Anesthesia and analgesia
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Anesthesia and analgesia · Jun 1999
Randomized Controlled Trial Clinical TrialEpidural phenylephrine attenuates hypotension induced by alkalinized lidocaine epidural anesthesia.
In this double-blinded, randomized study, we examined the hemodynamic effects of lumbar epidural injection of alkalinized lidocaine with phenylephrine in 81 patients undergoing inguinal herniorrhaphy. Patients assigned to four equal groups received 20 mL of alkalinized lidocaine (17 mL of 2% lidocaine + 3 mL of 7% sodium bicarbonate) with one of four doses of phenylephrine: 0 (Group 1), 50 (Group 2), 100 (Group 3), or 200 microg (Group 4) injected via a lumbar epidural catheter. Blood pressure, heart rate, and skin temperature on the foot were recorded every 5 min for 1 h after injection and were compared among groups. Hypotension was defined as mean arterial pressure < 80% of baseline. The incidence of hypotension was 45%, 55%, 35%, and 15% in Groups 1-4, respectively. Patients in Group 4 showed the smallest reduction in blood pressure compared with Groups 1 and 2 (one-sided Fisher's exact test, P < 0.05). We conclude that the 200-microg dose of epidural phenylephrine (1:100,000 concentration) reduced the incidence of hypotension after epidural anesthesia with alkalinized lidocaine. ⋯ Hypotension after epidural anesthesia is common in general clinical practice. Phenylephrine administered epidurally in combination with alkalinized lidocaine may reduce the incidence of hypotension.
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Anesthesia and analgesia · Jun 1999
Multicenter Study Clinical TrialMiddle latency auditory evoked responses and electroencephalographic derived variables do not predict movement to noxious stimulation during 1 minimum alveolar anesthetic concentration isoflurane/nitrous oxide anesthesia.
The electroencephalogram (EEG) and middle latency auditory evoked responses (MLAER) have been proposed for assessment of the depth of anesthesia. However, a reliable monitor of the adequacy of anesthesia has not yet been defined. In a multicenter study, we tested whether changes in the EEG and MLAER after a tetanic stimulus applied to the wrist could be used to predict subsequent movement in response to skin incision in patients anesthetized with 1 minimum alveolar anesthetic concentration (MAC) isoflurane in N2O. We also investigated whether the absolute values of any of these variables before skin incision was able to predict subsequent movement. After the induction of anesthesia with propofol and facilitation of tracheal intubation with succinylcholine, 82 patients received 1 MAC isoflurane (0.6%) in N2O 50% without an opioid or muscle relaxant. Spontaneous EEG and MLAER to auditory click-stimulation were recorded from a single frontoparietal electrode pair. MLAER were severely depressed at 1 MAC isoflurane. At least 20 min before skin incision, a 5-s tetanic stimulus was applied at the wrist, and the changes in EEG and MLAER were recorded. EEG and MLAER values were evaluated before and after skin incision for patients who did not move in response to tetanic stimulation. Twenty patients (24%) moved after tetanic stimulation. The changes in the EEG or MLAER variables were unable to predict which patients would move in response to skin incision. Preincision values were not different between patients who did and did not move in response to skin incision for any of the variables. MLAER amplitude increased after skin incision. We conclude that it is unlikely that linear EEG measures or MLAER variables can be of practical use in titrating isoflurane anesthesia to prevent movement in response to noxious stimulation. ⋯ Reliable estimation of anesthetic adequacy remains a challenge. Changes in spontaneous or auditory evoked brain activity after a brief electrical stimulus at the wrist could not be used to predict whether anesthetized patients would subsequently move at the time of surgical incision.
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Anesthesia and analgesia · Jun 1999
ReviewHypothesis: volatile anesthetics produce immobility by acting on two sites approximately five carbon atoms apart.
All series of volatile and gaseous compounds contain members that can produce anesthesia, as defined by the minimum alveolar anesthetic concentration (MAC) required to produce immobility in response to a noxious stimulus. For unhalogenated n-alkanes, cycloalkanes, aromatic compounds, and n-alkanols, potency (1 MAC) increases by two-to threefold with each carbon addition in the series (e.g., ethanol is twice as potent as methanol). Total fluorination (perfluorination) of n-alkanes essentially eliminates anesthetic potency: only CF4 is anesthetic (MAC = 66.5 atm), which indicates that fluorine atoms do not directly influence sites of anesthetic action. Fluorine may enhance the anesthetic action of other moieties, such as the hydrogen atom in CHF3 (MAC = 1.60 atm), but, consistent with the notion that the fluorine atoms do not directly influence sites of anesthetic action, adding -(CF2)n moieties does not further increase potency (e.g., CHF2-CF3 MAC = 1.51 atm). Similarly, adding -(CF2)n moieties to perfluorinated alkanols (CH2OH-[CF2]nF) does not increase potency. However, adding a second terminal hydrogen atom (e.g., CHF2-CHF2 or CH2OH-CHF2) produces series in which the addition of each -CF2- "spacer" in the middle of the molecule increases potency two- to threefold, as in each unhalogenated series. This parallel stops at four or five carbon atom chain lengths. Further increases in chain length (i.e., to CHF2[CF2]4CHF2 or CHF2[CF2]5CH2OH) decrease or abolish potency (i.e., a discontinuity arises). This leads to our hypothesis that the anesthetic moieties (-CHF2 and -CH2OH) interact with two distinct, spatially separate, sites. Both sites must be influenced concurrently to produce a maximal anesthetic (immobility) effect. We propose that the maximal potency (i.e., for CHF2[CF2]2CHF2 and CHF2[CF2]3CH2OH) results when the spacing between the anesthetic moieties most closely matches the distance between the two sites of action. This reasoning suggests that a distance equivalent to a four or five carbon atom chain, approximately 5 A, separates the two sites. ⋯ Volatile anesthetics may produce immobility by a concurrent action on two sites five carbon atom lengths apart.
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Anesthesia and analgesia · Jun 1999
Randomized Controlled Trial Clinical TrialEpidural ropivacaine for the initiation of labor epidural analgesia: a dose finding study.
The purpose of our study was to determine the lowest concentration of ropivacaine that offers pain relief for the initiation of labor epidural analgesia. Women in active labor were enrolled in this prospective, randomized, double-blinded study to receive either ropivacaine 0.20% (Group I), ropivacaine 0.15% (Group II), or ropivacaine 0.10% (Group III). After placement of the epidural catheter, 13 mL of the study medication was administered. Fifteen minutes later, the adequacy of analgesia was assessed. If the woman reported that her degree of analgesia was not adequate, an additional 5 mL of the study medication was given, the degree of pain relief was reassessed 15 min later, and the study was concluded. A sequential study design was used to assess the success rates. We found that 26 of 28 (93%) women in Group I had adequate analgesia, compared with only 18 of 28 (64%) in Group II (P = 0.014) and 4 of 12 (33%) in Group III (P = 0.003). We conclude that ropivacaine 0.20% offers adequate analgesia significantly more often than either ropivacaine 0.15% or ropivacaine 0.10%. If one selects ropivacaine as the sole local anesthetic for the initiation of labor epidural analgesia, the minimal concentration should be 0.20%. ⋯ The lowest effective concentration of ropivacaine for the initiation of labor epidural analgesia has not been determined. We found that ropivacaine 0.20% offers adequate analgesia significantly more often than either ropivacaine 0.15% or ropivacaine 0.10%. If one selects ropivacaine as the sole local anesthetic for the initiation of labor epidural analgesia, the minimal concentration should be 0.20%.
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Anesthesia and analgesia · Jun 1999
Clinical TrialTissue heat content and distribution during and after cardiopulmonary bypass at 17 degrees C.
We measured afterdrop and peripheral tissue temperature distribution in eight patients cooled to approximately 17 degrees C during cardiopulmonary bypass and subsequently rewarmed to 36.5 degrees C. A nasopharyngeal probe evaluated trunk and head temperature and heat content. Peripheral tissue temperature (arm and leg temperature) and heat content were estimated using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. Peripheral tissue temperature decreased to 19.7+/-0.9 degrees C during bypass and subsequently increased to 34.3+/-0.7 degrees C during 104+/-18 min of rewarming. The core-to-peripheral tissue temperature gradient was -5.9+/-0.9 degrees C at the end of cooling and 4.7+/-1.5 degrees C at the end of rewarming. The core-temperature afterdrop was 2.2+/-0.4 degrees C and lasted 89+/-15 min. It was associated with 1.1+/-0.7 degrees C peripheral warming. At the end of cooling, temperatures at the center of the upper and lower thigh were (respectively) 8.0+/-5.2 degrees C and 7.3+/-4.2 degrees C cooler than skin temperature. On completion of rewarming, tissue at the center of the upper and lower thigh were (respectively) 7.0+/-2.2 degrees C and 6.4+/-2.3 degrees C warmer than the skin. When estimated systemic heat loss was included in the calculation, redistribution accounted for 73% of the afterdrop, which is similar to the contribution observed previously in nonsurgical volunteers. ⋯ Temperature afterdrop after bypass at 17 degrees C was 2.2+/-0.4 degrees C, with approximately 73% of the decrease in core temperature resulting from core-to-peripheral redistribution of body heat. Cooling and rewarming were associated with large radial tissue temperature gradients in the thigh.