Difference In The Hypnosedative And Analgesic Effect Of Potent Opioids

Opioids in general induce a dose-related hyposedative component, which is mirrored in the electroencephalogram by an increase of activity in the slow S- with concomitant decrease of power in the fast ^-domain. However, when giving a large bolus dose of fentanyl (7-10 pg/kg body weight) alfentanil (50 pg/kg body weight) morphine (3-10mg/kg body weight) or sufentanil (2-3 pg/kg body weight) an immediate dominance of delta-waves in the EEG becomes evident, being accompanied by sleep. For instance, such effects clinically are seen when high-dose opioid anesthesia is used in cardiac patients for the induction of anesthesia. Such a sleep-inducing effect is due to a short-term blockade of all afferences being switched in the activating reticular system (ARS) of the mesencephalon. Aside from a blockade within the nucleus limitans a deep level of analgesia is initiated [90]. Such a "narcotic component", with dominance of delta-activity in the EEG, and contrary to equi-analgesic doses of fentanyl, it is more apparent after sufentanil [91], which makes this agent more suitable for the induction of cardiac patients (Figure II-43).

Following induction with a potent p-ligand such as fentanyl or sufentanil the initial "narcotic component" later transforms into a "pure analgesic component". This is because the opioid is redistributed, which results in a lesser concentration within the CNS and a lesser binding in areas within the ARS. At this stage there is a

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Control 5 min post 1 min post 10 min post induction L&I L&I

Control 5 min post 1 min post 10 min post induction L&I L&I

Figure 11-43. Difference in the hynosedative effects of sufentanil and fentanyl following intravenous administration of equi-analgesic doses in cardiac patients undergoing laryngoscopy and intubation (L & I). Note, a pronounced delta activation after injection and a lesser arousal reaction induced by laryngoscopy and intubation, which in the sufentanil group reflected in a lesser decline of power in the slow delta-domain of the EEG. Adapted from [92]

dominance in the a-band (7—13 Hz) of the EEG, which is stable, not being affected by any nociceptive stimuli [93, 94]. Clinically, such an effect has been described for the precursor of fentanyl, the opioid phenoperidine [95] and for fentanyl [96]. After a period of 10-15 min the deep narcotic component changes into a sedative state, which is stable and cannot be reversed to desynchronization by any nociceptive stimulus. During such "analgesic state" the patient again is able to respond to verbal commands, while at the same time having a deep analgesic level (Figure II-44).

Without the addition of nitrous oxide, such patients are awake, however, nociceptive afferents are not able to modulate the ARS, the endotracheal tube is tolerated while at the same time nociception is only sensed as a touch. Such phenomena are due to afferents ascending along the spinothalamic tract, which directly ascend to the postcentral cortical area by which the impulse can be localized. Collaterals, which ascend through the nucleus limitans within the limbic system and convey nociception, are sufficiently blocked by the opioid and the patient does not perceive pain (Figure II-45).

The opioid receptor system bordering the fourth cerebral ventricle and the underlying activating reticular system is the relevant anatomical structure in mediating sedation. Selective perfusion of increasing concentrations of the opioid fentanyl in the awake canine induced a dose-related enlargement of slow-wave high amplitude delta-activity within the EEG, characterized by a sleep-like behavior (Figure II-46).

This effect was reversed by the levo-isomer of naloxone inducing an arousal reaction. It, however, was not reversible by the dextro-isomer of the antagonist [98]. The physiological significance of opioid receptors in the control of postcentral cortex thalamus the hypnotic component bf high dose ^opioids

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