Chalkias Athanasios, Laou Eleni, Papagiannakis Nikolaos, Spyropoulos Vaios, Kouskouni Evaggelia, Theodoraki Kassiani, Xanthos Theodoros
Department of Anesthesiology, Faculty of Medicine, University of Thessaly, 41500 Larisa, Greece.
Outcomes Research Consortium, Cleveland, OH 44195, USA.
J Pers Med. 2022 Apr 29;12(5):724. doi: 10.3390/jpm12050724.
The present work investigated the dynamic changes in stressed volume (Vs) and other determinants of venous return using a porcine model of hyperdynamic septic shock. Septicemia was induced in 10 anesthetized swine, and fluid challenges were started after the diagnosis of sepsis-induced arterial hypotension and/or tissue hypoperfusion. Norepinephrine infusion targeting a mean arterial pressure (MAP) of 65 mmHg was started after three consecutive fluid challenges. After septic shock was confirmed, norepinephrine infusion was discontinued, and the animals were left untreated until cardiac arrest occurred. Baseline Vs decreased by 7% for each mmHg decrease in MAP during progression of septic shock. Mean circulatory filling pressure (Pmcf) analogue (Pmca), right atrial pressure, resistance to venous return, and efficiency of the heart decreased with time (p < 0.001 for all). Fluid challenges did not improve hemodynamics, but noradrenaline increased Vs from 107 mL to 257 mL (140%) and MAP from 45 mmHg to 66 mmHg (47%). Baseline Pmca and post-cardiac arrest Pmcf did not differ significantly (14.3 ± 1.23 mmHg vs. 14.75 ± 1.5 mmHg, p = 0.24), but the difference between pre-arrest Pmca and post-cardiac arrest Pmcf was statistically significant (9.5 ± 0.57 mmHg vs. 14.75 ± 1.5 mmHg, p < 0.001). In conclusion, the baseline Vs decreased by 7% for each mmHg decrease in MAP during progression of hyperdynamic septic shock. Significant changes were also observed in other determinants of venous return. A new physiological intravascular volume existing at zero transmural distending pressure was identified, termed as the rest volume (Vr).
本研究使用高动力性感染性休克猪模型,调查了应激容量(Vs)及静脉回流其他决定因素的动态变化。对10头麻醉猪诱导败血症,在诊断出败血症诱导的动脉低血压和/或组织灌注不足后开始液体冲击。在连续3次液体冲击后,开始输注去甲肾上腺素以将平均动脉压(MAP)维持在65 mmHg。确认感染性休克后,停止输注去甲肾上腺素,动物不再接受治疗直至发生心脏骤停。在感染性休克进展过程中,MAP每降低1 mmHg,基线Vs下降7%。平均循环充盈压(Pmcf)类似物(Pmca)、右心房压力、静脉回流阻力和心脏效率随时间下降(所有p<0.001)。液体冲击未改善血流动力学,但去甲肾上腺素使Vs从107 mL增加至257 mL(140%),MAP从45 mmHg增加至66 mmHg(47%)。基线Pmca与心脏骤停后Pmcf无显著差异(14.3±1.23 mmHg对14.75±1.5 mmHg,p = 0.24),但心脏骤停前Pmca与心脏骤停后Pmcf之间的差异具有统计学意义(9.5±0.57 mmHg对14.75±1.5 mmHg,p<0.001)。总之,在高动力性感染性休克进展过程中,MAP每降低1 mmHg,基线Vs下降7%。在静脉回流的其他决定因素中也观察到显著变化。确定了一种在零跨壁扩张压力下存在的新的生理性血管内容量,称为静息容量(Vr)。