CHRONIC OBSTRUCTIVE PULMONARY DISEASE
DEFINITION
A disease state characterized by progressive airflow limitation that
is
not fully reversible.
It is often accompanied by airway hyper reactivity.
COPD has tremendous impact relating to epidemiology and burden of illness on individual and
nation
ENTITIES INCLUDED UNDER COPD
1. Emphysema,
2. Chronic bronchitis and
3. Small airway disease
Note :
• COPD evolves only if chronic airflow obstruction occurs
• Chronic bronchitis without chronic airflow obstruction is not COPD.
OUTLINE OF PATHOGENESIS
• Chronic bronchitis definition relates to clinical presentation
(long term daily cough or sputum production extending over 3mths for a period of atleast
2yrs.)
• Emphysema centers on pathology of lung itself.
(Characterized by destruction and permanent enlargement of lung alveoli)
This destruction diminishes the elasticity of
lung. leading to collapse of
bronchioles
As a result airflow out of alveoli is obstructed,”trapping air” in the alveoli specially in
expiration which is a passive process .
Because of trapped air more air cannot
be taken up during next inspiration
So exchange of gases in alveoli gets
impaired
Trapped air also compresses adjacent normal lung tissue impairing lung function further.
Gas
exchange takes place across the thin alveolar wall.
When alveolar wall destructed number of capillaries available
for
gas exchange get reduced.
Also on account of collapse of lung and loss of elastic recoil during expiration,
Work of
breathing increases
In summary
In Emphysema
Irreversible dilatation of alveoli+
Destructive changes in alveolar wall+
Bullae development
Loss of elastic recoil
Gas exchange across alveolar wall impaired with Co2 retension
Work of breathing increased.
In chronic bronchitis
Mucous glands of tracheobronchial tree become thick and so narrow the bronchial lumen.
Incidence
Chronic bronchitis accounts for majority of COPD cases
In lesser percentage emphysema
Still less often both are combined In chronic bronchitis
there is inflammation of
lining of airways
Inflammation stimulates production of sputum further obstructing the airway. This predisposes to bacterial lung infection
RISK FACTORS
Most critical
risk factor –SMOKING
Second hand smoke
Air pollution in work place/enviroment
Genetic factors- α1 antitrypsin
deficiency (in this COPD worsens rapidly)
Predisposition to respiratory infection in childhood
In older population- mucus hyper secretion,
respiratory infection
Concomitant cardio vascular conditions-
Ventricular /atrial
arrhythmias
SMOKING AND COPD
Smoking is responsible for COPD in (90%)
Smokers with COPD have higher death rate than non smokers with COPD. In them deterioration is more rapid than in non smokers
On quitting the habit,decline in lung function slows .
Pathology of chronic bronchitis and emphasema
CLASSIFICATION OF COPD ACCORDING TO SEVERITY
According to pulmonary functions based on FEV1
Staging of COPD by GOLD
(GOLD- Global initiative for chronic obstructive lung disease)
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| Classification of COPD as per GOLD |
Mechanism of
Lung
damage
Smoke an irritant attracts inflammatory cells
These release enzyme elastase which breaks down elastic fibers in the lung.
TYPICAL SYMPTOMS
Symptoms develop after significant lung damage has occurred.
I. Dyspnea on exertion initially ,at
rest later
Mostly irreversible
Develops many years after patient starts smoking(age 50-60) Reason:-Lung function start declining slowly with age
Normally at age 30 begin to lose lung function at the rate of 25-30mL/yr of
FEV1
Smokers lose at more rapid rate.Because lungs have considerable amount of reserve, large portion
must become non functional before symptoms occur. It takes
around 30 yrsor more
(If a person quits smoking lose of function slows to the rate of non smokers Quality of life can improve in quitters even if lung function has already declined.)
II. Productive Cough
Increased sputum production
( Due to inflammation and excessive mucus production)
III. Wheezing
Chronic wheeze or mainly during exacerbations
These symptoms occur chronically over years
And slowly worsen over time.
Other symptoms
Hemoptysis,weight loss,pedal edema
PHYSICAL SIGNS
Barrel shape chest
Low
diaphragm
Accessory muscles of respiration at work in severe cases
Diminished breath sounds
Rhonchi
Plus
Diminished FEV1
Increased Paco2
Marked hypoxemia(polycythemia and cyanosis) Signs of Rt heart failure in advanced cases
Posture in
COPD
Patient sits leaning forward with arms supported on a surface in front or on knees
This stabilizes upper chest and shoulder thus allowing accessory muscles to work efficiently.
Pursed lip
breathing
Because air flow out of lung is limited expiration takes longer.
Also since alveoli lose their elasticity patient tries to shorten the time of exhalation by forcefully exhaling. But forced exhalation increases pressure on lungs and causes structurally weakened airways to collapse. To prevent airways from closing during forced exhalation pursed lip
breathing is used. Lips are narrowed together which slows exhalation at mouth.This keeps
positive pressure in the airways, thus preventing their collapse allowing some forced exhalation.
DIAGNOSIS
Thorough medical history
Current or past smokers age >40yr with dyspnea,
productive cough,
wheeze. Physical exams showing barrel chest,rhonchi, diminished breath sounds Signs of rt
sided heart failure
Signs of infections of lung,pneumonia
Along with investigations
COPD is diagnosis of history in Ch.bronchitis,
Diagnosis of anatomy in emphysema
COMPLICATIONS
Pulmonary hypertension
Rt heart failure called cor pulmonale
Hemoptysis causes1.damage to blood vessels 2.Lung cancer
INVESTIATIONS
1.Pulmonary function tests
2.Oximetry
3.Radiological procedures
4.Arterial blood gas analysis
5.Alpha 1 antitrypsin level
Four components of Pulmonary function test
1.Spirometry
2.Post broncho dilator spirometry
3.Lung volumes
4.Diffusion capacity
5.
Xray chest
(in Severe cases of emphysema) Hyper translucent lung
Flattened diaphragm
Decreased lung markings indicating destruction of
lung
tissue.
May also show bullae and area of destroyed lung tissue that show
large air sacs
Xray chest in Chronic Bronchitis
Increased lung markings indicating thickened .inflammed and scarred airways
Xray chest is an imprecise method of diagnosis of COPD It ia abnormal only in severe cases
CT scan lung is more sensitive (not always needed) CT
shows 1.extent of emphysema 2.Early lung cancer
In addition pneumonia can be diagnosed by xray chest. CT
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EMPHYSEMA vs CHRONIC BRONCHITIS
PREVENTION
Inspite of
lot of risk factors COPD is largely preventable since main cause is smoking
Nature of
treatment
Treatment is palliative and not curative
Longevity cannot be improved much except in cases with hypoxia who benefit fro supplemental
oxygen
KEY COMPONENTS OF COPD TREATMENT
I.Medical treatment
2.Behavioural treatment
3.Surgical treatment
4.Other treatment
Medical
1.Point of critical importance is cessation of
smoking
For withdrawal symptoms:-
Anti depressant Buproprion is used alone or in combination with
Nicotine replacement therapy
Nicotine patches,inhalers,nasal sprays
Broncho dilator Antibiotics Mucolytics Supplemental oxygen
In the end stage-Mechanical ventilator
Medications List
• Fast acting broncho dilator Beta2 agonists e.g.albuterol
• Anticholenergic (ipratropium/oxitropium)-block
the broncho constrictor effect of acetyl
Choline on muscarinic receptors
• Theophyllin derivatives
views on exact effect are controversial.
• Long acting broncho dilators
• Inhaled or oral cortico steroids
• Above
4 are most effective as inhalers( except theophyllin)
• There are several delivery methods of inhaled medications
o Metered dose inhaler
o Breath actuated inhalers
o Dry powdered inhaler
o Nebulisers
• β2 agonists
Relax
the
smooth muscles,clear the mucus ,enhance the endurance of resp.muscles
Short acting used only when needed Long acting used for daily requirement
Both may be combined
• Anticholinergics
Iptra tropium
Has greater broncho dilatory effect than β2 agonists
Used if patients have symptoms daily.
• Theophylline
Action-Broncho dilator and anti inflammatory
Use contravertial
Has narrow therapeutic range (use decided on case by case basis)
Specially effective in relieving nocturnal symptoms
Numerous drug interaction raise this drugs level causing arrhythmias and seizures
• Cortico steroids
o Treat inflamed airways;long term benefit not known
o In some patient reduce the number of exacerbations
o Oral corticosteroids
- are used when dose requirement is higher than it can be delivered by inhalation
o In acute exacerbations –oral or inhaled steroid used
o It is difficult to wean patients off ,so patients are often left
on inhaled steroids
o COPD case when put on c.steroids for more than 1yr or more run risk of pneumonia
Mucolytics
Guaifenesin, potassium iodide N-acetylcysteine are likely to benefit
Guaifenesin, potassium iodide taken orally
N acetyl cysteine –as nebulizer
These are tried on case by case basis
N acetyl cysteine- can cause bronchospasm
Antibiotics
Antibiotics at the first sign of respiratory infection
Used in acute exacerbations with purulent sputum
In patients who develop frequent exacerbations in a year
with
purulent sputum
Placed on a schedule of prophylactic treatment with antibiotics for first 10 days of each
month.This is done for special cases only.
Leukotriene inhibitors
Not all are approved by FDA
yet
Behavioral/rehabilitation therapy
Smoking cessation
Exercise programme,
Disease
management training,
Nutritional and psychological counseling
Oxygen to treat COPD
Oxygen is the only agent which increases survival
Indication
ArterialPaO2 <50mm of Hg or O2 saturation falls to 88%
Corpulmonale +o2 saturation of 88%
Polycythemia
If does not
fall under above category O2 used only during exercise and sleep.
Nasal cannula is most useful device
O2 source-portable or non portable
OTHER THERAPIES
Exercise to strengthen the muscles Drugs for associated conditions
Diuretics
To be used with caution are -Pain killers,cough suppresants and sedatives
Chronic systemic steroids –
risk of serious side effects ;reserved for acute exacerbations only.
Further management
Avoiding
Cigrettes,dust,airpollusion,smoke,work related fumes,contact with patients with respiratory
infections,excessive heat,cold or high altitudes
Maintaining
Healthy diet, exercise programme, regular monitoring with spirometer tests
Additional treatment options
Regular immunization for flu,pneumococcal pneumonia
Pulmonary rehabilitation to improve exercise tolerance
Supplemental oxygen in late stages (nocturnal non invasive Ventilation)
Surgery-
• Bullectomy
• Lung volume reduction surgery (currently experimental)
• Lung transplant
For Alpha 1 anti
tripsin deficiency –AAT replacement –life long and gene
therapy.
End stage disease
Mechanical ventilation for short term or long term
Some may become ventilator dependant until death.
Patients consent is important
Emerging treatment
Reactive oxidant species Proteases
Neutrophil chemotactics, Monoclonal antibodies; Retinoids
POINT OF IMPORTANCE TO PRACTIONER COPD EXACERBATION
Exacerbation is worsening of previous stable situation,
Acute in onset
Necessitating change in regular medication
Is of important to practitioner
Worsening dyspnea,
Increase in sputum volume and purulence
Causes of
COPD exacerbation:
Respiratory
viruses
Bacteria
Pollutants
Temperature
Signs of Severe exacerbation:
Severe dyspnea impairing speech
Confusion and impaired sensorium
(requires immediate hospitalization) Paradoxical chest wall movement Worsening central cyanosis
Rt heart failure Hemodynamic instability
Coma,
Cardiac arrhythmias
Fever-suspect pneumonia
Frequency of
exacerbations
Once a year in moderate and severe cases
Lab test to
assess severe exacerbation
Spirometry (but at times under estimates severity)
Assess arteria O2 saturation Sao2
CXR to detect pneumonia,pneumothorax,pleral effusion, CCF
Risks of dying from exacerbation is related to
1.Respiratory acidosis
2.Significant comorbidities
3.Need for ventilator support
4. Arrhythmias
Low dose macrolide erythromycin reduces exacerbations
Severity of exacerbation is graded as mild,moderate and severe.
Assessing severity of
COPD is important from management point of
view
History taking in acute exacerbation
Take h/o risk factors exposure
Time of onset
Severity of presenting exacerbation and previous attacks
Medication use
Comorbidities
Prior hospitalization History of respiratory failure
Recognising changes in signs and symptoms of
COPD Exacerbation
Knowing when symptoms are changing is helpful to begin treatment and interventions
Early treatment is effective
Severe symptoms –begin appropriate treatment promptly. Decide if home therapy/tmt in clinic or in ICU is to be given
Change or increase in severity of symptoms could be warning sign
Increase in amount or thickness of sputum.purulent sputum blood in sputum
Increase in severity of symptom-dyspnea,wheeze,cough
Symptoms like-pedal edema,insomnia,altered sensorium, morning headaches,dizziness,
Advise the patient not do the following on his own
Not to take extra dose of
theophyllin,codein,OTC nasal spray for more than 3days,
Not increase rate of prescribed oxygen flow,notto smoke,
Diet
Should have nutritious food with adequate calories to meet increased work of breathing
Limit salt
intake,caffeinated drinks, avoid food which can cause bloating
If patient is on cannula .continue same during eating –and after meals
-eating and digestion requires energy.
DIFFERENTIAL DIAGNOSIS FOR COPD EXACERBATION
Bronchial Asthma
CCF
Small pulmonary embolism
Hyperventilation syndrome
Numerous upper airway obstruction
(laryngeal spasm,Foreign body aspiration,,SVC obstruction)
Management of
COPD
in Elderly
Changes occur in lung function in normal elderly non smokers
If these are compounded with effects of smoking morbidity /mortality rises
COPD is very common in elderly
DD of COPD and asthma in elderly is more difficult than in younger age group.
Compared to middle aged, elderly are more likely to have COPD and cardiovascular disease
Both of these are associated with cigarette smoking and symptoms like Asthma
Objective pulmonary function tests are very useful in these situations
LUNG FUNCTIONS AND AGEING
LUNG FUNCTIONS EFFECTS OF AGEING
Airway reactivity
increased
Chest wall compliance Less
compliant (stiffer) Diffusing capacity (oxygen uptake ) Lower
FRC AND RV
Increased
Vital capacity
Lower
Total lung capacity Stable
Lung tissue compliance Inceased(loss of lung recoil)
Maximal expiratory flows LowerFEV1,FEV1/FVC,FEF75%
PO2 and spo2 Lower as a result of V/Q mismatch( but in PCO2)
Respiratory muscle strength Lower
Respiratory drive Reduced
ANTIBIOTICS FOR ACUTE EXACERBATIONS
Treatment includes antibiotics
50% acute exacerbation due to bacteria
Streptococcus pneumonia,hemophilis influenza,Moraxella catarrhalis
Numerous effectively treat these infections
MEDICATIONS TO TREAT ACUTE EXACERBATION
Corticosteroids- IV if hospitalized
Increase broncho dilator dosage
Theophillyne may be used.
OXYGEN THERAPY
Supplemental O2 is required in acute exacerbation
MECHANICAL VENTILATION
Indicated in Respiratory failure
Non invasive ventilation
Used in conscious cooperative patient
Advantage
Mask can be periodically removed
Secretions getting into lungs can be prevented
Most patients can be successfully weaned Small percentage not so.
No way to predict this out come
Invasive ventilation
For patients unconscious or heavily sedated
Decision as to go for ventilation is to be made by patient
Another decision whether to discontinue ventilator or be allowed to die is to be made by patient
COPD AND CHRONIC VENTILATION
A small percentage of
people may be unable to be weaned from ventilator.going for chronic ventilation.If after 2weeks if still
dependent on ventilator a tracheostomy is to be performed
which gives more stable
airway,facilitates movement of patient and oral care.
With tracheostomy they can be maintained on ventilator indefinitely.
In
one study average survival rate was found to be 7 months
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