title: Cerebral oxygenation during cardiopulmonary resuscitation with epinephrine and vasopressin in pigs.
abstract: OBJECTIVE
  Administration of vasopressin during cardiopulmonary resuscitation (CPR) improves vital organ blood flow compared with epinephrine, but the effect of vasopressin on cerebral oxygenation and cerebral venous hypercarbia during CPR has not previously been studied.
  
  
  METHODS
  Fourteen pigs were allocated to receive either epinephrine (0.2 mg/kg) or vasopressin (0.4 U/kg) after 4 minutes of ventricular fibrillation and 3 minutes of CPR. Cerebral blood flow was determined by radiolabeled microspheres, and arterial and cerebral venous blood gases were measured.
  
  
  RESULTS
  Cerebral blood flow, measured before and 90 seconds and 5 minutes after drug administration, was 9 (3; 12), 25 (19; 27), and 18 (10; 23) mL/min per 100 g (median and 25th and 75th percentiles, respectively) in the epinephrine group and 12 (5; 16), 51 (48; 70), and 53 (45; 63) mL/min per 100 g in the vasopressin group (P<.05 at 90 seconds, P<.01 at 5 minutes between groups). Five minutes after drug administration, cerebral venous Pco2 was 63 (59; 68) mm Hg in the epinephrine group and 47 (43; 55) mm Hg in the vasopressin group (P<.01); at the same time cerebral venous pH was 7.18 (7.17; 7.20) and 7.26 (7.22; 7.36) (P<.01) in the epinephrine and vasopressin groups, respectively. Cerebral oxygen extraction ratio, calculated before and 90 seconds and 5 minutes after drug administration, was 0.42 (0.32; 0.57), 0.47 (0.41; 0.57), and 0.56 (0.56; 0.64) in the epinephrine group and 0.43 (0.38; 0.45), 0.38 (0.25; 0.44), and 0.35 (0.33; 0.49) in the vasopressin group (P<.05 at 90 seconds and 5 minutes).
  
  
  CONCLUSIONS
  Compared with epinephrine, vasopressin not only increases cerebral blood flow but also improves cerebral oxygenation and decreases cerebral venous hypercarbia when administered during CPR in pigs.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, University of Ulm, Germany.
authors.forename: A W
authors.initials: AW
authors.lastname: Prengel
authors.forename: K H
authors.initials: KH
authors.lastname: Lindner
authors.forename: A
authors.initials: A
authors.lastname: Keller
mesh_terms: D000136:Acid-Base Equilibrium; D000322:Adrenergic Agonists / Q000627:therapeutic use*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D016887:Cardiopulmonary Resuscitation; D002550:Cerebral Veins / Q000187:drug effects; D002552:Cerebral Ventricles / Q000098:blood supply; D002560:Cerebrovascular Circulation; D003392:Cranial Sinuses / Q000378:metabolism; D004837:Epinephrine / Q000627:therapeutic use*; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000097:blood / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects; D013552:Swine; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014667:Vasopressins / Q000627:therapeutic use*; D014693:Ventricular Fibrillation / Q000628:therapy
chemical_list: D000322:Adrenergic Agonists; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D002245:Carbon Dioxide; D010100:Oxygen; D004837:Epinephrine