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)
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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