The study protocol and main results have been published earlier. Six ICUs in Finland and one in Denmark participated in the COMACARE study that was conducted from March 2016 to March 2017. 3–5 poor), and we hypothesised that CVR would be impaired in patients with poor outcome. The primary outcome in this post-hoc analysis was the association between TOx and six-month neurological outcome dichotomised by cerebral performance category (CPC1-2 good vs. All patients were monitored with the same type of NIRS device over the first 48 h of ICU care enabling an estimation of CVR over time. In the multicentre randomised controlled pilot study COMACARE, 120 adult comatose mechanically ventilated survivors of OHCA with an initial rhythm of ventricular fibrillation/tachycardia were treated with low- or high-normal targets for MAP, arterial oxygen (P aO 2) and carbon dioxide (P aCO 2) tension. Impaired CVR monitored by TO x is associated with poor neurological outcomes in acute neurocritical conditions and in OHCA, as suggested by smaller, single-centre, observational cohort studies. This technique has known limitations but provides a non-invasive method to estimate CVR at the bedside. Near-infrared spectroscopy (NIRS) may be used to monitor spontaneous low-frequency oscillations in cerebral tissue oxygenation (cStO 2) that reflect CBF and, when correlated with simultaneous changes in MAP, allow for the tissue oxygenation index (TO x) to be derived as an index of dynamic CVR. The specific aspect of CVR related to MAP is commonly referred to as cerebral autoregulation. Cerebrovascular reactivity (CVR) refers to the ability of the brain vasculature to change flow resistance in response to fluctuating blood tension of oxygen and carbon dioxide and varying mean arterial blood pressure (MAP) levels, aiming to maintain a relatively constant CBF. On suggested mechanism of HIBI is ongoing cerebral hypoxia related to insufficient cerebral blood flow (CBF) after return of spontaneous circulation (ROSC). Out-of-hospital cardiac arrest (OHCA) carries a high overall mortality rate related to hypoxic-ischaemic brain injury (HIBI). Decreased upper MAP bound and a narrower MAP range for maintained CVR were associated with poor outcome and more severe brain injury assessed with NfL.

Impaired CVR over 48 h was more common in patients with chronic hypertension and associated with poor outcome. NfL concentrations were higher in patients with impaired CVR compared to those with intact CVR (43 IQR vs 20 IQR pg/ml, p = 0.042). The MAP range of maintained CVR was narrower in all time intervals and intervention groups ( p < 0.05). Patients with poor outcomes had a decreased upper MAP bound of CVR over time ( p = 0.001), including the high-normal oxygen ( p = 0.002), carbon dioxide ( p = 0.012) and MAP ( p = 0.001) groups. Integrated TO x for 0–48 h was higher in patients with poor outcome than in patients with good outcome (0.89 95% CI vs.

In 108 patients with sufficient data to calculate TO x, 76 patients (70%) had impaired CVR and among these, chronic hypertension was more common (58% vs. Secondary outcomes included associations with MAP bounds for CVR and biomarkers of brain injury. The primary outcome was the association between TO x and six-month functional outcome dichotomised by the cerebral performance category (CPC1-2 good vs. TO x was analysed in the 0–12, 12–24, 24–48 h time-periods and integrated over 0–48 h. The tissue oximetry index (TO x) generated by the moving correlation coefficient between cerebral tissue oxygenation measured by NIRS and MAP was used as a dynamic index of CVR with TO x > 0 indicating impaired reactivity and TO x > 0.3 used to delineate the lower and upper MAP bounds for disrupted CVR. MethodsĪ post-hoc analysis of 120 comatose OHCA patients continuously monitored with NIRS and randomised to low- or high-normal oxygen, carbon dioxide and mean arterial blood pressure (MAP) targets for 48 h. We studied the incidence and features of CVR by near infrared spectroscopy (NIRS) and associations with outcome and biomarkers of brain injury. Impaired cerebrovascular reactivity (CVR) is one feature of post cardiac arrest encephalopathy.

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