Anesthesia and analgesia
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Anesthesia and analgesia · Jan 2000
Clinical TrialSequential changes of arterial oxygen tension in the supine position during one-lung ventilation.
To investigate how surgical positions affect the severity and progress of hypoxemia during one-lung ventilation (OLV), we studied 33 adult patients undergoing right thoracotomy with left OLV. The patients were divided into three groups according to the positions during surgery as follows: the supine position (SP) group (n = 11), the left semilateral decubitus position (LSD) group (n = 9), and the left lateral decubitus position (LLD) group (n = 13). Analysis of arterial blood gases was sequentially determined every 5 min for 30 min during OLV (fractional ratio of inspiratory oxygen = 1.0) in each position. OLV was promptly terminated and switched to bi-lung ventilation if Spo2 declined to 90%. Pao2 progressively decreased with time in all three groups (P < 0.01). The incidence of termination of OLV within 30 min was higher in the SP group (82%), compared with that in the LSD (11%) and LLD (8%) groups (P < 0.01). Final Pao2 (65+/-12 mm Hg, mean +/- SD, P < 0.01 versus LLD, P < 0.05 versus LSD) and SaO2 (91%+/-4%, P < 0.01 versus LLD and LSD) at the termination of OLV in the SP group were the lowest. There was no difference between these values in the LSD and LLD groups (128+/-54 mm Hg, 96%+/-2%, and 167+/-69 mm Hg, 97%+/-4%, respectively) 30 min after the start of OLV. The time for Pao2 to decrease to 200 mm Hg calculated from each regression curve was 354 s in the SP group, 583 s in the LSD group, and 798 s in the LLD group. The time for Pao2 to decline to 100 mm Hg was 794 s in the SP group. In the regression curves of the LSD and LLD groups, the Pao2 did not decrease to 100 mm Hg. Heart rate was slow at baseline in the SP group (P < 0.05 versus LSD), but other hemodynamic variables did not differ among the three groups throughout this study. The LSD was as effective as the LLD in avoiding life-threatening hypoxemia during OLV. ⋯ Close observation and prompt counteractions including termination of one-lung ventilation (OLV) are crucial for patients under OLV in the supine position, because life-threatening hypoxemia frequently occurs approximately 10 min after starting OLV, even under 100% oxygen inhalation. The left semilateral decubitus position was as effective as the left lateral decubitus position in avoiding life-threatening hypoxemia during OLV.
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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
The anticonvulsant effects of volatile anesthetics on penicillin-induced status epilepticus in cats.
Volatile anesthetics may be used to treat status epilepticus when conventional drugs are ineffective. We studied 30 cats to compare the inhibitory effects of sevoflurane, isoflurane, and halothane on penicillin-induced status epilepticus. Anesthesia was induced and maintained with one of the three volatile anesthetics in oxygen. Penicillin G was injected into the cisterna magna, and the volatile anesthetic discontinued. Once status epilepticus was induced (convulsive period), the animal was reanesthetized with 0.6 minimum alveolar anesthetic concentration (MAC) of the volatile anesthetic for 30 min, then with 1.5 MAC for the next 30 min. Electroencephalogram and multiunit activity in the midbrain reticular formation were recorded. At 0.6 MAC, all anesthetics showed anticonvulsant effects. Isoflurane and halothane each abolished the repetitive spike phase in one cat; isoflurane reduced the occupancy of the repetitive spike phase (to 27%+/-22% of the convulsive period (mean +/- SD) significantly more than sevoflurane (60%+/-29%; P < 0.05) and halothane (61%+/-24%; P < 0.05), and the increase of midbrain reticular formation with repetitive spikes was reduced by all volatile anesthetics. The repetitive spikes were abolished by 1.5 MAC of the anesthetics: in 9 of 10 cats by sevoflurane, in 9 of 9 cats by isoflurane, and in 9 of 11 cats by halothane. In conclusion, isoflurane, sevoflurane, and halothane inhibited penicillin-induced status epilepticus, but isoflurane was the most potent. ⋯ Convulsive status epilepticus is an emergency state and requires immediate suppression of clinical and electrical seizures, but conventional drugs may be ineffective. In such cases, general anesthesia may be effective. In the present study, we suggest that isoflurane is preferable to halothane and sevoflurane to suppress sustained seizure.
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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.