Abstract

Introduction: Coronary perfusion pressure (CPP) guided CPR improves survival over guideline CPR. EtCO2 has also been used to guide CPR. These efforts reflect that one-size-fits-all CPR is sub-optimal, but assume that CPP and EtCO2 guidance will result in similar definitions of “high quality” chest compressions (CC). A mechanistic study of the interaction between CC, blood flow, CPP, and EtCO2 has not been done. Methods: CPR was performed on 21 domestic swine (~30 Kg) using standard physiological monitoring. Flow was measured in the abdominal aorta, the inferior vena cava (IVC), the right renal artery and vein, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical CC were started after ten minutes of VF. CC waveforms varied so that sternal release occurred over 100 ms, 200 ms, or 300 ms. CC were delivered at a rate of 100 per minute and at a depth of 1.25” (n=9), 1.9” (n=8), or 1.9” with vasopressor use (n=4) for a total of 54 min. CC release times changed every 2 min and were randomized. Results: In the first 18 min of CPR, EtCO2 was optimized by a 100 ms release (27.2±2.5 mmHg) vs. a 200 ms (24.7±2.5 mmHg; p = .005) or 300 ms release (25.1±2.5 mmHg; p= 0.03). CPP was optimized by a 200 ms release (6.7±1.0 mmHg) vs. a 100 ms (5.7±1.0 mmHg; p = 0.03) or 300 ms (4.9±1.0 mmHg; p < 0.01) release. Deeper CC increased blood flow in the IVC (1.5±0.2 vs. 0.12±0.2 mL/comp: p<0.001) and carotid artery (0.4±0.03 vs. 0.2±0.03 mL/comp: p<0.001) and changed the distribution of blood flow. In prolonged CPR, CC efficacy decayed with time, particularly with 1.25” CC, and resulted in distinct periods of to and fro flow (sloshing). Vasopressor effects appeared to be time dependent, but trended towards improved CPP at the expense of significantly reduced carotid blood flow. Conclusions: CPP and EtCO2 provide insight into two distinct aspects of CC generated blood flow, and consequently cannot be simultaneously optimized. CC generated blood flow transitions from forward blood flow to sloshing as a function of time and CC depth. Pressure measurements are insufficient to titrate vasopressor use, as tissue perfusion can collapse while maintaining the CPP. We currently lack the monitoring and the physiological understanding required to personalize CPR.

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