Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest

Abstract

Introduction: Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival. Hypothesis: Incomplete chest wall recoil during the decompression phase of standard CPR increases intrathoracic pressure and right atrial pressure, impedes venous return, decreases compression-induced aortic pressures and results in a decrease of mean arterial pressure, coronary and cerebral perfusion pressure. Methods: Nine pigs in ventricular fibrillation (VF) for 6 min, were treated with an automated compression/decompression device with a compression rate of 100 min −1, a depth of 25% of the anterior–posterior diameter, and a compression to ventilation ratio of 15:2 with 100% decompression (standard CPR) for 3 min. Compression was then reduced to 75% of complete decompression for 1 min of CPR and then restored for another 1 min of CPR to 100% full decompression. Coronary perfusion pressure (CPP) was calculated as the diastolic (aortic (Ao)–right atrial (RA) pressure). Cerebral perfusion pressure (CerPP) was calculated multiple ways: (1) the positive area (in mmHg s) between aortic pressure and intracranial pressure (ICP) waveforms, (2) the coincident difference in systolic and diastolic aortic and intracranial pressures (mmHg), and (3) CerPP = MAP − ICP. ANOVA was used for statistical analysis and all values were expressed as mean ± S.E.M. The power of the study for an alpha level of significance set at 0.05 was >0.90. Results: With CPR performed with 100%–75%–100% of complete chest wall recoil, respectively, the CPP was 23.3 ± 1.9, 15.1 ± 1.6, 16.6 ± 1.9, p = 0.003; CerPP was: (1) area: 313.8 ± 104, 89.2 ± 39, 170.5 ± 42.9, p = 0.03, (2) systolic aortic minus intracranial pressure difference: 22.8 ± 3.6, 16.5 ± 4, 23.7 ± 4.5, p = n.s., and diastolic pressure difference: 5.7 ± 3, −2.4 ± 2.4, 3.2 ± 2.5, p = 0.04 and (3) mean: 14.3 ± 3, 7 ± 2.9, 12.4 ± 2.9, p = 0.03, diastolic aortic pressure was 28.1 ± 2.5, 20.7 ± 1.9, 20.9 ± 2.1, p = 0.0125; ICP during decompression was 22.8 ± 1.7, 23 ± 1.5, 19.7 ± 1.7, p = n.s. and mean ICP was 37.1 ± 2.3, 35.5 ± 2.2, 35.2 ± 2.4, p = n.s.; RA diastolic pressure 4.8 ± 1.3, 5.6 ± 1.2, 4.3 ± 1.2 p = 0.1; MAP was 52 ± 2.9, 43.3 ± 3, 48.3 ± 2.9, p = 0.04; decompression endotracheal pressure, −0.7 ± 0.1, −0.3 ± 0.1, −0.75 ± 0.1, p = 0.045. Conclusions: Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures.