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      Correlation of Venous Blood Gas and Pulse Oximetry With Arterial Blood Gas in the Undifferentiated Critically Ill Patient

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d13370046e237">Rationale</h5> <p id="P1">Blood gas analysis is often used to assess acid–base, ventilation, and oxygenation status in critically ill patients. Although arterial blood gas (ABG) analysis remains the gold standard, venous blood gas (VBG) analysis has been shown to correlate with ABG analysis and has been proposed as a safer less invasive alternative to ABG analysis. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d13370046e242">Objective</h5> <p id="P2">The purpose of this study was to evaluate the correlation of VBG analysis plus pulse oximetry (SpO <sub>2</sub>) with ABG analysis. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d13370046e250">Methods</h5> <p id="P3">We performed a prospective cohort study of patients in the emergency department (ED) and intensive care unit (ICU) at a single academic tertiary referral center. Patients were eligible for enrollment if the treating physician ordered an ABG. Statistical analysis of VBG, SpO <sub>2</sub>, and ABG data was done using paired <i>t</i> test, Pearson χ <sup>2</sup>, and Pearson correlation. </p> </div><div class="section"> <a class="named-anchor" id="S4"> <!-- named anchor --> </a> <h5 class="section-title" id="d13370046e264">Main Results</h5> <p id="P4">There were 156 patients enrolled, and 129 patients completed the study. Of the patients completing the study, 53 (41.1%) were in the ED, 41 (31.8%) were in the medical ICU, and 35 (27.1%) were in the surgical ICU. The mean difference for pH between VBG and ABG was 0.03 (95% confidence interval: 0.03–0.04) with a Pearson correlation of 0.94. The mean difference for pCO <sub>2</sub> between VBG and ABG was 4.8 mm Hg (95% confidence interval: 3.7–6.0 mm Hg) with a Pearson correlation of 0.93. The SpO <sub>2</sub> correlated well with PaO <sub>2</sub> (the partial pressure of oxygen in arterial blood) as predicted by the standard oxygen–hemoglobin dissociation curve. </p> </div><div class="section"> <a class="named-anchor" id="S5"> <!-- named anchor --> </a> <h5 class="section-title" id="d13370046e278">Conclusion</h5> <p id="P5">In this population of undifferentiated critically ill patients, pH and pCO <sub>2</sub> on VBG analysis correlated with pH and pCO <sub>2</sub> on ABG analysis. The SpO <sub>2</sub> correlated well with pO <sub>2</sub> on ABG analysis. The combination of VBG analysis plus SpO <sub>2</sub> provided accurate information on acid–base, ventilation, and oxygenation status for undifferentiated critically ill patients in the ED and ICU. </p> </div>

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          Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.

          Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking. To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality. Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO(2) on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO(2) of 300 mm Hg or greater; hypoxia, PaO(2) of less than 60 mm Hg (or ratio of PaO(2) to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia. In-hospital mortality. Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
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            Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest

            Introduction Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients. Methods We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined 'hyperoxia' as PaO2 of 300 mmHg or greater, 'hypoxia/poor O2 transfer' as either PaO2 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21). Conclusions Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.
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              Accuracy of pulse oximetry in the intensive care unit.

              Pulse oximetry (SpO2) is a standard monitoring device in intensive care units (ICUs), currently used to guide therapeutic interventions. Few studies have evaluated the accuracy of SpO2 in critically ill patients. Our objective was to compare pulse oximetry with arterial oxygen saturation (SaO2) in such patients, and to examine the effect of several factors on this relationship. Observational prospective study. A 26-bed medical ICU in a university hospital. One hundred two consecutive patients admitted to the ICU in whom one or serial arterial blood gas analyses (ABGs) were performed and a reliable pulse oximeter signal was present. For each ABG, we collected SaO2, SpO2, the type of pulse oximeter, the mode of ventilation and requirement for vasoactive drugs. Three hundred twenty-three data points were collected. The mean difference between SpO2 and SaO2 was -0.02% and standard deviation of the differences was 2.1%. From one sample to another, the fluctuations in SpO2 to arterial saturation difference indicated that SaO2 could not be reliably predicted from SpO2 after a single ABG. Subgroup analysis showed that the accuracy of SpO2 appeared to be influenced by the type of oximeter, the presence of hypoxemia and the requirement for vasoactive drugs. Finally, high SpO2 thresholds were necessary to detect significant hypoxemia with good sensitivity. Large SpO2 to SaO2 differences may occur in critically ill patients with poor reproducibility of SpO2. A SpO2 above 94% appears necessary to ensure a SaO2 of 90%.
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                Author and article information

                Journal
                Journal of Intensive Care Medicine
                J Intensive Care Med
                SAGE Publications
                0885-0666
                1525-1489
                May 10 2017
                June 09 2016
                : 33
                : 3
                : 176-181
                Article
                10.1177/0885066616652597
                5885755
                27283009
                6747cb7d-0d52-4233-9feb-03eb9337300f
                © 2016

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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