Validation of direct intraabdominal pressure measurement using a continuous indwelling compartment pressure monitor.

BACKGROUND: According to recommendations, intraabdominal pressure should be monitored every 8 hours for patients at high risk of abdominal compartment syndrome. Continuous intraabdominal pressure monitoring may be valuable for these patients. METHODS: For 15 patients undergoing laparoscopic surgery, a pressure monitor was introduced after formation of pneumoperitoneum. During the procedure, the laparoscopic insufflator pressure was varied. The pressure monitor values and the time to equilibrium were recorded. RESULTS: Altogether, 152 pressure recordings were taken for the patients studied. The measurements from the insufflator and pressure monitor were compared using a Bland-Altman plot. The mean difference between the techniques was 0.04 +/- 3.8, and 95% of the points from the pressure monitor were within two standard deviations of the mean difference. Pressure changes were essentially "real time." CONCLUSIONS: The intracompartmental pressure monitor provides accurate, rapid, and direct measurement of intraabdominal pressure, and may be a useful tool for continuous intraabdominal pressure measurement among patients at risk of abdominal compartment syndrome.

Liver tissue partial pressure of oxygen and carbon dioxide during partial hepatectomy.

BACKGROUND: Data on tissue oxygen partial pressure (PtO2) and carbon dioxide partial pressure (PtCO2) in human liver tissue are limited. We set out to measure changes in liver PtO2 and PtCO2 during changes in ventilation and a 10 min period of ischaemia in patients undergoing liver resection using a multiple sensor (Paratrend Diametrics Medical Ltd, High Wycombe, UK). METHODS: Liver tissue oxygenation was measured in anaesthetized patients undergoing liver resection using a sensor inserted under the liver capsule. PtO2 and PtCO2 were recorded with FIO2 values of 0.3 and 1.0, at end-tidal carbon dioxide partial pressures of 3.5 and 4.5 kPa and 10 min after the onset of liver ischaemia (Pringle manoeuvre). RESULTS: Data are expressed as median (interquartile range). Increasing the FIO2 from 0.3 to 1.0 resulted in the PtO2 changing from 4.1 (2.6-5.4) to 4.6 (3.8-5.2) kPa, but this was not significant. During the 10 min period of ischaemia PtCO2 increased significantly (P<0.05) from 6.7 (5.8-7.0) to 11.5 (9.7-15.3) kPa and PtO2 decreased, but not significantly, from 4.3 (3.5-12.0) to 3.3 (0.9-4.1) kPa. CONCLUSION: PtO2 and PtCO2 were measured directly using a Paratrend sensor in human liver tissue. During anaesthesia, changes in ventilation and liver blood flow caused predictable changes in PtCO2.

Does neostigmine increase gastric emptying in the critically ill?--results of a pilot study.

OBJECTIVE: Based on the successful use of neostigmine for the treatment of acute colonic pseudo-obstruction, we hypothesised that neostigmine would increase gastric emptying and improve tolerance to enteral feeding in the critically ill patient. METHODS: Eleven patients intolerant of enteral feeds due to high gastric aspirates, were randomised to receive a 'study infusion' consisting of either neostigmine (0.4 mg/hr) or 0.9% saline. If, after 12 hours the patient was deemed intolerant of the nasogastric feed, the rate of the 'study infusion' was doubled. Those who remained intolerant after 24 hours of the 'study infusion' were 'crossed-over' and continued on the other infusion for a further 24 hours. Gastric emptying was assessed in each group before and after the infusion by measuring the hourly rates of feed "absorption" [(delivery rate + returned aspirates) - total aspirates] and paracetamol absorption using the area under a time-concentration curve at 120 minutes (AUC120). Differences within and between groups were analysed using Students t test and one-way analysis of variance. RESULTS: Six patients received neostigmine first and 5 received the placebo first. Four of the 6 patients receiving the neostigmine first compared with all of those receiving placebo first required to be 'crossed-over' to the other infusion. While the hourly rates of feed "absorption" were greater for patients receiving neostigmine than for placebo, these differences did not achieve statistical significance. The mean paracetamol AUC120 for all patients who received neostigmine was 3996 mg/min/L while that for placebo was 1929 mg/min/L (p = 0.21). CONCLUSIONS: These data suggest that while neostigmine may have a positive effect on gastric emptying and enteral feed absorption in critically ill patients, the results did not reach statistical significance and an adequately powered study will be required to confirm this effect.

Effects of propofol and nitrous oxide on middle cerebral artery flow velocity and cerebral autoregulation.

We studied the effects of adding 50% nitrous oxide to propofol anaesthesia administered by target-controlled infusion on middle cerebral artery flow velocity and autoregulatory indices derived from transient hyperaemic response tests. Nine healthy (ASA 1) adult patients scheduled to undergo elective surgery were recruited. A standardised anaesthetic comprising alfentanil 10 microg x kg(-1), propofol via a target-controlled infusion pump and vecuronium 0.1 mg x kg(-1) was used. Transcranial Doppler ultrasonography was used to measure middle cerebral artery (MCA) blood flow velocity and the transient hyperaemic response test was used to assess cerebral autoregulation. These measurements were performed while awake and then at an induction target concentration of propofol (the target at which consciousness was lost, mean 6.2 (SD 1.1) microg x ml(-1)). The measurements were repeated after the addition of 50% nitrous oxide to the breathing gas mixture. Propofol caused a significant decrease in MCA flow velocity and a significant increase in the strength of autoregulation. The addition of nitrous oxide had no significant effect on MCA flow velocity or cerebral autoregulation. These results suggest that addition of 50% nitrous oxide does not influence propofol-induced changes in cerebral haemodynamics.

Effects of desflurane on cerebral autoregulation.

The aim of this study was to determine the effects of desflurane, at 1 and 1.5 MAC, on cerebral autoregulation. Data were analysed from eight patients undergoing non-neurosurgical procedure. The blood flow velocity in the middle cerebral artery was measured by transcranial Doppler ultrasound and cerebral autoregulation was assessed by the transient hyperaemic response test. Partial pressure of the end-tidal carbon dioxide (PE'(CO(2))) and mean arterial pressure were measured throughout the study. Anaesthesia was induced with propofol and was maintained with desflurane at end-tidal concentrations of 7.4% (1 MAC) or 10.8% (1.5 MAC). The order of administration of the desflurane concentrations was determined randomly and a period of 15 min was allowed for equilibration at each concentration. The transient hyperaemic response tests were performed before induction of anaesthesia and after equilibration with each concentration of desflurane. An infusion of phenylephrine was used to maintain pre-induction mean arterial pressure and ventilation was adjusted to maintain the pre-induction value of PE'(CO(2)) throughout the study. Two indices derived from the transient hyperaemic response test (the transient hyperaemic response ratio and the strength of autoregulation) were used to assess cerebral autoregulation. Desflurane resulted in a marked and significant impairment in cerebral autoregulation; at concentrations of 1.5 MAC, autoregulation was almost abolished.

A comparison of the transient hyperemic response test and the static autoregulation test to assess graded impairment in cerebral autoregulation during propofol, desflurane, and nitrous oxide anesthesia.

UNLABELLED: The transient hyperemic response (THR) test has been used to assess cerebral autoregulation in anesthesia and intensive care. To date it has not been compared with the static autoregulation test for assessing graded changes in cerebral autoregulation. We compared the two tests during propofol, desflurane, and nitrous oxide anesthesia. Seven subjects were studied. For the THR test, changes in the middle artery blood flow velocity were assessed during and after a 10-s compression of the ipsilateral common carotid artery. Two indices of autoregulation--THR ratio (THRR) and strength of autoregulation (SA)--were calculated. For the test of static autoregulation, changes in the middle cerebral artery flow velocity after a phenylephrine-induces increase in mean arterial pressure were assessed, and the static rate of regulation (sROR) was calculated. The tests were performed before induction and after equilibrium at 0.5 minimum alveolar anesthetic concentration (MAC) and then at 1.5 MAC of desflurane. THRR, SA and sROR decreased significantly (P < 0.001) at 0.5 MAC and then at 1.5 MAC desflurane. CHanges in THRR and SA reflected the changes in sROR with a sensitivity of 100%. IMPLICATIONS: When compared with the established test of static autoregulation, the transient hyperemic response test provides a valid method for assessing graded impairment in cerebral autoregulation.

Video imaging to assess neuromuscular blockade at the larynx.

UNLABELLED: We describe video imaging as a technique for assessing neuromuscular blockade at the larynx. We sought to determine the stability and reproducibility of this technique and to compare the effect of succinylcholine at the adductor pollicis and the larynx. Ten patients were studied. Anesthesia was induced and maintained with propofol. The recurrent laryngeal nerve was stimulated superficially and movements of the vocal cords were recorded on videotape by using a fiberoptic bronchoscope passed via a laryngeal mask airway. Neuromuscular function was recorded at the adductor pollicis by using a mechanomyograph. Twenty images of the vocal cords were examined repeatedly by one investigator and by ten independent observers. The mean difference between the two sets of observations was 0.86 degrees with a correlation coefficient (r) of 0.997. For 3 min before the administration of relaxant the coefficient of variation in the cord movement during supramaximal stimulation ranged from 1%-4% (median 2.7%). After the administration of succinylcholine 1 mg. kg(-1) the times to loss of T1 at the larynx and hand were 63 +/- 15 s and 63 +/- 12 s respectively. Times to 25% recovery were 215 +/- 36 s at the larynx and 436 +/- 74 s at the hand and times to 75% recovery were 285 +/- 55 s and 525 +/- 85 s respectively. These results indicate that video imaging may be a useful research technique for estimating neuromuscular blockade at the larynx and that the time to onset of succinylcholine at the larynx is similar to that at the hand, whereas the duration of blockade is significantly shorter at the larynx. IMPLICATIONS: Assessment of neuromuscular blockade at the larynx is possible by using a video imaging technique. By using this technique, the time to onset of neuromuscular blockade at the larynx is similar to that at the hand after the administration of succinylcholine; this finding is different from previously published data obtained by using a cuff pressure measurement technique.

New developments in anaesthesia for neurological surgery.

The present review concentrates on the advances that have been made in three areas. First, the cerebrovascular effects of anaesthetic agents used for neurological surgery are considered. Second, recent data relating to the use of remifentanil are reviewed. Finally, two recent papers that have examined the place of anticoagulation in patients undergoing neurological surgery are evaluated.

Influence of metoclopramide on plasma cholinesterase and duration of action of mivacurium.

Mivacurium is metabolized by plasma cholinesterase (PCHE). Metoclopramide inhibits PCHE in vitro and in vivo. We have assessed the effect of metoclopramide on duration of action of mivacurium and measured PCHE at baseline and at the time of maximal block. In a randomized, double-blind study, 30 patients received metoclopramide 0.15 mg kg-1 i.v. or saline, followed by propofol anaesthesia and mivacurium 0.15 mg kg-1. Using a TOF-Guard accelerometer, times to recovery of TI to 25%, 75% and 90% were 13.4, 19.3 and 21.9 min in the saline group and 17.8, 25.3 and 28.8 min in the metoclopramide group (P < 0.01, P < 0.05, P < 0.05, respectively). There were no differences in onset time or recovery index between the groups. PCHE activity at the time of maximum block decreased within each group (P < 0.01) but there was no difference between groups. In a second biochemical study of eight patients, a small decrease in PCHE activity was detected after metoclopramide 0.15 mg kg-1, but before administration of mivacurium (P < 0.025). We conclude that metoclopramide prolongs the duration of action of mivacurium.

Effect of cricoid pressure on gastro-oesophageal reflux in awake subjects.

This study aimed to evaluate whether cricoid pressure is associated with a high risk of gastro-oesophageal reflux. Fifteen awake, fasted volunteers were studied. A cricoid pressure of 44 N was applied for 60 s by resting a padded yoke over the cricoid cartilage. Using continuous oesophageal pH monitoring, no volunteer had gastro-oesophageal reflux during cricoid pressure, although one subject had a reflux spike soon after relieving cricoid pressure. We conclude with 95% confidence that the incidence of gastro-oesophageal reflux during cricoid pressure is not more than 20%.

The effects of sevoflurane and nitrous oxide on middle cerebral artery blood flow velocity and transient hyperemic response.

UNLABELLED: We studied the effects of sevoflurane, with and without nitrous oxide, on the indices of cerebral autoregulation (transient hyperemic response ratio and the strength of autoregulation) derived from the transient hyperemic response (THR) test. Twelve patients (ASA physical status I or II) aged 18-40 yr presenting for routine non-neurosurgical procedures were recruited. The middle cerebral artery blood flow velocity was continuously recorded using transcranial Doppler ultrasonography. Preinduction THR tests were performed before the patients were anesthetized with alfentanil, propofol, and vecuronium. End-tidal carbon dioxide concentration and mean arterial pressure (to within 10% with a phenylephrine infusion) were maintained at their preinduction values. THR tests were performed sequentially at the following end-tidal sevoflurane concentrations: 2.2% in oxygen, 3.4% in oxygen, 3.4% with 50% nitrous oxide in oxygen, and 2.2% with 50% nitrous oxide in oxygen. Neither 2.2% nor 3.4% sevoflurane significantly affected cerebral autoregulation. The addition of 50% nitrous oxide to the 2.2%, but not the 3.4%, concentration of sevoflurane increased middle cerebral artery blood flow velocity and decreased autoregulatory indices significantly. IMPLICATIONS: Transient hyperemic response is preserved during sevoflurane anesthesia but is significantly impaired when nitrous oxide is added to the lower concentration of sevoflurane (2.2%). These findings have implications for neurosurgical patients undergoing general anesthesia.

The effects of nitrous oxide and oxygen on transient hyperemic response in human volunteers.

UNLABELLED: The aim of this study was to determine the effects of breathing 100% oxygen or 50% nitrous oxide in oxygen on the indices of cerebral autoregulation derived from the transient hyperemic response (THR) test in human volunteers. Data were analyzed from nine healthy subjects. Middle cerebral artery (MCA) blood flow velocity (FV) was measured by transcranial Doppler ultrasound, and the THR test was performed using 10-s compression of the common carotid artery. Continuous measurement of P(ETCO2) and expired fractions of oxygen (F(ETO2)) and nitrous oxide (F(ETN2O)) was established, and mean arterial pressure (MAP) was recorded at 2-min intervals. All measurements were performed while the volunteers were breathing room air and were repeated 10 min after achieving F(ETO2) >0.95 and 10 min after achieving F(ETN2O) 0.48-0.52. Two indices derived from the THR test, the transient hyperemic response ratio (THRR) and strength of autoregulation (SA), were used to assess cerebral autoregulation. P(ETCO2) and mean arterial pressure did not change significantly throughout the study period. Breathing 100% oxygen did not change MCA FV, THRR, or SA. Inhalation of nitrous oxide resulted in a marked and significant increase in the MCA FV (from 48+/-9 to 72+/-8 cm/s; mean +/- SD) and a significant decrease in the THRR (from 1.5+/-0.2 to 1.2+/-0.1) and the SA (from 1.0+/-0.1 to 0.8+/-0.1) (P<0.05 for all). We conclude that breathing 50% nitrous oxide in oxygen results in both a significant increase in MCA FV and impairment of transient hyperemic response. IMPLICATIONS: Our study suggests that nitrous oxide impairs cerebral autoregulation and may have implications for its use in neurosurgical anesthesia and for interpretation of the results from studies of anesthetics in which nitrous oxide is used in the background.

Assessing neuromuscular block at the larynx: the effect of change in resting cuff pressure and a comparison with video imaging in anesthetized humans.

UNLABELLED: Neuromuscular block (NMB) at the larynx has been assessed by measuring the cuff pressure (CP) in an endotracheal tube (ETT) placed between the vocal cords. In this study, we evaluated the decrease in resting cuff pressure (RCP) after the administration of rocuronium and the effect of this decrease on the assessment of NMB, and we compared CP measurement with an alternative technique, video imaging (VI). In 20 patients, NMB was determined at the hand by mechanomyography and at the larynx initially by CP and subsequently by VI, recording images using a fiberoptic bronchoscope via a laryngeal mask. Train-of-four stimuli were applied at both sites. After baseline measurements, the ETT was replaced, and rocuronium was infused to achieve a steady-state 50% (n = 10) or 75% (n = 10) block at the hand. CP measurements were recorded before and after restoration of RCP to prerocuronium pressure, followed by further VI measurements. The mean RCP decreased from 21 +/- 4 to 12 +/- 5 mm Hg after rocuronium. At 50% block at the hand, the CP estimate of block at the larynx with reduced RCP was 62% +/- 18%, and that after restoring RCP was 29% +/- 13%; VI estimated 27% +/- 14% block. At 75% block at the hand, CP and VI estimated 52% +/- 11% and 46% +/- 9% block, respectively (RCP maintained). We conclude that RCP decreases after the administration of rocuronium, that restoring RCP significantly alters CP estimates of NMB, and that VI is in agreement with CP measurement if RCP is maintained at prerelaxant values. IMPLICATIONS: In this study, we show that a muscle relaxant-induced decrease in resting tension at the larynx may confound the assessment of neuromuscular block by cuff pressure measurement. The preliminary data suggest that video imaging may provide a suitable alternative to cuff pressure measurement to assess neuromuscular block at the larynx.

Effects of target-controlled infusion of propofol on the transient hyperaemic response and carbon dioxide reactivity in the middle cerebral artery.

The transient hyperaemic response (THR) of blood flow velocity in the middle cerebral artery (vmca), measured by transcranial Doppler ultrasonography (TCD), can be used to assess cerebral autoregulation. We have studied the effects of propofol administered by target-controlled infusion on vmca, THR and carbon dioxide reactivity. We studied 20 healthy adult patients undergoing elective surgery. A standardized anaesthetic comprising alfentanil 10 micrograms kg-1, propofol via a target-controlled infusor and vecuronium 0.1 mg kg-1 was used in both parts of the study. In the first part, THR tests were performed on 10 subjects while awake and then at an 'induction' target concentration of propofol (the target at which consciousness was lost, mean 6.7 (SD 1.1) micrograms ml-1). In the carbon dioxide study, reactivity was tested in 10 patients while awake and at the 'induction' target concentration of propofol by altering the end-tidal carbon dioxide partial pressure by 1 kPa either side of baseline. Propofol caused a significant decrease in vmca but indices of autoregulation, THR ratio and strength of autoregulation increased significantly. Propofol had no effect on carbon dioxide reactivity. These results suggest that propofol may have a beneficial effect on cerebral haemodynamics.

Alfentanil-mediated analgesia during propofol injection: no evidence for a peripheral action.

We have investigated if alfentanil acts via peripheral opioid receptors to relieve the pain which occurs on injection of propofol. Thirty seconds before induction of anaesthesia and immediately after a tourniquet at 50 mm Hg greater than systolic pressure was inflated on the upper arm, patients were given either placebo (n = 22), alfentanil 1 mg (n = 22) or lignocaine 40 mg (n = 22) via an i.v. cannula in the dorsum of the hand. Pain during injection of propofol was assessed using a three-point verbal rating scale, recorded at 8-s intervals. We found a significant reduction in pain after lignocaine compared with the two other groups (P < 0.001), but there was no difference between the placebo and alfentanil groups. We conclude that alfentanil does not relieve pain on injection with propofol via an action on peripheral opioid receptors when alfentanil is limited to the forearm for 30 s before induction of anaesthesia.

The effect of stabilization on the onset of neuromuscular block when assessed using accelerometry.

Accelerometry is increasingly being used for neuromuscular monitoring. We sought to determine whether this system is sensitive to the period of stabilization of muscle twitch prior to the administration of neuromuscular relaxant. We recruited 20 patients. No premedication was given, and anesthesia was induced with propofol and alfentanil and maintained by a propofol infusion. An accelerometer was attached to each wrist. One of the ulnar nerves was stimulated for 20 min and the other for 3 min using a train-of-four pattern at 15-s intervals. Ten patients then received vecuronium 0.1 mg/kg and a subsequent 10 received atracurium 0.5 mg/kg. The time to onset of maximum block was recorded. The data collected was subjected to a paired t-test with P < 0.05 taken as significant. The mean onset times for patients who received vecuronium was 148.5s for the arms stabilized for 3 min and 151.5s for the arms stabilized for 20 min, and in those who received atracurium it was 138.0s and 130.5s, respectively. We conclude that there is no significant difference in the onset of neuromuscular block with either vecuronium or atracurium after stabilization periods of 3 or 20 min when assessed by accelerometry.