A randomized comparison of manual, mechanical and high-impulse chest compression in a porcine model of prolonged ventricular fibrillation.
BACKGROUND
Elevated coronary perfusion pressure (CPP) during CPR is associated with return of spontaneous circulation (ROSC). We compared CPP achieved with three methods of chest compression: manual (MAN), mechanical (MECH) and high-impulse mechanical (HI) in a porcine model of prolonged ventricular fibrillation (VF). We hypothesized that HI (very rapid acceleration of the down-stroke) would produce greater CPPs than MAN or MECH, and that HI would also produce a higher rate of ROSC.


METHODS
Twenty-eight domestic swine (mean 27.8 kg) were randomly assigned to three methods of chest compression. Animals were instrumented under anesthesia, and VF was induced and untreated for 8 min. After 2 min of CPR, epinephrine (adrenaline) (0. 1 mg/kg), vasopressin (40 U) and propranolol (1.0 mg) were administered. CPR continued for three more minutes, after which up to three rescue shocks were delivered. CPP was determined in an automated fashion by measuring the difference between aortic and right atrial pressures 0.1s prior to the down-stroke of each compression (i.e. end-relaxation). ROSC was defined as a systolic pressure greater than 80 mmHg sustained for at least 1 min. We analyzed CPP and ROSC using repeated measures ANOVA and Fisher's exact test.


RESULTS
Over the 5 min of CPR, CPP increased more with HI compression than with MAN compression (p=0.017). ROSC was attained in 4/9 MAN, 6/9 MECH and 10/10 HI (HI versus MAN p=0.01).


CONCLUSIONS
Over the course of CPR, HI compression increased CPP more than MAN compression. HI compression produced a significantly higher rate of ROSC than MAN, but not MECH compression.
Department of Emergency Medicine, University of Pittsburgh School of Medicine, 230 McKee Place, Suite 400, Pittsburgh, PA 15213, USA. aeb40@pitt.edu
Amy E
AE
Betz
James J
JJ
Menegazzi
Eric S
ES
Logue
Clifton W
CW
Callaway
Henry E
HE
Wang
D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D002560:Cerebrovascular Circulation / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D004837:Epinephrine / Q000494:pharmacology; D010477:Perfusion; D011312:Pressure / Q000009:adverse effects; D011433:Propranolol / Q000008:administration & dosage / Q000494:pharmacology; D011897:Random Allocation; D012016:Reference Values; D012039:Regional Blood Flow; D034421:Sus scrofa; D035441:Thoracic Wall / Q000503:physiopathology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology; D014667:Vasopressins / Q000008:administration & dosage / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000503:physiopathology*
D000316:Adrenergic alpha-Agonists; D000319:Adrenergic beta-Antagonists; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D011433:Propranolol; D004837:Epinephrine