The Cardiac Physiology Underpinning Exsanguination Cardiac Arrest: Targets for Endovascular Resuscitation. Issue 1 (January 2021)

• Record Type: Journal Article
• Authors: Madurska, Marta J.; Abdou, Hossam; Leung, Lai Yee; Richmond, Michael J.; Elansary, Noha N.; Scalea, Thomas M.; Hu, Peter; Morrison, Jonathan J.
• Is Part Of: Shock. Volume 55:Issue 1(2021)
• Publication Date: 2021-01
• Subjects: Exsanguination -- hemorrhage -- hypovolemic shock -- resuscitation -- selective aortic arch perfusion; Shock -- Periodicals; Shock -- Periodicals; Choc (Pathologie) -- Périodiques; Shock; Periodicals; 616.0475
• DOI: 10.1097/SHK.0000000000001607
• Languages: English
• ISSNs: 1073-2322

Abstract

Abstract : ABSTRACT: Exsanguination leading to cardiac arrest is the terminal phase of uncontrolled hemorrhage. Resuscitative interventions have focused on preload and afterload support. Outcomes remain poor due to several factors but poor coronary perfusion undoubtedly plays a role. The aim of this study is to characterize the relationship between arterial pressure and flow during hemorrhage in an effort to better describe the terminal phases of exsanguination. Male swine weighing 60 kg to 80 kg underwent splenectomy and instrumentation followed by a logarithmic exsanguination until asystole. Changes in hemodynamic parameters over time were compared using one-way, repeated measures analysis of variance. Nine animals weighing 69 ± 15 kg were studied. Asystole occurred at 53 ± 13 min when 52 ± 11% of total blood volume has been shed. The greatest fall in mean hemodynamic indices were noted in the first 15 min: SBP (80–42 mm Hg, P = 0.02), left ventricular end-diastolic volume (94–52 mL, P = 0.04), cardiac output (4.8–2.4 L/min, P = 0.03), coronary perfusion pressure (57–30 mm Hg, P = 0.01), and stroke volume (60–25 mL, P = 0.02). This corresponds to the greatest rate of exsanguination. Organized cardiac activity was observed until asystole without arrythmias. Coronary flow was relatively preserved throughout the study, with a precipitous decline once mean arterial pressure was less than 20 mm Hg, leading to asystole. In this model, initial hemodynamic instability was due to preload failure, with asystole occurring relatively late, secondary to failure of coronary perfusion. Future resuscitative therapies need to directly address coronary perfusion failure if effective attempts are to be made to salvage these patients.