Definitions:

 Asthma: It's a chronic respiratory condition that

causes the airways to constrict become inflamed
and collect mucus. It can be triggered by natural
allergens, cigarette smoke, pets, exercise or
emotional stress.
 COPD: is characterized by air flow obstruction.
The airflow obstruction is usually progressive, not
fully reversible and doesn't change markedly over
several months. The disease is predominantly
caused by smoking.
Diagnosis of COPD
 It should be considered in patients over the age of
35 who have a risk factor, generally smoking, and
who present with exertional dyspnoea, chronic
cough, regular sputum production, frequent
winter bronchitis or wheeze. The presence of
airflow obstruction should be confirmed by
performing spirometry.
All health professionals should be competent
in the interpretation of the results
Faktor – faktor resiko
Kebiasaan merokok merupakan satu - satunya penyebab kausal yang terpenting, jauh lebih penting
dari faktor penyebab lainnya.

• a. Riwayat merokok
• - Perokok aktif
• - Perokok pasif
• - Bekas perokok

• b. Derajat berat merokok dengan Indeks Brinkman (IB), yaitu perkalian jumlah rata-rata batang
rokok dihisap sehari dikalikan lama merokok dalam tahun :
- Ringan : 0-200
- Sedang : 200-600
- Berat : >600

• 2. Riwayat terpajan polusi udara di lingkungan dan tempat kerja

• 3. Hipereaktiviti bronkus
• 4. Riwayat infeksi saluran napas bawah berulang
• 5. Defisiensi antitripsin alfa - 1, umumnya jarang terdapat di Indonesia
Pathogenesis
 Three processes:
 Chronic inflammation
 Imbalance of proteinases and anti-proteinases
 Oxidative stress
Chronic Inflammation
 Chronic inflammation in airways, parenchyma,
pulmonary vasculature
 Inflammatory cells involved are:
 Macrophages leukotriene B4
 T-lymphocytes (CD8) interleukin 8
 Neutrophils TNF-α
 Pathology
 Central Airways:
 Enlarged mucus secreting
glands
 Increase in goblet cells

 Mucus hypersecretion
 Peripheral Airways
 Repeated cycles of injury
and repair

 Increased collagen/scarring
in airway wall
Pathology
 Pulmonary vascular changes

 Thickening of vessel wall (intima)

 Increase in smooth muscle

 Infiltration of vessel wall by inflammatory cells

 As COPD worsens, more smooth muscle, proteoglycans
and collagen further thicken the vessel wall
Pathophysiology
Mucus hypersecretion

Ciliary dysfunction

Airflow limitation

Pulmonary hyperinflation

Gas exchange abnormalities

Pulmonary hypertension

Cor pulmonale

 Mucus hyperserection & ciliary dysfunction → cough, sputum production

Diagnosis
• A. Gambaran klinis
a. Anamnesis
• - Keluhan
• - Riwayat penyakit
• - Faktor predisposisi
b. Pemeriksaan fisis

B. Pemeriksaan penunjang
a. Pemeriksaan rutin
b. Pemeriksaan khusus
 Physical Examination
 Thorax:
 Barrel chest
 Lungs
 Decreased breath sounds
 Wheezing
 Cardiac
 Right-sided heart failure
 Edema, tender liver,
distended abdomen

 Physical signs are rarely apparent

until significant impairment of lung
function has occurred
 Diagnostic Tests
 Chest X-ray
 Flattened diaphragms
 Use to exclude other diagnoses
 High resolution CT
 Not routinely recommended
 If in doubt about diagnosis of
COPD
 If considering bullectomy or lung
volume reduction surgery
 CBC
 May see increased
hemoglobin/hematocrit secondary
to hemoconcentration
 ABG
 Spirometry
Spirometry
 Measure of FVC and FEV1
 FVC = forced vital capacity
 Maximum volume of air forcibly exhaled from the point of maximal
inhalation
 FEV1 = forced expiratory volume in 1 second
 Volume of air exhaled in the 1st second of the FVC maneuver
 Calculate the FVC/FEV1 ratio
 Normal ratio = 70/80%
 COPD ratio = <70% pre-bronchodilator FVC & FEV are
 COPD ratio = <80% post-bronchodilator both decreased
 Essential to making the diagnosis of COPD
Spirometry
 Bronchodilator Reversibility Testing
 Perform in the initial assessment of COPD in order to:
 Exclude asthma
 Establish best attainable lung function
 Gauge patient prognosis
 Guide treatment decisions
Arterial Blood Gas (ABG)
 Obtain in patients with FEV1 < 40% predicted OR
 Clinical signs of respiratory or right heart failure
 Central cyanosis, ankle swelling, increase in jugular
venous pressure (JVP) OR
 Respiratory Failure:
 PaO2 < 60 mm Hg with or without PaCO2 > 45 mm Hg
while breathing air at sea level
 Technique:
 Obtain by arterial puncture; DO NOT USE finger or ear
oximeters
Other Tests
 Alpha-1 antitrypsin
 Consider in patients with COPD < age 45
 Strong family hx of early COPD or with alpha-1
antitrypsin deficiency
Differential Diagnosis of COPD
 Asthma
 Reversible airflow limitation
 Early onset (childhood)
 Symptoms vary day to day
 Congestive heart failure
 Volume restriction, NOT airflow
limitation
 CXR with dilated heart, pulmonary
edema
 Bronchiectasis
 Large volumes of purulent sputum
 Commonly associated with bacterial
infection
 Bronchial dilation and bronchial
wall thickening on CXR or CT
 Tuberculosis
 Onset at all ages
 Chest x-ray with infiltrate or nodular
lesions
 Obliterative bronchiolitis
 Younger patients/non-smokers
 May have a hx of rheumatoid
arthritis or fume exposure
 CT shows hypodense areas with
expiration
 Diffuse panbronchiolitis
 Male/non-smokers
 Chronic sinusitis
 CXR and high resolution CT show
diffuse small centrilobular nodular
opacities and hyperinflation
Medications
 Goals
 Prevent and control symptoms
 Reduce frequency and severity of exacerbations
 Improve health status
 Improve exercise tolerance
 No existing medications can modify the long-term decline
in lung function
 Reduction of therapy once symptom control occurs is not
normally possible
 COPD is progressive and over time will require progressive
introduction of more treatments to attempt to limit the
impact of these changes
Bronchodilators
 Central to symptom management
 Used in all stages of COPD severity
 Inhaled forms are preferred
 Can be prescribed as needed OR regularly to prevent or reduce
symptoms
 Long-acting inhaled bronchodilators are more effective and convenient
(but are more expensive)
 Combining drugs with different mechanisms and durations of action
may increase the degree of bronchodilation for equivalent or lesser side
effects
 All categories of bronchodilators have been show to increase exercise
capacity without necessarily producing significant changes in FEV1
Bronchodilators
 Beta2-agonists
 Short-acting: albuterol
 Long-acting: salmeterol (Serevent™), formoterol (Foradil™)
 Anticholinergics
 Short acting: ipratropium bromide (Atrovent™)
 Long acting: tiotropium bromide (Spiriva™)
 Methylxanthines (Theophylline™)
 Combination bronchodilators
 Fenoterol/ipratropium (Duovent™)
 Salbutamol/ipratropium (Combivent™)

GOLD Pocket Guide to COPD Diagnosis, Management, and Preve

Glucocorticosteroids
 Use if FEV1 < 50% predicted and repeated exacerbations, e.g. three in
the last three years
 Severe COPD and Very Severe COPD
 Does not modify the long-term decline in FEV1 BUT does reduce the
frequency of excacerbations and improves health status
 The combination of a long-acting beta2-agonist and an inhaled
glucocorticosteroid is more effective than the individual components
 Long-term treatment with oral glucocorticoids is NOT recommended
 Glucocorticosteroid (inhaled) reversibility testing
 Treatment trial of inhaled glucocorticosteroids for 6 to 12 weeks then repeat
spirometry with and without bronchodilators
 Patients most likely to respond to inhaled steroids have an FEV1 increase of
200 mL and 15% above baseline post-bronchodilator

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Inhaled Glucocorticoids
 Beclomethasone (Vanceril™)
 Budesonide (Pulmicort™)
 Fluticasone (Flovent™)
 Triamcinolone (Azmacort™)

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Immunizations
 Vaccines
 Influenza yearly
 Reduces serious illness and death in COPD patients by
approximately 50%
 Give once yearly: autumn OR twice yearly: autumn and
winter
 Pneumovax
 Sufficient data to support its general use in COPD is lacking,
but it is commonly used
Other Medications?
 Alpha-1 Antitrypsin Augmentation Therapy
 Only if this deficiency is present in an individual should they undergo
treatment
 Antibiotics
 Prophylactic use is NOT recommended
 Can be used in the treatment of infectious exacerbations of COPD
 Mucolytic agents
 Overall benefits are small, so currently not recommended for widespread
use
 Types:
 Ambroxol
 Erdosteine (Erdostin, Mucotec)
 Carbocysteine (Mucodyne)
 Iodinated gylerol (Expigen)

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Other Medications?
 Antioxidant agents
 N-acetylcysteine (Bronkyl, Fluimucil, Mucomyst)
 Have been shown to reduce the frequency of exacerbations and could have a role in
the treatment of patients with recurrent exacerbations
 More studies are needed
 Immunoregulators
 Not recommended at this time
 No reproducible studies are available
 Antitussives
 Regular use is contraindicated in stable COPD since cough has a significant
protective role
 Vasodilators
 Inhaled nitric oxide
 Can worsen gas exchange because of altered hypoxic regulation of ventilation-perfusion
balance and is contraindicated in stable COPD

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention

Other Medications?
 Respiratory stimulants
 Doxapram (IV)
 Almitrine bismesylate
 Not recommended in stable COPD

 Narcotics
 Oral and parenteral opioids are effective for treating dyspnea in patients
with advanced COPD
 Use this with caution; benefits may be limited to a few sensitive subjects
 nebulized opioids: insufficient evidence re: efficacy
 Miscellaenous:
 Nedocromil
 Leukotriene modifiers
 Alternative healing methods
 None have been adequately studied in COPD patients at this time

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention