Published on March 1, 2014
Anaesthesia and COPD Presenter: D. Sivaramakrishnan Moderator: 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 Disease Feature 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 COPD Feature Chronic bronchitis Pulmonary emphysema Mech. 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 spirometry Chronic 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. Thromboprophylaxis increased risk of developing venous thromboembolism, so thromboprophylaxis is imp with early mobilisation and adequate hydration.
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