title: Potential negative effects of epinephrine on carotid blood flow and ETCO2 during active compression-decompression CPR utilizing an impedance threshold device.
abstract: OBJECTIVE
  This study examines the effects of IV epinephrine administration on carotid blood flow (CBF) and end tidal CO(2) (ETCO(2)) production in a swine model of active compression-decompression CPR with an impedance threshold device (ACD-CPR+ITD).
  
  
  METHODS
  Six female swine (32 ± 1 kg) were anesthetized, intubated and ventilated. Intracranial, thoracic aorta and right atrial pressures were measured via indwelling catheters. CBF was recorded. ETCO(2), SpO(2) and EKG were monitored. V-fib was induced and went untreated for 6 min. Three minutes each of standard CPR (STD), STD-CPR+impedance threshold device (ITD) and active compression-decompression (ACD)-CPR+ITD were performed. At minute 9 of the resuscitation, 40 μg/kg of IV Epinephrine was administered and ACD-CPR+ITD was continued for 1 min. Statistical analysis was performed with a paired t-test. p values of <0.05 were considered statistically significant and all values are reported in mmHg unless otherwise noted.
  
  
  RESULTS
  Aortic pressure, cerebral and coronary perfusion pressures increased from STD<STD+ITD<ACD-CPR+ITD (p<0.001). Epinephrine administered during ACD-CPR+ITD signficantly increased mean aortic pressure (29 ± 5 vs 42 ± 12, p = 0.01), cerebral perfusion pressure (12 ± 5 vs 22 ± 10, p = 0.01), and coronary perfusion pressure (8 ± 7 vs 17 ± 4, p = 0.02); however, mean CBF and ETCO(2) decreased (respectively 29 ± 15 vs 14 ± 7.0 ml/min, p = 0.03; 20 ± 7 vs 18 ± 6, p = 0.04).
  
  
  CONCLUSIONS
  In this model, administration of epinephrine during ACD-CPR+ITD significantly increased markers of macrocirculation, while significantly decreasing carotid blood flow and ETCO(2). This calls into question the ability of calculated perfusion pressures to accurately reflect oxygen delivery to end organs. The administration of epinephrine during ACD-CPR+ITD does not improve cerebral tissue perfusion.
authors.affiliation: Department of Emergency Medicine, Regions Hospital, Saint Paul, MN, United States. Aaron.M.Burnett@healthpartners.com
authors.forename: Aaron M
authors.initials: AM
authors.lastname: Burnett
authors.forename: Nicolas
authors.initials: N
authors.lastname: Segal
authors.forename: Joshua G
authors.initials: JG
authors.lastname: Salzman
authors.forename: M Scott
authors.initials: MS
authors.lastname: McKnite
authors.forename: Ralph J
authors.initials: RJ
authors.lastname: Frascone
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists / Q000009:adverse effects*; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000295:instrumentation*; D017097:Electric Impedance; D004837:Epinephrine / Q000009:adverse effects*; D005260:Female; D006323:Heart Arrest / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics / Q000187:drug effects*; D013552:Swine
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D004837:Epinephrine