Class of hemorrhagic shock is associated with progressive diastolic coronary flow reversal and diminished left ventricular function

Abstract

Introduction: The relationship between coronary artery flow and left ventricular (LV) function during hemorrhagic shock remains unknown. The aim of this study was to quantify coronary artery flow directionality alongside left ventricular function through the four classes of hemorrhage shock.Methods: Following baseline data collection, swine were exsanguinated into cardiac arrest via the femoral artery using a logarithmic bleed, taking each animal through the four classes of hemorrhagic shock based on percent bleed (class I: 15%; class II: 15%–30%; class III: 30%–40%; class IV: >40%). Telemetry data, left ventricular pressure-volume loops, and left anterior descending artery flow tracings over numerous cardiac cycles were collected and analyzed for each animal throughout.Results: Five male swine (mean 72 ± 12 kg) were successfully exsanguinated into cardiac arrest. Mean left ventricular end-diastolic volume, end-diastolic pressure, and stroke work decreased as the hemorrhagic shock class progressed (p < 0.001). The proportion of diastole spent with retrograde coronary flow was also associated with class of hemorrhagic shock (mean 5.6% of diastole in baseline, to 63.9% of diastole in class IV; p < 0.0001), worsening at each class from baseline through class IV. Preload recruitable stroke work (PRSW) decreased significantly in classes II through IV (p < 0.001). Systemic Vascular Resistance (SVR) is associated with class of hemorrhage shock (p < 0.001).Conclusion: With progressive classes of hemorrhagic shock left ventricular function progressively decreased, and the coronary arteries spent a greater proportion of diastole in retrograde flow, with progressively more negative total coronary flow. Preload recruitable stroke work, a load-independent measure of inotropy, also worsened in severe hemorrhagic shock, indicating the mechanism extends beyond the drop in preload and afterload alone.

Technical and analytical approach to biventricular pressure-volume loops in swine including a completely endovascular, percutaneous closed-chest large animal model

“…We have used these techniques in swine weighing up to 90 kg. 9 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 If swine weighing less than 40 kg are used, we recommend imaging their external iliac artery diameter to confirm that it will support instrumentation. 29 , 30 We chose the gender of the animals based on availability and cost, and ultimately, only male animals were included in the study.…”

Investigating the variability in pressure–volume relationships during hemorrhage and aortic occlusion

“…Currently, there is sparse research investigating cardiac performance during diastole in response to hemorrhage (38) first reported coronary artery measurements in response to REBOA and found that the total coronary flows were almost three times higher during a full aortic occlusion than baseline, and subsequently decreased with a partial occlusion, proportional to increases in E es . Then, Elansary et al (46) examined the directionality of coronary artery flow waveform and LV function in progressive levels of hemorrhagic shock and found that the coronary arteries spent a greater proportion of diastole in retrograde flow. The findings from these studies indicate that future investigations incorporating both LV function and coronary flow would lead to a more holistic understanding of the underlying cardiovascular physiology of hemorrhagic shock and EHC interventions.…”

Inhibition of integrin alpha v/beta 5 mitigates the protective effect induced by irisin in hemorrhage

“…The initial physiologic response to hemorrhage is the activation of the sympathetic nervous system, which regulates cardiac performance and vasoconstriction to maintain blood pressure and preserve the perfusion of essential organs ( Koyama et al, 1988 ; Skoog et al, 1985 ). This is closely associated with diminished cardiac function, multi-organ ischemia ( Elansary et al, 2022 ; Kvarstein et al, 2003 ), and a triggered inflammatory cascade ( Hierholzer et al, 1998 ). The inability to recover cardiac function following hemorrhage leads to cardiovascular collapse and mortality ( Chatpun and Cabrales, 2011 ).…”