Anaesthesia and COPD
Presenter: D. Sivaramakrishnan
Moderator: Prof. S. Sarat Singh
• Chronic Obstructive Pulmonary Disease (COPD) is generally a
progressive inflammatory disease of the lungs characterised
by airflow limitation that is not fully reversible and mainly
related to smoking.
• The risk factors for development of COPD are
(1) cigarette smoking;
(2) respiratory infection;
(3) occupational exposure to dust, especially in coal
mining, gold mining, and the textile industry; and
(4) genetic factors such as α1-antitrypsin deficiency.
• Combination of inflammatory small airways disease
(obstructive bronchiolitis) and parenchymal destruction
• Small airways disease leads to obstruction and air trapping.
• Loss of lung parenchyma decreases gas transfer reduces the
pulmonary capillary bed and worsens VQ mismatching.
• End result of VQ mismatching, decrease gas transfer and
alveolar hyperventilation is hypoxemia and sometimes
hypercarbia. The hyperinflation causes marked dyspnoea even
without a fall in PO2
• Extra pulmonary – Cor pulmonale, resp and skeletal muscle
wasting and weight loss.
Clinical features of COPD
• Dyspnoea, wheeze and cough with or without sputum
• A diagnosis of COPD should be considered in all patients > 40
yrs. with a significant smoking history (>10 pack years)
• In early stages dyspnoea – associated with exertion.
• Diff. from asthma by lack of nocturnal symptoms ( in early
COPD ), a lack of diurnal variability, a lack of association with
allergy and its persistent and progressive nature.
• Predominant chronic bronchitis – chronic productive cough
• Predominant emphysema – dyspnoea
• Orthopnoea – advanced COPD
• Combination of Chronic Bronchitis and reversible
bronchospasm is referred to as asthmatic bronchitis.
• Pulmonary Function Tests
• Decreases in the FEV1/ forced vital capacity (FVC) ratio and even
greater decreases in (FEF25%-75%)
• Chest radiograph
• Hyperlucency and hyperinflation – emphysema
• If bullae – emphysema is certain
• CT chest useful for diagnosis of emphysema
• Arterial Blood Gases
• Pink Puffers – PaO2 > 60 mmHg and PaCO2 normal
• Blue Bloaters – PaO2 < 60 mmHg and PaCO2 chronically increased to
more than 45 mmHg
• Blue bloaters – pulmonary hyp, secondary erythrocytosis,
rt.ventricular hyp and cor pulmonale
• Pink puffers - PaO2 is minimally depressed, so pulmonary
vasoconstriction is minimal and sec erythrocytosis does not occur
Signs and symptoms of Chronic
Obstructive Pulmonary Disease
Increased lung markings
Normal to slightly
Comparative features of COPD
Mech. of airway obstr.
lumen due to mucus
Loss of elastic recoil
Normal to decreased
• Smoking cessation and chronic oxygen administration
• Ch. Oxygen administration is recommended if the PaO2
is < 55 mmHg, Hct > 55% or evidence of cor pulmonale.
• Goal – achieve PaO2 between 60 and 80 mmHg – nasal
cannula at 2L/min
• Mainstay of treatment is bronchodilation for maintenance and
• Both ß- agonists and anti-cholinergics (ipratropium bromide
and tiotropium bormide) are used.
• Long term inhaled steroids – severe COPD, repeated
exacerbations and co – existent asthma
• Oral steroids – no role in maintenance of COPD
• History and examination:
• Exercise tolerance
• Frequency of exacerbations, hospital admissions
• Smoking history
• Cough and particularly sputum production
• History regarding co-morbid conditions
• Sypmtoms and signs of active infection – green or purulent
sputum, increased dyspnoea, wheeze and signs of consolidation
• CXR – exclude active infection and occult malignancy
• ECG – rt. Heart disease – echo
• Simple exercise tests – stair climbing and the 6 minute walk
test – correlate well with formal exercise testing
• Arterial blood gas measurement
Spirometric classification of the severity of COPD
0: at risk
Chronic symptoms(cough, sputum production)
I: mild COPD
FEV₁≥80% predicted, ± chronic symptoms
II: moderate COPD
50%≤ FEV₁, <80% predicted, ± chronic symptoms
III: severe COPD
30%≤ FEV₁, < 50% predicted, ± chronic symptoms
IV: very severe COPD FEV₁/FVC <70%
FEV₁ < 30% predicted or FEV₁ <50% predicted plus
chronic respiratory failure, i.e., PaO₂ <60 mm Hg
and/ or PCO₂ > 50 mm Hg
• Smoking cessation: – atleast 6-8 weeks before surgery
• Improved ciliary and small airway function and deceased sputum
production occur slowly over a period of time.
• Return of normal immune function requires at least 6 weeks of
abstinence from smoking,
• It likely takes 6 weeks for hepatic enzyme activity to return to
normal following cessation of smoking.
Disadvantage to smoking cessation in immediate post operative
period: increase in sputum production, a fear of inability to
handle stress, nicotine withdrawal symptoms – irritability,
restlessness, sleep disturbances and depression.
• Optimal drug treatment: Almost all patients benefit from at
least one dose of nebulised bronchodilator preopratively.
• Caution – exacerbate tachyarrhythmia's and cause hypokalemia
• Nebulised anticholinergics – can increase sputum viscosity
• Treatment of infection/ exacerbation : current infection and
exacerbations are a contraindication to anaesthesia. Treated
with both ß-agonist and anticholinergic therapy, in nebulised
form and systemic steroids
• Sings of active infection – treated preoperatively with antibiotics
• Oral steroids are not recommended for stable patients
• Physiotherapy: imp to clear any retained sputum.
• Regional Anaesthesia – suitable for operations that do not
invade peritoneum and for Sx on extremeties.
• RA that produce sensory anaesthesia above T6 are not
recommended because such high blocks can impair ventilatory
• General anaesthesia – with volatile anaesthetics- rapidly
eliminated – produce bronchodilation.
• Nitrous oxide – pass into bullae – enlargement or even
rupture – tension pneumothorax. It also limits the inspired
• Opioids are less useful – associated with prolonged ventilatory
• Humidification and use of low gas flows are needed
• Controlled mech. Ventilation
• Large tidal volumes ( 10-15ml/kg) + slow inspiratory flow rates
for complete exhalation to occur – imp if air trapping is to be
minimized. Allow sufficient time for venous return and are less
likely to be associated with undesirable degrees of
hyperventilation. Detrimental effects of PEEP is avoided.
• Bronchospasm may occur – avoidance of endotracheal
intubation if possible. Extubation should be carried out with
the patient awake and sitting up.
• V/Q mismatch increases under GA and in supine position –
• Supplemental oxygen and positive pressure ventilation
• Sputum plugging – may lead to lobar collapse , ventilatory
failure and high airway pressure. Saline nebulisation,
suctioning and physiotherapy
Post operative management
Maintaining adequate lung volumes – FRC and facilitating and
• Lung expansion maneuvers:
Deep breathing exercises,
Positive – pressure breathing techniques
These techniques decrease the risk of atelectasis by increasing
• Post – operative neuraxial analgesia with opioid may permit
early tracheal extubation. It is recommended after high-risk
thoracic, abdominal, and major vascular surgery.
• Mechanical ventilation:
Continued post operative mech ventilation – necessary in patients
with severe COPD – major abdominal or intrathoracic surgery.
• Patients with preoperative FEV1/FVC ratio less than 0.5 or with a
preoperative PaCO2 of more than 50 mmHg are likely to need
some post-operative mechanical ventilation.
• If the PaCO2 has been chronically increased, it is important not to
correct the hypercarbia too quickly.
• Ventilator settings should be adjusted to maintain the PaO2
between 60 and 100 mmHg and the PaCO2 in a range that
maintains the pH at 7.35 to 7.45
• Chest physiotherapy:
A combination of chest physiotherapy and postural drainage plus
deep-breathing exercises decrease the incidence of postoperative
increased risk of developing venous thromboembolism,
so thromboprophylaxis is imp with early mobilisation and