Changes in systemic and cerebral blood flow and metabolism after cardio-pulmonary-cerebral resuscitation.

DOI
  • Oku Ken-ichi
    Internal Medicine, Hanwa Memorial Hospital
  • Safar Peter
    International Resuscitation Research Center, University of Pittsburgh
  • Sterz Fritz
    International Resuscitation Research Center, University of Pittsburgh
  • Leonov Yuval
    International Resuscitation Research Center, University of Pittsburgh
  • Tisherman Samuel
    International Resuscitation Research Center, University of Pittsburgh
  • Obrist Walter
    Neurosurgery, University of Pittsburgh

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Other Title
  • 心肺脳蘇生後における全身および脳の血流と代謝の変化

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Description

Cerebral and systemic metabolic changes after cardiac arrest are complex and unclear. We postulate that post-arrest monitoring of arterial, systemic and cerebral mixed venous oxygen (O2), lactate (L), and glucose (G) contents might help guide life support. We used our standardized dog model with ventricular fibrillation (VF), 12.5min of no flow, brief (2∼3min) cardio-pulmonary bypass (CPB), and controlled ventilation for 24hr (n=8). We monitored systemic and cerebral pressure variables including cardiac output (CO), intracranial pressure (ICP), arterial (a) and sagittal sinus (ss) O2, L, and G, and pulmonary arterial (pa) O2. CO was stable except for a 30% reduction at 4hr post-arrest. ICP remained normal for 24hr. The cerebral a-v O2 content difference (Ca-ssO2) was almost doubled at 1∼24hr post-arrest (worst at 4hr), whereas the systemic a-v difference (Ca-PaO2) was only slightly increased at 4∼12hr. These results implied the mismatching of cerebral metabolism/blood flow. Calculated cerebral O2 extraction ratio (OER) was 0.34 pre-arrest; decreased transiently to 0.06 during hyperemia; and increased post-arrest during hypoperfusion to a peak of 0.74 at 4hr. Simultaneous systemic OER was 0.16 pre-arrest, and changed little post-arrest. Cerebral a-vG values (a-ssG) were not consistent. Cerebral v-a values for L (a-ssL) were increased from reperfusion to 2hr. Oxygen glucose, lactate glucose, and lactate oxygen indices (OGI, LGI, LOI) were calculated. OGI and LGI varied considerably between dogs. LOI was more consistent; it reflected severe cerebral lactacidosis between 0∼2hr post-arrest. Post-arrest cerebral O2 deprivation seemed more severe than systemic deprivation in this model. Monitoring LOI early and CeOER early and late might be valuable for clinically guiding post-arrest therapy.

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