Biomedical subjects

W E Hoffman

Publications and source records attributed to W E Hoffman.

At least 19 recordsLinked to original sources

PubMed2003

Glyburide decreases myocardial oxygen pressure in dogs.

BACKGROUND: Reports show that glyburide, an adenosine triphosphate sensitive potassium (K+ATP) channel blocker, will reverse the myocardial protective effect of inhalational anesthesia. We evaluated the effect of glyburide on myocardial tissue oxygen pressure (PmO2) in dogs anesthetized with desflurane. METHODS: Twelve dogs were anesthetized with 8% end-tidal desflurane for baseline anesthesia. A flow probe was placed on the left anterior descending (LAD) artery. A probe that measured PmO2 was inserted into the middle myocardium in the LAD region. After baseline measures, six dogs received i.v. 1 mg kg(-1) of glyburide and six dogs received sham vehicle treatment. After the glyburide or sham treatment, each dog received an i.v. infusion of adenosine 0.1 microg kg(-1) x min(-1), sodium nitroprusside (SNP) 2-4 microg kg(-1) x min(-1) and 14% end-tidal desflurane in random order. RESULTS: Glyburide decreased LAD artery flow from 59 +/- 9 ml min(-1) to 30 +/- 6 ml min(-1) (P < 0.05) and PmO2 from 44 +/- 16 mmHg to 30 +/- 9 mmHg (P < 0.05). Adenosine infusion increased LAD artery blood flow 180% in the sham-treated dogs but produced no change in the glyburide-treated dogs. Sodium nitroprusside infusion increased LAD artery flow and decreased PmO2 in both the glyburide- and sham-treated dogs. Desflurane (14%) did not reverse the glyburide-induced vasoconstriction but increased PmO2 to 38 +/- 20 mmHg (P < 0.05). CONCLUSION: Glyburide produced myocardial tissue hypoxia, which was not changed by adenosine, worsened by SNP and improved by 14% desflurane. The improvement in PmO2 with desflurane occurred without a change in myocardial blood flow.

Adenosine↗

PubMed2001

Sodium nitroprusside compared with isoflurane-induced hypotension: the effects on brain oxygenation and arteriovenous shunting.

UNLABELLED: We compared sodium nitroprusside (SNP)-induced hypotension with 3% isoflurane-induced hypotension with regard to brain tissue oxygen pressure (PtO(2)), middle cerebral artery (MCA) blood flow, and cerebral arteriovenous shunting. Eight dogs were anesthetized with 1.5% isoflurane. After a craniotomy, a probe was inserted into the left frontoparietal brain cortex to mea-sure tissue gases and pH. Blood flow was measured in a secondary branch of the MCA by a flowprobe. Measurements were made during baseline 1.5% isoflurane, during 1.5% isoflurane and SNP-induced hypotension or 3% isoflurane-induced hypotension to a mean pressure of 60-65 mm Hg, and during continued treatment with SNP or 3% isoflurane with blood pressure support to baseline levels with phenylephrine. Shunting was calculated from arterial, sagittal sinus, and tissue (indicating capillary) oxygen content. During hypotension with SNP, PtO(2) decreased 50%, and shunting increased 50%. During hypotension with 3% isoflurane, PtO(2) and shunting did not change. Blood pressure support increased PtO(2) and MCA flow during both SNP and 3% isoflurane treatment. These results show that SNP is a cerebrovasodilator but that hypotension will decrease PtO(2), probably because of an increase in arteriovenous shunting and a decrease in capillary perfusion. IMPLICATIONS: We measured brain arteriovenous shunting and tissue oxygen pressure(PtO(2))during a 40% decrease in blood pressure induced by sodium nitroprusside (SNP)or 3% isoflurane. Large-dose isoflurane maintainedPtO(2) with no change in shunting. SNP infusion decreasedPtO(2) 50%and increased shunting 50%. This suggests that SNP-induced hypotension decreases PtO(2) because of a decrease in capillary perfusion.

Anesthetics, Inhalation↗

PubMed2001

Combining median electroencephalography frequency and sympathetic activity in an index to evaluate opioid detoxification in patients.

During rapid opioid detoxification, increased sympathetic activity and a greater median frequency (MF) of activity on electroencephalography (EEG) have been reported. The purpose of this study was to evaluate a new index for detoxification that combines sympathetic activity and MF data. After informed consent was obtained, eight patients were sedated with propofol. The MF of EEG activity derived from frontal electrodes was determined. Heart rate variability was evaluated in 256-second segments by power spectral analysis, and sympathetic activity was determined by the low frequency component. The Hoffman Index for narcotic detoxification was weighted 70% to sympathetic activity and 30% to MF to normalize the difference in scales and to provide adequate weight to the sympathetic component. Opioid detoxification was produced by infusion of 25 mg naloxone for 30 minutes, followed by a 24-hour infusion of 1 mg per hour. The MF showed a rapid increase during high-dose infusion of naloxone, but the peak response occurred 1 to 2 hours later. Sympathetic activation and the Hoffman Index increased more slowly after the start of naloxone infusion, but peak increases in all components occurred at approximately the same time. The peak increases in Hoffman Index (110% of baseline), MF (260%), and sympathetic activity (304%) during administration of naloxone were significant and correlated with respect to time (r = 0.89-0.94). The Hoffman Index showed an early increase related to MF and a well-defined peak response indicative of sympathetic and MF activity. The behavior of the Hoffman Index in relation to the MF and sympathetic activity more clearly indicated the onset of opioid detoxification and the maximum response to opioid reversal than did MF or sympathetic activity alone.

Electrocardiography↗

PubMed2001

Brain compared to heart tissue oxygen pressure during changes in arterial carbon dioxide in the dog.

Myocardial tissue oxygen pressure (PmO2 ) and left anterior descending (LAD) artery blood flow were measured in dogs anesthetized with 1.5% isoflurane, and were then compared to brain tissue oxygen pressure (PbO2 ) and middle cerebral artery (MCA) blood flow during normocapnia, hypocapnia, and hypercapnia. A craniotomy was performed and a tissue probe (Codman, Inc.) that measures PO2, PCO2, and pH was inserted into the brain cortex in the MCA region (n = 8). Separately, after a thoracotomy, a probe was inserted into the middle myocardium of the left ventricle, within the distribution of the LAD, in eight dogs. Blood flow probes were placed on the LAD or MCA. Blood flow and tissue gases were measured during normocapnia (PaCO2 = 38 mm Hg), hypocapnia (PaCO2 = 26 mm Hg), and hypercapnia (PaCO2 = 53 mm Hg). Mean arterial pressure, heart rate, arterial gases, and pH were not different between brain and heart measurements. PbO2 was 21 +/- 9 mm Hg (mean +/- SD ), 40 +/- 16 mm Hg, and 47 +/- 11 mm Hg. PmO2 was 35 +/- 12 mm Hg, 40 +/- 14 mm Hg, and 48 +/- 15 mm Hg during hypocapnia, normocapnia, and hypercapnia respectively. During hypercapnia, LAD and MCA flow increased 50% and tissue oxygenation increased 20% ( P < .05). During hypocapnia, MCA flow and PbO2 decreased 50% ( P < .05), but LAD flow and PmO2 did not significantly change. These results indicated that LAD flow and myocardial PO2 were less responsive to hypocapnia than MCA flow and PbO2.

Animals↗

PubMed2000

Brain tissue PO(2), PCO(2), and pH during cerebral vasospasm.

BACKGROUND: The purpose of the present study was to assess brain tissue monitoring for detection of ischemia due to vasospasm in aneurysmal subarachnoid hemorrhage (SAH) patients. METHODS: After obtaining informed consent, a burr hole was made in 10 patients and a Neurotrend 7 probe was inserted ipsilateral to the region of SAH. In eight patients the probe was inserted during surgery for clipping the aneurysm and in two patients the probe was inserted in the neurosurgery ICU. Brain tissue gases and pH were collected over 6-hour periods for 7 to 10 days until the termination of monitoring. The onset of vasospasm was confirmed by angiography and xenon computed tomography (Xe/CT) cerebral blood flow studies. RESULTS: Seven patients did not develop vasospasm during monitoring and were considered as controls. In this group, brain tissue oxygen pressure (PO(2)) remained above 20 mmHg, carbon dioxide pressure (PCO(2)) stabilized at 40 mmHg and pH remained between 7.1 and 7.2. In three patients who developed vasospasm during monitoring, PO(2) was not different from the control group. However, PCO(2) increased to 60 mmHg and pH decreased to 6.7 (p < 0.001). CONCLUSION: In this study, patients with SAH who developed vasospasm had significantly lower brain tissue pH and higher PCO(2) compared to controls. However, there was no significant change in PO(2) levels associated with vasospasm. Brain tissue monitoring can provide an indication of ischemia during vasospasm.

Aged↗

PubMed2000

Cerebral oxygen reactivity in the dog.

Brain tissue oxygen reactivity is a measure of the increase in tissue oxygen pressure (PtO2) relative to an increase in arterial oxygen pressure (PaO2). Clinical studies show that PtO2 reactivity is increased after cerebral injury. However, the impact of patient ventilation on these measures is not known. We determined whether changes in end tidal carbon dioxide pressure (ETCO2) would affect PtO2 reactivity in dogs. After a craniotomy, a Neurotrend probe that measures PtO2 was inserted into the cerebral cortex of eight dogs. PtO2 reactivity was measured at five concentrations of inspired oxygen (room air, 40%, 60%, 80%, 95%) at three levels of ETCO2 (20 mmHg, 40 mmHg, 60 mmHg) in random order. PtO2 reactivity at ETCO2 of 20 mmHg was 0.2 and increased to 0.3 when ETCO2 was 40 mmHg was 0.4 when ETCO2 was 60 mmHg (p < 0.05). These results show that PtO2 reactivity increases from hypocapnia to normocapnia. It is important to consider the ventilation state of each patient when evaluating PtO2.

Animals↗

PubMed2000

Comparison of brain tissue and local cerebral venous gas tensions and pH.

Neurosurgical monitoring devices have recently become available which are capable of measuring cerebral tissue gas tensions and pH. Brain tissue sensors have not been conclusively demonstrated to correlate with other measurements of regional cerebral gas tensions or pH. The present study was undertaken to correlate sensor values for pO2, pCO2 and pH with blood samples taken concurrently from local cerebral veins. Adult mongrel dogs were anesthetized and a craniotomy was performed. A small gyral vein was isolated and cannulated. Adjacent to the venous catheter tip, a Neurotrend brain tissue probe was inserted in an intracortical location. Each subject received a sequence of manipulations in inspired oxygen and end tidal carbon dioxide conditions. Under each experimental condition, samples of arterial and gyral venous blood were obtained and blood gas analysis performed. Concurrent brain probe measurements of tissue pO2, pCO2 and pH were recorded. Statistical analysis determined that local tissue and cerebral venous blood values for pO2, pCO2 and pH were highly correlated (R(s) = 0.62-0.82; p < 0.001). This indicates that there exists a confirmable monotonic relationship between tissue values and conditions in the post-capillary venous bed. Tissue sensors such as the Neurotrend probe can offer reliable trend indications in brain tissue gas tensions and pH.

Animals↗

PubMed2000

Isoflurane increases brain oxygen reactivity in dogs.

UNLABELLED: We tested the possibility that large-dose isoflurane will produce a loss of brain tissue oxygen regulation in dogs. A total of 12 dogs were anesthetized with isoflurane, a craniotomy was performed, and a probe was inserted to measure brain tissue oxygen pressure (PtO(2)), carbon dioxide, and pH. Baseline measures were made during 1.5% end-tidal isoflurane with 30% oxygen ventilation, followed by 95% oxygen ventilation. Six dogs (Group 1) were treated with 3% isoflurane and 30% oxygen, followed by a second oxygen challenge with 95% O(2). Six dogs (Group 2) received propofol to produce a similar suppression of the electroencephalogram as in Group 1, followed by 95% oxygen ventilation. Brain tissue oxygen reactivity was calculated by the increase in PtO(2) divided by the increase in arterial PO(2). During 1.5% isoflurane and propofol anesthesia, PtO(2) increased from 42 to 62 mm Hg with oxygen ventilation, and brain tissue oxygen reactivity was 0.14% per mm Hg(-1). Brain tissue oxygen reactivity did not change during propofol anesthesia. With 3% isoflurane, PtO(2) increased from 52 to 113 mm Hg and brain tissue oxygen reactivity was 0.36% per mm Hg(-1) (P: < 0.05). These results suggest that the cerebrovasodilator and vasoplegic effects of large-dose isoflurane attenuate brain oxygen regulation. IMPLICATIONS: We evaluated the ability of oxygen ventilation to increase brain tissue oxygen pressure in dogs anesthetized with 1.5% and 3% isoflurane and propofol. Increases in tissue oxygen were significantly greater during 3% isoflurane compared with 1.5% isoflurane and propofol.

Algorithms↗

PubMed2000

Hypoxic brain tissue following subarachnoid hemorrhage.

BACKGROUND: Subarachnoid hemorrhage can lead to cerebral ischemia and irreversible brain injury. The purpose of this study was to determine whether subarachnoid hemorrhage produces changes in brain tissue oxygen pressure, carbon dioxide pressure, or pH during surgery for cerebral aneurysm clipping. METHODS: After institutional review board approval and patient consent, 30 patients undergoing craniotomy for cerebral aneurysm clipping were studied, 15 without and 15 with subarachnoid hemorrhage. Patients with subarachnoid hemorrhage were prospectively separated into groups with modest (Fisher grade 1 or 2; n = 8) and severe bleeds (Fisher grade 3; n = 7). After a craniotomy, a probe was inserted into cortex tissue supplied by the artery associated with the aneurysm. Baseline measures were made in the presence of a 4% end-tidal desflurane level. The end-tidal desflurane level was increased to 9% before clipping of the aneurysm, and a second tissue measurement was made. RESULTS: The median time of surgery after subarachnoid hemorrhage was 2 days, ranging from 1 to 13 days. During baseline anesthesia, brain tissue oxygen pressure was 17+/-9 mm Hg (mean +/- SD) in control patients, 13+/-9 mm Hg in those with Fisher grade 1 or 2 hemorrhage, and 7+/-6 mm Hg in those with Fisher grade 3 hemorrhage (P<0.05 compared with control). Brain tissue pH was 7.10+/-0.10 in control patients, 7.14+/-0.13 in those with Fisher grade 1 or 2 hemorrhage, and 6.95+/-0.18 in those with with Fisher grade 3 hemorrhage (P<0.05). At a 9% end-tidal desflurane level, brain tissue oxygen pressure increased to 19+/-9 mm Hg and brain tissue pH increased to 7.11+/-0.11 in patients with Fisher grade 3 hemorrhage (P<0.05 for both increases). CONCLUSION: These results show that subarachnoid hemorrhage can significantly decrease brain tissue oxygen pressure and pH related to the severity of the bleed. Increasing the desflurane concentration to 9% increased brain tissue oxygen pressure in all patients and brain tissue pH in patients with subarachnoid hemorrhage with baseline acidosis.

Adult↗

PubMed2000

Enhancement of brain tissue oxygenation during high dose isoflurane anesthesia in the dog.

It is reported that high dose desflurane can increase brain tissue oxygen pressure (PtO2) in patients during cerebral aneurysm surgery. The purpose of this study was to determine whether high dose isoflurane anesthesia can produce a similar effect in dogs and the importance of cerebral perfusion pressure in mediating this effect. Six dogs were anesthetized, and ventilated with isoflurane inspired oxygen concentration of 40%. Following a craniotomy, a catheter was inserted into the sagittal sinus for cerebral venous blood samples and a Neurotrend probe was inserted into cortex brain tissue to measure PtO2, carbon dioxide pressure (PtCO2), and pH (pHt). Brain tissue and arterial and sagittal sinus blood gas tensions and pH were measured under the following conditions: 1 = baseline 1.5% isoflurane, 2 = 1.5% isoflurane + increase mean arterial pressure (MAP) by 50 mm Hg, 3 = 3% isoflurane anesthesia, 4 = 3% isoflurane anesthesia + increase MAP 55 mm Hg, 5 = 1.5% isoflurane anesthesia, 6 = 1.5% isoflurane anesthesia + increase MAP 35 mm Hg. In the first and second trial with 1.5% end-tidal isoflurane, PtO2 increased 15% during an increase in MAP without a change in sagittal sinus oxygenation. At 3% isoflurane, PtO2 increased 90% and sagittal sinus PO2 increased 38% during an increase in MAP. These results show that the cerebral metabolic depression and cerebrovasodilatory effects of high dose isoflurane can enhance brain tissue oxygenation. Normal brain vascular regulation that limits hyperperfusion and hyperoxygenation of brain tissue is antagonized by high dose isoflurane.

Anesthesia, Inhalation↗

PubMed2000

Plasma naltrexone during opioid detoxification.

Orogastric naltrexone is used for opioid detoxification, but it is not known how gastric absorption affects plasma concentrations of the drug. We measured plasma naltrexone during orogastric naltrexone, given in repeated doses of 12.5 mg, 25 mg, 50 mg and 50 mg. Plasma naltrexone was measured after each naltrexone dose. The increase in plasma naltrexone was highly variable between patients during orogastric administration. Adequate detoxification was questioned in 4 of 10 patients because plasma naltrexone did not increase above 5 ng/ml. There was a negative correlation between plasma naltrexone and the presence of withdrawal symptoms on the day after the procedure (r = -0.78, P < 0.05). These results show that the increase in plasma naltrexone is variable during orogastric administration and this may impair successful detoxification.

Administration, Oral↗

PubMed1999

What does measurement of brain tissue pO2, pCO2 & pH add to neuromonitoring?

In this paper the rationale behind utilizing the brain tissue measurements of oxygen, carbon dioxide, pH and temperature is evaluated in the context of ischemia. These parameters were measured using an intraparenchymal multi-parametric brain tissue monitor (Paratrend 7). The need to establish the relevance of this type of monitoring becomes acute as further experience is gained using this kind of technology. Our experience with such a device is presented and is illustrated with two clinical cases. The potential caveats and areas of possible future work are also delineated.

Acute Disease↗

PubMed1999

Measurement of ischemia by changes in tissue oxygen, carbon dioxide, and pH.

BACKGROUND: We evaluated the ability of brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2), and pH to detect regional ischemia produced by temporary brain artery occlusion, compared with a group without artery occlusion. METHODS: Patients undergoing craniotomy for cerebrovascular surgery were recruited for this study. A 0.5-mm-diameter probe was inserted into brain tissue to measure PO2, PCO2, and pH continuously. Group 1 (n = 15) did not receive brain artery occlusion during their surgical procedure. In Group 2, brain artery occlusion was produced for aneurysm clipping (n = 10) or extracerebral to intracerebral artery bypass (n = 3). Mean arterial pressure was maintained above 90 mmHg in both groups. Measurements were made after artery occlusion or sham treatment and compared with baseline. RESULTS: Under baseline conditions, tissue PO2, PCO2, and pH were not different between the groups. In Group 2, brain artery occlusion for a median time of 7 minutes (range, 2-48 min) significantly decreased PO2 and pH and increased PCO2 compared with baseline. There were no significant changes in Group 1. During artery occlusion, PO2 decreased below 10 mmHg and/or pH decreased below 7.0 in 8 of 13 patients. CONCLUSIONS: Regional brain ischemia can be consistently detected and treated by monitoring tissue metabolism. It will be necessary in the future to identify critical levels and duration of decreases in PO2 and pH that lead to irreversible neuronal injury.

Brain↗

PubMed1999

Cerebral venous and tissue gases and arteriovenous shunting in the dog.

UNLABELLED: Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (P(CO2)) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures P(O2), P(CO2), pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue P(O2) and Pco2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal Pco2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and C(O2) content in artery, vein, and tissue, representing capillary. Tissue P(CO2) was 8 mm Hg greater than vein Pco2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein P(O2) was 8 mm Hg higher than tissue P(O2) during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%-20% during hypocapnia to 50%-60% during hypercapnia. These results show that brain vein and tissue P(O2) and P(CO2) differ because of arteriovenous shunting and this difference is increased as end-tidal P(CO2) increases. IMPLICATIONS: We found, in dogs, that the gradient between brain venous and tissue P(O2) and PCO2 is increased with increased arterial P(CO2). The divergence between tissue and venous gases can be described by arterial to venous shunting.

Animals↗

PubMed1999

Measurement of intracerebral oxygen pressure: practicalities and pitfalls.

Two probes, using different technologies, are currently available to measure tissue oxygen pressure. One of these also measures oxygen pressure, carbon dioxide pressure, pH and temperature. Research has delineated normal brain tissue oxygen pressure as 25-45 mmHg and ischemic thresholds of less than 10 mmHg that are related to ischemic injury. Oxygen pressure measures are correlated with other indicators of brain oxygenation such as jugular bulb oxygen saturation and near infrared spectroscopy, but are more reliable for detecting regional ischemic events. Oxygen pressure is correlated with local blood flow in the brain, and treatments that enhance tissue perfusion improve oxygenation.

Journal Article↗

PubMed1999

The effect of anticonvulsant therapy on two doses of rocuronium-induced neuromuscular blockade.

Larger and more frequent doses of steroidal neuromuscular blocking agents are required to paralyze patients taking anticonvulsants (carbamazepine and phenytoin). We compared the effects of rocuronium on onset, duration, and speed of recovery from neuromuscular blockade (NMB) in anticonvulsant-treated (Tx) and untreated (C or control) patients. Thirty-eight neurosurgical patients were enrolled: 11 Tx and 8 C patients received 0.6 mg/kg rocuronium; 9 Tx and 10 C patients received 1.2 mg/kg rocuronium. Anesthesia was induced with midazolam, fentanyl, and thiopental, and maintained with N2O and isoflurane in O2. The evoked compound electromyograph (EMG) of the hypothenar eminence was recorded (train-of-four supramaximal stimulus at 2 Hz every 20 seconds). Rocuronium was administered after baseline EMG was recorded. Data = mean +/- SD. Rocuronium 1.2 mg/kg significantly shortened onset time [depression of baseline height of first twitch (T1) to 10% of baseline] of NMB versus rocuronium 0.6 mg/kg in both Tx (2.5+/-2 versus 3.3+/-2 minutes) and C (1.3+/-1 versus 2.8+/-1 minute) patients. Duration (recovery to 25% of T1) of NMB was significantly shorter in the Tx patients than in the C patients who received rocuronium 0.6 mg/kg (21+/-9 versus 45+/-20 minutes), but similar in Tx and C patients who received 1.2 mg/kg rocuronium (56+/-24 versus 69+/-21 minutes). The speed of recovery (time from 10 to 25% recovery of T1) was significantly slower in Tx patients who received 1.2 mg/kg rocuronium (9+/-5 minutes) than in those who received 0.6 mg/kg (5+/-3 minutes) and not different from controls who received 0.6 (9+/-4 minutes) or 1.2 mg/kg (12+/-7 minutes) rocuronium. We recommend the use of rocuronium 1.2 mg/kg and very frequent monitoring of NMB in anticonvulsant-treated patients to avoid premature and extremely rapid recovery after the standard 0.6 mg/kg rocuronium.

Adult↗

PubMed1999

Heart rate variability and plasma catecholamines in patients during opioid detoxification.

It has been shown that rapid opioid detoxification is associated with increased sympathetic activity (SYMP) and plasma catecholamines. Heart rate (HR) variability may provide a noninvasive method of evaluating withdrawal and sympathetic activation caused by the reversal of opioid binding in patients who are opioid dependent. The purpose of this study was to evaluate the relationship between HR variability and plasma catecholamines during opioid detoxification. Patients were anesthetized with propofol, intubated, paralyzed with rocuronium infusion, and ventilated. The bispectral index (BIS) of the electroencephalogram was recorded with the patient awake as well as during propofol anesthesia. SYMP was determined by power spectral analysis of HR variability. Plasma epinephrine and norepinephrine were measured at baseline propofol anesthesia and during naltrexone treatment in eight opioid-dependent patients. Nonopioid-dependent controls (n = 7) were monitored during surgery without naltrexone treatment or measurement of plasma catecholamines. Compared with an awake status, propofol anesthesia significantly decreased the BIS and SYMP in both groups of patients. Controls showed no change from baseline anesthetized levels during surgery. Plasma norepinephrine and epinephrine as well as SYMP increased 300 to 400% (P < .05) during naltrexone treatment in opioid-dependent patients, and the time to peak increase in plasma norepinephrine correlated with the increase in SYMP (r = 0.89, P < .01). These results confirm that opioid detoxification increases plasma catecholamines and SYMP in a similar manner. HR rate variability may provide a low-cost real-time noninvasive method of evaluating the reversal of opioid binding in opioid-dependent patients.

Adult↗

PubMed1999

Median EEG frequency is more sensitive to increases in sympathetic activity than bispectral index.

Sympathetic heart rate variability is correlated with the increase in plasma catecholamines during rapid opioid detoxification. We evaluated whether the bispectral index, median frequency, or 95% spectral edge of the electroencephalogram are sensitive to the sympathetic response seen during reversal of opioid dependence. Eight patients undergoing rapid opioid detoxification gave informed consent. Two-channel frontal electroencephalogram was measured. Sympathetic heart rate variability was measured in 256 second segments by Fourier transform of continuous heart rate and the low frequency segment (0.02-0.13 Hz) analyzed for sympathetic function. Patients were anesthetized with propofol infusion. After a 30-60 min steady state, naloxone was infused intravenously at a rate of 25 mg/30 min, followed by an infusion of 1 mg/hr. During induction of anesthesia, sympathetic heart rate variability decreased from 1.80 to 0.3, bispectral index from 86 to 47, median frequency from 10.2 to 3.4, spectral edge from 23.5 to 16.7 (all P<.05). During naloxone infusion, the median percent increase in sympathetic heart rate variability was 487% (P<.05), median frequency increased 163% (P<.05), bispectral index (10%), and spectral edge (7%) did not significantly change. The increase in median frequency was delayed compared to sympathetic heart rate variability and median frequency remained elevated after sympathetic heart rate variability returned to anesthetized baseline in 5 of 8 cases. Our results show that median frequency and sympathetic heart rate variability increase during opioid detoxification, but the time course of each response is different. Median frequency is a more sensitive electroencephalogram indicator of opioid reversal than bispectral index or spectral edge.

Anesthesia, Intravenous↗