Anaesthesia and COPDPresenter: D. SivaramakrishnanModerator: Prof. S. Sarat Singh

Introduction• 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.

Pathophysiology • Combination of inflammatory small airways disease

(obstructive bronchiolitis) and parenchymal destruction (emphysema).

• 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

production.

• 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 DiseaseFeature Chronic Bronchitis Emphysema

Cough Frequent With exertion

Sputum Copious Scant

Hematocrit Elevated Normal

PaCO2 Often elevated(>40) Usually normal(<40)

Cheast radiograph Increased lung markings Hyperinflation

Elastic recoil Normal Decreased

Airway resistance Increased Normal to slightly increased

Cor pulmonale Early Late

Comparative features of COPDFeature Chronic bronchitis Pulmonary

emphysemaMech. of airway obstr. Decreased airway

lumen due to mucus and inflammation

Loss of elastic recoil

Dyspnea Moderate Severe

FEV₁ Decreased Decreased

PaO₂ Marked decreased‘blue bloater’

Modest decrease‘pink puffer’

PaCO₂ Increased Normal to decreased

Diffusing capacity Normal Decreased Hematocrit Increased Normal Cor pulmonale Marked Mild Prognosis Poor Good

Treatment• 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 for exacerbations.

• 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

Management of anaesthesia

Pre-operative management• 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

Investigations

• CXR – exclude active infection and occult malignancy

• ECG – rt. Heart disease – echo

• Spirometry

• 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

Stage Characteristics

0: at risk Normal spirometryChronic symptoms(cough, sputum production)

I: mild COPD FEV₁/FVC <70%FEV₁≥80% predicted, ± chronic symptoms

II: moderate COPD FEV₁/FVC <70%50%≤ FEV₁, <80% predicted, ± chronic symptoms

III: severe COPD FEV₁/FVC <70%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

Preoperative optimisation• 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.

Intraoperative management• 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 functions.

• 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 oxygen concentration

• Opioids are less useful – associated with prolonged ventilatory depression

• 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 – reduces FRC.

• 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 effective cough• Lung expansion maneuvers: • Deep breathing exercises,• Incentive spirometry,• Chest physiotherapy,• Positive – pressure breathing techniques

These techniques decrease the risk of atelectasis by increasing lung volumes• 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 pulmonary complications.

Thromboprophylaxisincreased risk of developing venous thromboembolism,

so thromboprophylaxis is imp with early mobilisation and adequate hydration.

Thank You