Chronic exposure to cigarette smoke produces profound changes in physiology that may alter responses to perioperative interventions and contribute to perioperative morbidity Because of smoke-free policies in healthcare facilities, all smokers undergoing surgery are abstinent from cigarettes for at least some period of time so that all are in various stages of recovery from the effects of smoke Understanding this recovery process will help perioperative physicians better treat these patients This review examines current knowledge regarding how both short-term (duration ranging from hours to weeks) and long-term smoking cessation affects selected physiology and pathophysiology of particular relevance to perioperative outcomes and how these changes affect perioperative risk It will also consider current evidence regarding how nicotine replacement therapy, a valuable adjunct to help patients maintain abstinence, may affect perioperative physiology

Perioperative abstinence from cigarettes: physiologic and clinical consequences.

BACKGROUND Tracheal intubation frequently results in reversible bronchoconstriction. Propofol has been reported to minimize this response in healthy patients and in asthma patients, but may be unsuitable for hemodynamically unstable patients for whom etomidate may be preferable. The current study examined respiratory resistance after tracheal intubation after induction with either thiopental, etomidate, or propofol. A supratherapeutic dose of etomidate was used to test the hypothesis that the bronchoconstrictive response could be minimized by deep intravenous anesthesia. METHODS Seventy-seven studies were conducted in 75 patients. Anesthesia was induced with either 2.5 mg/kg propofol, 0.4 mg/kg etomidate, or 5 mg/kg thiopental. Respiratory resistance was measured at 2 min after induction. RESULTS Respiratory resistance at 2 min was 8.1 +/- 3.4 cmH2O.1(-1).s (mean +/- SD) for patients receiving propofol versus 11.3 +/- 5.3 for patients receiving etomidate and 12.3 +/- 7.9 for patients receiving thiopental (P < or = 0.05 for propofol vs. either etomidate or thiopental). CONCLUSIONS Respiratory resistance after tracheal intubation is lower after induction with propofol than after induction with thiopental or after induction with high-dose etomidate.

Comparison of the Effects of Etomidate, Propofol, and Thiopental on Respiratory Resistance After Tracheal Intubation

Background:After tracheal intubation, lung resistance and therefore respiratory system resistance (Rrs) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparin

The effect of isoflurane, halothane, sevoflurane, and thiopental/nitrous oxide on respiratory system resistance after tracheal intubation.

Background: In patients with bronchial hyperreactivity, airway instrumentation can evoke life-threatening bronchospasm. However, the best strategy for the prevention of bronchospasm has not been defined. Therefore, in a randomized, prospective, placebo-controlled study, the authors tested whether prophylaxis with either combined salbutamol‐methylprednisolone or salbutamol alone (1) improves lung function and (2) prevents wheezing after intubation. Methods: Thirty-one patients with partially reversible airway obstruction (airway resistance > 180%, forced expiratory volume in 1 s [FEV1] 10% after two puffs of salbutamol), who were naive to antiobstructive treatment, were randomized to receive daily for 5 days either 3 2 puffs (0.2 mg) of salbutamol alone (n 16) or salbutamol combined with methylprednisolone (40 mg/day orally) (n 15). Lung function was evaluated daily. Another 10 patients received two puffs of salbutamol 10 min before anesthesia. In all patients, wheezing was assessed before and 5 min after tracheal intubation. Results: Within 1 day, both salbutamol and salbutamol‐methylprednisolone treatment significantly improved airway resistance (salbutamol, 4.3 2.0 [SD] to 2.9 1.3 mmHg ·s·l 1 ; salbutamol‐methylprednisolone, 5.5 2.9 to 3.4 1.7 mmHg ·s·l 1 ) and FEV1 (salbutamol, 1.79 0.49 to 2.12 0.61 l; salbutamol‐methylprednisolone, 1.58 0.66 to 2.04 1.05 l) to a steady state, with no difference between groups. However, regardless of whether single-dose salbutamol preinduction or prolonged salbutamol treatment was used, most patients (8 of 10 and 7 of 9) experienced wheezing after intubation. In contrast, only one patient receiving additional methylprednisolone experienced wheezing (P 0.0058). Conclusions: Pretreatment with either salbutamol alone or salbutamol combined with methylprednisolone significantly and similarly improves lung function within 1 day. However, only combined salbutamol‐methylprednisolone pretreatment decreases the incidence of wheezing after tracheal intubation. Therefore, in patients with bronchial hyperreactivity, preoperative treatment with combined corticosteroids and salbutamol minimizes intubation-evoked bronchoconstriction much more effectively than the inhaled 2-sympathomimetic salbutamol alone. IN patients with bronchial hyperreactivity, airway instrumentation by tracheal intubation may evoke life-threatening bronchospasm, perioperative complications, and prolonged intensive care treatment. 1– 6 In particular, patients with active signs of obstructive airway disease are at a higher risk for perioperative complications. 4 Therefore, treatment in patients with previously undiagnosed bronchial hyperreactivity should intuitively be an important goal to improve lung function and to mitigate evoked bronchoconstriction. However, it is unknown which drugs should be used as first-line treatment, what the effects are, and how many days should elapse before anesthesia and surgery can proceed safely.

Corticosteroids and inhaled salbutamol in patients with reversible airway obstruction markedly decrease the incidence of bronchospasm after tracheal intubation.

Background: Propofol and ketamine have been purported to decrease bronchoconstriction during induction of anesthesia and intubation. Whether they act on airway smooth muscle or through neural reflexes has not been determined. We compared propofol and ketamine to attenuate the direct activation of airway smooth muscle by methacholine and limit neurally mediated bronchoconstriction (vagal nerve stimulation). Methods: After approval from the institutional review board, eight sheep were anesthetized with pentobarbital, paralyzed, and ventilated. After left thoracotomy, the bronchial artery was cannulated and perfused. In random order, 5 mg/ml concentrations of propofol, ketamine, and thiopental were infused into the bronchial artery at rates of 0.06, 0.20, and 0.60 ml/min. After 10 min, airway resistance was measured before and after vagal nerve stimulation and methacholine given via the bronchial artery. Data were expressed as a percent of baseline response before infusion of drug and analyzed by analysis of variance with significance set at P ≤ 0.05. Results: Systemic blood pressure was not affected by any of the drugs (P > 0.46). Baseline airway resistance was not different among the three agents (P = 0.56) or by dose (P = 0.96). Infusion of propofol and ketamine into the bronchial artery caused a dose-dependent attenuation of the vagal nerve stimulation-induced bronchoconstriction to 26 ± 11% and 8 ± 2% of maximum, respectively (P < 0.0001). In addition, propofol caused a significant decrease in the methacholine-induced bronchoconstriction to 43 ± 27% of maximum at the highest concentration (P = 0.05) Conclusions: The local bronchoprotective effects of ketamine and propofol on airways is through neurally mediated mechanisms. Although the direct effects on airway smooth muscle occur at high concentrations, these are unlikely to be of primary clinical relevance.

Mechanisms of bronchoprotection by anesthetic induction agents : Propofol versus ketamine

BACKGROUND After induction of anesthesia, lung resistance increases. We hypothesized that prophylactic bronchodilator treatment before tracheal intubation would result in a lower lung resistance after placement of the endotracheal tube. METHODS Forty-two adult patients were randomized to receive one of three inhaled medications 1 h before surgery. All patients first underwent pulmonary function tests. Patients then received either inhaled albuterol (360 micrograms) (n = 12), inhaled ipratropium bromide (72 micrograms) (n = 15) or a placebo inhalation (n = 15). Two, 5, and 15 min after tracheal intubation, lung resistance was measured using the method of von Neergard and Wirtz. RESULTS Patients who received either bronchodilator had significantly lower lung resistance after intubation than those receiving placebo. At 2 min, lung resistances were 12.7 +/- 1.4 cmH2O.l-1.s-1 (mean +/- SEM) for the placebo group, 6.4 +/- 3.1 cmH2O.l-1.s-1 for the ipratropium-treated group (P < 0.05 vs. placebo), and 7.2 +/- 0.8 cmH2O.l-1.s-1 for the albuterol-treated group (P < 0.05 vs. placebo). The differences in lung resistance persisted through the final measurement at 15 min. Three of fifteen placebo-treated patients developed audible wheezing whereas no patients developed wheezing in either bronchodilator-treated group (P < 0.05 by Fisher's exact test). Although smokers and nonsmokers in the placebo group developed similar resistances after intubation, bronchodilator treatment resulted in lower resistance in nonsmokers than in smokers (P < 0.05). CONCLUSIONS Prophylactic treatment with either an inhaled beta 2-adrenergic agonist or an inhaled cholinergic antagonist produced lower lung resistance after intubation when compared with an inhaled placebo medication. The effect was more pronounced in nonsmokers than in smokers.

G. Alec Rooke

Papers

Effect of prophylactic bronchodilator treatment on lung resistance after tracheal intubation.