Anesthesia and analgesia
-
Anesthesia and analgesia · Mar 2001
Case ReportsIntraoperative monitoring of the recurrent laryngeal nerve during single-lung ventilation in esophagectomy.
We describe the use of a surface electrode attached to a double-lumen endobronchial tube to identify and monitor the recurrent laryngeal nerve during esophagectomy in single-lung ventilation. The technique is demonstrated in the case of a patient with carcinoma of the distal esophagus.
-
Anesthesia and analgesia · Mar 2001
Thromboelastography for monitoring prolonged hypercoagulability after major abdominal surgery.
Despite clinical and laboratory evidence of perioperative hypercoagulability, there are no consistent data evaluating the extent, duration, and specific contribution of platelets and procoagulatory proteins by in vitro testing. We tested the hypothesis that the parallel use of standard and abciximab-cytochalasin D-modified thromboelastography (TEG) can assess 7 days' postoperative hypercoagulability and can estimate the independent contribution of procoagulatory proteins and platelets. Thromboelastograms were performed before surgery, at the end of surgery, 6 h after surgery, and on postoperative days 1, 2, 3, and 7; they were analyzed for the reaction time and the maximal amplitude (MA). We calculated the elastic shear modulus of standard MA (G(t)) and modified MA (G(c)), which reflect total clot strength and procoagulatory protein component, respectively. The difference was an estimate of the platelet component (G(p)). There was a 10% perioperative increase of standard MA, corresponding to a 50% increase of G(t) (P < 0.0001) and an 86%-90% contribution of the calculated G(p) to G(t). We conclude that serial standard and modified thromboelastography may reveal prolonged postoperative hypercoagulability and the independent contribution of platelets and procoagulatory proteins to clot strength. ⋯ Postoperative hypercoagulability, occurring for at least 1 wk after major abdominal surgery, may be demonstrated by standard and modified thromboelastography. This hypercoagulability is not reflected by standard coagulation monitoring and seems to be predominantly caused by increased platelet reactivity.
-
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.
-
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.
-
Anesthesia and analgesia · Mar 2001
The effects of olprinone (a phosphodiesterase III inhibitor) on hepatic vascular bed in a porcine model of endotoxemia.
Decreased hepatic blood flow, and impaired hepatic oxygen delivery caused by endotoxin, result in hepatic metabolic deterioration followed by liver dysfunction and multiple organ failure. Among phosphodiesterase III inhibitors, only olprinone increases hepatosplanchnic blood flow. We evaluated the effects of olprinone on systemic hemodynamics, hepatic circulation, and hepatic oxygen delivery in a porcine model of endotoxemia. Fifteen pigs received a continuous infusion (1.7 microg. kg(-1). h(-1)) of endotoxin (lipopolysaccharide [LPS]) via the portal vein for 240 min. Seven of these pigs received olprinone infusion (0.3 microg. kg(-1). min(-1)) via a central vein from t = 150 min to t = 240 min, whereas the eight remaining pigs served as LPS controls. Continuous infusion of LPS caused significant reductions in hemodynamic variables and a significant increase in arterial lactate. After the administration of olprinone during the LPS infusion, portal venous flow and hepatic oxygen delivery were increased and were higher than in the LPS group. Furthermore, olprinone prevented any further increase in arterial lactate. We conclude that the administration of olprinone halted the disturbances in the hepatic circulation, especially in portal venous flow and hepatic oxygen delivery, in a porcine model of endotoxemia. ⋯ Endotoxin is a causative factor in peripheral vascular failure, resulting in a hemodynamic depression that includes a reduction in liver blood flow. The administration of olprinone (phosphodiesterase III inhibitor) improves the liver blood flow circulation in a porcine model of endotoxemia.