Critical Care Medicine最新文献

Objectives: To standardize optic nerve sheath diameter (ONSD) point-of-care ultrasonography (POCUS) and improve its research and clinical utility by developing the ONSD POCUS Quality Criteria Checklist (ONSD POCUS QCC).

Design: Three rounds of modified Delphi consensus process and three rounds of asynchronous discussions.

Setting: Online surveys and anonymous asynchronous discussion.

Subjects: Expert panelists were identified according to their expertise in ONSD research, publication records, education, and clinical use. A total of 52 panelists participated in the Delphi process.

Interventions: None.

Measurements and main results: Three Delphi rounds and three asynchronous discussion rounds generated consensus on quality criteria (QC). This started with 29 QC in addition to other QC proposed by expert panelists. The QC items were categorized into probe selection, safety, body position, imaging, measurement, and research considerations. At the conclusion of the study, 28 QC reached consensus to include in the final ONSD POCUS QCC. These QC were then reorganized, edited, and consolidated into 23 QC that were reviewed and approved by the panelists.

Conclusions: ONSD POCUS QCC standardizes ONSD ultrasound imaging and measurement based on international consensus. This can establish ONSD ultrasound in clinical research and improve its utility in clinical practice.

Objectives: Hyperkalemia is a common life-threatening condition causing severe electrophysiologic derangements and arrhythmias. The beneficial effects of calcium (Ca 2+ ) treatment for hyperkalemia have been attributed to "membrane stabilization," by restoration of resting membrane potential (RMP). However, the underlying mechanisms remain poorly understood. Our objective was to investigate the mechanisms underlying adverse electrophysiologic effects of hyperkalemia and the therapeutic effects of Ca 2+ treatment.

Design: Controlled experimental trial.

Setting: Laboratory investigation.

Subjects: Canine myocytes and tissue preparations.

Interventions and measurements: Optical action potentials and volume averaged electrocardiograms were recorded from the transmural wall of ventricular wedge preparations ( n = 7) at baseline (4 mM potassium), hyperkalemia (8-12 mM), and hyperkalemia + Ca 2+ (3.6 mM). Isolated myocytes were studied during hyperkalemia (8 mM) and after Ca 2+ treatment (6 mM) to determine cellular RMP.

Main results: Hyperkalemia markedly slowed conduction velocity (CV, by 67% ± 7%; p < 0.001) and homogeneously shortened action potential duration (APD, by 20% ± 10%; p < 0.002). In all preparations, this resulted in QRS widening and the "sine wave" pattern observed in severe hyperkalemia. Ca 2+ treatment restored CV (increase by 44% ± 18%; p < 0.02), resulting in narrowing of the QRS and normalization of the electrocardiogram, but did not restore APD. RMP was significantly elevated by hyperkalemia; however, it was not restored with Ca 2+ treatment suggesting a mechanism unrelated to "membrane stabilization." In addition, the effect of Ca 2+ was attenuated during L-type Ca 2+ channel blockade, suggesting a mechanism related to Ca 2+ -dependent (rather than normally sodium-dependent) conduction.

Conclusions: These data suggest that Ca 2+ treatment for hyperkalemia restores conduction through Ca 2+ -dependent propagation, rather than restoration of membrane potential or "membrane stabilization." Our findings provide a mechanistic rationale for Ca 2+ treatment when hyperkalemia produces abnormalities of conduction (i.e., QRS prolongation).

Objectives: To validate a mathematical model using porous media theory for alveolar CO2 determination in ventilated patients.

Design: Mathematical modeling study with prospective clinical validation to simulate CO2 exchange from bloodstream to airway entrance.

Setting: ICU.

Patients: Thirteen critically ill patients without chronic or acute lung disease.

Interventions: None.

Measurements and main results: Model outcomes compared with patient data showed correlations for end-tidal CO2 (EtCO 2 ), area under the CO2 curve, and Pa CO2 of 0.918, 0.954, and 0.995. Determination coefficients ( R2 ) were 0.843, 0.910, and 0.990, indicating precision and predictive power.

Conclusions: The mathematical model shows potential in pulmonary critical care. Although promising, practical application demands further validation, clinician training, and patient-specific adjustments. The path to clinical use will be iterative, involving validation and education.

Objective: The Efficacy of Inhaled Hydrogen on Neurologic Outcome Following Brain Ischemia During Post-Cardiac Arrest Care (HYBRID) II trial (jRCTs031180352) suggested that hydrogen inhalation may reduce post-cardiac arrest brain injury (PCABI). However, the combination of hypothermic target temperature management (TTM) and hydrogen inhalation on outcomes is unclear. The aim of this study was to investigate the combined effect of hydrogen inhalation and hypothermic TTM on outcomes after out-of-hospital cardiac arrest (OHCA).

Design: Post hoc analysis of a multicenter, randomized, controlled trial.

Setting: Fifteen Japanese ICUs.

Patients: Cardiogenic OHCA enrolled in the HYBRID II trial.

Interventions: Hydrogen mixed oxygen (hydrogen group) versus oxygen alone (control group).

Measurements and main results: TTM was performed at a target temperature of 32-34°C (TTM32-TTM34) or 35-36°C (TTM35-TTM36) per the institutional protocol. The association between hydrogen + TTM32-TTM34 and 90-day good neurologic outcomes was analyzed using generalized estimating equations. The 90-day survival was compared between the hydrogen and control groups under TTM32-TTM34 and TTM35-TTM36, respectively. The analysis included 72 patients (hydrogen [ n = 39] and control [ n = 33] groups) with outcome data. TTM32-TTM34 was implemented in 25 (64%) and 24 (73%) patients in the hydrogen and control groups, respectively ( p = 0.46). Under TTM32-TTM34, 17 (68%) and 9 (38%) patients achieved good neurologic outcomes in the hydrogen and control groups, respectively (relative risk: 1.81 [95% CI, 1.05-3.66], p < 0.05). Hydrogen + TTM32-TTM34 was independently associated with good neurologic outcomes (adjusted odds ratio 16.10 [95% CI, 1.88-138.17], p = 0.01). However, hydrogen + TTM32-TTM34 did not improve survival compared with TTM32-TTM34 alone (adjusted hazard ratio: 0.22 [95% CI, 0.05-1.06], p = 0.06).

Conclusions: Hydrogen + TTM32-TTM34 was associated with improved neurologic outcomes after cardiogenic OHCA compared with TTM32-TTM34 monotherapy. Hydrogen inhalation is a promising treatment option for reducing PCABI when combined with TTM32-TTM34.