Discussion
EEG-verified, OHCA, hypoperfusion, post-cardiac arrest, cardiac arrest, comatose, Secondary brain injury, reperfusion injury, mitochondrial dysfunction, cerebral ischemia
HYPOPERFUSION, BRAIN HYPOXIA, CARDIAC ARREST, COMATOSE, TRANSIENT CEREBRAL ISCHEMIA, SECONDARY, SEPARATION, MITOCHONDRIAL DYSFUNCTION, HYPERTENSION, CEREBRAL ISCHEMIA
This double-blinded randomized trial compared two blood pressure targets in comatose patients resuscitated from OHCA. Targeting a higher MAP (77 vs. 63 mmHg) did not significantly improve cerebral energy metabolism within 96 h of post-resuscitation care. No secondary outcomes, including cerebral oxygenation (rSOBedside monitoring of global cerebral energy metabolism is a novel technique. It is based on experimental studies in pigs showing that microdialysis of the draining venous cerebral blood gives semi-quantitative information of cerebral interstitial levels of lactate, pyruvate and LP ratio at cerebral ischemia [Secondary brain injury seems to occur in the early period after OHCA and is driven by complex pathophysiological mechanisms such as reperfusion injury with mitochondrial dysfunction, impaired autoregulation and delayed hypoperfusion during the first 12 to 24 h after cardiac arrest [Despite a clinically significant separation between MAP groups (Fig. Compromised cerebral metabolism and brain hypoxia probably depend on several factors. Despite optimized MAP and oxygen delivery, diffusion limitations of oxygen [Interestingly, JBM revealed that jugular bulb lactate, LP ratio, and glycerol correlated negatively to the corresponding MAP in all patients. Moreover, we were able to discriminate specific subgroups (preexisting hypertension), benefiting more from an augmented MAP on cerebral metabolism.Cerebral reperfusion after OHCA is complex and there is a lack of data regarding the first hours after ROSC. In both MAP groups, a majority exhibited severe disturbance in cerebral energy metabolism with markedly increased LP ratio up to 20 h after the start of JBM (Fig. In experimental studies, near-normalization of LP ratio is obtained 60–120 min after recirculation in animals exposed to 30 min of complete cerebral ischemia [Though the LP ratio may return to a near-normal level after transient cerebral ischemia, the insult often causes lasting mitochondrial dysfunction [Although JBM did not start until about 260 min after ROSC, significant differences were obtained between the two outcome groups (CPC 1–2 vs. CPC 3–5) for variables related to oxidative energy metabolism (lactate, pyruvate, LP ratio) (Fig. In the CPC 3–5 group, lactate and pyruvate remained higher than in the CPC 1–2 group for up to 60 h (Fig. Identifying patients bedside suffering from severe mitochondrial dysfunction using JBM might optimize prognostication and individualize (improving oxygen utilization) the treatment of post-cardiac arrest patients and improve outcome.
Moreover, JBM revealed significantly higher pyruvate levels with EEG-verified epileptiform activity during the first 48 h (CPC 3–5).Glycerol was significantly increased in the low MAP group during a prolonged period (Fig. No difference in rSOOn the other side the non-significant difference between MAP groups could reflect an intact cerebral autoregulation. However, irrespective of chronic hypertension, no significant differences in rSO