Acta Anaesthesiol &and 1990: 34, Supplementum 92: 65-69
The respiratory effects of reversing midazolarn sedation with flumazenil in the presence or absence of narcotics A. WEINBRUM and E. GELLER Department of Anesthesiology and ICU, Ichilov Hospital, Tel-Aviv Medical Center and the Sackler School of Medicine, Tel-Aviv University, Israel
The purpose of this study was to determine the effects of reversal of sedation with flumazenil (F), in the presence or absence of opiates, on arterial oxygen saturation (Sao,) and end-tidal CO, (Eso,). Twenty-four patients undergoing surgery and epidural anaesthesia were studied. Twelve patients (Group A) were orally premedicated with diazepam and 0.1 mg . kg-' morphine i.m. Intraoperative sedation consisted of midazolam 0.1 mg. kg-' and pethidine 0.7 mg. kg-' i.v. Twelve patients (Group B) were premedicated with diazepam and sedated intraoperatively with 0.1 m g . kg-' midazolam. I n the recovery room, six patients in each group were randomly allocated to receive 1 rng offlumazenil while the others were allowed to awaken spontaneously (control). Sedation (eyes open vs closed), Sao,, E.,co,, respiratory rate, blood pressure and pulse were noninvasively monitored for 90 rnin. Administration of flumazenil resulted in a statistically significant increase in the number of patients with eyes open in both groups at 5 min, lasting 15 min in Group A and 30 rnin in Group B patients. An increase in Sao, from 15-45 min after injection of flumazenil was observed only in Group B. No significant difference between groups in any other parameter was found. We concluded that reversal of benzodiazepine (BZ) sedation with flumazenil improved Sao, in patients sedated with only BZ; in the presence of BZ and opiates, flumazenil did not affect respiratory parameters.
K g words: Benzodiazepine antagonist; flumazenil; regional anesthesia; respiratory effects.
Benzodiazepines (BDZ) are frequently used for sedation of patients undergoing surgery under local or regional anaesthesia as well as for induction and maintenance of general anaesthesia. Opiates are often added as pre-medication or intravenous supplementation for analgesia. BDZ have previously been shown to cause depression of the ventilatory responses to carbon dioxide (CO,) (1, 2) as well as depression of hypoxic ventilatory responses (3). Recently it has been suggested that flumazenil, when used to antagonise the sedative effects of BDZ, may cause arterial oxygen desaturation (4)and either a worsening (5) or full reversal (6) of the depressed ventilatory responses to carbon dioxide. I n the present study arterial O2 saturation (Sao,) and end-tidal CO, were monitored in patients recovering from surgery under regional anaesthesia with BDZ and opioid sedation, reversed with flumazenil.
in Table 1. Approval of the study by the ethics committee and written informed consent from each patient were obtained. The patients were divided into two equal groups: Group A (12 patients) were premedicated with diazepam 5-10 mg orally and 0.1 mg. kg-' morphine i.m. 1 h before surgery. For intra-operative sedation pethidine 0.7 mg.kg-' and rnidazolam 0.1 mg.kg-' i.v. were given. Group B (12 patients) were sedated with only BDZ: diazepam 5-10 mg orally 1 h before surgery and midazolam 0.1 mg . kg-' i.v. for intra-operative sedation. I n the recovery room all patients were observed for 15 min and then, in a random order, half of the patients in each group were slowly injected with 1 mg of flumazenil i.v., while the other half (control) were allowed to awaken spontaneously. All patients were then studied for 90 min. The following parameters were continuously measured and recorded, every 5 min: Sao, by pulse oximetry, end tidal GO,, respiratory rate, blood pressure and pulse (Cardiocap, Datex Corporation, Finland). Sedation was assessed as: eyes open - awake, eyes closed asleep. Patients requiring supplemental oxygen to relieve hypoxaemia were excluded from the study. Statistical analysis consisted of analysis of variance to detect significant differences (P
The respiratory effects of reversing midazolarn sedation with flumazenil in the presence or absence of narcotics A. WEINBRUM and E. GELLER Department of Anesthesiology and ICU, Ichilov Hospital, Tel-Aviv Medical Center and the Sackler School of Medicine, Tel-Aviv University, Israel
The purpose of this study was to determine the effects of reversal of sedation with flumazenil (F), in the presence or absence of opiates, on arterial oxygen saturation (Sao,) and end-tidal CO, (Eso,). Twenty-four patients undergoing surgery and epidural anaesthesia were studied. Twelve patients (Group A) were orally premedicated with diazepam and 0.1 mg . kg-' morphine i.m. Intraoperative sedation consisted of midazolam 0.1 mg. kg-' and pethidine 0.7 mg. kg-' i.v. Twelve patients (Group B) were premedicated with diazepam and sedated intraoperatively with 0.1 m g . kg-' midazolam. I n the recovery room, six patients in each group were randomly allocated to receive 1 rng offlumazenil while the others were allowed to awaken spontaneously (control). Sedation (eyes open vs closed), Sao,, E.,co,, respiratory rate, blood pressure and pulse were noninvasively monitored for 90 rnin. Administration of flumazenil resulted in a statistically significant increase in the number of patients with eyes open in both groups at 5 min, lasting 15 min in Group A and 30 rnin in Group B patients. An increase in Sao, from 15-45 min after injection of flumazenil was observed only in Group B. No significant difference between groups in any other parameter was found. We concluded that reversal of benzodiazepine (BZ) sedation with flumazenil improved Sao, in patients sedated with only BZ; in the presence of BZ and opiates, flumazenil did not affect respiratory parameters.
K g words: Benzodiazepine antagonist; flumazenil; regional anesthesia; respiratory effects.
Benzodiazepines (BDZ) are frequently used for sedation of patients undergoing surgery under local or regional anaesthesia as well as for induction and maintenance of general anaesthesia. Opiates are often added as pre-medication or intravenous supplementation for analgesia. BDZ have previously been shown to cause depression of the ventilatory responses to carbon dioxide (CO,) (1, 2) as well as depression of hypoxic ventilatory responses (3). Recently it has been suggested that flumazenil, when used to antagonise the sedative effects of BDZ, may cause arterial oxygen desaturation (4)and either a worsening (5) or full reversal (6) of the depressed ventilatory responses to carbon dioxide. I n the present study arterial O2 saturation (Sao,) and end-tidal CO, were monitored in patients recovering from surgery under regional anaesthesia with BDZ and opioid sedation, reversed with flumazenil.
in Table 1. Approval of the study by the ethics committee and written informed consent from each patient were obtained. The patients were divided into two equal groups: Group A (12 patients) were premedicated with diazepam 5-10 mg orally and 0.1 mg. kg-' morphine i.m. 1 h before surgery. For intra-operative sedation pethidine 0.7 mg.kg-' and rnidazolam 0.1 mg.kg-' i.v. were given. Group B (12 patients) were sedated with only BDZ: diazepam 5-10 mg orally 1 h before surgery and midazolam 0.1 mg . kg-' i.v. for intra-operative sedation. I n the recovery room all patients were observed for 15 min and then, in a random order, half of the patients in each group were slowly injected with 1 mg of flumazenil i.v., while the other half (control) were allowed to awaken spontaneously. All patients were then studied for 90 min. The following parameters were continuously measured and recorded, every 5 min: Sao, by pulse oximetry, end tidal GO,, respiratory rate, blood pressure and pulse (Cardiocap, Datex Corporation, Finland). Sedation was assessed as: eyes open - awake, eyes closed asleep. Patients requiring supplemental oxygen to relieve hypoxaemia were excluded from the study. Statistical analysis consisted of analysis of variance to detect significant differences (P
