Acute recurrent bradycardia with evoked potential loss during transforaminal lumbar interbody fusion.

During a transforaminal lumbar interbody fusion a patient experienced acute intermittent bradycardia with manipulation of the intervertebral body space, followed by loss of somatosensory evoked potentials that did not recover. Postoperative evaluation revealed new bilateral lower extremity sensory and motor deficits. We postulate an afferent reflex arc to explain this and other reported instances of bradycardia and asystole during transforaminal lumbar interbody fusion surgery. Awareness of the association between bradycardia during lumbar spine surgery may alert anaesthetists, surgeons and neuromonitoring teams to impending neurological harm.

Prolonging viability of swine muscle biopsy specimens in malignant hyperthermia testing.

In North America, the caffeine halothane contracture test (CHCT) is the standard test for the diagnosis of malignant hyperthermia (MH). Current CHCT protocol recommends that the test be completed within 5 h of muscle excision. The purpose of this study was to investigate whether the period of skeletal muscle viability could be extended to 24 h. We tested the gracilis muscle from normal (n = 8) and MH-susceptible swine (n = 8). After baseline (1-2 h after excision) CHCT, the remaining muscles were placed into one of the following four treatment groups. In Groups 1 and 2, the muscles remained under tension and were stored in Krebs buffer (pH 7.4) at 23 degrees C-25 degrees C (clamped-warm) and 4 degrees C (clamped-cold), respectively. In Groups 3 and 4, the muscle strips were dissected, and the ends were tied with silk sutures, cut from the clamp, and placed in Krebs buffer at 23 degrees C-25 degrees C (free-warm) and 4 degrees C (free-cold), respectively. The responses of the treatment groups to halothane (3%) and caffeine (0.5-32 mM) were tested 22-26 h after excision. The clamped-warm storage was the only storage method to correctly diagnose MH susceptibility in all muscle strips tested. This finding was also confirmed in muscle stored under clamped-warm conditions and shipped overnight to another testing center for a parallel CHCT.

Pyruvate improves cerebral metabolism during hemorrhagic shock.

Pyruvate (PYR) improves cellular and organ function hypoxia and ischemia by stabilizing the reduced nicotinamide adenine dinucleotide redox state and cytosolic ATP phosphorylation potential. In this in vivo study, we evaluated the effects of intravenous pyruvate on neocortical function, indexes of the cytosolic redox state, cellular energy state, and ischemia during a prolonged (4 h) controlled arterial hemorrhage (40 mmHg) in swine. Thirty minutes after the onset of hemorrhagic shock, sodium PYR (n = 8) was infused (0.5 g x kg(-1) x h(-1)) to attain arterial levels of 5 mM. The volume and osmotic effects were matched with 10% NaCl [hypertonic saline (HTS)] (n = 8) or 0.9% NaCl [normal saline (NS)] (n = 8). During the hemorrhage protocol, the time to peak hemorrhage volume was significantly delayed in the PYR group compared with the HTS and NS groups (94 +/- 5 vs. 73 +/- 6 and 72 +/- 4 min, P < 0.05). In addition to the early onset of the decompensatory phase of hemorrhagic shock, the complete return of the hemorrhage volume during decompensatory shock resulted in the death of five and four animals, respectively, in the HTS and NS groups. In contrast, in the PYR group, reinfusion of the hemorrhage volume was slower and all animals survived the 4-h hemorrhage protocol. During hemorrhage, the PYR group also exhibited improved cerebral cortical metabolic and function status. PYR slowed and reduced the rise in neocortical microdialysis levels of adenosine, inosine, and hypoxanthine and delayed the loss of cerebral cortical biopsy ATP and phosphocreatine content. This improvement in energetic status was evident in the improved preservation of the electrocorticogram in the PYR group. PYR also prevented the eightfold increase in the excitotoxic amino acid glutamate observed in the HTS group. The findings show that PYR administered after the onset of hemorrhagic shock markedly improves cerebral metabolic and functional status for at least 4 h.

Ascorbate reduces superoxide production and improves mitochondrial respiratory chain function in human fibroblasts with electron transport chain deficiencies.

The present paper attempts to ascertain the role of ascorbate on the generation of superoxide radicals in skin fibroblasts of patients with deficiency of mitochondrial respiratory chain enzymes. Fibroblast cell lines were grown with or without ascorbate for the last 48 h of their growth period. The amount of superoxide radical production in cells was measured by the reduction of nitroblue tetrazolium and the activities of respiratory chain enzymes were examined in isolated fibroblast mitochondria. The results indicated a significant inverse correlation between the amount of superoxide radicals and the specific activities of complexes I-III and II-III of the respiratory chain. The ascorbate treatment of fibroblasts from control subjects did not show any effect on either superoxide radical production or respiratory chain enzymes' activities. While in patient's fibroblasts, this vitamin significantly decreased the superoxide radicals and increased the specific activities of I-III and II-III complexes but not complex IV. These observations indicate that superoxide radicals are increased in patients with deficient respiratory chain enzymes in their fibroblasts and ascorbate can prevent the loss of these enzymes by acting on the selected sites in the respiratory chain, which are related to the production of free radicals.

Monitoring of somatosensory and motor evoked potentials during open reduction and internal fixation of pelvis and acetabular fractures.

Monitoring of motor and somatosensory evoked potentials provides instantaneous intraoperative assessment of a patient's neurologic status. Monitoring of the sciatic nerve through motor and somatosensory evoked potentials can be used during open reduction and internal fixation of pelvic and acetabular fractures. A review of 12 pelvic and acetabular fractures treated with open reduction and internal fixation was conducted and assessed with a combination of intraoperative motor and somatosensory evoked potential monitoring. Results revealed intraoperative motor evoked potential monitoring was 100% sensitive and 100% specific in predicting postoperative sciatic nerve deficits, whereas somatosensory evoked potentials were not accurate in predicting postoperative sciatic nerve deficits. Combined monitoring of the sciatic nerve with motor and somatosensory evoked potentials is beneficial at predicting postoperative sciatic nerve deficits during open reduction and internal fixation of pelvic and acetabular fractures.

Intravenous pyruvate prolongs survival during hemorrhagic shock in swine.

Pyruvate improves cellular and organ function during hypoxia and ischemia and stabilizes the NADH redox state and cytosolic ATP phosphorylation potential. In this in vivo study, we evaluated the effects of intravenous pyruvate on cardiovascular and neocortical function, indexes of the cytosolic redox state (lactate/pyruvate ratio, L/P) and cellular energy state (adenosine and degradative products hypoxanthine and inosine, ADO + HX + Ino) during controlled arterial hemorrhage (40 mmHg) in sedated swine (45 kg). Na+ pyruvate was infused 1 h before (1 g. kg(-1). h(-1)) and 2 h during (0.5 g. kg(-1). h(-1)) hemorrhage to attain arterial pyruvate levels of 6 mM. Volume (0.9% NaCl) and osmotic (10% NaCl) effects were matched in controls. Time to peak hemorrhage (57 min) and peak hemorrhage volume (43 ml/kg) were similar in all groups. The volume and osmotic groups experienced spontaneous cardiovascular decompensation between 60 and 90 min, with an average time until death of 82.7 +/- 5.5 and 74.8 +/- 8.2 min. In contrast, survival in the pyruvate group was 151.2 +/- 10.0 min (P < 0.001). During hemorrhage, the pyruvate group had better cardiovascular and cerebrovascular function with significantly higher systemic and cerebral oxygen consumption and less attenuation of the amplitude and frequency of the electrocorticogram. In addition, pyruvate prevented metabolic acidosis and stabilized the L/P. Pyruvate slowed the rise in neocortical microdialysis levels of ADO + HX + Ino, and prevented the net efflux of ADO + HX + Ino into the sagittal sinus. The findings reveal considerable metabolic and functional enhancement by pyruvate during severe hemorrhagic shock with a 75-min delay in spontaneous cardiovascular decompensation and death.

Hemodynamic changes induced by liposomes and liposome-encapsulated hemoglobin in pigs: a model for pseudoallergic cardiopulmonary reactions to liposomes. Role of complement and inhibition by soluble CR1 and anti-C5a antibody.

BACKGROUND: Intravenous administration of some liposomal drugs can trigger immediate hypersensitivity reactions that include symptoms of cardiopulmonary distress. The mechanism underlying the cardiovascular changes has not been clarified. METHODS AND RESULTS: Anesthetized pigs (n=18) were injected intravenously with 5-mg boluses of large multilamellar liposomes, and the ensuing hemodynamic, hematologic, and laboratory changes were recorded. The significant (P<0.01) alterations included 79+/-9% (mean+/-SEM) rise in pulmonary arterial pressure, 30+/-7% decline in cardiac output, 11+/-2% increase in heart rate, 236+/-54% increase in pulmonary vascular resistance, 71+/-27% increase in systemic vascular resistance, and up to a 100-fold increase in plasma thromboxane B2. These changes peaked between 1 and 5 minutes after injection, subsided within 10 to 20 minutes, were lipid dose-dependent (ED50=4. 5+/-1.4 mg), and were quantitatively reproducible in the same animal several times over 7 hours. The liposome-induced rises of pulmonary arterial pressure showed close quantitative and temporal correlation with elevations of plasma thromboxane B2 and were inhibited by an anti-C5a monoclonal antibody (GS1), by sCR1, or by indomethacin. Liposomes caused C5a production in pig serum in vitro through classic pathway activation and bound IgG and IgM natural antibodies. Zymosan- and hemoglobin-containing liposomes and empty liposomes caused essentially identical pulmonary changes. CONCLUSIONS: The intense, nontachyphylactic, highly reproducible, complement-mediated pulmonary hypertensive effect of minute amounts of intravenous liposomes in pigs represents a unique, unexplored phenomenon in circulation physiology. The model provides highly sensitive detection and study of cardiopulmonary side effects of liposomal drugs and many other pharmaceutical products due to "complement activation-related pseudoallergy" (CARPA).

The anesthetic and physiologic effects of an intravenous administration of a halothane lipid emulsion (5% vol/vol)

UNLABELLED: The i.v. administration of < or = 9 mL of nonvaporized liquid halothane causes significant pulmonary damage, cardiovascular decompensation, and death. To determine whether liquid halothane mixed in a lipid emulsion would alter these toxic effects, six swine were evaluated in a randomized cross-over study. The pulmonary, analgesic, hemodynamic, and histopathologic effects of liquid halothane (25 mL) mixed with a liquid carrier (475 mL, Liposyn III 20%) and administered by constant infusion were compared with halothane administered by a calibrated vaporizer. Three swine received the halothane lipid emulsion (HLE), followed by inhaled halothane. Three additional swine received inhaled halothane, followed by the HLE. There were no changes in pulmonary compliance or arterial blood gases during or after the administration of equivalent volumes of halothane (13.75 mL) either by infusion of HLE or by inhalation of halothane. The end-tidal halothane concentration for the minimum alveolar anesthetic concentration was 0.79% +/- 0.08% during HLE administration and 1.13% +/- 0.12% for inhaled halothane (P < 0.001). Hemodynamic variables and blood halothane levels by gas chromatography were measured at end-tidal concentrations of 0.6%, 1.2%, and 1.8%. Blood halothane levels (mg/mL) were significantly higher (P < 0.05) after the administration of HLE at end-tidal halothane concentrations of 1.2% (0.49 +/- 0.19 vs 0.82 +/- 0.18) and 1.8% (0.79 +/- 0.17 vs 1.29 +/- 0.34). When compared at equivalent blood levels, HLE caused fewer changes in the left ventricular end-diastolic pressure, mean arterial pressure, and dP/dt than inhaled halothane. There was no evidence of pulmonary histopathologic damage 4-8 h after the infusion of 500-700 mL of HLE. This novel method of delivery of a volatile anesthetic seems to lack the toxicity of direct i.v. administration of liquid halothane. It may be a useful alternative to traditional administration via a vaporizer. IMPLICATIONS: Halothane causes pulmonary dysfunction and death when given i.v. in liquid form. Six swine received a halothane lipid emulsion i.v. to evaluate the anesthetic and physiologic effects. No pulmonary toxicity or deaths were associated with the halothane lipid emulsion. The anesthetic profile was similar to delivery of halothane via a vaporizer.

Tranexamic acid and aprotinin reduce postoperative bleeding and transfusions during primary coronary revascularization.

UNLABELLED: We evaluated the blood conservation effects of tranexamic acid (TA) or aprotinin administered before and during cardiopulmonary bypass (CPB) in a prospective, randomized, double-blind study of 150 adult patients undergoing primary coronary artery bypass grafting surgery. Patients received either TA (2 g) or large-dose aprotinin (7 million KIU). Thirty additional untreated patients otherwise managed in a similar fashion were included from a recently completed study for comparison of outcomes. Demographic, medical, surgical, laboratory, mediastinal chest tube drainage (MCTD), transfusion, and outcome data were collected. Allogeneic blood product administration was tightly controlled. The demographic, medical, and surgical characteristics did not significantly differ between the two therapy groups. The median postoperative MCTD loss in the TA group did not significantly differ from that in the aprotinin-treated group (708 vs 600 mL). The percentage of patients that received no allogeneic blood products was 25% for the TA group and 27% for the aprotinin group (P = not significant). The median number of allogeneic blood products administered to the TA group (0 U) did not significantly differ from that administered to the aprotinin group (0 U). The percentage of patients with excessive MCTD (>1000 mL/24 h) did not significantly differ between groups (19% and 17%, respectively). In comparison, the control group had a significantly greater (P < 0.05) median MCTD (1020 mL), median allogeneic blood product exposure (4.5 U), and incidence of excessive MCTD (66%) and transfusion therapy (66%). These data help to support the use of pharmacologic methods to improve clinically relevant indicators of blood conservation for primary CPB procedures. Furthermore, the data show that TA is equivalent to aprotinin for blood conservation in patients at risk of excessive post-CPB bleeding and transfusion therapy. IMPLICATIONS: In a randomized, blind trial, we evaluated the effects of tranexamic acid or aprotinin on blood conservation after primary cardiopulmonary bypass surgery. Both drugs were equally effective in reducing blood loss, the incidence of transfusion, and the amount of blood products transfused compared with placebon.

Tranexamic acid is effective in decreasing postoperative bleeding and transfusions in primary coronary artery bypass operations: a double-blind, randomized, placebo-controlled trial.

UNLABELLED: We evaluated the effects of tranexamic acid (TA) administered before and after cardiopulmonary bypass (CPB) in a prospective, randomized, placebo-controlled, double-blind study of adult patients undergoing primary coronary artery bypass grafting surgery. Patients received placebo (n = 30) or TA 15 mg/kg before CPB, followed by a TA infusion of 1 mg x kg(-1) x h(-1) for 5 h (n = 30) or TA 15 mg/kg after CPB, followed by a TA infusion of 1 mg x kg(-1) x h(-1) for 5 h (n = 30). Demographic, medical, surgical, laboratory, mediastinal chest tube drainage (MCTD), hemoglobin loss, transfusion, and outcome data were collected. Allogenic blood product administration was tightly controlled. The demographic, medical, and surgical characteristics were similar in all three groups. The median postoperative MCTD and hemoglobin loss in the pre-CPB TA group (710 mL, 8.6 g) was significantly less (P < 0.001) compared with the control (1202 mL, 44.2 g) and post-CPB TA groups (1020 mL, 23.4 g). The percentage of patients who received no allogenic blood products was 27% for the pre-CPB TA group and 33% for the post-CPB TA group (not significant). These percentages were significantly lower than those in the placebo group (66%, P < 0.001). The median number of allogenic blood products administered to the pre-CPB TA group (0 units) was significantly less compared with the control group (4.5 units). The thromboelastogram and fibrinogen split product levels in the pre-CPB TA group indicated better platelet function and less activation of the fibrinolytic system compared with the other two groups (P < 0.05). There were no intergroup differences in reoperation, myocardial infarction, stroke, infections, or death. These data support the use of pre-CPB TA to decrease patient exposure to postcardiopulmonary bypass allogenic blood products. IMPLICATIONS: In this randomized, placebo-controlled trial, we investigated the efficacy of tranexamic acid to decrease bleeding and blood transfusions after open-heart operations. Tranexamic acid administered before and during the operation was effective in decreasing both bleeding and transfusions. When tranexamic acid was administered immediately after the operation, it had a minor beneficial effect.

Profound normovolemic hemodilution: hemostatic effects in patients and in a porcine model.

Previous systematic investigations of the hemostatic effects of normovolemic hemodilution (NHD) have not explored the influence of hematocrits less than 20% in humans or animals. However, clinical interest in maximizing the perioperative conservation of erythrocytes may involve profound NHD beyond traditionally accepted empiric end points. We report here on coagulation data in eight healthy adolescent patients undergoing profound NHD in concert with surgical correction of idiopathic scoliosis, and in 29 swine undergoing experimental stepwise NHD until death. Blood was replaced with 5% albumin in 0.9% saline in our patients, and with 5% albumin in lactated Ringer's solution in our pigs. A 75% blood volume exchange in our patients yielded a platelet count (PLT) of 158 +/- 26 x 10(3)/microL, fibrinogen concentration (FIB), 50 +/- 7 mg/dL, prothrombin time (PT), 25.4 +/- 2.6 s, activated partial thromboplastin time (aPTT), 87 +/- 15s, and a nadir hemoglobin of 2.8 +/- 0.2 g/dL; however, global oxygen delivery as assessed by body oxygen consumption remained adequate. Coagulation during the experimental porcine hemodilution was assessed by measuring PLT, FIB, PT, and aPTT, as well as by measurement of coagulation factor activities. In neither species did clinically significant thrombocytopenia (PLT < 100 x 10(3)/ microL) become manifest prior to clinical or other laboratory evidence of coagulopathy. Rather, a combined deficiency of coagulation factors explains the coagulopathy developing during NHD in both patients and swine. Abnormal hemostasis develops prior to compromise of global tissue oxygenation, assessed by mixed venous oxygen saturation and total body oxygen consumption, during NHD in healthy patients anesthetized as described. Therefore, NHD may be more limited by preservation of normal coagulation than of global oxygen delivery and consumption.

Intravenous ketorolac tromethamine worsens platelet function during knee arthroscopy under spinal anesthesia.

Ketorolac prolongs bleeding time and inhibits platelet aggregation and platelet thromboxane production in healthy, awake volunteers. However, platelet function was recently shown not to worsen after ketorolac was given during general anesthesia. The purpose of this study was to investigate platelet function changes during a standardized spinal anesthetic and surgery, as well as after a single intraoperative dose of intravenous (IV) ketorolac. The study comprised 30 ASA physical status I patients undergoing spinal anesthesia for knee arthroscopy. Subjects were randomized to receive either ketorolac 60 mg IV 15 min after skin incision or placebo IV. Platelet function testing consisted of an Ivy bleeding time, platelet aggregometry with adenosine diphosphate (ADP) and collagen, thromboelastography (TEG), and serum thromboxane B2 (TxB2) assays. Platelet function testing was performed: 1) 15 min prior to the performance of spinal anesthesia; 2) 10 min after surgical skin incision; and 3) 45 min after administration of study drug. The placebo group demonstrated no changes in any platelet function variable during spinal anesthesia and surgery relative to preoperative values. The ketorolac group, however, demonstrated a significant increase in bleeding time from postincision to poststudy drug data points (213 +/- 60s to 275 +/- 85s, mean +/- SD; P < 0.01). Further, platelet aggregometry to collagen was diminished in the ketorolac group from preoperative to poststudy drug data points (90.8% +/- 7.6% to 60.5% +/- 32.5%; P < 0.01). Platelet aggregometry with ADP, however, was unchanged in the ketorolac group. Platelet TxB2 production decreased dramatically in the ketorolac group from preoperative to poststudy drug data points (157.2 +/- 129.4 to 0.3 +/- 0.3 ng/mL; P < 0.01). Platelet function does not appear to be accentuated during spinal anesthesia as it is during general anesthesia. Unlike during general anesthesia, platelet function during spinal anesthesia is impaired, with respect to bleeding time and platelet aggregometry to collagen, by a single intraoperative dose of IV ketorolac.

Evaluation of a double-lumen multiorifice catheter for resuscitation of swine from lethal venous air embolism.

BACKGROUND: A double-lumen multiorifice catheter has been developed to potentially enhance accurate electrocardiographic central venous localization and resuscitation from a massive venous air embolism (VAE). This double-lumen multiorifice catheter was compared to a Bunegin-Albin multiorifice catheter for flow characteristics, air aspiration efficiency, and efficacy in resuscitating swine from a lethal VAE. METHODS: Flow characteristics of both catheters were determined by aspirating both agitated and unagitated citrated swine blood with a 50-ml syringe. Swine were anesthetized with halothane and positioned to approximate a modified sitting craniotomy position (45-degree elevation). By a random block method, 24 swine were assigned to either catheter (n = 12 each catheter) for the initial air aspiration. Catheters were positioned, using intravenous electrocardiography, with the distal aspiration orifice in the high right atrium. A 5-ml/kg air embolism was administered over 30 s into the sagittal sinus, and the swine were resuscitated by aspirating air through the multiorifice catheters and then positioning the swine horizontally. Surviving animals were allowed to recover for 60 min. The initial catheter was exchanged and repositioned in the high right atrium using intravenous electrocardiography. A 5-ml/kg air embolus was administered, and the swine were resuscitated as in the first challenge. Surviving swine recovered for 60 min, repositioned, and administered a third 5-ml/kg air embolism. On this final challenge, no attempt was made to resuscitate the animal by aspirating the multiorifice catheter. RESULTS: Flow characteristics of both catheters were similar in the unagitated blood (195.3 +/- 1.9 vs. 196.7 +/- 2.5 ml/min). The flow rate of agitated blood through the double-lumen multiorifice catheter was 14% greater than through the Bunegin-Albin catheter (136.3 +/- 6.8 vs. 117 +/- 5.9 ml/min, P = 0.001). Forty-three air embolism trials were conducted at 5 ml/kg. All nine trials at 5 ml/kg without air aspiration resulted in death. Five animals died during the embolism dose determination trials, and four died during the third embolism challenge. The use of a multiorifice catheter for aspiration after a VAE enhanced survival after a 5-ml/kg sagittal sinus air embolus (14/34 vs. 0/9, P = 0.02). Although the double-lumen multiorifice catheter was more efficient than the Bunegin-Albin catheter in percentage of air retrieved (37.7 +/- 12.0 vs. 29.7 +/- 10.1, P = 0.042). Aspiration of the VAE with the double-lumen multiorifice catheter successfully rescued 9 of the 15 trials, and aspiration using the Bunegin-Albin catheter resuscitated 5 of the 19 (P = 0.08). CONCLUSIONS: Multiorifice catheters are effective in resuscitating swine from a lethal VAE. The double-lumen multiorifice catheter evaluated aspirated a larger percentage of the VAE but was not statistically more effective than the Bunegin-Albin catheter in resuscitating the animals. Based on these findings of improved flow rate and efficiency in air aspiration, further investigation of this double-lumen multiorifice catheter is warranted.

Intravenous ketorolac tromethamine does not worsen platelet function during knee arthroscopy under general anesthesia.

Ketorolac (KT) prolongs bleeding time and inhibits platelet aggregation and platelet thromboxane production in healthy, awake volunteers. However, platelet function may be accentuated during the stress of general anesthesia (GA) and surgery. The purpose of this study was to investigate platelet function changes during a standard GA technique and surgery, as well as after a single intraoperative dose of intravenous (i.v.) KT. The study comprised 30 ASA physical status I patients undergoing GA for knee arthroscopy. Subjects were randomized to receive either KT 60 mg IV 15 min after skin incision or placebo i.v. Platelet function testing consisted of an Ivy bleeding time (BT), platelet aggregometry (PA) with adenosine diphosphate (ADP) and collagen, thromboelastography (TEG), and serum thromboxane B2 assays (TxB2). Platelet function testing was performed: 1) 15 min prior to the induction of GA, 2) 10 min after skin incision, and 3) 45 min after administration of study drug. BT decreased significantly in the placebo group from 263 +/- 133 s (mean +/- SD) preoperatively to 207 +/- 89 s postincision. BT did not change in the KT group. PA was unchanged after IV KT. TEG data was unchanged in both groups during anesthesia and surgery. TxB2 levels decreased markedly in the KT group from 106.9 +/- 96.2 ng/mL preoperatively to 0.4 +/- 1.2 ng/mL poststudy drug, P = 0.002. Platelet function appears to be accentuated during GA and surgery as evaluated by BT in the placebo group. Further, platelet function by BT, PA, and TEG was not inhibited after i.v. KT despite near complete abolition of TxB2 production.

Oxygen consumption and cardiovascular function in children during profound intraoperative normovolemic hemodilution.

The clinically acceptable limit of acute normovolemic, normothermic hemodilution, a standard procedure in scoliosis surgery, is not yet well defined. Eight ASA class I patients undergoing idiopathic scoliosis correction were administered a standard anesthetic with 100% oxygen and controlled ventilation. Hemodilution was accomplished by exchanging whole blood for 5% albumin in 0.9% saline. Blood gases, acid-base status, and circulatory variables were recorded prior to and after hemodilution, and every 30 min throughout surgery. The impact of hemodilution was judged by mixed venous oxygen saturation which was maintained at > or = 60%, while intravascular volume was maintained with the 5% albumin solution. Reinfusion of the autologous blood was completed by the end of surgery. In the eight controlled cases in which normovolemic hemodilution was studied, hemoglobin levels decreased from 10.0 +/- 1.6 g/dL to 3.0 +/- 0.8 g/dL. Mixed venous oxygen saturation decreased from 90.8% +/- 5.4% to 72.3% +/- 7.8%. Oxygen extraction ratio increased from 17.3% +/- 6.2% to 44.4% +/- 5.9%. Oxygen delivery decreased from 532.1 +/- 138.1 mL.min-1.m-2 to 260.2 +/- 57.1 mL.min-1.m-2, while global oxygen consumption did not decrease and plasma lactate did not appreciably increase. Central venous pressure increased and peripheral resistance decreased during hemodilution. Cardiac index increased, heart rate remained essentially constant, and left ventricular stroke work index did not decrease significantly. No patients suffered clinically adverse outcomes. Global oxygen transport and myocardial work can be maintained at extreme normovolemic anemia. Our evidence suggests that stages of normovolemic hemodilution more severe than previously reported may be clinically acceptable for young, healthy patients during normocarbic anesthesia.

Onset of action of mivacurium chloride. A comparison of neuromuscular blockade monitoring at the adductor pollicis and the orbicularis oculi.

BACKGROUND: The optimal site for monitoring neuromuscular blockade for intubations facilitated with mivacurium chloride has not been established. The primary purpose of this evaluation was to determine the difference in onset of neuromuscular blockade between the orbicularis oculi and adductor pollicis in patients administered mivacurium chloride. We also evaluated intubating conditions when intubation was timed to maximal neuromuscular blockade at either the orbicularis oculi or the adductor pollicis. The results for patients administered mivacurium chloride were compared with those for a control group administered succinylcholine. METHODS: In a double-blind randomized design, the time to loss of the compound muscle action potential at the orbicularis oculi and adductor pollicis was monitored in 20 patients administered mivacurium chloride and ten patients administered succinylcholine. After administration of mivacurium chloride (0.15 mg.kg-1), ten patients underwent tracheal intubation at maximal depression of the orbicularis oculi (group 2) and ten patients at maximal depression of the adductor pollicis (group 3). In an additional ten patients the trachea was intubated 60 s after administration of succinylcholine (1 mg.kg-1) (group 1, control). Intubation and evaluation of conditions was performed by one investigator blinded to patient treatments. RESULTS: Loss of compound muscle action potential at the orbicularis oculi and adductor pollicis was more rapid in group 1, and intubation was completed at 86 +/- 26 s. In the patients administered mivacurium chloride, the orbicularis oculi compound muscle action potential was lost 3 min earlier than the adductor pollicis compound muscle action potential. Subsequently, intubation was completed at 134 +/- 50 s in the orbicularis oculi group, whereas the time to intubation was 321 +/- 57 s in the adductor pollicis group. There was no significant differences in intubation conditions between the mivacurium chloride groups. CONCLUSIONS: When monitoring 95% twitch height depression of the orbicularis oculi muscle, intubation can be accomplished in approximately 2 min after administration of mivacurium chloride (0.15 mg.kg-1). Because intubating conditions were comparable to the patients administered succinylcholine or intubated during monitoring of the twitch height depression of the adductor pollicis, we believe that optimal site for monitoring during intubation using mivacurium chloride is the orbicularis oculi muscle.

Spinal evoked potentials are predictive of neurologic function in a porcine model of aortic occlusion.

The limitations of somatosensory evoked potentials during aortic occlusion stimulated us to evaluate the sensitivity and specificity of spinal (T10 and L4) evoked potentials (SpEPs) in predicting neurologic function after aortic occlusion. Thirty-six swine were assigned randomly to three equal groups (Group 1, control; Group 2, cerebrospinal fluid (CSF) drainage; Group 3, CSF drainage with 20-mg intrathecal papaverine). After induction of anesthesia and initiation of physiologic monitoring, a left-sided thoracotomy was performed to provide access to the descending aorta. SpEPs were generated by stimulating the thoracic spinal cord and recording the conducted response at the T10 and L4 level. After baseline measurements were recorded, the descending aorta was occluded 1 cm distal to the left subclavian artery. SpEPs were recorded every 2.5 min and physiologic variables every 5 min. The aorta was unclamped 10, 15, or 20 min after loss of the L4 SpEP. If the L4 SpEP was not lost, the aortic occlusion interval was terminated at 90 min. Attenuation of the SpEPs occurred earlier at the L4 level. Group 1 experienced the earliest loss of the L4 SpEP (18.3 +/- 7.8 min, P < 0.005). Loss of the L4 SpEP in Group 2 (49.3 +/- 27.8 min) was earlier than in Group 3 (73.7 +/- 26.1 min, P < 0.05). Early postoperative motor function (modified Tarlov scale) correlated with time from loss of the L4 SpEP until reperfusion of the distal aorta (r = 0.93). The sensitivity, specificity, and accuracy of the L4 SpEP in predicting neurologic dysfunction was 92.8% (13 abnormal/14 predicted), 90.9% (20/22), and 91.7% (33/36).(ABSTRACT TRUNCATED AT 250 WORDS)

An assessment of the duration of cephapirin-induced coagulation abnormalities as measured by thromboelastography.

Cephalosporin antibiotics are used prophylactically in cardiothoracic surgery to prevent postoperative infection. In 30 patients undergoing primary elective coronary artery bypass grafting, the whole blood coagulation system was prospectively evaluated before, and 10 and 30 minutes after administration of 1 g of cephapirin (Cefadyl, Bristol Laboratory, Evansville, IN). All patients had normal preoperative coagulation studies and had not received anticoagulant or antiplatelet therapy within 7 days of surgery. At 10 minutes after cephapirin administration, 23 of 30 patients had a significant change in all phases of whole blood coagulation as monitored by thromboelastography (TEG). Thirty minutes after cephapirin administration there was no statistical difference compared with the baseline TEG. It is concluded that cephapirin can cause a significant but transient change in the viscoelastic properties of blood. Coagulation parameters of the TEG should be measured prior to cephapirin administration to prevent errors in establishing baseline values prior to cardiopulmonary bypass.

Intravenous anesthetic alterations on the spinal-sciatic evoked response in swine.

Sciatic evoked responses (ScER) are used to monitor the integrity of the anterior spinal cord during spinal surgery. To evaluate the effects of intravenous anesthetics on the lumbar spinal evoked potential (SpEP) and ScER, 28 swine were anesthetized with halothane and an intravenous infusion of ketamine. After experimental preparation, anesthesia was maintained with ketamine, and the swine were divided into four equal groups (n = 7). The evoked responses were generated by delivering an electrical stimuli to the interspinous ligaments caudal to T1 and T2. The lumbar SpEP was recorded from the interspinous ligaments caudal to L2 and L3. The ScERs were recorded bilaterally from electrodes placed adjacent to the sciatic nerves. In Group 1 the effects of bolus dose administration of ketamine were evaluated. In Groups 2-4 anesthesia was maintained with ketamine by continuous infusion and the effects of fentanyl, sufentanil, and propofol on the L2 SpEP and ScER were evaluated. There was no significant change in either the amplitude or latency of the L2 SpEP with any anesthetic studied. Ketamine administered in bolus doses (2.5, 5, and 10 mg/kg) did not alter the ScER. After bolus doses of fentanyl 10 micrograms/kg or sufentanil 1 micrograms/kg, there was a similar decrement in the amplitude of the ScER (P < 0.05) that recovered at 10 min without changes in latency. There were no changes in the ScER associated with infusion of fentanyl 1-5 micrograms.kg-1 x h-1 or sufentanil 0.1-0.5 microgram.kg-1 x h-1.(ABSTRACT TRUNCATED AT 250 WORDS)