title: Intra-cardiopulmonary resuscitation hypothermia with and without volume loading in an ischemic model of cardiac arrest.
abstract: BACKGROUND
  We investigated the effects of intra-cardiopulmonary resuscitation (CPR) hypothermia with and without volume loading on return to spontaneous circulation and infarction size in an ischemic model of cardiac arrest.
  
  
  RESULTS
  Using a distal left anterior descending artery occlusion model of cardiac arrest followed by resuscitation with a total of 120 minutes of occlusion and 90 minutes of reperfusion, we randomized 46 pigs into 5 groups and used myocardial staining to define area at risk and myocardial necrosis. Group A had no intervention. Immediately after return of spontaneous circulation, group B received surface cooling with cooling blankets and ice. Group C received intra-CPR 680+/-23 mL of 28 degrees C 0.9% normal saline via a central venous catheter. Group D received intra-CPR 673+/-26 mL of 4 degrees C normal saline followed by surface cooling after return of spontaneous circulation. Group E received intra-CPR and hypothermia after return of spontaneous circulation with an endovascular therapeutic hypothermia system placed in the right atrium and set at a target of 32 degrees C. Intra-CPR volume loading with room temperature (group C) or iced saline (group D) significantly (P<0.05) decreased coronary perfusion pressure (group C, 12.8+/-4.78 mm Hg; group D, 14.6+/-9.9 mm Hg) compared with groups A, B, and E (20.6+/-8.2, 20.1+/-7.8, and 21.3+/-12.4 mm Hg). Return of spontaneous circulation was significantly improved in group E (9 of 9) compared with groups A plus B and C (10 of 18 and 1 of 8). The percent infarction to the area at risk was significantly reduced with intra-CPR hypothermia in groups D (24.3+/-4.2%) and E (4+/-3.4%) compared with groups A (72+/-5.1%) and B (67.3+/-4.2%).
  
  
  CONCLUSIONS
  Intra-CPR hypothermia significantly reduces myocardial infarction size. Elimination of volume loading further improves outcomes.
authors.affiliation: Cardiology Division, University of Minnesota, Mayo Mail Code 508, 420 Delaware St SE, Minneapolis, MN 55455, USA. yanno001@umn.edu
authors.forename: Demetris
authors.initials: D
authors.lastname: Yannopoulos
authors.forename: Menekhem
authors.initials: M
authors.lastname: Zviman
authors.forename: Valeria
authors.initials: V
authors.lastname: Castro
authors.forename: Aravindan
authors.initials: A
authors.lastname: Kolandaivelu
authors.forename: Ravi
authors.initials: R
authors.lastname: Ranjan
authors.forename: Robert F
authors.initials: RF
authors.lastname: Wilson
authors.forename: Henry R
authors.initials: HR
authors.lastname: Halperin
mesh_terms: D000818:Animals; D001775:Blood Circulation / Q000502:physiology; D001794:Blood Pressure; D016887:Cardiopulmonary Resuscitation / Q000295:instrumentation / Q000379:methods*; D002404:Catheterization / Q000295:instrumentation / Q000379:methods; D004195:Disease Models, Animal; D005263:Femoral Artery / Q000502:physiology; D006323:Heart Arrest / Q000628:therapy*; D007036:Hypothermia, Induced / Q000295:instrumentation / Q000379:methods*; D009203:Myocardial Infarction / Q000473:pathology; D013552:Swine; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology