Biomedical subjects

E Kochs

Publications and source records attributed to E Kochs.

At least 145 records · Page 8Linked to original sources

PubMed1991

Cerebral autoregulation in awake versus isoflurane-anesthetized rats.

We evaluated regional cerebral and spinal cord blood flow in rats during isoflurane anesthesia. Tissue blood flow was measured in cerebral cortex, subcortex, midbrain, and spinal cord using radioactive microspheres. Blood flow autoregulation was measured within the following arterial blood pressure ranges (mm Hg): 1 = less than 50, 2 = 50-90, 3 = 90-130, 4 = 130-170, 5 = greater than 170. Arterial blood pressure was increased using phenylephrine infusion and decreased with ganglionic blockade and hemorrhage. Three treatment groups were studied: 1 = awake control, 2 = 1.0 minimum alveolar anesthetic concentration (MAC) isoflurane, 3 = 2.0 MAC isoflurane. Autoregulation was seen in awake rats from 50 to 170 mm Hg in all tissues. The autoregulatory coefficient (change in blood flow/change in blood pressure) was increased in midbrain and spinal cord during 1.0 MAC isoflurane and in all tissues during 2.0 MAC isoflurane (P less than 0.05). Within the arterial blood pressure range of 90-130 mm Hg, isoflurane produced the following changes in tissue blood flow (percent of awake control): 1.0 MAC isoflurane: cortex = 87% +/- 8% (P greater than 0.30), subcortex = 124% +/- 11% (P greater than 0.05), midbrain = 263% +/- 20% (P less than 0.001), spinal cord = 278% +/- 19% (P less than 0.001); 2.0 MAC isoflurane: cortex = 137% +/- 13% (P less than 0.05), subcortex = 272% +/- 24% (P less than 0.001), midbrain = 510% +/- 53% (P less than 0.001), spinal cord = 535% +/- 50% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

PubMed1991

Somatosensory evoked responses during and after graded brain ischaemia in goats.

Somatosensory evoked potentials (SEPs) were studied during graded incomplete cerebral ischaemia in eight goats and for the following 2 h. Anaesthesia was maintained with etomidate 1-1.5 mg kg-1 h-1 and 50% nitrous oxide in oxygen. Global cerebral blood flow (gCBF) was measured by a magnetic flow transducer at one internal maxillary artery after surgical occlusion of all other major extracranial cerebral arteries. CBF was reduced every 30 min by 25% with a lower limit of 15-20 ml 100 g-1 min-1. Regional cerebral blood flow (rCBF) in the brainstem and cortex was measured by the microsphere technique. The main findings were: (a) a graded decline in cortical SEP and a concurrent prolongation of the central conduction time (CCT) at gCBF values below 35 ml 100 g-1 min-1 and (b) an incomplete recovery of cortical SEP components during recirculation. Reduction of gCBF affected cortical rCBF more severely than brainstem rCBF. As a result, only cortical SEPs were changed. Our data suggest that reduced cerebral perfusion may result in altered cortical brain electrical activity that may be monitored by SEP recordings.

Animals↗

PubMed1991

[Spontaneous and evoked electroencephalograms in experimental incomplete cerebral ischemia].

In the present study changes in spontaneous EEG and somatosensory evoked potentials (SEP) under incomplete cerebral ischaemia and in the following reperfusion phase were examined in 8 goats. The neurophysiological parameters were compared with global cerebral blood flow (CBF). At CBF values below 37 ml/100 g/min significant reduction in the EEG power density occurred with a shift of the dominant frequency to lower frequencies. The cortical SEP amplitudes increased significantly with simultaneous increases in latencies. In contrast subcortical components were not affected. In the reperfusion period no complete remission of EEG and SEP changes occurred despite occasional CBF values above the baseline values. The study demonstrates that neurophysiological monitoring can show early functional changes in cases of incomplete cerebral ischaemia.

Animals↗

PubMed1990

Alterations in brain electrical activity may indicate the onset of malignant hyperthermia in swine.

The time course of changes in brain electrical activity during halothane anesthesia was examined in 12 malignant hyperthermia-susceptible (MHS) and 14 normal (nMHS) swine. Power densities in selected frequency bands were calculated from the electroen-cephalogram (EEG). EEG and systemic variables were determined over a period of 60 min after starting halothane (1% inspired). Malignant hyperthermia (MH) was triggered in all susceptible pigs. Initial changes in the EEG during development of MH consisted of a decrease in total power and a shift to lower frequencies (delta-theta activity) in all animals. These EEG alterations were noted when there was an increase in heart rate, but other systemic variables were still normal. EEG changes in all MHS animals started at an arterial oxygen tension (PaO2) greater than 90 mmHg and an arterial carbon dioxide tension (PaCO2) less than 50 mmHg. In 5 MHS animals EEG became isoelectric at a PaO2 of 61-82 mmHg and a PaCO2 of 53-68 mmHg. Mean arterial blood pressure at this time was 54-66 mmHg. To determine the effects of hypoxia on the EEG in 7 nMHS animals, oxygen was decreased over a period of 45-60 min to 7% inspired. In 7 other nMHS animals, hypercarbia was produced by admixture of carbon dioxide to the fresh gas supply to achieve incremental increases of PaCO2 to 110-120 mmHg. Significant EEG changes during hypoxia comparable to those seen at the onset of MH were noted at a PaO2 below 40 mmHg and during hypercarbia at a PaCO2 greater than 68 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗

PubMed1990

Dose-dependent blood flow velocity changes in the Basal cerebral arteries following low-dose ketamine.

The effects of low-dose ketamine on blood flow velocity and pulsatility index (PI) in the basal cerebral arteries were studied in two groups of healthy volunteers (group A: 0.25 mg/kg, n = 10; group B: 0.5 mg/kg, n = 10) by means of a 2 MHz pulsed transcranial Doppler ultrasonic system (TCD) for an observation period of 70 min. In addition, mean arterial pressure (MAP), heart rate (HR), end-tidal CO2 (petCO2), and oxygen saturation (saO2) were recorded. The mean blood flow velocity (Vmean) increased significantly by 28% in group A and by 68% in group B within 2-9 min. In group B, the PI was reduced by 32% for a period of 2-7 min (p < 0.05). MAP (group A: -20%; group B: -26%) and HR (group A: -39%; group B: -54%) increased significantly (p < 0.05). Vmean and PI were significantly different between groups A and B, suggesting a dose-dependent stimulation of cerebral hemodynamics. The flow velocity increases cannot be entirely explained by systemic hemodynamic changes since there was no intergroup difference with respect to MAP and HR. No significant differences were observed with regard to petCO2 and saO2. With the assumption that the diameter of the insonated vessel is not changed by ketamine, the dose-dependent increase in Vmean with a concomitant decrease in PI may be interpreted as indicating an increase in cerebral blood flow.

Journal Article↗

PubMed1990

Transcranial Doppler sonography as a supplement in the detection of cerebral circulatory arrest.

The effects of compromised cerebral hemodynamics on intracranial blood flow velocity patterns (BFV) were studied by noninvasive transcranial Doppler sonography (TCD). Pulsatility index (PI) as an estimation of peripheral cerebral vascular resistance was additionally analyzed. TCD patterns were determined in 19 mechanically ventilated brain dead patients (group A) and 8 resuscitated or severely head injured patients (group B) with intermittent elevated intracranial pressure (ICP). Group A and B TCD data were compared to control measurements obtained in 20 healthy volunteers (group C). Normal TCD recordings (group C) were characterized by anterograde Doppler wave-forms with a predominantly high diastolic flow pattern and PI values of <1. In brain dead patients (group A), flow velocity profiles were significantly decreased. The flow curve consisted of low systolic anterograde spikes, while early diastolic flow components of low amplitudes revealed retrograde phases with a late diastolic zero flow. In some cases, total diastolic circulatory arrest was obtained. PI in brain dead patients was increased by a factor of 10 and was infinite in situations of zero net flow. The low systolic spikes and retrograde diastolic flow may be explained by the effects of reduced intracranial compliance due to increased intracranial pressure (ICP). The detection of bidirectional signals, indicating anterograde and retrograde movements of the blood column or low systolic spikes without diastolic signals, seems to be specific for the condition of brain death. Insonation of the basilar artery should be performed in order to exclude preserved perfusion of infratentorial brain regions during supratentorial circulatory arrest and vice versa. In group B patients, episodes of increased ICP predominantly affected the diastolic flow velocity component. In these patients, resistive Doppler signals with normal or reduced systolic peaks and decreased diastolic flow velocities were expressed as increases in PI. Noninvasive transcranial Doppler sonography appears to confirm cerebral circulatory arrest. Additionally, TCD may be of value for the early detection of impaired cerebral hemodynamics due to changes in intracranial compliance.

Journal Article↗

PubMed1990

Midazolam and flumazenil in neuroanaesthesia.

Of the numerous benzodiazepines currently available, only a few are used in anaesthetic practice. Midazolam is utilised as a premedicant, sedative, and an induction agent and produces minimal depression of ventilation or of the cardiovascular system. The anticonvulsant activity is similar to that of diazepam. In neuroanaesthesia midazolam may be an acceptable alternative to other intravenous induction agents like barbiturates or etomidate in patients with compromised intracranial compliance. Midazolam produces dose-related reductions in cerebral blood flow and cerebral oxygen consumption. However, midazolam does not necessarily prevent increases in intracranial pressure during induction of anaesthesia. In the electroencephalogram (EEG) midazolam produces a reduction in alpha-activity, an increase in theta-delta-activity and low-voltage beta-activity. Midazolam like other benzodiazepines does not affect early components of auditory and somatosensory evoked responses, whereas late cortical responses may be suppressed. Flumazenil, a specific benzodiazepine antagonist, has been demonstrated to be effective in reversing benzodiazepine-induced sedation. In the EEG midazolam-induced changes vanish almost instantaneously. Flumazenil is also effective in restoring the amplitudes of cortical auditory and somatosensory evoked responses. However, as has been demonstrated in head-injured patients and animal experiments after incomplete cerebral ischaemia, increases in cerebral blood flow and intracranial pressure cannot be excluded after flumazenil administration. When utilising flumazenil for wake-up procedures in midazolam-sedated patients with pathological intracranial compliance, flumazenil has to be titrated very carefully in low doses over prolonged periods.

Anesthesia, Intravenous↗

PubMed1990

Modulation of pain-related somatosensory evoked potentials by general anesthesia.

The aim of the present study was to assess if late somatosensory evoked cerebral potentials (SEPs) in response to painful electrical stimuli are a sensitive indicator for analgesic treatment during general anesthesia. For this purpose, a pain model developed for the quantification of drug-induced analgesia in awake volunteers was used in 10 patients scheduled for elective abdominal hysterectomy. Before induction of anesthesia, stimuli were adjusted to two and three times the pain threshold for each individual. Late auditory evoked potentials (AEPs, 30 dB hearing level) and spontaneous electroencephalogram were also evaluated. After control recordings, anesthetic treatments were varied in the following sequences: (a) 0.8% (end-tidal) halothane with 70% nitrous oxide (HN); (b) 0.8% halothane in oxygen (H1); (c) same anesthetic condition as in H1, but the SEP and AEP stimulus intensities were increased to 15 times pain threshold and to 70 dB hearing level, respectively (H2); and (d) fentanyl (0.25 mg) was given with 0.8% halothane in oxygen with no further change in stimulus intensities (HF). In treatments HN and H1, blood pressure and heart rate increases to pain stimuli were abolished, and SEPs and AEPs were both suppressed. Increasing the somatosensory stimulus intensity (treatment H2) stimulated heart rate and arterial pressure responses and again elicited the SEPs. However, AEP components remained suppressed with increased auditory stimulus intensity. Addition of fentanyl (HF) suppressed SEP amplitudes and stimulus-induced hemodynamic responses. Our results suggest that late SEPs in response to painful stimuli change with different analgesic levels.

Adult↗

PubMed1990

[The effect of postural changes on cerebral hemodynamics during general anesthesia].

Anesthesia may compromise the regulation of systemic and cerebral hemodynamics following changes in body position. Sudden decreases in cerebral perfusion pressure due to changes from a horizontal to a head-elevated position may cause decreases in cerebral blood flow (CBF), particularly in patients with preexisting cerebrovascular disease. Transcranial Doppler sonography (TCD) permits on-line measurement of blood flow velocity (BFV) in human basal cerebral arteries, and there is evidence that monitoring of BFV may indicate relative changes in CBF. The present study compares the effects of changes from a horizontal to a head-elevated position on blood flow velocity in the middle cerebral artery (MCA) in 30 patients (ASA I) with different levels of steady state anesthesia (group A: n = 20, isoflurane = 1.0 vol% end-tidal; group B: n = 10, isoflurane = 0.4 vol% end-tidal; O2/N2O; FiO2: 0.3; 6 1/min). The MCA was insonated by transtemporal approach using a 2 MHz Doppler ultrasound system (TC2-64 B, EME) with a range-gating mechanism, adjustable sample volume depth, and flow direction discrimination. Systolic (Vsyst, cm/s) and mean flow velocity (Vmean, cm/s), pulsatility index (PI), mean arterial blood pressure (MAP, mmHg), heart rate (HR, b/min) and end-tidal CO2 (pet-CO2, mmHg) were recorded with the subjects lying flat (baseline values) and for 5 min following adjustment to a 35-40 degrees head-elevated position. There was a significant reduction of 25% for Vsyst from 79 +/- 17 cm/s (baseline) to 59 +/- 13 cm/s and a 33% decrease for Vmean from 52 +/- 9 cm/s (baseline) to 35 +/- 9 cm/s in group A immediately after repositioning.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[The effect of positive end expiratory pressure on the blood flow velocity in the basal cerebral arteries during general anesthesia].

The effects of incremental positive end-expiratory pressure (PEEP) on middle cerebral artery (MCA) blood flow velocity and pulsatility index were studied in 20 patients scheduled for minor elective surgery. Transcranial Doppler sonography (TCD) was used to measure systolic (Vsyst) and mean flow velocity (Vmean) and the pulsatility index (PI). Heart rate (HR), mean arterial blood pressure (MAP), end-tidal CO2(PetCO2) and TCD parameters were recorded at control (PEEP = O) and following PEEP of 5 cm H2O, 10 cm H2O and 15 cm H2O for a period of 5 minutes for each PEEP level. Vsyst and Vmean were significantly reduced with each increment of PEEP. PI increased stepwise in response to each PEEP level. MAP decreased with PEEP 10 and 15 while HR and PetCO2 remained constant over time. These data suggest that PEEP-induced decreases in MCA blood flow velocity may represent decreases in CBF due to impairment of the intracranial venous flow if the diameter of the insonated vascular segment remains constant.

Adult↗

PubMed1990

[Characteristics of cerebral blood flow and the electroencephalogram during experimental malignant hyperthermia].

It is generally assumed that the brain is not primarily involved in the development of a malignant hyperthermia syndrome (MH). However, spontaneous brain electrical activity (EEG) has not been related temporally to the development of haemodynamic, respiratory and metabolic changes during a fulminant MH crisis. In the present study cerebral blood flow (CBF) and spontaneous electroencephalogram (EEG) were recorded in 8 pigs susceptible (MHS) for the development of malignant hyperthermia and 8 non-susceptible pigs (nMHS) after exposure to 1% halothane. Power densities in selected frequency bands were calculated from the EEG. Additionally, body temperature and haemodynamic and blood gas parameters were studied over a period of 60 min. MH was triggered in all MHS animals. Following exposure to halothane initial EEG changes were noted after 20 to 30 min. They consisted of a decrease in total power and a shift to lower frequencies (delta-theta activity). At this time, CBF was significantly increased compared to control. In 4 animals an isoelectric EEG was noted at a PaO2 of 65-78 mmHg and PaCO2 of 52 to 64 mmHg. Characteristic changes for the development of an MH syndrome in haemodynamic and respiratory parameters as well as a rise in body temperature occurred after first EEG changes were seen. Our results do not support the hypothesis that early EEG changes during MH occur as a result of systemic hypotension, hypoxaemia, hypercapnia or cerebral ischaemia. Our data indicate that EEG monitoring in combination with monitoring of haemodynamic, respiratory and metabolic parameters may be of value for an early detection of an MH-crisis.

Animals↗

PubMed1989

[Effects of low molecular weight hydroxyethyl starch (HES 40) in comparison with Ringer solution on oxygen tension in skeletal muscles of infected patients].

Volume expansion for the establishment of normal to slightly hyperdynamic systemic circulation has become part of a standard concept in the treatment of septicemic patients. The goal is an improvement of microcirculation with beneficial effects on tissue oxygen supply. This study investigates the effect of hydroxyethyl starch solution (HES 6%: mean molecular weight = 40,000) versus ringer's solution on tissue oxygen tensions in human skeletal muscle during periods of septicemia in 10 mechanically ventilated ICU-patients. Measurement of tissue oxygen tension was achieved by a polarographic pO2-sensitive flexible probe. After computer assisted analysis pO2-histograms were calculated out of 200 single pO2-values measured consecutively within a time period of 4 min. Infusions of 500 ml ringer's solution or 500 ml HES were given over 60 min in each patient in a randomized order. The second infusion was begun when the pO2-histogram had reproducibly regained control values as measured before treatment. Measurements were made every 30 min after starting the infusion for a total period of 150 min. As a result the median pO2 improved by 24.5% 90 min after the infusion of HES was begun with a simultaneous significant (30 to 150 min; p less than 0.05) drop in hematocrit from 34.3% to 32.4%. In contrast ringer's solution had no significant effect on tissue pO2 whereas the hematocrit was comparable to the HES group in the time period of 30-60 min. In both groups no linear correlation between hematocrit and pO2-tensions could be established. It remains unclear if pO2-tensions during and after HES infusion can be correlated to an improved capillary perfusion. However, as was clearly demonstrated, different types of solutions used for volume expansion may exert different effects on pO2-tissue tension in septic patients.

Adult↗

PubMed1989

[Acoustic and somatosensory evoked cortical potentials in sedation with midazolam and drug antagonism with flumazenil].

The effect of many intravenous sedative and hypnotic drugs on subcortical and early cortical evoked responses has been investigated by many authors. Because of the great inter- and intraindividual variabilities late cortical evoked components (EP) are thought to be unable to reflect the degree of anesthetic depth. However the impact of centrally acting anesthetic drugs on EP has not been thoroughly studied. The present study investigates the influence of midazolam and the specific benzodiazepine antagonist flumazenil on acoustical (AEP) and somatosensory (SEP) evoked cortical responses. In addition the following parameters were recorded: heart frequency, mean arterial blood pressure, arterial oxygen saturation and in approximation the end-expiratory carbon dioxide tension. In 12 healthy volunteers (age: 25-36 y) the following combinations of drugs were given in several sessions: Midazolam-flumazenil, midazolam-ringer's solution, ringer's solution-flumazenil. In 6 subjects the study was performed according to a double blind placebo-controlled experimental protocol. Midazolam led to a suppression and a prolongation of latencies of components: N1/P2; P2/N2 (AEP); P100/N150; N150/P220 (SEP). Flumazenil (0.3 mg) led to a prompt restoration of all cortical components with however still reduced amplitudes compared to control. At the end of the observation period, 50 min after application of the second drug, EP-components did not differ significantly between the groups given midazolam-ringer's solution and midazolam-flumazenil. Flumazenil given alone had no significant effect on the AEP- and SEP-recordings, so no intrinsic activity of flumazenil could be substantiated.

Adult↗

PubMed1989

[Increase in blood flow velocity in the middle cerebral artery following low-dose ketamine].

Low-dose ketamine is recommended in patients requiring sufficient analgetic support in emergency situations. There is still controversy in the discussion on ketamine-induced effects on cerebral blood flow and intracranial pressure. We investigated the effect of 0.25 mg x kg-1 ketamine i.v. on the blood flow velocity in the basal cerebral arteries in 10 healthy volunteers by transcranial Doppler sonography (TCD). Peak and mean blood flow velocities, pulsatility index, arterial blood pressure, heart rate, oxygen saturation and end tidal carbon dioxide tension were measured during the study. There was a significant increase in the hemodynamic parameters and in blood flow velocities, paralleled by a decrease in pulsatility index and constant values for oxygen saturation and CO2-tensions following injection of ketamine. The results indicate a transient stimulation of the cardiocirculatory system with a concomitant reduction of the cerebral vascular resistance. The question of informative detection of intracranial hemodynamics following application of intravenous anesthetics will be discussed.

Adult↗

PubMed1988

[Neurophysiological monitoring (electroencephalogram, evoked potentials) and the effects of benzodiazepines].

Since the introduction of diazepam, flunitrazepam and midazolam into clinical practice benzodiazepines have been increasingly used for premedication, induction of anesthesia, and long-term sedation in the intensive care unit utilizing their anxiolytic and sedative components. Intraoperative monitoring of central nervous structures has to take into account the effects of benzodiazepines on the electroencephalogram (EEG) and evoked potentials (EP) before their contribution to alterations in brain electrical activity during balanced anesthesia with combination of different drugs can be evaluated. EEG reflects the spontaneous brain electrical activity whereas EP are the averaged time-locked electrical responses to external stimulation. They are thus able to assess the functional integrity of afferent neuronal pathways from peripheral nerves to cortical areas. The specific benzodiazepine antagonist flumazenil binds competitively to benzodiazepine receptors and is able to induce a change in pharmacodynamic parameters, which i.e. can be measured by EEG- and EP-recordings. Characteristical changes in the EEG after benzodiazepine medication consist in an activation of higher EEG-frequencies simultaneous to a decrease in alpha-activity. A facultative increase in delta-activity seems to be dependent on the absolute dose administered and on the speed for intravenous injection. Benzodiazepine-induced EEG-alterations can be reversed by flumazenil almost completely but in the time course will change again in correspondence to the plasma levels of the benzodiazepines and the half-time of flumazenil. Cortical EP-components are suppressed by benzodiazepines whereas subcortical generated potentials are not altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1988

[Effect of flumazenil on global cerebral blood flow and on intracranial pressure in the reperfusion phase following incomplete global cerebral ischemia].

Sedation with benzodiazepines in intensive care patients with head injuries has become part of a standard concept in controlling intracranial pressure (ICP) and metabolic demands of an injured brain. The specific benzodiazepine antagonist flumazenil, which is supposed to exert no direct effect on cerebral blood flow (CBF) in healthy volunteers, suggests that rapid reversal from midazolam sedation might be achieved without any deleterious side effects. It remains however ambiguous if the same holds true in subjects with head trauma. This study describes the effect of flumazenil on CBF, ICP and cerebral perfusion pressure (CPP) during the reperfusion period after incomplete global ischemia in 10 goats. After preparation progressively decreasing CBF in 7 goats was achieved by stepwise external occlusion of the a. max. interna. 90-120 min after reestablishment of CBF 15 mg midazolam i.v. were given followed by 0.5 mg flumazenil i.v. 5 min later. Within 60 sec after application of the antagonist an increase of CBF by 30-165% and of ICP by 25-310% was noted in 5 goats. Simultaneous changes in arterial pressure, CBF and ICP suggest a severe impact of the benzodiazepine antagonist after midazolam sedation on ICP and CBF during periods of impaired cerebral autoregulation. Until the cerebrovascular and cerebral metabolic effects of flumazenil have been elaborated in detail, it is recommended to titrate the effect of flumazenil over long intervals in head injured patients.

Animals↗

PubMed1988

[The electroencephalogram and somatosensory evoked potentials following intravenous administration of 0.5 mg/Kg ketamine].

UNLABELLED: Because of its analgesic potency without affecting consciousness, low-dose ketamine (0.5 mg/kg) has been advocated for traumatized patients in order to ensure the possibility of neurological assessment. This study describes the effects of 0.5 mg/kg ketamine on spontaneous and evoked brain electrical activity. METHODS: Nine unpremedicated, healthy volunteers aged 22-35 years and free of CNS-active drugs took part in the study. The EEG was recorded from C3P3, C4P4, and vertex versus linked earlobes (Cz/A1-A2) (bandpass: 1-45 Hz). For artefact control the electro-oculogram (EOG) was recorded from supra- and infraorbital electrodes with the same filter settings. EEG and EOG were stored on magnetic tape and were digitized off-line (sampling rate: 100/s) followed by Fourier transformation (epoch-length: 5.2 s). Somatosensory evoked potentials (SEP) were elicited by constant current pulses at the median nerve near the wrist. Recording sites were at the cervical spine (Cv6), the ipsi- and contralateral somatosensory projection area, and the vertex (Cz) vs a frontal reference (Fz). Bandpass: 10-2000 Hz, stimulation frequency: 4 Hz, twofold motor threshold, analysis time: 100 ms. Electrocardiogram, blood pressure, and arterial oxygen saturation (pulse oximeter) were monitored continuously. After an adaptation session of 30-45 min, 0.5 mg ketamine was administered intravenously. EEG and SEP were recorded for the following 45-60 min. Data were subjected to analysis of variance (ANOVA) and Scheffé-test if appropriate (P less than or equal to 0.05). RESULTS: All subjects lost consciousness within 45-110 s (mean: 70 s) after administration of ketamine. Mean blood pressure levels increased by about 20% and heart rate by about 10% after 5-10 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

[Evoked potentials and intravenous anesthetics].

In contrast to the electroencephalogram, which is a collection of the spontaneous brain electrical potentials generated by the cerebral cortex, evoked potentials are the electrical signals generated by the nervous system in response to brief extrinsic sensory stimuli. They can be used to establish objective evidence of an abnormality when clinical signs and symptoms are equivocal. Moreover they prove useful to define the anatomical level of lesions in the afferent pathway tested. They have been successfully applied during anesthesia and operations when pathways amenable to evoked potential recording were at risk. The most practical techniques in common intraoperative evoked response monitoring involve stimulation of visual, auditory and somatosensory pathways. As could be clearly demonstrated alterations of evoked responses can not only be found with diminished regional blood flow but in a graded manner depend on the used anesthetics as well. The potential application of evoked responses to monitor depth of anesthesia has been demonstrated by several groups. In contrast to visual, auditory and somatosensory cortical evoked potentials which show a large inter- and intraindividual variance acoustical evoked brainstem and somatosensory evoked subcortical potentials are very robust under general anesthesia. Drug-induced effects on shape, amplitude and latencies of evoked responses during balanced anesthesia must be well documented in order to establish evoked responses as sensitive indicators of systemic problems that may threaten the viability of the central nervous system. There is evidence that the effects on evoked responses during deep anesthetic states can be mimicked by several life-threatening conditions (e.g.: hypoxia, ischemia). This review describes the effects of intravenously used anesthetic drugs on visual, auditory and somatosensory evoked potentials and the alterations in evoked responses by abnormal systemic conditions as seen under hypotension, hypoxia, ischemia.

Anesthesia, Intravenous↗