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Cerebral oxygenation in mechanically ventilated early cardiac arrest survivors: The impact of hypercapnia

  • Glenn M. Eastwood
    Correspondence
    Corresponding author at: Department of Intensive Care, Austin Hospital, 145 Studley Road, Heidelberg, Melbourne 3084, VIC, Australia. Fax: +61 3 9496 3932.
    Affiliations
    Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia

    Australian and New Zealand Intensive Care Research Centre, Melbourne, VIC, Australia

    School of Nursing and Midwifery, Faculty of Health, Deakin University, Melbourne, Australia
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  • Aiko Tanaka
    Affiliations
    Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia

    Department of Anesthesiology and Intensive Care, Osaka University Graduate School of Medicine, Suita, Osaka, Japan
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  • Rinaldo Bellomo
    Affiliations
    Department of Intensive Care, Austin Hospital, Melbourne, VIC, Australia

    Australian and New Zealand Intensive Care Research Centre, Melbourne, VIC, Australia
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      Abstract

      Background

      Optimal cerebral oxygenation is considered fundamental to cerebral protection in cardiac arrest (CA) patients. Hypercapnia increases cerebral blood flow and may also improve cerebral oxygenation. It is uncertain, however, whether this effect occurs in mechanically ventilated early survivors of CA.

      Methods

      We enrolled mechanically ventilated resuscitated patients within 36 h of their cardiac arrest. We performed a prospective double cross-over physiological study comparing the impact of normocapnia (PaCO2 35–45 mmHg) vs. mild hypercapnia (PaCO2 45–55 mmHg) on regional cerebral tissue oxygen saturation (SctO2) assessed by near infrared spectroscopy (NIRS).

      Results

      We studied seven adult CA patients with a median time to return of spontaneous circulation of 28 min at a median of 26 h and 30 min after CA. During normocapnia (median EtCO2 of 32 mmHg [30–41 mmHg] and PaCO2 of 37 mmHg [32–45 mmHg]) the median NIRS-derived left frontal SctO2 was 61% [52–65%] and the right frontal SctO2 was 61% [54–68%]. However, during mild hypercapnia (median EtCO2 of 49 mmHg [40–57 mmHg] and PaCO2 of 52 mmHg [43–55 mmHg) the median left frontal SctO2 increased to 69% [59–78%] and the right frontal SctO2 increased to 73% [61–76%])(p = 0.001, for all comparisons).

      Conclusion

      During the early post-resuscitation period, in mechanically ventilated CA patients, mild hypercapnia increases cerebral oxygenation as assessed by NIRS. Further investigations of the effect of prolonged mild hypercapnia on cerebral oxygenation and patient outcomes appear justified.

      Keywords

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