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Tytuł oryginału: Effects of acute hypoxemia/ischemia on EEG and evoked responses at normothermia and hypothermia in humans.
Autorzy: Stecker Mark M., Escherich Alison, Patterson Terry, Bavaria Joseph E., Cheung Albert T.
Źródło: Med. Sci. Monitor 2002: 8 (4) s.CR223-CR228, il., tab., bibliogr. 25 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca kazuistyczna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • dorośli 19-44 r.ż.
  • dorośli 45-64 r.ż.
  • płeć męska
  • płeć żeńska

    Streszczenie angielskie: Background: Hypothermia is used clinically to prevent neurologic injury but the degree of protection which it affords at various levels of the nervous system in humans is difficult to establish. Material/Methods: The temporal changes in EEG amplitude and somatosensory evoked potential (SEP) amplitudes in a patient experiencing acute normothermic hypoxemia, a patient experiencing acute circulatory arrest at moderate hypothermia and a collection of patients undergoing deep hypothermic circulatory arrest were analyzed to determine the rate at which changes occur during acute lack of oxygen delivery at various temperatures. Results: In each case, it was found that more rostrally geneated potentials disappeared more quickly than more peripheral potentials. All potentials decayed more slowly during acute normothermic hypoxemia than during circualtory arrest. During circulatory arrest at 14.4řC, the amplitude of the Erb's point, 13 and N18 potentials in th SEP took 5 times longer to drop to 50 p.c. of their value at the onset of ischemia than with circulatory arrest at 30.9řC. Conclusions: The longer times to disappearance of the SEP potentials during deep hypothermia compared to moderate hypotheramia was consistent with the predicted 3.5 - 6.5 fold reduction in metabolic activity at deep hypothermia compared to moderate hypothermia. The prolonged time to disappearance of the SEP during normothermic hypoxemia demonstrates that even with reduced oxygen delivery the continued delivery of metabolic substrate can be critical to neural function.

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