Anesthesia and analgesia
-
Anesthesia and analgesia · May 1998
Randomized Controlled Trial Clinical TrialTracheal intubation with rocuronium using the "timing principle".
We compared the endotracheal intubating conditions after rocuronium, using the "timing principle," with those after succinylcholine. The timing principle entails administration of a single bolus dose of nondepolarizing muscle relaxant, followed by an induction drug at the onset of clinical weakness. Forty-five patients were randomly assigned to three groups. Patients allocated to Groups 1 and 2 received rocuronium 0.6 mg/kg. At the onset of clinical weakness (onset of ptosis), anesthesia was induced with thiopental 4-6 mg/kg; intubation was accomplished after 45 s in Group 1 and after 60 s in Group 2. Patients in Group 3 received vecuronium (0.01 mg/kg) 3 min before the administration of thiopental and succinylcholine 1.5 mg/kg, and their tracheas were intubated 60 s later by a blind anesthesiologist. Intubating conditions were assessed according to a grading scale and were either good (5 patients in Groups 1 and 2, 4 patients in Group 3) or excellent (10 patients in Groups 1 + 2, 11 patients in Group 3) in all patients. Patients were interviewed postoperatively, and all were satisfied with the induction of anesthesia. We conclude that rocuronium 0.6 mg/kg provides good to excellent intubating conditions 45 and 60 s after the induction of anesthesia using the timing principle. ⋯ We compared the ease with which a breathing tube could be placed in patients using three techniques. The standard technique (succinylcholine) was compared with two others in which a muscle-relaxing drug (rocuronium) was administered just before the anesthetic drug (so-called timing principle). No difference among the techniques was observed.
-
Anesthesia and analgesia · May 1998
Randomized Controlled Trial Comparative Study Clinical TrialQuantifying oral analgesic consumption using a novel method and comparison with patient-controlled intravenous analgesic consumption.
-
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.
-
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.