Anesthesia and analgesia
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Anesthesia and analgesia · Jul 1999
Randomized Controlled Trial Clinical TrialNitrous oxide increases endotracheal cuff pressure and the incidence of tracheal lesions in anesthetized patients.
The pressure in air-filled endotracheal cuffs increases steadily throughout general anesthesia with nitrous oxide (N2O). High cuff pressures can be responsible for local ischemia, which may induce tracheal mucosal injury. In this study, cuff pressure was monitored in anesthetized patients, and postanesthesia endotracheal lesions were assessed by endoscopy. Sixty-five patients undergoing general anesthesia with tracheal intubation >1 h in duration were randomized into two groups. The endotracheal tube cuff was inflated to 30-40 cm H2O with air in Group 1 (n = 33) and with a gas mixture (N2O 50% in oxygen) in Group 2 (n = 32). At the time of tracheal extubation, a fiberoptic examination via the endotracheal tube was performed by an independent observer. Aspects of trachea at the level of cuff contact area were scored as 0 = normal, 1 = mucosal erythema or edema, 2 = mucosal erosion or hemorrhage, 3 = mucosal erosion or hemorrhage on both anterior and posterior tracheal walls. Cuff pressure increased throughout the procedure (P<0.01) in Group 1 and remained stable in Group 2. In Group 1, tracheal lesions in the area of the cuff were more frequent than they were in Group 2 (79% vs. 37%; P<0.001). Tracheal injury was correlated to cuff pressure (r = 0.62, P<0.001). No postoperative respiratory complication was observed in any patient. In patients anesthetized with N2O, the inflation of the tracheal tube cuff with a gas mixture of the same composition as the inhaled mixture can prevent excessive cuff pressure and reduce the incidence of tracheal injury. ⋯ In patients anesthetized with nitrous oxide, the inflation of the tracheal tube cuff with a gas mixture of the same composition as the inhaled mixture can prevent excessive cuff pressure and reduce the incidence of tracheal injury.
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Anesthesia and analgesia · Jul 1999
Randomized Controlled Trial Clinical TrialPropofol anesthesia enhances pressor response to ephedrine in patients given clonidine.
We studied the hemodynamic effects of ephedrine in patients with or without clonidine premedication during either isoflurane or propofol anesthesia. Forty adult patients were randomly assigned to one of two groups: 20 patients received famotidine 20 mg orally (control group) and 20 received clonidine 3 microg/kg and famotidine 20 mg orally (clonidine group). Within each group, 10 patients were then anesthetized with isoflurane and 10 with propofol. Hemodynamic measurements were taken at 1-min intervals for 10 min after a bolus injection of ephedrine 0.1 mg/kg. The magnitude of the maximal pressor response to ephedrine was no different whether patients without clonidine were anesthetized with isoflurane (increase 5+/-7 mm Hg) or propofol (3+/-9 mm Hg); however, this response was greater (P<0.05) with propofol (17+/-6 mm Hg) versus isoflurane (6+/-5 mm Hg) in patients given clonidine. The arterial blood pressure increase in clonidine-premedicated patients with propofol anesthesia was the largest among the four subgroups. The heart rate response to ephedrine was not significant in patients anesthetized with isoflurane and was small but significant in those anesthetized with propofol. The present results, together with previous studies on the effect of ephedrine in patients medicated with clonidine, suggest that the interaction between clonidine and ephedrine is modulated by the anesthetic used. ⋯ We evaluated the pressor response to ephedrine during isoflurane or propofol anesthesia with or without clonidine premedication. Our study suggests that, in anesthetized patients premedicated with clonidine, decreases in blood pressure may be easier to reverse with ephedrine with some types of anesthesia (e.g., propofol) than with others (e.g., isoflurane).
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Anesthesia and analgesia · Jul 1999
The effects of nitrous oxide and oxygen on transient hyperemic response in human volunteers.
The aim of this study was to determine the effects of breathing 100% oxygen or 50% nitrous oxide in oxygen on the indices of cerebral autoregulation derived from the transient hyperemic response (THR) test in human volunteers. Data were analyzed from nine healthy subjects. Middle cerebral artery (MCA) blood flow velocity (FV) was measured by transcranial Doppler ultrasound, and the THR test was performed using 10-s compression of the common carotid artery. Continuous measurement of P(ETCO2) and expired fractions of oxygen (F(ETO2)) and nitrous oxide (F(ETN2O)) was established, and mean arterial pressure (MAP) was recorded at 2-min intervals. All measurements were performed while the volunteers were breathing room air and were repeated 10 min after achieving F(ETO2) >0.95 and 10 min after achieving F(ETN2O) 0.48-0.52. Two indices derived from the THR test, the transient hyperemic response ratio (THRR) and strength of autoregulation (SA), were used to assess cerebral autoregulation. P(ETCO2) and mean arterial pressure did not change significantly throughout the study period. Breathing 100% oxygen did not change MCA FV, THRR, or SA. Inhalation of nitrous oxide resulted in a marked and significant increase in the MCA FV (from 48+/-9 to 72+/-8 cm/s; mean +/- SD) and a significant decrease in the THRR (from 1.5+/-0.2 to 1.2+/-0.1) and the SA (from 1.0+/-0.1 to 0.8+/-0.1) (P<0.05 for all). We conclude that breathing 50% nitrous oxide in oxygen results in both a significant increase in MCA FV and impairment of transient hyperemic response. ⋯ Our study suggests that nitrous oxide impairs cerebral autoregulation and may have implications for its use in neurosurgical anesthesia and for interpretation of the results from studies of anesthetics in which nitrous oxide is used in the background.
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Anesthesia and analgesia · Jul 1999
Voiding in patients managed with or without ultrasound monitoring of bladder volume after outpatient surgery.
The goal of this study was to determine whether recovery room monitoring of bladder volume would affect patient outcome after ambulatory surgery. Incidence of urinary retention and times to void and to discharge were compared in 161 patients managed with ultrasound bladder monitoring versus 173 controls without bladder monitoring. Urinary retention was diagnosed by clinical means or by ultrasound, confirmed by bladder catheterization. Patients were required to void or were catheterized before discharge. In the control patients without underlying risk factors for retention, median time to void was 95 min, and retention occurred in 0.8%, which was not significantly different from the ultrasound group (80 min and 0%, respectively). After hernia/anal surgery or spinal/epidural anesthesia, voiding was delayed (130 and 213 min), incidence of retention was increased (17% and 13%), and there was a trend toward earlier voiding (168+/-99 vs. 138+/-68 min) with bladder monitoring. We conclude that most patients at low risk of retention void within 3 h of outpatient surgery; their outcome is unaffected by bladder monitoring. After hernia/anal surgery and spinal/ epidural anesthesia, the likelihood of urinary retention is increased, and ultrasound monitoring facilitates deciding whether such patients should be catheterized. ⋯ Incidence of bladder catheterization and urinary retention were compared in patients managed with and without ultrasound monitoring of bladder volume after outpatient surgery. Monitoring did not alter outcome in patients at low risk of retention, but it facilitated determining when to catheterize patients at high risk of retention (hernia/anal surgery, spinal/epidural anesthesia).
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Anesthesia and analgesia · Jul 1999
The spinal antinociceptive effects of a novel competitive AMPA receptor antagonist, YM872, on thermal or formalin-induced pain in rats.
Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonists have spinally mediated analgesic effects on acute nociception; however, their current formulations are not water-soluble and have toxic side effects. A new competitive AMPA antagonist, YM872 (2,3-dioxo-7-[1H-imidazol-1-yl]-6-nitro-1,2,3,4-tetrahydro-1-quinoxal inyl acetic acid) is water-soluble and may have fewer side effects. The purpose of this study was to investigate the analgesic effects of YM872 on both acute thermal and irritant-induced pain. Sprague-Dawley rats were implanted with chronic lumbar intrathecal catheters and were tested for their tail withdrawal response by the tail flick test and for their paw flinches by formalin injection after the intrathecal administration of YM872. The tail flick latency increased dose-dependently with a 50% effective dose (ED50) value of 1.0 microg. The number of flinches in both Phase 1 and Phase 2 of the formalin test decreased with increasing dose of YM872. ED50 values were 0.24 microg in Phase 1 and 0.21 microg in Phase 2. YM872 10 and 30 microg induced motor disturbance and flaccidity. In rats, the intrathecal administration of YM872 had analgesic effects on both acute thermal and formalin-induced nociceptions. Transient motor disturbance and flaccidity occurred only with large doses. YM872 may have potential in the clinical management of both acute and chronic pain. ⋯ A novel alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist, YM872, may have an analgesic effect on both acute and chronic pain when administered intrathecally.