In the United States, cigarette smoking has been identified as the leading cause of preventable disease and death. Recent data from the Centers of Disease Control shows that 15% of US adults smoke cigarettes and more than 16 million Americans suffer from a smoking-related disease. As such, the diligent anesthesiologist must be aware of the multisystem perioperative considerations of smoking in today’s practice environment.
Cessation of smoking is the most evidence-based and effective preoperative respiratory intervention to reduce pulmonary mortality and morbidity during the perioperative period (Table 151-1). Perioperative pulmonary complications, such as pneumonia, pneumothorax, exacerbation of existing respiratory illness, and atelectasis, occur in up to 80% of surgical patients. The causative mechanisms include respiratory secretions, shallow breathing, splinting, aspiration, and trauma secondary to mechanical ventilation. Not only do these pulmonary complications significantly increase morbidity and mortality, but they increase length of hospitalization and medical resource utilization. Cessation of smoking 4–8 weeks prior to surgery is one of the few preoperative lifestyle modifications that results in a significantly decreased rate of perioperative pulmonary complications.
TABLE 151-1Cessation of Smoking: Temporal Benefits ||Download (.pdf) TABLE 151-1 Cessation of Smoking: Temporal Benefits
|6–12 hours ||2–4 weeks ||6–8 weeks |
|Decreased carboxyhemoglobin levels ||Increased mucociliary function ||Improved pulmonary immune system function |
|Right shift of oxyhemoglobin curve ||Decreased sputum production (by 4 wk) ||Normalization of hepatic enzyme function |
The pulmonary complications associated with smoking demand particular attention by the anesthesiologist, as they have the potential to affect oxygenation, ventilation, and oxygen utilization. Smoking increases airway irritability and secretions, decreases mucociliary transport function, decreases forced vital capacity (FVC) and forced expiratory flow (FGF) 25%–75%, and increases closing capacity. Noxious environmental stimuli, of which smoking is the most common, cause a persistent state of inflammation of lung tissue, leading to mucus metaplasia. This process is a major determinant of small airway inflammation and impairment of expiratory airflow in chronic obstructive pulmonary disease (COPD).
COPD is a chronic respiratory illness that is one of the leading causes of mortality and morbidity worldwide, affecting 175 million people and causing 3 million deaths annually. The delineations of chronic bronchitis and emphysema are no longer accepted, as most patients suffer elements of both intrapulmonary processes. Chronic bronchitis is currently considered a separate pathology defined by chronic cough and sputum production, and its primary risk factor is smoking. Chronic bronchitis in patients with COPD is associated with increased mortality and increased COPD exacerbations. Treatment of chronic bronchitis includes medications (eg, beta agonists, glucocorticoids, anticholinergics), physical mucus clearance maneuvers, and perhaps most importantly, smoking cessation.
Smoking also results in changes at the cellular level. Smoking causes increased carbon monoxide levels, which decreases tissue oxygen perfusion via a left shift of the oxyhemoglobin curve. Further, cyanide levels increase, which creates a state of metabolic acidosis via inhibition of mitochondrial oxidative phosphorylation. ...