title: Coronary perfusion pressure during experimental cardiopulmonary resuscitation.
abstract: Systemic blood flow during cardiopulmonary resuscitation may result from alterations in intrapleural pressure (IPP), with the heart serving only as a passive conduit. Chest compression with simultaneous lung inflation (C + SI) or with abdominal binding may also increase vascular pressures and cerebral flow. Our study was done to evaluate the effects of C + SI with and without abdominal binding on coronary perfusion pressure (CPP) during CPR. Micromanometric pressures were recorded in 7 dogs during ventricular fibrillation (VF) and CPR to evaluate CPP (aortic minus right atrial pressure). During chest compression alone, aortic (AoP) and right atrial (RAP) pressures did not differ significantly. During relaxation, AoP (15 +/- 4 mm Hg) was greater than RAP (3 +/- 2 mm Hg; P less than 0.001) and diastolic CPP averaged 12 +/- 4 mm Hg. C + SI significantly increased AoP, RAP, and IPP, but did not improve systolic or diastolic CPP. Tight abdominal binding during chest compression alone or during C + SI also increased AoP and RAP and caused a slight but insignificant decrease in diastolic CPP. Extravascular resistance to coronary flow during VP has been shown to average 28 mm Hg in the in vitro heart. Our study indicates that CPPs calculated during CPR do not reach sufficient values to overcome the resistance offered by the fibrillating myocardium. Interventions which increase IPP, intravascular pressures, and carotid flow do not improve CPP or, by inference, coronary flow.
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D016275:Atrial Function; D001794:Blood Pressure; D003326:Coronary Circulation; D003971:Diastole; D004285:Dogs; D006336:Heart Massage; D008365:Manometry; D008954:Models, Biological; D012151:Resuscitation; D013599:Systole; D014655:Vascular Resistance