Anaesthesia in copd Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics Ph D physiology. Mahatma gandhi medical college and research institute, puducherry, India
Definition GOLD • Global Initiative for Chronic Obstructive Lung Disease • as a disease state characterized by airflow limitation that is not fully reversible
Definitions • COPD includes emphysema, an anatomically defined condition characterized by destruction and enlargement of the lung alveoli; • chronic bronchitis, a clinically defined condition with chronic cough and phlegm; and small airways disease, a condition in which small bronchioles are narrowed.
COPD is present only if chronic airflow obstruction occurs; chronic bronchitis without chronic airflow obstruction is not included within COPD. • Dutch hypothesis • British hypothesis
HOW MUCH IT IS?? Factors • 4 – 10 % • Cigarette smoking • Age • 20 pack years + age more than 60 • Repeated respiratory infections • general exposure to dust at work • Less fruits and antioxidants in diet • Genetic (alpha 1 antitrypsin deficiency) • Low birth weight
Leads on to • Pulmonary hypertension • Pulmonary thrombosis may develop sec. to airway inflammation. • Skeletal muscle changes – myopathy, defective muscle protein synthesis • Weight loss • Osteopenia – excess osteoclastic activity • CAD and increased CRP ,fibrinogen • COPD is a systemic inflammatory illness
Chronic bronchitis Emphysema Loss – elastic recoil Severe FEV 1 decrease Moderate less better • Decreased airway lumen • Dyspnea moderate • FEV 1 decrease • PaO2 severe • Dif. Capa. N • Corpulmonale more • Prog. bad
Treatment options • Smoking cessation • Bronchodilators – theo and beta 2 agonists • Steroids – oral and inhaled • Inhaled – tiotropium • PDE 4 inhibitors – noflumilast • Cromolyn ,Mucokinetics ,retinoids • Antibiotics ,rehabilitation , home oxygen • Alpha 1 antitrysin • Vaccines
Differences between asthma and COPD • Age < 30 • Atopy yes • Reversibility – yes • Chest wheezy • Cough – nonproductive , episodic • Nocturnal – yes • Smoking – no • Steroids yes • BAL - eosinophil • Age > 50 • Atopy no • Irreversible • Chest silent • Cough productive • No nocturnal • Smoking yes • Steroids – poor response • BAL – neutrophil
Anaesthesia • Optimize preop • Bounding pulse and hand flap – hypercarbia • History – smoking , CCF, cough , dyspnea exercise tolerance • Diuretics, digoxin, heparin • Other routine history • Premed = humidified oxygen
Clinical examination • RS • Breath sounds • Added sounds • Steth in trachea • Breathing pattern • Cylindrical chest • P2 in CVS • Dynamic hyperinflation • Specific --- Don’t miss others
CxR usually may not help • Radiographic abnormalities may be minimal, • Hyperlucencydue to arterial vascular deficiency in the lung periphery and hyperinflation (flattening of the diaphragm with loss of its normal domed appearance and a very vertical cardiac silhouette) suggest the diagnosis of emphysema. • If bullae are present, the diagnosis of emphysema is certain.
Preop care • smoking cessation, • 12 hours – CO and tachycardia • 6-8 weeks all benefits • treatment of bronchospasm, • eradication of bacterial infection.
Preop • ECG ,Urinalysis ,CBC • Electrolytes • Drugs • Cardiac evaluation • Preop PFT ??? • Major thoraco abdominal surgeries , lung resections • Preop PFT should not be used to make patients unfit.
Bad indicators • Dyspnea at rest • Cyanosis ( PaO2 less than 60 ) • PaCO2 more than 45 • Persistent heavy smoking • Poor response to broncho dilators and steroids • Pulmonary hypertension • PFT FEV1 < 50 % and FEV1/FVC < 70%
Cardiac Effects of Smoking • 1. Smoking is a risk factor for development of cardiovascular disease • 2. Carbon monoxide decreases oxygen delivery and increases myocardial work • 3. Smoking releases catecholamines and causes coronary vasoconstriction • 4. Smoking decreases exercise capacity
Respiratory Effects of Smoking • 1. Smoking is the major risk factor for development of chronic pulmonary disease • 2. Smoking decreases mucociliaryactivity • 3. Smoking results in hyper reactive airways • 4. Smoking decreases pulmonary immune function • Other Organ System Effects 1. Smoking impairs wound healing
Other preop measures • Inhaled and systemic steroids • Antibiotics • Antisialogogues ??, ranitidine ? • Narcotics, sedatives < beware • Droperidol and diphenhydramine are safe • Lung expansion education- deep breathing or CPAP
Anaesthetic technique • Lower limb / lower abdominal surgeries – spinal - • Sedatives - aware of side effects . • Brachial plexus blocks – satisfactory • High spinals are associated with desaturation • Neuraxial opioids – post op pain relief • Nasogastric drainage – useful in selected cases • IV morphine - no
Regional • Spinal epidural below thoracic – no effect on respiratory function except in obese 20 % reduction in FEV1 • TEA – 10 % decrease in inspiratory capacity • but no effect on bronchial smooth muscle, HPV ventilatory response to hypoxia and hypercarbia • It also confers cardio protection
General • Propofol induction • Thio – may increase bronchospasm • Etomidate is not all useful • IV – not spray of lignocaine • If active wheezing, ketamine is an induction agent of choice • Sure - it is noncardiac acute wheezing
Relaxants • Vecuronium • Rocuronium • Cisatracurium • Atra , doxa, pancuronium – no • DTC – worst • Neostigmine – danger of wheezing • Residual neuro muscular block – predictor of PPC
Agents • Halo – yes – no airway irritation • But – sensitivity to catecholamines • Sevo and des – ok • Iso better but think of airway spasm • Nitrous – increase bulla size – CT bulla – beware
LMA or tube • Introduction of LMA proseal • airway manipulation is less – but active wheezing patients – may not be ideal • Tube is replaced by LMA proseal in COPD ?? • (Nasogastric tube) • ET has definite indications
Clinical tips in GA • Humidification of inspired gas • PCV with decelerating flow • High tidal volumes with less rate. • Adequate depth • Head lift and open eyes may not be of use • To add TEA or paravertebral block
Intraop wheezing • Kinked ET tube • Pulmonary edema • Wheezing • secretions thick • Pneumo – bulla rupture • Endobronchial • Treatment • Check, deepen, relaxants, salb, steroids, FiO2
GA in COPD • Diaphragmatic function is well preserved during anesthesia in patients with COPD due to ‘length adaptation’ phenomenon and they experience little decrement in gas exchange. • Therefore general anesthesia with controlled ventilation need not be considered an evil that has to be avoided at all costs. However, one should pay attention to the pattern of ventilation in these patients.
Recruitment maneuvers • consisting of sustained (8 to 15 seconds) application of high airway pressures (30 to 40 cm H2O), • followed by positive end-expiratory pressure [PEEP] and limited inspired oxygen concentration, may minimize dependent lung atelectasis and improve intraoperative oxygenation
IV fluids • Hemodynamic goal directed • Liberal • Restricted
Post op • Institute lung volume expansion maneuvers (voluntary deep breathing, incentive spirometry, continuous positive airway pressure) Maximize analgesia (neuraxial opioids, intercostal nerve blocks, patient-controlled analgesia) No NSAIDs
PPCs • atelectasis or pneumonia and death • PPCs have been reported to occur in 5%-10% and • in 4%-22% of patients undergoing abdominal surgery • In COPD patients [with FEV1 ≤ 1.2 L and FEV1/FVC < 75%] undergoing non-cardiothoracic surgery, an incidence of 37% [excluding atelectasis] and a 2-year mortality rate of 47%
PPCs • death, pneumonia, prolonged intubation, refractory bronchospasm, and prolonged intensive care unit (ICU) stay. • ASA physical status ≥ IV, FEV1 < 1 Liter were significant preoperative risk factors and emergency operation, abdominal incision, anesthesia duration • [> 3h] and general anesthesia, were the intraoperative risk factors.
Permissive hypercapnia and hypoxemia • Pao2 of around 60 • PaCO2 of 45
Post op • Care for prevention and cure of PPCs • Analgesia by blocks, paracetomol, opioids • IV fluids tuned to that patient. • Early ambulation • Neuraxial opioids
Continued mechanical ventilation in the postoperative period may be necessary in patients with severe COPD who have undergone major abdominal or intrathoracic surgery. • Patients with preoperative FEV1/FVC ratios less than 0.5 or with a preoperative PaCO2 of more than 50 mm Hg are likely. • If the PaCO2 has been chronically increased, it is important not to correct the hypercarbia too quickly • Lead on arrythmias or seizures may result
Post op • A combination of chest physiotherapy and postural drainage plus deep-breathing exercises taught during the preoperative period may decrease the incidence of postoperative pulmonary complications. • vibrationsproduced on the chest wall by physiotherapy result in dislodgment of mucus plugs from peripheral airways. Appropriate positioning facilitates elimination of loosened mucus
Summary • Definition of COPD • Types • Clinical features – systemic • Treatment • Preop – smoking, infections, B’dilations, other systems • Intraop – FiO2, nitrous, SEVO, tube/LMA, rocu, vec. neo/sugammadex • PPCs – avoid and treat PPC, use blocks, neuraxial opioids
In anaesthesia • Minimal invasion • Or • maximal support