BACKGROUND: Our previous research proved that vagus nerve stimulation (VNS) improved the neurological outcome after cardiopulmonary resuscitation (CPR) by activating α7 nicotinic acetylcholine receptor (α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains unclear.

METHODS: In vivo, we established a mouse model of cardiac arrest (CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion (I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2 (JAK2) and toll-like receptor 4 (TLR4) /nuclear factor-κB (NF-κB).

RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation (ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha (TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 antagonists.

CONCLUSION: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway.

BACKGROUND: The ion shift index (ISI) as a prognostic indicator that can show the severity of hypoxic-ischemic injury. We aimed to evaluate the performance of the ISI in predicting unfavorable neurological outcomes at hospital discharge in cardiac arrest (CA) patients following extracorporeal cardiopulmonary resuscitation (ECPR) and to compare its performance to other prognostic predictors.
METHODS: This was a retrospective observational study including adult CA patients treated with ECPR between January 2018 and December 2022 in a tertiary hospital. Data regarding clinical characteristics and laboratory parameters were collected from medical records. The ISI was determined based on the first available serum electrolyte levels after ECPR. The primary outcome was unfavorable neurological status at hospital discharge, defined as Cerebral Performance Categories 3-5. Comparisons of the characteristics between the two groups were made using the χ² test for categorical variables and the t-test or non-parametric Mann-Whitney U-test for continuous variables, as appropriate. Correlation analysis was performed using Spearman’s rank correlation coefficient. A two-tailed P-value <0.05 was considered statistically significant.
RESULTS: Among the 122 patients involved, 46 (37.7%) had out-of-hospital CA, and 88 had unfavorable neurological outcomes. The ISI was significantly higher in the unfavorable outcome group than in the favorable outcome group (3.74 [3.15-4.57] vs. 2.69 [2.51-3.07], P<0.001). A higher ISI level was independently related to unfavorable outcome (odds ratio=6.529, 95% confidence interval 2.239-19.044, P=0.001). An ISI level >3.12 predicted unfavorable outcomes with a sensitivity and specificity of 74.6% and 85.2%, respectively (P<0.001). The prognostic performance of ISI (area under the curve [AUC]=0.887) was similar to that of other predictors, such as gray-to-white matter ratio (AUC=0.850, P=0.433) and neuron-specific enolase (AUC=0.925, P=0.394).
CONCLUSION: ISI may be used as a prognostic biomarker to predict neurological outcomes in CA patients following ECPR.

BACKGROUND: Blood pressure (BP) monitoring is essential for patient care. Invasive arterial BP (IABP) is more accurate than non-invasive BP (NIBP), although the clinical significance of this difference is unknown. We hypothesized that IABP would result in a change of management (COM) among patients with non-hypertensive diseases in the acute phase of resuscitation.

METHODS: This prospective study included adults admitted to the Critical Care Resuscitation Unit (CCRU) with non-hypertensive disease from February 1, 2019, to May 31, 2021. Management plans to maintain a mean arterial pressure >65 mmHg (1 mmHg=0.133 kPa) were recorded in real time for both NIBP and IABP measurements. A COM was defined as a discrepancy between IABP and NIBP that resulted in an increase/decrease or addition/discontinuation of a medication/infusion. Classification and regression tree analysis identified significant variables associated with a COM and assigned relative variable importance (RVI) values.

RESULTS: Among the 206 patients analyzed, a COM occurred in 94 (45.6% [94/206]) patients. The most common COM was an increase in current infusion dosages (40 patients, 19.4%). Patients receiving norepinephrine at arterial cannulation were more likely to have a COM compared with those without (45 [47.9%] vs. 32 [28.6%], P=0.004). Receiving norepinephrine (relative variable importance [RVI] 100%) was the most significant factor associated with a COM. No complications were identified with IABP use.

CONCLUSION: A COM occurred in 94 (45.6%) non-hypertensive patients in the CCRU. Receiving vasopressors was the greatest factor associated with COM. Clinicians should consider IABP monitoring more often in non-hypertensive patients requiring norepinephrine in the acute resuscitation phase. Further studies are necessary to confirm the risk-to-benefit ratios of IABP among these high-risk patients.