败血症
医学
重症监护医学
器官功能障碍
重症监护室
内科学
作者
Julie‐Kathryn Graham,Anova Westcott,Simon A. Smith,Elizabeth A. Mann,Ron Daniels,M. Quillin-Mcewan,Angel Bahena,David Bello,Christina Kelley
出处
期刊:Critical care nursing quarterly
[Ovid Technologies (Wolters Kluwer)]
日期:2024-12-02
卷期号:48 (1): 8-14
标识
DOI:10.1097/cnq.0000000000000540
摘要
Sepsis remains a major concern in health care globally. Despite decades of research, incidence is on the rise, and mortality remains high. Costs are staggering. Additionally, the outdated sepsis bundle established based on SIRS, remains the standard by which providers are held accountable. It is now accepted that organ dysfunction in sepsis is secondary to cellular metabolic dysregulation. Technology for metabolic monitoring should be explored for improved, early recognition of sepsis. We sought to investigate the underlying metabolic profile of patients with sepsis, to determine the value of continuous metabolic monitoring technology. The investigators partnered with industry, to trial noninvasive monitoring of the cellular metabolite carbon dioxide, under a prospective, observational design. During the 6-month trial, the investigators collected data from the electronic medical record of patients using the technology, to determine the specific metabolic differences between patients with and without sepsis. The investigators found serum carbon dioxide (paCO 2 ) was significantly lower in patients with sepsis, and, low paCO 2 had a significant inverse relationship to serum lactate. This finding supports the notion that paCO 2 is low in sepsis secondary to metabolic dysregulation and not hyperventilation, which had historically explained low paCO 2 under the SIRS model. Metabolic monitoring is available, easy to apply and manage, and contributes valuable information in the detection of sepsis. Further research should be done to understand trends in serum CO 2 and its relationship to the development of sepsis. This study also provides important further support for the emerging understanding of the dysregulated host response in sepsis.
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