SEARCH RESULTS FOR: COPD

COPD: Pathogenesis

COPD: Clinical Findings

COPD: Findings on Investigations

COPD: Complications

Pulsus Paradoxus

Yu Yan - Pulsus Paradoxus - FINAL.pptx Lungs are hyperinflated, and vascular beds are more expanded? BP on inspiration (<10mmHg)Pulsus ParadoxusThrombi in the pulmonary arteries ? blood filling pulmonary vasculatureLegend:Published January 21, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsAuthor: Yan YuReviewers:Sean SpenceLaura CraigNanette Alvarez** MD at time of publication? ? ? forward blood flow from lungs into left heartWith cardiac pathology external to myocardium(Cardiac tamponade, or rarely with constrictive pericarditis)? Right heart filling, ? blood flow into lung vesselsMore blood returns to R heart ? more blood enters and pools in pulmonary vasculature? blood returns to the left heart, ? its fillingWith obstructive lung diseases (i.e. COPD)With vascular pathology (rare):InspirationNormally:? lung volume ? ? intra-vascular volume within pulmonary blood vessels ? ? lung capacitance for blood, ? R heart afterloadPulsus Paradoxus:Exaggerated ?in systolic BP on inspiration (>10mmHg)? left heart stroke volume/cardiac outputOn inspiration, ? ? ? blood enter lungs and pools within pulmonary vasculature? ? ? left heart stroke volume/cardiac outputAbnormally:On inspiration, as pulmonary intra-vasculature volume expands and blood pools within, flow into the left heart ? ? ? Pulmonary embolism? venous return to R heartVena cava obstructionBy thrombi, or external compression by masses/ fibrosis (from obesity, pregnancy) As ? blood fills R heart on inspiration, external constraints on myocardium ? cardiac expansion, interventricular septum is pushed into LVThere is no room in the pericardial sac for the LV to expand and maintain normal end diastolic volume (i.e. ? LV filling) 98 kB / 233 words

Bronchiectasis Pathogenesis and clinical findings

Bronchiectasis: Pathogenesis and clinical findings Acquired immunodeficiency Lymphoma, HIV, transplant Autoimmune Lupus, inflammatory bowel disease, rheumatoid arthritis Congenital/Genetic Cystic fibrosis, A1AT deficiency, Marfan, immunoglobulin deficiency, Kartagener syndrome, Young syndrome Endobronchial obstruction Neoplasm, foreign body, lymph node compression Other Inhalation exposure (smoke, ammonia), MAC complex infection, COPD, allergic bronchopulmonary aspergillosis, chronic infections Irreversibly dilated bronchi Chronic bronchial infection and inflammation 1 Easily collapsible airways I Bronchiectasis (persistent and progressive damage to lungs) Chronic cough (mucopurulent) Defect in immunity and/or mucus clearance Persistent bacteria in airway (commonly Pseudomonas/Staph aureus) Inflammatory response Rhinosinusitis Abbreviations: • A1AT — Alpha-1-antitrypsin • COPD — Chronic Obstructive Pulmonary Disease • HIV — Human Immunodeficiency Virus • MAC — Membrane Attack Complex • VQ— Ventilation/Perfusion ratio Legend: Pathophysiology Mechanism Fever Sign/Symptom/Lab Finding Failure to thrive (children) Authors: Rebecca (Becky) Phillips Reviewers: Midas (Kening) Kang Usama Malik Eric Leung* * MD at time of publication Notes: • Can be focal (single lobe/segment) or diffuse (both lungs) • Mainly in elderly • 1% prevalence in children Tissue damage Epithelial destruction of airways Further impairment of bacterial clearance Persistent inspiratory adventitious sounds (crackles > wheezing) Complications Structural damage to bronchial walls Obstructive pulmonary function tests Hemoptysis Chest pain VQ mismatch and 4, gas exchange 4, oxygenation Digital clubbing (rare) Fatigue Dyspnea Cyanosis (uncommon)

Secondary Polycythemia

Secondary Polycythemia: Pathogenesis Authors: Noriyah Al Awadhi, Yan Yu, Peter Duggan* Reviewers: Crystal Liu, Kara Hawker, Paul Ratti, Man-Chiu Poon*, Lynn Savoie* * MD at time of initial publication Chronic lung disease (ILD, COPD) Poor lung function Renal artery stenosis ↓ blood flow to kidney Kidney senses ↓ O2 High affinity Hb or CO poisoning Hb does not easily unload O2 Tissues become hypoxic Tumors (e.g. renal, hepatic, lung) Secretes EPO in an unregulated way, as a “paraneoplastic syndrome” High altitude Obstructive sleep apnea Episodic airway obstruction during sleep Intermittent hypoxia Cyanotic heart disease Shunting of blood Venous and arterial blood mixes Poorly oxygenated blood ↓ O2 partial pressure ↑ EPO production independent of O2 (inappropriate response) ↑ EPO production due to hypoxia (appropriate response) Abbreviations: • Hb- Hemoglobin • EPO- Erythropoietin • ILD- Interstitial Lung Disease • COPD- Chronic Obstructive Pulmonary Disease “Endogenous causes” of high EPO Secondary Polycythemia “Exogenous causes” of high EPO Testosterone therapy Iatrogenic EPO (results in ↑ EPO synthesis administration within the body) Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published May 5, 2019 on www.thecalgaryguide.com

A1AT-Deficiency

α1AT Deficiency: Pathophysiology and Clinical Findings Authors: Sean Spence Reviewers: Danny Guo Yan Yu Merna Adly Crystal Liu Sam Lee* * MD at time of publication Abnormal α1-Anti-Trypsin (α1AT) allele(s) Accumulation of mutant α1AT protein as ordered polymers in endoplasmic reticulum of hepatocytes ↓ α1AT inhibition of Hepatocyte Injury tissue proteases (Mechanism unclear) ↓ release from hepatocytes Cirrhosis, chronic hepatitis, hepatocellular carcinoma ↓ lung elasticity, ↓ ability for lung to expel air on expirationà gas trapping, hyperinflation, airway collapse over time Role of Genetics: Low serum α1AT In the skin: Subcutaneous proteases > Anti- proteases Unopposed proteolysis in subcutaneous tissues Panniculitis (Rare, most cases associates with ZZ Genotype) Lung Proteases > Anti-proteases àproteolytic destruction of lung parenchymaàpanacinar emphysema (accelerated by smoking) Stigmata of chronic liver disease (ascites, jaundice, spider nevi, petechiae, etc.) Symptoms of chronic obstructive pulmonary disease (COPD): barrel chest/High residual volume (RV), low vital capacity (VC), wheezes on auscultation, etc) – see relevant slide Degree of α1AT deficiency dependent on genotype: • MM gives normal α1AT levels • MZ genotype produces levels ~ 35% of normal • ZZ genotype produces severe deficiency ( <10% of normal) • Null phenotype is completely deficient of α1AT N.B. Heterozygotes almost never develop phenotypic α1AT deficiency syndromes. Even some homozygotes don’t manifest the disease. Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published January 12, 2020 on www.thecalgaryguide.com

copd-overview-and-definitions

Defining “Chronic Obstructive Pulmonary Disease (COPD)” Author: Yan Yu Reviewers: Jason Baserman, Jennifer Au, Ciara Hanly, Zesheng Ye (叶泽生), Yonglin Mai (麦泳琳)*, Naushad Hirani*, Juri Janovcik* * MD at time of publication Cystic Fibrosis Multisystem disease due to CFTR gene mutation, that presents in the lungs as bronchiectasis Bronchiectasis, Cystic Fibrosis, etc COPD Systemic disease, largely manifesting as an airflow-obstructing respiratory disorder; can manifest in the form of any of the following disorders: Emphysema Lung tissue destruction & abnormal, permanent enlargement of lung acini: airspaces distal to terminal bronchioles Chronic Bronchitis Chronic, productive cough for a total duration of 3 months per year, over 2 continuous years Asthma Asthma that does not remit completely with treatment (thus, chronic airflow obstruction) is defined as asthma-COPD overlap syndrome (ACOS) Emphysema Bronchiectasis Destruction and widening of large airways, resulting in mucus hyper-secretion and recurrent infections Chronic Bronchitis Most common COPD manifestations (most patients suffer from a combination of emphysema and chronic bronchitis) Clinically, COPD is seen as: • Progressive, partially reversible airflow obstruction and lung hyperinflation (causing respiratory symptoms like cough, sputum production, and dyspnea) • Post-bronchodilator spirometry results: FEV1/FVC ratio <0.7 (FEV1 is not a defining feature of COPD, but a marker of severity) • ↑ frequency & severity of acute exacerbations • Systemic manifestations such as deconditioning and muscle weakness Chronic Obstructive Pulmonary Disease (COPD) Asthma Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013, updated October 5, 2021 on www.thecalgaryguide.com

COPD Acute Exacerbations

COPD Acute Exacerbations: Triggers and Signs/Symptoms Authors: Brianne McDonald, Yan Yu* Reviewers: Nilani Sritharan, Sean Doherty, Zihong Xie (谢梓泓), Zesheng Ye (叶泽生), Yonglin Mai (麦泳琳)*, Kerri Johannson* * MD at time of publication Notes: • The triggers for acute exacerbations of COPD are unknown in approximately 1/3 of cases • Changes in pulmonary function (e.g. FEV1) are poorly sensitive in the individual diagnosis of acute exacerbations of COPD due to individual variability Acute Bacterial Infection Activation of proinflammatory cytokines and recruitment of neutrophils Acute Viral Infection Epithelial cell secretion of cytokines and ↑ airway lymphocythemia Acute ↑ in airway inflammation (accumulation of inflammatory cells and release of harmful mediators, such as reactive oxygen species and proteases, into the lung tissue/airways) Air pollution (including cigarette smoke) ↑ reactive oxygen species in lungs Airway inflammation ↑ secretions that accumulate in the airway lumen Airway wall edema Limits outflow of air from lungs on expiration Airway bronchoconstriction in response to inflammation Constricted airways create audible turbulent airflow on expiration Systemic spread of inflammatory markers via the bloodstream cause inflammation throughout the body ↑ Cardiac Morbidity ↑ CRP Worsening of respiratory symptoms Irritation of cough reflexes in airways Cough ↑ Sputum production and sputum purulence ↑ Wheeze Unexpired air becomes trapped in the lungsàDynamic Hyperinflation Bloodflow to lungs continue to perfuse under- ventilated regions of lungs àV/Q Mismatch Lungs are larger àmore blood remains in lungs à↓ preload Acute Respiratory Failure Tachypnea ↑ Dyspnea Accessory Muscle Use Attempts to restore normal arterial CO2 and O2 levels Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published April 21, 2019, updated October 6, 2021 on www.thecalgaryguide.com

Pneumonie: Pathogenese und klinische Befunde

Pneumonie: Pathogenese und klinische Befunde Autoren: Laura Byford-Richardson Rezensenten: *Yan Yu, Sadie Kutz, Natalie Morgunov, *Kerri Johannson Übersetzung: Sarah Schwarz Übersetungsprüfung: Gesche Tallen* *MD zum Zeitpunkt der Veröffentlichung Anmerkungen: • Pathogene können Bakterien, Viren, Pilze oder Parasiten sein • Die Pneumonie ist eine Entzündung der unteren Atemwege (im Gegensatz zur Entzündung der oberen Atemwege z.B. die Bronchitis) und kann unterteilt werden in: Ambulant erworbene, nosokomial (im Krankenhaus) erworbene Pneumonie Die Immunantwort variiert je nach eingedrungenem Erreger (z.B. Pneumokokken verursachen ein lobär betontes, H. influenzae ein interstitiell betontes Entzündungsbild) Rauchen unterdrückt die Funktionsfähigkeit der neutrophilen Granulozyten und schädigt das Lungenepithel Chronische Lungenerkrankungen z.B. COPD, Asthma oder Lungenkrebs zerstören das Lungengewebe und bieten Krankheitserregern mehr Angriffsfläche für Infektionen Durch Immunsuppression z.B. bei HIV, Sepsis, Glucocorticoid- oder Chemotherapie wird die Immunantwort eingeschränkt Systemisch kommt es zu einer inflammatorischen Immunantwort Durch systemische Zytokinfreisetzung wird die hypothalamische Thermoregulation beeinträchtigt Erregersexposition durch Inhalation, Aspiration, Kontakt- oder hämatologische Übertragung Anfällige Person und/oder virulenter Erreger Proliferation des Erregers in unteren Atemwegen und Alveolen Lokal reagiert das Alveolarepithel mit einer Chemokinausschüttung um neutrophile Granulozyten an den Entzündungsort zu mobilisieren LOBÄR betont: Lokal begrenzte Akkumulation von neutrophilen Granulozyten und Plasmaexudat in Alveolen INTERSTITIELL betont: Zelluläre Infiltrate (Immunzellen und Immunzellfragmente) in den Alveolarwänden (zwischen Alveolen und Kapillaren) Fieber Anmerkungen: Schüttelfrost Irritation der Atemwege mit Hustenreiz Flüssige Infiltrate in Alveolen führen zur Schleimbildung Produktiver Husten Das Exudat vermindert die Röntgenstrahlendur chlässigkeit, entzündete Areale erscheinen im Röntgenbild heller/weiß. Verschattung im Röntgen Alveolen sind durch Flüssigkeitsansamml ungen blockiert Verdickung der Alveolarwände, Diffusionsstrecke ↑ Irritation der Alveolarwände mit Hustenreiz Bei ausschließlich interstitieller Infiltration -> Husten ohne Schleimproduktion Trockener Husten • Andere Symptome der Pneumonie sind: Brustschmerzen, Nutzung der Atemhilfsmuskulatur, auskultatorisch Rasselgeräusche, Müdigkeit • Diese Symptome sind jedoch unspezifisch O2 und CO2- Austausch vermindert Hypoxie Periphere & zentrale Chemorezeptoren werden aktiviert, Atemfrequenz ↑ Luftnot Legende: Pathophysiologie Mechanismen Symptome/Klinische Befunde Komplikationen Veröffentlicht: 26. September 2016 auf www.thecalgaryguide.com

COPD-发病机制

COPD: 发病机制 作者: Yan Yu 审稿人:Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人:Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 /012 (如a1-抗胰蛋白酶缺乏) 阻止肺组织损伤的能力↓ +,-. (如长期吸烟、环境污染、感染) 肺内产生自由基 34*5 肺抗蛋白酶的失活 ↑氧化应激，炎性细胞因子，蛋白酶功能 支气管的持续、反复损伤 炎性细胞浸润， 杯状细胞增殖， 气道上皮纤毛 尤其中性粒细 黏液产生↑ 细胞死亡 气道弹性↓ (弹性回缩 肺实质的蛋白水解破坏↑ 维持气道开放 肺泡永久性异常 的结构支持↓ 扩张 胞 力) 肺气体潴留 气道狭窄与 肺过度 肺大泡 气道黏液潴留，成为感染 狭窄 病灶 塌陷 充气 肺气肿 (容易肺泡 破裂) 气道纤维化和 %&'()* 慢性阻塞性肺疾病(COPD) 临床表现 并发症 (参阅相关幻灯片) (参阅相关幻灯片) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Clinical Findings Lung tissue Chronic Obstructive Pulmonary Disease (COPD) damage ↓ elastic recoil to push air out of lungs on expiration Lungs don’t fully empty, air is trapped in alveoli (lung hyperinflation) ↑ lung volume means diaphragm is tonically contracted (flatter) If occurring around airways Airflow obstruction ↑ mucus production ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) Chronic cough with sputum Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction ↓ ventilation of alveoli ↓ oxygenation of blood (hypoxemia) ↓ perfusion of body tissues (i.e. brain, muscle) Fatigue; ↓ exercise tolerance Total expiration time takes longer than normal Prolonged expiration More effort needed to ventilate larger lungs Respiratory muscles must work harder to breathe Turbulent airflow in narrower airways is heard on auscultation Expiratory Wheeze Diaphragm can’t flatten much further to generate deep breaths To breathe, chest wall must expand out more Dyspnea Shortness of breath, especially on exertion Breathes are rapid & shallow If end-stage: Chronic fatigue causes deconditioning Muscle weakness & wasting Barrel chest If end-stage: diaphragm will be “flat”. Continued Patient tries to expire against higher mouth air pressure, forcing airways to open wider Pursed-lip breathing Patient breathes with accessory muscles as well as diaphragm to try to improve airflow inspiratory effort further contracts diaphragmà pull the lower chest wall inwards Hoover’s sign (paradoxical shrinking of lower chest during inspiration) Tripod sitting position (activates pectoral muscles) Neck (SCM, scalene) muscles contracted Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: ! 45 (on ABGs) Ventilation- perfusion mismatch High A-a gradient (calculated from ABGs) Low, flat diaphragm, >10 posterior ribs (on frontal CXR) High TLC and VC (on spirometry) • • PaO2: partial pressure of O2 in arterial blood PaCO2: partial pressure of CO2 in arterial blood • In the setting of fever and productive cough, especially if lung field opacifications are seen on CXR: consider sputum gram stain and culture to rule out pneumonia. Air does not block X-ray beams, will appear black on X-ray film Chronic hypercapnia makes breathing centers less sensitive to the high PaCO2 stimulus for breathing, & more reliant on the low PaO2 stimulus (“CO2 retention”) Give O2 carefully to these patients (high PaO2 may suppress patients’ hypoxic respiratory drive, ↓ their breathing, & ↑↑↑ PaCO2) ↑ retrosternal air space (on lateral CXR) Hyper-lucent (darker) lung fields, ↓ lung markings (on frontal CXR) • Arterial Blood Gasses (ABGs) • Chest X-Ray (CXR): frontal and lateral Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 气流阻塞 肺泡通气↓ 呼气时，胸膜腔正压挤压气 道à 阻塞↑ 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者:Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 慢性阻塞性肺疾病 (COPD) 肺组织损伤 没有弹性回缩力将 气体排出肺 肺实质与血管分布减少导 致气体交换面积↓ 弥散功能↓ (肺功能检查) 更多的CO2残留 并扩散到血液中 高碳酸血症: PaCO2 > 45 (动脉血气) 血流灌注通气不良的肺泡 时无法获得足够的氧气 总呼气时长较正常长 FEV1/FEV < 0.7 (肺功能检查) 肺无法完全排空 更多空气潴留在肺部 (肺过度充气) 低氧血症: PaO2 < 70mmHg (动脉血气) 通气-灌注不匹配 肺泡-动脉氧分压差↑ (可通过动脉血气分析计算得出) 横膈低平， 下移至第10肋后端 及以下部位 (胸部正位片) TLC与VC增大 (肺功能检查) 缩写: • • FEV1: 1秒用 • VC:肺活量 PaO2: 动脉血 力呼气量 氧分压 空气不会阻挡X射线， 在X光片上呈现为黑色 慢性高碳酸血症使呼吸中枢对PaCO2 刺激呼吸的敏感性下降 & 更依赖于低PaO2的刺激 (“二氧化碳潴留”) 给患者吸氧时需注意(高PaO2 可能会抑制患者低氧时对呼吸的 刺激，使呼吸驱动↓ & PaCO2↑↑↑ ) • FVC: 用力肺 • 活量 • TLC:肺总量 慢阻肺相关检查 : PaCO2: 动脉 血二氧化碳 分压 胸骨后间隙↑ (胸部侧位片) 肺纹理↓ • 肺功能检查 • 动脉血气分析(Arterial Blood Gasses, ABGs) • 胸部正侧位片 • 当患者发热和湿咳，特别是胸片上见肺野不清晰时: 肺透亮度↑, (胸部正位片) 考虑进行痰革兰氏染色及痰培养以排除肺炎可能 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Complications Lung inflammation Chronic Obstructive Pulmonary Disease (COPD) Airway obstruction ↓ inhaled air in alveoli and terminal bronchioles Rupture of emphasematous bullae on surface of lung Inhaled air leaks into pleural cavity and is trapped there Pneumothorax Feeling a loss of control over one’s life, and hopelessness for the future Goblet cell proliferation, ↑ mucus production Death of airway epithelium ciliated cells ↓ oxygenation of the blood passing through the lungs Chronic hypoxemia Kidneys compensate by ↑ erythropoietin (EPO) production ↑ Hemoglobin and red blood cell synthesis Polycythemia (secondary) Hypoxic alveoli cause the pulmonary arterioles perfusing them to reflexively vasoconstrict Since most alveoli in the lungs are hypoxic, hypoxic vasoconstriction occurs across entire lung Vasoconstriction ↑ blood pressure within lung vasculature Pulmonary hypertension ↑ workload of the right ventricle (to pump against higher pressures) To compensate, the right ventricle progressively hypertrophies and dilates, but over time its output ↓ Cor pulmonale (Right heart failure in isolation, not due to Left heart failure) Mucus trapped in airways, serve as nidus for infection Acute exacerbation of COPD (AECOPD) Pneumonia The chronic, systemic inflammation in COPD is a hyper-metabolic state that consumes calories Macro-nutrient deficiency Trouble with respiration lead to inactivity and deconditioning Wasting, muscle atrophy More inactivity and deconditioning perpetuates the cycle Depression Author: Yan Yu Reviewers: Jason Baserman Naushad Hirani* Juri Janovcik* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"# 肺部炎症 杯状细胞增殖， 气道上皮纤毛 粘液产生↑ 细胞死亡 黏液潴留呼吸道，成为感 染的病灶 慢性阻塞性肺疾病 (COPD) 气道阻塞à 吸入肺泡和终末细 肺大疱破裂 吸入的空气渗入 并潴留于胸腔 气胸 感觉生活失控，对未 来感到绝望 抑郁 作者: Yan Yu 审稿人: Jason Baserman, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 支气管的空气 ↓ 流经肺的血液进行气 缺氧的肺泡à灌注肺泡的肺小动 慢性阻塞性肺疾 病急性加重期 (AECOPD) 肺炎 体交换↓ 慢性低氧血症 肾脏合成促红细胞 生成素进行代偿↑ 血红蛋白与红 细胞合成↑ 红细胞增多症 (继发性) 脉发生反射性血管收缩 肺大部分肺泡缺氧à整个肺 都出现缺氧性血管收缩 肺血管收缩 à 肺血管压力↑ 肺动脉高压 ↑ 右心室负荷(泵血时对抗高压) 为了代偿，右心室逐渐肥大和扩张， 但随着病程进展，右心室输出量 ↓ 肺心病 (单独出现右心衰竭，非左心衰) COPD所致的慢性全身 呼吸困难导致活 性炎症会使机体处于高 动量减少和活动 代谢状态，消耗能量 耐量降低 宏量营养 素缺乏症 消瘦，肌肉萎缩 运动量下降和活动耐量 的降低造成恶性循环 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com " title="COPD: 发病机制 作者: Yan Yu 审稿人:Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人:Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 /012 (如a1-抗胰蛋白酶缺乏) 阻止肺组织损伤的能力↓ +,-. (如长期吸烟、环境污染、感染) 肺内产生自由基 34*5 肺抗蛋白酶的失活 ↑氧化应激，炎性细胞因子，蛋白酶功能 支气管的持续、反复损伤 炎性细胞浸润， 杯状细胞增殖， 气道上皮纤毛 尤其中性粒细 黏液产生↑ 细胞死亡 气道弹性↓ (弹性回缩 肺实质的蛋白水解破坏↑ 维持气道开放 肺泡永久性异常 的结构支持↓ 扩张 胞 力) 肺气体潴留 气道狭窄与 肺过度 肺大泡 气道黏液潴留，成为感染 狭窄 病灶 塌陷 充气 肺气肿 (容易肺泡 破裂) 气道纤维化和 %&'()* 慢性阻塞性肺疾病(COPD) 临床表现 并发症 (参阅相关幻灯片) (参阅相关幻灯片) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Clinical Findings Lung tissue Chronic Obstructive Pulmonary Disease (COPD) damage ↓ elastic recoil to push air out of lungs on expiration Lungs don’t fully empty, air is trapped in alveoli (lung hyperinflation) ↑ lung volume means diaphragm is tonically contracted (flatter) If occurring around airways Airflow obstruction ↑ mucus production ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) Chronic cough with sputum Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction ↓ ventilation of alveoli ↓ oxygenation of blood (hypoxemia) ↓ perfusion of body tissues (i.e. brain, muscle) Fatigue; ↓ exercise tolerance Total expiration time takes longer than normal Prolonged expiration More effort needed to ventilate larger lungs Respiratory muscles must work harder to breathe Turbulent airflow in narrower airways is heard on auscultation Expiratory Wheeze Diaphragm can’t flatten much further to generate deep breaths To breathe, chest wall must expand out more Dyspnea Shortness of breath, especially on exertion Breathes are rapid & shallow If end-stage: Chronic fatigue causes deconditioning Muscle weakness & wasting Barrel chest If end-stage: diaphragm will be “flat”. Continued Patient tries to expire against higher mouth air pressure, forcing airways to open wider Pursed-lip breathing Patient breathes with accessory muscles as well as diaphragm to try to improve airflow inspiratory effort further contracts diaphragmà pull the lower chest wall inwards Hoover’s sign (paradoxical shrinking of lower chest during inspiration) Tripod sitting position (activates pectoral muscles) Neck (SCM, scalene) muscles contracted Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 慢性阻塞性肺疾病 (COPD) 如果出现在气道周围 气流阻塞 肺不能完全排空 气体，气体潴留 于肺泡(肺过度 充气) 总呼气时长大于 正常时长 呼气相延长 肺组织损伤 呼气时，将空气排出肺外 的弹性回缩力↓ 肺不能完全排空气体， 气体潴留于肺泡内 (肺过度充气) 肺容积↑，膈肌紧张 性收缩(膈肌平坦) 呼气时，胸膜腔正压挤压气道 à 气道阻塞↑ 肺泡通气↓ 血液氧合↓ (低 氧血症) 身体组织灌注 量↓ (比如脑、 肌肉) 疲劳; 运动耐量↓ 黏液生成↑ 清除黏液的上皮纤 毛细胞数量↓ (受 气道炎症损伤) 慢性咳嗽伴咳 痰 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 容积较大 的肺需要 更加努力 才能通气 呼吸肌必须 更用力才能 呼吸 听诊闻及狭窄气 道中的湍流气流 呼气喘鸣音 呼吸困难 气促，尤其是劳累 膈肌无法进一步收缩以 产生深呼吸 呼吸浅快 为了呼吸， 胸壁必须延 展得更大 桶状胸 晚期病人: 患者试图在较高的口 慢性疲劳导致 患者动用辅助呼吸肌和膈肌呼吸， 腔内气压下进行呼气， 活动耐量下降 从而使气道更开放 以改善气流 晚期病人:膈肌 “平坦” ，持续吸气进一步压 缩膈肌à 向内拉季肋部胸壁 胡佛征 (吸气时，胸廓下侧季肋部内收) 缩唇呼吸 肌肉无力 & 消瘦 端坐呼吸 (调动胸肌) 颈部肌肉收 缩(胸锁乳 突肌、斜角 肌) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Findings on Investigations Chronic Obstructive Pulmonary Disease (COPD) Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication Airflow obstruction Lung tissue damage ↓ ventilation of alveoli Blood perfusing ill- ventilated alveoli does not receive normal amounts of oxygen During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction) No elastic recoil to push air out of lungs Loss of lung parenchyma and vasculature ↓ surface area for gas exchange ↓ diffusion capacity (on spirometry) Hypoxemia: PaO2 < 70mmHg (on ABGs) Abbreviations: • FEV1: Forced expiratory volume in 1 second • FVC: Forced vital capacity • TLC: Total lung capacity • VC: Vital Capacity Investigations for COPD : • Spirometry (Pulmonary function test) Total expiration time takes longer than normal FEV1/FEV < 0.7 (on spirometry) Lungs don’t fully empty More air trapped within lungs (hyperinflation) More CO2 remains and diffuses into the blood Hypercapnia: PaCO2 > 45 (on ABGs) Ventilation- perfusion mismatch High A-a gradient (calculated from ABGs) Low, flat diaphragm, >10 posterior ribs (on frontal CXR) High TLC and VC (on spirometry) • • PaO2: partial pressure of O2 in arterial blood PaCO2: partial pressure of CO2 in arterial blood • In the setting of fever and productive cough, especially if lung field opacifications are seen on CXR: consider sputum gram stain and culture to rule out pneumonia. Air does not block X-ray beams, will appear black on X-ray film Chronic hypercapnia makes breathing centers less sensitive to the high PaCO2 stimulus for breathing, & more reliant on the low PaO2 stimulus (“CO2 retention”) Give O2 carefully to these patients (high PaO2 may suppress patients’ hypoxic respiratory drive, ↓ their breathing, & ↑↑↑ PaCO2) ↑ retrosternal air space (on lateral CXR) Hyper-lucent (darker) lung fields, ↓ lung markings (on frontal CXR) • Arterial Blood Gasses (ABGs) • Chest X-Ray (CXR): frontal and lateral Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 气流阻塞 肺泡通气↓ 呼气时，胸膜腔正压挤压气 道à 阻塞↑ 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者:Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 慢性阻塞性肺疾病 (COPD) 肺组织损伤 没有弹性回缩力将 气体排出肺 肺实质与血管分布减少导 致气体交换面积↓ 弥散功能↓ (肺功能检查) 更多的CO2残留 并扩散到血液中 高碳酸血症: PaCO2 > 45 (动脉血气) 血流灌注通气不良的肺泡 时无法获得足够的氧气 总呼气时长较正常长 FEV1/FEV < 0.7 (肺功能检查) 肺无法完全排空 更多空气潴留在肺部 (肺过度充气) 低氧血症: PaO2 < 70mmHg (动脉血气) 通气-灌注不匹配 肺泡-动脉氧分压差↑ (可通过动脉血气分析计算得出) 横膈低平， 下移至第10肋后端 及以下部位 (胸部正位片) TLC与VC增大 (肺功能检查) 缩写: • • FEV1: 1秒用 • VC:肺活量 PaO2: 动脉血 力呼气量 氧分压 空气不会阻挡X射线， 在X光片上呈现为黑色 慢性高碳酸血症使呼吸中枢对PaCO2 刺激呼吸的敏感性下降 & 更依赖于低PaO2的刺激 (“二氧化碳潴留”) 给患者吸氧时需注意(高PaO2 可能会抑制患者低氧时对呼吸的 刺激，使呼吸驱动↓ & PaCO2↑↑↑ ) • FVC: 用力肺 • 活量 • TLC:肺总量 慢阻肺相关检查 : PaCO2: 动脉 血二氧化碳 分压 胸骨后间隙↑ (胸部侧位片) 肺纹理↓ • 肺功能检查 • 动脉血气分析(Arterial Blood Gasses, ABGs) • 胸部正侧位片 • 当患者发热和湿咳，特别是胸片上见肺野不清晰时: 肺透亮度↑, (胸部正位片) 考虑进行痰革兰氏染色及痰培养以排除肺炎可能 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Complications Lung inflammation Chronic Obstructive Pulmonary Disease (COPD) Airway obstruction ↓ inhaled air in alveoli and terminal bronchioles Rupture of emphasematous bullae on surface of lung Inhaled air leaks into pleural cavity and is trapped there Pneumothorax Feeling a loss of control over one’s life, and hopelessness for the future Goblet cell proliferation, ↑ mucus production Death of airway epithelium ciliated cells ↓ oxygenation of the blood passing through the lungs Chronic hypoxemia Kidneys compensate by ↑ erythropoietin (EPO) production ↑ Hemoglobin and red blood cell synthesis Polycythemia (secondary) Hypoxic alveoli cause the pulmonary arterioles perfusing them to reflexively vasoconstrict Since most alveoli in the lungs are hypoxic, hypoxic vasoconstriction occurs across entire lung Vasoconstriction ↑ blood pressure within lung vasculature Pulmonary hypertension ↑ workload of the right ventricle (to pump against higher pressures) To compensate, the right ventricle progressively hypertrophies and dilates, but over time its output ↓ Cor pulmonale (Right heart failure in isolation, not due to Left heart failure) Mucus trapped in airways, serve as nidus for infection Acute exacerbation of COPD (AECOPD) Pneumonia The chronic, systemic inflammation in COPD is a hyper-metabolic state that consumes calories Macro-nutrient deficiency Trouble with respiration lead to inactivity and deconditioning Wasting, muscle atrophy More inactivity and deconditioning perpetuates the cycle Depression Author: Yan Yu Reviewers: Jason Baserman Naushad Hirani* Juri Janovcik* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"# 肺部炎症 杯状细胞增殖， 气道上皮纤毛 粘液产生↑ 细胞死亡 黏液潴留呼吸道，成为感 染的病灶 慢性阻塞性肺疾病 (COPD) 气道阻塞à 吸入肺泡和终末细 肺大疱破裂 吸入的空气渗入 并潴留于胸腔 气胸 感觉生活失控，对未 来感到绝望 抑郁 作者: Yan Yu 审稿人: Jason Baserman, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 支气管的空气 ↓ 流经肺的血液进行气 缺氧的肺泡à灌注肺泡的肺小动 慢性阻塞性肺疾 病急性加重期 (AECOPD) 肺炎 体交换↓ 慢性低氧血症 肾脏合成促红细胞 生成素进行代偿↑ 血红蛋白与红 细胞合成↑ 红细胞增多症 (继发性) 脉发生反射性血管收缩 肺大部分肺泡缺氧à整个肺 都出现缺氧性血管收缩 肺血管收缩 à 肺血管压力↑ 肺动脉高压 ↑ 右心室负荷(泵血时对抗高压) 为了代偿，右心室逐渐肥大和扩张， 但随着病程进展，右心室输出量 ↓ 肺心病 (单独出现右心衰竭，非左心衰) COPD所致的慢性全身 呼吸困难导致活 性炎症会使机体处于高 动量减少和活动 代谢状态，消耗能量 耐量降低 宏量营养 素缺乏症 消瘦，肌肉萎缩 运动量下降和活动耐量 的降低造成恶性循环 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com " />

COPD-临床表现

COPD: 临床表现 作者: Yan Yu 审稿人:Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人:Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 /012 (如a1-抗胰蛋白酶缺乏) 阻止肺组织损伤的能力↓ +,-. (如长期吸烟、环境污染、感染) 肺内产生自由基 34*5 肺抗蛋白酶的失活 ↑氧化应激，炎性细胞因子，蛋白酶功能 支气管的持续、反复损伤 炎性细胞浸润， 杯状细胞增殖， 气道上皮纤毛 尤其中性粒细 黏液产生↑ 细胞死亡 气道弹性↓ (弹性回缩 肺实质的蛋白水解破坏↑ 维持气道开放 肺泡永久性异常 的结构支持↓ 扩张 胞 力) 肺气体潴留 气道狭窄与 肺过度 肺大泡 气道黏液潴留，成为感染 狭窄 病灶 塌陷 充气 肺气肿 (容易肺泡 破裂) 气道纤维化和 %&'()* 慢性阻塞性肺疾病(COPD) 临床表现 并发症 (参阅相关幻灯片) (参阅相关幻灯片) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Clinical Findings Lung tissue Chronic Obstructive Pulmonary Disease (COPD) damage ↓ elastic recoil to push air out of lungs on expiration Lungs don’t fully empty, air is trapped in alveoli (lung hyperinflation) ↑ lung volume means diaphragm is tonically contracted (flatter) If occurring around airways Airflow obstruction ↑ mucus production ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) Chronic cough with sputum Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction ↓ ventilation of alveoli ↓ oxygenation of blood (hypoxemia) ↓ perfusion of body tissues (i.e. brain, muscle) Fatigue; ↓ exercise tolerance Total expiration time takes longer than normal Prolonged expiration More effort needed to ventilate larger lungs Respiratory muscles must work harder to breathe Turbulent airflow in narrower airways is heard on auscultation Expiratory Wheeze Diaphragm can’t flatten much further to generate deep breaths To breathe, chest wall must expand out more Dyspnea Shortness of breath, especially on exertion Breathes are rapid & shallow If end-stage: Chronic fatigue causes deconditioning Muscle weakness & wasting Barrel chest If end-stage: diaphragm will be “flat”. Continued Patient tries to expire against higher mouth air pressure, forcing airways to open wider Pursed-lip breathing Patient breathes with accessory muscles as well as diaphragm to try to improve airflow inspiratory effort further contracts diaphragmà pull the lower chest wall inwards Hoover’s sign (paradoxical shrinking of lower chest during inspiration) Tripod sitting position (activates pectoral muscles) Neck (SCM, scalene) muscles contracted Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: ! 45 (on ABGs) Ventilation- perfusion mismatch High A-a gradient (calculated from ABGs) Low, flat diaphragm, >10 posterior ribs (on frontal CXR) High TLC and VC (on spirometry) • • PaO2: partial pressure of O2 in arterial blood PaCO2: partial pressure of CO2 in arterial blood • In the setting of fever and productive cough, especially if lung field opacifications are seen on CXR: consider sputum gram stain and culture to rule out pneumonia. Air does not block X-ray beams, will appear black on X-ray film Chronic hypercapnia makes breathing centers less sensitive to the high PaCO2 stimulus for breathing, & more reliant on the low PaO2 stimulus (“CO2 retention”) Give O2 carefully to these patients (high PaO2 may suppress patients’ hypoxic respiratory drive, ↓ their breathing, & ↑↑↑ PaCO2) ↑ retrosternal air space (on lateral CXR) Hyper-lucent (darker) lung fields, ↓ lung markings (on frontal CXR) • Arterial Blood Gasses (ABGs) • Chest X-Ray (CXR): frontal and lateral Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 气流阻塞 肺泡通气↓ 呼气时，胸膜腔正压挤压气 道à 阻塞↑ 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者:Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 慢性阻塞性肺疾病 (COPD) 肺组织损伤 没有弹性回缩力将 气体排出肺 肺实质与血管分布减少导 致气体交换面积↓ 弥散功能↓ (肺功能检查) 更多的CO2残留 并扩散到血液中 高碳酸血症: PaCO2 > 45 (动脉血气) 血流灌注通气不良的肺泡 时无法获得足够的氧气 总呼气时长较正常长 FEV1/FEV < 0.7 (肺功能检查) 肺无法完全排空 更多空气潴留在肺部 (肺过度充气) 低氧血症: PaO2 < 70mmHg (动脉血气) 通气-灌注不匹配 肺泡-动脉氧分压差↑ (可通过动脉血气分析计算得出) 横膈低平， 下移至第10肋后端 及以下部位 (胸部正位片) TLC与VC增大 (肺功能检查) 缩写: • • FEV1: 1秒用 • VC:肺活量 PaO2: 动脉血 力呼气量 氧分压 空气不会阻挡X射线， 在X光片上呈现为黑色 慢性高碳酸血症使呼吸中枢对PaCO2 刺激呼吸的敏感性下降 & 更依赖于低PaO2的刺激 (“二氧化碳潴留”) 给患者吸氧时需注意(高PaO2 可能会抑制患者低氧时对呼吸的 刺激，使呼吸驱动↓ & PaCO2↑↑↑ ) • FVC: 用力肺 • 活量 • TLC:肺总量 慢阻肺相关检查 : PaCO2: 动脉 血二氧化碳 分压 胸骨后间隙↑ (胸部侧位片) 肺纹理↓ • 肺功能检查 • 动脉血气分析(Arterial Blood Gasses, ABGs) • 胸部正侧位片 • 当患者发热和湿咳，特别是胸片上见肺野不清晰时: 肺透亮度↑, (胸部正位片) 考虑进行痰革兰氏染色及痰培养以排除肺炎可能 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Complications Lung inflammation Chronic Obstructive Pulmonary Disease (COPD) Airway obstruction ↓ inhaled air in alveoli and terminal bronchioles Rupture of emphasematous bullae on surface of lung Inhaled air leaks into pleural cavity and is trapped there Pneumothorax Feeling a loss of control over one’s life, and hopelessness for the future Goblet cell proliferation, ↑ mucus production Death of airway epithelium ciliated cells ↓ oxygenation of the blood passing through the lungs Chronic hypoxemia Kidneys compensate by ↑ erythropoietin (EPO) production ↑ Hemoglobin and red blood cell synthesis Polycythemia (secondary) Hypoxic alveoli cause the pulmonary arterioles perfusing them to reflexively vasoconstrict Since most alveoli in the lungs are hypoxic, hypoxic vasoconstriction occurs across entire lung Vasoconstriction ↑ blood pressure within lung vasculature Pulmonary hypertension ↑ workload of the right ventricle (to pump against higher pressures) To compensate, the right ventricle progressively hypertrophies and dilates, but over time its output ↓ Cor pulmonale (Right heart failure in isolation, not due to Left heart failure) Mucus trapped in airways, serve as nidus for infection Acute exacerbation of COPD (AECOPD) Pneumonia The chronic, systemic inflammation in COPD is a hyper-metabolic state that consumes calories Macro-nutrient deficiency Trouble with respiration lead to inactivity and deconditioning Wasting, muscle atrophy More inactivity and deconditioning perpetuates the cycle Depression Author: Yan Yu Reviewers: Jason Baserman Naushad Hirani* Juri Janovcik* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"# 肺部炎症 杯状细胞增殖， 气道上皮纤毛 粘液产生↑ 细胞死亡 黏液潴留呼吸道，成为感 染的病灶 慢性阻塞性肺疾病 (COPD) 气道阻塞à 吸入肺泡和终末细 肺大疱破裂 吸入的空气渗入 并潴留于胸腔 气胸 感觉生活失控，对未 来感到绝望 抑郁 作者: Yan Yu 审稿人: Jason Baserman, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 支气管的空气 ↓ 流经肺的血液进行气 缺氧的肺泡à灌注肺泡的肺小动 慢性阻塞性肺疾 病急性加重期 (AECOPD) 肺炎 体交换↓ 慢性低氧血症 肾脏合成促红细胞 生成素进行代偿↑ 血红蛋白与红 细胞合成↑ 红细胞增多症 (继发性) 脉发生反射性血管收缩 肺大部分肺泡缺氧à整个肺 都出现缺氧性血管收缩 肺血管收缩 à 肺血管压力↑ 肺动脉高压 ↑ 右心室负荷(泵血时对抗高压) 为了代偿，右心室逐渐肥大和扩张， 但随着病程进展，右心室输出量 ↓ 肺心病 (单独出现右心衰竭，非左心衰) COPD所致的慢性全身 呼吸困难导致活 性炎症会使机体处于高 动量减少和活动 代谢状态，消耗能量 耐量降低 宏量营养 素缺乏症 消瘦，肌肉萎缩 运动量下降和活动耐量 的降低造成恶性循环 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com " title="COPD: 临床表现 作者: Yan Yu 审稿人:Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人:Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 /012 (如a1-抗胰蛋白酶缺乏) 阻止肺组织损伤的能力↓ +,-. (如长期吸烟、环境污染、感染) 肺内产生自由基 34*5 肺抗蛋白酶的失活 ↑氧化应激，炎性细胞因子，蛋白酶功能 支气管的持续、反复损伤 炎性细胞浸润， 杯状细胞增殖， 气道上皮纤毛 尤其中性粒细 黏液产生↑ 细胞死亡 气道弹性↓ (弹性回缩 肺实质的蛋白水解破坏↑ 维持气道开放 肺泡永久性异常 的结构支持↓ 扩张 胞 力) 肺气体潴留 气道狭窄与 肺过度 肺大泡 气道黏液潴留，成为感染 狭窄 病灶 塌陷 充气 肺气肿 (容易肺泡 破裂) 气道纤维化和 %&'()* 慢性阻塞性肺疾病(COPD) 临床表现 并发症 (参阅相关幻灯片) (参阅相关幻灯片) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Clinical Findings Lung tissue Chronic Obstructive Pulmonary Disease (COPD) damage ↓ elastic recoil to push air out of lungs on expiration Lungs don’t fully empty, air is trapped in alveoli (lung hyperinflation) ↑ lung volume means diaphragm is tonically contracted (flatter) If occurring around airways Airflow obstruction ↑ mucus production ↓ number of epithelial ciliated cells to clear away the mucus (the cells have been killed by airway inflammation) Chronic cough with sputum Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction ↓ ventilation of alveoli ↓ oxygenation of blood (hypoxemia) ↓ perfusion of body tissues (i.e. brain, muscle) Fatigue; ↓ exercise tolerance Total expiration time takes longer than normal Prolonged expiration More effort needed to ventilate larger lungs Respiratory muscles must work harder to breathe Turbulent airflow in narrower airways is heard on auscultation Expiratory Wheeze Diaphragm can’t flatten much further to generate deep breaths To breathe, chest wall must expand out more Dyspnea Shortness of breath, especially on exertion Breathes are rapid & shallow If end-stage: Chronic fatigue causes deconditioning Muscle weakness & wasting Barrel chest If end-stage: diaphragm will be “flat”. Continued Patient tries to expire against higher mouth air pressure, forcing airways to open wider Pursed-lip breathing Patient breathes with accessory muscles as well as diaphragm to try to improve airflow inspiratory effort further contracts diaphragmà pull the lower chest wall inwards Hoover’s sign (paradoxical shrinking of lower chest during inspiration) Tripod sitting position (activates pectoral muscles) Neck (SCM, scalene) muscles contracted Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 慢性阻塞性肺疾病 (COPD) 如果出现在气道周围 气流阻塞 肺不能完全排空 气体，气体潴留 于肺泡(肺过度 充气) 总呼气时长大于 正常时长 呼气相延长 肺组织损伤 呼气时，将空气排出肺外 的弹性回缩力↓ 肺不能完全排空气体， 气体潴留于肺泡内 (肺过度充气) 肺容积↑，膈肌紧张 性收缩(膈肌平坦) 呼气时，胸膜腔正压挤压气道 à 气道阻塞↑ 肺泡通气↓ 血液氧合↓ (低 氧血症) 身体组织灌注 量↓ (比如脑、 肌肉) 疲劳; 运动耐量↓ 黏液生成↑ 清除黏液的上皮纤 毛细胞数量↓ (受 气道炎症损伤) 慢性咳嗽伴咳 痰 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 容积较大 的肺需要 更加努力 才能通气 呼吸肌必须 更用力才能 呼吸 听诊闻及狭窄气 道中的湍流气流 呼气喘鸣音 呼吸困难 气促，尤其是劳累 膈肌无法进一步收缩以 产生深呼吸 呼吸浅快 为了呼吸， 胸壁必须延 展得更大 桶状胸 晚期病人: 患者试图在较高的口 慢性疲劳导致 患者动用辅助呼吸肌和膈肌呼吸， 腔内气压下进行呼气， 活动耐量下降 从而使气道更开放 以改善气流 晚期病人:膈肌 “平坦” ，持续吸气进一步压 缩膈肌à 向内拉季肋部胸壁 胡佛征 (吸气时，胸廓下侧季肋部内收) 缩唇呼吸 肌肉无力 & 消瘦 端坐呼吸 (调动胸肌) 颈部肌肉收 缩(胸锁乳 突肌、斜角 肌) 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Findings on Investigations Chronic Obstructive Pulmonary Disease (COPD) Author: Yan Yu Reviewers: Jason Baserman Jennifer Au Naushad Hirani* Juri Janovcik* * MD at time of publication Airflow obstruction Lung tissue damage ↓ ventilation of alveoli Blood perfusing ill- ventilated alveoli does not receive normal amounts of oxygen During expiration, positive pleural pressure squeezes on airwaysà↑ obstruction) No elastic recoil to push air out of lungs Loss of lung parenchyma and vasculature ↓ surface area for gas exchange ↓ diffusion capacity (on spirometry) Hypoxemia: PaO2 < 70mmHg (on ABGs) Abbreviations: • FEV1: Forced expiratory volume in 1 second • FVC: Forced vital capacity • TLC: Total lung capacity • VC: Vital Capacity Investigations for COPD : • Spirometry (Pulmonary function test) Total expiration time takes longer than normal FEV1/FEV < 0.7 (on spirometry) Lungs don’t fully empty More air trapped within lungs (hyperinflation) More CO2 remains and diffuses into the blood Hypercapnia: PaCO2 > 45 (on ABGs) Ventilation- perfusion mismatch High A-a gradient (calculated from ABGs) Low, flat diaphragm, >10 posterior ribs (on frontal CXR) High TLC and VC (on spirometry) • • PaO2: partial pressure of O2 in arterial blood PaCO2: partial pressure of CO2 in arterial blood • In the setting of fever and productive cough, especially if lung field opacifications are seen on CXR: consider sputum gram stain and culture to rule out pneumonia. Air does not block X-ray beams, will appear black on X-ray film Chronic hypercapnia makes breathing centers less sensitive to the high PaCO2 stimulus for breathing, & more reliant on the low PaO2 stimulus (“CO2 retention”) Give O2 carefully to these patients (high PaO2 may suppress patients’ hypoxic respiratory drive, ↓ their breathing, & ↑↑↑ PaCO2) ↑ retrosternal air space (on lateral CXR) Hyper-lucent (darker) lung fields, ↓ lung markings (on frontal CXR) • Arterial Blood Gasses (ABGs) • Chest X-Ray (CXR): frontal and lateral Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"#$ 气流阻塞 肺泡通气↓ 呼气时，胸膜腔正压挤压气 道à 阻塞↑ 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者:Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 慢性阻塞性肺疾病 (COPD) 肺组织损伤 没有弹性回缩力将 气体排出肺 肺实质与血管分布减少导 致气体交换面积↓ 弥散功能↓ (肺功能检查) 更多的CO2残留 并扩散到血液中 高碳酸血症: PaCO2 > 45 (动脉血气) 血流灌注通气不良的肺泡 时无法获得足够的氧气 总呼气时长较正常长 FEV1/FEV < 0.7 (肺功能检查) 肺无法完全排空 更多空气潴留在肺部 (肺过度充气) 低氧血症: PaO2 < 70mmHg (动脉血气) 通气-灌注不匹配 肺泡-动脉氧分压差↑ (可通过动脉血气分析计算得出) 横膈低平， 下移至第10肋后端 及以下部位 (胸部正位片) TLC与VC增大 (肺功能检查) 缩写: • • FEV1: 1秒用 • VC:肺活量 PaO2: 动脉血 力呼气量 氧分压 空气不会阻挡X射线， 在X光片上呈现为黑色 慢性高碳酸血症使呼吸中枢对PaCO2 刺激呼吸的敏感性下降 & 更依赖于低PaO2的刺激 (“二氧化碳潴留”) 给患者吸氧时需注意(高PaO2 可能会抑制患者低氧时对呼吸的 刺激，使呼吸驱动↓ & PaCO2↑↑↑ ) • FVC: 用力肺 • 活量 • TLC:肺总量 慢阻肺相关检查 : PaCO2: 动脉 血二氧化碳 分压 胸骨后间隙↑ (胸部侧位片) 肺纹理↓ • 肺功能检查 • 动脉血气分析(Arterial Blood Gasses, ABGs) • 胸部正侧位片 • 当患者发热和湿咳，特别是胸片上见肺野不清晰时: 肺透亮度↑, (胸部正位片) 考虑进行痰革兰氏染色及痰培养以排除肺炎可能 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com COPD: Complications Lung inflammation Chronic Obstructive Pulmonary Disease (COPD) Airway obstruction ↓ inhaled air in alveoli and terminal bronchioles Rupture of emphasematous bullae on surface of lung Inhaled air leaks into pleural cavity and is trapped there Pneumothorax Feeling a loss of control over one’s life, and hopelessness for the future Goblet cell proliferation, ↑ mucus production Death of airway epithelium ciliated cells ↓ oxygenation of the blood passing through the lungs Chronic hypoxemia Kidneys compensate by ↑ erythropoietin (EPO) production ↑ Hemoglobin and red blood cell synthesis Polycythemia (secondary) Hypoxic alveoli cause the pulmonary arterioles perfusing them to reflexively vasoconstrict Since most alveoli in the lungs are hypoxic, hypoxic vasoconstriction occurs across entire lung Vasoconstriction ↑ blood pressure within lung vasculature Pulmonary hypertension ↑ workload of the right ventricle (to pump against higher pressures) To compensate, the right ventricle progressively hypertrophies and dilates, but over time its output ↓ Cor pulmonale (Right heart failure in isolation, not due to Left heart failure) Mucus trapped in airways, serve as nidus for infection Acute exacerbation of COPD (AECOPD) Pneumonia The chronic, systemic inflammation in COPD is a hyper-metabolic state that consumes calories Macro-nutrient deficiency Trouble with respiration lead to inactivity and deconditioning Wasting, muscle atrophy More inactivity and deconditioning perpetuates the cycle Depression Author: Yan Yu Reviewers: Jason Baserman Naushad Hirani* Juri Janovcik* * MD at time of publication Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published January 7, 2013 on www.thecalgaryguide.com COPD: !"# 肺部炎症 杯状细胞增殖， 气道上皮纤毛 粘液产生↑ 细胞死亡 黏液潴留呼吸道，成为感 染的病灶 慢性阻塞性肺疾病 (COPD) 气道阻塞à 吸入肺泡和终末细 肺大疱破裂 吸入的空气渗入 并潴留于胸腔 气胸 感觉生活失控，对未 来感到绝望 抑郁 作者: Yan Yu 审稿人: Jason Baserman, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 支气管的空气 ↓ 流经肺的血液进行气 缺氧的肺泡à灌注肺泡的肺小动 慢性阻塞性肺疾 病急性加重期 (AECOPD) 肺炎 体交换↓ 慢性低氧血症 肾脏合成促红细胞 生成素进行代偿↑ 血红蛋白与红 细胞合成↑ 红细胞增多症 (继发性) 脉发生反射性血管收缩 肺大部分肺泡缺氧à整个肺 都出现缺氧性血管收缩 肺血管收缩 à 肺血管压力↑ 肺动脉高压 ↑ 右心室负荷(泵血时对抗高压) 为了代偿，右心室逐渐肥大和扩张， 但随着病程进展，右心室输出量 ↓ 肺心病 (单独出现右心衰竭，非左心衰) COPD所致的慢性全身 呼吸困难导致活 性炎症会使机体处于高 动量减少和活动 代谢状态，消耗能量 耐量降低 宏量营养 素缺乏症 消瘦，肌肉萎缩 运动量下降和活动耐量 的降低造成恶性循环 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com " />

COPD-检查结果

COPD: 检查结果 气流阻塞 肺泡通气↓ 呼气时，胸膜腔正压挤压气 道à 阻塞↑ 作者: Yan Yu 审稿人: Jason Baserman, Jennifer Au, Naushad Hirani*, Juri Janovcik* 译者:Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 慢性阻塞性肺疾病 (COPD) 肺组织损伤 没有弹性回缩力将 气体排出肺 肺实质与血管分布减少导 致气体交换面积↓ 弥散功能↓ (肺功能检查) 更多的CO2残留 并扩散到血液中 高碳酸血症: PaCO2 > 45 (动脉血气) 血流灌注通气不良的肺泡 时无法获得足够的氧气 总呼气时长较正常长 FEV1/FEV < 0.7 (肺功能检查) 肺无法完全排空 更多空气潴留在肺部 (肺过度充气) 低氧血症: PaO2 < 70mmHg (动脉血气) 通气-灌注不匹配 肺泡-动脉氧分压差↑ (可通过动脉血气分析计算得出) 横膈低平， 下移至第10肋后端 及以下部位 (胸部正位片) TLC与VC增大 (肺功能检查) 缩写: • • FEV1: 1秒用 • VC:肺活量 PaO2: 动脉血 力呼气量 氧分压 空气不会阻挡X射线， 在X光片上呈现为黑色 慢性高碳酸血症使呼吸中枢对PaCO2 刺激呼吸的敏感性下降 & 更依赖于低PaO2的刺激 (“二氧化碳潴留”) 给患者吸氧时需注意(高PaO2 可能会抑制患者低氧时对呼吸的 刺激，使呼吸驱动↓ & PaCO2↑↑↑ ) • FVC: 用力肺 • 活量 • TLC:肺总量 慢阻肺相关检查 : PaCO2: 动脉 血二氧化碳 分压 胸骨后间隙↑ (胸部侧位片) 肺纹理↓ • 肺功能检查 • 动脉血气分析(Arterial Blood Gasses, ABGs) • 胸部正侧位片 • 当患者发热和湿咳，特别是胸片上见肺野不清晰时: 肺透亮度↑, (胸部正位片) 考虑进行痰革兰氏染色及痰培养以排除肺炎可能 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症 2013年1月7日发布于 www.thecalgaryguide.com

COPD-并发症

COPD: 并发症 肺部炎症 杯状细胞增殖， 气道上皮纤毛 粘液产生↑ 细胞死亡 黏液潴留呼吸道，成为感 染的病灶 慢性阻塞性肺疾病 (COPD) 气道阻塞à 吸入肺泡和终末细 肺大疱破裂 吸入的空气渗入 并潴留于胸腔 气胸 感觉生活失控，对未 来感到绝望 抑郁 作者: Yan Yu 审稿人: Jason Baserman, Naushad Hirani*, Juri Janovcik* 译者: Zihong Xie (谢梓泓) 翻译审稿人: Yonglin Mai (麦泳琳), Zesheng Ye (叶泽生) * 发表时担任临床医生 支气管的空气 ↓ 流经肺的血液进行气 缺氧的肺泡à灌注肺泡的肺小动 慢性阻塞性肺疾 病急性加重期 (AECOPD) 肺炎 体交换↓ 慢性低氧血症 肾脏合成促红细胞 生成素进行代偿↑ 血红蛋白与红 细胞合成↑ 红细胞增多症 (继发性) 脉发生反射性血管收缩 肺大部分肺泡缺氧à整个肺 都出现缺氧性血管收缩 肺血管收缩 à 肺血管压力↑ 肺动脉高压 ↑ 右心室负荷(泵血时对抗高压) 为了代偿，右心室逐渐肥大和扩张， 但随着病程进展，右心室输出量 ↓ 肺心病 (单独出现右心衰竭，非左心衰) COPD所致的慢性全身 呼吸困难导致活 性炎症会使机体处于高 动量减少和活动 代谢状态，消耗能量 耐量降低 宏量营养 素缺乏症 消瘦，肌肉萎缩 运动量下降和活动耐量 的降低造成恶性循环 图注: 病理生理 机制 体征/临床表现/实验室检查 并发症

copd-komplikationen

copd-diagnostik

copd-klinische-befunde

copd-pathogenese

Chronic Cough Pathogenesis_2021

Chronic Cough: Pathogenesis ACE Inhibitors Protussive mediator accumulation (bradykinin, substance P) Infection IP; likely chronic ↑ cough receptors commonly pertussis- related or post-viral Asthma ↑ EDN ↑ MBP levels in RT Neoplasm Bronchiectasis COPD GERD Allergic Rhinitis ↑ sputum production and accumulation Damage from chronic inflammation causes poor mucus clearance Inhalants trigger ↑ cytokines ↑ mucus Aspiration of refluxed microdroplets Irritation by post- nasal drip ↑ inflammatory mediators in RT Mechanical obstructions (i.e. mediastinal masses, neoplasms) Foreign body Presence irritation of irritants Stimulation of sensory nerve receptors expressed on nerve endings penetrating the epithelia of the upper RT Abbreviations: • RT: respiratory tract • IP: indefinite pathophysiology • GERD: Gastro-esophageal reflux disease • EDN: Eosinophil-derived neurotoxin • MBP: Major basic protein • COPD: Chronic Obstructive Pulmonary Disease Complications: Syncope, insomnia, hemoptysis, rib fractures Slowly adapting receptors Respond to mechanical forces during breathing Stimulation of the vagus nerve Activation of nucleus tractus solitarius in central respiratory generator (brainstem) Generation of efferent cough signal Chronic cough: Cough of over 8 weeks duration with no dyspnea or fever C-fibre receptors Respond to chemical stimuli (bradykinin, capsaicin, acid/alkaline solutions, mannitol, hypertonic saline, and other inhaled irritants) Authors: Arsalan Ahmad Lance Bartel Reviewers: Midas (Kening) Kang Usama Malik Ciara Hanly Yonglin Mai (麦泳琳) Yan Yu*, Eric Leung* * MD at time of publication Rapidly adapting receptors Responds to mechanical stimuli, such as physical obstruction of the airways Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Feb 06, 2018, updated Dec 4, 2021 on www.thecalgaryguide.com

慢性阻塞性肺疾病简称copd定义

慢性阻塞性肺疾病简称copd定义

copd-诱发因素和体征-急性加重的症状

copd-诱发因素和体征-急性加重的症状

adult-pneumonia-pathogenesis-and-clinical-findings

Adult Pneumonia: Pathogenesis and clinical findings Author: Laura Byford-Richardson Reviewers: Tara Shannon, *Yan Yu, Sadie Kutz , Natalie Morgunov, *Kerri Johannson, *Julie Carson *MD at time of publication Smoking à suppressed neutrophil function and damaged lung epithelium Chronic lung conditions e.g. COPD, asthma, lung canceràdestroys lung tissue and offers pathogen more niduses for infection Immune suppression e.g. HIV, sepsis, glucocorticoids, chemotherapyà suppression of immune response Systemic inflammatory response towards invading microbe Systemic cytokine release leads to a disruption in hypothalamic thermoregulation Exposure to a pathogen via inhalation, aspiration, contiguous Notes: or hematological mechanism Susceptible host and/or virulent pathogen Proliferation of microbe in lower airways and alveoli Local response by alveolar epithelial cells release chemokines into surrounding tissue to recruit neutrophils to the site of inflammation • Pathogens can be bacteria, viruses, fungi and parasites • Pneumonia is a lower respiratory tract infection (in contrast to upper respiratory tract infections such as bronchitis) and can be further classified by location of exposure: community, health- care, hospital acquired Inflammatory response varies depending on type of invading pathogen (i.e. S. Pneumonia causes a lobar pattern and Influenza A & B cause an interstitial pattern) LOBAR: Accumulation of neutrophils and plasma exudate from capillaries into alveoli specific to a lung area/lobe INTERSTITIAL: Accumulation of infiltrates (i.e. inflamed cellular debris) in the alveolar walls (i.e. space between the alveolar spaces and bloodstream) Fever Notes: • Other signs and symptoms of pneumonia exist such as chest pain, accessory muscle use, crackles on auscultation and fatigue • These signs and symptoms are less specific to the ones outlined on this slide Irritation and attempted clearance of airways Fluid infiltrates are inside alveoli, airway clearance leads to phlegm production Productive Cough Fluid build up does not allow X-rays to pass through à white opacity on plain film at site of fluid buildup Consolidation on CXR Alveolar sacs blocked by fluid accumulation Thickening of alveolar walls ↑ diffusion distance between alveoli & capillaries Irritated alveolar walls trigger cough reflex Since fluid infiltrates are NOT in the alveoli, attempts to empty the alveoli through coughing doesn’t lead to production of fluid Dry Cough Chills/Rigors ↓ Exchange of CO2 and O2 Hypoxemia Triggers peripheral and central chemoreceptors to ↑ respiratory drive Dyspnea Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Sept 26 2016, updated Feb 9, 2022 on www.thecalgaryguide.com

chest-exam-findings-of-lung-pleural-diseases

Chest Exam Findings of Lung & Pleural Diseases Note: Please see slides on pathogenesis of Transudative and Exudative Pleural Effusions, Primary and Tension Pneumothorax, Adult Pneumonia, Acute Respiratory Distress Syndrome (ARDS), Chronic Obstructive Pulmonary Disease (COPD), Heart Failure, and Kidney Disease Authors: Sravya Kakumanu Reviewers: Ben Campbell, *Tara Lohmann, *Yan Yu * MD at time of publication Interstitial Lung Disease Pneumothorax Rupture of visceral pleura Build-up of air within pleural space Pleural Effusion Atelectasis Consolidation ↑ Hydrostatic pressure pushes fluid into pleural space ↑ Capillary permeability = fluid leaks into pleural space ↓ Oncotic pressure = fluid moves into pleural space Bronchus obstructed Scarring/infiltration of lung tissue Surfactant dysfunction (ex. ARDS) Loss of contact between visceral and parietal pleura (ex. effusion, pneumothorax) Parenchymal compression (ex. loculated effusion, mass) ↑ Hydrostatic pressure pushing fluid into alveoli (ex. cardiogenic pulmonary edema) ↑ Capillary permeability allowing fluid to move into alveoli (ex. pneumonia) Idiopathic Connective tissue diseases Sarcoidosis, Amyloidosis Chronic medical diseases (ex. COPD, heart failure, kidney disease, etc) Occupational or environmental exposures (ex. silicosis, organic dusts, metals, gases, aerosols, etc) Accumulation of fluid in pleural space Collapse of alveoli Accumulation of fluid within alveoli Pulmonary fibrosis (scarring of alveoli bilaterally) Breath Sounds Lung unable to inflate fully Fluid in pleural space Collapsed lung unable to inflate Airspace filled with fluid and unable to fill with air dampens sound ↓ Breath sounds ipsilaterally Scarred alveoli unable to expand to fill with air ↓ Breath sounds bilaterally (may not be noticeable) Chest Rising on Inspiration Chest cavity filled with air, but lung Lung unable to inflate fully Scarred alveoli unable to expand to fill with air unable to inflate fully ↑ Chest size, ↓ Rising ipsilaterally ↓ Chest rising ipsilaterally ↓ Chest rising bilaterally (may not be noticeable) Percussion Sound resonates through air in pleural space Ipsilateral hyperresonance on percussion Sound unable to resonate through pleural fluid Sound unable to resonate through compacted lung tissue Ipsilateral dullness on percussion Sound unable to resonate through fluid-filled alveoli Diffuse scarring of alveoli No notable changes on percussion Tracheal Deviation Air pushes trachea Fluid pushes trachea ↓ Pressure within chest wall pulls trachea No pushing or pulling of trachea Contralateral tracheal deviation Ipsilateral tracheal deviation No tracheal deviation Adventitious Lung Sounds Alveoli not impacted (i.e. not collapsed or fluid-filled) Sudden opening of collapsed alveoli filling with air Fine inspiratory crackles Air movement through fluid-filled alveoli Coarse inspiratory crackles Fluid-filled alveoli can’t dampen breath sounds from larger central airways Bronchial breath sounds all over consolidated area (harsh, ↑ pitch with expiratory phase > inspiratory; only normal when heard centrally over trachea + bronchi) Scarred inelastic alveoli suddenly open on inspiration Fine inspiratory crackles No crackles No abnormal breath sounds Severe pneumothorax or effusion pushing against lung parenchyma Other sounds Amplification of patient voice through fluid-filled alveoli Tactile fremitus (↑ vibrations felt by hand placed on chest wall when patient speaks) *Whispers also sound louder on auscultation Fluid-filled alveoli only allow certain sound frequencies to be audible Egophony (“E” sounds like “A” on auscultation) Legend: Pathophysiology Mechanism Physical Exam Findings Complications Published October 9, 2022 on www.thecalgaryguide.com

copd-findings-on-posterior-anterior-and-lateral-chest-x-ray-findings

Authors: Shayan Hemmati COPD: Findings on Posterior-Anterior and Lateral Chest X-ray Findings Reviewers: Reshma Sirajee, Sravya Kakumanu, Tara Shannon, *Stephanie Nguyen, *MD at time of publication Chronic Obstructive Pulmonary Disease (COPD) See Pathogenesis of COPD Slides Findings of COPD may not be apparent on chest X-ray early within the disease Lung inflammation causes proteolytic destruction of lung parenchyma (part of lungs involved in gas exchange) Alveolar walls are damagedàformation of fragile enlarged sacs of air called bullae Rupture of bullae due to weak alveolar walls Air leaves alveola and enters pleural space Pneumothorax See Primary Spontaneous Pneumothorax slide Vasoconstriction of pulmonary arteries to shunt blood to better ventilated areas Pulmonary hypertension See Pathogenesis of Pulmonary Hypertension slide ↑ Pressure within pulmonary arteries Enlargement of pulmonary arteries Hilar enlargement Lung hyperinflation (defined as 10 posterior ribs above the diaphragm level on the midclavicular line) ↑ Lucency of the lung field, ↓ lung markings (unless COPD is of chronic bronchitis phenotype) ↑ Size of retrosternal airspace ↑ Anterior – posterior (AP) diameter (“Barrel Chest”) Flattening of hemidiaphragms 12 3 4 5 6 7 8 9 10 Poorly ventilated areas of lung Hyperinflation as air becomes trapped in damaged lungs ↑ Total volume of air within the chest Airway fibrosisà bronchial wall thickening (yellow arrow heads) Air is less dense than soft tissue and vessels so it appears black ↑ Pressure anteriorly on sternum ↑ Pressure posteriorly on thoracic wall ↑ Pressure posteriorly on diaphragms PA Bullae sometimes visible on X-ray (focal areas of lucency with spread out vascular markings) Image credit: Bronchial wall thickening image courtesy of Dr. Ashley Davidoff Image credit: Radiopaedia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published October 26, 2022 on www.thecalgaryguide.com

COPD: Treatments and Common Side Effects

COPD: Treatments and Common Side Effects Note: Please see various slides on COPD related to pathogenesis and findings • Relievers: Used as needed to ↓ symptoms during attacks • Controllers: Used daily to ↓ frequency and severity of attacks • Exacerbation: Used emergently in acute exacerbation (relievers also often used) Short-acting Beta Agonists (SABA) Reliever Long-acting Beta Agonists (LABA) Controller Long-acting Muscarinic Antagonists Controller Inhaled Corticosteroids (ICS) Controller Phosphodiesterase Inhibitors (PDE4i) Controller Short-acting Muscarinic Antagonists Reliever Systemic Corticosteroids Exacerbation Antibiotic therapy Exacerbation + Controller Binds to beta-2 adrenergic receptors in bronchial smooth muscle cells Activation of intracellular signal cascade in bronchial smooth muscle Off-target binding occurs in other systemic cells Prevent phosphodiesterase enzymes from breaking down secondary messenger molecules such as cyclic adenosine monophosphate (cAMP) cAMP binds to other cell signaling proteins Bronchial smooth muscle cells have ↓ Ca2+ release from intracellular stores (i.e. from sarcoplasmic reticulum) Inhibition of muscarinic acetylcholine receptors in airway muscle cells ↓ Activation of the inositol triphosphate (IP3) intracellular pathway (IP3 pathway normally functions to mobilize intracellular Ca2+ stores) Steroid binds to nuclear receptors within cells ↓ Gene expression/ synthesis of immune mediators (ex. cytokines) Frequent moderate-severe exacerbations despite maximal therapy Prophylactic macrolide treatment in outpatients Certain macrolides have anti- inflammatory properties ↓ Infection risk = ↓ exacerbation risk COPD exacerbations often triggered by respiratory infections Empiric antibiotic therapy in hospitalized patients with acute exacerbations ↓ Infection in lungs ↓ Sputum production ↓ Respiratory distress Stimulation of Na/K ATPase (which transports K into cells) Hypokalemia Palpitations Tachycardia Muscle cramps Tremor Inadvertent sympathetic nervous system activation ↓↓ Cytoplasmic Ca2+ Myosin (muscle protein) unable to be activated for muscle contraction ↓ Smooth muscle contraction in bronchioles Bronchodilation ICS ↓ immune cell activity in the oropharynx Susceptibility to infection and irritation of the oropharynx due to inhaled particles and pathogens Hoarseness Thrush Systemic steroids cause ↓ immune cell activity in whole body ↑ Susceptibility to any infection (and many other side effects) ↓ Release of inflammatory cytokines (↓ Type 2 inflammatory response in airways) ↓ Permeability of airway vasculature ↓ Microvascular leakage into airway Authors: Reshma Sirajee, Chunpeng Nie Reviewers: Sravya Kakumanu, Ben Campbell, Tara Lohmann* * MD at time of publication Similar effects on other muscles in the body outside bronchi Dry mouth Urinary retention Constipation ↓ Airway mucus ↓ Mucosal edema Legend: Pathophysiology Mechanism Treatment Effect Side Effects Published November 15, 2022 on www.thecalgaryguide.com

Death Cardiovascular Respiratory and Neurologic Mechanisms

Death: Cardiovascular, Respiratory and Neurologic Mechanisms Mitochondria in tissues unable to utilize O2 Reduced hemoglobin in blood to carry O2 Low oxygen content in blood (CaO2) Hypoxemia (Type I Respiratory Failure): low dissolved oxygen in blood (PaO2) Lungs can’t oxygenate blood fast enough Lungs can’t rid blood of CO2 fast enough Hypercapnia / hypercarbia (Type II Respiratory Failure): elevated dissolved CO2 in blood (PaCO2) Cerebral vasodilation Toxins: e.g. cyanide, pesticides, arsenic Severe anemia Distributive problems: Systemic inflammation (sepsis, anaphylaxis, pancreatitis), adrenal insufficiency, vasodilatory drugs Obstructive problems: Cardiac tamponade*, tension pneumothorax* or massive pulmonary embolism* Hypovolemic* problems (low blood volume): Hemorrhage, dehydration, widespread skin disruption or burns Cardiac valve dysfunction Myocardial infarction* or cardiomyopathy Cardiac arrhythmia or heart block Disturbed electrical activity in cardiomyocytes Peripheral metabolic disturbances Hypokalemia*, Hyperkalemia* Acidosis* (including renal failure) Hypothermia* Toxins* (e.g. cocaine, beta blockers, tricyclics) Severe thyroid derangement Inappropriate systemic vasodilation Adjacent forces impair heart filling Low cardiac preload Low stroke volume (SV; depends on valves, contractility, preload) Decreased systemic vascular resistance (SVR) Low blood pressure (BP = CO x SVR) Decreased cardiac output (CO = SV x HR) Disseminated intravascular coagulationàwidespread thrombi that occlude blood flow (also causes hemorrhage, see relevant box at left) Methemoglobinemia: some hemoglobin gets stuck in a state that can’t carry O2 Hemoglobin has reduced capacity to carry or release O2 Drugs: e.g. dapsone, nitrates Carbon monoxide poisoning Circulatory collapse / shock: inadequate perfusion of tissue with blood Respiratory collapse: blood has insufficient useable O2 content Ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) Hypoxia*: inadequate O2 delivery or utilization in tissues Hypoxia creates metabolic disturbances that impair cardiac cells. Alternatively, any of the preceding conditions marked with (*) can directly trigger cardiac arrest first Pulseless Electrical Activity (PEA): organized activity on ECG with no cardiac output (can be preceded or mimicked by pseudo-PEA, in which there is still some output on ultrasound) Low atmospheric pressure or oxygen content Severe lung disease Asthma, COPD, interstitial lung disease, congestive heart failure, pulmonary hypertension, pulmonary embolism, lung collapse / atelectasis Acute respiratory distress syndrome Pneumonia, aspiration pneumonitis, inhalational injury, systemic inflammation, drowning Severe hypoventilation Respiratory fatigue, advanced COPD, chest wall disorders, neuromuscular disorders, upper airway obstruction, toxins (e.g. opioids, botulism) Can degenerate at any time Asystole: no cardiac electrical activity or output Death Respiratory arrest: cessation of breathing Inability to protect airway Decreased level of consciousness Note This is a broad overview of the many scenarios that can result in death. For detailed explanations of the various disease mechanisms, refer to the corresponding slides. * = reversible causes of cardiac arrest (Hs and Ts) Author: Ben Campbell Reviewers: Yan Yu* Huma Ali* * MD at time of publication Bradycardia (low heart rate, HR) Unopposed parasympathetic stimulation of heart (can also cause vasodilation, see Distributive problems) Disruption of spinal cord sympathetic control Injury to cervical or upper thoracic spinal cord Irreversible cessation of cardiac, respiratory, and brain function Prolonged seizure initially causes increased cardiovascular activity, until the system fatigues Disruption of respiratory control center in medulla Expanding skull contents squeeze brainstem (herniation) Increased intracranial pressure Edema from intracranial hemorrhage, trauma, brain mass Edema, inflammation, hypoxia and/or metabolic derangements cause diffuse neuron dysfunction Central nervous system infection Dementia, particularly with delirium Massive ischemic stroke Seizure activity prevents or alters breathing Metabolic disturbances that affect the central nervous system Hypoglycemia Hypocalcemia, hypercalcemia Hyponatremia, hypernatremia Uremia Acute liver failure (hyperNH4) Many drugs / toxins Withdrawal (e.g. EtOH) Status epilepticus Brainstem lesion (e.g. stroke, neoplasm, inflammatory) Nervous System Insult Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 11, 2023 on www.thecalgaryguide.com Respiratory System Insult Cardiovascular System Insult Cardiogenic problems

COPD - بیماریزایی

COPD - بیماریزایی

COPD - یافتھ ھای بالینی

COPD - یافتھ ھای بالینی

COPD - یافتھ ھای تشخیصی

COPD - یافتھ ھای تشخیصی

COPD - عوارض و عواقب

COPD - عوارض و عواقب

Anesthetic Considerations One Lung Ventilation

Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated Shunt: Non- dependent lung unventilated Perfusion but no ventilation to collapsed lung Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung Right to left intrapulmonary shunt with some perfusion to non- dependent lung V/Q mismatch causes ↑ hypoxemia Increase FiO2 to 1 to maintain SpO2 ≥ 90% Increased FiO2 can allow for toleration of shunt Optimize cardiac output and shunt fraction to maximize PaO2 Author: Aly Valji Reviewers: Jasleen Brar Ryden Armstrong* * MD at time of publication Relative indications Surgical exposure for pulmonary resection, mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Double lumen tube (gold standard) Endotracheal tube (ETT) with two lumens (bronchial and tracheal) Insert longer side to a mainstem bronchus, shorter side ends in distal trachea Absolute Indications Isolation of healthy from contaminated lung (unilateral infection, hemorrhage) Control unilateral disruption of ventilation (bronchopleural fistula, unilateral bullae) Video assisted thoracoscopic surgery Unilateral lung lavage Airway Technique Anesthetic Technique General anesthetic with neuromuscular blockade ↓ Inspiratory muscle tone Intraabdominal contents push up on diaphragm ↓ Functional residual capacity (FRC) ↑ Atelectasis if closing capacity > FRC ↑ Hypoxemia Optimize Altered gravitational forces on thorax ↓ Compliance of dependent lung ↑ Airway pressure required ↑ Risk of lung barotrauma due to ↑ pressure ↑ Perfusion to dependent lung. ↑ Ventilation to nondependent lung (prior to lung isolation) Collapse of nondependent lung using lung isolation causes ↓ ventilation to this lung Optimize tidal volume (6-8 mL/kg), respiratory rate (maintain PaCO2 35-40 mmHg), PEEP (5-10 cm H2O) based on clinical picture Univent tube Single lumen ETT with movable endobronchial blocker in wall Blocker steered after intubation into a mainstem bronchus with fiberoptic bronchoscope Endotracheal tube in mainstem bronchus Single lumen ETT pushed into a mainstem bronchus Bronchial blocker Shaft with an inflatable balloon on distal end Inserted through single lumen ETT into a mainstem bronchus, after intubation positive end- expiratory pressure (PEEP) of 5-10 cm H2O Recruitment of dependent, atelectatic lung with positive pressure Optimize FiO2 ↓ Absorptive atelectasis (from ↑ partial pressure O2 and ↓ N2) Cuff inflated in a mainstem bronchus to isolate respective lung. Placement should be verified using fiberoptic bronchoscope if possible after positioning ↓ Atelectasis and ↑ FRC ↓ Hypoxemia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Management Published December 5, 2023 on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated Shunt: Non- dependent lung unventilated Perfusion but no ventilation to collapsed lung Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung Right to left intrapulmonary shunt with some perfusion to non- dependent lung V/Q mismatch from shunt causes ↑ hypoxemia Increase FiO2 to 1 to maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for shunt to non- dependent lung ↓ V/Q mismatch Author: Aly Valji Reviewers: Jasleen Brar Dr. Armstrong* * MD at time of publication Relative indications Surgical exposure for pulmonary resection, mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Double lumen tube (DLT) Two endotracheal tubes (ETT) bonded together Insert longer side to a mainstem bronchus, shorter side ends in distal trachea Absolute Indications Isolation of healthy from contaminated lung (unilateral infection, hemorrhage) Control unilateral disruption of ventilation (bronchopleural fistula, unilateral bullae) Video assisted thoracoscopic surgery Unilateral lung lavage Airway Technique Anesthetic Technique General anesthetic with neuromuscular blockade ↓ Inspiratory muscle tone Intraabdominal contents push up on diaphragm ↓ Functional residual capacity (FRC) ↑ Atelectasis if closing capacity > FRC ↑ Hypoxemia Optimize Altered gravitational forces on thorax ↑ Elastance of dependent lung ↑ Airway pressure required ↑ Risk of lung barotrauma due to ↑ pressure ↑ Perfusion to dependent, ventilated lung ↓ Ventilation- perfusion (V/Q) mismatch ↓ Hypoxemia Optimize tidal volume (6-8 mL/kg), respiratory rate (maintain PaCO2 35-40 mmHg), PEEP (5-10 cm H2O) based on clinical picture Univent tube Single lumen ETT with movable endobronchial blocker in wall Blocker steered after intubation into a mainstem bronchus with fiberoptic bronchoscope Endotracheal tube in mainstem bronchus Single lumen ETT pushed into a mainstem bronchus Bronchial blocker Shaft with an inflatable balloon on distal end Inserted through single lumen ETT into a mainstem bronchus, after intubation positive end- expiratory pressure (PEEP) of 5-10 cm H2O Recruitment of dependent, atelectatic lung with positive pressure Optimize FiO 2 ↓ Absorptive atelectasis (from ↑ partial pressure O2 and ↓ N2) Cuff inflated in a mainstem bronchus to isolate respective lung. Placement should be verified using fiberoptic bronchoscope if possible after positioning ↓ Atelectasis and ↑ FRC ↓ Hypoxemia Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Management Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Author: Aly Valji Reviewers: Jasleen Brar Name* * MD at time of publication Non-dependent lung unventilated Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung Right to left intrapulmonary shunt with some perfusion to non- dependent lung V/Q mismatch from shunt causes ↑ hypoxemia Increase FiO2 to maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for shunt to non- dependent lung Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated Indications Anesthetic General anesthetic with neuromuscular blockade ↓ Inspiratory muscle tone Relative indications Surgical exposure for pulmonary resection, mediastinal, esophageal, vascular, thoracic spine surgery Absolute Indications Isolation of healthy from contaminated lung (Unilateral infection or hemorrhage) Control unilateral disruption of ventilation (Bronchopleural fistula, unilateral bullae) Video assisted thoracoscopic surgery Unilateral lung lavage Intraabdominal contents push up on diaphragm ↓ FRC ↑ Atelectasis if closing capacity > FRC ↑ Hypoxemia Altered gravitational forces on thorax Shaft with an inflatable balloon on distal end. Inserted through a single lumen ETT after intubation into a mainstem bronchi Single lumen ETT pushed into a mainstem bronchus Optimize positive end-expiratory pressure (PEEP)) Recruitment of dependent, atelectatic lung with positive pressure ↑ Elastance of dependent lung ↑ Airway pressure required ↑ Risk of lung barotrauma due to ↑ pressure ↑ Perfusion to dependent, ventilated lung ↓ Ventilation- perfusion (V/Q) mismatch ↓ Hypoxemia Optimize tidal volume, respiratory rate, PEEP based on clinical picture Bronchial blocker Endotracheal tube in mainstem bronchus Technique Univent tube Double lumen tube (DLT) Optimize FiO2 ↓ Absorptive atelectasis (from ↑ partial pressure O2 and ↓ N2) Single lumen ETT with movable endobronchial blocker housed in wall of ETT. Blocker maneuvered after intubation into a mainstem bronchus Two endotracheal tubes (ETT) bonded together. Longer side goes into a mainstem bronchus, shorter side ends in distal trachea ↓ Atelectasis and ↑ FRC ↓ V/Q mismatch Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Author: Aly Valji Reviewers: Jasleen Brar Name* * MD at time of publication Non-dependent lung unventilated Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung Right to left intrapulmonary shunt with some perfusion to non- dependent lung V/Q mismatch from shunt causes ↑ hypoxemia Increase FiO to 2 maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for shunt to non- dependent lung ↓ V/Q mismatch Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated Indications Anesthetic General anesthetic with neuromuscular blockade ↓ Inspiratory muscle tone Comorbidity: Likely underlying pulmonary disease Pre-operative evaluation Pulmonary function testing Overall clinical picture, forced expiratory volume (FEV1), and diffusion capacity (DLCO) Multidisciplinary determination of fitness for surgery Pulmonary hemorrhage Whole lung lavage Unilateral infection Bronchopleural fistula Isolation of affected lung from unaffected lung Pulmonary resection Mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Operative lung deflated to expose surgical site Intraabdominal contents push up on diaphragm ↓ FRC ↑ Atelectasis if closing capacity > FRC ↑ Hypoxemia Optimize positive Altered gravitational forces on thorax Contraindications ↑ Elastance of dependent lung ↑ Airway pressure required ↑ Risk of lung barotrauma due to ↑ pressure ↑ Perfusion to dependent, ventilated lung ↓ Ventilation- perfusion (V/Q) mismatch ↓ Hypoxemia Optimize tidal volume, respiratory rate, PEEP based on clinical picture Bilateral lung ventilation dependency Hemodynamic instability Severe hypoxia Severe COPD Severe pulmonary hypertension Potentially unable to tolerate one lung ventilation Intraluminal airway obstruction/mass Known difficult airway Risk of dislodging mass and inability to secure airway Pursue more advanced airway techniques end-expiratory pressure (PEEP) Recruitment of dependent, atelectatic lung with positive pressure Optimize FiO2 ↓ Absorptive atelectasis (from ↑ partial pressure O and ↓ N ) 2 2 ↓ Atelectasis and ↑ FRC Post-operative pain management Thoracotomy or VATS procedure causing ↑ pain along thoracic dermatomes Epidural Paravertebral block Anesthetic injected into epidural space Anesthetic injected into paravertebral spaces Bilateral spinal nerve blockade below desired spinal level Ipsilateral spinal nerve and sympathetic chain blockade in thoracic dermatomes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Author: Aly Valji Reviewers: Jasleen Brar Name* * MD at time of publication Non-dependent lung unventilated Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung Right to left intrapulmonary shunt with some perfusion to non- dependent lung V/Q mismatch from shunt causes ↑ hypoxemia Increase FiO2 to maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for shunt to non- dependent lung ↓ V/Q mismatch Indications Anesthetic General anesthetic with neuromuscular blockade ↓ Inspiratory muscle tone Comorbidity: Likely underlying pulmonary disease Pre-operative evaluation Pulmonary function testing Overall clinical picture, forced expiratory volume (FEV1), and diffusion capacity (DLCO) Multidisciplinary determination of fitness for surgery Anesthetic injected into epidural space Anesthetic injected into paravertebral spaces Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated Pulmonary hemorrhage Whole lung lavage Unilateral infection Bronchopleural fistula Isolation of affected lung and unaffected lung Pulmonary resection Mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Operative lung deflated to expose surgical site Intraabdominal contents push up on diaphragm ↓ FRC ↑ Atelectasis ↑ Hypoxemia Optimize positive end- expiratory pressure (PEEP) Recruitment of dependent, atelectatic lung with positive pressure ↓ Atelectasis and ↑ FRC Altered gravitational forces on thorax Contraindications ↑ Elastance of dependent lung ↑ Airway pressure required ↑ Risk of lung barotrauma due to ↑ pressure Optimize tidal volume, respiratory rate, PEEP based on clinical picture ↑ Perfusion to dependent, ventilated lung ↓ Ventilation- perfusion (V/Q) mismatch ↓ Hypoxemia Bilateral lung ventilation dependency Hemodynamically unstable Severe hypoxia Severe COPD Severe pulmonary hypertension Unable to tolerate one lung ventilation Intraluminal airway obstruction/mass Known difficult airway Risk of dislodging mass and inability to secure airway Pursue more advanced airway techniques Post-operative pain management Thoracotomy or VATS procedure causing ↑ pain along thoracic dermatomes Epidural Paravertebral block Bilateral spinal nerve blockade below desired spinal level Ipsilateral spinal nerve and sympathetic chain blockade in thoracic dermatomes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Mechanical separation of the lungs to allow for individualized ventilation of only one lung Author: Aly Valji Reviewers: Name* * MD at time of publication Indication Contraindications Comorbidity: Likely underlying pulmonary disease Positioning: Lateral decubitus position (patient on their side) with dependent lung ventilated General anesthetic with neuromuscular blockade Post-operative pain management Pulmonary resection, mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Pulmonary hemorrhage, whole lung lavage, bronchopleural fistula, or unilateral infection Operative lung deflated to expose surgical site Isolation of affected lung and unaffected lung Dependency on bilateral lung ventilation, hemodynamically unstable, severe hypoxia, severe COPD, or severe pulmonary hypertension Unable to tolerate one lung ventilation Intraluminal airway obstruction/mass or known difficult Pursue more advanced Risk of dislodging mass and inability to secure airway Multidisciplinary determination of fitness for surgery airway Pulmonary function testing Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung airway techniques Overall clinical picture, forced expiratory volume (FEV1), and diffusion capacity (DLCO) Pre-operative evaluation Non- dependent lung not ventilated Altered gravitational forces on thorax Intraabdominal contents push up on diaphragm ↓ Inspiratory muscle tone Likely procedure is thoracotomy or VATS causing ↑ pain along thoracic dermatomes Right to left intrapulmonary shunt with some perfusion to non- dependent lung still present V/Q mismatch from shunt causes ↑ hypoxemia Increase FiO2 to maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for shunt to non- dependent lung ↓ V/Q mismatch ↓ Hypoxemia Intervention: Optimize tidal volume, respiratory rate, PEEP based on clinical picture ↓ Atelectasis and ↑ FRC ↑ Perfusion to dependent, ventilated lung ↑ Elastance of dependent lung ↓ FRC ↓ Functional residual capacity (FRC) ↓ Ventilation-perfusion (V/Q) mismatch ↑ Airway pressure required ↑ Atelectasis ↑ Hypoxemia ↑ Risk of lung barotrauma due to ↑ pressure Intervention: Optimize positive end-expiratory pressure (PEEP) Recruitment of dependent, atelectatic lung with positive pressure Epidural Paravertebral block Anesthetic injected into epidural space Bilateral spinal nerve blockade below desired spinal level Anesthetic injected into Ipsilateral spinal nerve and sympathetic chain blockade in thoracic paravertebral spaces dermatomes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic Considerations: One-lung ventilation Author: Aly Valji Reviewers: Name* * MD at time of publication One lung ventilation: mechanical separation of the lungs to allow for individualized ventilation of only one lung Indication Pulmonary resection, mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Pulmonary hemorrhage, whole lung lavage, bronchopleural fistula, or unilateral infection Exposure of surgical site by deflation of operative lung Isolation of affected lung and unaffected lung Dependency on bilateral lung ventilation, Contraindications hemodynamically unstable, severe hypoxia, severe COPD, or severe pulmonary hypertension Intraluminal airway obstruction/mass or known difficult airway Pursue more advanced airway techniques Unable to tolerate one lung ventilation Risk of dislodging mass and inability to secure airway Likely underlying Pre-operative Pulmonary pulmonary disease evaluation function testing Overall clinical picture, forced expiratory Determination of volume (FEV1), and diffusion capacity (DLCO) fitness for surgery Right to left intrapulmonary shunt as some perfusion to non- dependent lung is still present ↑ Perfusion to dependent, ventilated lung ↑ Elastance of dependent lung ↓ FRC Non- dependent lung not ventilated Hypoxic vasoconstriction decreases but does not stop perfusion to non- dependent lung V/Q mismatch from shunt increases hypoxemia Intervention: Increase FiO2 to maintain SpO2 ≥ 90% Vasodilation of dependent lung vasculature to compensate for non-dependent lung ↓ V/Q mismatch ↓ Hypoxemia Intervention: Optimize tidal volume, respiratory rate, PEEP ↓ Atelectasis and ↑ FRC Positioning: Lateral position with dependent lung ventilated Altered gravitational forces on thorax ↓ Ventilation-perfusion (V/Q) mismatch General anesthetic with neuromuscular blockade Intraabdominal contents push up on diaphragm ↑ Airway pressure required ↑ Atelectasis ↑ Hypoxemia ↑ Risk of lung barotrauma Intervention: Optimize positive end-expiratory pressure (PEEP) Recruitment of dependent, atelectatic lung from PEEP ↓ Inspiratory muscle tone ↓ Functional residual capacity (FRC) Post- operative pain management Thoracotomy or VATS causes pain along thoracic dermatomes Epidural Paravertebral block Bilateral spinal nerve blockade below desired Anesthetic injected into epidural space spinal level Anesthetic injected into Ipsilateral spinal nerve and sympathetic chain blockade in paravertebral spaces thoracic dermatomes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com Anesthetic considerations: one-lung ventilation Author: Aly Valji Reviewers: Name* * MD at time of publication One lung ventilation: mechanical separation of the lungs to allow for individualized ventilation of only one lung Indication Pulmonary resection, mediastinal, esophageal, vascular, thoracic spine, or cardiac valve surgery Pulmonary hemorrhage, whole lung lavage, bronchopleural fistula, or unilateral infection Exposure of surgical site by deflation of one lung Isolation of one lung from other Dependency on bilateral lung ventilation, Contraindications hemodynamically unstable, severe hypoxia, severe COPD, or severe pulmonary hypertension Intraluminal airway obstruction/mass or known difficult airway Pursue more advanced airway techniques Unable to tolerate one lung ventilation Risk of dislodging mass and inability to secure airway Pre-operative evaluation given likely Pulmonary Forced expiratory volume (FEV1) Determination of underlying pulmonary disease function testing Diffusion capacity (DLCO) fitness for surgery Non- dependent lung not ventilated Hypoxic vasoconstriction decreases but does not stop perfusion of non- dependent lung Vasodilation of dependent lung pulmonary vasculature Right to left intrapulmonary shunt causes V/Q mismatch ↑ Perfusion to dependent, ventilated lung ↑ Elastance of dependent lung ↓ FRC ↑ Hypoxemia Intervention: Increase FiO2 to maintain SpO2 ≥ 90% ↓ V/Q mismatch ↓ Hypoxemia Intervention: Optimize tidal volume, respiratory rate, PEEP ↓ Atelectasis and ↑ FRC Positioning: Lateral decubitus with dependent lung ventilated Altered gravitational forces on thorax ↓ Ventilation-perfusion (V/Q) mismatch General anesthetic with neuromuscular blockade Intraabdominal contents push up on diaphragm ↑ Airway pressure required ↑ Atelectasis ↑ Hypoxemia ↑ Risk of lung barotrauma Intervention: Optimize positive end-expiratory pressure (PEEP) Recruitment of dependent lung ↓ Inspiratory muscle tone ↓ Functional residual capacity (FRC) Post- operative pain management Thoracotomy or VATS causes pain along thoracic dermatomes Epidural Paravertebral block Bilateral spinal nerve blockade below desired Anesthetic injected into epidural space spinal level Anesthetic injected into Ipsilateral spinal nerve and sympathetic chain blockade in paravertebral spaces thoracic dermatomes Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complication/Intervention Published MONTH, DAY, YEAR on www.thecalgaryguide.com

تعریف-بیماری-انسدادی-مزمن-ریھ

تعریف ”بیماری انسدادی مزمن ریھ

MPOC Resultats des radiographies du thorax

MPOC: Résultats des radiographies du thorax