Cerebral oximetry in cerebral resuscitation

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Cerebral oximetry in cerebral resuscitation

  1. 1. Cerebral Oximetry in Cerebral Resuscitation After Cardiac Arrest A. Ahn, J. et al. Presented by: Mohamed A. Kotb Lecturer of Anesthesia, ASU Intensivest KFHJ
  2. 2. Pathophysiology of Post-CPR state • Cardiac arrest represents a state of generalized whole-body ischemia resulting from either a no-flow or a low-flow state that culminates in inadequate organ perfusion and oxygen delivery (DO2) leading to cellular damage and death. • On-going inflammatory responses and cellular damage continue even after return of spontaneous circulation (ROSC), and are confounded by the problem of ischemia-reperfusion injury because of a combination of neurological and cardiac dysfunction. • Limitation in current practice is the inability to measure and optimize end-organ perfusion in real-time due to lack of a clear physiological marker to guide the quality of care to vital organ and in particular brain perfusion. • Adjustments in CPR could then improve coronary and cerebral perfusion and ultimately outcome.
  3. 3. Monitoring during CPR • End tidal carbon dioxide (etCO2): proposed recently as a general marker of effective overall circulation and perfusion as well as ROSC during cardiac arrest, but does not indicate the quality of cerebral perfusion or DO2. • Electroencephalogram (EEG) : Used during procedures such as cardiac and neurosurgery as an indicator of cortical activity. limitations during CPR: -No real-time DO2 and brain tissue perfusion. - Technical limitations. • Bispecteral Index: Unreliable ,movement artifacts
  4. 4. Cerebral Oximetry: Near-infrared Spectroscopy
  5. 5. Cerebral Oximetry:a Prognosticator and RealTime Marker of Cerebral Perfusion During CPR • works by non-invasively transmitting and detecting harmless near-infrared light through sensors that are placed on the patient’s forehead, and is not susceptible to motion artifact. • Cerebral oximetry relies on near-infrared spectroscopy (NIRS), which is based on the Beer Lambert law. • Since 70–80 % of blood in the measured areas of brain tissue is venous, these data represent mainly cerebral venous saturation . normal range-60-80% .
  6. 6. Why we chosen NIR light ? Electromagnetic spectrum  Penetrate the biological tissue deeper  Property : Oxygenated hemoglobin and deoxygenated hemoglobin both absorb light differently in this region.  At 780 nm, deoxygenated blood has a higher absorption, whereas at 830 nm, oxygenated blood has a higher absorption.
  7. 7. Comparison between NIRS and Pulse oximetry Different wavelengths are used in both these techniques  NIRS is far more penetrating effect than Pulse oximeter because sources of light is in NIR wavelength  NIRS characterize more chromophores than Pulse oximeter NIRS - assessment of all the vascular compartments (Arterial, Venous and capillary). • Pulse oximeter - only compartment by time Measure hemo dynamics, metabolic and fast neuronal responses to brain activation • Measure relative changes in pulsatile components of the cerebral blood flow and cerebral blood volume . • Used in patients with low perfusion states an. It gives exact oxygen level in the blood. the arterial gating the measurements • Reliable and commonly used to monitor systemic oxygen supply only. • Pulse oximeter utilizes the arterial oscillations to extract arterial oxygen • saturation SaO2 and does not exploit all of the information from the heartbeat oscillations •
  8. 8. Validation Studies of Cerebral Oximetry Using NIRS :Baseline Variables • Different body positions: no effect except in high ICP, decrease cerebral DO2 and perfusion. • Age, Hb concentration, and sensor location did alter saturation values. • Gender, weight, height, and head size: Did not impact on rSO2 values • Hyperbilirubinemia may directly alter cerebral oximetry readings and interfere with cerebral oxygen saturation in patients with icterus.
  9. 9. The Effect of Oxygen, Carbon Dioxide, Sedatives and Neuromuscular Blocking Drugs on NIRS • CO2: CBF and perfusion are linearly related to PaCO2; cerebral VD occurs during hypercapnia and VC during hypocapnia. • O2: Cerebral oximetry values decrease following induced hypoxia. The administration of oxygen increases mean cerebral saturation. • The administration of sedatives, general anesthetics and MR will enhance O2 effect, that could have a significant impact on preserving neuronal tissue lying at the ischemic threshold following cardiac arrest and in other brain injury states.
  10. 10. The Effect of Low Cardiac Output and Hypothermia on NIRS • NIRS has been validated in both low cardiac output states and hypothermia. • Reduced COP decreases systemic DO2, which leads to increased brain oxygen extraction and lower cerebral oxygen saturation as measured using NIRS. • Hypothermia is another factor that independently affects cerebral metabolism and the balance between oxygen supply and demand leading to increased cerebral oxygen saturation because of reduced cerebral metabolism and oxygen uptake.
  11. 11. Application of NIRS During Cardiac Arrest • NIRS has been used extensively in patients with different medical specialties including neurology and neurosurgery, trauma, vascular and cardiac surgery. • There have been few studies of cerebral oximetry during cardiac arrest. These studies indicate that cerebral saturation may correlate with outcome .
  12. 12. Conclusion • Cerebral oximetry using NIRS may prove to be a valuable real-time monitor of the quality of CPR, and in particular cerebral resuscitation. It may also provide data that can contribute to prognostication in individual patients. • Further studies are needed to understand the utility of this technology during CPR and in the post resuscitation period.
  13. 13. THANKS

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