title: Mild hypothermia after cardiac arrest in dogs does not affect postarrest cerebral oxygen uptake/delivery mismatching.
abstract: OBJECTIVE
  To compare measurements of cerebral arteriovenous oxygen content differences (oxygen extraction ratios, oxygen utilization coefficients) in dogs after cardiac arrest, resuscitated under normothermia vs. mild hypothermia for 1-2 h or 12 h.
  
  
  METHODS
  In 20 dogs, we used our model of ventricular fibrillation (no blood flow) of 12.5 min, reperfusion with brief cardiopulmonary bypass, and controlled ventilation, normotension, normoxemia, and mild hypocapnia to 24 h. We compared a normothermic control Group I (37.5 degrees C) (n = 8); with brief mild hypothermia in Group II (core and tympanic membrane temperature about 34 degrees C during the first hour after arrest) (n = 6); and with prolonged mild hypothermia in Group III (34 degrees C during the first 12 h after arrest) (n = 6).
  
  
  RESULTS
  In Group I, the cerebral arteriovenous O2 content difference was 5.6 +/- 1.6 ml/dl before arrest; was low during reperfusion (transient hyperemia) and increased (worsened) significantly to 8.8 +/- 2.8 ml/dl at 1 h, remained increased until 18 h, and returned to baseline levels at 24 h after reperfusion. These values were not significantly different in hypothermic Groups II and III. The cerebral venous (saggital sinus) PO2 (PssO2) was about 40 mmHg (range 29-53) in all three groups before arrest and decreased significantly below baseline values, between 1 h and 18 h after arrest; the lowest mean values were 19 +/- 19 mmHg in Group I, 15 +/- 8 in Group II (NS), and 21 +/- 3 in Group III (NS). Postarrest PssO2 values of < or = 20 mmHg were found in 6/8 dogs in Group I, 5/6 in Group II and 4/6 in Group III. Among the 120 values of PssO2 measured between 1 h and 18 h after arrest, 32 were below the critical value of 20 mmHg.
  
  
  CONCLUSIONS
  After prolonged cardiac arrest, critically low cerebral venous O2 values suggest inadequate cerebral O2 delivery. Brief or prolonged mild hypothermia after arrest does not mitigate the postarrest cerebral O2 uptake/delivery mismatching.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh Medical Center, PA 15260.
authors.forename: K
authors.initials: K
authors.lastname: Kuboyama
authors.forename: P
authors.initials: P
authors.lastname: Safar
authors.forename: K
authors.initials: K
authors.lastname: Oku
authors.forename: W
authors.initials: W
authors.lastname: Obrist
authors.forename: Y
authors.initials: Y
authors.lastname: Leonov
authors.forename: F
authors.initials: F
authors.lastname: Sterz
authors.forename: S A
authors.initials: SA
authors.lastname: Tisherman
authors.forename: S W
authors.initials: SW
authors.lastname: Stezoski
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000503:physiopathology / Q000517:prevention & control*; D004285:Dogs; D005260:Female; D006323:Heart Arrest / Q000503:physiopathology / Q000628:therapy*; D007036:Hypothermia, Induced; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology*; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D012151:Resuscitation / Q000379:methods*; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000628:therapy