The pitfalls of bedside regional cerebral oxygen saturation in the early stage of post cardiac arrest

Abstract

It remains uncertain whether neuromonitoring reliably predicts outcome in adult post-cardiac arrest patients in the early stage treated with therapeutic hypothermia. Recent reports demonstrated a regional cerebral oxygen saturation of cardiac arrest patients on hospital arrival could predict their neurological outcome. There has been little discussion about the significance of regional cerebral oxygen saturation in patients with post-cardiac arrest syndrome. Amplitude-integrated electroencephalography monitoring may also provide early prognostic information for post-cardiac arrest syndrome. However, even when the initial electroencephalography is flat after the return of spontaneous circulation, good neurological outcome may still be obtainable if the electroencephalography shifts to a continuous pattern. The electroencephalography varied from flat to various patterns, such as flat, epileptic, or continuous during the first 24 h, while regional cerebral oxygen saturation levels varied even when the electroencephalography was flat. It is therefore difficult to estimate whether regional cerebral oxygen saturation accurately indicates the coupling of cerebral blood flow and metabolism in the early stage after cardiac arrest. Careful assessment of prognosis is necessary when relying solely on regional cerebral oxygen saturation as a single monitoring modality.

Regional cerebral oxygen saturation in cardiac arrest survivors undergoing targeted temperature management 36 °C versus 33 °C: A randomized clinical trial

“…From the results of previous studies, we assumed that the mean difference in the absolute rSO 2 level at 72 h between the 36°C and 33°C groups would be 3% with 4% standard deviation. 6,15…”

“…13,14 Of these, the CMRO 2 depends on body temperature and brain injury severity. 15 CBF depends on mean arterial pressure (MAP), intracranial pressure (ICP), and cerebral vessel diameter which is regulated in part by the arterial partial pressure of carbon dioxide (PaCO 2 ). 13,14 In a variety of clinical conditions, potential influences of these factors can alter the rSO 2 level and make it difficult to establish the usefulness of rSO 2 monitoring in cardiac arrest survivors.…”

“…13,14 In a variety of clinical conditions, potential influences of these factors can alter the rSO 2 level and make it difficult to establish the usefulness of rSO 2 monitoring in cardiac arrest survivors. [13][14][15][16] In particular, the effects of induced hypothermia on the rSO 2 level remain uncertain .…”

Effects of therapeutic hypothermia on cerebral tissue oxygen saturation in a swine model of post‑cardiac arrest

“…Due to the absence of baseline measurements and uncontrolled experiments, as well as the generally limited numbers of samples, there has been minimal discussion regarding sequential changes in S ct O 2 following ROSC (10). Hypothermic therapy is the only treatment with proven efficacy in terms of neurological outcome after cardiac arrest (11,12).…”

“…Hypothermic therapy is the only treatment with proven efficacy in terms of neurological outcome after cardiac arrest (11,12). S ct O 2 remains uncertain due to hypothermic reduction of the cerebral metabolic rate of oxygen (10). Although NIRS monitoring is growing in popularity, definitive data regarding the benefits of its use remain sparse.…”