title: Cardiopulmonary resuscitation with a novel chest compression device in a porcine model of cardiac arrest: improved hemodynamics and mechanisms.
abstract: OBJECTIVE
  The goal of this study was to determine the magnitude and mechanisms of hemodynamic improvement of an automated, load-distributing band device (AutoPulse, Revivant Corp., Sunnyvale, California) compared with conventional cardiopulmonary resuscitation (C-CPR).
  
  
  BACKGROUND
  Improved blood flow during cardiopulmonary resuscitation (CPR) enhances survival from cardiac arrest.
  
  
  METHODS
  AutoPulse CPR (A-CPR) and C-CPR were performed on 30 pigs (16 +/- 4 kg) 1 min after induction of ventricular fibrillation. Aortic and right atrial pressures were measured with micromanometers. Regional flows were measured with microspheres; A-CPR and C-CPR were performed with 20% anterior-posterior chest compression, with (n = 10) and without (n = 10) epinephrine. A pressure transducer was advanced down the airways during chest compressions (n = 10), and magnetic resonance imaging (MRI) was performed.
  
  
  RESULTS
  AutoPulse CPR improved coronary perfusion pressure (CPP) (aortic - right atrial pressure) without epinephrine (A-CPR 21 +/- 8 mm Hg vs. C-CPR 14 +/- 6 mm Hg, mean +/- SD, p < 0.0001) and with epinephrine (A-CPR 45 +/- 11 mm Hg vs. C-CPR 17 +/- 6 mm Hg, p < 0.0001). AutoPulse CPR improved myocardial flow without epinephrine and cerebral and myocardial flow with epinephrine (p < 0.05). AutoPulse CPR also produced greater myocardial flow at every CPP (p < 0.01). With A-CPR, high airway pressure was noted distal to the carina, which corresponded to an area of airway collapse on MRI, and which was not present with C-CPR.
  
  
  CONCLUSIONS
  AutoPulse CPR improved hemodynamics over C-CPR in this pig model. AutoPulse CPR with epinephrine can produce pre-arrest levels of myocardial and cerebral flow. The improved hemodynamics with A-CPR appear to be mediated through airway collapse, which likely impedes airflow and helps maintain higher levels of intrathoracic pressure.
authors.affiliation: Johns Hopkins University, Department of Medicine, Baltimore, Maryland, USA. hhalper@jhmi.edu
authors.forename: Henry R
authors.initials: HR
authors.lastname: Halperin
authors.forename: Norman
authors.initials: N
authors.lastname: Paradis
authors.forename: Joseph P
authors.initials: JP
authors.lastname: Ornato
authors.forename: Menekhem
authors.initials: M
authors.lastname: Zviman
authors.forename: Jennifer
authors.initials: J
authors.lastname: Lacorte
authors.forename: Albert
authors.initials: A
authors.lastname: Lardo
authors.forename: Karl B
authors.initials: KB
authors.lastname: Kern
mesh_terms: D000818:Animals; D001794:Blood Pressure; D016887:Cardiopulmonary Resuscitation / Q000295:instrumentation* / Q000379:methods; D003326:Coronary Circulation; D006323:Heart Arrest / Q000628:therapy*; D012039:Regional Blood Flow; D013552:Swine