Anesthesia and analgesia
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Anesthesia and analgesia · Apr 1998
Randomized Controlled Trial Clinical TrialPropofol concentration required for endotracheal intubation with a laryngoscope or fiberscope and its interaction with fentanyl.
The administration of fentanyl with propofol reduces the blood concentration of propofol required to achieve adequate anesthesia for tracheal intubation. However, different intubation procedures have variable intensities of noxious stimulation and may require different levels of anesthesia. The goal of this study was to determine the propofol blood concentration at which 50% of patients did not respond to stimulation (Cp50) for laryngoscopy, intubation with a laryngoscope, insertion of a slotted oral-pharyngeal airway (Ovassapian airway), and intubation with a fiberscope when administered in conjunction with fentanyl. Patients undergoing elective surgery were given varying amounts of propofol or propofol with fentanyl, and their responses to the four procedures listed above were assessed. These experiments demonstrated that the propofol concentration required for intubation with a laryngoscope was similar to that for intubation with a fiberscope, and that the required level was reduced by fentanyl. Hemodynamic responses to intubation were lower with a fiberscope than with a laryngoscope. We conclude that almost the same concentrations of propofol or fentanyl are necessary for suppressing both of the somatic responses to tracheal intubation with a fiberscope or a laryngoscope. Hemodynamic responses were attenuated more during intubation with a fiberscope. ⋯ The propofol blood concentrations at which 50% of patients did not respond to stimulation for laryngoscopy, tracheal intubation with a laryngoscope, and tracheal intubation with a fiberscope were 10.9, 19.6, and 19.9 microg/mL, respectively. These were reduced by fentanyl. Hemodynamic responses to intubation were less with a fiberscope than with a laryngoscope.
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Anesthesia and analgesia · Apr 1998
Comparative StudyCardiovascular and central nervous system effects of intravenous levobupivacaine and bupivacaine in sheep.
Commercially available bupivacaine is an equimolar mixture of R(+)- and S(-)-bupivacaine. S(-)-bupivacaine (i.e., levobupivacaine) is currently undergoing preclinical evaluation. Cross-over studies with i.v. levobupivacaine and bupivacaine were conducted in two groups of seven conscious sheep. Doses were chosen to avoid convulsions (smaller dose 6.25-37.5 mg/min) or to be potentially toxic (larger dose 75-200 mg/3 min). In subconvulsive doses, both drugs produced similar time- and dose-dependent depression of left ventricular systolic contractility (dP/dt(max)). Convulsions occurred consistently with > or = 75 mg of bupivacaine and > or = 100 mg of levobupivacaine, producing an abrupt reversal of dP/dt(max) depression. Subconvulsive doses produced minor cardiovascular effects on heart rate and blood pressure, whereas both were increased by convulsions. Cardiac output and myocardial blood flow were decreased with larger doses of both drugs. Doses > 75 mg of bupivacaine or > 100 mg of levobupivacaine induced QRS widening and ventricular arrhythmias, but significantly fewer and less deleterious arrhythmias were induced by levobupivacaine. Three animals died after 150, 150, and 200 mg of bupivacaine from the sudden onset of ventricular fibrillation. These doses of levobupivacaine produced nonfatal arrhythmias that automatically returned to sinus rhythm. We conclude that levobupivacaine could offer a greater margin of clinical safety than bupivacaine. ⋯ Levobupivacaine comprises 50% of commercially available bupivacaine and is being considered for use in its own right. Local anesthetics can cause toxicity to the cardiovascular and central nervous systems. As a part of a preclinical evaluation of levobupivacaine, this study compared the toxic effects of levobupivacaine and bupivacaine in sheep.
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Anesthesia and analgesia · Apr 1998
The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.
Adhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. ⋯ This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful.
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Anesthesia and analgesia · Apr 1998
Comparative StudyComparison of ketamine and dextromethorphan in potentiating the antinociceptive effect of morphine in rats.
We compared the efficacy of two clinically available drugs with N-methyl-D-aspartate receptor antagonist properties, dextromethorphan and ketamine, in potentiating morphine-induced antinociception. Ketamine alone at 0.3-3 mg/kg had no effect on the hot plate test and at 10 mg/kg caused sedation/motor deficits. The antinociceptive effect of 5 mg/kg morphine was slightly enhanced by 1 mg/kg, but not 0.3 or 3 mg/kg, ketamine. Dextromethorphan alone at 45 mg/kg had no effect, but at 60 mg/kg caused sedation/motor deficit. At 15-45 mg/kg, dextromethorphan significantly and dose-dependently increased the magnitude and duration of morphine-induced antinociception. Dextromethorphan also potentiated morphine at doses that, by themselves, did not cause antinociception (1-2 mg/kg). ⋯ Dextromethorphan was more effective than ketamine in potentiating morphine-induced antinociception. Dextromethorphan may thus be the drug of choice for testing the interactions between N-methyl-D-aspartate antagonists and morphine clinically.
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Anesthesia and analgesia · Apr 1998
The dose-response relationship of ketorolac as a component of intravenous regional anesthesia with lidocaine.
Ketorolac (K) is a useful addition to lidocaine for i.v. regional anesthesia (IVRA). However, the minimal dose of K that is effective for this purpose has not been established. We added 0, 5, 10, 15, 20, 30, and 60 mg of K to 0.5% lidocaine IVRA for either carpal tunnel release or tenolysis. Pain was assessed in the postanesthesia care unit by using a visual analog scale. The duration of analgesia (time to first request for pain relief) and the use of Tylenol No. 3 tablets (T3) were measured. A linear dose-response relationship was observed between the dose of K and the duration of analgesia (r = 0.988) up to 20 mg of K. Similarly, the number of T3 tablets used was inversely related to the dose of K (r = 0.960) over the same range. There were no significant differences among the groups who received 20, 30, or 60 mg of K. We conclude that 20 mg of K is the optimal dose for inclusion with 0.5% lidocaine for IVRA under the conditions of our study. ⋯ The antiinflammatory drug ketorolac is a useful addition to lidocaine for i.v. regional anesthesia. This study showed that 20 mg of ketorolac is equally effective as 60 mg in this context. However, smaller doses provided less effective pain relief, and a linear dose-response relationship was demonstrated.