1. Chronic obstructive pulmonary disease (COPD) is a preventable and treatable lung disease characterized by airflow limitation caused by cigarette smoking.
2. COPD symptoms include cough, sputum production, and breathlessness. It is a major cause of death and disability worldwide and is expected to be the third leading cause of death by 2020.
3. COPD is diagnosed based on symptoms and spirometry showing airflow limitation that is not fully reversible. The two main phenotypes are chronic bronchitis and emphysema.
This document provides information about COPD (chronic obstructive pulmonary disease). It defines COPD as a preventable and treatable lung disease characterized by persistent airflow limitation. The primary cause is cigarette smoking. COPD is the 4th leading cause of death and is expected to rise to 3rd by 2020. The document discusses the clinical presentation, diagnosis through spirometry testing, and management through smoking cessation and bronchodilator medications.
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.
This document discusses restrictive interstitial lung diseases. Restrictive lung diseases are caused by loss of lung volume from conditions affecting the lungs, chest wall, or pleura. Interstitial lung diseases involve thickening of alveolar walls due to inflammation, granulomas, hemorrhage or fibrosis. Specific restrictive interstitial diseases covered include sarcoidosis, cryptogenic fibrosing alveolitis, pneumoconioses caused by organic or inorganic dust exposure, and lung diseases associated with connective tissue disorders or systemic inflammation.
This document defines acute respiratory distress syndrome (ARDS) and discusses its pathophysiology, risk factors, diagnosis, management, and ventilator strategies. ARDS is defined as acute onset bilateral pulmonary infiltrates, hypoxemia, and no heart failure. It was initially defined in 1971 and revised definitions in 1988 and 1994 established clearer criteria. Common causes are pneumonia, aspiration, and sepsis. Management involves treating the underlying cause, supportive ICU care, and lung protective ventilation with low tidal volumes (6 ml/kg) and moderate PEEP levels. Adjuncts like conservative fluid management, prone positioning, and recruitment maneuvers may provide benefits.
This document discusses a case of acute respiratory failure in a 300 kg patient who presented with sudden severe hypoxia and unconsciousness. It then provides an overview of acute respiratory failure, distinguishing between hypercapnic and hypoxemic respiratory failure. Various causes of each type are described in detail. The case is specifically focused on acute respiratory distress syndrome (ARDS), explaining its pathogenesis, risk factors, complications, and management including a landmark ARMA clinical trial showing benefit of lower tidal volumes.
This document discusses the treatment of acute exacerbations of asthma and COPD. For asthma, treatment involves high doses of inhaled bronchodilators, systemic corticosteroids, oxygen therapy, and intravenous fluids. For COPD, treatment focuses on oxygenation, ventilation support using non-invasive ventilation if needed, nebulized short-acting bronchodilators, corticosteroids, and antibiotics for bacterial infections. Lung volumes measured via spirometry can differentiate obstructive disorders like COPD and asthma from restrictive disorders. Obstructive disorders show reduced airflow and FEV1/FVC ratio, while restrictive disorders have normal ratio but reduced lung volumes. Emergent tests for diagnosis include ECG, arterial blood gases,
This document discusses restrictive lung diseases including interstitial lung fibrosis and asbestosis. It defines interstitial pulmonary fibrosis as a chronic, fibrosing interstitial pneumonia of unknown cause typically affecting adults over 50. Usual interstitial pneumonia is the most common form and has a median survival of 3 years. Asbestosis is an occupational lung disease caused by inhalation of asbestos fibers, which can lead to pleural thickening, effusions, rounded atelectasis or fibrosis. Prevention focuses on never disturbing asbestos materials and smoking cessation.
This document provides information about COPD (chronic obstructive pulmonary disease). It defines COPD as a preventable and treatable lung disease characterized by persistent airflow limitation. The primary cause is cigarette smoking. COPD is the 4th leading cause of death and is expected to rise to 3rd by 2020. The document discusses the clinical presentation, diagnosis through spirometry testing, and management through smoking cessation and bronchodilator medications.
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.
This document discusses restrictive interstitial lung diseases. Restrictive lung diseases are caused by loss of lung volume from conditions affecting the lungs, chest wall, or pleura. Interstitial lung diseases involve thickening of alveolar walls due to inflammation, granulomas, hemorrhage or fibrosis. Specific restrictive interstitial diseases covered include sarcoidosis, cryptogenic fibrosing alveolitis, pneumoconioses caused by organic or inorganic dust exposure, and lung diseases associated with connective tissue disorders or systemic inflammation.
This document defines acute respiratory distress syndrome (ARDS) and discusses its pathophysiology, risk factors, diagnosis, management, and ventilator strategies. ARDS is defined as acute onset bilateral pulmonary infiltrates, hypoxemia, and no heart failure. It was initially defined in 1971 and revised definitions in 1988 and 1994 established clearer criteria. Common causes are pneumonia, aspiration, and sepsis. Management involves treating the underlying cause, supportive ICU care, and lung protective ventilation with low tidal volumes (6 ml/kg) and moderate PEEP levels. Adjuncts like conservative fluid management, prone positioning, and recruitment maneuvers may provide benefits.
This document discusses a case of acute respiratory failure in a 300 kg patient who presented with sudden severe hypoxia and unconsciousness. It then provides an overview of acute respiratory failure, distinguishing between hypercapnic and hypoxemic respiratory failure. Various causes of each type are described in detail. The case is specifically focused on acute respiratory distress syndrome (ARDS), explaining its pathogenesis, risk factors, complications, and management including a landmark ARMA clinical trial showing benefit of lower tidal volumes.
This document discusses the treatment of acute exacerbations of asthma and COPD. For asthma, treatment involves high doses of inhaled bronchodilators, systemic corticosteroids, oxygen therapy, and intravenous fluids. For COPD, treatment focuses on oxygenation, ventilation support using non-invasive ventilation if needed, nebulized short-acting bronchodilators, corticosteroids, and antibiotics for bacterial infections. Lung volumes measured via spirometry can differentiate obstructive disorders like COPD and asthma from restrictive disorders. Obstructive disorders show reduced airflow and FEV1/FVC ratio, while restrictive disorders have normal ratio but reduced lung volumes. Emergent tests for diagnosis include ECG, arterial blood gases,
This document discusses restrictive lung diseases including interstitial lung fibrosis and asbestosis. It defines interstitial pulmonary fibrosis as a chronic, fibrosing interstitial pneumonia of unknown cause typically affecting adults over 50. Usual interstitial pneumonia is the most common form and has a median survival of 3 years. Asbestosis is an occupational lung disease caused by inhalation of asbestos fibers, which can lead to pleural thickening, effusions, rounded atelectasis or fibrosis. Prevention focuses on never disturbing asbestos materials and smoking cessation.
Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of bilateral pulmonary infiltrates and hypoxemia leading to respiratory failure. It is caused by acute diffuse inflammatory lung injury from a direct or indirect pulmonary insult. Diagnosis requires excluding left heart failure and evaluating for underlying causes. Pathologically, it involves diffuse alveolar damage and pulmonary edema. Treatment focuses on supportive care including mechanical ventilation, fluid management, and treatment of underlying conditions. While mortality has decreased in recent decades, ARDS still carries a significant risk of death.
Chronic obstructive pulmonary diseases (COPD) include chronic bronchitis and emphysema. Chronic bronchitis involves long-term inflammation of the airways that leads to excessive mucus production and chronic cough. Emphysema causes permanent enlargement of the airspaces in the lungs due to destruction of lung tissue, which reduces elastic recoil and increases air trapping. Asthma is a chronic inflammatory disease characterized by variable and recurring symptoms of wheezing, coughing, chest tightness and shortness of breath. Treatment for these conditions focuses on reducing symptoms through bronchodilators and corticosteroids.
Acute Respiratory Distress Syndrome (ARDS) is a clinical syndrome characterized by hypoxemia, bilateral pulmonary infiltrates, and respiratory failure. The document defines ARDS and discusses its etiology, pathophysiology, clinical features, diagnosis, and evidence-based treatment recommendations. Key points include low tidal volume ventilation to minimize lung injury, conservative fluid management, use of PEEP to recruit alveoli while limiting pressures, and treating the underlying cause of ARDS. Outcomes remain poor with high mortality rates, though some patients fully recover lung function over time.
The document compares mechanical ventilation strategies for acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). For ARDS, the strategies aim to prevent volutrauma and barotrauma by limiting tidal volumes and airway pressures. Positive end-expiratory pressure (PEEP) is used to recruit alveoli and keep airways open. For COPD, the goal is to increase oxygen levels while allowing longer expiration to prevent auto-PEEP. Non-invasive ventilation can help both conditions but invasive ventilation may be needed for severe COPD exacerbations or if non-invasive methods fail.
Acute Respiratory Distress Syndrome (ARDS) is a sudden, progressive form of respiratory failure characterized by severe dyspnea, hypoxemia, and decreased lung compliance. It develops from direct or indirect lung injuries and is thought to be caused by stimulation of the inflammatory and immune systems, resulting in leakage of fluid into the lungs. The clinical progression of ARDS involves exudative, proliferative, and fibrotic phases that can lead to respiratory failure if not promptly treated with oxygen supplementation, mechanical ventilation, and other supportive therapies.
Acute respiratory distress syndrome (ARDS) is defined as acute lung inflammation and increased permeability causing hypoxemia. It is characterized by bilateral infiltrates and low PaO2/FiO2 ratio with no cardiac cause. ARDS can be caused directly by lung injury or indirectly. It has three stages - exudative, proliferative, and recovery. Mechanical ventilation can worsen ARDS through barotrauma, atelectotrauma, and volutrauma. Lung protective ventilation aims to prevent further injury through small tidal volumes, high respiratory rate, low pressures and adequate PEEP. The prone position and ECMO may be rescue therapies for moderate-severe ARDS when conventional measures fail.
Slideshow is from the University of Michigan Medical School's M2 Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Resp
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.
1) Pediatric ARDS is caused by conditions like sepsis, pneumonia, trauma, and noninfectious lung injuries. It is characterized by diffuse lung inflammation and fluid buildup in the lungs.
2) Traditional management focuses on gentle mechanical ventilation with low tidal volumes and permissive hypercapnia to prevent further lung injury. New therapies under investigation include prone positioning, high frequency oscillatory ventilation, inhaled nitric oxide, surfactant, and steroids.
3) While no single therapy has proven definitively effective for pediatric ARDS outcomes, a multimodal approach tailored to the individual patient shows the most promise based on current research.
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 acute respiratory distress syndrome (ARDS). It begins by defining ARDS and describing its signs and symptoms. It then discusses the history of ARDS definitions and criteria. It outlines the pathophysiology and three phases of ARDS. Treatment strategies covered include mechanical ventilation, monitoring, infection control, and specific therapies. Prognosis and risk factors are also summarized.
The document provides information about Acute Respiratory Distress Syndrome (ARDS) including its definition, pathophysiology, diagnosis, management, and prognosis. ARDS is defined as rapid onset hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. It is caused by direct lung injury from conditions like pneumonia or indirect injury from sepsis or trauma. Diagnosis involves criteria of acute onset, hypoxemia with PaO2/FiO2 ≤200, and no heart failure. Management focuses on treating the underlying cause and providing ventilator support using low tidal volumes per the ARDSNet protocol to reduce ventilator-induced lung injury. Prognosis depends on risk factors and mortality ranges from 26-44%.
This document discusses the diagnosis of chronic obstructive pulmonary disease (COPD). It covers the clinical, spirometric, and radiological aspects of diagnosis. Clinically, COPD should be considered in patients with dyspnea, chronic cough or sputum production who have a history of risk factor exposure. Spirometry is required to diagnose COPD, with a post-bronchodilator FEV1/FVC ratio below 70% confirming persistent airflow limitation. Radiological examinations can identify emphysema and airway abnormalities associated with COPD. Spirometry values should be compared to age-related normal values and reversibility testing with bronchodilators can distinguish COPD from asthma.
The document provides information about acute respiratory distress syndrome (ARDS). It begins with a brief history of ARDS and provides the clinical definition. It describes the diagnostic criteria and etiology, including that most cases are caused by sepsis, pneumonia, or trauma. It then discusses the normal lung physiology and pathophysiology of ARDS, which involves three phases: exudative, proliferative, and fibrotic. The management section outlines the principles of therapy to provide adequate gas exchange while avoiding secondary injury, including mechanical ventilation protocols, fluid management, and other strategies. It concludes with a discussion of prognosis and recent advances in ARDS management such as protective ventilation strategies.
This document summarizes acute respiratory distress syndrome (ARDS) by defining it, describing its severity, pathophysiology, etiology, risk factors, goals of therapy, and ventilator strategies. ARDS is defined by timing, radiographic changes, and origin of edema not due to heart failure. Severity is based on oxygenation. The pathophysiology involves diffuse alveolar damage and endothelial injury. Common causes are sepsis, aspiration, and trauma. Treatment aims to allow lung healing while avoiding further injury through strategies like low tidal volumes and positive end-expiratory pressure to reduce volutrauma, barotrauma, and atelectrauma.
This document discusses acute respiratory distress syndrome (ARDS), including its definition, causes, pathogenesis, management challenges, and treatment strategies. ARDS is characterized by acute lung injury leading to hypoxemia. Common causes include pneumonia, sepsis, and trauma. The lung injury progresses through exudative, proliferative, and fibrotic phases. Conservative fluid management, low tidal volume ventilation, and positive end-expiratory pressure are the primary treatment approaches.
This document discusses chronic obstructive pulmonary disease (COPD) and considerations for anesthesia. It defines COPD and describes related conditions like chronic bronchitis and emphysema. It covers risk factors, pathogenesis, pathophysiology including airway obstruction, hyperinflation, and gas exchange impairment. Clinical features, investigations, disease classification, and treatment approaches including smoking cessation and bronchodilators are summarized. Key points for anesthetists regarding airway challenges, ventilation/perfusion abnormalities, and development of auto-PEEP are highlighted.
Updates on Acute respiratory distress syndromeHamdi Turkey
The document provides an overview of acute respiratory distress syndrome (ARDS). It begins with a case presentation of a patient exhibiting symptoms of ARDS and then outlines the learning objectives which include understanding the definition, pathology, ventilation strategies, and adjunct therapies for ARDS. It reviews the history and evolving definitions of ARDS from 1967 to the current Berlin Definition from 2012. Key aspects of the Berlin Definition are described. The document discusses the incidence, outcomes, risk factors, pathophysiology involving different phases, clinical features, investigations, management goals and therapies for ARDS. Images are included showing histology, chest x-rays and CT scans of ARDS patients.
The document defines acute hypoxaemic respiratory failure and ARDS according to the Berlin Definition. It then discusses issues with the Berlin definition and the old criteria. The direct and indirect causes of ARDS are outlined. Details are provided about the pathophysiology, effects, biomarkers, outcomes, and various treatment strategies for ARDS including ventilation measures, prone positioning, recruitment maneuvers, and oxygenation targets. Mortality rates associated with ARDS are also summarized.
This document provides information on chronic obstructive pulmonary disease (COPD). It discusses the epidemiology, definition, risk factors, pathogenesis, pathology, classification, management, and exacerbations of COPD. Key points include: cigarette smoking is the primary cause of COPD worldwide; the disease involves inflammation in the lungs from noxious particles leading to airflow limitation; emphysema and chronic bronchitis are the major pathological changes; severity is classified based on lung function tests; and management involves reducing risk factors, treating stable COPD, and managing exacerbations.
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation caused by exposure to noxious particles or gases. It includes chronic bronchitis and emphysema. Clinically, patients are either "blue bloaters", with predominantly bronchitis, or "pink puffers" with predominantly emphysema. Diagnosis is confirmed by spirometry showing FEV1/FVC <70% and severity is classified based on post-bronchodilator FEV1. Management involves smoking cessation, bronchodilators, corticosteroids, oxygen therapy, and surgery in some cases. Acute exacerbations are managed with oxygen, nebulized bronchodilators, oral
Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of bilateral pulmonary infiltrates and hypoxemia leading to respiratory failure. It is caused by acute diffuse inflammatory lung injury from a direct or indirect pulmonary insult. Diagnosis requires excluding left heart failure and evaluating for underlying causes. Pathologically, it involves diffuse alveolar damage and pulmonary edema. Treatment focuses on supportive care including mechanical ventilation, fluid management, and treatment of underlying conditions. While mortality has decreased in recent decades, ARDS still carries a significant risk of death.
Chronic obstructive pulmonary diseases (COPD) include chronic bronchitis and emphysema. Chronic bronchitis involves long-term inflammation of the airways that leads to excessive mucus production and chronic cough. Emphysema causes permanent enlargement of the airspaces in the lungs due to destruction of lung tissue, which reduces elastic recoil and increases air trapping. Asthma is a chronic inflammatory disease characterized by variable and recurring symptoms of wheezing, coughing, chest tightness and shortness of breath. Treatment for these conditions focuses on reducing symptoms through bronchodilators and corticosteroids.
Acute Respiratory Distress Syndrome (ARDS) is a clinical syndrome characterized by hypoxemia, bilateral pulmonary infiltrates, and respiratory failure. The document defines ARDS and discusses its etiology, pathophysiology, clinical features, diagnosis, and evidence-based treatment recommendations. Key points include low tidal volume ventilation to minimize lung injury, conservative fluid management, use of PEEP to recruit alveoli while limiting pressures, and treating the underlying cause of ARDS. Outcomes remain poor with high mortality rates, though some patients fully recover lung function over time.
The document compares mechanical ventilation strategies for acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). For ARDS, the strategies aim to prevent volutrauma and barotrauma by limiting tidal volumes and airway pressures. Positive end-expiratory pressure (PEEP) is used to recruit alveoli and keep airways open. For COPD, the goal is to increase oxygen levels while allowing longer expiration to prevent auto-PEEP. Non-invasive ventilation can help both conditions but invasive ventilation may be needed for severe COPD exacerbations or if non-invasive methods fail.
Acute Respiratory Distress Syndrome (ARDS) is a sudden, progressive form of respiratory failure characterized by severe dyspnea, hypoxemia, and decreased lung compliance. It develops from direct or indirect lung injuries and is thought to be caused by stimulation of the inflammatory and immune systems, resulting in leakage of fluid into the lungs. The clinical progression of ARDS involves exudative, proliferative, and fibrotic phases that can lead to respiratory failure if not promptly treated with oxygen supplementation, mechanical ventilation, and other supportive therapies.
Acute respiratory distress syndrome (ARDS) is defined as acute lung inflammation and increased permeability causing hypoxemia. It is characterized by bilateral infiltrates and low PaO2/FiO2 ratio with no cardiac cause. ARDS can be caused directly by lung injury or indirectly. It has three stages - exudative, proliferative, and recovery. Mechanical ventilation can worsen ARDS through barotrauma, atelectotrauma, and volutrauma. Lung protective ventilation aims to prevent further injury through small tidal volumes, high respiratory rate, low pressures and adequate PEEP. The prone position and ECMO may be rescue therapies for moderate-severe ARDS when conventional measures fail.
Slideshow is from the University of Michigan Medical School's M2 Respiratory sequence
View additional course materials on Open.Michigan:
openmi.ch/med-M2Resp
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.
1) Pediatric ARDS is caused by conditions like sepsis, pneumonia, trauma, and noninfectious lung injuries. It is characterized by diffuse lung inflammation and fluid buildup in the lungs.
2) Traditional management focuses on gentle mechanical ventilation with low tidal volumes and permissive hypercapnia to prevent further lung injury. New therapies under investigation include prone positioning, high frequency oscillatory ventilation, inhaled nitric oxide, surfactant, and steroids.
3) While no single therapy has proven definitively effective for pediatric ARDS outcomes, a multimodal approach tailored to the individual patient shows the most promise based on current research.
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 acute respiratory distress syndrome (ARDS). It begins by defining ARDS and describing its signs and symptoms. It then discusses the history of ARDS definitions and criteria. It outlines the pathophysiology and three phases of ARDS. Treatment strategies covered include mechanical ventilation, monitoring, infection control, and specific therapies. Prognosis and risk factors are also summarized.
The document provides information about Acute Respiratory Distress Syndrome (ARDS) including its definition, pathophysiology, diagnosis, management, and prognosis. ARDS is defined as rapid onset hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. It is caused by direct lung injury from conditions like pneumonia or indirect injury from sepsis or trauma. Diagnosis involves criteria of acute onset, hypoxemia with PaO2/FiO2 ≤200, and no heart failure. Management focuses on treating the underlying cause and providing ventilator support using low tidal volumes per the ARDSNet protocol to reduce ventilator-induced lung injury. Prognosis depends on risk factors and mortality ranges from 26-44%.
This document discusses the diagnosis of chronic obstructive pulmonary disease (COPD). It covers the clinical, spirometric, and radiological aspects of diagnosis. Clinically, COPD should be considered in patients with dyspnea, chronic cough or sputum production who have a history of risk factor exposure. Spirometry is required to diagnose COPD, with a post-bronchodilator FEV1/FVC ratio below 70% confirming persistent airflow limitation. Radiological examinations can identify emphysema and airway abnormalities associated with COPD. Spirometry values should be compared to age-related normal values and reversibility testing with bronchodilators can distinguish COPD from asthma.
The document provides information about acute respiratory distress syndrome (ARDS). It begins with a brief history of ARDS and provides the clinical definition. It describes the diagnostic criteria and etiology, including that most cases are caused by sepsis, pneumonia, or trauma. It then discusses the normal lung physiology and pathophysiology of ARDS, which involves three phases: exudative, proliferative, and fibrotic. The management section outlines the principles of therapy to provide adequate gas exchange while avoiding secondary injury, including mechanical ventilation protocols, fluid management, and other strategies. It concludes with a discussion of prognosis and recent advances in ARDS management such as protective ventilation strategies.
This document summarizes acute respiratory distress syndrome (ARDS) by defining it, describing its severity, pathophysiology, etiology, risk factors, goals of therapy, and ventilator strategies. ARDS is defined by timing, radiographic changes, and origin of edema not due to heart failure. Severity is based on oxygenation. The pathophysiology involves diffuse alveolar damage and endothelial injury. Common causes are sepsis, aspiration, and trauma. Treatment aims to allow lung healing while avoiding further injury through strategies like low tidal volumes and positive end-expiratory pressure to reduce volutrauma, barotrauma, and atelectrauma.
This document discusses acute respiratory distress syndrome (ARDS), including its definition, causes, pathogenesis, management challenges, and treatment strategies. ARDS is characterized by acute lung injury leading to hypoxemia. Common causes include pneumonia, sepsis, and trauma. The lung injury progresses through exudative, proliferative, and fibrotic phases. Conservative fluid management, low tidal volume ventilation, and positive end-expiratory pressure are the primary treatment approaches.
This document discusses chronic obstructive pulmonary disease (COPD) and considerations for anesthesia. It defines COPD and describes related conditions like chronic bronchitis and emphysema. It covers risk factors, pathogenesis, pathophysiology including airway obstruction, hyperinflation, and gas exchange impairment. Clinical features, investigations, disease classification, and treatment approaches including smoking cessation and bronchodilators are summarized. Key points for anesthetists regarding airway challenges, ventilation/perfusion abnormalities, and development of auto-PEEP are highlighted.
Updates on Acute respiratory distress syndromeHamdi Turkey
The document provides an overview of acute respiratory distress syndrome (ARDS). It begins with a case presentation of a patient exhibiting symptoms of ARDS and then outlines the learning objectives which include understanding the definition, pathology, ventilation strategies, and adjunct therapies for ARDS. It reviews the history and evolving definitions of ARDS from 1967 to the current Berlin Definition from 2012. Key aspects of the Berlin Definition are described. The document discusses the incidence, outcomes, risk factors, pathophysiology involving different phases, clinical features, investigations, management goals and therapies for ARDS. Images are included showing histology, chest x-rays and CT scans of ARDS patients.
The document defines acute hypoxaemic respiratory failure and ARDS according to the Berlin Definition. It then discusses issues with the Berlin definition and the old criteria. The direct and indirect causes of ARDS are outlined. Details are provided about the pathophysiology, effects, biomarkers, outcomes, and various treatment strategies for ARDS including ventilation measures, prone positioning, recruitment maneuvers, and oxygenation targets. Mortality rates associated with ARDS are also summarized.
This document provides information on chronic obstructive pulmonary disease (COPD). It discusses the epidemiology, definition, risk factors, pathogenesis, pathology, classification, management, and exacerbations of COPD. Key points include: cigarette smoking is the primary cause of COPD worldwide; the disease involves inflammation in the lungs from noxious particles leading to airflow limitation; emphysema and chronic bronchitis are the major pathological changes; severity is classified based on lung function tests; and management involves reducing risk factors, treating stable COPD, and managing exacerbations.
Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation caused by exposure to noxious particles or gases. It includes chronic bronchitis and emphysema. Clinically, patients are either "blue bloaters", with predominantly bronchitis, or "pink puffers" with predominantly emphysema. Diagnosis is confirmed by spirometry showing FEV1/FVC <70% and severity is classified based on post-bronchodilator FEV1. Management involves smoking cessation, bronchodilators, corticosteroids, oxygen therapy, and surgery in some cases. Acute exacerbations are managed with oxygen, nebulized bronchodilators, oral
Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by airflow limitation that is usually progressive. It is the third leading cause of death in the United States. The two main conditions that make up COPD are chronic bronchitis and emphysema. Cigarette smoking is the leading risk factor. Symptoms include dyspnea, chronic cough, and sputum production. Diagnosis is confirmed by spirometry showing airflow limitation. Management focuses on smoking cessation, bronchodilators, glucocorticoids, pulmonary rehabilitation, oxygen therapy, and managing exacerbations and comorbidities.
This document discusses pneumonia, including its definition, causes, classification, prevalence, and treatment. Key points include:
- Pneumonia is an inflammatory lung disease that can be caused by bacteria, viruses, fungi or other particles. The most common type is bacterial pneumonia.
- Risk factors for pneumonia include aging, smoking, underlying diseases, and immunosuppression. It is classified based on location (lobar, foliar, interstitial), cause (bacterial, viral, fungal), and place of infection (community-acquired, hospital-acquired).
- Common bacterial causes are Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. Diagn
Obstructive and restrictive pulmonary diseases can be categorized based on pulmonary function tests. Obstructive diseases like emphysema and chronic bronchitis involve airflow limitation due to airway obstruction. Restrictive diseases like pulmonary fibrosis involve reduced lung expansion and capacity. Chronic obstructive pulmonary disease (COPD) encompasses chronic bronchitis and emphysema, both of which involve irreversible airway obstruction. Emphysema is defined as abnormal enlargement of airspaces distal to terminal bronchioles due to alveolar wall destruction. The main types are centriacinar and panacinar emphysema. Emphysema results from an imbalance between proteases and antiproteases degrading lung tissue in heavy smokers.
Respiratory failure is characterized by severe dysfunction of pulmonary ventilation and/or oxygenation caused by various diseases, resulting in hypoxia and retention of carbon dioxide. It is defined as a PaO2 of less than 8.0 kPa (60 mmHg), and/or a PaCO2 of greater than 6.67 kPa (50 mmHg). The main causes are ventilation dysfunction due to airway obstruction or limitation, and oxygenation dysfunction due to pulmonary edema, interstitial lung disease, or ARDS. The key pathophysiological changes are hypoxia, retention of carbon dioxide, and acidosis, which can affect multiple organ systems and lead to complications.
1) The patient presents with a history of recurrent chest infections and inspiratory crackles on examination. Imaging and pulmonary function tests are required to diagnose interstitial lung disease.
2) Idiopathic pulmonary fibrosis is a chronic, progressive form of interstitial lung disease of unknown cause characterized by fibrosis of the lungs. It carries a poor prognosis with median survival of 3 years.
3) Diagnosis requires ruling out other causes through history, imaging showing reticular opacities and honeycombing, and lung biopsy if imaging is not definitive. Treatment focuses on managing complications, vaccination, oxygen therapy and consideration of lung transplantation in advanced cases.
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is usually progressive and associated with an abnormal inflammatory response in the lungs. The most common causes of COPD are cigarette smoking and exposure to occupational dusts and fumes. Spirometry is required for diagnosis and shows airflow limitation defined as a reduced FEV1/FVC ratio. The severity of COPD is classified based on post-bronchodilator FEV1 levels. Management involves smoking cessation, vaccinations, rehabilitation, pharmacotherapy including bronchodilators and inhaled corticosteroids, and long-term oxygen therapy in severe cases.
This document discusses several pulmonary conditions including pleural effusion, acute respiratory distress syndrome (ARDS), bronchial asthma, chronic obstructive pulmonary disease (COPD), and lung abscess. For pleural effusion, it describes the causes, signs and symptoms, investigations including pleural fluid analysis, and treatments including thoracentesis. For ARDS, it provides the definition, precipitating factors, symptoms, investigations, and management including supportive care and treating the underlying cause. It also summarizes the definitions, common triggers, signs and symptoms, diagnosis, investigations, and treatment including bronchodilators and corticosteroids for bronchial asthma and COPD.
Pneumocystis pneumonia (PCP) is caused by Pneumocystis jiroveci and is an opportunistic infection affecting those with weakened immune systems. It is diagnosed through microscopic visualization of the organism in samples obtained noninvasively through induced sputum or bronchoalveolar lavage, or invasively through lung biopsy. Common symptoms include dyspnea, fever, and cough. Chest imaging often shows bilateral infiltrates and laboratory tests like lactate dehydrogenase are elevated. Treatment involves anti-fungal medications.
Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction that is not fully reversible. The two main conditions that cause COPD are chronic bronchitis and emphysema. Chronic bronchitis involves a long-term cough with mucus, while emphysema involves destruction of lung tissue leading to fewer and larger air spaces. The primary risk factor is cigarette smoking. Symptoms include cough, sputum production, wheezing and shortness of breath. Diagnosis is made based on history of symptoms and spirometry showing airflow limitation. Treatment focuses on smoking cessation and medications to relieve symptoms.
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 provides information on chronic obstructive pulmonary disease (COPD) including its definition, risk factors, pathophysiology, clinical manifestations, medical management, nursing management, and surgical options. COPD is characterized by persistent airflow limitation that is not fully reversible. It is mostly caused by smoking and results in changes like thickening of the airways and inflammation that narrow the lungs over time. Management involves treatments to improve ventilation and remove secretions, as well as strategies to prevent complications and promote overall health.
The document summarizes chronic obstructive pulmonary disease (COPD). It covers the general considerations, epidemiology, risk factors, pathogenesis, clinical findings, differential diagnosis, diagnostic testing including spirometry and imaging, and treatment including smoking cessation, oxygen therapy, bronchodilators, corticosteroids, and antibiotics. COPD is characterized by airflow obstruction due to chronic bronchitis or emphysema and is generally progressive. Cigarette smoking is the most important risk factor.
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.
Presentation1.pptx, radiological imaging of restrictive lung diseases.Abdellah Nazeer
1. Restrictive lung diseases are characterized by diffuse involvement of the pulmonary connective tissue leading to stiff lungs and reduced expansion.
2. Fibrosis results in the stiffening of the lung tissue, predominantly in the delicate alveolar walls.
3. Common restrictive lung diseases include idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, and pneumoconiosis.
mechanical ventilation in restrictive lung disease.pptxnigatendalamaw2
1. The document discusses mechanical ventilation in restrictive pulmonary diseases. It outlines causes of restrictive diseases including lung parenchyma disorders, pleural disorders, and extra-pulmonary disorders.
2. Lung parenchyma disorders discussed in detail include interstitial lung diseases like sarcoidosis and hypersensitivity pneumonitis, occupational lung diseases, and atelectatic disorders like ARDS.
3. The key characteristics of restrictive diseases are decreased vital capacity, total lung capacity, and gas exchange. Ventilator settings for restrictive diseases aim to use low tidal volumes and pressures to prevent further lung injury.
COPD is a common lung disease characterized by persistent airflow limitation caused by damage to the lungs, usually from smoking. It is the fourth leading cause of death. Symptoms include shortness of breath, chronic cough, and sputum production. Diagnosis is confirmed by pulmonary function tests showing airflow limitation that is not fully reversible. Treatment focuses on reducing symptoms and exacerbations through bronchodilators, inhaled corticosteroids, pulmonary rehabilitation, oxygen therapy, and managing comorbidities.
Pneumothorax is the presence of air in the pleural space and can occur spontaneously or due to injury. It is classified as primary, occurring without lung disease, or secondary, occurring in patients with lung diseases like COPD. Symptoms include chest pain and breathlessness. Diagnosis is made through chest x-ray showing lung edge and lack of markings between lung and chest wall. Small primary pneumothorax may resolve on its own but others require chest tube placement and hospital monitoring. Recurrent spontaneous pneumothorax requires pleurodesis surgery after second occurrence to prevent future episodes.
This document discusses a case of lung consolidation seen in a patient. It provides definitions and causes of lung consolidation, including pneumonia, malignancy, and infarction. Differential diagnoses for consolidation are discussed. The document also contains sections on carcinoma of the lung, bronchial carcinoma, clinical features of lung cancer, investigations for lung cancer, and management of lung cancer. Secondary tumors of the lung and classifications of pneumonia are also summarized.
This document defines pulmonary embolism and describes its causes, risk factors, symptoms, diagnostic tests, and treatment options. Pulmonary embolism is caused by blockage of the pulmonary arteries, most commonly by blood clots originating in the deep veins of the lower extremities. It can be diagnosed based on risk factors, symptoms of dyspnea and chest pain, and tests including D-dimer, CT scans, ventilation/perfusion scans and pulmonary angiography. Treatment involves blood thinners, thrombolytic drugs, or occasionally surgery to restore blood flow in severe cases.
This very short document does not contain enough content to create a meaningful 3 sentence summary. The document only contains an instruction to "Type a quote here" but does not include any actual quote or other substantive information.
Tracheal auscultation is recommended as part of the routine clinical assessment for asthma patients due to hyperinflated lungs making wheezes easier to hear over the trachea. Chest X-rays are only necessary for severe asthma to rule out other conditions like pneumonia. Allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to fungal spores in the airway wall that can complicate asthma in 1-2% of patients and cystic fibrosis in 5-10% of patients. Management of allergic bronchopulmonary aspergillosis includes regular low-dose oral corticosteroids with itraconazole to reduce steroids in some patients.
L1 introduction to respiratory medicinebilal nuaman
The document appears to be a date range from 2017 to 2018. It does not provide any other context or details within the single line of text. The year range of 2017 to 2018 is the only information given.
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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.
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TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
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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.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. DefinitionDefinition
Chronic obstructive pulmonary disease (COPD) isChronic obstructive pulmonary disease (COPD) is
a preventable and treatable disease statea preventable and treatable disease state
characterized by airflow limitation that ischaracterized by airflow limitation that is notnot
fully reversiblefully reversible..
The airflow limitation is usuallyThe airflow limitation is usually progressiveprogressive andand
is associated with an abnormal inflammatoryis associated with an abnormal inflammatory
response of the lungs, primarily caused byresponse of the lungs, primarily caused by
cigarette smoking.cigarette smoking.
Although COPD affects the lungs, it alsoAlthough COPD affects the lungs, it also
producesproduces significant systemic consequencessignificant systemic consequences..
22
4. ➢Major cause of death and disabilityMajor cause of death and disability
➢44thth
leading cause of deathleading cause of death
➢COPD is the only chronic disease that isCOPD is the only chronic disease that is
showing progressive upward trend in bothshowing progressive upward trend in both
mortalitymortality andand morbiditymorbidity
➢It is expected to be theIt is expected to be the thirdthird leading cause ofleading cause of
death by 2020death by 2020
COPDCOPD
GENERAL FACTSGENERAL FACTS
44
5. % Change in Age Adjusted Death Rate% Change in Age Adjusted Death Rate
55
7. ➢ COPD should be suspected in any patientCOPD should be suspected in any patient
over the age of 35 years who presents withover the age of 35 years who presents with
symptoms of persistent cough and sputumsymptoms of persistent cough and sputum
production and/or breathlessness.production and/or breathlessness.
➢ Depending on the presentation importantDepending on the presentation important
differential diagnoses include asthma,differential diagnoses include asthma,
tuberculosis, bronchiectasis and congestivetuberculosis, bronchiectasis and congestive
cardiac failure.cardiac failure.
77
8. ➢ BreathlessnessBreathlessness usually heralds the first presentation tousually heralds the first presentation to
the health professional.the health professional.
➢ In advanced disease, the presence ofIn advanced disease, the presence of edemaedema andand
morning headachesmorning headaches indicative ofindicative of hypercapniahypercapnia..
➢ CracklesCrackles may accompany infection but if persistent raisemay accompany infection but if persistent raise
the possibility of bronchiectasis.the possibility of bronchiectasis.
➢ Finger clubbingFinger clubbing isis not consistentnot consistent with COPD and shouldwith COPD and should
alert the physician to potentially more serious pathology.alert the physician to potentially more serious pathology.
(CA Lung)(CA Lung)
88
9. ➢ Some patients with severe COPD maySome patients with severe COPD may
demonstrate signs consistent withdemonstrate signs consistent with corpulmonalecorpulmonale
(raised jugular venous pressure, loud P2 due to(raised jugular venous pressure, loud P2 due to
pulmonary hypertension, tricuspid regurgitation,pulmonary hypertension, tricuspid regurgitation,
pitting peripheral edema and hepatomegaly) andpitting peripheral edema and hepatomegaly) and
its presence usually indicates a poor prognosis.its presence usually indicates a poor prognosis.
99
10. Skeletal muscle wasting and cachexia maySkeletal muscle wasting and cachexia may
occur in advanced disease, while someoccur in advanced disease, while some
patients may also be overweight.patients may also be overweight.
The body mass index (BMI; weight/height²)The body mass index (BMI; weight/height²)
should be calculated during the initialshould be calculated during the initial
examination.examination.
1010
16. Pink PuffersPink Puffers
➢Thin andThin and
dyspnic , anddyspnic , and
maintain PaCO2maintain PaCO2
until the lateuntil the late
stage ofstage of
disease.disease.
➢EMPHESEMAEMPHESEMA
1616
17. PPursed liursed lipp breathing occur inbreathing occur in
emempphysemahysema not in chronic bronchitisnot in chronic bronchitis
1717
22. Clinical FeaturesClinical Features
➢No cyanosisNo cyanosis (pink)(pink)
➢Presents withPresents with severe dyspneasevere dyspnea (puffer)(puffer)
➢Have aHave a barrel chestbarrel chest..
➢X-ray showsX-ray shows large volume lung, Heartlarge volume lung, Heart isis
seems buried and diaphragm pushed down.seems buried and diaphragm pushed down.
Alveoli can ruptureAlveoli can rupture pneumothorax.pneumothorax.
➢Don’t usually have cough or expectorationDon’t usually have cough or expectoration
PINK PUFFERPINK PUFFER
2222
23. BLUE BLOATERBLUE BLOATER
Develop andDevelop and
toleratetolerate
hypercapniahypercapnia
earlier and mayearlier and may
develop edemadevelop edema
and 2‘and 2‘
polycythemia.polycythemia.
CHRONICCHRONIC
BRONCHITICBRONCHITIC
2323
24. CHRONIC BRONCHITISCHRONIC BRONCHITIS
➢DefinedDefined clinicallyclinically
Persistent cough with sputumPersistent cough with sputum
production forproduction for at least 3 monthsat least 3 months inin
at leastat least 2 consecutive2 consecutive yearsyears, with, with
exclusion of other causes likeexclusion of other causes like
Bronchiectasis .Bronchiectasis .
2424
25. PATHOGENESISPATHOGENESIS
SMOKINGSMOKING
4-10 times more common in heavy smokers4-10 times more common in heavy smokers
✓ a smoking history of more than 20 pack yearsa smoking history of more than 20 pack years
➢ Smoke and other irritants causeSmoke and other irritants cause
Hypertrophy of submucosal glands--- hypersecretionHypertrophy of submucosal glands--- hypersecretion
of mucusof mucus
Increase in goblet cellsIncrease in goblet cells
↑↑predisposition to infectionpredisposition to infection
2525
26. Clinical FeaturesClinical Features
➢CyanosedCyanosed ((Blue)Blue)
➢EdematousEdematous ((Bloater)Bloater)
➢Productive CoughProductive Cough
➢CorPulmonale – heart failureCorPulmonale – heart failure
➢Usually dyspnea triggered by infectionUsually dyspnea triggered by infection
➢Respiratory acidosisRespiratory acidosis
Blue bloaterBlue bloater
2626
30. 2-Negative reversibility test2-Negative reversibility test (Post-(Post-
bronchodilator FEV1 <15%bronchodilator FEV1 <15% (200ML)(200ML)
increase following administration ofincrease following administration of
bronchodilator or trial ofbronchodilator or trial of
corticosteroids) .corticosteroids) .
3030
31. DLCO: Transfer FactorDLCO: Transfer Factor
• AsthmaAsthma highhigh
• Chronic bronchitisChronic bronchitis normalnormal
• EmphysemaEmphysema lowlow
3131
32. Other testsOther tests
➢ Hemoglobin level and packed cell volume (PCV)Hemoglobin level and packed cell volume (PCV) cancan
be elevated as a result of persistent hypoxemiabe elevated as a result of persistent hypoxemia
causing secondary polycythemia.causing secondary polycythemia.
➢ Arterial blood gases (ABGs)Arterial blood gases (ABGs) determine the degree ofdetermine the degree of
hypoxia and hypercapnia.hypoxia and hypercapnia.
➢ CXRCXR can be normal or show hyper-expanded lungcan be normal or show hyper-expanded lung
fields with low flattened diaphragms and the presencefields with low flattened diaphragms and the presence
of bullae (emphysema).of bullae (emphysema).
➢ ECGECG can show advanced cor pulmonalecan show advanced cor pulmonale
➢ Alpha-antitrypsin level and phenotypeAlpha-antitrypsin level and phenotype may be helpfulmay be helpful
(young non smokers, lower lobe emphysema, a family(young non smokers, lower lobe emphysema, a family
history of chest problems).history of chest problems). 3232
34. Disease Progression of a Patients withDisease Progression of a Patients with
COPDCOPD
Symptoms
Exacerbations
Exacerbations
Exacerbations
Deterioration
End of Life
3434
39. Smoking cessationSmoking cessation
➢The onlyThe only
interventionintervention
proven toproven to
decelerate thedecelerate the
decline indecline in
FEV1.FEV1. 3939
41. BronchodilatorsBronchodilators
Short Acting BetaShort Acting Beta22 Agonist (SABA)Agonist (SABA)
➢e.g. Salbutamole.g. Salbutamol
➢Improve pulmonary function/SOB/exerciseImprove pulmonary function/SOB/exercise
performanceperformance
➢Combination SABA’s and anticholinergicsCombination SABA’s and anticholinergics
produce better bronchodilationproduce better bronchodilation
➢For patients with MILD symptomsFor patients with MILD symptoms
●
SOB on exertionSOB on exertion
4141
42. BronchodilatorsBronchodilators
Long Acting BetaLong Acting Beta22 Agonist (LABA)Agonist (LABA)
➢e.g.– Formoterol, Salmeterole.g.– Formoterol, Salmeterol
➢For patients who still have symptomsFor patients who still have symptoms
on SABA’s (MODERATE disease)on SABA’s (MODERATE disease)
➢More sustained effect on PFT’s, chronicMore sustained effect on PFT’s, chronic
SOBSOB
➢Early evidence these may prolong timeEarly evidence these may prolong time
between exacerbationsbetween exacerbations
4242
43. Inhaled anticholinergicsInhaled anticholinergics
inhaled ipratropium bromide is preferred over
beta-2 agonists by many as the bronchodilator of
choice in COPD for the following reasons:
➢Its minimal cardiac stimulatory effects compared
to those of beta agonists
➢Its greater effectiveness than either beta agonist
or methylxanthine bronchodilators in most studies
of patients with COPD
4343
45. SteroidsSteroids
Inhaled steroidInhaled steroid
➢ Not recommended as first line therapyNot recommended as first line therapy
➢ No consistent effect on decreasing inflammationNo consistent effect on decreasing inflammation
➢ Consider inhaled form in those with mod-severeConsider inhaled form in those with mod-severe
diseasedisease
➢ Consider in those who have maximalConsider in those who have maximal
bronchodilator therapybronchodilator therapy
➢ Inhaled corticosteroids are currentlyInhaled corticosteroids are currently
recommended inrecommended in severe disease( FEV1 <50%) whosevere disease( FEV1 <50%) who
report two or more exacerbations requiringreport two or more exacerbations requiring
antibiotics or oral steroids per yearantibiotics or oral steroids per year .. 4545
48. Additional measuresAdditional measures
➢ Vaccines. Patients with COPD should receive a singleVaccines. Patients with COPD should receive a single
ddose of the polyvalent pneumococcal polysaccharideose of the polyvalent pneumococcal polysaccharide
vaccine and yearly influenza vaccinations.vaccine and yearly influenza vaccinations.
➢ a1-Antitrypsin replacement. Weekly or monthlya1-Antitrypsin replacement. Weekly or monthly
Infusions of a1-antitrypsin have been recommended forInfusions of a1-antitrypsin have been recommended for
patients with serum levels below 310mg/L andpatients with serum levels below 310mg/L and
abnormal lung function. 1abnormal lung function. 1
➢ Heart failure should be treated with diuretics .Heart failure should be treated with diuretics .
➢ Secondary polycythemia requires venesection if theSecondary polycythemia requires venesection if the
PCV is >55%.PCV is >55%.
4848
49. SURGERYSURGERY
➢ BullectomyBullectomy : young with emphysema: young with emphysema
➢ Lung Volume reduction surgery (LVRS)Lung Volume reduction surgery (LVRS)::
emphysemaemphysema
➢ Lung transplantLung transplant
Have been used for severe COPDHave been used for severe COPD
4949
50. 5050
Emergency treatment
Emergency treatment
Exacerbations of COPD are characterized by an acute
worsening of symptoms, with
increased breathlessness,
sputum volume and
sputum purulence.
They may occur spontaneously or as a result of infections.
Mild exacerbations can be managed at home but patients with
severe exacerbations require admission to hospital.
key adverse features that indicate a severe exacerbation :
(confusion, cyanosis, severe respiratory distress).
51. 5151
Patients admitted to hospital should have
• Chest X-ray,
• Arterial blood gas measurement,
• ECG (to exclude comorbidities),
• Full blood count and
• Urea and electrolyte measurements.
• Culture of sputum
• Blood cultures should be taken if the patient is
pyrexial and
• Theophylline level should be measured in patients
on theophylline therapy.
53. ORAL STEROIDSORAL STEROIDS
ORAL STEROIDS are useful during exacerbationsORAL STEROIDS are useful during exacerbations
(rule of 15)(rule of 15)
PREDINSOLONPREDINSOLON 1515 mgmg TWICE DAILY GIVENTWICE DAILY GIVEN FORFOR 1515
DAYSDAYS MAY BENEFITMAY BENEFIT 1515%% OF PATIENTS WITHOF PATIENTS WITH
COPD EXACERBATIONCOPD EXACERBATION
5353
54. 5454
Antibiotics
Common bacteria associated with COPD exacerbation
include
Haemophilus inluenzae,
Streptococcus pneumoniae and
Moraxella catarrhalis.
Treatment
Augmentin(amoxicillin and clavulanic acid),
or doxycycline, or ciprofloxacin or clarithromycin.
57. BRONCHIECTASISBRONCHIECTASIS
A destructive lung disease characterized by:A destructive lung disease characterized by:
●
Abnormal & permanent dilatation of medium sizedAbnormal & permanent dilatation of medium sized
bronchibronchi
●
An associated, persistent and variable inflammatoryAn associated, persistent and variable inflammatory
process producing damage to bronchial elastic andprocess producing damage to bronchial elastic and
muscular elementsmuscular elements
5757
58. PATHOLOGYPATHOLOGY
Neutrophil proteasesNeutrophil proteases
(acute infection in a normal or compromised host)(acute infection in a normal or compromised host)
⇩⇩
Epithelial injuryEpithelial injury
++
Structural protein damageStructural protein damage
⇩⇩
Damaged, dilated airwayDamaged, dilated airway
⇩⇩
Mucous retention / chronic, recurrent infectionMucous retention / chronic, recurrent infection
⇩⇩
Ongoing inflammation / tissue damage / repairOngoing inflammation / tissue damage / repair
5858
62. Physical signsPhysical signs
➢ 1-normal chest exam1-normal chest exam. If bronchiectatic airways. If bronchiectatic airways
do not contain secretions and there is nodo not contain secretions and there is no
associated lobar collapse .associated lobar collapse .
➢ 2-coarse crackles2-coarse crackles if there is secretions .if there is secretions .
➢ 3- deviated trachea toward side of lesion ,3- deviated trachea toward side of lesion ,
dullness ,↓breath sounddullness ,↓breath sound if there is collapse .if there is collapse .
➢ 4- bronchial breathing4- bronchial breathing : advanced scarring .: advanced scarring .
6262
63. INVESTIGATIONSINVESTIGATIONS
1-Sputum culture1-Sputum culture
For pseudomonas aeruginosa , fungi , andFor pseudomonas aeruginosa , fungi , and
mycobacteria .mycobacteria .
2- Radiology2- Radiology
CXR : early stage normalCXR : early stage normal
Advanced thickened airway walls , cysticAdvanced thickened airway walls , cystic
spaces , pneumonic consolidation or collapse .spaces , pneumonic consolidation or collapse .
SPIRAL CT SCAN of chest is much more sensitiveSPIRAL CT SCAN of chest is much more sensitive
..
3-Assessment of ciliary function3-Assessment of ciliary function
6363
64. managementmanagement
➢ 1-airway obstruction1-airway obstruction :: inhaled bronchodilators andinhaled bronchodilators and
corticosteroids .corticosteroids .
➢ 2-2- physiotherapyphysiotherapy
Patients should adopt a position in which the lobePatients should adopt a position in which the lobe
to be drained is uppermost.to be drained is uppermost.
Deep breathing followed by forced expiratoryDeep breathing followed by forced expiratory
maneuvers (the 'active cycle of breathing'maneuvers (the 'active cycle of breathing'
technique) is of help in allowing secretions in thetechnique) is of help in allowing secretions in the
dilated bronchi to gravitate towards the trachea,dilated bronchi to gravitate towards the trachea,
from which they can be cleared by vigorousfrom which they can be cleared by vigorous
coughing.coughing.
6464
65. 'Percussion' of the chest wall with cupped'Percussion' of the chest wall with cupped
hands may help to dislodge sputum, and ahands may help to dislodge sputum, and a
number of mechanical devices are availablenumber of mechanical devices are available
which cause the chest wall to oscillate, thuswhich cause the chest wall to oscillate, thus
achieving the same effect.achieving the same effect.
The optimum duration and frequency ofThe optimum duration and frequency of
physiotherapy depends on the amount ofphysiotherapy depends on the amount of
sputum but 5-10 minutes once or twice dailysputum but 5-10 minutes once or twice daily
is a minimum for most patients.is a minimum for most patients.
6565
67. 3- antibiotics3- antibiotics
Oral ciprofloxacin 500-750 mg bidOral ciprofloxacin 500-750 mg bid
Or ceftazidime by IV inj. Or infusion 1-2 gm 8-Or ceftazidime by IV inj. Or infusion 1-2 gm 8-
hourly.hourly.
4- surgery4- surgery
Only in unilateral , single lobe in young patientOnly in unilateral , single lobe in young patient
6767
Diagnosis of COPD is based on a history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, with or without the presence of symptoms.
Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea.
For the diagnosis and assessment of COPD, spirometry is the gold standard.
Health care workers involved in the diagnosis and management of COPD patients should have access to spirometry.