Anesthesia and analgesia
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To examine the physicochemical stability of combinations of propofol-lidocaine mixtures frequently used in clinical practice, we added lidocaine 5, 10, 20, or 40 mg to commercially available 1% propofol 20 mL. To assess chemical stability, propofol concentrations were determined by gas chromatography assay for 24 h after preparation of the mixture. In addition, scanning electron microscopy was used to determine the maximum detectable droplet size in randomly selected fields. Macroscopically, separate, colorless layers were first seen at 3 and 24 h after the addition of 40 and 20 mg of lidocaine to propofol, respectively, whereas the mixture with 5 or 10 mg of lidocaine was macroscopically stable. Propofol concentrations in the mixture with 40 mg of lidocaine decreased linearly and significantly from 4 to 24 h after preparation, whereas those combined with other lidocaine doses were unchanged compared with baseline concentrations. Scanning electron microscopy showed that droplets with diameters >or=5 microm first appeared 30 min after the addition of 40 mg of lidocaine to propofol, and the emulsion droplets were enlarged in a time- and dose-dependent fashion. Our results indicate that the addition of lidocaine to propofol results in a coalescence of oil droplets, which finally proceeds to a visible separate layer. Depending on the dose of lidocaine and the duration between its preparation and administration, this combination may pose the risk of pulmonary embolism. ⋯ The addition of lidocaine to propofol results in time- and dose-dependent increases in oil droplet diameters in emulsion. This mixture is physicochemically unstable over time and may cause pulmonary embolism, depending on the dose of lidocaine.
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Anesthesia and analgesia · Dec 2003
Case ReportsThe use of the LMA-ProSeal in airway resuscitation.
Insufflation of the stomach with air can be a complication of face mask ventilation in the case of airway obstruction. Although the laryngeal mask airway has proven value in airway resuscitation, it has two major failings: a relatively low seal pressure and lack of access to the alimentary tract. ⋯ The patient was resuscitated with a LMA-ProSeal, which permitted ventilation with high airway pressures. Return of oxyhemoglobin saturation occurred after decompression of the stomach with a gastric tube inserted via the LMA-ProSeal's gastric drain.
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Anesthesia and analgesia · Dec 2003
Propofol suppresses the cortical somatosensory evoked potential in rats.
The dose-response curve for the effect of volatile anesthetics on the somatosensory evoked potential (SEP) is well described, but for propofol, the large dose segment of the curve is undefined. We describe the effect of increasing plasma concentrations of propofol on cortical SEPs in 18 rats. After surgical preparation under ketamine anesthesia, a remifentanil infusion was begun at 2.5, 5, or 10 microg x kg(-1) x min(-1). After 20 min, the propofol infusion was initiated at 20 mg x kg(-1) x h(-1) and was increased to 40, 60, and 80 mg x kg(-1) x h(-1) at 20-min intervals. SEP was recorded before remifentanil infusion, before propofol infusion rate changes, and 30 min after discontinuing propofol infusion. In six additional rats, the plasma concentrations of propofol after each 20-min infusion were measured using gas chromatography. Remifentanil did not have a significant effect, but propofol significantly depressed the SEP amplitude and prolonged the latency at infusion rates of 40 mg x kg(-1) x h(-1) and more. Propofol's effect was dose-dependent, but even at 80 mg x kg(-1) x h(-1) with an estimated plasma concentration of 31.6 +/- 3.4 microg/mL (10.8 50% effective concentration), a measurable response was present in 44.5% of rats. These results suggest that even at large doses, propofol and remifentanil provide adequate conditions for SEP monitoring. ⋯ Rats demonstrate dose-dependent somatosensory evoked potential (SEP) suppression with propofol but not with remifentanil. However, SEP suppression by 50% occurred only at large (1.5 EC(50)) concentrations of propofol, and a measurable SEP was present in 8 of 18 rats, even at 10.8 EC(50).
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Anesthesia and analgesia · Dec 2003
The effects of vasopressin on systemic and splanchnic hemodynamics and metabolism in endotoxin shock.
We compared the effects of vasopressin and norepinephrine on systemic and splanchnic circulation and metabolism in endotoxin shock in pigs. Twenty-one pigs were randomized to endotoxin shock (Escherichia coli endotoxin infusion) (n = 6), endotoxin and vasopressin (VASO; n = 6), endotoxin and norepinephrine (NE; n = 6), and controls (n = 3). Endotoxin infusion was increased to induce hypotension, after which vasopressin or norepinephrine was started to keep systemic mean arterial blood pressure >70 mm Hg. Regional blood flows and arterial and regional lactate concentrations were measured. Tonometers with microdialysis capillaries were inserted into the stomach, jejunum, and colon. Systemic mean arterial blood pressure >70 mm Hg was achieved in the VASO and NE groups. Vasopressin decreased cardiac output, superior mesenteric artery, and portal vein blood flow, whereas hepatic arterial blood flow increased. Arterial lactate concentration increased from 2.0 mM (1.6-2.1 mM) to 4.7 mM (4.7-4.9 mM) (P = 0.007). Systemic and mesenteric oxygen delivery and consumption decreased and oxygen extraction increased in the VASO group. Vasopressin increased mucosal-arterial PCO(2) gradients in all three locations, whereas luminal lactate release occurred only in the jejunum. Animals in the NE group remained stable. Vasopressin reversed hypotension but decreased systemic and gut blood flow. This was associated with hyperlactatemia, signs of visceral dysoxia, and jejunal luminal lactate release. ⋯ Although vasopressin induces vasoconstriction in visceral region, its effects on splanchnic circulation and metabolism during septic-endotoxin shock are still poorly characterized. We evaluated the metabolic and hemodynamic effects of vasopressin and norepinephrine within the splanchnic area in porcine endotoxin shock.
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Anesthesia and analgesia · Dec 2003
Clinical TrialMonitoring renal oxygen supply in critically-ill patients using urinary oxygen tension.
Critically-ill patients are at risk of developing renal disorders as a consequence of systemic hypoperfusion. Ischemic acute tubular necrosis and resulting acute renal failure are caused by hypotension or therapeutic management. In this study, we tested the change of O(2) availability induced by fenoldopam mesylate using the continuous measurement of urinary oxygen tension (PuO(2)), a relatively noninvasive technique that could provide potentially important real-time data regarding renal oxygenation in intensive care unit patients. Fenoldopam was administered at different doses (0.03, 0.06, and 0.09 microg x kg(-1) x min(-1)) to 50 stable critically-ill patients. Urine output was collected every hour to assess volume and urinary electrolytes. Heart rate, mean arterial blood pressure, cardiac output, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption index were analyzed after fenoldopam dose modifications and at infusion end. PaO(2) and PuO(2) continuous measurements were obtained through two sensors inserted in the radial artery and in the bladder. After a fenoldopam dose increase, PuO(2) significantly increased (P < 0.05), whereas PaO(2) remained unchanged. During the study, heart rate, mean arterial blood pressure, cardiac output, central venous pressure, pulmonary artery occlusion pressure, arterial oxygen delivery index, and oxygen consumption remained unchanged. Dose-dependent PuO(2) increases, unrelated to indexes of systemic perfusion and cardiac function, demonstrate that fenoldopam affects the balance between renal oxygen supply and demand in stable critically-ill patients. ⋯ Acute renal failure in critically-ill patients is associated with frequent mortality. Prolonged renal hypoperfusion cannot be detected by current systemic hemodynamic indexes. Using continuous measurement of urinary oxygen tension, which could indirectly provide real-time data regarding renal oxygenation, our study showed that fenoldopam increases the ratio between oxygen supply and demand.