SummaryPain after craniotomy remains a significant problem. The effect of morphine and tramadol patient‐controlled analgesia (PCA) on arterial carbon dioxide tension is unknown in patients having such surgery. Sixty craniotomy patients were randomly allocated to receive morphine PCA, tramadol PCA or codeine phosphate 60 mg intramuscularly. Baseline values of pain score (0–10), sedation and arterial carbon dioxide tension were recorded at the time of first analgesic administration and at 30 min, 1, 4, 8, 12, 18 and 24 h. Patient satisfaction was assessed at 24 h. There were no differences in arterial carbon dioxide tension or sedation between groups at any time, but in all three groups some patients had rises greater than 1 kPa. Morphine produced significantly better analgesia than tramadol at all time points (p < 0.005) and better analgesia than codeine at 4, 12 and 18 h. Patients were more satisfied with morphine than with codeine or tramadol (p < 0.001). Vomiting and retching occurred in 50% of patients with tramadol, compared with 20% with morphine and 29% with codeine.

SummaryXenon anaesthesia is thought to have minimal haemodynamic side-effects. It is, however, expensive and requires special delivery systems for economic use. In this randomised cross-over study, we: (i) investigated the haemodynamic profile and recovery characteristics of xenon compared with propofol sedation in postoperative cardiac surgery patients, and (ii) evaluated a fully closed breathing system to minimise xenon consumption. We demonstrated a significantly faster recovery from xenon (3 min 11 s) than propofol sedation (25 min 23 s). Relative to propofol, xenon sedation produced no change in heart rate or mean arterial pressure and there were significantly higher mean values for central venous pressure (10.6 vs. 8.9 mmHg), pulmonary artery occlusion pressure (11.2 vs. 9.5 mmHg), mean pulmonary artery pressure (20.1 vs. 18.3 mmHg) and systemic vascular resistance index (2170 vs. 1896 dyn.s.cm 25 .m 22 ). The haemodynamic profile seen with propofol reflected its known vasodilator effects. This was supported by the almost identical left ventricular stroke work indexes seen with both methods of sedation.

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Editor-We commend Eissa and colleagues' 1 review article; however, we wish to draw attention to the selection of induction agent for septic patients. The ideal haemodynamic properties of etomidate use in this population are countered by lingering concerns about subsequent impaired adrenal steroidogenesis with its attendant consequences-a situation described as an ultimate Faustian bargain. 2 Two recent systematic reviews have examined effects of single-dose etomidate in critically ill patients, 3 and those with suspected sepsis. 4 They both conclude that single-dose etomidate is associated with transient suppression of the adrenal axis. However, neither study reported a significant effect of etomidate on mortality. In fact, no prospective randomized trials to date have reported that etomidate has a significant adverse effect on mortality in patients with sepsis. 5 We feel that while uncertainty remains, consideration should be given to using alternative induction agents, such as ketamine, in the patient with severe sepsis. 1 Eissa D, Carton EG, Buggy DJ. Anaesthetic management of patients with severe sepsis. Br J Anaesth 2010; 105: 734-43 2 Hofer J, Nunnally M. Taking the septic patient to the operating room. Anesthesiol Clin 2010; 28: 13-24 3 Hohl CM, Kelly-Smith CH, Yeung TC, et al. The effect of a bolus dose of etomidate on cortisol levels, mortality, and health services utilization: a systematic review. Ann Emerg Med 2010; 56: 105-13 4 Edwin SB, Walker PL. Controversies surrounding the use of etomidate for rapid sequence intubation in patients with suspected sepsis.

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