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Background: Intravenous drugs active via gamma-aminobutyric acid receptors to produce memory impairment during conscious sedation. Memory function was assessed using event-related potentials (ERPs) while drug was present.Methods: The continuous recognition task measured recognition of photographs from working (6 s) and long-term (27 s) memory while ERPs were recorded from Cz (familiarity recognition) and Pz electrodes (recollection recognition). Volunteer participants received sequential doses of one of placebo (n = 11), 0.45 and 0.9 microg/ml propofol (n = 10), 20 and 40 ng/ml midazolam (n = 12), 1.5 and 3 microg/ml thiopental (n = 11), or 0.25 and 0.4 ng/ml dexmedetomidine (n = 11). End-of-day yes/no recognition 225 min after the end of drug infusion tested memory retention of pictures encoded on the continuous recognition tasks.Results: Active drugs increased reaction times and impaired memory on the continuous recognition task equally, except for a greater effect of midazolam (P < 0.04). Forgetting from continuous recognition tasks to end of day was similar for all drugs (P = 0.40), greater than placebo (P < 0.001). Propofol and midazolam decreased the area between first presentation (new) and recognized (old, 27 s later) ERP waveforms from long-term memory for familiarity (P = 0.03) and possibly for recollection processes (P = 0.12). Propofol shifted ERP amplitudes to smaller voltages (P < 0.002). Dexmedetomidine may have impaired familiarity more than recollection processes (P = 0.10). Thiopental had no effect on ERPs.Conclusion: Propofol and midazolam impaired recognition ERPs from long-term memory but not working memory. ERP measures of memory revealed different pathways to end-of-day memory loss as early as 27 s after encoding. [ABSTRACT FROM AUTHOR]

Background: Propofol may produce amnesia by affecting encoding. The hypothesis that propofol weakens encoding was tested by measuring regional cerebral blood flow during verbal encoding.Methods: Seventeen volunteer participants (12 men; aged 30.4 +/- 6.5 yr) had regional cerebral blood flow measured using H2O positron emission tomography during complex and simple encoding tasks (deep vs. shallow level of processing) to identify a region of interest in the left inferior prefrontal cortex (LIPFC). The effect of either propofol (n = 6, 0.9 microg/ml target concentration), placebo with a divided attention task (n = 5), or thiopental at sedative doses (n = 6, 3 microg/ml) on regional cerebral blood flow activation in the LIPFC was tested. The divided attention task was expected to decrease activation in the LIPFC.Results: Propofol did not impair encoding performance or reaction times, but impaired recognition memory of deeply encoded words 4 h later (median recognition of 35% [interquartile range, 17-54%] of words presented during propofol vs. 65% [38-91%] before drug; P < 0.05). Statistical parametric mapping analysis identified a region of interest of 6.6 cm in the LIPFC (T = 7.44, P = 0.014). Regional cerebral blood flow response to deep encoding was present in this region of interest in each group before drug (T > 4.41, P < 0.04). During drug infusion, only the propofol group continued to have borderline significant activation in this region (T = 4.00, P = 0.063).Conclusions: If the amnesic effect of propofol were solely due to effects on encoding, activation in the LIPFC should be minimal. Because LIPFC activation was not totally eliminated by propofol, the amnesic action of propofol must be present in other brain regions and/or affect other memory processes. [ABSTRACT FROM AUTHOR]

Background: Detailed understanding of the association between intraoperative left atrial and left ventricular diastolic function and postoperative atrial fibrillation is lacking. In this post hoc analysis of the Posterior Left Pericardiotomy for the Prevention of Atrial Fibrillation after Cardiac Surgery (PALACS) trial, we aimed to evaluate the association of intraoperative left atrial and left ventricular diastolic function as assessed by transesophageal echocardiography (TEE) with postoperative atrial fibrillation., Methods: PALACS patients with available intraoperative TEE data (n = 402 of 420; 95.7%) were included in this cohort study. We tested the hypotheses that preoperative left atrial size and function, left ventricular diastolic function, and their intraoperative changes were associated with postoperative atrial fibrillation. Normal left ventricular diastolic function was graded as 0 and with lateral e' velocity 10 cm/s or greater. Diastolic dysfunction was defined as lateral e' less than 10 cm/s using E/e' cutoffs of grade 1, E/e' 8 or less; grade, 2 E/e' 9 to 12; and grade 3, E/e' 13 or greater, along with two criteria based on mitral inflow and pulmonary wave flow velocities., Results: A total of 230 of 402 patients (57.2%) had intraoperative diastolic dysfunction. Posterior pericardiotomy intervention was not significantly different between the two groups. A total of 99 of 402 patients (24.6%) developed postoperative atrial fibrillation. Patients who developed postoperative atrial fibrillation more frequently had abnormal left ventricular diastolic function compared to patients who did not develop postoperative atrial fibrillation (75.0% [n = 161 of 303] vs. 57.5% [n = 69 of 99]; P = 0.004). Of the left atrial size and function parameters, only delta left atrial area, defined as presternotomy minus post-chest closure measurement, was significantly different in the no postoperative atrial fibrillation versus postoperative atrial fibrillation groups on univariate analysis (-2.1 cm2 [interquartile range, -5.1 to 1.0] vs. 0.1 [interquartile range, -4.0 to 4.8]; P = 0.028). At multivariable analysis, baseline abnormal left ventricular diastolic function (odds ratio, 2.02; 95% CI, 1.15 to 3.63; P = 0.016) and pericardiotomy intervention (odds ratio, 0.46; 95% CI, 0.27 to 0.78, P = 0.004) were the only covariates independently associated with postoperative atrial fibrillation., Conclusions: Baseline preoperative left ventricular diastolic dysfunction on TEE, not left atrial size or function, is independently associated with postoperative atrial fibrillation. Further studies are needed to test if interventions aimed at optimizing intraoperative left ventricular diastolic function during cardiac surgery may reduce the risk of postoperative atrial fibrillation., (Copyright © 2023 American Society of Anesthesiologists. All Rights Reserved.)

Background: Anesthesiologists' contribution to perioperative healthcare disparities remains unclear because patient and surgeon preferences can influence care choices. Postoperative nausea and vomiting is a patient- centered outcome measure and a main driver of unplanned admissions. Antiemetic administration is under the sole domain of anesthesiologists. In a U.S. sample, Medicaid insured versus commercially insured patients and those with lower versus higher median income had reduced antiemetic administration, but not all risk factors were controlled for. This study examined whether a patient's race is associated with perioperative antiemetic administration and hypothesized that Black versus White race is associated with reduced receipt of antiemetics., Methods: An analysis was performed of 2004 to 2018 Multicenter Perioperative Outcomes Group data. The primary outcome of interest was administration of either ondansetron or dexamethasone; secondary outcomes were administration of each drug individually or both drugs together. The confounder-adjusted analysis included relevant patient demographics (Apfel postoperative nausea and vomiting risk factors: sex, smoking history, postoperative nausea and vomiting or motion sickness history, and postoperative opioid use; as well as age) and included institutions as random effects., Results: The Multicenter Perioperative Outcomes Group data contained 5.1 million anesthetic cases from 39 institutions located in the United States and The Netherlands. Multivariable regression demonstrates that Black patients were less likely to receive antiemetic administration with either ondansetron or dexamethasone than White patients (290,208 of 496,456 [58.5%] vs. 2.24 million of 3.49 million [64.1%]; adjusted odds ratio, 0.82; 95% CI, 0.81 to 0.82; P < 0.001). Black as compared to White patients were less likely to receive any dexamethasone (140,642 of 496,456 [28.3%] vs. 1.29 million of 3.49 million [37.0%]; adjusted odds ratio, 0.78; 95% CI, 0.77 to 0.78; P < 0.001), any ondansetron (262,086 of 496,456 [52.8%] vs. 1.96 million of 3.49 million [56.1%]; adjusted odds ratio, 0.84; 95% CI, 0.84 to 0.85; P < 0.001), and dexamethasone and ondansetron together (112,520 of 496,456 [22.7%] vs. 1.0 million of 3.49 million [28.9%]; adjusted odds ratio, 0.78; 95% CI, 0.77 to 0.79; P < 0.001)., Conclusions: In a perioperative registry data set, Black versus White patient race was associated with less antiemetic administration, after controlling for all accepted postoperative nausea and vomiting risk factors., (Copyright © 2023, the American Society of Anesthesiologists. All Rights Reserved.)

Background: Intravenous anesthetics have marked effects on memory function, even at subclinical concentrations. Fundamental questions remain in characterizing anesthetic amnesia and identifying affected system-level processes. The authors applied a mathematical model to evaluate time-domain components of anesthetic amnesia in human subjects., Methods: Sixty-one volunteers were randomized to receive propofol (n = 12), thiopental (n = 13), midazolam (n = 12), dexmedetomidine (n = 12), or placebo (n = 12). With drug present, subjects encoded pictures into memory using a 375-item continuous recognition task, with subsequent recognition later probed with drug absent. Memory function was sampled at up to 163 time points and modeled over the time domain using a two-parameter, first-order negative power function. The parietal event-related P2-N2 complex was derived from electroencephalography, and arousal was repeatedly sampled. Each drug was evaluated at two concentrations., Results: The negative power function consistently described the course of amnesia (mean R = 0.854), but there were marked differences between drugs in the modulation of individual components (P < 0.0001). Initial memory strength was a function of arousal (P = 0.005), whereas subsequent decay was related to the reaction time (P < 0.0001) and the P2-N2 complex (P = 0.007/0.002 for discrete components)., Conclusions: In humans, the amnesia caused by multiple intravenous anesthetic drugs is characterized by arousal-related effects on initial trace strength, and a subsequent decay predicted by attenuation of the P2-N2 complex at encoding. The authors propose that the failure of normal memory consolidation follows drug-induced disruption of interregional synchrony critical for neuronal plasticity and discuss their findings in the framework of memory systems theory.