OBJECTIVE: Hypotension after emergent endotracheal intubation is a serious complication related to in-hospital mortality. We investigated factors including modified shock index to predict the development of hypotension after emergent intubation. METHODS: This retrospective observational study was conducted between January 2011 and December 2016. The study population included intubated patients among all medical patients admitted to the emergency department (ED) except for patients whose systolic blood pressure was below 90 mmHg at any time before intubation. The postintubation hypotension (PIH) groups were compared with the non-PIH group. The secondary outcome was in-hospital mortality. RESULTS: A total of 285 patients were included in this study, of which 92 patients (32.3%) PIH. The age (odds ratio [OR], 1.04; 95% confidence interval [CI], 1.01–1.06; P=0.001), serum albumin level (OR, 0.62; 95% CI, 0.41–0.92; P=0.019), shock index (OR, 3.25; 95% CI, 1.26–8.38; P=0.015), and modified shock index (MSI) (OR, 2.18; 95% CI, 1.06–4.47; P=0.034) were more closely associated with PIH than any other factors. The average survival of the PIH group was significantly shorter than that of the non-PIH group (13.6±3.5 vs. 35.6±12.0, log-rank test P=0.019). CONCLUSION: Overall, 32.3% of hemodynamically stable medical patients developed PIH in ED. MSI was associated with PIH.
Blood Pressure ; Emergencies* ; Emergency Medical Services ; Emergency Service, Hospital* ; Hospital Mortality ; Humans ; Hypotension* ; Intubation ; Intubation, Intratracheal ; Mortality ; Observational Study ; Retrospective Studies ; Risk Factors ; Serum Albumin ; Shock*

In the brain, a reduction in extracellular osmolality causes water-influx and swelling, which subsequently triggers Cl⁻- and osmolytes-efflux via volume-regulated anion channel (VRAC). Although LRRC8 family has been recently proposed as the pore-forming VRAC which is activated by low cytoplasmic ionic strength but not by swelling, the molecular identity of the pore-forming swelling-dependent VRAC (VRAC(swell)) remains unclear. Here we identify and characterize Tweety-homologs (TTYH1, TTYH2, TTYH3) as the major VRAC(swell) in astrocytes. Gene-silencing of all Ttyh1/2/3 eliminated hypo-osmotic-solution-induced Cl⁻ conductance (I(Cl,swell)) in cultured and hippocampal astrocytes. When heterologously expressed in HEK293T or CHO-K1 cells, each TTYH isoform showed a significant I(Cl,swell) with similar aquaporin-4 dependency, pharmacological properties and glutamate permeability as I(Cl,swell) observed in native astrocytes. Mutagenesis-based structure-activity analysis revealed that positively charged arginine residue at 165 in TTYH1 and 164 in TTYH2 is critical for the formation of the channel-pore. Our results demonstrate that TTYH family confers the bona fide VRAC(swell) in the brain.
Arginine ; Astrocytes ; Brain ; Cytoplasm ; Glutamic Acid ; Humans ; Osmolar Concentration ; Permeability