Type 1 respiratory failure is defined as hypoxemia without hypercapnia, caused by conditions that impair oxygenation like pneumonia. Type 2 involves both hypoxemia and hypercapnia due to inadequate ventilation from issues like COPD.
Pulmonary embolism occurs when a blood clot lodges in the lungs, impairing gas exchange. Risk factors include leg injuries and surgeries. Diffuse alveolar hemorrhage results from widespread damage to small lung vessels, leading to blood in the alveoli. Causes include autoimmune disorders and infections. Pneumonia has multiple causes and presentations depending on patient factors. Proper diagnosis and treatment of underlying conditions are important for managing respiratory failure.
Thromboembolism refers to the blocking of blood vessels by particles that have broken away from clots in the body. It is common in patients with cardiac disease or impaired circulation. Intracardiac thrombi, which can be detected by echocardiogram, are especially common in patients with atrial fibrillation. Pulmonary embolism occurs when a thrombus breaks off and travels to the lung, often from a deep vein thrombosis. It can be treated with anticoagulants or thrombolytics. Pericardial effusion involves a buildup of fluid in the sac around the heart, which can lead to cardiac tamponade if pressure increases and compresses the heart.
This document discusses infarction, which is localized ischemic necrosis of tissue due to decreased blood supply. Infarction can be caused by thrombi, emboli, vasospasm, expansion of atheroma, extrinsic compression of vessels, vessel twisting, or traumatic vessel rupture. There are three main types of infarction: red (hemorrhagic), white (anemic), and septic. Factors that influence infarction development include vulnerability to hypoxia, blood oxygen content, rate of occlusion, and blood supply. Myocardial, pulmonary, and cerebral infarctions are provided as examples and their characteristics and outcomes described.
Pulmonary diseases of vascular origin(pulmonary embolism)imrana tanvir
The most probable diagnosis is Pulmonary Saddle embolus. The key points are:
- Prolonged bed rest following pelvic fracture which is a risk factor for deep vein thrombosis
- Sudden onset of chest pain and collapse
- Rapid demise of the patient
This fits with the clinical presentation of a large pulmonary embolism causing sudden death as described in the document.
All about arterial and venous embolectomy, thrombectomy and thrombo-embolectomy
basic definitions, diagrammatic differences, factors, Virchow's triad, signs and symptoms , investigations and treatments
This document discusses pulmonary edema, including its etiology, pathophysiology, clinical features, investigations, radiological features, and treatment. Pulmonary edema can be cardiogenic, caused by elevated pulmonary capillary pressure from various heart conditions, or non-cardiogenic. The pathophysiology involves fluid transudation from capillaries into the lungs' interstitium and alveoli. Treatment focuses on oxygenation, diuresis, vasodilation, and sometimes inotropes or ventilation support to reduce pulmonary pressures and fluid overload.
1) Myocardial infarction, cerebral infarction, pulmonary infarction, and gangrene of limbs are common examples of infarction that result from obstruction of blood flow.
2) Infarctions are typically wedge-shaped areas of ischemic necrosis caused by occlusion of the arterial blood supply or venous drainage of a tissue.
3) The development of an infarction depends on factors like the nature of the blood supply, the rate of occlusion, the tissue's vulnerability to hypoxia, and the oxygen content of the blood. Tissues with dual blood supplies are less likely to infarct.
PULMONARY EMBOLISM- Venous Diseases
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Pulmonary Embolism-PE.
• In this video, I discussed about the etio-pathogenesis, clinical features, investigations, Wells scoring, differential diagnosis, treatment and treatment algorithm of Pulmonary Embolism.
• I hope you will enjoy the video.
• You can watch all my teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video
Thromboembolism refers to the blocking of blood vessels by particles that have broken away from clots in the body. It is common in patients with cardiac disease or impaired circulation. Intracardiac thrombi, which can be detected by echocardiogram, are especially common in patients with atrial fibrillation. Pulmonary embolism occurs when a thrombus breaks off and travels to the lung, often from a deep vein thrombosis. It can be treated with anticoagulants or thrombolytics. Pericardial effusion involves a buildup of fluid in the sac around the heart, which can lead to cardiac tamponade if pressure increases and compresses the heart.
This document discusses infarction, which is localized ischemic necrosis of tissue due to decreased blood supply. Infarction can be caused by thrombi, emboli, vasospasm, expansion of atheroma, extrinsic compression of vessels, vessel twisting, or traumatic vessel rupture. There are three main types of infarction: red (hemorrhagic), white (anemic), and septic. Factors that influence infarction development include vulnerability to hypoxia, blood oxygen content, rate of occlusion, and blood supply. Myocardial, pulmonary, and cerebral infarctions are provided as examples and their characteristics and outcomes described.
Pulmonary diseases of vascular origin(pulmonary embolism)imrana tanvir
The most probable diagnosis is Pulmonary Saddle embolus. The key points are:
- Prolonged bed rest following pelvic fracture which is a risk factor for deep vein thrombosis
- Sudden onset of chest pain and collapse
- Rapid demise of the patient
This fits with the clinical presentation of a large pulmonary embolism causing sudden death as described in the document.
All about arterial and venous embolectomy, thrombectomy and thrombo-embolectomy
basic definitions, diagrammatic differences, factors, Virchow's triad, signs and symptoms , investigations and treatments
This document discusses pulmonary edema, including its etiology, pathophysiology, clinical features, investigations, radiological features, and treatment. Pulmonary edema can be cardiogenic, caused by elevated pulmonary capillary pressure from various heart conditions, or non-cardiogenic. The pathophysiology involves fluid transudation from capillaries into the lungs' interstitium and alveoli. Treatment focuses on oxygenation, diuresis, vasodilation, and sometimes inotropes or ventilation support to reduce pulmonary pressures and fluid overload.
1) Myocardial infarction, cerebral infarction, pulmonary infarction, and gangrene of limbs are common examples of infarction that result from obstruction of blood flow.
2) Infarctions are typically wedge-shaped areas of ischemic necrosis caused by occlusion of the arterial blood supply or venous drainage of a tissue.
3) The development of an infarction depends on factors like the nature of the blood supply, the rate of occlusion, the tissue's vulnerability to hypoxia, and the oxygen content of the blood. Tissues with dual blood supplies are less likely to infarct.
PULMONARY EMBOLISM- Venous Diseases
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Pulmonary Embolism-PE.
• In this video, I discussed about the etio-pathogenesis, clinical features, investigations, Wells scoring, differential diagnosis, treatment and treatment algorithm of Pulmonary Embolism.
• I hope you will enjoy the video.
• You can watch all my teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video
This document discusses pulmonary embolism (PE), which refers to obstruction of the pulmonary artery or its branches by a thrombus (blood clot). PE can be caused by factors that increase clotting like surgery, trauma, or heart failure. When a thrombus blocks a pulmonary vessel, it impairs gas exchange and increases pulmonary vascular resistance, raising pressure in the pulmonary artery and overworking the right ventricle. Diagnosis involves tests like ventilation-perfusion scans and treatment focuses on anticoagulation, thrombolytic drugs, or occasionally surgery to remove clots. Nursing care aims to prevent clots, monitor for complications, manage pain and oxygen therapy.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
Cardiogenic pulmonary edema is caused by increased hydrostatic pressure in the pulmonary veins due to cardiac dysfunction from various etiologies like mitral stenosis, congestive heart failure, cardiomyopathy, and myocardial infarction. Patients typically present with sudden shortness of breath, anxiety, coughing up pink frothy sputum, and other symptoms. Diagnosis involves blood tests, electrocardiogram, chest x-ray, and other exams. Treatment focuses on ventilatory support, reducing preload and afterload on the heart, and providing inotropic support. Prognosis varies greatly case by case.
This document discusses the case of a 62-year-old man presenting with acute dyspnea. On examination, the patient is pale, sweaty, coughing pink sputum, and in respiratory distress. His pulse is 140 BPM, respiratory rate is 30, and oxygen saturation is 85%. The document outlines potential causes of acute dyspnea including pulmonary edema and provides guidance on evaluating, diagnosing, and initially managing such a patient. Key factors to consider include the patient's medical history, signs of heart failure on examination, and portable chest x-ray findings suggestive of pulmonary edema. The goals of treatment are to place the patient in a sitting position, provide high-flow oxygen, administer diuretics and opioids,
Acute pulmonary edema refers to excess fluid in the lungs that can have cardiogenic or non-cardiogenic causes. Cardiogenic pulmonary edema is often due to left ventricular dysfunction that leads to increased pulmonary capillary pressure. Common causes of left ventricular dysfunction include congestive heart failure, myocardial infarction, cardiomyopathy, and valvular diseases. Pulmonary edema progresses through three stages as excess fluid builds up first in small blood vessels then the lung interstitium and alveoli, impairing gas exchange.
Thromboembolism refers to a blood clot or amniotic fluid that breaks off and travels through the bloodstream and lodges in a distant blood vessel. Virchow's triad identifies factors that increase thromboembolism risk: vessel injury, platelet adhesion, and aggregation. Risk factors include both acquired factors like surgery, trauma, cancers, and inherited factors like genetic clotting disorders. Clinical features depend on where the embolism lodges, such as lungs (difficulty breathing), heart (heart attack), or brain (stroke). Post-mortem analysis can determine the age and composition of an embolism.
Air embolism is a serious complication of central venous catheters that occurs when air enters the vasculature through an open catheter lumen or insertion site. Symptoms include cyanosis, respiratory distress, and hypotension. Treatment involves giving 100% oxygen and placing the patient on their left side to displace air from the heart. Prevention strategies include using luer-lock connections, avoiding tubing loops, covering sites after removal, and having patients hold their breath during catheter removal.
This document discusses hyperemia and congestion, two vascular events that involve an increased volume of blood in a particular tissue. Hyperemia is an active process of arteriolar dilation that increases blood volume on the arterial side, while congestion is a passive process caused by impaired venous outflow that increases blood volume on the venous side. Both lead to increased hydrostatic pressure and edema. Examples of congestion discussed include nutmeg liver seen in right-sided heart failure and pulmonary edema seen in left-sided heart failure. Microscopic findings of congestion in the liver include centrilobular necrosis and hemorrhage, while the lungs show engorged capillaries, edema, and hemorrhage.
Non invasive ventilation in cardiogenic pulmonary edemaSamiaa Sadek
Cardiogenic pulmonary edema (CPE) is caused by increased hydrostatic pressure in the pulmonary capillaries due to elevated left atrial pressure. This imbalance in hydrostatic and oncotic pressures across the capillary membrane leads to fluid filtration into the lungs. CPE progresses through three stages as fluid accumulates first in the lung interstitium then alveoli, impairing gas exchange. Treatment aims to reduce preload and afterload on the heart along with diuresis. Noninvasive ventilation with CPAP or BiPAP improves oxygenation and reduces workload of breathing by increasing lung volume while also decreasing cardiac preload and afterload.
This document provides an overview of pulmonary edema through defining it, discussing anatomy and physiology, epidemiology, classification, pathogenesis, staging, causes, clinical manifestations, diagnosis, medical management, nursing diagnosis, interventions, complications, and expected outcomes. It summarizes the key points of pulmonary edema for medical professionals.
Hyperaemia and congestion both refer to an increased volume of blood in vessels. Hyperaemia is an active process involving arteriolar dilation that brings more blood to an area, while congestion is passive with impaired drainage causing blood accumulation. There are physiological and pathological forms. Pathological hyperaemia can be acute or chronic, localized or generalized, and active via increased arterial flow or passive due to impaired venous drainage. Chronic passive hyperaemia develops slowly over time from obstructions like tumors or abscesses blocking venous drainage. Congestive heart failure is an example of chronic generalized passive hyperaemia. Hyperaemia is identifiable by tissue color changes and swelling due to increased blood volume.
Edema can be caused by increased hydrostatic pressure, increased vascular permeability, decreased colloid osmotic pressure, decreased protein synthesis or increased protein loss, or lymphatic obstruction. The major mechanisms are increased hydrostatic pressure, as seen in congestive heart failure, or increased vascular permeability during inflammation. Edema fluid is usually a protein-poor transudate when caused by hydrostatic or oncotic pressure changes, but is a protein-rich exudate with inflammatory causes due to higher vascular permeability.
Embolism occurs when a solid, liquid, or gaseous mass travels through the bloodstream and lodges in a blood vessel distant from the site of origin. Embolisms are classified based on direction of travel and composition. Pulmonary embolisms involve the lungs while systemic embolisms affect other organs. Common causes of embolism include blood clots, fat droplets, air bubbles, and infectious materials. Symptoms vary depending on the size and location of the embolism but may include dyspnea, chest pain, and coughing. Diagnosis involves blood tests, imaging, and scans. Consequences depend on factors like vessel size and collateral blood flow.
This document discusses different types of thromboembolism including pulmonary embolism, fat embolism, air embolism, and amniotic fluid embolism. It provides details on the definition, causes, risk factors, symptoms, diagnosis, treatment and prognosis of pulmonary embolism, which is the most common type of thromboembolism. The document also discusses the pathophysiology and mechanisms of the different embolism types.
This document provides information about aneurysms and peripheral vascular disorders. It defines different types of aneurysms including true aneurysms, false aneurysms, berry aneurysms, and aortic aneurysms. The causes of aneurysms are discussed, including conditions like atherosclerosis, smoking, and genetic factors. Diagnostic tests for aneurysms including CT scans, MRI, and angiograms are outlined. Treatment options for aneurysms include medications to control risk factors, surgical procedures like endovascular coiling and stent grafting, and rehabilitation after brain injury from rupture. Complications from ruptured aneurysms like re-bleeding and hydrocephalus are also noted.
An air embolism occurs when a gas bubble, usually air, lodges in the blood vessels blocking blood flow. Air embolisms can be venous or arterial. Venous air embolisms are more common during neurosurgeries performed in the sitting position when air can enter veins and travel to the heart. Clinical signs include decreased consciousness, seizures, and cardiac arrest. Treatment involves securing the airway, increasing oxygen levels, and administering fluids and medications to support circulation. Positioning the patient with the surgical site below the heart and stopping air entry can prevent worsening of the condition. Aspirating air from the heart through a central venous catheter can also help if placed correctly in the right atrium.
This document discusses cardiac tamponade and pericardial effusion. Pericardial effusion is an abnormal collection of fluid in the pericardial cavity. Cardiac tamponade is a clinical syndrome caused by excess accumulation of fluid in the pericardial space, reducing ventricular filling and causing hemodynamic compromise. Causes include rapidly developing issues like trauma or surgery, or long term issues like infections, tumors, or hypothyroidism. Symptoms include breathlessness, chest pain, and fatigue. Treatment for severe cases involves pericardiocentesis, while milder cases may be treated conservatively with oxygen, fluids, rest, and drugs.
This document provides an overview of pulmonary edema, including its definition, causes, pathophysiology, diagnosis, and treatment. Pulmonary edema is fluid accumulation in the lungs caused by increased pulmonary capillary pressure or decreased plasma oncotic pressure. It can be cardiogenic or non-cardiogenic in origin. Diagnosis involves physical exam, imaging, and labs. Treatment focuses on oxygen therapy, reducing preload with diuretics and vasodilators, and supporting ventilation if needed. Prognosis depends on severity but mortality can be up to 20% for cardiogenic pulmonary edema.
Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle.
Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes availed as synonyms, although this is technically much inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms [1, 2] (Fig: 1 &2).
Fig: 1. Coronary Thrombosis
Fig: 2. Heart with blood clot
Facts of Coronary Thrombosis
Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis, and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics and research are carried out to encounter problems in these fields
ARDS is a life-threatening form of respiratory failure characterized by diffuse lung inflammation and damage leading to hypoxemia. It has multiple causes but is commonly due to sepsis, pneumonia, or trauma. The pathology involves damage to the lung epithelium and endothelium, resulting in fluid accumulation in the alveoli. Treatment focuses on lung-protective ventilation with low tidal volumes, moderate levels of PEEP, and consideration of prone positioning. Other strategies include corticosteroids, neuromuscular blockade, and restrictive fluid management. More severe cases may require advanced support such as ECMO.
This document discusses pulmonary embolism (PE), which refers to obstruction of the pulmonary artery or its branches by a thrombus (blood clot). PE can be caused by factors that increase clotting like surgery, trauma, or heart failure. When a thrombus blocks a pulmonary vessel, it impairs gas exchange and increases pulmonary vascular resistance, raising pressure in the pulmonary artery and overworking the right ventricle. Diagnosis involves tests like ventilation-perfusion scans and treatment focuses on anticoagulation, thrombolytic drugs, or occasionally surgery to remove clots. Nursing care aims to prevent clots, monitor for complications, manage pain and oxygen therapy.
The document discusses various types of embolism and thrombosis. It describes the Virschow triad of factors that can lead to thrombosis - endothelial injury, changes in blood flow, and hypercoagulability. It then examines different causes and outcomes of thrombosis and embolism in various parts of the body, such as pulmonary embolism from deep vein thrombosis, systemic embolism from cardiac sources, and amniotic fluid embolism during childbirth.
An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
Cardiogenic pulmonary edema is caused by increased hydrostatic pressure in the pulmonary veins due to cardiac dysfunction from various etiologies like mitral stenosis, congestive heart failure, cardiomyopathy, and myocardial infarction. Patients typically present with sudden shortness of breath, anxiety, coughing up pink frothy sputum, and other symptoms. Diagnosis involves blood tests, electrocardiogram, chest x-ray, and other exams. Treatment focuses on ventilatory support, reducing preload and afterload on the heart, and providing inotropic support. Prognosis varies greatly case by case.
This document discusses the case of a 62-year-old man presenting with acute dyspnea. On examination, the patient is pale, sweaty, coughing pink sputum, and in respiratory distress. His pulse is 140 BPM, respiratory rate is 30, and oxygen saturation is 85%. The document outlines potential causes of acute dyspnea including pulmonary edema and provides guidance on evaluating, diagnosing, and initially managing such a patient. Key factors to consider include the patient's medical history, signs of heart failure on examination, and portable chest x-ray findings suggestive of pulmonary edema. The goals of treatment are to place the patient in a sitting position, provide high-flow oxygen, administer diuretics and opioids,
Acute pulmonary edema refers to excess fluid in the lungs that can have cardiogenic or non-cardiogenic causes. Cardiogenic pulmonary edema is often due to left ventricular dysfunction that leads to increased pulmonary capillary pressure. Common causes of left ventricular dysfunction include congestive heart failure, myocardial infarction, cardiomyopathy, and valvular diseases. Pulmonary edema progresses through three stages as excess fluid builds up first in small blood vessels then the lung interstitium and alveoli, impairing gas exchange.
Thromboembolism refers to a blood clot or amniotic fluid that breaks off and travels through the bloodstream and lodges in a distant blood vessel. Virchow's triad identifies factors that increase thromboembolism risk: vessel injury, platelet adhesion, and aggregation. Risk factors include both acquired factors like surgery, trauma, cancers, and inherited factors like genetic clotting disorders. Clinical features depend on where the embolism lodges, such as lungs (difficulty breathing), heart (heart attack), or brain (stroke). Post-mortem analysis can determine the age and composition of an embolism.
Air embolism is a serious complication of central venous catheters that occurs when air enters the vasculature through an open catheter lumen or insertion site. Symptoms include cyanosis, respiratory distress, and hypotension. Treatment involves giving 100% oxygen and placing the patient on their left side to displace air from the heart. Prevention strategies include using luer-lock connections, avoiding tubing loops, covering sites after removal, and having patients hold their breath during catheter removal.
This document discusses hyperemia and congestion, two vascular events that involve an increased volume of blood in a particular tissue. Hyperemia is an active process of arteriolar dilation that increases blood volume on the arterial side, while congestion is a passive process caused by impaired venous outflow that increases blood volume on the venous side. Both lead to increased hydrostatic pressure and edema. Examples of congestion discussed include nutmeg liver seen in right-sided heart failure and pulmonary edema seen in left-sided heart failure. Microscopic findings of congestion in the liver include centrilobular necrosis and hemorrhage, while the lungs show engorged capillaries, edema, and hemorrhage.
Non invasive ventilation in cardiogenic pulmonary edemaSamiaa Sadek
Cardiogenic pulmonary edema (CPE) is caused by increased hydrostatic pressure in the pulmonary capillaries due to elevated left atrial pressure. This imbalance in hydrostatic and oncotic pressures across the capillary membrane leads to fluid filtration into the lungs. CPE progresses through three stages as fluid accumulates first in the lung interstitium then alveoli, impairing gas exchange. Treatment aims to reduce preload and afterload on the heart along with diuresis. Noninvasive ventilation with CPAP or BiPAP improves oxygenation and reduces workload of breathing by increasing lung volume while also decreasing cardiac preload and afterload.
This document provides an overview of pulmonary edema through defining it, discussing anatomy and physiology, epidemiology, classification, pathogenesis, staging, causes, clinical manifestations, diagnosis, medical management, nursing diagnosis, interventions, complications, and expected outcomes. It summarizes the key points of pulmonary edema for medical professionals.
Hyperaemia and congestion both refer to an increased volume of blood in vessels. Hyperaemia is an active process involving arteriolar dilation that brings more blood to an area, while congestion is passive with impaired drainage causing blood accumulation. There are physiological and pathological forms. Pathological hyperaemia can be acute or chronic, localized or generalized, and active via increased arterial flow or passive due to impaired venous drainage. Chronic passive hyperaemia develops slowly over time from obstructions like tumors or abscesses blocking venous drainage. Congestive heart failure is an example of chronic generalized passive hyperaemia. Hyperaemia is identifiable by tissue color changes and swelling due to increased blood volume.
Edema can be caused by increased hydrostatic pressure, increased vascular permeability, decreased colloid osmotic pressure, decreased protein synthesis or increased protein loss, or lymphatic obstruction. The major mechanisms are increased hydrostatic pressure, as seen in congestive heart failure, or increased vascular permeability during inflammation. Edema fluid is usually a protein-poor transudate when caused by hydrostatic or oncotic pressure changes, but is a protein-rich exudate with inflammatory causes due to higher vascular permeability.
Embolism occurs when a solid, liquid, or gaseous mass travels through the bloodstream and lodges in a blood vessel distant from the site of origin. Embolisms are classified based on direction of travel and composition. Pulmonary embolisms involve the lungs while systemic embolisms affect other organs. Common causes of embolism include blood clots, fat droplets, air bubbles, and infectious materials. Symptoms vary depending on the size and location of the embolism but may include dyspnea, chest pain, and coughing. Diagnosis involves blood tests, imaging, and scans. Consequences depend on factors like vessel size and collateral blood flow.
This document discusses different types of thromboembolism including pulmonary embolism, fat embolism, air embolism, and amniotic fluid embolism. It provides details on the definition, causes, risk factors, symptoms, diagnosis, treatment and prognosis of pulmonary embolism, which is the most common type of thromboembolism. The document also discusses the pathophysiology and mechanisms of the different embolism types.
This document provides information about aneurysms and peripheral vascular disorders. It defines different types of aneurysms including true aneurysms, false aneurysms, berry aneurysms, and aortic aneurysms. The causes of aneurysms are discussed, including conditions like atherosclerosis, smoking, and genetic factors. Diagnostic tests for aneurysms including CT scans, MRI, and angiograms are outlined. Treatment options for aneurysms include medications to control risk factors, surgical procedures like endovascular coiling and stent grafting, and rehabilitation after brain injury from rupture. Complications from ruptured aneurysms like re-bleeding and hydrocephalus are also noted.
An air embolism occurs when a gas bubble, usually air, lodges in the blood vessels blocking blood flow. Air embolisms can be venous or arterial. Venous air embolisms are more common during neurosurgeries performed in the sitting position when air can enter veins and travel to the heart. Clinical signs include decreased consciousness, seizures, and cardiac arrest. Treatment involves securing the airway, increasing oxygen levels, and administering fluids and medications to support circulation. Positioning the patient with the surgical site below the heart and stopping air entry can prevent worsening of the condition. Aspirating air from the heart through a central venous catheter can also help if placed correctly in the right atrium.
This document discusses cardiac tamponade and pericardial effusion. Pericardial effusion is an abnormal collection of fluid in the pericardial cavity. Cardiac tamponade is a clinical syndrome caused by excess accumulation of fluid in the pericardial space, reducing ventricular filling and causing hemodynamic compromise. Causes include rapidly developing issues like trauma or surgery, or long term issues like infections, tumors, or hypothyroidism. Symptoms include breathlessness, chest pain, and fatigue. Treatment for severe cases involves pericardiocentesis, while milder cases may be treated conservatively with oxygen, fluids, rest, and drugs.
This document provides an overview of pulmonary edema, including its definition, causes, pathophysiology, diagnosis, and treatment. Pulmonary edema is fluid accumulation in the lungs caused by increased pulmonary capillary pressure or decreased plasma oncotic pressure. It can be cardiogenic or non-cardiogenic in origin. Diagnosis involves physical exam, imaging, and labs. Treatment focuses on oxygen therapy, reducing preload with diuretics and vasodilators, and supporting ventilation if needed. Prognosis depends on severity but mortality can be up to 20% for cardiogenic pulmonary edema.
Coronary thrombosis is formation of a blood clot inside a blood vessel of heart. Thrombosis in the heart can pave to a myocardial infarction. Coronary Thrombosis is general in high blood pressure patient, diabetic, and victims of atherosclerosis. The treatment is decreasing pain, improving blood flow to the heart muscle, and preventing irreversible damage to the heart muscle.
Coronary Thrombosis in the heart can pave to a myocardial infarction. Coronary thrombosis and myocardial infarction are sometimes availed as synonyms, although this is technically much inaccurate as the thrombosis refers to the blocking of blood vessels, while the infarction refers to the tissue death due to the consequent loss of blood flow to the heart tissue. The heart comprises many connecting blood vessels, and depending upon the location of the thrombosis, the infarction may cause no symptoms [1, 2] (Fig: 1 &2).
Fig: 1. Coronary Thrombosis
Fig: 2. Heart with blood clot
Facts of Coronary Thrombosis
Studies in Thrombosis and Hemostasis, Thrombosis and Haemostasis, Arteriosclerosis, Thrombosis, and Vascular Biology, Clinical and Applied Thrombosis/Hemostasis were a key investigation topics and research are carried out to encounter problems in these fields
ARDS is a life-threatening form of respiratory failure characterized by diffuse lung inflammation and damage leading to hypoxemia. It has multiple causes but is commonly due to sepsis, pneumonia, or trauma. The pathology involves damage to the lung epithelium and endothelium, resulting in fluid accumulation in the alveoli. Treatment focuses on lung-protective ventilation with low tidal volumes, moderate levels of PEEP, and consideration of prone positioning. Other strategies include corticosteroids, neuromuscular blockade, and restrictive fluid management. More severe cases may require advanced support such as ECMO.
This document discusses respiratory failure, including its classification, pathophysiology, clinical presentation, evaluation, complications, and management. Respiratory failure is classified as type 1 (hypoxemic) or type 2 (hypercapnic) based on blood gas abnormalities. Common causes include lung disease, disorders of the nervous system or respiratory muscles. Signs may include dyspnea, cyanosis, confusion. Evaluation includes blood gases, imaging, and tests to identify the underlying cause. Complications affect multiple organ systems. Management focuses on correcting hypoxemia and hypercapnia through supportive measures like oxygen supplementation or mechanical ventilation, as well as treating the underlying condition.
This document provides an overview of Acute Respiratory Distress Syndrome (ARDS). It defines ARDS as sudden acute respiratory failure caused by damage to the alveolar capillary membrane, resulting in pulmonary edema. The document outlines the etiology, pathology, clinical presentation, diagnosis, and management of ARDS. It describes the exudative, proliferative, and fibrotic stages of ARDS and emphasizes the importance of supportive care including mechanical ventilation with low tidal volumes to prevent further lung injury. The mortality rate for ARDS is reported to be 40-60% despite advances in understanding its pathogenesis.
Respiratory failure occurs when the lungs cannot effectively exchange oxygen and carbon dioxide, resulting in hypoxemia (low blood oxygen) and hypercapnia (high blood carbon dioxide). Acute respiratory failure develops suddenly in patients without preexisting lung disease, while chronic respiratory failure is caused by conditions like COPD. Treatment involves oxygen therapy, ventilation if needed, treating the underlying cause, and monitoring vital signs.
This document provides information about chronic obstructive pulmonary disease (COPD) including its definition, causes, diagnosis, management, and related conditions like emphysema and bronchiectasis. COPD is a progressive lung disease characterized by limited airflow in the lungs. The primary cause is cigarette smoking which leads to an abnormal inflammatory response in the lungs. Symptoms include breathlessness, chronic cough, and sputum production. Spirometry is required for diagnosis and shows airflow limitation. Management involves smoking cessation, bronchodilators, steroids, vaccines, and oxygen supplementation during exacerbations. Related conditions like emphysema and bronchiectasis are also discussed.
The document presents information about a seminar on Acute Respiratory Distress Syndrome (ARDS). The seminar aims to provide in-depth knowledge of ARDS including defining it, describing the pathophysiology and management. ARDS is a life-threatening condition that prevents enough oxygen from entering the blood. It occurs when the lungs become severely inflamed and fluid builds up in the tiny air sacs of the lungs. The seminar will discuss etiology, risk factors, clinical manifestations, diagnostic evaluation, complications, and the nurse's role in management.
1) Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by direct or indirect injury to the lungs whereby the alveolar capillary membrane becomes damaged and permeable, resulting in pulmonary edema.
2) ARDS is characterized by hypoxemia, reduced lung compliance, and diffuse pulmonary infiltrates seen on chest imaging.
3) Treatment involves supportive care in an intensive care unit including mechanical ventilation, supplemental oxygen, and positioning therapies like prone positioning to improve oxygenation.
1. The document discusses respiratory failure, describing it as a failure to maintain adequate gas exchange resulting in hypoxemia and potentially hypercapnia.
2. Types of respiratory failure are classified as type 1 (hypoxemic) or type 2 (hypercapnic), and common causes of each type are provided.
3. Diagnostic testing and management approaches are outlined, focusing on arterial blood gas analysis, oxygen therapy using devices like nasal cannulas or Venturi masks, and treating the underlying cause.
1. Respiratory failure occurs when the respiratory system fails in its gas exchange function, resulting in low oxygen and high carbon dioxide levels in the blood.
2. It can be acute, coming on suddenly from conditions like pneumonia, or chronic from ongoing diseases like COPD.
3. Treatment depends on the type of failure - oxygen therapy for hypoxemic respiratory failure and ventilation support like non-invasive ventilation for hypercapnic respiratory failure. Physiotherapy focuses on clearing secretions, maintaining strength, and mobilization to facilitate weaning from ventilation.
Definition
abnormal accumulation of extravascular fluid in the lung parenchyma.
diminished gas exchange at alveolar level,
potentially causing respiratory failure.
Etiology
cardiogenic
noncardiogenic
ACUTE RESPIRATORY FAILURE MAGDI SASI 2015cardilogy
1. Acute respiratory failure is defined as a severe form of respiratory insufficiency resulting in a PaO2 of less than 60 mmHg or a PaCO2 of more than 50 mmHg.
2. There are two main types - type 1 with low PaO2 and normal or low PaCO2, and type 2 with low PaO2 and high PaCO2.
3. Major causes include diffuse airway obstruction, central airway obstruction, restrictive lung disease, pulmonary vascular disease, pleural and chest wall diseases, and neuromuscular diseases.
This document discusses breathlessness (dyspnea) and tachycardia. It defines breathlessness and describes scales to assess severity. Positional breathlessness is discussed. Causes of acute, subacute and chronic dyspnea are provided. Tachycardia is evaluated based on ECG findings of QRS duration and rhythm regularity. Common adult tachycardias like sinus tachycardia, atrial fibrillation, atrial flutter, SVT are summarized. Management of various tachycardias is outlined.
Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function.
Acute Respiratory Distress Syndrome (ARDS) is an acute hypoxemic respiratory failure following a lung or systemic insult without heart failure. It involves diffuse bilateral lung infiltrates, normal heart functioning, and profound hypoxemia. Common causes include pneumonia, aspiration, and sepsis. Patients experience rapid onset of labored breathing and hypoxemia. Chest imaging shows bilateral infiltrates. Treatment focuses on supportive care, mechanical ventilation with low tidal volumes, and treating the underlying condition. While the mortality rate is high, especially with sepsis, outcomes have improved in recent decades.
Acute Respiratory Distress Syndrome (ARDS) is an acute hypoxemic respiratory failure following a lung or systemic insult without heart failure. It involves diffuse bilateral lung infiltrates, normal heart functioning, and profound hypoxemia. Common causes include pneumonia, aspiration, and sepsis. Patients experience rapid onset of labored breathing and hypoxemia. Chest imaging shows bilateral infiltrates. Treatment focuses on supportive care, mechanical ventilation with low tidal volumes, and treating the underlying condition. While the mortality rate is high, especially with sepsis, outcomes have improved in recent decades.
This document discusses respiratory failure, which occurs when the respiratory system fails in gas exchange. It defines two main types - hypoxemic respiratory failure, defined as low blood oxygen, and hypercapnic respiratory failure, defined as high blood carbon dioxide. The document then covers the anatomy and physiology of respiration, diagnostic evaluation of respiratory failure, treatment including mechanical ventilation, and specific causes of respiratory failure like infection, airway obstruction, and cardiac issues.
Similar to Dyspnea, Diffuse Alveolar Hemorrhage, Pulmonary Embolism, Respiratory Failure (20)
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3. RESPIRATORY FAILURE
It occurs when pulmonary gaseous exchange fails to
maintain normal arterial oxygen and carbon dioxide
levels
There are two types I and II which are defined by the
absence or presence of hypercapnia(increased partial
pressures of carbon dioxide)
4. TYPE 1(HYPOXEMIC) RESPIRATORY FAILURE
Defined as a low level of oxygen in blood(hypoxemia)or (Pa02 <60 mm Hg)without an increased level of
carbon dioxide (the partial pressures of CO2 maybe normal or low) hypoxemia without hypercapnia
It’s mainly caused by a ventilation perfusion mismatch ie volume of air flowing in and out of the lungs is
not matched with the flow of blood to the lungs
It’s caused by conditions that affect oxygenation
● Low ambient oxygen like in high altitudes.
● V/Q mismatch from pulmonary embolism,Alveolar hypo-ventilation in acute neuromuscular diseas
● Shunts (atrio-septal defects)
● Diffuse problem from pneumonia and acute respiratory distress syndrome
5. TYPE II RESPIRATORY FAILURE
Defined as the buildup of carbon dioxide levels in the body due to failure of expulsion. PaCO2 >50
mmHg, hypoxemia with hypercapnia
It’s caused by
● inadequate alveolar ventilation from drug overdose,brain stem lesion,extreme obesity.
● Neuromuscular problems like Guillian Barre syndrome,motor neuron diseases
● Chestwall abnormalities like kyphoscoliosis,ankylosing spondylitis or flail chest.
● Increased airway resistance like COPD,asthma,suffocation.
7. PATHOPHYSIOLOGY
When disease impairs ventilation of part of a lung,perfusion of that region results in hypoxic and
carbon dioxide laden (deoxygenated) blood to enter the pulmonary veins
The neighboring regions(which are still normal) eventually increase their ventilation thus accelerate the
excretion of the accumulation carbon dioxide in the pulm.veins
This corrects the arterial carbon dioxide to normal but can’t augment oxygen uptake because the
hemoglobin flowing through the normal regions is already saturated
Mixture of blood from the underventilated and normal regions results in hypoxia with normocapnia
(normal partial pressures of carbon dioxide ). This is type I respiratory failure
Arterial hypoxia with hypercapnia( increased partial pressures of carbon dioxide)results into Type II
respiratory failure
8. CLINICAL PRESENTATION
Pulmonary findings- pulmonary edema,asthma,COPD,pneumonia
Neurological manifestations-restlessness,confusion,seizures or coma
Asterixis(type II)
Tachycardia and arrhythmias from hypoxemia and acidosis
Peripheral and central cyanosis
Dyspnea-uncomfortable sensation of breathing
Pulmonary hypertension ( from pulmonary arteriolar constriction caused by alveolar hypoxemia
potentiated by hypercapnia)
9. INVESTIGATIONS
• Do full medical history and physical exam
• Pulse oximetry test for oxygen saturation rate
• Pulmonary function tests
• Arterial blood gas test I.e CBC (to establish severity of
hypoxemia,hypercapnia,acidemia,bicarbonate or polycythemia
• LFTs and RFTs to provide etiology of the respiratory failure
• Imaging tests like Chest X-ray, CT scans.
• Echocardiogram to rule out any cardiovascular cause,detect dysrythmias
from severe hypoxemia or acidosis
• Serum electrolytes test because potassium,Magnesium and Phosphate
may aggravate respiratory failure
• Bronchoscopy.
10. MANAGEMENT OF ACUTE RESPIRATORY FAILURE
Prompt diagnosis and management of the underlying cause is important
In type 1, high concentrations of oxygen (40-60% by mask) will usually relive hypoxia by increasing
the alveolar P02. O2 for SPO2 <93% on room air
In severe cases, mechanical ventilation may be needed to relieve hypoxia. If high concentrations of
oxygen for more than a few hours should receive humidified oxygen
NB; No opioids because they suppress ventilatory drive
11. PULMONARY EMBOLISM (PE)
Definition - lodging of a blood clot in the pulmonary arterial tree with subsequent increase in
pulmonary vascular resistance, impaired V/Q matching, and possibly reduced pulmonary blood
flow
12. ETIOLOGY AND PATHOPHYSIOLOGY
• One of the most common causes of preventable death in the hospital
• Proximal leg thrombi (popliteal, femoral, or iliac veins) are the source of most clinically
recognized pulmonary emboli
• Thrombi often start in calf, but must propagate into proximal veins to create a sufficiently large
thrombus for a clinically significant PE. Fewer than 30% of patients have clinical evidence of DVT
(e.g. Leg swelling, pain, or tenderness)
• Suspect PE if patient develops fever, sudden dyspnea, chest pain, or collapse 1-2 wk after surgery
16. MGT
• General Measures: Prompt recognition is life saving
• Provide sufficient oxygen to hypoxaemic patients so as to keep the SpO2 >90%
• Fluid resuscitation with intravenous fluids and volume expanders for patients with circulatory shock
• Avoid diuretics and vasodilators because they reduce the cardiac output
• Give opioids to relieve pain and distress but carefully used in hypotensive patients. External massage may be
good in moribund patients for it dislodges and breaks up the central embolus
• Give anticoagulation therapy eg. LMWH, UFH, DAOA
• Thrombolysis and surgical therapy-Thrombolysis is for patients with acute massive PE and cardiogenic shock
plus those with right ventricular dilatation and hypokinesis or severe hypoxia. Surgical pulmonary embolectomy
may be done for patients that may have high mortality
• Caval filters- for patients with severe hemorrhage on using anticoagulants or recurrent VTE. Retrievable filters
should be used in patients with temporary risk factors and used till patient is stable on anticoagulants.
17. DIFFUSE ALVEOLAR HEMORRHAGE
Diffuse alveolar hemorrhage is persistent or recurrent pulmonary hemorrhage.
Diffuse alveolar hemorrhage results from widespread damage to the pulmonary small vessels,
leading to blood collecting within the alveoli. If enough alveoli are affected, gas exchange is
disrupted. The specific pathophysiology and manifestations vary depending on cause.
18. ETIOLOGY
● Autoimmune disorders (Goodpasture syndrome, antiphospholipid antibody syndrome,
connective tissue disorders) MOST COMMON
● Pulmonary infections (eg, hantavirus infection, covid)
● Toxic exposures (eg,certain pesticides)
● Drug reactions (eg, amiodarone, methotrexate, nitrofurantoin
● Cardiac disorders (eg, mitral stenosis)
● Coagulation disorders caused by diseases or anticoagulant drugs
● Idiopathic pulmonary hemosiderosis
● Hematopoietic stem cell transplantation or solid organ transplantation
19. CONT’D
Features; Dyspnea,Cough, Features of anemia, Hemoptysis, Fever
Dx
● Chest x-ray ie features of diffuse bilateral alveolar infiltrates and a suspicion of diffuse
alveolar hemorrhage
● Bronchoalveolar lavage
● Serologic and other tests to diagnose the cause ie (antinuclear antibody, anti–double-
stranded DNA [anti-dsDNA], antiglomerular basement membrane [anti-GBM] antibodies,
antineutrophil cytoplasmic antibodies [ANCA], antiphospholipid antibody)
20. MGT
● Corticosteroids
● Sometimes cyclophosphamide, rituximab, or plasma exchange/plasmapheresis
● Supportive measures
Treatment involves correcting the cause.
Corticosteroids and possibly cyclophosphamide are used to treat vasculitides, connective tissue
disorders, and Goodpasture syndrome .
Cyclophosphamide- chemotherapeutic used to treat cancers and autoimmune diseases.
21. MGT ...
Plasma exchange may be used to treat Goodpasture syndrome.
Several studies have reported successful use of recombinant activated human factor VII in treating
severe unresponsive alveolar hemorrhage, but such therapy is controversial because of possible
thrombotic complications.
Other possible management measures include supplemental oxygen, bronchodilators, reversal of
any coagulopathy, and intubation with protective strategies as for acute respiratory distress
syndrome (ARDS) and mechanical ventilation .
22. PNEUMONIA
Acute infection and inflammation of the lungs alveoli.
There are two major types:
● Bronchopneumonia: involves both the lung parenchyma and the bronchi. Common in
children and the elderly
● Lobar pneumonia: involves one or more lobes of the lung. Common in young people
Causative agents can be viral, bacterial or parasitic.
23. CAUSES
Pathogens vary according to age, patient’s condition and whether infection was acquired in the
community or hospital (Gram negative are more common in hospital).
● Neonates: group B streptococcus, Klebsiella, E.coli, Chlamydia and S. aureus
● Children <5 years: Pneumococcus, Haemophilus influenzae, less frequently: S. aureus, M.
catarrhalis, M. Pneumoniae, viruses (RSV, influenza, measles)
● Adults and children >5 years: most commonly S.pneumoniae, followed by atypical bacteria,
e.g. Mycloplasma pneumoniae, viruses
● Immunosuppressed: Pneumocystis (in HIV infected)
24. PREDISPOSING FACTORS
● Malnutrition
● Old age
● Immunosuppression (HIV,
cancer, alcohol dependence)
● Measles, pertussis
● Pre existing lung or heart
diseases, diabetes
25. PRESENTATIONS
● Fever, chest pain, cough (with or without sputum), rapid breathing (> 30 bpm), chest
indrawing for children and severe cases
● If severe; Pulse >120/minute Temperature > 39.5 o C, Low BP < 90/60 mmHg, Oxygen
saturation less than 90
● Extrapulmonary features, e.g. confusion or disorientation, may predominate and may be the
only signs of pneumonia in elderly or immunosuppressed patients
26. INVESTIGATIONS
● Do a chest X-ray and look for complications, e.g. –
Pneumothorax, pyothorax – Pneumonitis suggestive of
pneumocystis jiroveci pneumonia (PCP) – Pneumatocoeles
(cavities filled with air) suggestive of staphylococcal
pneumonia
● Sputum: For Gram stain, Ziehl-Neelsen (ZN) stain, culture for
AFB
● Blood: Complete blood count
28. PNEUMOCYSTIS PNEUMONIA, PCP
● Interstitial pneumonitis caused by
the parasite/fungus
Pneumocystis jirovecii (formerly
carinii). It is common in severely
immunosuppressed patients (e.g.
in HIV).
30. DYSPNEA
Definition.
Is a term general applied to sensations experienced by individuals who complain of unpleasant
or uncomfortable respiratory sensation or simply difficult, laboured, uncomfortable breathing
Or Sensation of feeling breathless or experiencing air hunger. Its It's a subjective sensation of
breathing that varies from mild discomfort to feeling of suffocation.
31. MECHANISM OF DYSPNEA.
Dyspnea occurs when there is a mismatch between afferent and efferent signalings.
As the brain receives afferent ventilation information, it is able to compare it to the current level
of respiration by the efferent signals.
If the level of respiration is inappropriate for the body status and need , the dyspnea occurs.
32. PATHOPHYSIOLOGY OF DYSPNEA.
There are many theories as regards dyspnea. however the most attractive unifying theory is that
dyspnea results from dissociation or a mismatch between central respiratory motor activity and
incoming afferent information from receptors in the airway, lungs and chest wall structures.
The afferent feed back from peripheral sensory receptors may allow the brain to assess the
effectiveness of the motor command issued to the ventilatory muscles I.e the appropriateness
of the response in terms of the flow and volume for the command.
33. ,,,
When changes in respiratory pressure, airflow , or movement of the lungs and chest wall are not
appropriate for outgoing command , the intensity of dyspnea is heightened
In other words, a dissociation between the motor command and the mechanical response of the
respiratory system may produce a sensation of respiratory discomfort.
When the motor signals are sent to chest wall from the respiratory centre, the sensory cortex is
simultaneously activated, resulting into conscious sensation of muscular effort and
breathlessness.
There is a strong psychological component to dyspnea, as some people may become aware of
their breathing in such circumstances but not experience the distress typical of the condition.
34. CAUSES OF DYSPNEA.
There are generally four categories.
1. Cardiac
○ Congestive cardiac failure
○ Coronary artery disease
○ Cardiomyopathy
○ Valvular dysfunction
○ Pericarditis
○ Arrhythmias
2. Pulmonary
○ COPD
○ Asthma
○ Restrictive lung disease
○ Pneumothorax.
3. Cardiac + pulmonary.
● COPD with pulmonary hypertension and
corpulmonale
● Chronic pulmonary emboli.
4. Non cardiac , non pulmonary causes.
● Metabolic conditions ( acidosis)
● Pain in the chest wall
● Neuro vascular disorders
● Otorhinolaryngeal disorder.
35.
36. HISTORY ( ONSET AND CAUSE)
Ask about the onset and the cause of dyspnea to the client whether it's a chronic or acute issue
Acute causes ( within minutes)
Respiratory
● Acute exacerbation of asthma
● Pneumothorax
● Pulmonary embolism
● Foreign body
● Laryngeal oedema
37. SUB ACUTE CAUSES.
Within hours.
● Asthma
● Left heart failure
● Pneumonia.
Within days.
● Pneumonia
● ARDS
● Left heart failure.
Within weeks.
● Pleural effusion
● Anaemia
● Muscles weakness
● Tumours
Pleural =Effusion, Malignancy, Fibrosis
Parenchyma = Interstitial lung disease
Vascular = Vasculitis, A-V malformations.
38. HISTORY ( POSITION AT WHICH THE DYSPNEA OCCURS).
Orthopnea
Shortness of breath which occurs when lying flat , causing the person to have to sleep propped up in
bed or sitting in a chair.
Causes
● CCF
● Left ventricular heart failure
● COPD
● Bronchial asthma
● Massive pleural effusion
● Ascites
● GERD.
39. OTHERS
Platypnea - Shortness of breath that is relieved when lying down and worsens when sitting or
standing. Its It's the opposite of orthopnea
Causes
• Left atrial myxoma
• Massive pulmonary embolism
• Paralysis of intercostal muscles
• Hepato pulmonary symdrome .
Trepopnea - Shortness of breath that is sensed while lying on one side but not on the other ( lateral
recumbent position.
Common causes
• Diseases one lung or bronchi
• Congestive cardiac failure
40. HISTORY ( TIMING OF DYSPNEA)
1. Nocturnal onset dyspnea. Dyspnea that occurs mostly at night.
● Congestive cardiac failure
● COPD
● Bronchial asthma
● Sleep apnea
2. Severity of the nocturnal onset dyspnea, if its severe enough that awakens the person from sleep.
Making them sit or stand ( suspect underlying heart failure.
3. Post prandial dyspnea
● GERD
● Aspiration
● Food allergy.
41. GRADING OF THE DYSPNEA. ( HISTORY)
mMRC dyspnea scale. ( modified from medical research council for dyspnea scale)
Grade. Dyspnea related to activity.
0 Breathless only on strenuous exercise.
1. Breathless when hurrying on the level or walking up a slight hill.
2. Walks slower than other people of the same age on the same level due to shortness of
breath or need to stop for breath when walking on her own phase.
3. Shortness of breath after walking few minutes on the level or about 100yards ( 90
meters).
4. Too breathless to leave the house or breathless when dressing or undressing.
42. NYHA( NEW YORK HEART ASSOCIATION) CLASSIFICATION.
Class1.
● Ordinary physical activity doesn't cause undue fatigue, palpitation , dyspnea and / or
angina.
Class II .
● Ordinary physical activity does cause undue fatigue, palpitation , dyspnea and / or angina.
Class III
● Less than ordinary physical activity causes undue fatigue.
Class IV.
● Fatigue, palpitations , dyspnea and /or angina occur at rest.
44. RELIEVING FACTORS.
● Rest
● Medication.
Associated symptoms.
● Chest pain ( central, pleuritic or pericardial)
● Wheeze
● Fever
● Cough ( sputum production and colour)
● Change in pitch of voice
● Heart burn
● Hemoptysis.
● Muscle weakness or myalgia.
● Palpitation , syncope etc.
45. PHYSICAL EXAMINATIONS ( WHAT TO LOOK FOR).
General inspection.
● Anxiety may indicate anxiety disorder.
● Respiratory distress
● Ability to speak. Complete a sentence, unable to speak.
● Is there any audible wheeze or stridor ?. Is the voice Hoarse.
● Patient position
● Cyanosis or pallor.
● Mental status, it may be altered in hypoxemic and hypercapnic situations.
46. …
Vital signs.
Pulse : usually tachycardia , only bradycardia is in severe hypoxemia.
Respiratory rate .tachypnea danger if > 35 -40 beats per minute or below 10-12 beats per
minute.
Temperature . Is there fever.
Blood pressure, may increase if dyspnea is significant . Decrease may indicate life threatening
problem .
Pulseoximetry for any evidence of dessaturation
47. WHAT ELSE TO LOOK FOR IN GENERAL EXAMINATION.
Finger clubbing (CA bronchus, Pulmonary fibrosis, Bronchietasis, Lung Abscess, Pleural
empyema, CHF, IE)
Peripheral cyanosis- ( Cyanosis and clubbing may Indicate chronic severe hypoxia)
Nasal polyps, septal deviation. Dyspnea due to nasal obstruction.
Post nasal discharge- asthma/ allergy
Jugular vein distension. Congestive heart failure , pulmonary oedema.
Lower limb oedema . Cardiac problems
48. CHEST EXAMINATIONS.
● Normal chest is elliptical, increased in anterioposterior chest diameter ( may I dictate,
emphysema or COPD.
● Contraction of accessory muscles of respiration suggest severe difficulty in breathing.
● Retraction of supra clavicular fossa implies , tracheal stenosis.
● Pursed lip breathing and a prolonged expiratory phase are signs of outflow obstruction.
● Retraction of intercostal muscles on inspiration is characteristic of emphysema.
● Percuss for dullness or hyper resonance.
49. …
● Auscultate for wheeze (asthma, pulmonary oedema), quality of breath sounds.
● Crackles suggest fluid in the airway as it occurs with bronchitis, pneumonitis and CHF.
● Rhonchi, diminished breath sounds , rales.
NOTE. Normal chest examination findings does not rule out pulmonary pathology but only
lessen the likelihood that it is severe.
50. CARDIOVASCULAR EXAMINATION
Focus on :
● Signs of left sided heart failure
● Precordial impulse
● Detection of murmurs.( LHF , valvular dysfunction, S3- congestive HF.
● Signs of pulmonary hypertension and its consequences.
● Extremities for oedema and cyanosis.
Per abdomen.
Rule of ascites
Hepatojugular reflex.
51. INVESTIGATIONS.
1. Complete blood count. Assess for anemia and white cell counts.
2. Blood culture and sensitivity- identify probable pathogens
3. Sputum - Zn stain or Gene expert to rule out TB.
4. Arterial blood gas analysis- To assess the acid base status of the patient.
5. Electrolytes, BUN, creatinine, blood glucose. ( to ass6 metabolic derangement.
52. OTHER RELEVANT SPECIAL INVESTIGATIONS.
Chest xray.
● These has a great potential in aiding the diagnosis of many lung disorders that could have caused the
disorder and chest pain. ( consolidation, infiltrates masses ,cardiac size, hyperinflation, pneumonia, ILD
pleural effusion) etc.
Electocardiography
The ECG might be abnormal incase of structural heart disease. ( to assess left ventricular function and
pulmonary artery pressure) and if necessary a cardiopulmonary exercise test.
● Spirometry (lung volumes
● D.Dimers to rule of pulmonary embolism
● Ultra sound scan. To rule out acute cardiogenic pulmonary oedema.
If you suspect respiratory pump or gas exchange abnormalities , do a pulmonary function test . If diffusion
capacity reduced , consider CT angiogram.
53. MANAGEMENT OF A PATIENT WITH DYSPNEA.
Management strategy.
1. Reduce ventilatory demand
2. Decrease sense of effort
3. Improve respiratory muscle function
4. Pulmonary rehabilitation.
54. TREATMENT OF UNSTABLE PATIENT.
● Administer oxygen
● Consider intubation of the patient if gasping, apniec , or non unresponsive.
● Tension pneumothorax- thoracentesis
● Obstructive pulmonary disease - Bronchodilators
● Pulmonary oedema- IV / IM frusemide.
If the patient has stabilised.
● Reassess the patients airway, mental status , ability to speak and breathing effort.
● Check vital signs.
● Redo , thorough history taking , physical examination.
55. AFTER THE PATIENT HAS BEEN STABILISED
1. Reassess the patients airway, mental status, ability to speak and breathing efforts.
2. Check vital signs
3. Thorough history taking and physical examinations ( I.e breath sounds and observe skin
colour.
56. HOW DO WE REDUCE VENTILATORY DEMANDS .
Treat the underlying causes
● Infections
● Pleural effusion
● Pneumothorax
● Pulmonary embolism
● Congestive heart failure
The best method for assessing hypoxaemia is the ratio of the PaO2 (measured by blood gas) to the fractional inspired oxygen delivered (PaO2/FiO2). This ‘PF’ ratio is lower, the more severe the disease.
Other pulmonary function tests
Body plesthmography- airtight chamber
Cardiopulmonary exercise stress test- evaluation of dyspnea (to rule out cardiac dz)
Lung volumes
Diffusion capacity