TY - JOUR
T1 - The cardiac physiology underpinning exsanguination cardiac arrest
T2 - targets for endovascular resuscitation
AU - Madurska, Marta J.
AU - Abdou, Hossam
AU - Leung, Lai Yee
AU - Richmond, Michael J.
AU - Elansary, Noha N.
AU - Scalea, Thomas M.
AU - Hu, Peter
AU - Morrison, Jonathan J.
N1 - Publisher Copyright:
Copyright ß 2020 by the Shock Society
PY - 2021/1
Y1 - 2021/1
N2 - 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 ¼ 0.02), left ventricular end-diastolic volume (94–52 mL, P ¼ 0.04), cardiac output (4.8–2.4 L/min, P ¼ 0.03), coronary perfusion pressure (57–30 mm Hg, P ¼ 0.01), and stroke volume (60–25 mL, P ¼ 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.
AB - 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 ¼ 0.02), left ventricular end-diastolic volume (94–52 mL, P ¼ 0.04), cardiac output (4.8–2.4 L/min, P ¼ 0.03), coronary perfusion pressure (57–30 mm Hg, P ¼ 0.01), and stroke volume (60–25 mL, P ¼ 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.
KW - Exsanguination
KW - Hemorrhage
KW - Hypovolemic shock
KW - Resuscitation
KW - Selective aortic arch perfusion
UR - http://www.scopus.com/inward/record.url?scp=85098744174&partnerID=8YFLogxK
U2 - 10.1097/SHK.0000000000001607
DO - 10.1097/SHK.0000000000001607
M3 - Article
C2 - 33337788
AN - SCOPUS:85098744174
SN - 1073-2322
VL - 55
SP - 83
EP - 89
JO - Shock
JF - Shock
IS - 1
ER -