了解呼吸紊乱的酸碱反应:体内碱过量的发现和临床应用。

Q4 Medicine
Critical care explorations Pub Date : 2024-12-16 eCollection Date: 2024-12-01 DOI:10.1097/CCE.0000000000001191
Micah L A Heldeweg, Kenrick Berend, Patrick Schober, František Duška
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引用次数: 0

摘要

目的:探讨急性体内二氧化碳变化时的碱过量反应。设计:对来自实验研究的个体参与者数据进行二次分析。背景:三个实验研究急性体内呼吸紊乱对酸碱变量的影响。受试者:89例(犬类和人类)二氧化碳暴露。干预措施:通过环境室或机械通气进行动脉二氧化碳滴定。测量和主要结果:对于每个受试者,使用碳酸氢盐和pH计算碱过量,使用固定缓冲功率为16.2。使用线性回归进行分析,包括动脉二氧化(预测因子)、基础过量(结果)和研究(相互作用项)。所有的研究都显示了不同二氧化碳滴定方法中碱过量的基线和斜率的不同。个体受试者在高碳酸血症范围内表现出大量且可能具有临床相关性的碱性过度反应变化。通过对10,000个缓冲功率系数的数学模拟,我们确定系数为12.1 (95% CI, 9.1-15.1)而不是16.2,对于一般临床应用来说,更有利于在概念上更合适的体内基础过剩方程。结论:体内二氧化碳的变化导致碱过量的变化,这可能与个体患者的临床相关。缓冲功率系数16.2在体内可能不合适,需要在一系列临床环境中进行外部验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Understanding the Acid-Base Response to Respiratory Derangements: Finding, and Clinically Applying, the In Vivo Base Excess.

Objectives: To evaluate the base excess response during acute in vivo carbon dioxide changes.

Design: Secondary analysis of individual participant data from experimental studies.

Setting: Three experimental studies investigating the effect of acute in vivo respiratory derangements on acid-base variables.

Subjects: Eighty-nine (canine and human) carbon dioxide exposures.

Interventions: Arterial carbon dioxide titration through environmental chambers or mechanical ventilation.

Measurements and main results: For each subject, base excess was calculated using bicarbonate and pH using a fixed buffer power of 16.2. Analyses were performed using linear regression with arterial dioxide (predictor), base excess (outcome), and studies (interaction term). All studies show different baselines and slopes for base excess across carbon dioxide titrations methods. Individual subjects show substantial, and potentially clinically relevant, variations in base excess response across the hypercapnic range. Using a mathematical simulation of 10,000 buffer power coefficients we determined that a coefficient of 12.1 (95% CI, 9.1-15.1) instead of 16.2 facilitates a more conceptually appropriate in vivo base excess equation for general clinical application.

Conclusions: In vivo changes in carbon dioxide leads to changes in base excess that may be clinically relevant for individual patients. A buffer power coefficient of 16.2 may not be appropriate in vivo and needs external validation in a range of clinical settings.

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来源期刊
CiteScore
5.70
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