Key result
Intravenous lipopolysaccharide-induced endotoxic septic shock increased dynamic arterial elastance from 0.73 to 1.70, which subsequently decreased following hemodynamic resuscitation.
Why the study?
Dynamic arterial elastance (Ea dyn) has been suggested as a surrogate of arterial load, but the effects of endotoxic septic shock and hemodynamic resuscitation on Ea dyn remained to be determined.
Does endotoxic septic shock and hemodynamic resuscitation alter dynamic arterial elastance in an experimental rabbit model?
Does endotoxic septic shock and hemodynamic resuscitation alter dynamic arterial elastance in an experimental rabbit model?
In an experimental rabbit model, dynamic arterial elastance increased during endotoxic septic shock and decreased with hemodynamic resuscitation, effectively tracking cardiovascular efficiency.
Answers are grounded in this paper and cite their sources.
Ea dyn tracks efficiency in rabbit endotoxic shock; hypothesis-generating for human sepsis trials.
Abstract Background: Dynamic arterial elastance (Ea dyn ), the ratio between pulse pressure variation (PPV) and stroke volume variation (SVV), has been suggested as a functional parameter that is a surrogate of arterial load. We aimed to determine the effects of endotoxic septic shock and hemodynamic resuscitation on Ea dyn . Results: Experimental randomized study in a university animal research laboratory with 18 New Zealand rabbits. Animals received placebo (SHAM, n=6) or intravenous lipopolysaccharide (LPS, Escherichia coli serotype 055:B5, 1 mg·kg -1 ) with or without (EDX-R, n=6; EDX-NR, n=6) hemodynamic resuscitation (fluid bolus of 20 ml·kg -1 and norepinephrine for restoring mean arterial pressure). Continuous arterial pressure and aortic blood flow measurements were obtained simultaneously. Cardiovascular efficiency was evaluated by the oscillatory power fraction (%Osc: oscillatory work / left ventricular (LV) total work) and the energy efficiency ratio (EER = LV total work/cardiac output). The LPS-induced endotoxic shock produced a hyperdynamic shock with high cardiac output and arterial hypotension. Ea dyn increased in septic animals (from 0.73 to 1.70; p=0.012) and dropped after hemodynamic resuscitation. Ea dyn was related with the %Osc and EER [estimates: -0.101 (-0.137 – -0.064) and -9.494 (-11.964 – -7.024); p<0.001, respectively]. So, the higher the Ea dyn, the better the cardiovascular efficiency (lower %Osc and EER). Conclusions: In this experimental model, Ea dyn increased during endotoxic septic shock and decreased with hemodynamic resuscitation. Sepsis resulted in a reduced oscillatory power fraction and lowered EER, reflecting a better cardiovascular efficiency that was tracked by Ea dyn . Ea dyn could be a potential index of cardiovascular efficiency during septic shock.
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García et al. (2020) studied Endotoxic septic shock (n=18). Intravenous lipopolysaccharide (LPS) and hemodynamic resuscitation vs. Placebo (SHAM) was evaluated on Dynamic arterial elastance (Eadyn) (p=0.012). Intravenous lipopolysaccharide-induced endotoxic septic shock increased dynamic arterial elastance from 0.73 to 1.70, which subsequently decreased following hemodynamic resuscitation.
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