Anesthesia and analgesia
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Anesthesia and analgesia · May 1998
Randomized Controlled Trial Clinical TrialThe effect of varied doses of epinephrine on duration of lidocaine spinal anesthesia in the thoracic and lumbosacral dermatomes.
The efficacy of epinephrine in prolonging spinal analgesia has recently been confirmed in the lumbosacral but not in the thoracic, segments. Most previous studies used doses of epinephrine smaller than 0.3 mg. We studied the effects of 0.2, 0.4, or 0.6 mg of epinephrine added to hyperbaric lidocaine 60 mg in 7.5% dextrose solution for spinal anesthesia. Eighty patients were randomly divided into four groups: Group A received lidocaine without epinephrine, Group B received lidocaine plus 0.2 mL (0.2 mg) of epinephrine 1:1000 solution, Group C received lidocaine plus 0.4 mL (0.4 mg) of epinephrine, and Group D received lidocaine plus 0.6 mL (0.6 mg) of epinephrine. The maximal cephalad sensory level was between T2 and T3 for all groups. The median times for analgesia to regress two and four segments were significantly prolonged in Group D, but not in either Group B or C, compared with those in Group A. Times for regression to T12 and L3 were significantly prolonged in Groups B, C, and D compared with Group A. We conclude that the dose-dependent relationship of spinal analgesia can be applied to epinephrine, and that larger doses prolong lidocaine spinal anesthesia in the thoracic as well as the lumbosacral dermatomes. ⋯ Prolongation of lidocaine spinal analgesia by intrathecal epinephrine is established in the lumbosacral, but not in the thoracic, dermatomes. Three doses of epinephrine--0.2, 0.4, and 0.6 mg--were compared. A dose-dependent response and significant prolongation with the 0.6-mg dose in the thoracic dermatomes were confirmed.
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Uptake of inhaled anesthetics may be measured as the amount of anesthetic infused to maintain a constant alveolar concentration of anesthetic. This method assumes that the patient absorbs all of the infused anesthetic, and that none is lost to circuit components. Using a standard anesthetic circuit with a 3-L rebreathing bag simulating the lungs, and simulating metabolism by input of carbon dioxide, we tested this assumption for halothane, isoflurane, and sevoflurane. Our results suggest that after washin of anesthetic sufficient to eliminate a material difference between inspired and end-tidal anesthetic, washin to other parts of the circuit (probably the ventilator) and absorbent (soda lime) continued to remove anesthetic for up to 15 min. From 30 min to 180 min of anesthetic administration, circuit components absorbed trivial amounts of isoflurane (12 +/- 13 mL vapor at 1.5 minimum alveolar anesthetic concentration, slightly more sevoflurane (39 +/- 15 mL), and still more halothane (64 +/- 9 mL). During this time, absorbent degraded sevoflurane (321 +/- 31 mL absorbed by circuit components and degraded by soda lime). The amount degraded increased with increasing input of carbon dioxide (e.g., the 321 +/- 31 mL increased to 508 +/- 48 mL when carbon dioxide input increased from 250 mL/min to 500 mL/min). Measurement of anesthetic uptake as a function of the amount of anesthetic infused must account for these findings. ⋯ Systems that deliver inhaled anesthetics may also remove the anesthetic. Initially, anesthetics may diffuse into delivery components and the interstices of material used to absorb carbon dioxide. Later, absorbents may degrade some anesthetics (e.g., sevoflurane). Such losses may compromise measurements of anesthetic uptake.
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Anesthesia and analgesia · May 1998
The arterial to end-tidal carbon dioxide gradient increases with uncorrected but not with temperature-corrected PaCO2 determination during mild to moderate hypothermia.
End-tidal carbon dioxide (PETCO2) monitoring is recommended as a basic standard of care and is helpful in adjusting mechanical ventilation. Gas solubility changes with temperature, which might affect the PaCO2 and thereby the gradient between PaCO2 and PETCO2 (PA-ETCO2) under hypothermic conditions. We investigated whether the PA-ETCO2 changes during mild to moderate hypothermia (36 degrees C-32 degrees C) using PaCO2 measured at 37 degrees C (uncorrected PaCO2) and PaCO2 corrected to actual body temperature. We preoperatively investigated 19 patients. After anesthesia had been induced, controlled ventilation was established to maintain normocarbia using constant uncorrected PaCO2 to adjust ventilation (alpha-stat acid-base regimen). Body core temperature was reduced without surgical intervention to 32 degrees C by surface cooling. Continuous PETCO2 was monitored with a mainstream PETCO2 module. The PA-ETCO2 was calculated using the uncorrected and corrected PaCO2 values. During body temperature reduction from 36 degrees C to 32 degrees C, the gradient between PETCO2 and uncorrected PaCO2 increased 2.5-fold, from 4.1 +/- 3.7 to 10.4 +/- 3.8 mm Hg (P < 0.002). The PA-ETCO2 remained unchanged when the corrected PaCO2 was used for the calculation. We conclude that when the alpha-stat acid-base regimen is used to adjust ventilation, the PA-ETCO2 calculated with the uncorrected PaCO2 increases and should be added to the differential diagnosis of widened PA-ETCO2. In contrast, when the corrected PaCO2 is used for the calculation of the PA-ETCO2, the PA-ETCO2 remains unaltered during hypothermia. ⋯ We investigated the impact of induced hypothermia (36 degrees C-32 degrees C) on the gradient between PaCO2 and PETCO2 (PA-ETCO2). The PA-ETCO2 increased 2.5-fold when CO2 determinations were not temperature-corrected. Hypothermia should be added to the differential diagnosis of an increased PA-ETCO2 when the alpha-stat acid-base regimen is used.
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Anesthesia and analgesia · May 1998
The effects of age and gender on the optimal premedication dose of intramuscular midazolam.
We conducted a double-blind study on the effects of age and gender on the optimal premedication dose of i.m. midazolam. We randomly divided 100 male and 100 female patients in each of three age groups: A = 20-39 yr, B = 40-59 yr, and C = 60-79 yr (total 600 patients) into five groups according to midazolam dosage: 0.04, 0.06, 0.08, 0.10, and 0.12 mg/kg. Midazolam was injected i.m. with atropine 0.01 mg/kg 15 min before the induction of anesthesia. Blood pressure (BP), heart rate, respiratory rate, oxygen saturation (SpO2), sedation level, tongue root depression, eyelash reflex, and anterograde amnesia were monitored. There were no significant differences between male and female patients in any variables in any age. Decrease of SpO2 and loss of eyelash reflex were seen with midazolam 0.10 mg/kg in Group A, and with 0.08 mg/kg in Group B. In Group C, decreases in BP and SpO2, loss of eyelash reflex, and depression of the tongue root were observed with midazolam 0.06 mg/kg. In conclusion, the optimal doses of i.m. midazolam administered 15 min before the induction of anesthesia in male or female patients were 0.08, 0.06, and 0.04 mg/kg for Groups A, B, and C, respectively. ⋯ Midazolam is the most widely used preoperative anxiolytic drug. Our purpose was to evaluate the optimal dose of i.m. midazolam that would maximize the desired effects and minimize the side effects in a common clinical setting. Results indicate that age, but not gender, should affect the i.m. midazolam dose selected for premedication.