Low-dose Propofol Infusion Research Articles

Effects of Propofol on Cortical Electroencephalograms in the Operation of Glioma-Related Epilepsy

A cortical electroencephalogram (ECoG) is often used for the intraoperative monitoring of epilepsy surgery, and propofol is an important intravenous anesthetic, but its effect on EEGs is unclear. To further clarify the effect of propofol on cortical ECoGs during glioma-related epilepsy surgery and to clarify the possible clinical value. A total of 306 patients with glioma were included in the study. Two hundred thirty-nine with glioma-related epilepsy were included in the epilepsy group, and 67 without glioma-related epilepsy were included in the control group. All patients experienced continuous, real-time ECoG monitoring and long-term follow-up after surgery. After injection of low-dose propofol, the rate of activated ECoGs in the epilepsy group (74%) was significantly higher than in the control group (9%). Furthermore, compared with patients in the untreated group, patients in the treated group had lower rates of early and long-term postoperative seizure frequencies and fewer interictal epileptiform discharges (IEDs). Low-dose infusion of propofol can specifically activate ECoGs in epilepsy patients. Therefore, activated ECoGs might provide an accurate and reliable method for identifying potential epileptic zones during glioma-related epilepsy surgery, resulting in better early and long-term prognoses after epilepsy surgery.

Successful treatment of propofol-related infusion syndrome in critically ill patient receiving low-dose propofol infusion.

Propofol is widely used to sedate agitated patients in intensive care units. However, it can cause a rare but fatal complication, propofol-related infusion syndrome (PRIS). The pathophysiology of PRIS is not clear, and there is no definitive diagnosis and treatment. We report a successfully treated case of PRIS in a critically ill patient receiving low-dose propofol infusion. A 59-year-old male patient complaining of sudden chest pain repeatedly collapsed in an ambulance and the emergency room, and veno-arterial extracorporeal membrane oxygenation was delivered. He was diagnosed with a total occluded left anterior descending coronary artery in coronary angiography. On day 20, he showed arrhythmia, increased creatinine kinase (CK), and increased CK-MB and troponin I, accompanied by unstable hemodynamic status despite high-dose vasopressors. He was administered propofol for 20 days at an average dose of 1.3 mg/kg/hr owing to issues with agitation and ventilator synchrony. We strongly suspected PRIS and immediately discontinued propofol infusion, and he was successfully treated with aggressive supportive care. PRIS can occur in patients administered propofol for a prolonged period at low doses. Thus, clinicians should use propofol with caution for PRIS and change to alternative sedatives for long-term sedation.

Reducing postoperative nausea and vomiting in pediatric patients undergoing anterior cruciate ligament reconstruction: A quality report.

Postoperative nauseaand vomiting after elective outpatient surgery can complicate discharge and increase patient suffering. Within our hospital system, there was variability in the use ofpostoperative nausea and vomiting prophylaxis for patients undergoing anterior cruciate ligament reconstruction, which resulted in variable outcomes. To address this variability, we designed and implemented a standardized postoperative nausea and vomitingprophylaxis guideline for the care of this surgical population. We sought to develop and implement a standardized postoperative nausea and vomitingprophylaxis guideline for all patients presenting for elective ambulatory anterior cruciate ligament reconstruction with the goal of reducing the rate of emesis to ≤5%. We convened a multidisciplinary team to develop a postoperative nausea and vomitingprophylaxis guideline which included administration of dexamethasone, ondansetron, and a low-dose propofol infusion in addition to a femoral and sciatic nerve block and routine ketorolac administration for pain control. Our primary outcome, emesis rate, was tracked using a P-chart. Process measures included use of guideline medications and balancing measures included opioid administration, pain scores, and emergence time. We analyzed postoperative nausea and vomitingoutcomes for 817 patients from January 1, 2014, to December 31, 2018. The baseline postoperative emesis rate for all anesthetizing locations was 17%. Following, guideline implementation, the emesis rate decreased to 5%. Opioid administration was decreased following guideline implementation. The percentage of patients managed without any perioperative opioids increased from 16% in the baseline group to 38% following guideline implementation. The P-chart suggests that the observed reduction in emesis rate represents special cause variation and this reduction was sustained over a two-year period. Implementation of standard postoperative nausea and vomitingguidelines for adolescents undergoing outpatientanterior cruciate ligament reconstruction was associated with lower emesis rates. This reduction in emesis rate may have been due to the concurrent reduction in opioids we observed following guideline implementation.

Nitrous oxide anesthetic versus total intravenous anesthesia for functional endoscopic sinus surgery.

Functional endoscopic sinus surgery is a common procedure for sinonasal disease, frequently performed in the outpatient setting. General anesthesia maintained with total intravenous anesthesia (TIVA) with propofol has been shown to give superior surgical conditions compared to inhaled anesthetics. This study evaluated the effects of TIVA versus a predominantly nitrous oxide (N2 O)-based anesthetic with a low-dose propofol and remifentanil infusion on sinus surgery. Patients were randomized to either a N2 O-based (nitrous oxide with propofol and remifentanil) or TIVA (propofol and remifentanil without nitrous oxide) group. The surgeon was blinded to the anesthetic technique. Surgical field grading was performed in real time by the otolaryngologist every 15 minutes with the Boezaart grading system. There were no statistically significant differences between the Boezaart scores, duration of surgery, or estimated blood loss between the two anesthetic techniques. However, the use of N2 O provided a statistically significant, 38% reduction in time from surgery end to extubation. The TIVA group had significantly decreased mean and median pain scores in the post-anesthesia care unit (PACU). There was no difference in the rate of postoperative nausea and vomiting between the two groups. A N2 O-based anesthetic for functional endoscopic sinus surgery provides similar intraoperative and postoperative conditions when compared to TIVA, while being superior in terms of time to extubation. Although the TIVA group had significantly decreased pain scores, this did not lead to a decrease in pain medicine received in the PACU, and there was no difference between groups in time to discharge. 1b Laryngoscope, 130:E299-E304, 2020.

Awake craniotomy anesthetic management using dexmedetomidine, propofol, and remifentanil.

IntroductionAwake craniotomy allows continuous monitoring of patients’ neurological functions during open surgery. Anesthesiologists have to sedate patients in a way so that they are compliant throughout the whole surgical procedure, nevertheless maintaining adequate analgesia and anxiolysis. Currently, the use of α2-receptor agonist dexmedetomidine as the primary hypnotic–sedative medication is increasing.MethodsNine patients undergoing awake craniotomy were treated with refined monitored anesthesia care (MAC) protocol consisting of a combination of local anesthesia without scalp block, low-dose infusion of dexmedetomidine, propofol, and remifentanil, without the need of airways management.ResultsThe anesthetic protocol applied in our study has the advantage of decreasing the dose of each drug and thus reducing the occurrence of side effects. All patients had smooth and rapid awakenings. The brain remained relaxed during the entire procedure.ConclusionIn our experience, this protocol is safe and effective during awake brain surgery. Nevertheless, prospective randomized trials are necessary to confirm the optimal anesthetic technique to be used.

Fascia iliaca block associated only with deep sedation in high-risk patients, taking P2Y12 receptor inhibitors, for intramedullary femoral fixation in intertrochanteric hip fracture: a series of 3 cases

ObjectiveWe present a series of 3 cases in which the impact in outcome was, first of all, related to the capacity to offer early and safer treatment to some hip fracture high-risk patients using a fascia iliaca block (FIB; ropivacaine 0,5% 20 cc and mepivacaine 1,3% 15 cc, given 30 minutes before incision) associated only with deep sedation, contributing to better practice and outcome. Case reportsAll elderly patients were American Society of Anesthesiologists IV patients, under P2Y12 receptor inhibitors, suffering from an intertrochanteric fracture, and purposed for intramedullary femoral fixation (IMF). All patients have been managed successfully through a deep sedation using a low-dose infusion of propofol and bolus of fentanyl without face mask ventilation, supraglottic device placement, or endotracheal intubation after an FIB. Bispectral index was always greater than 75, and no CO2 retention or respiratory depression was present. No signs of pain or hemodynamic instability were observed. ConclusionsIn these cases, surgery would be postponed if the choice was neuroaxial anesthesia, particularly because of P2Y12 receptor inhibitors' effect.FIB puncture site is distal to the fracture and incision site, but proximal local anesthetic migration through the interfascial planes allows for constant block of femoral nerve and lateral cutaneous of femur nerve and, less constantly, block of obturator. FIB may reduce the risk of perineural hematoma associated with several injections in nerve vicinity of different lumbar plexus branches.Frequently, indications for extramedullary or IMF are overlapping, but IMF is associated with less blood loss and may be managed using a low anesthetic depth if an FIB is done, increasing safety. This way, these less invasive surgical techniques combined with an adjusted anesthetic technique may have a crucial role in high-risk patients, particularly if taking P2Y12 receptor inhibitors. In these cases of IMF, surgical manipulation of sciatic and/or inferior subcostal nerves territories was managed with systemic analgesia and deep sedation.

The Effect of General Anesthesia on the Microelectrode Recordings From Pallidal Neurons in Patients With Dystonia.

The most common anesthetic technique for patients undergoing insertion of deep brain stimulators (DBS) is local anesthesia with or without conscious sedation as this facilitates intraoperative microelectrode recordings (MERs) for target localization. However, general anesthesia (GA) may be needed in some of the patients especially those with dystonia. The purpose of our study was to determine the effects of GA on MERs from pallidal neurons in patients with dystonia undergoing DBS implantation surgery. After IRB approval, we retrospectively reviewed the medical records of all patients who had insertion of DBS from January 2009 to December 2013. Data collected and analyzed included demographics, indications for DBS, targets of insertion, MER, and anesthetic management. From the records we identified patients with dystonia who received GA for DBS insertion. We then compared the MER data under GA with the data from patients who had surgery under local anesthesia only during the same time period. Because of the small sample size, the effects of various anesthetic regiments on MER and localization of target nuclei were compared qualitatively. Of the 435 patients who underwent DBS insertion during the study period, 20 (4.3%) patients had GA for the procedure. Dystonia was the most common indication for GA (16/20 patients, 80%). Good-quality MER data obtained from 10 patients with dystonia under GA was compared with 8 patients who had no sedation for the procedure. Administration of GA made target localization difficult due to suppression of both spontaneous and evoked neuronal discharges from internal globus pallidus. Although not studied systematically, propofol (>100 mcg/kg/min) seemed to suppress pallidal discharges more than GA with a lower dose of propofol (<75 mcg/kg/min), remifentanil, and 0.2% to 0.4% end-tidal sevoflurane or desflurane. Our retrospective review suggests that there was a difference in spontaneous and evoked neuronal discharges with MER performed under GA compared with no sedation. MER recordings during GA appeared most robust during a combination of anesthetics including low-dose propofol infusion, remifentanil, and a low concentration of either sevoflurane or desflurane. Our findings can inform a power analysis to determine the sample size that would be required to prospectively test the hypothesis that there is a difference in spontaneous and evoked neuronal discharges with MER performed under GA compared with no sedation.

Propofol differentially inhibits the release of glutamate, γ-aminobutyric acid and glycine in the spinal dorsal horn of rats.

Propofol (2, 6-diisopropylphenol) is an intravenous anesthetic that is commonly used for the general anesthesia. It is well known that the spinal cord is one of the working targets of general anesthesia including propofol. However, there is a lack of investigation of the effects of propofol on spinal dorsal horn which is important for the sensory transmission of nociceptive signals. The objective of this study was to investigate the effects of increasing dosage of propofol on the release of glutamate (Glu), γ-aminobutyric acid (GABA) and glycine (Gly) in the spinal dorsal horn. The efflux of Glu, GABA or Gly in the spinal dorsal horn of rats was detected using transverse spinal microdialysis under an awake condition and various depths of propofol anesthesia. The infusion rates of propofol were, in order, 400 µg/(kg·min), 600 µg/(kg·min) and 800 µg/(kg·min), with a 20 min infusion period being maintained at each infusion rate. Propofol decreased the glutamate efflux within spinal dorsal horn in a dose-dependent manner, and the maximum decrease was 56.8 ± 6.0% at high-dose propofol infusion producing immobility. The inhibitory GABA and Gly efflux was also decreased about 15-20% at low-dose propofol infusion only producing sedation, but did not continue to drop with higher doses of propofol. Propofol decreased both excitatory and inhibitory amino acids efflux in spinal dorsal horn, and the preferential suppression of the excitatory amino acid might be associated with the analgesic effect of propofol.

Hemiarthroplasty performed under transversus abdominis plane block in a patient with severe cardiorespiratory disease

This report describes the use of a transversus abdominis plane block as the main anaesthetic technique for the performance of a hemiarthroplasty in a patient with severe cardiac and respiratory dysfunction, for whom both general and spinal anaesthesia carried considerable risks. The block was performed in the triangle of Petit posterior to the mid-axillary line, using a landmark technique. A combination of lidocaine 1% (20 ml) and bupivacaine 0.5% (20 ml) was administered. A low-dose propofol infusion was used intra-operatively to relieve anxiety, although the patient breathed spontaneously throughout the procedure and responded to voice commands. The surgery was completed successfully without the need for further analgesia. The patient was alert and comfortable in recovery. First opioid administration was 12 h after surgery. The patient was subsequently discharged to a nursing home, where he succumbed to his primary respiratory disease six months later.

Propofol-induced violent coughing in a patient with Becker′s muscular dystrophy

Propofol anesthesia is often associated with decreased incidence of gagging, coughing or laryngospasm, and provides intense suppression on airway reflex during tracheal intubation and laryngeal mask airway insertion. Propofol pretreatment is also effective in reducing the occurrence of opioid-induced coughing. These benefits are often attributed to bronchodilator and sedative effects of propofol. However, severe coughing following sedative doses of 1% propofol has not been reported so far. We report a rare case of violent coughing following low-dose propofol infusion in a patient with Becker's muscular dystrophy.

Behaviour of spectral entropy, spectral edge frequency 90%, and alpha and beta power parameters during low-dose propofol infusion

BackgroundIn this study we analyse the behaviour, potential clinical application and optimal cortical sampling location of the spectral parameters: (i) relative alpha and beta power; (ii) spectral edge frequency 90%; and (iii) spectral entropy as monitors of moderate propofol-induced sedation. MethodsMulti-channel EEG recorded from 12 ASA 1 (American Society of Anesthesiologists physical status 1) patients during low-dose, target effect-site controlled propofol infusion was used for this analysis. The initial target effect-site concentration was 0.5 μg ml−1 and increased at 4 min intervals in increments of 0.5 to 2 μg ml−1. EEG parameters were calculated for 2 s epochs in the frequency ranges 0.5–32 and 0.5–47 Hz. All parameters were calculated in the channels: P4–O2, P3–O1, F4–C4, F3–C3, F3–F4, and Fp1–Fp2. Sedation was assessed clinically using the OAA/S (observer’s assessment of alertness/sedation) scale. ResultsRelative beta power and spectral entropy increased with increasing propofol effect-site concentration in both the 0.5–47 Hz [F(18, 90) = 3.455, P<0.05 and F(18, 90) = 3.33, P<0.05, respectively] and 0.5–32 Hz frequency range. This effect was significant in each individual channel (P<0.05). No effect was seen of increasing effect-site concentration on relative power in the alpha band. Averaged across all channels, spectral entropy did not outperform relative beta power in either the 0.5–32 Hz [Pk=0.79 vs 0.814 (P>0.05)] or 0.5–47 Hz range [Pk=0.81 vs 0.82 (P>0.05)]. The best performing indicator in any single channel was spectral entropy in the frequency range 0.5–47 Hz in the frontal channel F3–F4 (Pk=0.85). ConclusionsRelative beta power and spectral entropy when considered over the propofol effect-site range studied here increase in value, and correlate well with clinical assessment of sedation.

Spectral Entropy as a Monitor of Depth of Propofol Induced Sedation

The aim of this prospective, observational study was to evaluate State and Response entropy (Entropy(TM) Monitor, GE Healthcare, Finland), indices as measures of moderate ("conscious") sedation in healthy adult patients receiving a low dose propofol infusion. Sedation was evaluated using: (I) the responsiveness component of the OAA/S scale (Observer's Assessment of Alertness/Sedation scale) and (II) multi-channel electroencephalogram (EEG) interpretation by a clinical expert. 12 ASA I patients were recruited. A target-controlled infusion of propofol was administered (using Schnider's pharmacokinetic model) with an initial effect site concentration set to 0.5 microg ml(-1). A 4 minute equilibrium period was allowed. This concentration was increased at 4 minute intervals by 0.5 microg ml(-1) to a maximum of 2.0 microg ml(-1). State (SE) and Response (RE), entropy values were recorded for each 4 minute epoch together with clinical sedation scores (OAA/S) and continuous multi-channel EEG. The multi-channel EEG recorded during the final minute of each 4 minute epoch or "patient/time unit" was presented to a neurophysiologist who assigned a label "sedated/not sedated". SE/RE values were compared in patient/time units with clinical or EEG evidence of sedation versus those without. Mean SE and RE values were less in patient/time units when clinical evidence of sedation was present, [mean = 86.8 (95% CI, 84.0-88.3) and 94.3 (95%CI, 92-96.1)], P = 0.002 and P = 0.001, respectively. In patient/time units assigned the label "sedated" by the clinical neurophysiologist assessing the multi-channel EEG, SE and RE values were less [mean = 87.5 (95% CI, 86.3-88.4) and 95.0 (95% CI, 93.8-96.1)] P = 0.001 and P < 0.001, respectively. A statistically significant decrease in SE and RE values was demonstrated in patient/time units in which clinical or EEG evidence of sedation was present. We conclude that spectral entropy offers potential as a monitor of propofol induced sedation.

The Effect of Electroencephalogram-Targeted High- and Low-Dose Propofol Infusion on Histopathological Damage After Traumatic Brain Injury in the Rat

Propofol is commonly used to sedate patients after traumatic brain injury. However, the dose-dependent neuroprotective effects of propofol after head trauma are unknown. We compared histopathological damage after 6 h of electroencephalogram-targeted high- and low-dose propofol infusion in rats subjected to controlled cortical impact (CCI). Animals were randomly assigned to CCI/propofol with electroencephalogram burst-suppression-ratio 1%-5% (CCI/lowprop), CCI/propofol with burst-suppression-ratio 30%-40% (CCI/highprop), control group CCI/1.0 vol % halothane (CCI/halo), or sham group with halothane anesthesia (SHAM/halo). Brain slices were stained with kresyl violet (KV) and hematoxylin/eosin (HE) to evaluate lesion volume, number of eosinophilic cells, and activation of caspase-3 in the hippocampus. Lesion volume (mm3) and number of eosinophilic cells in the hippocampus did not differ significantly [lesion volumes: CCI/lowprop 31.55 +/- 14.66 (KV) and 53.77 +/- 8.62 (HE); CCI/highprop 33.81 +/- 10.57 (KV) and 52.30 +/- 11.55 (HE); CCI/halo 36.42 +/- 17.06 (KV) and 57.95 +/- 8.49 (HE)]. Activation of caspase-3 occurred in the ipsilateral hippocampus in all CCI-groups. Despite different levels of cortical neuronal function, there were no relevant differences in the short-term histopathological damage. These results challenge the view that the neuroprotective effect of propofol relates to the suppression of cerebral metabolic demand.

Influence of EEG-Targeted High and Low Dose Propofol Infusion on Acute Histopathological Damage After Controlled Cortical Impact in the Rat Brain

s: 33rd Annual Meeting of the Society of Neurosurgical Anesthesia and Critical Care: CEREBRAL PROTECTION/TECHNIQUES

Low-dose Propofol Infusion for Controlling Acute Hyperspasticity after Withdrawal of Intrathecal Baclofen Therapy

Low-dose Propofol Infusion for Controlling Acute Hyperspasticity after Withdrawal of Intrathecal Baclofen Therapy

Left Ventricular Function After Cardiopulmonary Bypass Is Related to the Length-Dependent Regulation of Myocardial Function: In Response

We thank Drs. de Hert and Van der Linden for their insightful comments on our article (1) and we would like to respond on some of the issues brought forward. The aim of our study was two-fold: first, to describe our approach to quantify perioperative LV function, and second, to obtain a reference data set for future studies in patients undergoing cardiac surgery. The comments of de Hert and Van der Linden focus on the latter aspect of our study. We fully agree that the published literature indicates a substantial variability in recovery of LV function after cardiopulmonary bypass, and we acknowledge the extensive list of possible factors influencing this variable outcome. In fact, this is exactly the reason why we felt it was necessary to generate a data set that would be applicable to the anesthetic and cardioprotective approach followed in our institute. Specifically, we use low-dose target-controlled infusion of propofol, remifentanil, and sufentanil, and intermittent antegrade warm-blood cardioplegic arrest during normothermic cardiopulmonary bypass. The metabolic advantages of this approach have already been published, but few data are available on the acute hemodynamic effects. Our study was performed in patients with relatively preserved LV function undergoing elective CABG, to ensure that the possible changes in LV function could be contributed mainly to the effects of anesthesia and cardioplegic arrest, rather than to the surgical intervention. This selection may partly explain the preserved postoperative systolic function in our patient group. However, de Hert et al. studied a similar patient group and reported a more variable outcome that could not be explained by preoperative LV function (2). Therefore, differences in anesthesia and cardioplegic approaches between our study and the studies by de Hert et al. may need to be considered. One such difference is the use of normothermic arrest with blood cardioplegia in our study, whereas the studies of de Hert et al. included the use of hypothermia and crystalloid cardioplegia. This may be important because recent studies indicate less myocardial cell damage after normothermic blood cardioplegia (3). Furthermore, the use of propofol in both studies may not be comparable, because hypothermia has an important influence on propofol pharmacokinetics (4). However, we certainly agree that extrapolation of our findings to patients with poor baseline LV function and prolonged cardiac arrest should be done with caution. But despite this, we would still conclude that the new data provided by our study constitute valuable background information when interpreting the acute hemodynamic effects of complex surgical interventions such as LV reconstruction in heart failure patients in whom the same anesthesia and cardioplegia approach is used. Sven A. F. Tulner Robert J. M. Klautz Gerda L. van Rijk-Zwikker Frank H. M. Engbers Jeroen J. Bax Jan Baan Ernst E. van der Wall Robert A. Dion Paul Steendijk

Propofol in paediatric anaesthesia

In this review we intend to ascertain trends in propofol administration for paediatric anaesthesia and sedation. Propofol is being 'discovered' by non-anaesthesiologist practitioners of paediatric sedation. However it appears that the drug is not infrequently administered alone for painful procedures, necessitating large doses that result in uncontrolled general anaesthesia with a high potential for adverse events. An elegant technique comprises small doses of short-acting opioid (e.g. fentanyl 1 mug/kg) with low-dose propofol infusion. This does not result in worsening of pre-existing right-to-left intracardiac shunts. The dilemma is to educate non-anaesthesiologists about propofol pharmacokinetics and pharmacodynamics and in particular about the advantages of combined drug therapy. A paediatric target-controlled system for propofol has undergone preliminary clinical evaluation and it is hoped that administration according to pharmacokinetic principles will refine administration to infants and children. Sporadic cases of the propofol infusion syndrome in patients receiving prolonged sedation in intensive care units continue to be reported (characterized by metabolic acidosis, rhabdomyolysis and myocardial failure). It appears that one mechanism may be a deficiency of mitochondrial oxidative processes possibly induced by a dialyzable substance, perhaps a propofol metabolite. Propofol has been used with some success in treating postoperative laryngospasm and for tracheal intubation without muscle relaxants. Propofol should be used with extreme caution for prolonged sedation in intensive care unit patients, at dose rates of below 5 mg/kg per h, while maintaining extreme vigilance for signs of developing propofol infusion syndrome. If used correctly propofol is a suitable drug for sedation outside the operating room.

Effects of subhypnotic doses of propofol on gastric emptying in volunteers.

Drugs which accelerate gastric emptying (GE) decrease nausea and vomiting. This could contribute to the antiemetic potential of subhypnotic doses of propofol. On the contrary, subhypnotic doses of propofol used for sedation could decrease GE and thus favor regurgitation and pulmonary inhalation. Therefore, the aim of this study was to assess the effect of low-dose propofol infusion on GE. On three separate occasions, 10 volunteers received either a propofol infusion at a rate set to achieve a target plasma concentration of 0.5 microg/ml or equivalent volumes of 10% Intralipid(R) or 0.9% saline. GE for solids was measured by using the octanoic acid breath test. An acetaminophen absorption technique measured the GE rate for liquids. Blood samples were assayed for acetaminophen and propofol. Breath samples were analyzed for (13)CO(2) concentration by isotope-ratio mass spectrometry. Carbon dioxide production (VCO(2)) was measured instead of calculated by indirect calorimetry. Sedation was evaluated by the Bispectral Index of the electroencephalogram. Propofol blood concentrations were 0.32 +/- 0.20 and 0.45 +/- 0.18 microg/ml at 60 and 165 min, respectively. These concentrations were not sedative. Propofol or its solvent did not modify GE for solids or liquids. In all groups, differences in GE were obtained if measured VCO(2) was integrated in the formula instead of calculated VCO(2) (P < 0.002). Subhypnotic doses of propofol known to be antiemetic do not inhibit GE. These results suggest that the antiemetic properties of propofol are not peripheral and that propofol cannot be considered as a prokinetic agent. V(13)CO(2) must be measured instead of calculated to accurately determine GE.

Effect of low-dose propofol infusion on total-body oxygen consumption after coronary artery surgery

Objective: To investigate the effect of low-dose propofol infusion on total-body oxygen consumption (V0 2) after coronary artery bypass grafting (CABG) surgery. Design: A prospective, randomized, placebo-controlled, double-blind study. Setting: Cardiovascular intensive care unit in a university hospital. Participants: Thirty patients after elective, uncomplicated CABG surgery. Intervention: Patients were administered a continuous infusion of propofol with a fixed rate of 1 mg/kg/h (n = 15) or placebo (n = 15) during the spontaneous rewarming period of approximately 5 hours after surgery. A light level of sedation (Ramsay sedation score ≥2) was maintained by administering small doses of diazepam, 0.1 mg/kg, as required. Morphine, 0.05 mg/kg, was administered for analgesia as required. Measurements and Main Results: Total-body V0 2 was measured by indirect calorimetry. In addition, shivering (on a five-grade scale), hemodynamics, and plasma catecholamine and serum cortisol concentrations were measured. Diazepam, 5.6 ± 7.4 mg (mean ± standard deviation), was administered to the patients receiving propofol, and 16.1 ± 12.2 mg was administered to the patients receiving placebo ( p < 0.05). There was no difference in the dose of morphine between the groups (3.2 ± 3.9 v 4.2 ± 5.5 mg in the propofol and placebo groups, respectively). At any time during the study, V0 2 was not different between the groups. VO 2 increased from 130 ± 29 to 172 ± 29 mL/min/m 2 in the propofol group and from 118 ± 24 to 167 ± 27 mL/min/m 2 in the placebo group. Mean arterial pressure and heart rate were lower in the propofol group ( p < 0.05). Stress hormone levels did not differ between the groups. Conclusion: Low-dose propofol infusion and additional diazepam as required does not decrease total-body V02 compared with a pure diazepam bolus-dose technique when administered for light sedation during the immediate recovery period after CABG surgery.

The influence of nitrous oxide to supplement fentanyl/low-dose propofol anesthesia on transcranial myogenic motor-evoked potentials during thoracic aortic surgery

Objective: Intraoperative monitoring of myogenic motor evoked potentials to transcranial electrical stimulation (tc MEPs) is a new method to assess the integrity of the motor pathways. The authors studied the effects of 50% nitrous oxide (N 20) and a low-dose propofol infusion on tc MEPs paired electrical stimulation during fentanyl anesthesia with partial neuromuscular blockade. Design: Cross-over study. Setting: St Antonius Hospital, Nieuwegein, The Netherlands. Participants: Ten patients scheduled to undergo surgery on the thoracoabdominal aorta were studied; 6 women aged 54 to 69 years and 4 men aged 68 to 77 years. Interventions: After achieving a stable anesthetic state and before surgery, tc MEPs were recorded during four 15-minute periods: (I) air/oxygen (O 2; F IO 2 = 50%); propofol target blood concentration, 0.5 μg/mL; (II) N 2O/O 2 (F IO 2 = 50%); propofol target blood concentration, 0.5 μg/ mL; (III) N 2O/O 2 (F IO 2 = 50%; propofol target blood concentration, 1.0 μg/mL; and (IV) air/O 2 (F IO 2 = 50%); propofol target blood concentration, 1.0 μg/mL. Measurements and Main Results: Tc MEPs were recorded from the right extensor digitorum communis muscle and the right tibialis anterior muscle. The right thenar muscle was used for recording the level of relaxation; the T1 response was maintained at 40% to 70% of the control compound muscle action potential. There was no significant difference in onset latency among the four phases. The addition of N 2O and doubling the target propofol infusion to 1.0 μg/mL resulted in a 40% to 50% reduction of tc MEP amplitude recorded in the extensor digitorum communis muscle and tibialis anterior muscle ( p < 0.01). During each phase, tc MEPs could be elicited and interpreted, except in one patient, in whom no tc MEPs could be elicited in the leg because of technical problems. Conclusion: The data indicate that tc MEP monitoring is feasible during low-dose propofol, fentanyl/50% N 2O in O 2 anesthesia and partial neuromuscular blockade.