Copd 2012 pdf

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 FEATURES Symptoms

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, lit

ers

Time, sec

FVC 5

1

FEV1 = 4L

FVC = 5L

FEV1/FVC = 0.8

Spirometry: Obstructive Disease Volu

me, lit

ers

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


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)

OTHER PHARMACOLOGIC

TREATMENTS

• 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



OTHER PHARMACOLOGIC

TREATMENTS

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.



Patien

t

Characteristic Spirometric

Classification

Exacerbation

s per year

mMRC CAT

A Low Risk

Less Symptoms GOLD 1-2 ≤ 1 0-1 < 10

B Low Risk

More Symptoms GOLD 1-2 ≤ 1 > 2 ≥ 10

C High Risk

Less Symptoms GOLD 3-4 > 2 0-1 < 10

D High Risk

More Symptoms GOLD 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




Copd 2012 pdf

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