Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2001
Comparative StudyAn investigation of a new activated clotting time "MAX-ACT" in patients undergoing extracorporeal circulation.
Activated clotting time (ACT) is a test used in the operating room for monitoring heparin effect. However, ACT does not correlate with heparin levels because of its lack of specificity for heparin and its variability during hypothermia and hemodilution on cardiopulmonary bypass (CPB). A modified ACT using maximal activation of Factor XII, MAX-ACT (Actalyke MAX-ACT; Array Medical, Somerville, NJ), may be less variable and more closely related to heparin levels. We compared MAX-ACT with ACT in 27 patients undergoing CPB. We measured ACT, MAX-ACT, temperature, and hematocrit at six time points: baseline; postheparin; on CPB 30, 60, and 90 min; and postprotamine. Additionally, we assessed anti-Factor Xa heparin activity and antithrombin III activity at four of these six time points. With institution of CPB and hemodilution, MAX-ACT and ACT did not change significantly but had a tendency to increase, whereas concomitant heparin levels decreased (P = 0.065). Neither test correlated with heparin levels. ACT and MAX-ACT did not differ during normothermia but did during hypothermia, and ACT was significantly longer than MAX-ACT (P = 0.009). At the postheparin time point, ACT-heparin sensitivity (defined as [ACT postheparin - ACT baseline]/[heparin concentration postheparin - heparin concentration baseline]) was greater than MAX-ACT-heparin sensitivity (analogous calculation for MAX-ACT; 520 [266 - 9366] s. U(-1). mL(-1) vs 468 [203 - 8833] s. U(-1). mL(-1); P = 0.022). ⋯ MAX-ACT (a new activated clotting time [ACT] test) uses more maximal clotting activation in vitro and, although it is less susceptible to increase because of hypothermia and hemodilution than ACT, lack of correlation with heparin levels remains a persistent limitation.
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Anesthesia and analgesia · Mar 2001
Randomized Controlled Trial Comparative Study Clinical TrialThe release of antidiuretic hormone is appropriate in response to hypovolemia and/or sodium administration in children with severe head injury: a trial of lactated Ringer's solution versus hypertonic saline.
We conducted an open, randomized, and prospective study to determine the effect of hypertonic saline on the secretion of antidiuretic hormone (ADH) and aldosterone in children with severe head injury (Glasgow coma scale <8). Thirty-one consecutive patients at a level III pediatric intensive care unit at a children's hospital received either lactated Ringer's solution (Ringer's group, n = 16) or hypertonic saline (Hypertonic Saline group, n = 15) over a 3-day period. Serum ADH levels were significantly larger in the Hypertonic Saline group as compared with the Ringer's group (P = 0.001; analysis of variance) and were correlated to sodium intake (Ringer's group: r = 0.39, R(2) = 0.15, P = 0.02; Hypertonic Saline group: r = 0.42, R(2) = 0.18, P = 0.02) and volume of fluids given IV (Ringer's group: r = 0.38, R(2) = 0.15, P = 0.02; Hypertonic Saline group: r = 0.32, R(2) = 0.1, P = not significant). Correlation of ADH to plasma osmolality was significant if plasma osmolality was >280 mOsm/kg (r = 0.5, R(2) = 0.25, P = 0.06), indicating an osmotic threshold for ADH release. Serum aldosterone levels were larger on the first day than during Days 2 and 3 in both groups and inversely correlated to serum sodium levels only in the Ringer's group (r = -0.55, R(2) = 0.3, P < 0.001). This group received a significantly larger fluid volume on Day 1 (P = 0.05, Mann-Whitney U-test) than did patients in the Hypertonic Saline group, indicating hypovolemia during the first day. Head-injured children have appropriate levels of ADH. They may be hypovolemic during the first day of treatment, especially if they receive lactated Ringer's solution. ⋯ In head-injured patients, we recommend fluid restriction to avoid inappropriate secretion of antidiuretic hormone. In a prospective, randomized, and controlled study in 31 children, we were able to show that the antidiuretic hormone levels are appropriate in response to hypovolemia, sodium load, or both.
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Anesthesia and analgesia · Mar 2001
Randomized Controlled Trial Clinical TrialThe addition of morphine prolongs fentanyl-bupivacaine spinal analgesia for the relief of labor pain.
The combination intrathecal fentanyl (25 microg) and bupivacaine (2.5 mg) provides effective labor analgesia for approximately 90 minutes. The purpose of this prospective, randomized, double-blinded investigation was to determine if the addition of morphine (150 microg) to the intrathecal combination of fentanyl (25 microg) and bupivacaine (2.5 mg) would prolong labor analgesia. By using the combined spinal epidural technique, 95 healthy primiparous laboring women in early labor received 2 mL of one of the two intrathecal study solutions, either FB (n = 48): fentanyl (25 microg) and bupivacaine (2.5 mg); or FBM (n = 47): fentanyl (25 microg) and bupivacaine (2.5 mg) plus morphine (150 microg). The mean duration of labor analgesia was significantly longer in the FBM group than in the FB group (252 +/- 63 min vs 148 +/- 44 min, P < 0.01). There were no significant differences between the two groups regarding the sensory levels, the incidence of nausea, vomiting, pruritus, hypotension, or operative delivery. In conclusion, the addition of 150 microg of morphine to the intrathecal combination of fentanyl plus bupivacaine prolonged the duration of labor analgesia duration without increasing adverse effects. ⋯ The addition of morphine (150 microg) to intrathecal fentanyl (25 microg) and bupivacaine (2.5 mg) prolongs the duration of labor analgesia duration without increasing adverse effects.
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Anesthesia and analgesia · Mar 2001
The effect of epidural anesthesia on respiratory distress induced by airway occlusion in isoflurane-anesthetized cats.
The role of afferent information from the chest wall in the genesis of dyspnea is not fully elucidated. We have developed an animal model for the study of airway occlusion (AO) and proposed new concepts of minimum alveolar anesthetic concentration for AO (MACAOR) and the duration from the start of AO to the onset of the positive motor response (DOCCL) to evaluate respiratory distress quantitatively. We examined the effects of thoracic epidural anesthesia on respiratory distress by using our animal model. Adult cats (n = 24) were anesthetized with isoflurane, and an epidural catheter was placed after T9 laminectomy. After determination of MACAOR, DOCCL was measured. Animals were then randomly assigned into three groups: the EPD Group (n = 12) received epidural 1% lidocaine (0.4 mL/kg), IM saline (0.4 mL/kg), and saline infusion. The IM Group (n = 6) received epidural saline (0.4 mL/kg), IM 1% lidocaine (1 mL/kg), and saline infusion. The PHE Group (n = 6) received epidural 1% lidocaine (0.4 mL/kg) and IV phenylephrine (0.5-1 microg. kg(-1). min(-1)) to maintain a stable arterial blood pressure. DOCCL and MACAOR were measured in each animal at 15 min after the administration of drugs. Plasma lidocaine concentrations were measured before and after epidural or IM injection. DOCCL was significantly longer after epidural injection in all groups than before the injection. Although there was no significant difference in the values of MACAOR between before and after the epidural injection in the EPD Group, the IM administration of lidocaine in the IM Group significantly reduced MACAOR. Plasma concentrations of lidocaine were similar in all groups at all measurement points. Our data indicate that thoracic epidural anesthesia using 1% lidocaine significantly reduced respiratory distress induced by AO. This effect is most likely caused by a systemic effect of lidocaine rather than by reduced afferent information from the chest wall. ⋯ Thoracic epidural anesthesia reduced respiratory distress induced by airway occlusion. This effect is most likely caused by the systemic effect of lidocaine, rather than by the reduced afferent information from the chest wall.
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Anesthesia and analgesia · Mar 2001
The protective effect of acadesine on lung ischemia-reperfusion injury.
The purine precursor acadesine is highly effective in preventing ischemia-reperfusion (I-R) injury of the heart and intestine. The aim of this study was to test the effect of acadesine on I-R--induced lung injury. The lobar artery of the left lower lung lobe in intact-chest, spontaneously breathing cats was occluded for 2 h (Group 1, ischemia) and reperfused for 3 h (Group 2, I-R). Animals were subjected to one of the following three protocols: acadesine administered IV 15 min before ischemia (Group 3), 15 min before reperfusion (Group 4), or 30 min after reperfusion (Group 5). Acadesine was administered at an initial dose of 2.5 mg. kg(-1). min(-1) for 5 min, followed by 0.5 mg. kg(-1). min(-1) until the end of reperfusion. Injury was assessed by histologic examination. The right lower lobe served as control. Compared with the right lower lobe, which showed no abnormal findings in any group (percentage of injured alveoli, 2% +/- 1% to 4% +/- 2%), the left lower lung lobe in the I-R group revealed a disrupted alveolar structure with 63% +/- 9% injured alveoli. Ischemia alone did not produce alterations in alveolar structure. Acadesine significantly reduced the number of injured alveoli when given before ischemia (4% +/- 1%) or reperfusion (6% +/- 2%) but not when administered after reperfusion (62% +/- 8%). In conclusion, acadesine, when administered before ischemia or reperfusion, can blunt I-R-induced lung injury. The mechanism underlying the protection remains to be elucidated. ⋯ Acadesine reduces ischemia-reperfusion-induced lung injury in spontaneously breathing cats when administered before ischemia or reperfusion, but not after reperfusion.