Abstract
Brain tissue oxygen tension (PbtO2)-guided care, a therapeutic strategy to treat or prevent cerebral hypoxia through modifying determinants of cerebral oxygen delivery, including arterial oxygen tension (PaO2), end-tidal carbon dioxide (ETCO2), and mean arterial pressure (MAP), has recently been introduced. Studies have reported that cerebral hypoxia occurs after cardiac arrest in the absence of hypoxemia or hypotension. To obtain preliminary information on the degree to which PbtO2 is responsive to changes in the common target variables for PbtO2-guided care in conditions without hypoxemia or hypotension, we investigated the relationships between the common target variables for PbtO2-guided care and PbtO2 using data from an experimental study in which the animals did not experience hypoxemia or hypotension after resuscitation. We retrospectively analyzed 170 sets of MAP, ETCO2, PaO2, PbtO2, and cerebral microcirculation parameters obtained during the 60-min post-resuscitation period in 10 pigs resuscitated from ventricular fibrillation cardiac arrest. PbtO2 and cerebral microcirculation parameters were measured on parietal cortices exposed through burr holes. Multiple linear mixed effect models were used to test the independent effects of each variable on PbtO2. Despite the absence of arterial hypoxemia or hypotension, seven (70%) animals experienced cerebral hypoxia (defined as PbtO2 <20 mmHg). Linear mixed effect models revealed that neither MAP nor ETCO2 were related to PbtO2. PaO2 had a significant linear relationship with PbtO2 after adjusting for significant covariates (P = 0.030), but it could explain only 17.5% of the total PbtO2 variance (semi-partial R2 = 0.175; 95% confidence interval, 0.086–0.282). In conclusion, MAP and ETCO2 were not significantly related to PbtO2 in animals without hypoxemia or hypotension during the early post-resuscitation period. PaO2 had a significant linear association with PbtO2, but its ability to explain PbtO2 variance was small.
Highlights
Despite advances in the treatment of cardiac arrest, most cardiac arrest survivors fail to achieve meaningful neurological recovery due to brain injury [1,2,3]
Several studies have suggested associations between perturbations in cerebral oxygen delivery after restoration of spontaneous circulation (ROSC) and worse neurological outcome after cardiac arrest [4,5,6,7,8,9,10]. In line with these studies [4,5,6,7,8,9,10], recent post-cardiac arrest care guidelines have emphasized the importance of maintaining adequate arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2), and mean arterial pressure (MAP) to ensure sufficient cerebral oxygenation, which in turn prevents secondary hypoxic-ischemic brain injury [11, 12]
A total of 170 sets of MAP, ETCO2, PaO2, microvascular flow index (MFI), % Capillary number, and PbtO2 data were collected during the 60-min post-resuscitation period
Summary
Despite advances in the treatment of cardiac arrest, most cardiac arrest survivors fail to achieve meaningful neurological recovery due to brain injury [1,2,3]. Several studies have suggested associations between perturbations in cerebral oxygen delivery after ROSC and worse neurological outcome after cardiac arrest [4,5,6,7,8,9,10] In line with these studies [4,5,6,7,8,9,10], recent post-cardiac arrest care guidelines have emphasized the importance of maintaining adequate arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2), and mean arterial pressure (MAP) to ensure sufficient cerebral oxygenation, which in turn prevents secondary hypoxic-ischemic brain injury [11, 12]. No studies have evaluated the impact of increasing PaO2 and/or MAP on PbtO2 levels in non-hypoxemic, non-hypotensive cardiac arrest patients during the early post-resuscitation period
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