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