title: Ventilatory strategies affect gas exchange in a pig model of closed-chest cardiac compression.
abstract: OBJECTIVE
  To identify the arterial and mixed venous blood gas changes caused by different ventilatory strategies during resuscitation from ventricular fibrillation in a pig model of closed-chest cardiac compression.
  
  
  METHODS
  A prospective randomized animal study was performed using 27 domestic pigs (body weight, 30 to 35 kg). Pentobarbital-anesthetized pigs were assigned to receive one of three treatments: (1) chest compression without assisted ventilation (n = 8), (2) assisted ventilation with room air (n = 8), and (3) assisted ventilation with 100% oxygen (n = 8). A fourth group, with the airway completely blocked, was added at the end of the experiment (n = 3). After instrumentation, the ventricles were fibrillated, and chest compression was begun 30 seconds after fibrillation with the use of the Thumper Mechanical CPR system (Michigan Instruments). Arterial and mixed venous blood gas samples were collected at 1, 3, 10, and 20 minutes of resuscitation. Defibrillation was attempted after the 20-minute sample was taken.
  
  
  RESULTS
  Fibrillation followed by chest compression alone caused a significant drop in arterial and mixed venous partial pressure of oxygen (PO2) and a significant increase in arterial and mixed venous partial pressure of carbon dioxide (PCO2). Compared with the chest compression only, ventilation with room air significantly increased arterial and mixed venous PO2 and decreased arterial and mixed venous PCO2. Ventilation with 100% oxygen further increased arterial and mixed venous PO2 but did not affect PCO2, when compared with room air ventilation. The only successful defibrillations (3 animals) occurred in the group receiving 100% oxygen.
  
  
  CONCLUSIONS
  This study indicates that passive air movement during chest compression does not allow physiologically significant pulmonary gas exchange and that room air ventilation alone is not sufficient to maintain mixed venous PO2.
authors.affiliation: Department of Physiology, East Carolina University School of Medicine, Greenville, NC, USA.
authors.forename: M E
authors.initials: ME
authors.lastname: Whitehurst
authors.forename: A D
authors.initials: AD
authors.lastname: Blount
authors.forename: P E
authors.initials: PE
authors.lastname: Austin
authors.forename: R G
authors.initials: RG
authors.lastname: Carroll
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D003131:Combined Modality Therapy; D004195:Disease Models, Animal; D006336:Heart Massage / Q000295:instrumentation / Q000379:methods*; D010102:Oxygen Inhalation Therapy / Q000379:methods*; D011659:Pulmonary Gas Exchange; D011897:Random Allocation; D012121:Respiration, Artificial / Q000379:methods*; D013552:Swine; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*