Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2013
Case ReportsCase report: use caution when applying magnets to pacemakers or defibrillators for surgery.
The application of a magnet to a pacemaker (intended to cause asynchronous pacing) or implanted cardioverter defibrillator (intended to prevent shocks) during surgery without a clear understanding of actual magnet function(s) or precautions can have unexpected, untoward, or harmful consequences. In this report, we present 3 cases in which inadequate assessment of cardiac implanted electronic device (CIED) function, coupled with magnet application, contributed to or resulted in inappropriate antitachycardia pacing or shocks, CIED damage, or patient injury. Although these cases might be rare, they reinforce the need for a timely, detailed preoperative review of CIED function and programming as recommended by the American Society of Anesthesiologists and the Heart Rhythm Society.
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Anesthesia and analgesia · Aug 2013
Propofol stimulates noradrenalin-inhibited neurons in the ventrolateral preoptic nucleus by reducing GABAergic inhibition.
The cellular mechanisms underlying the sedative effect of general anesthetics are not completely understood. Accumulating evidence indicates that the ventrolateral preoptic area (VLPO) of the hypothalamus plays a critical role. The VLPO contains 2 major types of neurons, the noradrenalin-inhibited GABAergic projecting neurons (NA(-) neurons) and the noradrenalin-excited interneurons (NA(+) neurons) which are probably also γ-aminobutyric acid (GABA)-containing neurons. Our previous work suggests that NA(-) neurons are normally under the inhibitory control of NA(+) neurons. Previous studies also show that GABAergic agents including propofol activate GABAergic projecting neurons in the VLPO, which is believed to lead to the inhibition of the arousal-producing nuclei in the tuberomammillary nucleus and sedation. However, how propofol activates VLPO neurons remains unclear. We explored the possibility that propofol activates NA(-) neurons indirectly, by inhibiting GABAergic transmission including those from VLPO NA(+) neurons. ⋯ Propofol excites VLPO NA(-) neurons by reducing GABAergic transmission, at least in part by inhibiting VLPO NA(+) neurons. This may be a critical mechanism contributing to propofol-induced sedation.
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Anesthesia and analgesia · Aug 2013
Cardiac catheterization and postoperative acute kidney failure in congenital heart pediatric patients.
Acute renal failure (ARF) is a severe complication of cardiac operations in pediatric patients. Angiography with the exposure to contrast media is a risk factor for ARF. In the present study, we explored the association between timing of angiography, dose of contrast media, and the incidence of ARF after cardiac operations in pediatric patients. ⋯ Angiography before cardiac surgery is an important risk factor for ARF in pediatric patients. Being a modifiable risk factor, the contrast media dose should be limited to the lowest possible value, avoiding large doses of iodine which, together with other factors (age and postoperative low cardiac output), concur in the determinism of postoperative ARF.
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Anesthesia and analgesia · Aug 2013
What Is the Accuracy of the High-Fidelity METI Human Patient Simulator Physiological Models During Oxygen Administration and Apnea Maneuvers?
A widely used physiological simulator is generally accepted to give valid predictions of oxygenation status during disturbances in breathing associated with anesthesia. We compared predicted measures with physiological measurements available in the literature, or derived from other models. ⋯ Spo2 decreased much later during apnea on the METI simulator than in a clinical situation, whether preoxygenation was performed or not. The debriefing after simulation of critical situations or the use of the METI simulator to test a new equipment must consider these results.