Jongsiriyunyong K. EP rj
 Progressive        and Non fully reversible airflow    limitation   COPD is a disorder in which subsets have dominant  ...
   The Global Initiative for Chronic Obstructive    Lung Disease (GOLD) guidelines define COPD as a    disease state char...
1          1           2                       5                4         3                       8              6        ...
Histopathology of chronic bronchitis showing hyperplasia of mucous glandsand infiltration of the airway wall with inflamma...
Gross pathology of advanced emphysema. Large bullae are present on thesurface of the lung.
At high magnification, loss of alveolar walls and dilatation of airspaces inemphysema can be seen.
This phenomenon is called                      dynamic hyperinflationPathophysiological
   Cigarette smoking- 90%   Environmental factors     Biomass fuels with indoor cooking and heating     Traffic-relate...
   Immunodeficiency syndromes       Independent risk   Vasculitis syndrome       Hypocomplementemic vasculitis urticar...
   For assess an individual’s risk of death or    hospitalization   History   Multifactorial with       Individual lif...
4-year survival     0-2 points = 80%     3-4 points = 67%     5-6 points = 57%     7-10 points = 18%
   Typically combination of signs and symptoms of    chronic bronchitis, emphysema, and reactive    airway disease.   Co...
   Hx of more than 40 pack-yrs of smoking was the    best single predictor of airflow obstruction   If all 3 signs are a...
   Hyperinflation (barrel chest)   Wheezing – Frequently heard on forced and    unforced expiration   Diffusely decreas...
   obese                             thin with a barrel chest   Frequent cough and                little or no cough  ...
 Alpha1-Antitrypsin     def Bronchitis Emphysema Nicotine   Addiction Pulmonary    Embolism
   Pulmonary Function Tests       For diagnosis       Assessment of severity       Following its progress   ABG     ...
   CBC       Secondary polycythemia           Hct>52% in men or 47% in women   Alpha1-Antitrypsin       all patients ...
COPD: Hyperinflation, depressed diaphragm, increased retrosternal space,and hypovascularity of lung parenchyma are demonst...
Emphysema : increased AP diameter, increased retrosternal airspace, andflattened diaphragm on lateral chest radiograph.
A lung with emphysema shows increased anteroposterior (AP) diameter,increased retrosternal airspace, and flattened diaphra...
A computed tomography (CT) scan shows hyperlucency due to diffusehypovascularity and bullae formation, predominantly in th...
Severe bullous disease as seen on a computed tomography (CT) scan in apatient with chronic obstructive pulmonary disease (...
 Acute    exacerbation Stable   COPD    Rx base on severity of disease
Acute exacerbation Severity         evaluate    Mild to moderate             Hemodynamic stable                      ...
 Indication     for admit    Severe exarcerbation    Severe stage of COPD    New onset of : cyanosis, peripheral edema...
treatment
Acute exacerbation : 1-3 wk onset   Bronchodilator       Beta2-agonist       Anticholinergic       Methylxantine   Co...
Acute exacerbation : 1-3 wk onset   Short acting Beta2-agonist is first line but    recommended combine of SABA and    An...
Medication       type      Onset (min)     duration   Route            drug                                             (h...
Acute exacerbation : 1-3 wk onset Systemic         corticosteroid     Limited systemic inflammation and airway      infl...
Acute exacerbation : 1-3 wk onset   Oxygen       All pt with SpO2 < 90% keep SpO2 90-94%   Limited S/E of Oxygen supple...
Acute exacerbation : 1-3 wk onset   Machanical ventilation       Indication of NIPPV                            accesso...
Acute exacerbation : 1-3 wk onset Machanical  ventilation   Indication of Invasive mechanical    ventilation       Resp...
treatment
Stable COPD : base on severity   Bronchodilator       Beta2-agonist       Anticholinergic       Methylxantine   Corti...
Stable COPD : at ALL stage Avoidance   of risk factor(s) Influenza   vaccination Pneumococcal     vaccination
Stable COPD : Mild COPD   Short-acting bronchodilator when needed
Stable COPD : Moderate COPD   Short-acting bronchodilator when needed   Regular treatment with one or more long-acting  ...
Stable COPD : Severe COPD   Short-acting bronchodilator when needed   Regular treatment with one or more long-acting    ...
Combination            Dose(ug/dy)      Trade nameFluticasone/Salmeterol    500/100-1000/100   Seretide®Budesonide / Forme...
Medication       type      Onset (min)     duration   Route            drug                                             (h...
Stable COPD : Very severe COPD   Short-acting bronchodilator when needed   Regular treatment with one or more long-actin...
       3       Short-term therapy       Long-term continuous therapy       During exercise                     PaO2  ...
 Indication   for STOT     Recent Exacerbation with new hypoxemia Re-evaluate     at wk 4     Continue STOT if still h...
 Continue       Oxygen supplement > 15 hr/dy        mortality         exercise tolerance     Quality of life: psychoth...
Oxygen therapy via nasal cannula   Home supplemental oxygen
Bilevel positive airway pressure (BiPAP)
 Hemodynamic    stable Bronchodilator   supply less than every 4 hr SpO2   >90% w/o O2 supplement at least 24 hr
COPD review
COPD review
COPD review
COPD review
COPD review
COPD review
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  • This nonproportionalVenn diagram shows subsets of patients withchronic bronchitis, emphysema, and asthma (black circles). The subsetsdefined as COPD are shaded gray. Subset areas are not proportional toactual relative subset sizes. Asthma is, by definition, associated withreversible airflow obstruction; in variant asthma, special maneuvers maybe necessary to make the obstruction evident. Patients with asthmawhose airflow obstruction is completely reversible (subset 9) are notconsidered to have COPD. In many cases it is virtually impossible todifferentiate patients with asthma whose airflow obstruction does notremit completely from persons with chronic bronchitis and emphysemawho have partially reversible airflow obstruction with airwayhyperreactivity. Thus, patients with unremitting asthma are classified as
  • Figure 1. Pathophysiological Features of Airflow Obstruction in Chronic Obstructive Pulmonary Disease (COPD).Airflow obstruction in COPD is largely due to emphysema, characterized by disruption of the alveolar walls, along withinflammation of lung tissue, fibrosis, and mucus plugging in the distal airways (Panel A, normal distal airway surroundedby intact alveolar walls; Panel B, abnormal distal airway surrounded by disrupted alveolar walls). Alveolarattachments provide a radial tethering effect that is essential for keeping small airways patent in the normal lung.Airways narrow at smaller lung volumes because of decreased lung elasticity and weaker tethering effects. Consequently,maximal expiratory airflow decreases as the lung empties and ceases at 25 to 35% of total lung capacity.The remaining air is termed the residual volume. In patients with COPD who have emphysema, the disruption of alveolarattachments, coupled with distal airway disease, causes a substantial decrease in maximal expiratory airflow(Panel A, normal flow; Panel B, reduced flow). Residual volume may account for as much as 60 to 70% of predictedtotal lung capacity. Patients with COPD must breathe at larger lung volumes to optimize expiratory airflow, but thisrequires greater respiratory work because the lungs and chest wall become stiffer at larger volumes. These effects areaccentuated with exercise. A normal respiratory system meets the increased ventilatory demands of exercise by increasingboth tidal volume and respiratory rate, with little change in the final end-expiratory lung volume. In patientswith COPD, the respiratory rate does increase in response to exercise, but with insufficient expiratory time, breathsbecome increasingly shallow and end-expiratory lung volume progressively enlarges (Panel A, normal response to exercise;Panel B, response with COPD). This phenomenon is called dynamic hyperinflation and is thought to be animportant factor in the reduction of exercise capacity and the development of dyspnea.
  • Six-Minute Walking DistanceThe distance walked in 6 minutes (6MWD) is a good predictor of all-cause and respiratory mortality in patients with moderate COPD.[37, 38]Patients with COPD who desaturate during the 6MWD have a higher mortality rate than do those who do not desaturate.Consequently, this test is used as a part of the BODE index (body mass index, obstruction [FEV1], dyspnea [modified Medical Research Council dyspnea scale], and exercise capacity [6MWD]),[26] which was designed to help predict mortality in COPD patients.
  • Bronchodilatorช่วยให้อาการดีขึ้น แม้ FEV1ไม่ได้เพิ่มขึ้น ซึ่งส่วนหนึ่งมาจากหลอดลมที่ขยายตัวแม้ไม่มาก แต่ช่วยให้อากศที่ค้างอยู่ในปอดออกมาได้มากขึ้น(ลด synamic hyperinflation ทั้งในขณะพักและออกกำลัง) ทำให้คุณภาพชีวิตดีขึ้นยาขยายหลอดลมมี 3 กลุ่มคือB2agonist, anticholinergicและmethylxanthineหลักการให้ยาขยายดดยทั่วไป ในรายที่มีอาการเหนื่อยเพียงเล็กน้อยและนานๆครั้ง ควรเริ่มด้วยยาขยายหลอดลมออกฤทธิ์สั้นชนิดสูดเฉพาะเวลามีอาการ(short acting B2agonist, anticholinergic ) ห้างมีอาการเหนื่อยอาจใช้ นถ้ายักมีอาการเหนื่อยตลอดเวลา หลังจากประเมินแล้วว่าเกิดจาก COPD ไม่ใช่จากโรคร่วม อาจเพิ่มยาเช่น ให้สูดยาขยายหลอดลมชนิดออกฤทธ์สั้นวันละ 4 ครั้ง หลังจากนั้นหากยังมีอาการเหนื่อยอาจใช้ theophyllineขนาดต่ำ (ระดับยาในเลือด 5 mg/l) เช่น theophylline sustained-release 100 mg bid มี่ฤทธิ์ต้านการอักเสบช่วยลดการเกิดอาการกำเริบลงได้ หลังจากนี้ถ้ายังมีอาการอาจเพิ่มยาขยายหลอดลม long acting anticholinergicหรือ B2agonist ชนิดสูด ซึ่งยากลุ่มนี้มีประสิทธิภาพดีและสะดวกในการใช้มากกว่ายาที่ออกฤทธิ์สั้น แต่ยังมีราคาแพง สำหรับ LABA ในไทยไม่มียาเดี่ยวแต่อยู่ในรูปผสมกับ corticosteriodการใช้ยาขยายหลอดลมสองชนิดที่มีกลไกและระยะเวลาการออกฤทธิ์ต่างกัน อาจช่วยเสริมฤทธิ์ขยายหลอดลมหรือลดผลข้างเคียง เช่น ยาผสมระหว่าง SABA/anticholinergicทำให้ค่า FEV1 เพิ่มขึ้นมากกว่าและนานกว่าการใช้ยาเดี่ยวการบริหารยาควรใช้วิธีสูด โดยเลือก MDI (metered-dose inhaler) หรือ DPI (dry-powder inhaler) เป็นอันดับแรก เนื่องจากผลข้างเคียงน้อยกว่ายารับประทาน แต่ถ้าผู้ป่วยไม่สามารถใช้ยาแบบสูดได้ถูกวิธีหลังจากสอนหลายคร้งแล้ว อาจอนุโลมให้ใช้ยารับประทานได้ ในคนแก่อาจมีปัญหาในการใช้ MDI ให้ถูกวิธี ดังนั้นควรต้องสอนและตรวจสอบทุกครั้งที่ผู้ป่วยมารับการรักษา บางรายอาจต้องใช้ spacer ร่วมด้วย หรืออาจต้องเปลี่ยนเป็นใช้ยาสูดรูปแบบอื่นเช่น DPI ซึ่งใช้ง่ายกว่าแต่ข้อเสียคือต้องใช้แรงสูดมากซึ่งมีปัญหาในคนแก่ที่ไม่มีแรงพอ สำหรับ nebulizer ไม่แนะนำให้ใช้ใน stable COPD เนื่องจากแพงและต้องดูแลทำความสะอาด แต่อาจใช้ในกรณีผู้ป่วยไม่สามารถสูด MDI or DPI ได้อย่างมีประสิทธิภาพสิ่งสำคัญในการรักษาคือติดตามการตอบสนองต่อการรักษา พิจารณาปรับยาให้เหมาะสมกับผู้ป่วยแต่ละราย ผลข้างเคียงของยา ขึ้นกับปริมาณยาที่ใช้ ควรระวังโรคร่วมอื่นซึ่งอาจทำให้ผลข้างเคียงของยาเพิ่มขึ้น โดย S/E B2agonist : มือสั่น ใจสั่น ชีพจรเร็ว , anticholinergic : ปากแห้ง , theophylline : arrhythmia ชัก ปวดหัว นอนไม่หลับ N/V
  • goals of the program are to:Decrease and gain control of respiratory symptoms and complicationsImprove physical conditioning and exercise toleranceImprove general health and emotional well-beingEncourage self-management of symptoms and control of activities of daily livingReduce hospitalizations and improve quality of life
  • Transcript of "COPD review"

    1. 1. Jongsiriyunyong K. EP rj
    2. 2.  Progressive and Non fully reversible airflow limitation COPD is a disorder in which subsets have dominant features of  chronic bronchitis  chronic productive cough for 3 months during each of 2 consecutive years  emphysema, or asthma  permanent enlargement of the air spaces distal to the terminal bronchioles, without obvious fibrosis
    3. 3.  The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines define COPD as a disease state characterized by  Airflow limitation that is not fully reversible, is usually progressive, and  Associated with an abnormal inflammatory response of the lungs to inhaled noxious particles or gases
    4. 4. 1 1 2 5 4 3 8 6 7 9 10Venn diagram of chronic obstructive pulmonary disease (COPD).
    5. 5. Histopathology of chronic bronchitis showing hyperplasia of mucous glandsand infiltration of the airway wall with inflammatory cells
    6. 6. Gross pathology of advanced emphysema. Large bullae are present on thesurface of the lung.
    7. 7. At high magnification, loss of alveolar walls and dilatation of airspaces inemphysema can be seen.
    8. 8. This phenomenon is called dynamic hyperinflationPathophysiological
    9. 9.  Cigarette smoking- 90% Environmental factors  Biomass fuels with indoor cooking and heating  Traffic-related air pollution Airway hyperresponsiveness Alpha1-antitrypsin deficiency  Panacinar emphysema  Premature emphysema at an average age of 53 years for nonsmokers and 40 years for smokers Intravenous drug use  Pulmonary vascular damage  Insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate  Cocaine or heroin
    10. 10.  Immunodeficiency syndromes  Independent risk Vasculitis syndrome  Hypocomplementemic vasculitis urticaria syndrome (HVUS) Connective tissue disorders  Cutis laxa is a disorder of elastin , various forms of inheritance  Marfan syndrome is an autosomal dominant inherited disease of type I collagen  Ehlers-Danlos syndrome Salla disease  Autosomal recessive storage disorder , sialic acid
    11. 11.  For assess an individual’s risk of death or hospitalization History Multifactorial with  Individual lifestyle  Socioeconomic factors  Education / Knowledge
    12. 12. 4-year survival  0-2 points = 80%  3-4 points = 67%  5-6 points = 57%  7-10 points = 18%
    13. 13.  Typically combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease. Cough  Systemic manifestations worsening dyspnea  decreased fat-free mass progressive exercise  impaired systemic muscle intolerance function  Osteoporosis sputum production  Anemia alteration in mental status  Depression Productive cough or acute  pulmonary hypertension chest illness  cor pulmonale Breathlessness  left-sided heart failure Wheezing
    14. 14.  Hx of more than 40 pack-yrs of smoking was the best single predictor of airflow obstruction If all 3 signs are absent, airflow obstruction can be nearly ruled out  Self-reported smoking Hx of > 55 pack-yrs  Wheezing on auscultation  Self-reported wheezing
    15. 15.  Hyperinflation (barrel chest) Wheezing – Frequently heard on forced and unforced expiration Diffusely decreased breath sounds Hyperresonance on percussion Prolonged expiration phase
    16. 16.  obese  thin with a barrel chest Frequent cough and  little or no cough expectoration  Breathing may be assisted Use of accessory muscles by pursed lips of respiration is common  patients may adopt the Coarse rhonchi and tripod sitting position wheezing may be heard on  hyperresonant, and auscultation wheezing may be heard signs of right heart failure  Distant Heart sounds  Cor pulmonale  edema and cyanosis Chronic bronchitis Emphysema
    17. 17.  Alpha1-Antitrypsin def Bronchitis Emphysema Nicotine Addiction Pulmonary Embolism
    18. 18.  Pulmonary Function Tests  For diagnosis  Assessment of severity  Following its progress ABG  Hypoxemia / hypercapnia  Acidosis Serum Chemistries  Retain sodium /Lower potassium levels /bicarbonate  Chronic respiratory acidosis leads to compensatory metabolic alkalosis
    19. 19.  CBC  Secondary polycythemia  Hct>52% in men or 47% in women Alpha1-Antitrypsin  all patients < 40 yrs or Fm Hx of emphysema at early age Sputum Evaluation  Streptococcus pneumoniae  Haemophilus influenzae  Moraxella catarrhalis  Pseudomonas aeruginosa Chest Radiography +/- CT scan
    20. 20. COPD: Hyperinflation, depressed diaphragm, increased retrosternal space,and hypovascularity of lung parenchyma are demonstrated.
    21. 21. Emphysema : increased AP diameter, increased retrosternal airspace, andflattened diaphragm on lateral chest radiograph.
    22. 22. A lung with emphysema shows increased anteroposterior (AP) diameter,increased retrosternal airspace, and flattened diaphragm on posteroanteriorchest radiograph
    23. 23. A computed tomography (CT) scan shows hyperlucency due to diffusehypovascularity and bullae formation, predominantly in the upper lobes.
    24. 24. Severe bullous disease as seen on a computed tomography (CT) scan in apatient with chronic obstructive pulmonary disease (COPD).
    25. 25.  Acute exacerbation Stable COPD  Rx base on severity of disease
    26. 26. Acute exacerbation Severity evaluate  Mild to moderate   Hemodynamic stable  bronchodilator  Pred 30-40 mg/dy for 7dy  Moderate to severe  Risk for respiratory failure  AOC  Accessory muscle used: paradoxical chest/abd motion  SpO2 < 90% or PaO2 < 60 mmHg  PaCO2 > 45 mmHg or pH < 7.35
    27. 27.  Indication for admit  Severe exarcerbation  Severe stage of COPD  New onset of : cyanosis, peripheral edema  Unimprove after appropriated Tx  Multi-Comorbit : CAD, DM, HT  New onset Arrhythmia  Undefinite Diagnosis  Old age or Homeless
    28. 28. treatment
    29. 29. Acute exacerbation : 1-3 wk onset Bronchodilator  Beta2-agonist  Anticholinergic  Methylxantine Corticosteroid  Systemic corticosteroids Oxygen  All pt with SpO2 < 90% keep SpO2 90-94% Antibiotic  Cover Streptococcus pneumoniae, Hemophilus influenza, Morexella catarrhalis, Klebsiella pneumoniae ; Pseudomonas aeruginosa Machanical ventilation  Non-invasive positive pressure ventilation: NIPPV  Invasive mechanical ventilation
    30. 30. Acute exacerbation : 1-3 wk onset Short acting Beta2-agonist is first line but recommended combine of SABA and Anticholinergic for limited S/E (palpitation, tachycardia, tremor)  Fenoterol/Ipratropium bromide  Every 15-20 min in 1st hour then 4-6 hr interval  Addition SABA every 1-2 hr
    31. 31. Medication type Onset (min) duration Route drug (hour) Beta2agonist Short 3-5 4-6 Inhale Salbutamol(ventolin®) Oral Terbutaline IV Fenoterol 8-12 Inhale Procaterol Oral Long 30-45 > 12 Inhale Salmeterol FormoterolAnticholinergic Short 10-15 6-8 Inhale Ipratopium bromide Long 5 >24 Inhale Tiotropium (Spiriva®)Methylxanthine Uncertained in sustained release Oral Theophylline IV Aminophylline
    32. 32. Acute exacerbation : 1-3 wk onset Systemic corticosteroid  Limited systemic inflammation and airway inflammation  Decrease sputum eosinophil  Decrease serum CRP  Improve FEV1 and PaO2  Minimize treatment failure / Length of stay in Hospital/ Exacerbation  No improve of mortality  Prednisoline 30-40 mg/dy for 7-14 dy or  Dexamethasone 5- 10 mg q 6 hr or  Hydrocortisone 100-200 mg q 6 hr
    33. 33. Acute exacerbation : 1-3 wk onset Oxygen  All pt with SpO2 < 90% keep SpO2 90-94% Limited S/E of Oxygen supplement  hypoxic drive hypoventilation  ventilation / perfusion mismatch deadspace  Haldane effect  rightward displacement of the CO2-hemoglobin dissociation curve in the presence of increased oxygen saturation, increasing the amount of CO2 dissolved in blood
    34. 34. Acute exacerbation : 1-3 wk onset Machanical ventilation  Indication of NIPPV  accessory muscle with abd paradox  Acidosis pH 7.25-7.35 and/or PaCO2 > 45 mmHg  RR > 24 / min  C/I of NIPPV  Uncooperation    Cardiovascular instability  Life-threatening hypoxemia  Severe acidosis : pH < 7.25
    35. 35. Acute exacerbation : 1-3 wk onset Machanical ventilation  Indication of Invasive mechanical ventilation  Respiratory failure  Severe acidosis : pH < 7.25  RR > 35/min  Accessory muscle used  with  C/I for NIPPV  Fail NIPPV
    36. 36. treatment
    37. 37. Stable COPD : base on severity Bronchodilator  Beta2-agonist  Anticholinergic  Methylxantine Corticosteroid  inhaled corticosteroids Vaccination  Annual influenza vaccine  Pneumococcal vaccination Pulmonary rehabilitation  Improve quality of life Oxygen therapy  Short term  Long term sugery
    38. 38. Stable COPD : at ALL stage Avoidance of risk factor(s) Influenza vaccination Pneumococcal vaccination
    39. 39. Stable COPD : Mild COPD Short-acting bronchodilator when needed
    40. 40. Stable COPD : Moderate COPD Short-acting bronchodilator when needed Regular treatment with one or more long-acting bronchodilators Rehabilitation
    41. 41. Stable COPD : Severe COPD Short-acting bronchodilator when needed Regular treatment with one or more long-acting bronchodilators Rehabilitation Inhaled glucocorticoids if significant symptoms, lung function response, or if repeated exacerbations
    42. 42. Combination Dose(ug/dy) Trade nameFluticasone/Salmeterol 500/100-1000/100 Seretide®Budesonide / Formeterol 320/9-640/18 Symbicort®
    43. 43. Medication type Onset (min) duration Route drug (hour) Beta2agonist Short 3-5 4-6 Inhale Salbutamol(ventolin®) Oral Terbutaline IV Fenoterol 8-12 Inhale Procaterol Oral Long 30-45 > 12 Inhale Salmeterol FormoterolAnticholinergic Short 10-15 6-8 Inhale Ipratopium bromide Long 5 >24 Inhale Tiotropium (Spiriva®)Methylxanthine Uncertained in sustained release Oral Theophylline IV Aminophylline
    44. 44. Stable COPD : Very severe COPD Short-acting bronchodilator when needed Regular treatment with one or more long-acting bronchodilators Inhaled glucocorticoids if significant symptoms, lung function response, or if repeated exacerbations Treatment of complications : CHF, infection, nutrition Rehabilitation Long-term oxygen therapy if chronic respiratory failure Consider surgical treatment
    45. 45.  3  Short-term therapy  Long-term continuous therapy  During exercise PaO2 60 mmHg SaO2 90% O2
    46. 46.  Indication for STOT  Recent Exacerbation with new hypoxemia Re-evaluate at wk 4  Continue STOT if still hypoxemia Re-evaluate at Mo 3  Treat as LTOT
    47. 47.  Continue Oxygen supplement > 15 hr/dy  mortality  exercise tolerance  Quality of life: psychotherypy  Prevent pulmonary HT Ind for LTOT  PaO2 < 55 mmHg or SaO2 < 88%  PaO2 < 56-59 mmHg or SaO2 < 89% with sign of chronic hypoxemia  Pul HT  Peripheral edema CHF  Polycythemia (Hct > 55%)  Failed STOT
    48. 48. Oxygen therapy via nasal cannula Home supplemental oxygen
    49. 49. Bilevel positive airway pressure (BiPAP)
    50. 50.  Hemodynamic stable Bronchodilator supply less than every 4 hr SpO2 >90% w/o O2 supplement at least 24 hr
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