THE Confederate General “Stonewall” Jackson was one of the earliest known victims of a respiratory complication after surgery, dying of pneumonia 10 days after an otherwise successful ether anesthetic in 1863. Despite subsequent advances in anesthesia and surgical care, postoperative pulmonary complications (PPCs) still are a significant problem in modern practice. This commentary examines why PPCs occur and how the anesthesiologist can help prevent them.

Preventing postoperative pulmonary complications: the role of the anesthesiologist.

Etomidate is a carboxylated, imidazole-containing intravenous anesthetic agent introduced into clinical anesthesia practice in 1972. Its distinctive features that make it useful as an anesthetic induction include a lack of adverse effects on hemodynamic function as well as beneficial effects on cerebral blood flow and intracranial pressure. Because of these properties, its major role in anesthetic practice has been for the induction of anesthesia in patients with diminished cardiovascular function. As opposed to the considerable reported clinical experience with etomidate in the adult population, there remains limited reported information concerning its use in pediatric patients. This article reviews the specific end-organ effects of etomidate, the reports concerning its use in pediatric patients, and its adverse effect profile.

Dexmedetomidine: applications in pediatric critical care and pediatric anesthesiology.

T he use of electroconvulsive therapy (ECT) to provoke a generalized epileptic seizure was first described in 1938 and was performed without anesthesia for almost 30 yr (1). Now the number of ECT procedures performed each year under general anesthesia in the United States exceeds the number of coronary revascularization, appendectomy, and herniorrhaphy procedures (2). In recent years, ECT has assumed an increasingly important role in the treatment of severe and medicationresistant depression and mania, as well as in the treatment of schizophrenic patients with affective disorders, suicidal drive, delusional symptoms, vegetative dysregulation, inanition, and catatonic symptoms (2,3). Typically, the acute phase of ECT is performed three times a week for 6 to 12 treatments. In successful cases, initial clinical improvement is usually evident after three to five treatments (3,4). Maintenance therapy can be performed at progressively increasing intervals from once a week to once a month to prevent relapses. To optimize the anesthetic management of patients undergoing ECT, it is important to understand the physiologic responses to the electrical stimulus, the effect of anesthetic drugs on the ECT response, and the pharmacologic effects of the drugs used to attenuate the side effects related to ECT. In 1986, Gaines and Rees (5) published a comprehensive review regarding the psychiatric and anesthetic considerations in caring for patients undergoing ECT. More recently, Folk et al. (6) reviewed the preanesthetic management of ECT patients with coexisting diseases. This review article is intended to provide an update on the anesthetic management of patients undergoing ECT. Physiologic Responses to ECT

Anesthesia for electroconvulsive therapy.

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 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.

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

To compare the effects of propofol and thiopentone on tracheal intubation-induced bronchoconstriction, 37 patients were allocated randomly to anaesthesia with either thiopentone 4 mg kg-1 followed by a 15-mg kg-1 h-1 continuous infusion or propofol 3 mg kg-1 followed by a 9-mg kg-1 h-1 continuous infusion. Intubation was facilitated by vecuronium 0.1-0.2 mg kg-1. Respiratory system resistance (Rrs) was measured by a CP-100 pulmonary function monitor, 5 min after intubation. The 5-min post-intubation Rrs values were significantly lower in the propofol group (8.5 (SD 1.5) cm H2O litre-1 S-1) than in the thiopentone group (10.9 (3.2) cm H2O litre-1 S-1). Thirty minutes after commencing isoflurane-nitrous oxide anaesthesia, Rrs declined by 17.5 (SEM 3.6)% from baseline in the thiopentone group, but by only 1.6 (2.6)% in the propofol group. We conclude that the dose of propofol administered provided more protection against tracheal intubation-induced bronchoconstriction than an induction dose of thiopentone.

Michael J. Bishop

Papers

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

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

Comparative effects of thiopentone and propofol on respiratory resistance after tracheal intubation.

Anesthesia for patients with asthma : low risk but not no risk

Comparative Effects of Thiopentone and Propofol on Respiratory Resistance After Tracheal Intubation