This document discusses chronic obstructive pulmonary disease (COPD). It defines COPD as a progressive lung disease characterized by airflow limitation that is not fully reversible. The main phenotypes of COPD are chronic bronchitis and emphysema. The document discusses the pathogenesis and risk factors of COPD, as well as the clinical presentation and complications. It provides details on diagnosing COPD through pulmonary function tests, blood tests, imaging and other evaluations. Treatment options are outlined for acute exacerbations and management of stable COPD based on disease severity. Management includes bronchodilators, corticosteroids, pulmonary rehabilitation, oxygen therapy and occasionally surgery.

1. Jongsiriyunyong K. EP rj

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

4.  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

5. 1 1 2
5 4
3
8
6 7
9 10
Venn diagram of chronic obstructive pulmonary disease (COPD).

6. Histopathology of chronic bronchitis showing hyperplasia of mucous glands
and infiltration of the airway wall with inflammatory cells

7. Gross pathology of advanced emphysema. Large bullae are present on the
surface of the lung.

8. At high magnification, loss of alveolar walls and dilatation of airspaces in
emphysema can be seen.

9. This phenomenon is called
dynamic hyperinflation
Pathophysiological

10.  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

11.  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

12.  For assess an individual’s risk of death or
hospitalization
 History
 Multifactorial with
 Individual lifestyle
 Socioeconomic factors
 Education / Knowledge

13. 4-year survival
 0-2 points = 80%
 3-4 points = 67%
 5-6 points = 57%
 7-10 points = 18%

16.  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

17.  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

18.  Hyperinflation (barrel chest)
 Wheezing – Frequently heard on forced and
unforced expiration
 Diffusely decreased breath sounds
 Hyperresonance on percussion
 Prolonged expiration phase

19.  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

20.  Alpha1-Antitrypsin def
 Bronchitis
 Emphysema
 Nicotine Addiction
 Pulmonary Embolism

21.  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

22.  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

23. COPD: Hyperinflation, depressed diaphragm, increased retrosternal space,
and hypovascularity of lung parenchyma are demonstrated.

24. Emphysema : increased AP diameter, increased retrosternal airspace, and
flattened diaphragm on lateral chest radiograph.

25. A lung with emphysema shows increased anteroposterior (AP) diameter,
increased retrosternal airspace, and flattened diaphragm on posteroanterior
chest radiograph

26. A computed tomography (CT) scan shows hyperlucency due to diffuse
hypovascularity and bullae formation, predominantly in the upper lobes.

27. Severe bullous disease as seen on a computed tomography (CT) scan in a
patient with chronic obstructive pulmonary disease (COPD).

28.  Acute exacerbation
 Stable COPD
 Rx base on severity of disease

29. 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

30.  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

31. treatment

32. 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

33. 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

34. 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
Formoterol
Anticholinergic Short 10-15 6-8 Inhale Ipratopium bromide
Long 5 >24 Inhale Tiotropium (Spiriva®)
Methylxanthine Uncertained in sustained release Oral Theophylline
IV Aminophylline

35. 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

36. 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

37. 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

38. 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

39. treatment

40. 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

41. Stable COPD : at ALL stage
 Avoidance of risk factor(s)
 Influenza vaccination
 Pneumococcal vaccination

42. Stable COPD : Mild COPD
 Short-acting bronchodilator when needed

43. Stable COPD : Moderate COPD
 Short-acting bronchodilator when needed
 Regular treatment with one or more long-acting
bronchodilators
 Rehabilitation

44. 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

45. Combination Dose(ug/dy) Trade name
Fluticasone/Salmeterol 500/100-1000/100 Seretide®
Budesonide / Formeterol 320/9-640/18 Symbicort®

46. 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
Formoterol
Anticholinergic Short 10-15 6-8 Inhale Ipratopium bromide
Long 5 >24 Inhale Tiotropium (Spiriva®)
Methylxanthine Uncertained in sustained release Oral Theophylline
IV Aminophylline

47. 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

50.  3
 Short-term therapy
 Long-term continuous therapy
 During exercise
 PaO2 60 mmHg
SaO2 90%
O2

51.  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

52.  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

53. Oxygen therapy via nasal cannula Home supplemental oxygen

54. Bilevel positive airway pressure (BiPAP)

55.  Hemodynamic stable
 Bronchodilator supply less than every 4 hr
 SpO2 >90% w/o O2 supplement at least 24 hr