It is generally believed that COPD increases the risk of postoperative pulmonary complications. There are few or no data estimating the surgical risk in the asthmatic patient. Ideally, medical management is maximized prior to surgery. The patient should be free of wheezes and active infection. In one study, a forced vital capacity in 1 s (FEV.|) of less than 65 per cent of the predicted value and a forced vital capacity of less than 70 per cent of the predicted value resulted in a 100 per cent complication rate. However, there are also studies where patients with severe air-flow obstruction did not suffer any pulmonary complications. Other than in pulmonary resection, there is no level of pulmonary function that is an absolute contraindication to surgery. The preoperative test with the most utility in predicting postoperative complications is a reduced arterial PO2. In the case of a pulmonary resection, an FEVi below 800 ml contraindicates surgery.
COPD and asthma pose special ventilatory problems in the perioperative setting. Air-flow obstruction, inflammation, and increased secretions during acute episodes cause severe hypoxemia and hypercapnia as a result of ventilation-perfusion mismatch, atelectasis, increased work of breathing, and dysfunctional respiratory mechanics. Therapy is directed at correcting hypoxemia, reversing air-flow obstruction, treating infection, reducing inflammation, and in some instances providing ventilatory support. This is accomplished with chest physiotherapy, antibiotics, bronchodilators, corticosteroids, and both invasive and non-invasive mechanical ventilation.
Symptomatic COPD patients should be treated aggressively in the perioperative setting with antibiotics, bronchodilators, and corticosteroids. Bronchodilators and corticosteroids will decrease airway resistance. The reversibility of the air-flow obstruction will be variable, but every small advantage helps. Bronchodilators available include b-agonists, anticholinergics, and theophylline preparations. The b-agonists and the anticholinergics demonstrate greater bronchodilator action than theophylline. Studies of COPD patients suggest that anticholinergics have a slight advantage in both a stable setting and acute exacerbation. Maximal bronchodilation can be achieved with either drug in adequate doses. Adding the other agent does not improve bronchodilation further.
Beta-agonists available include metaproterenol (orciprenaline), albuterol (salbutamol), isoetheraine, pirbuterol, and bitolterol. They can be administered effectively via a nebulizer or metered dose inhaler. In the co-operative patient the metered dose inhaler with a spacer is the most cost-effective method of administering these medications. The spacer traps large particles that would deposit in the mouth and be absorbed, potentially increasing systemic side-effects. These agents can be dosed every 1 to 2 h if needed to achieve a beneficial effect.
Ipratroprium is the quarternary salt of atropine. Unlike atropine, it does not readily cross biological membranes. There are few systemic side-effects, and it has a longer duration of action. As with the b-agonists, it can be administered via a nebulizer or metered dose inhaler. During acute exacerbations there can be a benefit to increasing the dosing frequency from every 6 h to every 2 to 4 h. In contrast with COPD, ipratroprium is not considered a first line-drug in the therapy of asthma.
The role of theophylline in the management of COPD and asthma has come under scrutiny. In double-blind studies comparing its use with a placebo in patients already receiving b-agonists and corticosteroids, there was no significant improvement in dyspnea, spirometry, or arterial blood gases. More gastrointestinal side-effects occurred in the theophylline groups. Theophylline has a limited role as a bronchodilator in acute exacerbations of asthma and COPD. The beneficial effects seen in theophylline-treated patients are not the result of bronchodilation, but are due to its action as a respiratory stimulant, as a possible inotropic agent for the respiratory muscles, and as a mild diuretic. Dosing of theophylline should be adjusted according to blood levels. Its metabolism is variable, and it interacts with many commonly used drugs.
Corticosteroids are a cornerstone in the treatment of COPD exacerbations. The use of steroids is based on a single randomized study where patients received either methylprednisolone 0.5 mg/kg or placebo every 6 h for 3 days, in addition to standard therapy. The corticosteroid group demonstrated an improvement in FEV 1 after the first 12 h. Of the 40 corticosteroid-treated patients, 22 demonstrated a 40 per cent improvement in FEV v There were no differences in the arterial blood gases or the eventual outcome.
Adequate hydration is advocated empirically in both the asthmatic and the COPD patient. Respiratory secretions will be less viscous in the well-hydrated patient. The administration of fluid directly into the airway and the use of mucolytics have not been shown to have consistent benefit. Indeed, the mucolytic agent ^-acetylcysteine is an airway irritant, and may exacerbate the situation. In the attempt to mobilize secretions and treat atelectasis, chest physiotherapy, deep breathing, and cough offer the greatest benefit.
Mechanical ventilation will be required at times to support the patient with respiratory failure and asthma. The purpose is to support the patient while the disease process runs its course or the pharmacological intervention takes effect. The potential to do harm is great. Intubation predisposes to aspiration and nosocomial pneumonia. Increased work of breathing and respiratory muscle fatigue will occur in the setting of a small endotracheal tube and too little ventilator support. Air-flow obstruction by edema, bronchospasm, and mucus promote air trapping, auto-PEEP, and the risk of barotrauma. Auto-PEEP will also predispose to hypotension and increased work of breathing in triggering a machine breath. Hyperventilation of the patient can result in severe alkalemia. This promotes cardiac irritability and electrolyte disturbances, reduces cerebral blood flow, and suppresses the ventilatory drive. Strategies to minimize these complications include ventilating with tidal volumes of 5 to 10 ml/kg, increasing the peak flow to shorten inspiratory time, and applying extrinsic PEEP of the order of 5 to 10 cmH 2O to offset the effects of auto-PEEP. Additional strategies using non-invasive ventilation (continuous or bi-level positive airways pressure), where support is provided by facial or nasal masks, are being studied.
Was this article helpful?
If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.