We collected data from 641 consecutive patients undergoing coronary bypass surgery with cardiopulmonary bypass in 1991 at our institution. Prospective follow-up was through to July 2004.

In-hospital mortality was 2.7% (17 of 641). During follow-up, 248 (40%) patients discharged alive died (5 and 10 yr survival 90% and 70%, respectively). On univariate analysis, preoperative left ventricular dysfunction (ejection fraction <50%) and an increase in serum creatinine ≥25% in the first postoperative week were associated with long-term mortality. The associated mortality risk was additive in predominantly non-overlapping patients groups: the hazard ratio (HR) for renal function deterioration only was 1.41 [95% confidence interval (CI) 0.95–2.32, P=0.083; n=64] and for left ventricular dysfunction only 1.71 (95% CI 1.26–2.95, P=0.0026; n=73). In patients in whom both were present, HR was 3.23 (95% CI 2.52–20.28, P<0.0001; n=20). Although postoperative renal dysfunction was associated with left ventricular dysfunction (P=0.008), both left ventricular dysfunction and postoperative renal function deterioration were independently associated with long-term mortality on multivariate analysis, as were age and the use of venous conduits.

Both postoperative renal function deterioration and preoperative left ventricular dysfunction independently identify largely non-overlapping groups of patients with increased long-term mortality after coronary bypass surgery. In the group of patients with both factors present, the mortality risks appear additive.

Orthostatic tolerance and the cardiovascular response to sitting and standing were evaluated on the day before surgery and 6 and 22 h after operation in 16 patients. Non-invasive systolic (SAP) and diastolic arterial pressure (DAP) (Finometer®), heart rate, cardiac output (CO, Modelflow®), total peripheral resistance (TPR), and central venous oxygen saturation (Scv_o2) were monitored.

Before surgery, no patients had symptoms of orthostatic intolerance. In contrast, 8 (50%) and 2 (12%) patients were orthostatic intolerant at 6 and ~22 h after surgery, respectively. Before surgery, SAP, DAP, and TPR increased (P<0.05), whereas CO did not change (P>0.05) and Scv_o2 decreased (P<0.05) upon mobilization. At 6 h after operation, SAP and DAP declined with mobilization (P<0.05) and the arterial pressure response differed from the preoperative response both upon sitting (P<0.05) and standing (P<0.05) due to both impaired TPR and CO. At ~22 h, the SAP and DAP responses to mobilization did not differ from the preoperative evaluation (P>0.05).

The early postoperative postural cardiovascular response is impaired after radical prostatectomy with a risk of orthostatic intolerance, limiting early postoperative mobilization. The pathogenic mechanisms include both impaired TPR and CO responses.

Forty-two patients undergoing laparoscopic cholecystectomy were randomized to receive standard general anaesthetic either with (Group A, n=21) or without TAP block (Group B, n=21). Ultrasound-guided bilateral TAP block was performed with a high frequent linear ultrasound probe and an in-plane needle guidance technique with 15 ml bupivacaine 5 mg ml^–1 on each side. Intraoperative use of sufentanil and postoperative demand of morphine using a patient-controlled analgesia device were recorded.

Ultrasonographic visualization of the relevant anatomy, detection of the shaft and tip of the needle, and the spread of local anaesthetic were possible in all cases where a TAP block was performed. Patients in Group A received significantly more intraoperative sufentanil and postoperative morphine compared with those in Group B [mean (sd) 8.6 (3.5) vs 23.0 (4.8) µg, P<0.01, and 10.5 (7.7) vs 22.8 (4.3) mg, P<0.05].

Ultrasonographic guidance enables exact placement of the local anaesthetic for TAP blocks. In patients undergoing laparoscopic cholecystectomy under standard general anaesthetic, ultrasound-guided TAP block substantially reduced the perioperative opioid consumption.

A questionnaire on the use of guidelines was completed by 629 College Fellows. This presented three anaesthetic scenarios, each of which involved a deviation from a guideline, and asked respondents to rate their beliefs about the likely outcome of the violation, the level of social approval they would have for violating, the amount of control they would have over violating, and the practice of their peers with regard to violating.

In all three scenarios, beliefs about the outcome of violating and the amount of control over violating predicted respondents’ self-reported likelihood that they would commit the violation. In two scenarios, beliefs about the practice of peers predicted violating. Level of social approval predicted violating in one scenario only.

Anaesthetists’ decisions to follow or deviate from guidelines are influenced by the beliefs they hold about the consequences of their actions, the direct or indirect influence of others, and the presence of factors that encourage or facilitate particular courses of action.

Twenty-three ASA I–II grade female patients, aged 23–66 yr undergoing elective thyroidectomy were enrolled in this study. EC₅₀ and EC₉₅ of remifentanil for preventing cough were determined using Dixon's up-and-down method and probit analysis. Propofol effect site concentration at extubation, mean arterial pressure, and heart rate (HR) were compared in patients with smooth emergence and without smooth emergence.

Three out of 11 patients with remifentanil Ce of 1.5 ng ml^–1 and all seven patients with Ce of 2.0 ng ml^–1 did not cough during emergence; the EC₅₀ of remifentanil that suppressed coughing was 1.46 ng ml^–1 by Dixon's up-and-down method, and EC₉₅ was 2.14 ng ml^–1 by probit analysis. Effect site concentration of propofol at awakening was similar in patients with a smooth emergence and those without smooth emergence, but HR and arterial pressure were higher in those who coughed during emergence. Clinically significant hypoventilation was not seen in any patient.

We found that the EC₉₅ of effect site concentration of remifentanil to suppress coughing at emergence from anaesthesia was 2.14 ng ml^–1. Maintaining an established Ce of remifentanil is a reliable method of abolishing cough and thereby targeting smooth emergence from anaesthesia.

PFA-100^® with adenosine-5'-diphosphate (ADPCT) and epinephrine (EPICT) cartridges were measured before operation in consecutive patients undergoing elective total knee replacement and taking different COX inhibitors. Surgery and anaesthesia were performed by the same team using standardized techniques. Intraoperative blood loss and postoperative drain output were recorded by anaesthetists and nurses blinded to the PFA-100^® measurements. Surgeons, similarly blinded, were asked to rate the quality of haemostasis. Correlation was sought between these data and PFA-100^® measurements.

Thirty patients were studied, involving 51 knees. Preoperative PFA-100^® EPICT was correlated with drain output (r=0.30, P=0.03). The correlation becomes stronger when a 20% in vitro haemodiluted sample was used for measurement (r=0.42, P=0.01). Receiver-operating characteristic curve analysis using the diluted measurements [area under curve (AUC) 0.74 (95% CI 0.54–0.94)] suggested using a cut-off value of 188 s for EPICT, which will predict excessive drain output with 89% sensitivity, 54% specificity, and a likelihood ratio of 1.93. Diluted EPICT was also correlated with surgeon rating of haemostasis (r=0.36, P=0.04) although none of the measurements correlated with intraoperative blood loss.

Preoperative PFA-100^® prolongation is correlated with increased postoperative drain output. It can be a potentially useful preoperative measurement in patients taking COX inhibitors.

A blood products transfusion algorithm was developed using retrospective data from 42 elective patients (Group A). Two units of platelet concentrate were transfused after cardiopulmonary bypass, followed by 4 u of FFP if bleeding persisted, if platelet count was ≤100x10³ µl^–1 when removing the aortic clamp, and vice versa if platelet count was >100x10³ µl^–1. The trigger for each therapy step was ≥60 g blood absorbed from the mediastinal wound area by dry swabs in 5 min. Assignment to two prospective groups was neither randomized nor blinded; Group B (n=5) was treated according to the algorithm, Group C (n=10) received fibrinogen concentrate (Haemocomplettan^® P/Riastap, CSL Behring, Marburg, Germany) before the algorithm-based therapy.

A mean of 5.7 (0.7) g fibrinogen concentrate decreased blood loss to below the transfusion trigger level in all Group C patients. Group C had reduced transfusion [mean 0.7 (range 0–4) u vs 8.5 (5.3) in Group A and 8.2 (2.3) in Group B] and reduced postoperative bleeding [366 (199) ml vs 793 (560) in Group A and 716 (219) in Group B].

In this pilot study, FIBTEM-guided fibrinogen concentrate administration was associated with reduced transfusion requirements and 24 h postoperative bleeding in patients undergoing AV–AA.

Blood samples from six healthy volunteers were diluted 1:5 v/v with saline keeping haematocrit at 24% using red cell concentrates. We measured coagulation factors and thrombin generation in plasma at baseline and after dilution. Thromboelastometry was used to evaluate (i) speed and quality of clot formation in diluted samples supplemented with fibrinogen 50–300 mg dl^–1 and (ii) clot resistance to fibrinolysis. Diluted and undiluted samples with no added fibrinogen served as controls.

Coagulation parameters and platelets were reduced by 74–85% after dilution. Peak thrombin generation was reduced by 56%. Adding fibrinogen led to a concentration-dependent improvement of all thromboelastometric parameters. The half maximal effective concentration (EC50) for fibrinogen replacement in haemodiluted blood was calculated to be 125 mg dl^–1. Adding tissue plasminogen activator, 0.15 µg ml^–1, led to a decrease of clot firmness and lysis time.

The target plasma concentration for fibrinogen replacement was predicted by these in vitro results to be greater than 200 mg dl^–1 as only these concentrations optimized the rate of clot formation. This concentration is twice the level suggested by the current transfusion guidelines. Although improved, clots were prone to fibrinolysis indicating that the efficacy of fibrinogen therapy may be influenced by co-existing fibrinolytic tendency occurring during dilutional coagulopathy.

Three doses of norepinephrine (0.05, 0.1, and 0.15 µg kg^–1 min^–1 for 20 min each) were infused in nine healthy subjects [six males; 26 (6) yr, mean (sd)]. MAP, cerebral oxygenation characterized by frontal lobe oxygenation (Sc_o2) and internal jugular venous oxygen saturation (Sjv_o2), middle cerebral artery mean flow velocity (MCA Vmean), cardiac output (CO), and arterial partial pressure for carbon dioxide (Pa_co2) were evaluated.

MAP increased from 88 (79–101) [median (range)] to 115 (98–128) mm Hg with increasing doses of norepinephrine (P < 0.05), reflecting an increase in total peripheral resistance [20.3 (12.2–25.8) to 25.2 (16.4–28.5) mm Hg min litre^–1; P < 0.05] since CO remained at baseline values. Sc_o2 and Sjv_o2 decreased with increasing doses of norepinephrine, reaching statistical significance with norepinephrine infused at 0.1 µg kg^–1 min^–1 [Sc_o2: 78 (75–94) to 69 (61–83)%; P < 0.05; Sjv_o2: 67 (8) to 64 (7)%; P < 0.01]. MCA Vmean was reduced with each dose of norepinephrine [56.9 (11.2) to 55.0 (11.7) cm s^–1; P < 0.05] and Pa_co2 lowered from 5.4 (0.4) to 5.1 (0.4) kPa (P < 0.001).

This study suggests that infusion of norepinephrine at 0.1 µg kg^–1 min^–1 or higher may negatively affect cerebral oxygenation.

Seventy women were randomized in two groups to receive either phenylephrine at a rate of 16.6 µg min^–1 (concentration 1µg ml^–1) or ephedrine at a rate of 1.5 mg min^–1 (concentration 90 µg ml^–1). Patients received varying doses of hyperbaric bupivacaine with fentanyl 25 µg using a double-blinded, up-down sequential allocation design. Effective doses were defined as anaesthesia to touch with ethyl chloride spray to the xiphisternum within 20 min.

The ED50 estimates of bupivacaine were similar in the two groups: 7.8 mg [95% confidence interval (CI) 6.7–8.9] with phenylephrine and 7.6 mg (95% CI 6.8–8.4) with ephedrine. Systolic blood pressure control was similar (P=0.18) with vasopressors but heart rate was higher with ephedrine (P=0.0014).

Under the conditions of this study, we have shown that when phenylephrine or ephedrine were used to prevent post-spinal hypotension, the dosing requirement of hyperbaric bupivacaine was similar for intrathecal anaesthesia.

Forty-two women with severe pre-eclampsia were randomly assigned to receive either remifentanil 1 µg kg^–1 (n=21) or saline (n=21) over 30 s before induction of anaesthesia using thiopentone 4 mg kg^–1 and suxamethonium 1.5 mg kg^–1. Mean arterial pressure (MAP), heart rate (HR) and BIS values as well as plasma catecholamine concentrations were measured. Neonatal effects were assessed using Apgar scores and umbilical cord blood gas analysis.

Induction with thiopentone caused a reduction in MAP and BIS in both remifentanil and control groups. Following the tracheal intubation MAP and HR increased in both groups, the magnitude of which was lower in the remifentanil group. BIS values also increased, of which magnitude did not differ between the groups. Norepinephrine concentrations increased significantly following the intubation in the control, while remained unaltered in the remifentanil group. The neonatal Apgar scores at 1 min were significantly lower in the remifentanil group than in the control. However, Apgar scores at 5 min, and umbilical artery and vein blood gas values were similar between the groups.

These results suggest that a single bolus of 1 µg kg^–1 remifentanil effectively attenuates haemodynamic but not BIS responses to tracheal intubation in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia. However, its use was associated with maternal hypotension and neonatal respiratory depression requiring resuscitation.

Ninety children, <5 yr, undergoing catheterization through the right internal jugular vein were enrolled. The insertion depth was determined as follows. The insertion point was designated as ‘Point I’. The sternal head of the right clavicle was called ‘Point A’ and the midpoint of the perpendicular line drawn from Point A to the line connecting both nipples was called ‘Point B’. The insertion depth of CVC was determined by adding the two distances (from I to A and from A to B) and subtracting 0.5 cm from this. A chest radiography was taken and the distance of the CVC tip from the carina level was measured by the Picture Archiving and Communicating System.

The mean distance of the CVC tip from the carina level was 0.1 (1.0) (P=0.293) cm above the carina (95% CI 0.1 cm below the carina–0.3 cm above the carina). There was no specific relationship between the distance of the CVC tip from the carina level and the patients’ age, height, and weight.

The CVC tip could be placed near the carina by using the external landmarks without any formulae, images, and devices in children in our study.

Case studies were conducted comprising documentary review and semi-structured interviews (71) with anaesthetists, surgeons, nurses, other health professionals, and managers working in and around three broadly typical acute pain services.

Although the precise details differed to some degree, the three acute pain services all faced the same broad range of inter-related challenges identified in the organizational change literature (i.e. structural, political, cultural, educational, emotional, and physical/technological challenges). The services were largely isolated from wider organizational objectives and activities and struggled to engage other health professionals in improving postoperative pain management against a background of limited resources, turbulent organizational change, and inter- and intra-professional politics. Despite considerable efforts they struggled to address these challenges effectively.

The literature on organizational change and quality improvement in health care suggests that it is only by addressing the multiple challenges in a comprehensive way across all levels of the organization and health-care system that sustained improvements in patient care can be secured. This helps to explain why the hard work and commitment of acute pain services over the years have not always resulted in significant improvements in routine postoperative pain management for all surgical patients. Using this literature and adopting a whole-organization quality improvement approach tailored to local circumstances may produce a step-change in the quality of routine postoperative pain management.

Sixty patients with an adequate level of spinal block after standardized administration of plain bupivacaine 20 mg in men and of 17.5 mg in women were studied. To measure the CSF bupivacaine concentration, we performed a second lumbar spinal puncture and obtained a CSF sample at a randomized time point 5–45 min after the bupivacaine injection. In addition, we calculated the half-life of bupivacaine in the CSF and tested the hypothesis that the level of spinal block is related to the lumbar CSF bupivacaine concentration.

Men and women had CSF bupivacaine concentrations ranging from 95.4 to 773.0 µg ml^–1 (median 242.4 µg ml^–1) and from 25.9 to 781.0 µg ml^–1 (median 187.6 µg ml^–1), respectively. The large variability of bupivacaine concentrations obtained at similar times after subarachnoid administration made calculation of a meaningful half-life of bupivacaine in CSF impossible. There was no association between CSF bupivacaine concentration and spinal block level, and CSF bupivacaine concentrations for the same spinal block level differed between patients by six-fold.

There is a large variability of CSF bupivacaine concentrations in patients with an adequate level of spinal anaesthesia.

All patients with inadequate block after subarachnoid injection of plain bupivacaine 0.5% and in whom a second subarachnoid injection of LA was to be performed as a rescue technique were eligible for entry into this study. A CSF sample was withdrawn immediately before injection of the second dose of LA. Patients in whom failure was obviously due to technical problems or inadequate dosage were excluded. Bupivacaine concentrations were assessed with high-performance liquid chromatography.

During the study period of 15 months, 2600 spinal anaesthetics were performed. The failure rate was 2.7% (71 patients). In 20 patients (0.77%), CSF concentrations of bupivacaine were determined, which ranged from 3.36 to 1020 µg ml^–1.

Inadequate CSF concentration of LA is a common reason for FSA. However, in 12 of our 20 patients, concentrations were above 73 µg ml^–1, a concentration that should lead to an adequate block. In these patients, maldistribution of bupivacaine could be responsible for FSA. In view of the absence of sufficient block, despite adequate lumbar CSF concentrations of bupivacaine, concerns about neurotoxicity with repeat injections may be warranted.

We evaluated the feasibility of performing real-time US-guided paramedian epidural access with the epidural needle inserted in the plane of the US beam in 15 adults who were undergoing groin or lower limb surgery under an epidural or combined spinal–epidural anaesthesia.

The epidural space was successfully identified in 14 of 15 (93.3%) patients in 1 (1–3) attempt using the technique described. There was a failure to locate the epidural space in one elderly man. In 8 of 15 (53.3%) patients, studied neuraxial changes, that is, anterior displacement of the posterior dura and widening of the posterior epidural space, were seen immediately after entry of the Tuohy needle and expulsion of the pressurized saline from the LOR syringe into the epidural space at the level of needle insertion. Compression of the thecal sac was also seen in two of these patients. There were no inadvertent dural punctures or complications directly related to the technique described. Anaesthesia adequate for surgery developed in all patients after the initial spinal or epidural injection and recovery from the epidural or spinal anaesthesia was also uneventful.

We have demonstrated the successful use of real-time US guidance in combination with LOR to saline for paramedian epidural access with the epidural needle inserted in the plane of the US beam.

Forty-two patients scheduled for hallux valgus repair were studied. Sciatic block at the popliteal fossa was accomplished using nerve stimulation. When a motor response was elicited at <0.5 mA (2 Hz, 0.1 ms), 40 ml of local anaesthetic (LA) was injected. Using ultrasound (Titan, Sonosite, 5–10 MHz), the diameters and area of the SN were measured before and after the injection. The presence of nerve swelling and proximal or distal diffusion of LA were also assessed. Intraneural injection was defined as nerve area (NA) increase of ≥15% and one or more additional ultrasonographic markers (nerve swelling, proximal–distal diffusion within epineural tissue). Clinical neurological evaluation was performed 1 week after the block.

Post-injection NA increase ≥15% was seen in 32 (76%) patients [0.54 (sd 0.19) cm^–2 vs 0.76 (0.24) cm^–2; P<0.05]. Nerve swelling with fascicular separation was observed in 37 (88%) patients; proximal and distal diffusion of LA were present in six (14%) and 14 (38%) patients, respectively. Intraneural injection criteria were met in 28 (66%) patients. Greater NA increase was present in patients with fast block onset [61 (45) vs 25 (33)%; (Dif 35% 95% CI 61–9%); P<0.05]. No patient developed neurological complications.

Intraneural (subepineural) injection is a common occurrence after nerve stimulator-guided SN block at the popliteal fossa, yet it may not inevitably lead to neurological complications.

Sixty patients with BMI >30 kg m^–2 were randomized, after induction of pneumoperitoneum, to receive either PEEP of 10 cm H₂O (Group P), inspiratory pressure of 40 cm H₂O for 15 s once (Group R), Group R recruitment followed by PEEP 10 cm H₂O (Group RP), or Group RP recruitment but with the inspiratory manoeuvre repeated every 10 min (Group RRP). Static respiratory compliance and Pa_o2 were determined after intubation, 10 min after pneumoperitoneum (before lung recruitment), and every 10 min thereafter (after recruitment). Results are presented as mean (sd).

Pneumoperitoneum decreased respiratory compliance from 48 (3) to 30 (1) ml cm H₂O^–1 and decreased Pa_o2 from 12.4 (0.3) to 8.8 (0.3) kPa in all groups (P<0.01). Immediately after recruitment, compliance was 32 (1), 32 (2), 40 (2), and 40 (1) ml cm H₂O^–1 and Pa_o2 was 9.1 (0.3), 9.1 (0.1), 11.9 (0.1), and 11.9 (0.1) kPa in Groups P, R, RP, and RRP, respectively (P<0.01). Ten and 20 min later, Pa_o2 in Group R decreased to 9.2 (0.1) kPa and compliance in Group PR decreased to 33 (2) ml cm H₂O^–1, respectively (P<0.01).

Group RRP recruitment strategy was associated with the best intraoperative respiratory compliance and Pa_o2 in obese patients undergoing laparoscopic gastric banding.

In this prospective trial, 201 patients were randomized into six groups to receive rocuronium at a dose of 0.6 or 1.0 mg kg^–1 during propofol–remifentanil–nitrous oxide anaesthesia. The tracheal intubation was performed after maximal neuromuscular block by acceleromyography at the thumb (AP), the eyelid (OO), and the superciliary arch (CS). The onset time, intubating conditions, peak vital signs, and bispectral index were assessed.

The onset time of rocuronium in the OO and CS muscle was significantly shorter than in the AP muscle (P<0.001), but excellent intubating conditions were significantly increased in the AP (87%) and the CS (77%) compared with the OO (32%) after a dose of 0.6 mg kg^–1 of rocuronium (P<0.05).

After administration of rocuronium, twitch monitoring at the OO allows a faster intubation but is associated with an unacceptable incidence of inadequate intubating conditions. Excellent intubating conditions are observed most frequently with AP monitoring but with the longest delay before intubation is attempted. Monitoring of the CS allows intubation earlier than that of AP with fewer patients having excellent but no patients having inadequate intubating conditions.

(i) (a) A static test of 11 Whisperflow devices examining maximum flow generation with no load and with 2.5, 5, 7.5, 10, 15, and 20 cm H₂O valve loading, at varying Fi_o2. (b) CPAP valves (Accu-peep®, Vital Signs, Totowa, NJ, USA) were tested by measuring mean upstream pressure at varying flows in five valves (2.5, 5, 7.5, 10, 15, and 20 cm H₂O). (ii) We measured the mean and minimum inspiratory mask pressure generated by a representative Whisperflow device in a model of spontaneous respiration. Measurements were made with combinations of Fi_o2, ventilatory frequency, tidal volume, and valve loading similar to those encountered in clinical practice.

(i) (a) The flow generated by the Whisperflow valves decreases with increasing valve load and increasing Fi_o2 (from 140 to 20 litre min^–1). (b) The CPAP valves maintain the required pressure within acceptable limits against varying flow. (ii) At all permutations, the mean inspiratory mask pressure was significantly lower than that required. At high inspiratory flow rates, the minimum inspiratory pressure approached atmospheric pressure.

The Whisperflow may not perform as expected. Clinicians should be cautious when using this device, particularly with high Fi_o2 and CPAP valve load. The flow setting should be set at maximum. Failure of CPAP therapy may be due to failure of the generator. Further in vivo data are required.

Seventy-five patients were randomly assigned to receive tight heart rate (HR) control by a continuous infusion of: esmolol in combination with the PDE III inhibitor enoximone (esmolol+enoximone group), esmolol infusion alone (esmolol group), or standard therapy (control group) for a period of 48 h. Myocardial ischaemia and dysfunction were detected by serial plasma Troponin T (TnT) and B-type natriuretic peptide (BNP) measurements.

Cardiac index (CI) increased significantly only in esmolol+enoximone-treated patients [CI: from 2.4 (0.2) litre min^–1 m^–2 at baseline to 3.2 (0.2) litre min^–1 m^–2 at 24 h after surgery; P=0.001] and was significantly higher than in the esmolol [CI: from 2.5 (0.2) litre min^–1 m^–2 at baseline to 2.6 (0.2) litre min^–1 m^–2 at 24 h; P=0.18] and the control groups [CI: from 2.4 (0.2) litre min^–1 m^–2 at baseline to 2.7 (0.2) litre min^–1 m^–2 at 24 h; P=0.13]. A significant postoperative release of TnT was detected only in control patients. Plasma BNP levels increased towards the end of surgery in all patients. Peak plasma BNP concentrations were significantly higher in control patients [293 (98) pg ml^–1] than in esmolol [118 (71) pg ml^–1] and in esmolol+enoximone-treated patients [78 (21) pg ml^–1].

Inotropic therapy with the P