The accuracy of pulse oximetry in emergency department patients with severe sepsis and septic shock: a retrospective cohort study

<p>Abstract</p> <p>Background</p> <p>Pulse oximetry is routinely used to continuously and noninvasively monitor arterial oxygen saturation (SaO₂) in critically ill patients. Although pulse oximeter oxygen saturation (SpO₂) has been studied in several patient populations, including the critically ill, its accuracy has never been studied in emergency department (ED) patients with severe sepsis and septic shock. Sepsis results in characteristic microcirculatory derangements that could theoretically affect pulse oximeter accuracy. The purposes of the present study were twofold: 1) to determine the accuracy of pulse oximetry relative to SaO2 obtained from ABG in ED patients with severe sepsis and septic shock, and 2) to assess the impact of specific physiologic factors on this accuracy.</p> <p>Methods</p> <p>This analysis consisted of a retrospective cohort of 88 consecutive ED patients with severe sepsis who had a simultaneous arterial blood gas and an SpO₂value recorded. Adult ICU patients that were admitted from any Calgary Health Region adult ED with a pre-specified, sepsis-related admission diagnosis between October 1, 2005 and September 30, 2006, were identified. Accuracy (SpO₂- SaO₂) was analyzed by the method of Bland and Altman. The effects of hypoxemia, acidosis, hyperlactatemia, anemia, and the use of vasoactive drugs on bias were determined.</p> <p>Results</p> <p>The cohort consisted of 88 subjects, with a mean age of 57 years (19 - 89). The mean difference (SpO₂- SaO₂) was 2.75% and the standard deviation of the differences was 3.1%. Subgroup analysis demonstrated that hypoxemia (SaO₂< 90) significantly affected pulse oximeter accuracy. The mean difference was 4.9% in hypoxemic patients and 1.89% in non-hypoxemic patients (p < 0.004). In 50% (11/22) of cases in which SpO₂was in the 90-93% range the SaO2 was <90%. Though pulse oximeter accuracy was not affected by acidoisis, hyperlactatementa, anemia or vasoactive drugs, these factors worsened precision.</p> <p>Conclusions</p> <p>Pulse oximetry overestimates ABG-determined SaO₂by a mean of 2.75% in emergency department patients with severe sepsis and septic shock. This overestimation is exacerbated by the presence of hypoxemia. When SaO₂needs to be determined with a high degree of accuracy arterial blood gases are recommended.</p

Hydrogen Sulfide and Neurogenic Inflammation in Polymicrobial Sepsis: Involvement of Substance P and ERK-NF-κB Signaling

Hydrogen sulfide (H2S) has been shown to induce transient receptor potential vanilloid 1 (TRPV1)-mediated neurogenic inflammation in polymicrobial sepsis. However, endogenous neural factors that modulate this event and the molecular mechanism by which this occurs remain unclear. Therefore, this study tested the hypothesis that whether substance P (SP) is one important neural element that implicates in H2S-induced neurogenic inflammation in sepsis in a TRPV1-dependent manner, and if so, whether H2S regulates this response through activation of the extracellular signal-regulated kinase-nuclear factor-κB (ERK-NF-κB) pathway. Male Swiss mice were subjected to cecal ligation and puncture (CLP)-induced sepsis and treated with TRPV1 antagonist capsazepine 30 minutes before CLP. DL-propargylglycine (PAG), an inhibitor of H2S formation, was administrated 1 hour before or 1 hour after sepsis, whereas sodium hydrosulfide (NaHS), an H2S donor, was given at the same time as CLP. Capsazepine significantly attenuated H2S-induced SP production, inflammatory cytokines, chemokines, and adhesion molecules levels, and protected against lung and liver dysfunction in sepsis. In the absence of H2S, capsazepine caused no significant changes to the PAG-mediated attenuation of lung and plasma SP levels, sepsis-associated systemic inflammatory response and multiple organ dysfunction. In addition, capsazepine greatly inhibited phosphorylation of ERK1/2 and inhibitory κBα, concurrent with suppression of NF-κB activation even in the presence of NaHS. Furthermore, capsazepine had no effect on PAG-mediated abrogation of these levels in sepsis. Taken together, the present findings show that H2S regulates TRPV1-mediated neurogenic inflammation in polymicrobial sepsis through enhancement of SP production and activation of the ERK-NF-κB pathway

Acceptability of the Venting Wisely pathway for use in critically ill adults with hypoxaemic respiratory failure and acute respiratory distress syndrome (ARDS): a qualitative study protocol

Introduction Hypoxaemic respiratory failure (HRF) affects nearly 15% of critically ill adults admitted to an intensive care unit (ICU). An evidence-based, stakeholder-informed multidisciplinary care pathway (Venting Wisely) was created to standardise the diagnosis and management of patients with HRF and acute respiratory distress syndrome. Successful adherence to the pathway requires a coordinated team-based approach by the clinician team. The overall aim of this study is to describe the acceptability of the Venting Wisely pathway among critical care clinicians. Specifically, this will allow us to (1) better understand the user’s experience with the intervention and (2) determine if the intervention was delivered as intended.Methods and analysis This qualitative study will conduct focus groups with nurse practitioners, physicians, registered nurses and registered respiratory therapists from 17 Alberta ICUs. We will use template analysis to describe the acceptability of a multicomponent care pathway according to seven constructs of acceptability: (1) affective attitude;,(2) burden, (3) ethicality, (4) intervention coherence, (5) opportunity costs, (6) perceived effectiveness and (7) self-efficacy. This study will contribute to a better understanding of the acceptability of the Venting Wisely pathway. Identification of areas of poor acceptability will be used to refine the pathway and implementation strategies as ways to improve adherence to the pathway and promote its sustainability.Ethics and dissemination The study was approved by the University of Calgary Conjoint Health Research Ethics Board. The results will be submitted for publication in a peer-reviewed journal and presented at a scientific conference.Trial registration number ClinicalTrials.gov NCT04744298