Abstract 12018: Cardiac Ultrasound Performed During Cardiac Arrest has Potential to Detect Pulmonary Embolism as a Reversible Cause of Cardiac Arrest when Compared to Hypoxia and Ventricular Fibrillation - A Randomized Porcine Study

Abstract

Introduction: Survival from non-shockable cardiac arrest is unlikely unless a reversible cause is identified and treated. Guidelines state that ultrasound has the potential to identify reversible causes. Currently, ultrasonographic findings from patients with spontaneous circulation are extrapolated to patients in cardiac arrest. While right ventricular (RV) dilation is a finding normally associated with pulmonary embolism (PE), porcine studies have shown that RV dilation is also seen in ventricular fibrillation (VF) and severe hypoxia. No studies have investigated how causes of cardiac arrest affect RV size during resuscitation. Hypothesis: The RV diameter is larger during resuscitation of cardiac arrest caused by PE when compared to hypoxia and VF. Methods: Pigs were anesthetized and randomized to cardiac arrest induced by VF, hypoxia, or PE. Advanced life support (ALS) was preceded by 7 minutes of untreated cardiac arrest. Cardiac ultrasound images of the RV from a subcostal 5-chamber view were obtained during induction of cardiac arrest and ALS. The RV diameter was measured two centimeters from the aortic valve at end diastole. RV diameter at 3rd rhythm analysis was the primary endpoint. Based on pilot studies a sample size of 8 animals in each group was needed. Results: Eight animals were included in each group. RV diameter was not statistically different at baseline (mean (95%CI)) in VF: 19.8 (18.0-21.5) mm, hypoxia: 19.8 (16.6-22.9) mm, and PE: 21.8 (19.2-24.3) mm. During induction of cardiac arrest the RV diameter increased to 29.6 (27.3-31.9) mm in the hypoxia group and 38.0 (33.4-42.6) mm in the PE group (difference to baseline and between groups, both p<0.01). Induction of VF caused an immediate increase in the RV diameter to 25.0 (21.2-28.8) mm (difference to baseline p<0.01). At 3rd rhythm analysis, RV diameter was 32.4 (28.6-36.2) mm in the PE group, which was significantly larger than both the hypoxia group at 23.3 (19.5-27.0) mm and the VF group at 24.9 (22.2-27.5) mm (difference between groups p<0.01). Conclusions: Cardiac arrest due to VF, hypoxia, and PE all caused an increase in RV diameter. During resuscitation the RV was larger in PE compared to VF and hypoxia. Cardiac ultrasound thus has the potential to detect PE during resuscitation.