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Abstract Background There are few data to guide the intraoperative management of patients with reduced left ventricular ejection fraction (LVEF). This study aimed to describe how patients with reduced LVEF are managed differently and to identify and treatments had a different risk profile in this population. Methods We performed a retrospective cohort study of adult patients who underwent general anesthesia for non-cardiac surgery. The effect of anesthesia medications and fluid balance was compared between those with and without a reduced preoperative LVEF. The primary outcome was a composite of acute kidney injury, myocardial injury, pulmonary complications, and 30-day mortality. Multivariable logistic regression was used to adjust for confounders. Treatments that affected patients with reduced LVEF differently were defined as those associated with the primary outcome that also had a significant interaction with LVEF. Results A total of 9420 patients were included. Patients with reduced LVEF tended to have a less positive fluid balance. Etomidate, calcium, and phenylephrine were use more frequently, while propofol and remifentanil were used less frequently. Remifentanil affected patients with reduced LVEF differently than those without (interaction term OR 2.71, 95% CI 1.30–5.68, p = 0.008). While the use of remifentanil was associated with fewer complications in patients with normal systolic function (OR 0.54, 95% CI 0.42–0.68, p

Background: Reliable diagnosis of heart failure during preoperative evaluation is important for perioperative management and long-term care. We aimed to quantify preoperative heart failure diagnostic accuracy and explore characteristics of patients with heart failure misdiagnoses. Methods: We performed an observational cohort study of adults undergoing major noncardiac surgery at an academic hospital between 2015 and 2019. A preoperative clinical diagnosis of heart failure was defined using keywords from the history and clinical examination or administrative documentation. Across stratified subsamples of cases with and without clinically diagnosed heart failure, health records were intensively reviewed by an expert panel to develop an adjudicated heart failure reference standard using diagnostic criteria congruent with consensus guidelines. We calculated agreement among experts, and analysed performance of clinically diagnosed heart failure compared with the adjudicated reference standard. Results: Across 40 555 major noncardiac procedures, a stratified subsample of 511 patients was reviewed by the expert panel. The prevalence of heart failure was 9.1% based on clinically diagnosed compared with 13.3% (95% confidence interval [CI], 10.3–16.2%) estimated by the expert panel. Overall agreement and inter-rater reliability (kappa) among heart failure experts were 95% and 0.79, respectively. Based upon expert adjudication, heart failure was clinically diagnosed with an accuracy of 92.8% (90.6–95.1%), sensitivity 57.4% (53.1–61.7%), specificity 98.3% (97.1–99.4%), positive predictive value 83.5% (80.3–86.8%), and negative predictive value 93.8% (91.7–95.9%). Conclusions: Limitations exist to the preoperative clinical diagnosis of heart failure, with nearly half of cases undiagnosed preoperatively. Considering the risks of undiagnosed heart failure, efforts to improve preoperative heart failure diagnoses are warranted.

Background The variable presentations and different phenotypes of sepsis suggest that risk of sepsis comes from many genes each having a small effect. The cumulative effect can be used to create individual risk profile. The purpose of this study was to create a polygenic risk score and determine the genetic variants associated with sepsis. Methods We sequenced ~14 million single nucleotide polymorphisms with a minimac imputation quality R2>0.3 and minor allele frequency >10−6 in patients with Sepsis-2 or Sepsis-3. Genome-wide association was performed using Firth bias-corrected logistic regression. Semi-parsimonious logistic regression was used to create polygenic risk scores and reduced regression to determine the genetic variants independently associated with sepsis. Findings 2261 patients had sepsis and 13,068 control patients did not. The polygenic risk scores had good discrimination: c-statistic = 0.752 ± 0.005 for Sepsis-2 and 0.752 ± 0.007 for Sepsis-3. We found 772 genetic variants associated with Sepsis-2 and 442 with Sepsis-3, pConclusions Sepsis-2 and Sepsis-3 have both separate and shared genetic variants. Most genetic variants have small effects sizes, but cumulatively, the polygenic risk scores have good discrimination.

Purpose. To determine if left ventricular or inferior vena cava (IVC) measurements are easier to obtain on point-of-care ultrasound by anesthesiologists in preoperative patients, and to assess the relationship between preoperative cardiac dimensions and hypotension with the induction of general anesthesia. Methods. This prospective observational study was conducted at a large academic medical center. Sixty-three patients undergoing noncardiac surgeries under general anesthesia were enrolled. Ultrasound examinations were performed by anesthesiologists in the preoperative area. To ensure that hypotension represented both a relative and absolute decrease in blood pressure, both a mean arterial pressure (MAP) 30% from preoperative value defined this outcome. Results. Left ventricular measurements were more likely to be acquired than IVC measurements (97% vs. 79%). Subjects without adequate images to assess IVC collapsibility tended to have a higher body mass index (33.6 ± 5.5 vs. 28.5 ± 4.5, p=0.001). While high left ventricular end-diastolic diameter values were associated with a decreased odds of MAP 30% from baseline alone (OR: 0.25, 95% CI: 0.07–0.83, p=0.023), the primary endpoint of both relative and absolute hypotension was not associated with preoperative left ventricular dimensions. Conclusions. Preoperative cardiac ultrasound may be a more reliable way for anesthesiologists to assess patients’ volume status compared to ultrasound of the IVC, particularly for patients with a higher body mass index.

Abstract Background It is unknown if the plasma lipidome is a useful tool for improving our understanding of the acute respiratory distress syndrome (ARDS). Therefore, we measured the plasma lipidome of individuals with ARDS at two time-points to determine if changes in the plasma lipidome distinguished survivors from non-survivors. We hypothesized that both the absolute concentration and change in concentration over time of plasma lipids are associated with 28-day mortality in this population. Methods Samples for this longitudinal observational cohort study were collected at multiple tertiary-care academic medical centers as part of a previous multicenter clinical trial. A mass spectrometry shot-gun lipidomic assay was used to quantify the lipidome in plasma samples from 30 individuals. Samples from two different days were analyzed for each subject. After removing lipids with a coefficient of variation > 30%, differences between cohorts were identified using repeated measures analysis of variance. The false discovery rate was used to adjust for multiple comparisons. Relationships between significant compounds were explored using hierarchical clustering of the Pearson correlation coefficients and the magnitude of these relationships was described using receiver operating characteristic curves. Results The mass spectrometry assay reliably measured 359 lipids. After adjusting for multiple comparisons, 90 compounds differed between survivors and non-survivors. Survivors had higher levels for each of these lipids except for five membrane lipids. Glycerolipids, particularly those containing polyunsaturated fatty acid side-chains, represented many of the lipids with higher concentrations in survivors. The change in lipid concentration over time did not differ between survivors and non-survivors. Conclusions The concentration of multiple plasma lipids is associated with mortality in this group of critically ill patients with ARDS. Absolute lipid levels provided more information than the change in concentration over time. These findings support future research aimed at integrating lipidomics into critical care medicine.

Background: There are few data to guide the intraoperative management of patients with reduced left ventricular ejection fraction (LVEF). This study aimed to describe how patients with reduced LVEF are managed differently and to identify and treatments had a different risk profile in this population. Methods: We performed a retrospective cohort study of adult patients who underwent general anesthesia for non-cardiac surgery. The effect of anesthesia medications and fluid balance was compared between those with and without a reduced preoperative LVEF. The primary outcome was a composite of acute kidney injury, myocardial injury, pulmonary complications, and 30-day mortality. Multivariable logistic regression was used to adjust for confounders. Treatments that affected patients with reduced LVEF differently were defined as those associated with the primary outcome that also had a significant interaction with LVEF. Results: A total of 9420 patients were included. Patients with reduced LVEF tended to have a less positive fluid balance. Etomidate, calcium, and phenylephrine were use more frequently, while propofol and remifentanil were used less frequently. Remifentanil affected patients with reduced LVEF differently than those without (interaction term OR 2.71, 95% CI 1.30–5.68, p = 0.008). While the use of remifentanil was associated with fewer complications in patients with normal systolic function (OR 0.54, 95% CI 0.42–0.68, p < 0.001), it was associated with an increase in complications in patients with reduced LVEF (OR = 3.13, 95% CI 3.06–5.98, p = 0.026). Conclusions: Patients with a reduced preoperative LVEF are treated differently than those with a normal LVEF when undergoing non-cardiac surgery. An association was found between the use of remifentanil and an increase in postoperative adverse events that was unique to this population. Future research is needed to determine if this relationship is secondary to the medication itself or reflects a difference in how remifentanil is used in patients with reduced LVEF. [ABSTRACT FROM AUTHOR]

Objective: While endothelial dysfunction has been implicated in the widespread thromboinflammatory complications of COVID‐19, the upstream mediators of endotheliopathy remain, for the most part, unknown. This study was undertaken to identify circulating factors contributing to endothelial cell activation and dysfunction in COVID‐19. Methods: Human endothelial cells were cultured in the presence of serum or plasma from 244 patients hospitalized with COVID‐19 and plasma from 100 patients with non–COVID‐19–related sepsis. Cell adhesion molecules (E‐selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 [ICAM‐1]) were quantified using in‐cell enzyme‐linked immunosorbent assay. Results: Serum and plasma from COVID‐19 patients increased surface expression of cell adhesion molecules. Furthermore, levels of soluble ICAM‐1 and E‐selectin were elevated in patient serum and correlated with disease severity. The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID‐19 serum to activate endothelium. Depletion of total IgG from antiphospholipid antibody–positive serum markedly reduced the up‐regulation of cell adhesion molecules. Conversely, supplementation of control serum with patient IgG was sufficient to trigger endothelial activation. Conclusion: These data are the first to indicate that some COVID‐19 patients have potentially diverse antibodies that drive endotheliopathy, providing important context regarding thromboinflammatory effects of autoantibodies in severe COVID‐19. [ABSTRACT FROM AUTHOR]

Background: The variable presentations and different phenotypes of sepsis suggest that risk of sepsis comes from many genes each having a small effect. The cumulative effect can be used to create individual risk profile. The purpose of this study was to create a polygenic risk score and determine the genetic variants associated with sepsis. Methods: We sequenced ~14 million single nucleotide polymorphisms with a minimac imputation quality R2>0.3 and minor allele frequency >10−6 in patients with Sepsis-2 or Sepsis-3. Genome-wide association was performed using Firth bias-corrected logistic regression. Semi-parsimonious logistic regression was used to create polygenic risk scores and reduced regression to determine the genetic variants independently associated with sepsis. Findings: 2261 patients had sepsis and 13,068 control patients did not. The polygenic risk scores had good discrimination: c-statistic = 0.752 ± 0.005 for Sepsis-2 and 0.752 ± 0.007 for Sepsis-3. We found 772 genetic variants associated with Sepsis-2 and 442 with Sepsis-3, p<0.01. After multivariate adjustment, 100 variants on 85 genes were associated with Sepsis-2 and 69 variants in 54 genes with Sepsis-3. Twenty-five variants were present in both the Sepsis-2 and Sepsis-3 groups out of 32 genes that were present in both groups. The other 7 genes had different variants present. Most variants had small effect sizes. Conclusions: Sepsis-2 and Sepsis-3 have both separate and shared genetic variants. Most genetic variants have small effects sizes, but cumulatively, the polygenic risk scores have good discrimination. [ABSTRACT FROM AUTHOR]

Objective: Weaning parameters are well studied in patients undergoing first time extubation. Fewer data exists to guide re-extubation of patients who failed their first extubation attempt. It is reasonable to postulate that improved weaning parameters between the first and second extubation attempt would lead to improved rates of re-extubation success. To investigate, we studied a cohort of patients who failed their first extubation attempt and underwent a second attempt at extubation. We hypothesized that improvement in weaning parameters between the first and the second extubation attempt is associated with successful reextubation. Interventions: Rapid shallow breathing index (RSBI), maximum inspiratory pressure (MIP), vital capacity (VC), and the blood partial pressure of CO2 (PaCO2) were measured and recorded in the medical record prior to extubation along with demographic information. We examined the relationship between the change in extubation and re-extubation weaning parameters and re-extubation success. Measurements and main results: A total of 1283 adult patients were included. All weaning parameters obtained prior to re-extubation differed between those who were successful and those who required a second reintubation. Those with reextubation success had slightly lower PaCO2 values (39.5 ± 7.4 mmHg vs. 41.6 ± 9.1 mmHg, p = 0.0045) and about 13% higher vital capacity volumes (1021 ± 410 mL vs. 907 ± 396 mL, p = 0.0093). Lower values for RSBI (53 ± 32 breaths/min/L vs. 69 ± 42 breaths/min/L, p < 0.001) and MIP (-41 ± 12 cmH2O vs. -38 ± 13 cm H2O), p = 0.0225) were seen in those with re-extubation success. Multivariable logistical regression demonstrates lack of independent associated between the change in parameters between the 2 attempts and re-extubation success. Conclusions: The relationship between the changes in extubation parameters through successive attempts is driven primarily by the value obtained immediately prior to re-extubation. These findings do not support waiting for an improvement in extubation parameters to extubate patients who failed a first attempt at extubation if extubation parameters are compatible with success. [ABSTRACT FROM AUTHOR]

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Objective: To assess whether patients prescribed four‐factor prothrombin complex concentrate (4FPC) received less plasma during the following 24‐hour period than those treated for the same indications who received only plasma. Introduction: It is unclear whether 4FPC is associated with a reduction in subsequent plasma transfusion. This is important for minimising transfusion‐associated risks and for inventory management. Materials and Methods: We retrospectively studied patients treated for bleeding or coagulopathy. Individuals receiving 4FPC were matched by indication to patients treated with only plasma. Blood products received during 24‐hour follow up were compared between 4FPC and plasma‐only patients. Results: There was no difference in the number of patients receiving additional plasma (19 (21%) 4FPC patients vs 31 (34%) plasma‐only patients, P =.07) nor in the median number of additional plasma units received (0 units for both groups, interquartile range [0, 0] for 4FPC patients vs [0, 1] for plasma‐only patients, P =.09). Subgroup analysis comparing patients who received 4FPC for on‐label vs off‐label indications found no difference in the number of patients receiving plasma nor in the median number of plasma units received. Conclusion: 4FPC was prescribed to a diverse set of patients, and administration was not associated with reduced plasma transfusion at our institution. [ABSTRACT FROM AUTHOR]

Purpose. To determine if left ventricular or inferior vena cava (IVC) measurements are easier to obtain on point-of-care ultrasound by anesthesiologists in preoperative patients, and to assess the relationship between preoperative cardiac dimensions and hypotension with the induction of general anesthesia. Methods. This prospective observational study was conducted at a large academic medical center. Sixty-three patients undergoing noncardiac surgeries under general anesthesia were enrolled. Ultrasound examinations were performed by anesthesiologists in the preoperative area. To ensure that hypotension represented both a relative and absolute decrease in blood pressure, both a mean arterial pressure (MAP) < 65 mmHg and a MAP decrease of >30% from preoperative value defined this outcome. Results. Left ventricular measurements were more likely to be acquired than IVC measurements (97% vs. 79%). Subjects without adequate images to assess IVC collapsibility tended to have a higher body mass index (33.6 ± 5.5 vs. 28.5 ± 4.5, p = 0.001). While high left ventricular end-diastolic diameter values were associated with a decreased odds of MAP < 65 mmHg (OR: 0.24, 95% CI: 0.07–0.83, p = 0.023) or a MAP decrease of >30% from baseline alone (OR: 0.25, 95% CI: 0.07–0.83, p = 0.023), the primary endpoint of both relative and absolute hypotension was not associated with preoperative left ventricular dimensions. Conclusions. Preoperative cardiac ultrasound may be a more reliable way for anesthesiologists to assess patients' volume status compared to ultrasound of the IVC, particularly for patients with a higher body mass index. [ABSTRACT FROM AUTHOR]

Reflex cardiovascular responses to muscle contraction are mediated by mechanical and metabolic stimulation of thin muscle afferent fibers. Metabolic stimulants and receptors involved in responses are uncertain. Capsaicin depolarizes thin sensory afferent nerves that have vanilloid type 1 receptors (VR1). Among potential endogenous ligands of thin fibers, H+ has been suggested as a metabolite mediating the reflex muscle response as well as a potential stimulant of VR1. It has also been suggested that acid-sensing ion channels (ASIC) mediate H+, evoking afferent nerve excitation. We have examined the roles of VR1 and ASIC in mediating cardiovascular reflex responses to acid stimulation of muscle afferents in a rat model. In anesthetized rats, injections of capsaicin into the arterial blood supply of triceps surae muscles evoked a biphasic response (n = 6). An initial fall in mean arterial pressure (from baseline of 95.8 ± 9.5 to 70.4 ± 4.5 mmHg, P < 0.05 vs. baseline) was followed by an increase (to 131.6 ± 11.3 mmHg, P < 0.05 vs. baseline). Anandamide (an endogenous substance that activates VR1) induced the same change in blood pressure as did capsaicin. The pressor (but not depressor) component of the response was blocked by capsazepine (a VR1 antagonist) and section of afferent nerves. In decerebrate rats (n = 8), H+ evoked a pressor response that was not blocked by capsazepine but was attenuated by amiloride (an ASIC blocker). In rats (n = 12) pretreated with resiniferatoxin to destroy muscle afferents containing VR1, capsaicin and H+ responses were blunted. We conclude that H+ stimulates ASIC, evoking the reflex response, and that ASIC are likely to be frequently found on afferents containing VR1. The data also suggest that VR1 and ASIC may play a role in processing of muscle afferent signals, evoking the muscle pressor reflex. [ABSTRACT FROM AUTHOR]

Many cases of malignant hyperthermia triggered by volatile anesthetic agents have been described. However, to our knowledge, there has not been a report describing the precise changes in physiologic data of a human suffering from this process. Here we describe a case of malignant hyperthermia in which monitoring information was frequently and accurately captured by an anesthesia information management system. [ABSTRACT FROM AUTHOR]