Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2000
Cardiopulmonary resuscitation during severe hypothermia in pigs: does epinephrine or vasopressin increase coronary perfusion pressure?
The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo. ⋯ Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.
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Anesthesia and analgesia · Jan 2000
Clinical TrialMagnetic resonance imaging of the distribution of local anesthetic during the three-in-one block.
The three-in-one technique of simultaneously blocking the femoral, the lateral femoral cutaneous (LFC), and the obturator nerves by a single injection of a local anesthetic was first described in 1973, and it was suggested that the underlying mechanism was one of cephalad spread resulting in a blockade of the lumbar plexus. Today, the technique is widely used in surgery and pain management of the lower limb. Many investigators have, however, reported suboptimal analgesia levels, particularly in the obturator nerve. The purpose of this prospective study was to trace the distribution of a local anesthetic during a three-in-one block by means of magnetic resonance imaging (MRI). Seven patients scheduled for surgery of the lower limb were analyzed with the aid of a primary MRI and then received three-in-one blocks using 30 mL of bupivacaine 0.5% under the guidance of a nerve stimulator. A secondary MRI was performed to determine the distribution pattern of the local anesthetic. It emerged that the local anesthetic blocks the femoral nerve directly, the LFC nerve through lateral spread, and the anterior branch of the obturator nerve by slightly spreading in a medial direction. No involvement of the proximal and posterior portions of the obturator nerve was observed, nor was there any cephalad spread that could have resulted in a lumbar plexus blockade. We therefore conclude that the basis of the three-in-one block is confined to lateral, medial, and caudal spread of the local anesthetic, which effectively blocks the femoral and LFC nerves, as well as the distal anterior branch of the obturator nerve. ⋯ We demonstrate by using magnetic resonance imaging that the mechanism of a three-in-one block is one of lateral, caudal, and slight medial spread of a local anesthetic with subsequent blockade of the femoral, the lateral femoral cutaneous, and the anterior branch of the obturator nerves. It does not involve cephalad spread of the local anesthetic with blockade of the lumbar plexus.
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Anesthesia and analgesia · Jan 2000
Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts.
Eicosanoids and volatile anesthetics can influence cardiac reperfusion injury. Accordingly, we analyzed the effects of sevoflurane and isoflurane applied in clinically relevant concentrations on the myocardial production of prostacyclin and thromboxane A2 (TxA2) and on heart function. Isolated guinea pig hearts, perfused with crystalloid buffer, performed pressure-volume work. Between two working phases, hearts were subjected to 15 min of global ischemia followed by reperfusion. The hearts received no anesthetic, 1 minimum alveolar anesthetic concentration (MAC) isoflurane (1.2 vol%), or 0.5 and 1 MAC sevoflurane (1 vol% and 2 vol%), either only preischemically or pre- and postischemically. In additional groups, cyclooxygenase function was examined by an infusion of 1 microM arachidonic acid (AA) in the absence and presence of sevoflurane. The variables measured included the myocardial production of prostacyclin, TxA2 and lactate, consumption of pyruvate, coronary perfusion pressure, and the tissue level of isoprostane 8-iso-PGF2alpha. External heart work, determined pre- and postischemically, served to assess recovery of heart function. Volatile anesthetics had no impact on postischemic recovery of myocardial function (50%-60% recovery), perfusion pressure, lactate production, or isoprostane content. Release of prostacyclin and TxA2 was increased in the early reperfusion phase 5-8- and 2-4-fold, respectively, indicating enhanced AA liberation. Isoflurane and sevoflurane did not augment the eicosanoid release. Only 2 vol% sevoflurane applied during reperfusion prevented the increased eicosanoid formation in this phase. Infusion of AA increased prostacyclin production approximately 200-fold under all conditions, decreased pyruvate consumption irreversibly, and markedly attenuated postischemic heart work (25% recovery). None of these effects were mitigated by 2 vol% sevoflurane. In conclusion, only sevoflurane at 2 vol% attenuated the increased liberation of AA during reperfusion. Decreased eicosanoid formation had no effect on myocardial recovery in our experimental setting while excess AA was deleterious. Because eicosanoids influence intravascular platelet and leukocyte adhesion and activation, sevoflurane may have effects in reperfused tissues beyond those of isoflurane. ⋯ In an isolated guinea pig heart model, myocardial eicosanoid release was not increased by isoflurane or sevoflurane, either before or after ischemia. Sevoflurane (2 vol%) but not isoflurane attenuated the increased release of eicosanoids during reperfusion.
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Anesthesia and analgesia · Jan 2000
Randomized Controlled Trial Comparative Study Clinical TrialRecovery of cognitive function after remifentanil-propofol anesthesia: a comparison with desflurane and sevoflurane anesthesia.
We compared the recovery characteristics of remifentanil, desflurane, and sevoflurane when used for anesthesia in elective operative procedures. Sixty ASA physical status I and II patients, aged 18-65 yr, were randomly assigned to receive remifentanil-propofol, desflurane-N2O, or sevoflurane-N2O anesthesia. Before the induction of anesthesia, the patients of the desflurane and sevoflurane groups received fentanyl 2 microg/kg. In all groups, anesthesia was induced with propofol and maintained either with remifentanil 0.25 microg x kg(-1) x min(-1), desflurane, or sevoflurane 0.85 MAC with 65% nitrous oxide in oxygen. Anesthetics were titrated to achieve an adequate level of surgical anesthesia and to maintain mean arterial pressure within 20% of baseline values. Early recovery times and a modified Aldrete Recovery Score > 9 were recorded. Trieger Dot Test and Digit Substitution Test (DSST) were performed the day before surgery and in the postanesthesia care unit to evaluate intermediate recovery. The remifentanil-propofol group had a significantly faster emergence than desflurane or sevoflurane, with no difference between both inhaled anesthetics. Thirty min after anesthesia administration, patients in the remifentanil-propofol and in the desflurane groups gave significantly more correct responses in the DSST compared with sevoflurane (remifentanil 87%, desflurane 83%, sevoflurane 56%), the impairment in the sevoflurane patients corresponding to the effects of a blood alcohol level of approximately 0.1% and, thus, being of clinical importance. Ninety minutes after anesthesia administration, no significant difference could be demonstrated among the groups in the DSST scores. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration. ⋯ We compared awakening and intermediate recovery times after remifentanil-propofol anesthesia to desflurane-N2O and sevoflurane-N2O anesthesia. Emergence and return of cognitive function was significantly faster after remifentanil-propofol compared with desflurane and sevoflurane up to 60 min after anesthesia administration.