Abstract Body: Background:
Cardiac arrest care has had limited change to care over the last 50 years and remains a high cause of morbidity and mortality. In consideration of adjuvant treatment in cardiopulmonary arrest care, aortic compression in experimental models has emerged as a possibility Multiple animal models and human case reports suggest compression of the aorta enhances coronary perfusion pressure and augments cardiac output. Currently there is a paucity of data on the effect of Abdominal Aortic compression (AAo Comp) in human subjects. We developed a model of human volunteers to assess our hypothesis regarding safety and efficacy of AAo Comp with ultrasound. This study aimed to investigate the safety, feasibility ability to abdominal Aortic compression to effect cardiac output.


Methods:
A prospective, single-center cohort study of health subjects between the ages of 22 and 30 were place on a non-invasive hemodynamic monitor, NICOM (Non-invasive Cardiac Output Monitor Baxter Health) while abdominal aortic compression was performed with ultrasound. A blood pressure cuff measured the subjects' brachial pressure. After 1 minute of compression the US probe was removed. 1 minute later the same compression protocol was performed with 1 minute of compression time. Collected data included patient demographic data, cardiac output, stroke volume variation, peripheral resistance. The primary outcome was safety of compression on subjects. The secondary outcome was measuring difference in cardiac output after Ao compression.


Results
33 patients were included. 89% of the subjects had a change in cardiac output parameter. 85% of all subjects demonstrated the effect on cardiac output with AAo Comp. P value: The overall range of change of the Cardiac output was 3% - 15% with our AAo Comp intervention. 15% Subjects that discordant values of drop in cardiac output values.

Discussion:
Regarding safety data, our initial phase I sample of AAo compression demonstrated subjects reporting only mild transient abdominal tenderness (n= 30/33) and transient paresthesthesias of lower extremities (n- 5). 1 subject had CHD s/p surgical repair had a paradoxical response with hypotension when MAP recorded as low and greater than 20% with our intervention. The possible mechanisms for this observation include mismatched equipment size, CHD or surgically altered anatomy.