPercent
CardiomegalyCardiomegaly 27%27%
Normal studyNormal study 24%24%
AtelectasisAtelectasis 23%23%
Elevated HemidiaphragmElevated Hemidiaphragm 20%20%
Pulmonary Artery EnlargementPulmonary Artery Enlargement 19%19%
Pleural EffusionPleural Effusion 18%18%
Parenchymal Pulmonary InfiltrateParenchymal Pulmonary Infiltrate 17%17%
Am Heart J
1997;134:479-87
25. Radiographic signs of acute pulmonaryRadiographic signs of acute pulmonary
embolismembolism
Signs with relative high specificity but lowSigns with relative high specificity but low
sensitivity for acute pulmonary embolism:sensitivity for acute pulmonary embolism:
Decreased vascularity in the peripheral lungDecreased vascularity in the peripheral lung (Westermark sign).(Westermark sign).
Enlargement of the central pulmonary arteryEnlargement of the central pulmonary artery (Fleischner sign).(Fleischner sign).
Enlarged right descending pulmonary arteryEnlarged right descending pulmonary artery (Palla's sign)(Palla's sign)
Pleural based areas of increased opacity (Pleural based areas of increased opacity (Hampton humpHampton hump).).
Hemidiaphragm elevation.Hemidiaphragm elevation.
26. (Hampton hump)(Hampton hump)
•The classic radiographic findings of
pulmonary infarction
• a wedge-shaped, pleura-based
triangular opacity with an apex
pointing toward the hilus
30. D-dimerD-dimer
By-product of fibrinBy-product of fibrin
degradationdegradation
As clot degraded byAs clot degraded by
enzymes, Fibrinenzymes, Fibrin
Degradation ProductsDegradation Products
(FDP) are released, one(FDP) are released, one
of these is the D-dimerof these is the D-dimer
Little clots in body releaseLittle clots in body release
D-dimers, therefore if testD-dimers, therefore if test
+ve - do not know if it is+ve - do not know if it is
from a PE,from a PE,
But test is so sensitiveBut test is so sensitive
that if no D-dimer ( –ve)that if no D-dimer ( –ve)
you can rule out PEyou can rule out PE
31. CTPACTPA
Contrast injected into body,Contrast injected into body,
CT Scan obtained as this isCT Scan obtained as this is
occurringoccurring
Vessels viewed on end andVessels viewed on end and
seen if they light up withseen if they light up with
contrast.contrast.
If only partially light up withIf only partially light up with
contrast there may be a bloodcontrast there may be a blood
clot present stopping flowclot present stopping flow
Do not use if in renal failureDo not use if in renal failure
((Creatanine) (could useCreatanine) (could use
HCOHCO33 cover to stopcover to stop
nephrotoxic effect of contrast)nephrotoxic effect of contrast)
Unlike VQ Scan if patient hasUnlike VQ Scan if patient has
a pneumonia it will not affecta pneumonia it will not affect
resultsresults
32. CT findings of acute pulmonary embolismCT findings of acute pulmonary embolism
Vascular abnormalities:Vascular abnormalities:
Intraluminal filling defects that forms an acute angle withIntraluminal filling defects that forms an acute angle with
the vessel wall & may be surrounded by contrast materialthe vessel wall & may be surrounded by contrast material
(polo mint sign or railway sign).(polo mint sign or railway sign).
Total cutoff of vascular enhancement.Total cutoff of vascular enhancement.
Enlargement of the occluded vessel.Enlargement of the occluded vessel.
Ancillary findings:Ancillary findings:
Pleural based wedge shaped areas of increased attenuationPleural based wedge shaped areas of increased attenuation
with no contrast enhancement.with no contrast enhancement.
Linear atelectasis.Linear atelectasis.
33. Partial eccentric filling defect with acutePartial eccentric filling defect with acute
angle with the vessel wallangle with the vessel wall
36. V /Q lung scanning remains an option andV /Q lung scanning remains an option and
cancan be used when CTA is not available or isbe used when CTA is not available or is
contraindicated.contraindicated.
V /Q Scan
Advantages
relatively low radiation dose
no requirement for contrast
dye
Limitations
Unreliable in pts with COPD and
other conditions in which there is
structural Lung disease
When holding breath is difficult.
38. Probability of PEProbability of PE
Normal - Full ventilationNormal - Full ventilation
and perfusion seenand perfusion seen
Low Pobability for PE –Low Pobability for PE –
(<20%)(<20%)
Intermediate probabilityIntermediate probability
for PE-for PE- V andV and P inP in
same areasame area
(Matched deficit) (20-(Matched deficit) (20-
80%)80%)
High Probability for PE –High Probability for PE –
Normal V andNormal V and P (Un-P (Un-
Matched deficit) (>80%)Matched deficit) (>80%)
40. EchocardiographyEchocardiography
This modality generally hasThis modality generally has
limited accuracy in thelimited accuracy in the
diagnosis.diagnosis.
The overall sensitivity andThe overall sensitivity and
specificity for diagnosis ofspecificity for diagnosis of
central and peripheralcentral and peripheral
pulmonary embolism bypulmonary embolism by
ECHO is 59% and 77%.ECHO is 59% and 77%.
It may allow diagnosis ofIt may allow diagnosis of
other conditions that may beother conditions that may be
confused with pulmonaryconfused with pulmonary
embolism.embolism.
41. ECHO signs of PEECHO signs of PE
RV enlargementRV enlargement
Hypokinesis especially free wall hypokinesis, withHypokinesis especially free wall hypokinesis, with
sparing of the apexsparing of the apex (the McConnell’s sign)(the McConnell’s sign)
Interventricular septal flattening and paradoxicalInterventricular septal flattening and paradoxical
motion toward the LV resulting in a “D-shaped” LV inmotion toward the LV resulting in a “D-shaped” LV in
cross section.cross section.
Tricuspid regurgitationTricuspid regurgitation
Lack of inspiratory collapse of IVCLack of inspiratory collapse of IVC
Direct visualization of thrombusDirect visualization of thrombus
60/60 Sign-60/60 Sign- Acceleration time of RV ejection <60ms inAcceleration time of RV ejection <60ms in
the presence of TR pressure gradient </= 60mmHg.the presence of TR pressure gradient </= 60mmHg.
43. ECHOECHO
The severity of this PulmonaryThe severity of this Pulmonary
Artery Pressure (PAP) and theArtery Pressure (PAP) and the
severity of the clot, is found byseverity of the clot, is found by
looking at the tricuspid valvelooking at the tricuspid valve
and noting how much regurgeand noting how much regurge
occurs (Tricuspid jet)occurs (Tricuspid jet)
If tricuspid jet is high then PAPIf tricuspid jet is high then PAP
differential between RA anddifferential between RA and
RV is great and the clot burdenRV is great and the clot burden
is largeis large
All these tests may help in theAll these tests may help in the
possible diagnosis of a PE, butpossible diagnosis of a PE, but
are not definitive testsare not definitive tests
44.
45. UltrasoundUltrasound
Non-invasiveNon-invasive
Looks at lower limbsLooks at lower limbs
Doppler USS looks atDoppler USS looks at
vein for flow andvein for flow and
compressibilty to seecompressibilty to see
if clot presentif clot present
46. Magnetic resonance angiographyMagnetic resonance angiography
(MRA)(MRA)
MRA appears promising & avoids ionising radiation but has poor
sensitivity for subsegmental clot.
47. MRA findingsMRA findings
Visualization of the intravascular fillingVisualization of the intravascular filling
defect.defect.
Provide physiologic information includingProvide physiologic information including
the regional distribution of ventilation &the regional distribution of ventilation &
perfusion.perfusion.
49. Pulmonary angiographicPulmonary angiographic
findingsfindings
Primary signs:Primary signs:
The only primary sign of acute pulmonaryThe only primary sign of acute pulmonary
embolism is filling defect.embolism is filling defect.
Secondary signs:Secondary signs:
Abrupt occlusion of pulmonary artery.Abrupt occlusion of pulmonary artery.
Areas of oligemia with pruning of theAreas of oligemia with pruning of the
branching vessels.branching vessels.
50. cardiac troponinscardiac troponins
•Recently, cardiac troponins I and T have been
shown to be associated with early mortality and
a complicated hospital course in patients with
PE.
The assessment of cardiac plasma troponin
levels revealed ventricular injury, especially in
patients with massive PE who had hypotension
or shock.
51. B Natriuretic PeptideB Natriuretic Peptide
(BNP)(BNP)
•BNP is a neurohormone secreted from the
cardiac ventricles in response to dilatation or
an increase of pressure.
• BNP levels may increase with right ventricle
dysfunction when the patients is in bed and
decrease with treatment.
•Serum brain natriuretic peptide levels of > 90 pg/mL
have a sensitivity of 85% and a specificity of 75% for
predicting adverse clinical outcomes
54. Treatment optionsTreatment options
Symptomatic treatment:Symptomatic treatment:
– ABCD approachABCD approach
– OxygenOxygen
– AnalgesiaAnalgesia
Anticoagulation:Anticoagulation:
– IV HeparinIV Heparin
– S/C LMWH eg Enoxaparine, DalteparineS/C LMWH eg Enoxaparine, Dalteparine
– Oral WarfarinOral Warfarin
IVC filter:IVC filter: If there is contra-indications for anti-coagulationIf there is contra-indications for anti-coagulation
Thrombolysis:Thrombolysis: tPA eg Alteplase, TenectaplasetPA eg Alteplase, Tenectaplase
Surgical procedures:Surgical procedures: Pulmonary embolectomyPulmonary embolectomy
55. General MeasureGeneral Measure
Oxygen inhalationOxygen inhalation
Opiates to relieve painOpiates to relieve pain
Circulatory shock should be treated with I/V fluidCirculatory shock should be treated with I/V fluid
and plasma expenderand plasma expender
Inotropic agents have limited value as hypoxicInotropic agents have limited value as hypoxic
dilated right ventricle maximally stimulated bydilated right ventricle maximally stimulated by
endogenous catecolaminesendogenous catecolamines
Diuretics and vasodilator should be avoidedDiuretics and vasodilator should be avoided
because they reduce the cardiac output.because they reduce the cardiac output.
Precordial thump , which may dislodge thePrecordial thump , which may dislodge the
thrombusthrombus
56. AnticoagulationAnticoagulation
Ideally start Fast acting and slow acting anticoagulants,Ideally start Fast acting and slow acting anticoagulants,
when slow acting anticoagulants at desired level, stopwhen slow acting anticoagulants at desired level, stop
fast actingfast acting
Fast acting -Heparin productsFast acting -Heparin products
Heparin (IV) orHeparin (IV) or
Low Molecular Weight Heparin (S/C)Low Molecular Weight Heparin (S/C)
Slow acting – Vitamin K AntagonistsSlow acting – Vitamin K Antagonists
WarfarinWarfarin
57. HeparinHeparin
•The initial treatment of PE is LMWH or UHF for
at least 5 days, followed by warfarin.
•Dose of UFH: 80 U/kg bolus followed by18
U/kg/hour
. Monitoring by APTT(1.5-2.5 )times normal.
•It binds to endogenous antithrombin, This
heparin - antithrombin complex catalyzes the
inactivation of factor Xa and IIa (thrombin).
58. LMWHLMWH
.
•It should be used whenever possible for the
initial inpatient treatment of DVT & PE.
•Outpatient ttt of DVT, and possibly PE,is safe
and cost-effective for carefully selected
patients.
59. Adverse effect of heparinAdverse effect of heparin
•Adverse drug reactions include bleeding,
heparin-induced thrombocytopenia, and
osteoporosis .with prolonged use .
61. New oral anti coagulantNew oral anti coagulant
Oral direct thrombin inhibitor: DabigatranOral direct thrombin inhibitor: Dabigatran
It is as effective as warfarin for theIt is as effective as warfarin for the
treatment of acute VTE with similar safetytreatment of acute VTE with similar safety
profileprofile
Dabigatran was also not inferior to S/CDabigatran was also not inferior to S/C
enoxaparin in the prevention of VTEenoxaparin in the prevention of VTE
62. Oral direct factor X a inhibitor,Oral direct factor X a inhibitor,
RivaroxabanRivaroxaban
It has relatively short half life 5-9 hoursIt has relatively short half life 5-9 hours
and rapid onset of action 2.5 to 4 hoursand rapid onset of action 2.5 to 4 hours
It is not inferior to S/C enoxaparinIt is not inferior to S/C enoxaparin
followed by warfarin in the treatment offollowed by warfarin in the treatment of
acute symptomatic DVTacute symptomatic DVT
63. Duration of anticoagulationDuration of anticoagulation
•A patient with a first thromboembolic event occurring in the
setting of reversible risk factors, should receive warfarin therapy
for at least 3 months.
•Patients without a clearly defined predisposition to initial thrombo
embolism should be treated for 6 months or more.
•Patient who have active cancer or recurrent DVT require long
term ( indefinite period)
66. Indication of venacava filterIndication of venacava filter
Contra indication to anti coagulationContra indication to anti coagulation
Recurrent embolism while on adequateRecurrent embolism while on adequate
therapytherapy
Significant bleeding complication duringSignificant bleeding complication during
anti coagulationanti coagulation
67. Thrombolytic TherapyThrombolytic Therapy
•The ACCP guidelines recommend that thrombolytic therapy
should be used in
•patients with acute PE associated with hypotension (systolic BP<
90 mm HG) who do not have a high bleeding risk .
•select patients with acute PE not associated with hypotension
and with a low bleeding risk whose initial clinical presentation or
clinical course after starting anticoagulation suggests a high risk of
developing hypotension
•Tissue plasminogen activator (tPA) has a short
infusion time and has been recommended as the best
agent for this reason.
68.
69. EmbolectomyEmbolectomy
In case of massive life threateningIn case of massive life threatening
pulmonary embolismpulmonary embolism
Catheter EmbolectomyCatheter Embolectomy
Surgical EmbolectomySurgical Embolectomy
17/08/1717/08/17 6969
70. Catheter Embolectomy & FragmentationCatheter Embolectomy & Fragmentation
An alternative in high-risk PE patients when thrombolysis
is absolutely contraindicated or has failed
Kucher N Chest 2007;132:657-663
73. Intermittent pneumatic compression (IPC) devices
are used to help prevent blood clots in the deep
veins of the legs. The devices use cuffs around
the legs that fill with air and squeeze your legs.
This increases blood flow through the veins of
your legs and helps prevent blood clots.
75. Graduated compressionGraduated compression
stockingsstockings
Graduated compression stockings exertGraduated compression stockings exert
the greatest degree of compression at thethe greatest degree of compression at the
ankle, and the level of compressionankle, and the level of compression
gradually decreases up the garmentgradually decreases up the garment
They are often used to treat chronicThey are often used to treat chronic
venous disease and edemavenous disease and edema
78. Home messageHome message
Prevention is better than curePrevention is better than cure
Early diagnosis and treatment is lifeEarly diagnosis and treatment is life
savingsaving
Risk of pulmonary embolism significantlyRisk of pulmonary embolism significantly
increases with a flight distance more thanincreases with a flight distance more than
5000 km or duration more than 8 hours .5000 km or duration more than 8 hours .
Editor's Notes
Massive PE: obstructing more than 50% of pulmonary vasculature
Cardiomegaly was the most frequent finding in those with PE of In-patients
Out-patients, it seemed to be atelectasis in the above study.
Echocardiograms before and after Thrombolysis. A 29-year-old woman presented with progressive shortness of breath. A computed tomographic scan of the chest showed a central &quot;saddle&quot; pulmonary embolism. An echocardiogram (Panel A) showed an enlarged right ventricle and hypokinetic motion of the right ventricular free wall. After treatment with alteplase, the right ventricular size and wall motion returned to normal (Panel B). Echocardiograms courtesy of Scott D. Solomon, M.D., and Jose M. Rivero. (Videos of these images are available with the full text of this article at http://www.nejm.org.)
Figure 21-11. Pulmonary angiogram showing pulmonary embolism. Pulmonary angiography remains the diagnostic gold standard for pulmonary embolism. Access to the pulmonary artery is obtained via transvenous catheter placement. The diagnosis is confirmed by persistent filling defect or abrupt cut-off of flow. Abrupt cut-off of flow to the right and left upper lobe vessels is seen in this patient.
If anticoagulant or thrombolytic therapy is CI or fails to prevent thrombo-embolism, Patients with massive PE who survive (in whom a second PE may be fatal)
Greenfield filter inserted above the level of renal veins