Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Helmerhorst, Hendrik J. F.; Roos-Blom, Marie-José; Westerloo, David J. van; Abu‐Hanna, Ameen; Keizer, Nicolette F. de; Jonge, Evert de

doi:10.1186/s13054-015-1067-6

Cited by 112 publications

(102 citation statements)

References 40 publications

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“…Among 12,108 ICU patients in New Zealand, Bellomo, et al observed associations between hyperoxemia and hospital mortality, but these relatioships were not as strong on sensitivity analyses [10]. In a study of 5258 cardiac arrest patients admitted to 82 ICUs in the Netherlands, Helmermorst et al observed increased hospital mortality from all oxygen and carbon dioxide aberrancies [12]. Among 409 patients admitted to 21 ICUs in Finland, Vaahersalo, et al found no association between oxygen and carbon dioxide tensions and 12-month neurologic outcomes.…”

Section: Discussionmentioning

confidence: 99%

Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest

et al. 2017

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Objective To determine if arterial oxygen and carbon dioxide abnormalities in the first 24 h after return of spontaneous circulation (ROSC) are associated with increased mortality in adult out-of-hospital cardiac arrest (OHCA). Methods We used data from the Resuscitation Outcomes Consortium (ROC), including adult OHCA with sustained ROSC ≥1 h after Emergency Department arrival and at least one arterial blood gas (ABG) measurement. Among ABGs measured during the first 24 h of hospitalization, we identified the presence of hyperoxemia (PaO2 ≥ 300 mmHg), hypoxemia (PaO2 < 60 mmHg), hypercarbia (PaCO2 > 50 mmHg) and hypocarbia (PaCO2 < 30 mmHg). We evaluated the associations between oxygen and carbon dioxide abnormalities and hospital mortality, adjusting for confounders. Results Among 9186 OHCA included in the analysis, hospital mortality was 67.3%. Hyperoxemia, hypoxemia, hypercarbia, and hypocarbia occurred in 26.5%, 19.0%, 51.0% and 30.6%, respectively. Initial hyperoxemia only was not associated with hospital mortality (adjusted OR 1.10; 95% CI: 0.97–1.26). However, final and any hyperoxemia (1.25; 1.11–1.41) were associated with increased hospital mortality. Initial (1.58; 1.30–1.92), final (3.06; 2.42–3.86) and any (1.76; 1.54–2.02) hypoxemia (PaO2 < 60 mmHg) were associated with increased hospital mortality. Initial (1.89; 1.70–2.10); final (2.57; 2.18–3.04) and any (1.85; 1.67–2.05) hypercarbia (PaCO2 > 50 mmHg) were associated with increased hospital mortality. Initial (1.13; 0.90–1.41), final (1.19; 1.04–1.37) and any (1.01; 0.91–1.12) hypocarbia (PaCO2 < 30 mmHg) were not associated with hospital mortality. Conclusions In the first 24 h after ROSC, abnormal post-arrest oxygen and carbon dioxide tensions are associated with increased out of-hospital cardiac arrest mortality.

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Section: Discussionmentioning

confidence: 99%

Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest

et al. 2017

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“…Toxicity rose more rapidly as FiO 2 is increased above 0.6 and also as exposure time is prolonged (4,18,37,38). Available data showed a U-shaped relationship between mortality and arterial PaO 2 (52). Mortality sharply increased at PaO 2 <65 and >225 mmHg (1).…”

Section: Conservative O 2 Strategymentioning

confidence: 98%

Relationship between hyperoxemia and ventilator associated pneumonia

et al. 2017

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Previous studies suggest a relationship between hyperoxemia and ventilator-associated pneumonia (VAP). Hyperoxemia is responsible for denitrogenation phenomena, and inhibition of surfactant production, promoting atelectasis in mechanically ventilated patients. Further, hyperoxemia impairs the efficacy of alveolar macrophages to migrate, phagocyte and kill bacteria. Oxygen can also cause pulmonaryspecific toxic effect called hyperoxic acute lung injury leading to longer duration of mechanical ventilation.All these hyperoxic effects are well-known risk factors for VAP. A recent retrospective large single center study identified hyperoxemia as an independent risk factor for VAP. However, two recent randomized controlled trials evaluated the impact of conservative oxygen strategy versus a liberal strategy, but did not confirm the role of hyperoxemia in lower respiratory tract infection occurrence. In this review, we discuss animal and human studies suggesting a relationship between these two common conditions in mechanically ventilated patients and potential interventions that should be evaluated. Further large prospective studies in carefully selected groups of patients are required to confirm the potential role of hyperoxemia in VAP pathogenesis and to evaluate the impact of a conservative oxygen strategy vs. a conventional strategy on the incidence of VAP.

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“…Early oxygen administration can influence oxidative metabolism, respiratory markers, vasoconstrictive status and blood flow, and may thus be an important predictor of outcome [20]. Although it is intuitive that insufficient oxygen delivery can exacerbate cerebral anoxia, excessive oxygen delivery can also be harmful by increasing the amount of oxygen free radicals and subsequent reperfusion injury.…”

Section: Normoxia and Normocapniamentioning

confidence: 99%

“…Although it is intuitive that insufficient oxygen delivery can exacerbate cerebral anoxia, excessive oxygen delivery can also be harmful by increasing the amount of oxygen free radicals and subsequent reperfusion injury. Pure oxygen therapy after cardiac arrest has previously been shown to worsen neurological outcome in animal models and exposure to hypocapnia and hypercapnia after ROSC has been associated with poor neurological function at hospital discharge [20].…”

Section: Normoxia and Normocapniamentioning

confidence: 99%

Strategies of Neuroprotection after Successful Resuscitation

Kovács¹,

Zima²

2017

Resuscitation Aspects

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Post-cardiac arrest syndrome (PCAS) incorporates post-cardiac arrest brain injury, postcardiac arrest myocardial dysfunction, systemic ischemia/reperfusion syndrome and the precipitating pathology. Brain injury remains the leading cause of death in the postcardiac arrest period. One of our main goals during post-resuscitation care is to guide a proper neuroprotective strategy. We are going to summarize the tools of neuroprotection in post-cardiac arrest therapy. The role of normoxia/normocapnia, normoglycemia, seizure control, sedation and pharmacologic strategies will be discussed in brief. The handling of temperature management and the management of hemodynamic variables to secure satisfactory cerebral perfusion will be worked out in details. Targeted temperature management is the main tool of neuroprotection in post-cardiac arrest therapy. We are going to conclude the principles of temperature control after successful resuscitation pointing out its beneficial effects. This method has also several complications that are going to be discussed highlighting its hemodynamic impacts. There is no evidence about target hemodynamic parameters during post-cardiac arrest syndrome to maintain cerebral perfusion neither about the most effective hemodynamic monitoring system. We are presenting preliminary data of our study where we investigate the effect of PiCCO™ (Pulse index Continous Cardiac Output) monitoring on the outcome in this patient group.Keywords: post-cardiac arrest syndrome, post-cardiac arrest brain injury, post-resuscitation therapy, targeted temperature management, hemodynamic parameters IntroductionSudden cardiac arrest is one of the leading causes of death in Europe [1]. The outcome is still very poor: the hospital discharge varies between 7 and 10% after out-of-hospital cardiac arrest (OHCA) and it is approximately 25% after in-hospital cardiac arrest (IHCA) [1]. The chain of © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.survival describes links that lead to a successful resuscitation [2]. The fourth element covers proper post-resuscitation care to restore quality of life. It is well known that the management of post-resuscitation cardiac arrest syndrome affects outcome and it is an important part of the resuscitation process. Pointing out the growing importance of post-resuscitation therapy, the European Resuscitation Council (ERC) introduced a separate chapter about post-resuscitation care in the 2015 guidelines [3]. One of the key elements to improve survival rate after sudden cardiac arrest may be the enhancement of post-resuscitation therapy.The post-cardiac arrest brain injury remains the main cause of mortality in the post-cardiac arrest period, being as high as 68% after OHCA and 25% after IHCA [4]. These data show that one of our leading goa...

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Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Cited by 112 publications

References 40 publications

Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest

Post-resuscitation arterial oxygen and carbon dioxide and outcomes after out-of-hospital cardiac arrest

Relationship between hyperoxemia and ventilator associated pneumonia

Strategies of Neuroprotection after Successful Resuscitation

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