Energy balance can be estimated in tissues, body segments, individual subjects (the focus of the present article), groups of subjects and even societies. Changes in body composition in individual subjects can be translated into changes in the energy content of the body, but this method is limited by the precision of the techniques. The precision for measuring fat and fat-free mass can be as low as 0.5 kg when certain reference techniques are used (hydrodensitometry, air-displacement plethysmography, dual-energy X-ray absorptiometry), and approximately 0.7 kg for changes between two time points. Techniques associated with a measurement error of 0.7 kg for changes in fat and fat-free mass (approximately 18MJ) are of little or no value for calculating energy balance over short periods of time, but they may be of some value over long periods of time (18 MJ over 1 year corresponds to an average daily energy balance of 70 kJ, which is <1% of the normal dietary energy intake). Body composition measurements can also be useful in calculating changes in energy balance when the changes in body weight and composition are large, e.g. >5–10 kg. The same principles can be applied to the assessment of energy balance in body segments using dual-energy X-ray absorptiometry. Energy balance can be obtained over periods as short as a few minutes, e.g. during measurements of BMR. The variability in BMR between individuals of similar age, weight and height and gender is about 7–9%, most of which is of biological origin rather than measurement error, which is about 2%. Measurement of total energy expenditure during starvation (no energy intake) can also be used to estimate energy balance in a whole-body calorimeter, in patients in intensive care units being artificially ventilated and by tracer techniques. The precision of these techniques varies from 1 to 10%. Establishing energy balance by measuring the discrepancy between energy intake and expenditure has to take into consideration the combined validity and reliability of both components. The measurement error for dietary intake may be as low as 2–3% in carefully controlled environments, in which subjects are provided only with certain food items and bomb calorimetry can be undertaken on duplicate samples of the diet. Reliable results can also be obtained in hospitalised patients receiving enteral tube feeding or parenteral nutrition as the only source of nutrition. Unreliability increases to an unknown extent in free-living subjects eating a mixed and varied diet; thus, improved methodology is needed for the study of energy balance.

The bispectral index, a value derived from the electroencephalogram, has been proposed as a measure of anaesthetic effect. The aim of the present study was to evaluate the bispectral index during midazolam–fentanyl anaesthesia for cardiac surgery for its possible role as a predictor of increases in systolic blood pressure during endotracheal intubation and sternotomy. After institutional approval 15 consenting patients, scheduled for elective cardiac surgery, were selected for the study. Anaesthesia was induced in all patients with a loading dose of fentanyl 7.5–10 μg kg−1, midazolam 0.15 mg kg−1 and pancuronium 0.1 mg kg−1. After a further bolus dose of fentanyl 10–12.5 μg kg−1 prior to the start of incision and sternotomy, maintenance infusion rates of fentanyl 4–6 μg kg−1 h−1 and midazolam 0.1 mg kg−1 h−1 were started and continued through surgery at the discretion of the anaesthetist and guided by the presenting clinical and haemodynamic responses. The control of anaesthesia was never based on the value of the bispectral index. The mean bispectral index value decreased from 95.7 (3.1) at base-line to 59.5 (12.0) after induction of anaesthesia and then remained below 70 throughout surgery. However, there was an important interindividual variability in bispectral index values despite standardized dosages of fentanyl and midazolam. There was no significant correlation between the bispectral index values in the pre-intubation and pre-incision period and the changes in systolic blood pressure during endotracheal intubation and sternotomy, respectively. In conclusion, the large intersubject variability in the bispectral index values should be investigated further in the light of the great variability in the clinical effects of midazolam and fentanyl. The lack of significant correlation between the bispectral index values and the haemodynamic responses suggest that the bispectral index, which is a helpful monitor of anaesthetic depth, is not a very reliable monitor of global anaesthetic adequacy during total intravenous anaesthesia with a combination of midazolam and fentanyl in cardiac surgical patients.

After an intubating dose of rocuronium satisfactory intubating conditions are achieved before the onset time at the adductor pollicis. We examined the possibility that measurement of the relaxation of the masseter muscle is a more appropriate guide when determining the intubating time. Simultaneous accelerometry with a 0.1-Hz single twitch stimulation of the chin and thumb was performed in 20 patients after 0.6 mg kg=1 rocuronium. We observed a significantly more brief mean lag time and onset time at the masseter muscle (22.5 and 61 vs. 32.5 and 160 s). The corresponding mean relaxation at the onset time was also significantly more pronounced at the masseter muscle (99.6 vs. 97.6%). A mean onset time at the masseter muscle of 61 s as produced by rocuronium corresponds clinically with excellent or good intubating conditions. From these results, we suggest that measurement of the onset time of muscle relaxation at the masseter muscle appears to be a better predictor of good intubating conditions than measurements made using the adductor pollicis muscle after administration of rocuronium.

Sometimes progress is hard to see, when looking at the big picture, because there is very little of it. But sometimes progress is hard to see because the big picture is out of focus. When perioperative deaths ascribed to anaesthesia are in the order of 1 in 20 000 operations and even changes in major morbidity require massive sample sizes to detect, neuroanaesthesia's most emphatic yardstick of progress is too crude to measure advances that have occurred over the most recent decade. We clearly need to become more familiar with neuropsychological tests that can detect subtle changes. Today, for elective neurosurgery, we are primarily in the business of doing two things – pushing the envelope for surgical intervention to include cases that would have been considered too risky 15 years ago, and reducing the frequency of “Uncle-Joe-has-never-been-the-same-since-they-operated-on-his-brain syndrome”. Both of these areas of progress are empirically measurable, but we have not made much progress towards measuring them. Of course, this measurement problem plagues anaesthesiology generally, and we need to attend to it in general. Meanwhile, saying where we are relative to the recent past and the near future involves a lot of guesswork. What follows is my guesswork about progress in neurosurgical anaesthesiology.

Oxygen consumption (̇Vo2) measured by indirect calorimetry (Nellcor-Puritan-Bennett 7250; Carlsbad, CA, USA) has been compared with ̇Vo2 calculated by the Fick method in 22 volume-controlled ventilated general surgical patients in the early post-operative period. For 198 pairs of measurements, ̇Vo2 Fick and ̇Vo2 indirect calorimetry correlated significantly (y=1.00x–35.8, P=0.0001, r=0.77). ̇Vo2 indirect calorimetry was 212±32 mL min−1 and ̇Vo2 Fick was 177±41 mL min−1 (P=0.0001). The bias was 35±26 mL min−1. This difference represents 16±13% of the total body ̇Vo2. ̇Vo2 calculated by the Fick method did not accurately predict ̇Vo2 measured by indirect calorimetry, and the two methods were not interchangeable. ̇Vo2 calculated by the Fick method underestimated ̇Vo2 as measured by indirect calorimetry by a systematic quantity that could be attributed, in part, to ̇Vo2 of the lung. Indirect calorimetry should be the preferred method for measuring total body ̇Vo2 in mechanically ventilated surgical patients.

Tramadol is a centrally acting opioid with a low affinity resfor μ-opioid receptors, which has been claimed not to depress respiration as do the classic opioids. The respiratory effects of intravenous (i.v.) pethidine (0.6 mg kg−1) and tramadol (0.6 mg kg−1) were compared in 36 ASA Grade I–II patients in a placebo-controlled double-blind study. After induction of anaesthesia with propofol followed by suxamethonium-facilitated endotracheal intubation, the patients spontaneously breathed halothane in 70% nitrous oxide and oxygen via a non-rebreathing valve. Inspiratory and expiratory oxygen, and end-tidal carbon dioxide concentrations (PetCO2), tidal volume (VT), minute volume of ventilation (MV) and respiratory rate were monitored by a side-stream spirometry at an end-tidal halothane of 0.3%. The recordings were collected before surgery. Pethidine caused significant respiratory depression seen as an increase in fractional inspiratory–expiratory oxygen difference and PetCO2 and as a decrease in MV and respiratory rate. However, the effects of tramadol were similar to those of a placebo. Tidal volume was not affected by any study drug. In conclusion, tramadol 0.6 mg kg−1 was shown not to be associated with respiratory depression, unlike equipotent dose of pethidine in this setting.

The relation between left ventricular end-systolic wall stress (ESWS) and the velocity of circumferential fibre shortening (Vcfs) was examined in four non-random groups with 12 patients each. In group A, preload was increased by the administration of hydro- xyethylstarch 30 mL min−1. In group B, preload was reduced by administering nitroglycerine 4.0 ± 0.8 mg h−1. A change in pulmonary capillary wedge pressure by 3 mmHg was taken to be the end point for preload manipulation. To assess a change in the relation between ESWS and Vcfs, patients in group C received adrenaline at an infusion rate of 4 g min−1. Patients in group D served as the controls. Geometric variables of ESWS and Vcfs were determined by transoesophageal echocardiography. A linear model was used to assess the relation between ESWS and Vcfs within each group by regression analysis, and analysis of covariance performed to detect significance of intragroup and intergroup differences (P < 0.005). No significant changes were found during preload intervention. With adrenaline, Vcfs increased significantly for a given ESWS. It is concluded that the relation between ESWS and Vcfs, in a multiple patient setting, is independent of modest preload changes and may have the potential to indicate inotropic effects.

Cardiovascular responses after epidural alkalinized lignocaine and subarachnoid hyperbaric bupivacaine administration were studied using a non-invasive cardiac output measurement in 32 ASA Grade I–II patients undergoing orthopaedic leg surgery (hip hemi-arthroplasty or Ender nailing). All patients achieved adequate surgical anaesthesia. The block onset time was faster (P = 0.003), and the range of final sensory level wider (P = 0.006) in patients receiving spinal anaesthesia compared with the epidural group. Diastolic arterial pressure was significantly reduced when compared with base-line (P = 0.002) only in the spinal group. No significant changes in stroke volume, systemic vascular resistance or left ventricular stroke work were observed in either group. Heart rate and cardiac index were significantly reduced in the spinal group when compared both with base-line (P = 0.002; P = 0.04) and the epidural group (P = 0.001; P = 0.006). The results demonstrated that the block onset time and the cardiovascular effects produced by lumbar epidural anaesthesia, with alkalinized solutions, remain less than after spinal anaesthesia involving the same segments.

We studied the haemodynamic changes induced by pneumoperitoneum (PP) in elderly patients with increased cardiac risk (ASA class III; n = 10; age 72.3 ± 8.8 years, mean±SD, P < 0.05; group 2) and compared the results with patients at normal risk (ASA class I, II; n = 12; age 55.6 ± 11.8 years; group 1). Thermodilution measurements were performed after induction of general anaesthesia (T1), after onset of PP (T2, intraabdominal pressure 14 mmHg) and after additional 15° head-up tilt (T3). In both groups PP, as compared with T1, induced a significant increase in mean arterial pressure (MAP, mmHg, group 1:77 ± 14 to 96 ± 18, P < 0.05/group 2:75 ± 10 to 102 ± 18, P < 0.01), mean pulmonary artery pressure (MPAP, mmHg: 15 ± 5 to 22 ± 4, P < 0.01/18 ± 3 to 25 ± 5, P < 0.01), central venous pressure (CVP, mmHg: 7 ± 2 to 15 ± 3, P < 0.01/7 ± 2 to 12 ± 2, P < 0.01), pulmonary capillary wedge pressure (PCWP, mmHg: 9 ± 4 to 16.3, P < 0.01/8 ± 2 to 15 ± 6, P < 0.01) and in systemic vascular resistance (SVR, dynes s cm−5: 1415 ± 375 to 1873 ± 412, P < 0.01/1502 ± 360 to 2067 ± 647, P < 0.01). Cardiac index (CI, L min−1 m−2: 2.3 ± 0.3 to 1.9 ± 0.3, P < 0.05/2.2 ± 0.4 to 2.2 ± 0.5 P = 0.76) and oxygen delivery index (DO2I, mL min−1 m−2: 388 ± 54 to 324 ± 61, P < 0.05/358 ± 69 to 353 ± 82, P = 0.77) decreased in group 1 but not in group 2. Heart rate, stroke index, pulmonary vascular resistance, arteriovenous oxygen content difference and oxygen consumption index were unchanged. After head-up tilt MAP (mmHg, 92 ± 15, P < 0.05/101 ± 17, P < 0.01), MPAP (mmHg, 20 ± 3, P < 0.01/22 ± 4, P < 0.05), CVP (mmHg, 12 ± 2, P < 0.01/10 ± 2, P& lt; 0.01) and PCWP (mmHg, 12 ± 3, P < 0.05/12 ± 5, P < 0.05) remained elevated compared with T1 in both groups, SVR (dynes s cm−5, 1575 ± 372, P = 0.13/1793 ± 528, P < 0.01) in group 2 only. No complications occurred. The results indicate that PP is associated with significant but relatively benign haemodynamic changes. Anaesthesia for laparoscopic cholecystectomy may be performed safely also in elderly ASA class III patients with increased cardiac risk. An adequate haemoto dynamic monitoring is recommended.

The interaction of aprotinin with normal coagulation was studied in blood samples obtained from 10 healthy subjects. Each sample was simultaneously tested in four different preparations : NaCl-treated blood: 0.03 mL 0.9% NaCl in 0.33 mL blood; aprotinin treated blood : 0.33 mL blood+aprotinin in 0.03 mL in aliquots to obtain a final blood concentration of respectively 50 KIU mL−1; 100 KIU mL−1 and 200 KIU mL−1. The coagulation process was analysed by thromboelastography. R-time, reflecting intrinsic coagulation, increased in a dose dependent manner between NaCl-treated and aprotinin-treated blood. These findings suggest a dose dependent impairment of intrinsic coagulation by aprotinin.