Copd 2012

Department of Pulmonary Medicine

Chronic Obstructive Pulmonary Disease

(COPD)

Dr. Rahul Magazine

M.D. (Medicine); D.T.C.D.

Dept. of Pulmonary Medicine





DEFINITION

COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.


Chronic bronchitis has been defined as the presence of chronic productive cough for 3 months during each of two successive years in a patient in whom other causes of chronic cough have been excluded.

Emphysema is defined as a condition of the lung characterized by abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis.


EPIDEMIOLOGY

• COPD ranked sixth as the cause of death in 1990, but will become the third leading cause of death worldwide by 2020.

• The prevalence of COPD is appreciably higher in smokers and ex-smokers than in nonsmokers, in those over 40 years than those under 40, and in men than in women.


RISK FACTORS Exposure to particles Tobacco smoke Indoor air pollution from heating and cooking with biomass in poorly vented dwellings (among women in developing countries) Occupational dusts (organic and inorganic) Outdoor air pollution Genes (α1 anti-trypsin deficiency) Airway hyperresponsiveness Lung Growth and Development Oxidative stress Gender Age Respiratory infections Socioeconomic status


PATHOLOGY

• Large Airway Mucous gland enlargement and goblet cell

hyperplasia. • Small Airways Airway wall thickening Peribronchial fibrosis Luminal inflammatory exudate Airway narrowing (obstructive

bronchiolitis)


• Lung parenchyma Alveolar wall destruction Apoptosis of epithelial and endothelial cells• Pulmonary vasculature Thickening of intima Endothelial cell dysfunction,

INFLAMMATORY CELLS: Macrophages, T lymphocytes, few neutrophils or eosinophils


PATHOPHYSIOLOGY Peripheral airway obstruction

Air trapping during expiration

Hyperinflation

Functional Residual Capacity increased

PATHOPHYSIOLOGY

• Gas Exchange Abnormalities

• Mucus Hypersecretion

• Pulmonary Hypertension



PATHOGENESIS

The inflammation in the respiratory tract of COPD patients appears to be an amplification of the normal inflammatory response of the respiratory tract to chronic irritants such as cigarette smoke


Smoking

Lung Inflammation

Oxidative Stress

COPD Pathology

Proteinases


CLINICAL FEATURESSymptoms Breathlessness Progressive (worsens over time) Usually worse with exercise Persistent (present every day) Chronic cough, which is often, but not

invariably, productive. Wheeze


History of exposures to risk factors:

A smoking history of at least 20 pack

years is usual before symptoms develop

Smoke from home cooking and heating

fuels

Occupational dusts and chemicals Family history of COPD Weight loss and anorexia are features of severe

COPD Sleep quality is impaired in advanced COPD Hemoptysis


Clinical signs

General examination

• Tachypnoea,

• Prolonged forced expiratory time (more than 5 s)

• Adopting pursed lipped breathing on expiration which reduces expiratory airway collapse.


• Use of the accessory muscles of respiration• Adopt the position of leaning forward, supporting

themselves with their arms to fix the shoulder girdle

• Tar-stained fingers• Cyanosis in advanced disease • Flapping tremor• Weight loss• Finger clubbing is not a feature of COPD


Examination of Chest

Inspection and Palpation• Signs of overinflation: barrel-shaped with a

kyphosis and an apparent increased anterior/posterior diameter, horizontal ribs, prominence of the sternal angle, and a wide subcostal angle. Distance between the suprasternal notch and the cricoid cartilage (normally three finger-breadths) may be reduced.

• Pursed lip breathing, use of accessory muscles • An inspiratory tracheal tug • Hoover's sign


• Indrawing of the suprasternal and supraclavicular fossas and of the intercostal muscles

Percussion• Hyper resonant note• Decreased hepatic and cardiac dullness

Ausculatation• Breath sounds may have a prolonged expiratory

phase, or may be uniformly diminished• Wheeze• Crackles may be heard particularly at the lung bases


Cardiovascular Examination• Difficulty in localizing the apex beat• Signs of pulmonary artery hypertension• Signs of right heart failure

SYSTEMIC FEATURES: Skeletal muscle wasting Osteoporosis Anxiety and Depression Increased risk of cardiovascular disease, respiratory infections diabetes, lung cancer

Type A: Pink Puffer (Emphysema Predominant)

• Major complaint is dyspnea,

• Cough is rare, with scant clear, mucoid sputum.

• Patients are thin, with recent weight loss common.

• They appear uncomfortable, with evident use of accessory muscles of respiration.

• Chest is very quiet without adventitious sounds.

• No peripheral edema.


Type B: Blue Bloater (Bronchitis Predominant)

• Major complaint is chronic cough, productive of mucopurulent sputum

• Dyspnea usually mild, though patients may note limitations to exercise.

• Patients frequently overweight and cyanotic but seem comfortable at rest.

• Peripheral edema is common.

• Chest is noisy, with rhonchi invariably present



MANAGEMENT

Assessment

• COPD Assessment Test (CAT): An 8-item measure of health status impairment in COPD

• Breathlessness Measurement using the Modified British Medical Research Council (mMRC) Questionnairewell to other measures of health status and predicts future mortality risk.



INVESTIGATIONS

Hematocrit

Polycythemia can develop in the presence

of arterial hypoxemia, especially in continuing smokers, and can be identified by hematocrit > 55%.


• Spirometry: The presence of a postbronchodilator

FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus COPD

Spirometry: Normal Trace Showing FEV1 and FVC

1 2 3 4 5 6

1

2

3

4

Volu

me,

liters

Time, sec

FVC5

1

FEV1 = 4L

FVC = 5L

FEV1/FVC = 0.8

Spirometry: Obstructive Disease

Volu

me,

liters

Time, seconds

5

4

3

2

1

1 2 3 4 5 6

FEV1 = 1.8L

FVC = 3.2L

FEV1/FVC = 0.56

Normal

Obstructive

Christine Jenkins

Sue i have inserted a bracket and shifted the obstructive label. The FVC in this slide is about 3.4 by eyeball - shoudl be moved down to 3.2 or the numbers should be changed


Classification of Severity of Airflow Limitation in COPD

(Based on Post-Bronchodilator FEV1) In patients withFEV1/FVC < 0.70 GOLD I: Mild; FEV1 ≥ 80% predicted GOLD II: Moderate; 50% ≤ FEV1 < 80% predicted GOLD III: Severe; 30% ≤ FEV1 < 50% predicted GOLD IV: Very Severe; FEV1 < 30% predicted


• Imaging

Chest X-ray Signs of hyperinflation (flattened diaphragm and an increase in the volume of the retrosternal air space), hyperlucency of the lungs, and rapid tapering of the vascular markings.

Computed tomography (CT)


• Arterial blood gas measurement

• Exercise testing• Alpha-1 antitrypsin deficiency

screening (when COPD develops under 45 years or with a strong family history of COPD.)

• Other investigations, including electrocardiography, echocardiography, radionucleotide scintigraphy, and magnetic resonance imaging.


TREATMENT 1. Smoking Cessation• Counseling• Pharmacotherapy Nicotine replacement products (nicotine gum,

inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge)

Other pharmacotherapy:The antidepressants bupropion and nortriptyline. Varenicline, a nicotinic acetylcholine receptor partial agonist that aids smoking cessation by relieving nicotine withdrawal symptoms and reducing the rewarding properties of nicotine


Drugs Used in COPD

β2-agonists Short-acting

(Salbutamol, Terbutaline)

Long-acting

(Formoterol, Salmeterol)


Drugs Used in COPD

Anticholinergics

Short-acting

Ipratropium bromide

Oxitropium bromide Long-acting Tiotropium

Drugs Used in COPD

Combination short-acting β 2-agonists plus anticholinergic in one inhaler

Salbutamol/Ipratropium

Methylxanthines Aminophylline Theophylline (SR)



Drugs Used in COPD

Inhaled glucocorticosteroids Beclomethasone, Budesonide, Fluticasone, Triamcinolone

Combination long-acting β 2-agonists plus glucocorticosteroids in one inhaler

Formoterol/Budesonide Salmeterol/Fluticasone

Drugs Used in COPD

Phospodiesterase-4 inhibitor: Roflumilast

Systemic glucocorticosteroids Prednisone, Methyl-prednisolone



OTHER PHARMACOLOGIC TREATMENTS

• Alpha-1 antitrypsin augmentation therapy.

• Vaccines:

Influenza vaccine (reduces serious illness and

death)

Pneumococcal vaccine (reduces incidence of

CAP)


• Mucolytic agents (ambroxol, carbocysteine, iodinated glycerol)

Patients with viscous sputum may benefit

from mucolytics; overall benefits are very

small. • Antibioticsefits are very small• Antioxidant agents• Immunoregulators• Antitussives




Oxygen Therapy Can be administered in three ways: longterm

continuous therapy, during exercise, and to relieve acute dyspnea.

The primary goal of oxygen therapy is to increase the baseline PaO2 to at least 8.0 kPa (60 mm Hg) at sea level and rest, and/or produce an SaO2 at least 90%, which will preserve vital organ function by ensuring adequate delivery of oxygen.


The long-term administration of oxygen(> 15 h/d) to patients with chronic respiratory failure has been shown to increase survival.

Long-term oxygen therapy is generally introduced in patients with COPD, who have PaO2 at or below 55 mm Hg or SaO2 at or below 88%, with or without hypercapnia

OTHER TREATMENTS

• Non invasive ventilation with LTOT in

a some selected patients may improve

survival

• Rehabilitation



Surgical Treatments

Bullectomy

Lung volume reduction surgery

Lung transplantation

Only three interventions influence the natural history of patients with COPD.

1.Smoking cessation

2.Oxygen therapy in chronically hypoxemic patients

3.Lung volume reduction surgery in selected patients with emphysema.There is currently suggestive, but not definitive, evidence that the use of inhaled glucocorticoids may alter mortality rate.



Patient

Characteristic Spirometric Classification

Exacerbations per year

mMRC CAT

ALow Risk

Less SymptomsGOLD 1-2 ≤ 1 0-1 < 10

BLow Risk

More SymptomsGOLD 1-2 ≤ 1 > 2 ≥ 10

CHigh Risk

Less SymptomsGOLD 3-4 > 2 0-1 < 10

DHigh Risk

More SymptomsGOLD 3-4 > 2 > 2

≥ 10

Combined Assessment

Management of Stable COPD


Managing Stable COPD



MANAGE EXACERBATIONS

An exacerbation of COPD is defined as an event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.


The most common causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree. .

Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis are the most common bacterial pathogens involved in COPD exacerbations.


Inhaled bronchodilators (particularly inhaled Β 2-agonists with or without anticholinergics) and oral glucocorticosteroids are effective treatments for exacerbations of COPD.

Antibiotics if clinical signs of airway infection (e.g., increased sputum, purulence)


Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality.

Medications and education to help prevent future exacerbations should be considered as part of follow-up


OXYGEN THERAPY


INTRODUCTION

Oxygen is the substrate that cells use in the greatest quantity and upon which aerobic metabolism and cell integrity depend. Since the tissues have no storage system for oxygen, a continuous supply at a rate that matches changing metabolic requirements is necessary to maintain aerobic metabolism and normal cellular function.


PRINCIPLES

In general, maintain SaO2 >90%, though preferably >95%.


Devices For Providing Oxygen

• Oxygen supply (cylinder or wall unit)

• Nasal cannula

• Face mask

• Venturi mask


NASAL CANNULA• The nasal cannula is a low-flow oxygen administration

system designed to add oxygen to room air when the patient inspires.

• A nasal cannula provides up to 44% oxygen.• The ultimate inspired oxygen concentration is

determined by the oxygen flow rate through the cannula and how deeply the patient breathes (tidal volume).


• Increasing the oxygen flow by 1 L/min (starting with 1 L/min) will increase the inspired oxygen concentration by approximately 4%:

— 1 L/min: 21% to 24% — 2 L/min: 25% to 28% — 3 L/min: 29% to 32% — 4 L/min: 33% to 36% — 5 L/min: 37% to 40% — 6 L/min: 41% to 44%



FACE MASK

• A simple face mask delivers low oxygen flow to the patient’s nose and mouth. A partial rebreathing mask consists of a face mask with an attached reservoir bag


• A face mask can supply up to 60% oxygen with flow rates of 6 to 10 L/min. A face mask with oxygen reservoir nonrebreathing mask) provides up to 90% to 100% oxygen with flow rates of 9 to 15 L/min. In this system a constant flow of oxygen enters an attached reservoir.


Use a face mask with a reservoir for patients who Are seriously ill, responsive, and have adequate

ventilation but require high oxygen concentrations



VENTURI MASK• A Venturi mask enables a more reliable and

controlled delivery of oxygen concentrations from 24% to 50%. Use the Venturi mask for patients who retain carbon dioxide (CO2). Patients who have chronic high levels of CO2 in their blood and moderate-to-severe hypoxemia may develop respiratory depression if the drive stimulating them to breathe (oxygen) is reduced.


• Delivered oxygen concentrations can be adjusted to 24%, 28%, 35%, and 40% using a flow rate of 4-8 L/min and 40% to 50% using a flow rate of 10-12 L/min.


MONITORING

Adequacy and changes in arterial oxygen saturation can be continuously monitored by pulse oximetry and intermittent or continuous invasive blood gas analysis.


REFERENCES

• Harrison's Principles of Internal Medicine, 18th Edition

• GOLD. 2011 (revised) • Murray & Nadel's Textbook of Respiratory

Medicine, 4th ed. • CMDT 2010


THANK YOU




Health & Medicine

Copd 2012