Jong Seok Lee

Effects of fentanyl pretreatment on the QTc interval during propofol induction

Prolongation of the corrected QT (QTc) interval is associated with various anaesthetic drugs. The QTc prolongation may become more exacerbated during laryngoscopy and intubation, which is possibly caused by sympathetic stimulation. The aim of this study was to investigate the effects of fentanyl on the QTc interval during propofol induction in healthy patients. The patients were randomly allocated to receive either fentanyl (nu2003=u200325) or saline (nu2003=u200325) before induction. The QTc interval was significantly prolonged immediately after intubation in control group compared to preceding values, but it did not change in the fentanyl group. The number of patients with the prolonged QTc interval exceeding 20u2003ms immediately after intubation compared to the baseline values was 14 in the control group and seven in the fentanyl group. In conclusion, pretreatment with fentanyl 2u2003μg.kg−1 significantly attenuated QTc prolongation associated with laryngoscopy and tracheal intubation during propofol induction.

The effect of bolus administration of remifentanil on QTc interval during induction of sevoflurane anaesthesia.

Stimulation of the sympathetic nervous system associated with tracheal intubation causes corrected QT (QTc) interval prolongation. We postulated that the use of remifentanil during induction of anaesthesia might prevent this. Sixty unpremedicated, ASA gradeu20031 patients were selected and randomly allocated to receive either saline (group S), remifentanil 0.5u2003μg.kg−1 (group R 0.5) or remifentanil 1.0u2003μg.kg−1 (group R1.0) 1u2003min before laryngoscopy. The QTc interval was significantly prolonged immediately following intubation in group S and group R0.5, but it remained stable in group R1.0, compared with the QTc interval just before laryngoscopy. It is concluded that the administration of remifentanil 1.0u2003μg.kg−1 before intubation can prevent the prolongation of the QTc interval associated with tracheal intubation during induction of anaesthesia with sevoflurane.

Effects of target concentration infusion of propofol and tracheal intubation on QTc interval

This study was designed to evaluate the effect of target controlled infusion of propofol on QTc interval and tracheal intubation. Twenty‐five unpremedicated, ASA class I or II patients were selected and target concentration infusion of propofol at 5u2003μg.ml−1 was used throughout the study. The QTc interval was measured before anaesthetic induction (baseline, T1), 10u2003min after propofol infusion (T2), immediately after tracheal intubation (T3), and 1u2003min after tracheal intubation (T4). The QTc interval increased significantly at 10u2003min after the propofol infusion started compared to baseline (pu2003=u20030.003). After tracheal intubation, the QTc interval was further increased when compared to that at T2 (pu2003<u20030.0001). The increased QTc interval was within normal limit and no patient had an arrhythmia. In conclusion, although statistically significant, the increase in QTc interval was too small to be clinically significant during propofol infusion. However, the combination of propofol and tracheal intubation must be used carefully in patients with prolonged QTc interval.

Evaluation of radial and ulnar blood flow after radial artery cannulation with 20‐ and 22‐gauge cannulae using duplex Doppler ultrasound

This study evaluated ulnar and radial artery blood flow after radial artery cannulation during general anaesthesia using Doppler ultrasound. A total of 80 patients were randomly assigned to receive radial artery cannulation with either a 20‐G or 22‐G cannula. Arterial diameter, peak systolic velocity, end‐diastolic velocity, resistance index and mean volume flow were measured at four time points in both arteries: before anaesthesia; 5u2003min after intubation; immediately after cannulation; and 5u2003min after cannulation. After radial artery cannulation, ulnar diameters and blood flow were significantly increased, and persisted until 5u2003min after cannulation. Radial blood flow was decreased immediately after cannulation and recovered to pre‐cannulation values 5u2003min after cannulation. There were no statistical differences between groups at each time point. Radial artery cannulation causes compensatory increase in ulnar artery blood flow, and the difference in cannula size has minimal effect on this change.

A randomised, crossover comparison between the CobraPLA® and the LMA Classic™ in paralysed patients*

We performed a randomised, crossover study in 38 anaesthetised and paralysed patients to compare the performance of the CobraPLA® and the LMA Classic™ during controlled ventilation. The median (IQR [range]) airway leak pressure was 23.0 (20–24 [12–30]) cmH2O for the CobraPLA and 15.0 (12–19 [8–30]) cmH2O for the LMA Classic (pu2003< 0.001). The median (IQR [range]) insertion time was 15.0 (11–26 [9–31]) s for the CobraPLA and 22.5 (20–25 [15–50])u2003s for the LMA Classic (pu2003<u20030.001). There was no significant difference between the two devices for the number of insertion and reposition attempts, the anatomical position scored by fibreoptic bronchoscopy or the peak and plateau airway pressures. There were no adverse events during anaesthesia. The CobraPLA provides a better airway leak pressure and takes less time to insert than the LMA Classic in paralysed patients. Our data show that the CobraPLA can be used to secure a patent airway during controlled ventilation in selected patients.

Relationship between arterial and end‐tidal carbon dioxide pressures during anesthesia using a laryngeal tube

Background:u2002 The Laryngeal Tube® (LT), (VBM Medizintechnik, Sulz, Germany) is a relatively new supraglottic device for controlling the airway. Arterial carbon dioxide tension (PaCO2) can be estimated by monitoring the end‐tidal tension of carbon dioxide (PETCO2). The relationship between PETCO2 and PaCO2 during controlled ventilation via the LT has not been reported.

The effect of intrathecal fentanyl on Cerebral State Index-guided sedation during spinal anaesthesia*

This study investigated the effect of intrathecal fentanyl on the dose of propofol during sedation guided by Cerebral State Index monitoring. Seventy patients were randomly assigned to receive either fentanyl 25u2003μg (nu2003=u200335) or normal saline (nu2003=u200335) with hyperbaric bupivacaine 12.5u2003mg for spinal anaesthesia. Propofol was infused to maintain a Cerebral State Index value of 65–75 for 30u2003min. The propofol infusion time and dose required to reach a Cerebral State Index value of 75 were recorded together with the time required to reach a Cerebral State Index value higher than 90 after cessation of sedation. The onset time for sedation was faster and the recovery time was slower in the fentanyl group compared to those in the saline group (pu2003=u20030.018 and 0.027, respectively). The propofol doses required for onset and maintenance of sedation were significantly lower in the fentanyl group compared to those in the control group (pu2003=u20030.018 and <u20030.001, respectively). In conclusion, adding intrathecal fentanyl 25u2003μg during spinal anaesthesia significantly reduced the dose of propofol required for sedation and prolonged the subsequent recovery time.

Propofol–remifentanil and the ankle clonus test in scoliosis patients

Ankle clonus can be elicited in more than 80% of patients during emergence from inhalational anaesthesia [1–3]. The inability to elicit clonus during emergence has been described as a useful test for predicting neurological compromise of the spinal cord during spinal surgery [1]. We examined the incidence of inducible ankle clonus during emergence from propofol–remifentanil anaesthesia. Following institutional ethics committee approval and written informed consent, 30 patients aged 15–20 years, of ASA physical status 1–2, underwent surgical correction of idiopathic scoliosis. A target-controlled infusion pump (Fresenius Orchestra Base Primea; Fresenius Kabi, Bad Homburg, Germany) was used to deliver propofol and remifentanil. During surgery, the patients’ lungs were ventilated and anaesthesia was maintained with propofol at effect site concentrations of 3.0– 5.0 lg.ml and remifentanil at effect site concentrations of 2.0–6.0 ng.ml, with intermittent doses of rocuronium. At the end of surgery after neuromuscular transmission returned, as evaluated by train-of-four peripheral nerve stimulation, the propofol infusion was discontinued while maintaining the remifentanil at 1.0 ng.ml. With every decrease of 0.1 lg.ml of propofol, we performed an ankle clonus test until patients opened their eyes in response to verbal command. Bilateral ankle clonus was elicited in only 40% of patients (12 ⁄ 30), and no patients had demonstrable neurological impairment postoperatively. The median (IQR [range]) propofol effect site concentration for a positive ankle clonus test was 2.1 (2.4–1.7 [2.7– 0.7]) lg.ml. There have been no studies investigating the validity of the ankle clonus test during propofol–remifentanil anaesthesia, although this type of anaesthesia has benefits such as rapid recovery, minimal postoperative confusion and minimal effects on somatic evoked potentials [4]. During emergence from general anaesthesia, lower motor neuron function returns before cortical inhibitory impulses regain their normal function; this disinhibits lower motor neurons thereby allowing clonus to occur during testing [5]. Spinal reflex responses are suppressed at low concentrations of propofol and reflex activity of the spinal cord is less pronounced during propofol anaesthesia compared with sevoflurane anaesthesia [6, 7]. This suggests that propofol may more potently inhibit the appearance of ankle clonus compared with volatile anaesthetic agents. The limitations of our study include that there were no controls and the observers were not blinded to the study protocol. Our results suggest that anaesthesia maintained with propofol and remifentanil may suppress ankle clonus during emergence, thereby making it of limited use as a marker of spinal cord impairment.