Sustained abdominal compression during CPR raises coronary perfusion pressures as much as vasopressor drugs.
OBJECTIVE
This study investigated sustained abdominal compression as a means to improve coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR) and compared the resulting CPP augmentation with that achieved using vasopressor drugs.


METHODS
During electrically induced ventricular fibrillation in anesthetized, 30kg juvenile pigs, Thumper CPR was supplemented at intervals either by constant abdominal compression at 100-500mmHg using an inflated contoured cuff or by the administration of vasopressor drugs (epinephrine, vasopressin, or glibenclamide). CPP before and after cuff inflation or drug administration was the end point.


RESULTS
Sustained abdominal compression at >200mmHg increases CPP during VF and otherwise standard CPR by 8-18mmHg. The effect persists over practical ranges of chest compression force and duty cycle and is similar to that achieved with vasopressor drugs. Constant abdominal compression also augments CPP after prior administration of epinephrine or vasopressin.


CONCLUSIONS
During CPR noninvasive abdominal compression with the inflatable contoured cuff rapidly elevates the CPP, sustains the elevated CPP as long as the device is inflated, and is immediately and controllably reversible upon device deflation. Physical control of peripheral vascular resistance during CPR by abdominal compression has some advantages over pharmacological manipulation and deserves serious reconsideration, now that the limitations of pressor drugs during CPR have become better understood, including post-resuscitation myocardial depression and the need for intravenous access.
Lottes
Aaron E
AE
Weldon School of Biomedical Engineering, Purdue University, 206 S. Intramural Drive, West Lafayette, IN 47907-2032, USA.
Rundell
Ann E
AE
Geddes
Leslie A
LA
Kemeny
Andre E
AE
Otlewski
Michael P
MP
Babbs
Charles F
CF
D000005:Abdomen; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D003326:Coronary Circulation / Q000187:drug effects* / Q000502:physiology*; D004195:Disease Models, Animal; D011312:Pressure; D034421:Sus scrofa; D014655:Vascular Resistance / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014693:Ventricular Fibrillation / Q000628:therapy
D014662:Vasoconstrictor Agents