COPD – History/Symptoms/Signs
 History
o Risk factors
 Family history
 Smoking history
 Age at initiation
 Average amount smoked per day since initiation
 Date when stopped smoking or a current smoker
 Environmental history
 The chronologically taken environmental history may
disclose important risk factors for COPD.
 Symptoms
o Dyspnoea
 Ask about the amount of effort required to induce
uncomfortable breathing. Many individuals will deny
symptoms of dyspnea, but will have reduced their activity
levels substantially.
o Cough
 Cough with or without sputum production should be an
indication for spirometric testing. The presence of chronic
cough and sputum has been used to define chronic bronchitis.
o Wheezing
 Wheezing or squeaky noises occurring during breathing
indicate the presence of airflow obstruction.
o Acute chest illnesses
 Inquire about occurrence and frequency of episodes of
increased cough and sputum with wheezing, dyspnea, or fever.
 Physical examination
All physical findings are generally present only with severe disease.
o Chest
 The presence of emphysema (only when severe) is indicated
by: overdistention of the lungs in the stable state (chest held
near full inspiratory position at end of normal expiration, low
diaphragmatic position), decreased intensity of breath and
heart sounds, and prolonged expiratory phase.
 Evidence of airflow obstruction: wheezes during auscultation
on slow or forced breathing and prolongation of forced
expiratory time.
 Frequently observed with severe disease (characteristic, but
not diagnostic): pursed-lip breathing, use of accessory
respiratory muscles, retraction of lower interspaces.
o Other
 Unusual positions to relieve dyspnea at rest.
 Digital clubbing suggests the possibility of lung cancer or
bronchiectasis.
 Mild dependent edema may be seen in the absence of right
heart failure.
 Diagnosis of chronic obstructive pulmonary disease
o Spirometry
 Spirometry is the essential test to confirm the diagnosis and
establish the staging of COPD. If values are abnormal, a postbronchodilator test may be indicated. Reversibility following
bronchodilator would suggest asthma, and, if function reversed
to normal, would exclude COPD.
 The forced vital capacity, or its surrogate the FEV6, is needed
to establish the presence of obstruction.
o Lung volumes
 The inspiratory capacity may acutely decrease with tachypnea
due to dynamic hyperinflation. It is the best physiologic
correlate of dyspnea, but is not usually required to diagnose
COPD. Body plethysmography, which can asses other volumes,
is not necessary except in special instances.
o Carbon monoxide diffusing capacity
 Measurement of carbon monoxide diffusing capacity can help
establish the presence of emphysema, but is not necessary for
the routine diagnosis of COPD.
o Chest radiography
 Only diagnostic of severe emphysema, but always essential to
exclude other lung diseases.
o Arterial blood gases
 Mild (FEV1 >80 percent predicted) and moderate (FEV1 65 to
79 percent predicted) airflow obstruction - not needed.
 Moderately severe (FEV1 50 to 64 percent predicted) airflow
obstruction - arterial blood gas measurement is optional, but
oximetry should be done. Arterial blood gases should be
measured if oxygen saturation is ≥88 percent.
 Severe (FEV1 30 to 49 percent predicted) and very severe
(FEV1 <30 percent predicted) airflow obstruction - arterial
blood gases are essential and, with very severe airflow
obstruction, become the major monitoring tool.
CHRONIC AND 'ACUTE ON CHRONIC' TYPE II RESPIRATORY FAILURE
The most common cause of chronic type II respiratory failure is COPD.


Here CO2 retention may occur on a chronic basis, the acidaemia being
corrected by renal retention of bicarbonate, which results in the plasma
pH remaining within the normal range.
This 'compensated' pattern, which is also seen in some patients with
chronic neuromuscular disease or kyphoscoliosis, is maintained until
there is a further pulmonary insult such as an exacerbation of COPD
which precipitates an episode of 'acute on chronic' respiratory failure.
PROGRESSION OF CHRONIC RESPIRATORY FAILURE

If PaCO2 continues to rise or patient cannot achieve a safe PaO2
without severe hypercapnia and acidaemia,
o respiratory stimulants (e.g. doxapram) or
o mechanical ventilatory support
may be required