G. Barr

Entropy during propofol hypnosis, including an episode of wakefulness.

Depth of anaesthesia has proved to be a complex process to quantify. Monitors based on bispectral analysis of the electroencephalogram and auditory evoked potential have been available, but only recently has a monitor based on entropy become available. This study determined state entropy and response entropy in nine healthy volunteers during propofol hypnosis with a brief intervening period of wakefulness. Both the calculated entropy indices decreased with increasing levels of sedation (r2 = 0.58 and 0.61, respectively) and they showed a high correlation with each other (r2 = 0.94). However, an overlap was observed in real time indices between different stages of the Observers Assessment of Alertness/Sedation Scale. Only three of the nine volunteers had explicit memories from the episode of wakefulness. Electroencephalographic entropy monitors seem to have potential for staging clinical hypnotic effects.

Clinical comparison of three different anaesthetic depth monitors during cardiopulmonary bypass.

The lack of a gold standard complicates the evaluation and comparison of anaesthetic depth monitors. This randomised study compares three different depth‐of‐anaesthesia monitors during cardiopulmonary bypass (CPB) at 34 °C with fentanyl/propofol anaesthesia adjusted clinically and blinded to the monitors. Coronary artery bypass grafting patients (n = 21) were randomly assigned to all three possible paired combinations of three monitors: Bispectral Index (Aspect Medical), AAITM auditory evoked potential (Danmeter), EntropyTM (Datex‐Ohmeda). Indices were manually recorded every 5 min during CPB. Agreement between paired indices was classified as good, non‐, or disagreement. Anaesthesia was classed as adequate, inadequate, or excessive according to recommended index values. Of the 255 paired indices recorded, 62% showed good agreement, 33% showed non‐agreement, and 5% showed disagreement. Using good agreement between two monitors as a gold standard, a quarter of the measurements indicate inappropriate anaesthetic depth monitoring during CPB with clinically titrated anaesthetic depth.

The Influence of Glucose-Insulin-Potassium (GIK) on the GH/IGF-1/IGFBP-1 Axis During Elective Coronary Artery Bypass Surgery

OBJECTIVES To investigate the influence of glucose-insulin-potassium (GIK) on the growth hormone/insulin-like growth factor-1 axis. DESIGN Randomized clinical study. SETTING University hospital. PARTICIPANTS Twenty patients, without metabolic disorders, admitted for elective aortocoronary bypass surgery. INTERVENTIONS GIK therapy. Measurements and main results Blood samples were taken repeatedly during the day of surgery. Ejection fraction (EF) was determined by transesophageal echocardiography before and at the end of surgery. Blood samples were taken on the first postoperative day and at discharge (8 am and 8 pm). During coronary artery bypass graft (CABG) surgery, a rapid decrease (44%) in total IGF-1 occurred in both groups. Directly after cessation of extracorporeal circulation, there was a prompt rise in IGFBP-1. The mean peak value in the control group was more than 3 times higher than in the GIK group. GH secretion was stimulated by surgery in both groups and was enhanced by GIK. B-glucose was significantly higher in the control group during surgery. EF ( approximately 55% at baseline) was unchanged in both groups. Postoperatively, there were no differences between the groups (all parameters). At discharge, IGFBP-1 was unchanged, but insulin was elevated compared with preoperative levels. This was seen in both groups, reflecting a hepatic insulin resistance. Conclusions The authors conclude that GIK blunts the rise of IGFBP-1 and thereby increases the bioavailability of IGF-1. GIK also seems to speed up the return of IGF-1 to baseline. Both mechanisms could be of importance to catabolic high-risk patients with low IGF-1. Hence, GIK has favorable effects on the GH/IGF-1 axis during CABG surgery.

Effects of thoracic epidural analgesia on glucose homeostasis after cardiac surgery in patients with and without diabetes mellitus.

Background and objective: Even moderate hyperglycaemia increases mortality/morbidity after coronary artery bypass grafting, stroke and myocardial infarction. The goal of this prospective study was to determine if using thoracic epidural analgesia from start of surgery until the end of the third postoperative day would blunt postoperative hyperglycaemia. Methods: Forty‐four patients had diabetes mellitus, 60 did not; half of each group had an epidural with continuous local anaesthetics. All patients received continuous insulin infusions during the initial 24 h period beginning with surgery. Blood glucose was measured four times daily (fasting or 2‐3 h post‐prandial) until end of the third postoperative day. Results: For patients without diabetes, the epidural group had lower mean blood glucose and insulin requirements (P < 0.02) than controls during the initial 24 h period beginning with surgery. For patients with diabetes mellitus, thoracic epidural analgesia reduced mean blood glucose (P = 0.017) with unchanged insulin requirements. Epidural did not diminish the increase (vs. preoperative) in fasting blood glucose on the third postoperative day (32% vs. 22%, P < 0.001) for non‐diabetics. Epidural analgesia was not able to attenuate hyperglycaemia during the first 3 postoperative days. Conclusions: Epidural analgesia improved glucose homeostasis minimally during the initial 24 postoperative hours but did not attenuate hyperglycaemia during the subsequent 3 postoperative days.

Is endothelin-1 release at reperfusion of the ischaemic human heart due to cold-induced displacement of endothelin from binding sites ?

Following reperfusion of ischaemic human hearts subjected to cold (4 degrees C) cardioplegia during coronary bypass surgery, there was an increase in cardiac outflow of endothelin-1 but not the pro-peptide big endothelin-1. Furthermore, specific endothelin-1 binding in human lung membrane preparations was displaced by incubation in buffer medium at 4 degrees C. The present results thus indicate that cold-induced displacement of endothelin-1 binding, rather than increased synthesis, may explain the cardiac release of endothelium-1 following ischaemia during heart surgery in which cold cardioplegia has been used.