Abstract 301: Aortic and Central Venous Pressure Wave Synchronization in Pseudo-Pulseless Electrical Activity

Abstract

Introduction: Pseudo-Pulseless Electrical Activity (p-PEA) is a lifeless form of profound cardiac shock characterized by measurable cardiac mechanical activity without clinically detectable pulses. p-PEA may constitute up to 40% of reported cases of cardiac arrest and its etiologies and physiology are distinctly different from ventricular fibrillation or even true-PEA. In the normal physiologic state, there is an expected delay between the central venous (CV) and aortic (Ao) pressure waveforms corresponding to atrial kick and ventricular systole, respectively. We studied this relationship in hypoxic porcine p-PEA. Hypothesis: Development of p-PEA may be associated with changes in Ao and CV waveform synchronization. Methods: Female swine (N = 14) under intravenous anesthesia were instrumented with Ao and CV micromanometer catheters. ECG and ET-CO 2 were measured continuously. p-PEA was induced by ventilation with 6% oxygen in 94% nitrogen, and was defined as a systolic aortic pressure less than 40 mmHg. After 2 min. of p-PEA, 100% O 2 , CPR, and epinephrine were administered in a stepwise progression until ROSC was achieved. Results: One min. before the onset of hypoxia, the mean CV to Ao waveform delay was 0.161 sec. (SE ± 0.0015) across 52 experiments (n = 4797). This delay shortened during development of the p-PEA disease state (Figure 1), where the average delay decreased to 0.057 seconds (SE ± 0.0012) across 52 experiments (n = 3969, P < 10-6). There were statistically significant differences (P < 10-6) in waveform delays in between cohorts of animals who required more interventions to achieve ROSC, with shorter delay periods in both baseline and disease states correlating strongly with greater interventions. Conclusions: Development of the hypoxic p-PEA state may be associated with a loss of the normal CV to Ao pressure waveform delay. The degree of this loss may be associated with the severity of p-PEA disease state and predictive of the therapy required for ROSC.