Mid-Latency Auditory Evoked Potentials Differentially Predict Sedation and Drug Level Under Opioid and Hypnotic Agents
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Mid-Latency Auditory Evoked Potentials Differentially Predict Sedation and Drug Level Under Opioid and Hypnotic Agents. / Supp, Gernot G; Higgen, Focko L; Hipp, Joerg F; Engel, Andreas K; Siegel, Markus.
In: FRONT PHARMACOL, Vol. 9, 04.12.2018, p. 1427.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Mid-Latency Auditory Evoked Potentials Differentially Predict Sedation and Drug Level Under Opioid and Hypnotic Agents
AU - Supp, Gernot G
AU - Higgen, Focko L
AU - Hipp, Joerg F
AU - Engel, Andreas K
AU - Siegel, Markus
PY - 2018/12/4
Y1 - 2018/12/4
N2 - Background: Auditory-evoked brain potentials (AEPs) are widely used to assess depth of the sedative component of general anesthesia. Depth of sedation as induced by hypnotic drugs (e.g., propofol) is characterized by a gradual decline of mid-latency cortical AEPs (10-50 ms). Using the decline of mid-latency AEPs as a reliable index for sedation requires its robustness against confounding pharmaceutical influences, e.g., analgesic opioids such as remifentanil. Critically, in this context the following two questions remained unresolved so far: First, it is unclear whether opioids directly affect mid-latency AEPs. Second, high doses of opioids decrease arousal, but it is unknown whether opioid-induced sedation is reflected by the diminution of mid-latency AEPs. We hypothesized that opioids affect mid-latency AEPs and that these effects rely on different mechanisms compared to hypnotic agents. Methods: To address both questions, we performed a series of experiments under the participation of healthy human volunteers. We measured AEPs and quantified participants' sedation state by a standardized rating scale during stepwise increase of different pharmaceutical agents (remifentanil, propofol or placebo). Results: Our results revealed a decline of mid-latency AEPs during remifentanil medication. This decrease was predicted by drug dose, rather than sedation level. In contrast, attenuation of the mid-latency AEPs during propofol was predicted by sedation level and was not related to hypnotic drug dose. We did not find any drug-induced changes of brainstem AEPs (1-10 ms). Conclusion: As remifentanil reduced mid-latency AEPs without inducing strong sedation levels, a decrease of this evoked brain component does not constitute an unequivocal index for the depth of sedation. These results challenge the use of mid-latency AEPs as a reliable marker of depth of the sedative component of anesthesia if hypnotic drugs are combined with opioids.
AB - Background: Auditory-evoked brain potentials (AEPs) are widely used to assess depth of the sedative component of general anesthesia. Depth of sedation as induced by hypnotic drugs (e.g., propofol) is characterized by a gradual decline of mid-latency cortical AEPs (10-50 ms). Using the decline of mid-latency AEPs as a reliable index for sedation requires its robustness against confounding pharmaceutical influences, e.g., analgesic opioids such as remifentanil. Critically, in this context the following two questions remained unresolved so far: First, it is unclear whether opioids directly affect mid-latency AEPs. Second, high doses of opioids decrease arousal, but it is unknown whether opioid-induced sedation is reflected by the diminution of mid-latency AEPs. We hypothesized that opioids affect mid-latency AEPs and that these effects rely on different mechanisms compared to hypnotic agents. Methods: To address both questions, we performed a series of experiments under the participation of healthy human volunteers. We measured AEPs and quantified participants' sedation state by a standardized rating scale during stepwise increase of different pharmaceutical agents (remifentanil, propofol or placebo). Results: Our results revealed a decline of mid-latency AEPs during remifentanil medication. This decrease was predicted by drug dose, rather than sedation level. In contrast, attenuation of the mid-latency AEPs during propofol was predicted by sedation level and was not related to hypnotic drug dose. We did not find any drug-induced changes of brainstem AEPs (1-10 ms). Conclusion: As remifentanil reduced mid-latency AEPs without inducing strong sedation levels, a decrease of this evoked brain component does not constitute an unequivocal index for the depth of sedation. These results challenge the use of mid-latency AEPs as a reliable marker of depth of the sedative component of anesthesia if hypnotic drugs are combined with opioids.
KW - Journal Article
U2 - 10.3389/fphar.2018.01427
DO - 10.3389/fphar.2018.01427
M3 - SCORING: Journal article
C2 - 30564126
VL - 9
SP - 1427
JO - FRONT PHARMACOL
JF - FRONT PHARMACOL
SN - 1663-9812
ER -