Search PubMed⌕ Search

Biomedical subjects

C J Kalkman

Publications and source records attributed to C J Kalkman.

88 records · Page 5Linked to original sources
PubMed1994

Haemodynamic effects of pneumoperitoneum for laparoscopic surgery: a comparison of CO2 with N2O insufflation.

We studied the haemodynamic effects of intra-abdominal insufflation with either CO2 (n = 15) or N2O (n = 15) in patients undergoing laparoscopic surgery. Haemodynamic variables were measured at increasing levels of intra-abdominal pressure up to 20 mmHg. In the CO2 group cardiac index decreased from 2.6 +/- 0.6 to 2.0 +/- 0.4 litre min-1 m-2 (mean +/- SD, P < 0.001) and in the N2O group from 2.6 +/- 0.5 to 1.8 +/- 0.4 litre min-1 m-2 (P < 0.001)). In the CO2 group, this was accompanied by increases in mean arterial pressure, systemic vascular resistance index and central venous pressure without change in heart rate. In contrast, during N2O insufflation mean arterial pressure decreased (from 77 +/- 8 to 63 +/- 15 mmHg (P < 0.001)) without change in vascular resistance. No further changes in haemodynamic variables were observed during head-up tilt in both groups. After desufflation mean arterial pressure increased in the N2O group to pre-insufflation levels and cardiac index increased in both groups (P < 0.001), but reached pre-insufflation levels only in the CO2 group. In both groups central venous O2 tension and saturation decreased at maximum intra-abdominal pressure and increased after release of the pneumoperitoneum. The results indicate that laparoscopic insufflation with either CO2 or N2O results in cardiovascular depression. Insufflation with N2O may decrease blood pressure, whereas mean arterial pressure is better preserved with CO2 insufflation.

Adult↗
PubMed1993

Effect of ibuprofen on regional eicosanoid production and neuronal injury after forebrain ischemia in rats.

Post-ischemic metabolism of arachidonic acid by cyclooxygenase results in the elaboration of numerous eicosanoids and in the generation of free radicals. Accordingly, the effect of cyclooxygenase inhibition by ibuprofen on post-ischemic eicosanoid production and delayed neuronal death was evaluated in Wistar-Kyoto rats subjected to incomplete forebrain ischemia. In control (C) and ibuprofen-treated groups (n = 5 each), pre- and post-ischemic eicosanoid production in the caudate nucleus (CN) and dorsal hippocampus (HPC) were evaluated by microdialysis. The ibuprofen-treated animals were given ibuprofen, 15 mg/kg i.v., prior to insertion of microdialysis probes. Forebrain ischemia was induced by bilateral carotid artery occlusion (BCAO) for 10 min with simultaneous hypotension to 35 Torr. The concentrations of thromboxane B2 (TxB2), 6-keto-PGF1 alpha and PGF2 alpha in the microdialysate were measured by radioimmunoassay. In two additional concurrent groups of rats (n = 10 each), neuronal injury in the HPC, CN and cortex (parietal, temporal and entorhinal regions) was evaluated histologically three days after 10 min of forebrain ischemia with and without pre-ischemic ibuprofen administration. In the control microdialysis group, levels of TxB2, 6-keto-PGF1 alpha and PGF2 alpha increased in both CN and HPC after probe insertion. These probe related increases were substantially reduced in the ibuprofen group. After ischemia and reperfusion in the control group, the levels of TxB2 and PGF2 alpha increased in both CN and HPC. Levels of 6-keto-PGF1 alpha increased in the CN but not in the HPC. The administration of ibuprofen substantially reduced post-ischemic TxB2 and PGF2 alpha levels in both CN and HPC and decreased 6-keto-PGF1 alpha levels in the CN. The results of these initial microdialysis studies left the possibility that, in the ibuprofen group, the reduction in eicosanoid levels after probe penetration might have influenced the subsequent post-ischemic eicosanoid production. Therefore, in an additional group of animals (n = 5), ibuprofen was administered after probe insertion. Only PGF2 alpha levels were measured in this group. Increased levels of PGF2 alpha comparable to the original control group were detected after probe penetration. Nonetheless, after ibuprofen administration, the pre- and post-ischemic levels of PGF2 alpha were again significantly reduced. In the histologic evaluation groups, overall neuronal injury was significantly less in the ibuprofen treated animals. This protective effect of ibuprofen was most clearly evident in the CA3 sector of the HPC.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial electrical or magnetic stimulation in humans.

The effects of propofol, etomidate, midazolam, and fentanyl on motor evoked responses to transcranial stimulation (tc-MERs) were studied in five healthy human volunteers. Each subject, in four separate sessions, received intravenous bolus doses of propofol 2 mg.kg-1, etomidate 0.3 mg.kg-1, midazolam 0.05 mg.kg-1, and fentanyl 3 micrograms.kg-1. Electrical tc-MERs (tce-MERs) were elicited with anodal stimuli of 500-700 V. Magnetic tc-MERs (tcmag-MERs) were elicited using a Cadwell MES-10 magnetic stimulator at maximum output. Compound muscle action potentials were recorded from the tibialis anterior muscle. Duplicate tce-MERs and tcmag-MERs were recorded before and up to 30 min after drug injection. Reproducible baseline tce-MERs (amplitude 4.7 +/- 0.43 (SEM) mV, latency 29.4 +/- 0.35 ms) and tcmag-MERs (amplitude 3.7 +/- 0.43 mV, latency 31.1 +/- 0.39 ms) were obtained in all subjects. Pronounced depression of tce-MER amplitude to 2% of baseline values (P less than 0.01) was observed 2 min after injection of propofol. Thirty minutes after injection of propofol, amplitude depression to 44% of baseline (P less than 0.05) was still present, despite an apparent lack of sedation. Midazolam caused significant (P less than 0.01) amplitude depression, e.g., tcmag-MER to 16% of baseline values 5 min after injection. Significant depression persisted throughout the 30-min study period. Fentanyl did not cause any statistically significant amplitude changes in this small population. Etomidate caused significant but transient depression of tc-MER amplitude. However, there was considerable intersubject variability. Latency did not change significantly after any drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Pulmonary function and stress response after laparoscopic cholecystectomy: comparison with subcostal incision and influence of thoracic epidural analgesia.

Laparoscopic cholecystectomy (LPC) is increasingly used to treat symptomatic cholelithiasis. We compared the effects of cholecystectomy by subcostal incision to those of LPC on lung function and endocrine metabolic response. The effects of thoracic epidural analgesia for LPC were studied as well. Thirty patients undergoing elective cholecystectomy under general anesthesia were allocated to three study groups: group I, cholecystectomy by subcostal incision; group II, LPC; group III, LPC and epidural analgesia with 0.5% bupivacaine with epinephrine, followed by continuous epidural infusion of 6 mL of 0.5% bupivacaine. Forced vital capacity (FVC), peak expiratory flow, and forced expiratory volume in 1 s were measured with the patients in a half-sitting position. In all groups, sustained decreases in FVC, forced expiratory volume in 1 s, and peak expiratory flow were observed up to 24 h after surgery. Reduction of FVC was significantly more in group I compared with groups II and III (P less than 0.05). The FVC in group I decreased from 3.8 +/- 0.42 (SD) to 1.1 +/- 0.27 L (P less than 0.01), in group II from 3.6 +/- 1.46 to 2.1 +/- 0.94 L (P less than 0.05), and in group III from 3.8 +/- 0.92 to 2.8 +/- 0.90 L (P less than 0.05). In all groups, plasma glucose and cortisol increased after surgery compared with baseline levels (P less than 0.05). At 240 min after surgery, a small but significant decrease of cortisol was measured in group III (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Intraoperative monitoring of tibialis anterior muscle motor evoked responses to transcranial electrical stimulation during partial neuromuscular blockade.

We studied the feasibility of recording motor evoked responses to transcranial electrical stimulation (tce-MERs) during partial neuromuscular blockade (NMB). In 11 patients, compound muscle action potentials were recorded from the tibialis anterior muscle in response to transcranial electrical stimulation during various levels of vecuronium-induced NMB. The level of NMB was assessed by accelerometry of the adductor pollicis muscle after train-of-four stimulation of the ulnar nerve. The compound muscle action potential was also recorded from the tibialis anterior muscle after direct stimulation of the peroneal nerve (M-response) as an alternative means of assessing the degree of NMB. In all patients, tce-MERs could be recorded reliably during anesthesia with N2O and a continuous infusion of sufentanil (0.5 micrograms.kg-1.h-1). An intact train-of-four was present in all patients, and the amplitude of the first twitch was recorded and designated as the control value. Before administration of vecuronium, the M-response amplitude was 9.6 +/- 3.6 (mean +/- SD) mV, and the tce-MER amplitude was 1.21 +/- 0.66 mV. Although administration of vecuronium (0.05 mg/kg) resulted in loss of the mechanical adductor pollicis response in 8 of the 11 patients, the M-response and the tce-MER remained recordable. Subsequently, during an infusion of vecuronium, adjusted to maintain one or two mechanical responses to train-of-four stimulation, the average M-response to peroneal nerve stimulation was 5.2 +/- 2.5 mV (53% of the control value), and tce-MER amplitude was 0.59 +/- 0.36 mV (59% of the control value).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

A comparison of the effects of propofol and nitrous oxide on the electroencephalogram in epileptic patients during conscious sedation for dental procedures.

The influence of sedative doses of propofol or nitrous oxide on the electroencephalogram was studied in 11 mentally handicapped patients with treated epilepsy undergoing dental procedures. At one session, propofol was titrated to achieve conscious sedation. The mean (+/- SD) dose requirements were 5.5 +/- 1.1 mg.kg-1.h-1. In six patients, the electroencephalogram was unchanged during propofol administration. In three patients, there was a decrease in epileptic activity, and in two patients, paroxysmal discharges disappeared. At another session, nitrous oxide was administered by nasal mask. The mean (+/- SD) concentration of nitrous oxide needed was 43.6% +/- 4.8%. The electroencephalogram did not change in nine patients, whereas in two patients epileptic activity decreased. There were no clinical epileptoid or other adverse manifestations during any treatment or up to 48 h thereafter. The results of the present study suggest that propofol or nitrous oxide can be administered in subanesthetic doses for conscious sedation in mentally handicapped patients with treated epilepsy.

Adolescent↗
PubMed1991

Eliminating diathermy-induced artifacts during intraoperative monitoring of somatosensory-evoked potentials: a hardware solution.

Somatosensory-evoked potentials (SEPs) recorded intraoperatively are often contaminated by artifacts arising from unipolar diathermy. This increases variability in serial SEP recordings and decreases the reliability of SEPs for intraoperative monitoring. Rejection of single sweeps on the basis of a voltage criterion can only partially prevent the inclusion of sweeps containing artifacts. We describe a low-cost hardware system that will halt SEP acquisition automatically before diathermy becomes active. Activation of the diathermy switch will halt SEP acquisition by sending a digital inhibit signal to the evoked potential machine via a fiberoptic cable. A timer delays the activation of the diathermy until the last sweep has been completed. To allow the electroencephalographic amplifiers to recover from any overload condition resulting from the high-voltage/high-frequency input during diathermy, acquisition is resumed only after a user-selectable time interval. The system was evaluated in 50 patients. It effectively interrupted SEP acquisition each time diathermy was used. By eliminating diathermy noise from the averaged waveforms, the system will allow evoked potential monitoring even during periods of intensive use of diathermy.

Artifacts↗
PubMed1991

Differential effects of propofol and nitrous oxide on posterior tibial nerve somatosensory cortical evoked potentials during alfentanil anaesthesia.

We have studied differential effects of propofol and nitrous oxide on posterior tibial nerve somatosensory evoked potentials (PTN-SEP) during a continuous infusion of alfentanil. In study 1, 14 patients received initially 66% nitrous oxide in oxygen, which was replaced 90 min after incision by propofol 6 mg kg-1 h-1. This substitution resulted in a significant increase in mean P1N1 amplitude from 1.01 (SD 1.14) microV to 2.61 (2.17) microV (P less than 0.01), while amplitudes of later peaks were unaffected. Latencies of peaks N1, P2 and N2 increased after the substitution. In study 2, 30 patients undergoing spinal surgery received either alfentanil-nitrous oxide anaesthesia (group I, n = 15) or alfentanil-propofol anaesthesia (group II, n = 15). P1N1 amplitude was significantly greater in group II (3.24 (1.08) microV) than in group I (1.64 (0.97) microV) (P less than 0.01). Latencies of peaks P2 and N2 were of significantly greater duration in group II than in group I. Because early cortical PTN-SEP peaks were preserved better during alfentanil-propofol anaesthesia we conclude that this combination may be a suitable alternative to alfentanil-nitrous oxide anaesthesia, when spinal cord function monitoring with PTN-SEP is indicated.

Adolescent↗
PubMed1991

Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensory cortical evoked potentials during alfentanil/nitrous oxide anesthesia.

The effects of variation of arterial CO2 tension (PaCO2) on the electroencephalogram (EEG) and posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) during opioid/N2O anesthesia have not been well documented. We studied the effects of hypocapnia (PaCO2 approximately 23 mmHg) and hypercapnia (PaCO2 approximately 50 mmHg) during steady-state alfentanil/N2O anesthesia in 16 patients. EEG and PTN-SCEP were recorded continuously, while PaCO2 was altered in 15-min intervals by varying the inspired CO2 concentration. Hypocapnia caused significant increases in power in the delta, theta, and beta bands (P less than 0.01), with the greatest increase observed in the alpha band. Relative power increased in the alpha band but remained unchanged in the delta, theta, and beta bands. Median frequency and 95% spectral edge frequency were unaltered during hypocapnia. In contrast, hypercapnia caused a significant decrease of power in the alpha and beta bands, whereas delta and theta power remained unchanged. This was reflected in a significant decrease of the 95% spectral edge frequency, from 8.9 (6.7-11.6) to 7.0 (5.6-8.6) Hz. All EEG parameters returned to normal upon restoration of normocapnia. There was a significant negative correlation between power in the alpha band and end-tidal CO2 in all patients (r = 0.47 to -0.89). PTN-SCEP latencies and amplitudes were not significantly different from control values during hypocapnia and hypercapnia. It is concluded that variations in PaCO2 within the limits 20-50 mmHg produce substantial changes in the EEG power spectrum, especially in the alpha band (8-12 Hz), but do not alter PTN-SCEP.

Adult↗
PubMed1991

Variability of somatosensory cortical evoked potentials during spinal surgery. Effects of anesthetic technique and high-pass digital filtering.

The effects of anesthetic technique (nitrous oxide or propofol) and high-pass digital filtering on within-patient variability of posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) were compared prospectively in two groups of 20 patients undergoing spinal surgery. Average P1N1 amplitude was significantly higher and P1N1 amplitude variability lower during propofol/alfentanil anesthesia than during nitrous oxide/alfentanil anesthesia. Off-line 30-Hz high-pass digital filtering significantly reduced P1N1 amplitude variability without decreasing P1N1 amplitude. In 93 patients studied retrospectively, a significant negative logarithmic correlation (r = -0.77) was observed between P1N1 amplitude and P1N1 amplitude variability. This study shows the importance of maintaining the highest possible PTN-SCEP amplitudes during spinal surgery. Propofol/opioid anesthesia may be an alternative anesthetic technique to nitrous oxide/opioid anesthesia during spinal cord function monitoring.

Adult↗
PubMed1991

Effects of interpleurally administered bupivacaine 0.5% on opioid analgesic requirements and endocrine response during and after cholecystectomy: a randomized double-blind controlled study.

In 30 patients undergoing cholecystectomy, a randomized double-blind saline-controlled study was performed using interpleural 0.5% bupivacaine with or without epinephrine (5 micrograms.ml-1) in combination with 0.8% halothane inspired concentration in oxygen. The aim of the study was to investigate whether interpleural 0.5% bupivacaine could decrease the intraoperative opioid requirements and attenuate the metabolic endocrine response to surgical stress. Patients were randomly allocated to one of three groups: Group 1: 0.5% bupivacaine; Group 2: 0.5% bupivacaine with epinephrine (5 micrograms.ml-1); and Group 3: saline. The interpleural catheter was inserted after induction of anesthesia in the spontaneously breathing patient. The study drug was injected 30 min prior to surgery. Peak plasma bupivacaine concentrations in the respective groups were 1.30 +/- 0.78 and 1.16 +/- 0.48 micrograms.ml-1. In all patients concentrations were below suggested convulsive level. Two patients in Group 1 and two in Group 2 required intraoperative fentanyl (0.1 mg each). In contrast, eight patients in the saline group received an average of 0.21 mg (range 0.1 +/- 0.4 mg) fentanyl (P less than 0.05). Postoperatively, a second dose of the study drug was given. Subsequently, pain was assessed using a visual analog score and a verbal rating scale. Pain scores decreased significantly 30 min after the interpleural injection in both bupivacaine groups and remained unchanged in the saline group (P less than 0.05). Pain management by means of interpleural bupivacaine was successful in 17 of the 20 patients. In the saline group seven out of ten patients needed additional analgesics (P less than 0.05). Cortisol levels increased in response to surgery in all groups: maximum levels in Groups 1, 2 and 3 were: 1.09 +/- 0.29, 1.11 +/- 0.20 and 1.19 +/- 0.16 mumol.l-1, respectively. Plasma glucose concentrations increased significantly in all groups: maximum levels in Groups 1, 2 and 3 were: 7.6 +/- 1.3, 7.3 +/- 1.7 and 8.3 +/- 1.7 mmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Low concentrations of isoflurane abolish motor evoked responses to transcranial electrical stimulation during nitrous oxide/opioid anesthesia in humans.

To study the feasibility of noninvasive monitoring of motor pathways in anesthetized patients, we evaluated the effect of isoflurane on motor evoked responses to constant-voltage transcranial electrical stimulation (tce-MERs). Reproducible tce-MERs were recordable from the tibialis anterior muscle during nitrous oxide/opioid anesthesia in 11 patients. Before the introduction of isoflurane, tce-MER onset latency was 30.8 +/- 1.9 ms, and amplitude ranged from 19 microV to 2.6 mV (median, 209 microV). Operating conditions necessitated neuromuscular blockade in three patients before administration of isoflurane. In the remaining eight patients, introduction of isoflurane in low concentrations resulted in an immediate increase in the latency and a decrease in the amplitude of tce-MERs. The tce-MERs were completely obliterated in all subjects at end-tidal isoflurane concentrations between 0.2% and 0.6% (median, 0.24%). After discontinuation of isoflurane, the tce-MER returned in all patients. The authors conclude that, during nitrous oxide/opioid anesthesia, with the stimulus and recording variables used, isoflurane even at very low concentrations precludes recording of tce-MERs.

Adult↗
PubMed1988

Influence of high-dose opioid anesthesia on posterior tibial nerve somatosensory cortical evoked potentials: effects of fentanyl, sufentanil, and alfentanil.

The effects of high doses of fentanyl (group F), sufentanil (group S), and alfentanil (group A) on posterior tibial nerve somatosensory cortical evoked potentials were studied in 30 patients scheduled for elective valve replacement surgery. Anesthesia was induced with either fentanyl, 75 microg/kg, sufentanil, 5 microg/kg, or alfentanil, 125 microg/kg. The lungs were ventilated with oxygen/air. A bolus dose of fentanyl, 25 microg/kg, was given 30 minutes after induction of anesthesia in group F. Anesthesia was maintained with a continuous infusion of sufentanil, 5 microg/kg/h, in group S, or alfentanil, 500 microg/kg/h, in group A. Latencies of the peaks of the primary cortical complex (P1, N1, P2) increased by 1 to 2 ms after induction of anesthesia, although this was significant (P < 0.01) only for P1 and N1 in groups F and S. N2 latency increased significantly (P < 0.01) by 6 to 10 ms in all groups. P1-N1 amplitude did not change after induction of anesthesia. N1-P2 amplitude decreased significantly (P < 0.01) to 60%-70% of preinduction values in groups F and S. P2-N2 amplitude decreased significantly (P < 0.01) to 60%-70% of preinduction values in all groups. P1, N1 and P2 latencies did not change significantly from the post-induction values in the period preceding cardiopulmonary bypass (75 +/- 16 minutes) in groups F and S. In group A significant changes were observed only for N1 and P2 latency (P < 0.01). During this period there was a further gradual increase in N2 latency and amplitudes remained stable, except P1-N1 amplitude in group F, which decreased significantly (P < 0.05). A bolus dose of fentanyl, 25 microg/kg, given in group F at 30 minutes after induction of anesthesia did not change latencies and amplitudes. No significant differences in latency or amplitude were found at any time among the three study groups. It is concluded that anesthesia with high doses of fentanyl, sufentanil, or alfentanil is a suitable technique when intraoperative monitoring of posterior tibial nerve somatosensory cortical evoked potentials is indicated.

Adult↗
PubMed1986

Influence of moderate hypothermia on posterior tibial nerve somatosensory evoked potentials.

Posterior tibial nerve somatosensory evoked potentials (PTN-SSEP) were recorded in eight patients during cardiac surgery with cardiopulmonary bypass and moderate hypothermia (25-28 degrees C). There was no correlation between changes in amplitude and temperature; however, latencies of potentials recorded over the tibial nerve in the popliteal fossa, the lumbar spinal cord, and the cortex increased linearly as temperature decreased. Latency changes correlated well with nasopharyngeal temperature, but only poorly with rectal and lower limb muscle temperatures. During perioperative monitoring of spinal cord function by means of PTN-SSEP, an increase of the first positive cortical peak (P1) greater than 3 msec is considered an indication for intervention. In this study P1 prolonged 1.15 msec/degree C (r = 0.89, P less than 0.001). This implies that a temperature decrease of 2-3 degrees C may prolong P1 latency by more than 3 msec.

Adult↗