Anesthesiology
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Randomized Controlled Trial Multicenter Study
Intravenous Lidocaine Does Not Improve Neurologic Outcomes after Cardiac Surgery: A Randomized Controlled Trial.
Why is this interesting?
Lidocaine/lignocaine has been increasingly used intra- and perioperatively as an analgesic adjunct, with further research suggesting a potential neuroprotective effect. Cognitive decline is a common problem following cardiac surgery (40-50%), with lidocaine potentially offering a simple and safe intervention to reduce this complication. Past studies have showed conflicting results.
What did they do?
This Duke University team randomized 478 cardiac surgery patients across multiple centres to lidocaine intraoperatively (1 mg/kg bolus then decreasing infusions across 2.9 / 1.5 / 0.6 mg/kg/h over 48 hours) or blinded control. Cognitive function was assessed at 6 weeks and 1 year.
They found...
No difference in cognitive deficit between lidocaine infusion and saline control at either 6 weeks or 1 year.
Be smart
Intravenous lidocaine infusion remains relatively safe, practical and is still likely a useful analgesic adjunct. Similar to magnesium, which has been shown to be neuroprotective in premature infants but not adult cardiac patients, the problem for lidocaine may well be context rather than physiological benefit itself.
summary -
Anesthetic-induced loss of consciousness is accompanied by changes in functional connectivity within and between brain networks. ⋯ Anesthesia-induced alterations of functional connectivity are dynamic despite the stable and prolonged administration of isoflurane, in the absence of any noxious stimuli. Changes in connectivity over time will likely yield more information as a marker or mechanism of surgical anesthesia than any single pattern.
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Respiratory function is fundamental in the practice of anesthesia. Knowledge of basic physiologic principles of respiration assists in the proper implementation of daily actions of induction and maintenance of general anesthesia, delivery of mechanical ventilation, discontinuation of mechanical and pharmacologic support, and return to the preoperative state. ⋯ We review the path of oxygen from air to the artery and of carbon dioxide the opposite way, and we have the causes of hypoxemia and of hypercarbia based on these very footpaths. We present the actions of pressure, flow, and volume as the normal determinants of ventilation, and we review the resulting abnormalities in terms of changes of resistance and compliance.
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The antidepressant effect of ketamine is associated with increased activity in the reward circuitry of the brain and a suppression of circuitry that mediates perceptual processing of negative emotions. The duration of ketamine effect on these brain structures remains to be defined. ⋯ Single bolus ketamine administration rapidly triggers lasting changes in mesolimbic neural networks to improve pathologic reward and emotional processing in patients with major depressive disorder.
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A key feature of the human brain is its capability to adapt flexibly to changing external stimuli. This capability can be eliminated by general anesthesia, a state characterized by unresponsiveness, amnesia, and (most likely) unconsciousness. Previous studies demonstrated decreased connectivity within the thalamus, frontoparietal, and default mode networks during general anesthesia. We hypothesized that these alterations within specific brain networks lead to a change of communication between networks and their temporal dynamics. ⋯ These results suggest that (1) higher-order brain regions play a crucial role in the generation of specific between-network connectivity patterns and their dynamics, and (2) the capability to interact with external stimuli is represented by complex between-network connectivity patterns.