Effects of norepinephrine on dynamic variables of fluid responsiveness during hemorrhage and after resuscitation in a pediatric porcine model

Abstract

Eight anesthetized piglets were studied at normovolemia, after stepwise blood withdrawal (25 ml x kg(-1)), after infusion of NE to restore mean arterial pressure (MAP), after NE titration was stopped and shed blood was retransfused and finally again after NE titration. Stroke volume (SV) was measured using a thermodilution pulmonary artery catheter. GEDV was measured by transpulmonary thermodilution. PPV and SVV were monitored continuously by pulse contour analysis. In response to NE administration during hemorrhage, MAP significantly increased (P < 0.01), PPV significantly decreased (P = 0.02), whereas SVV, SV and GEDV remained unchanged. After retransfusion, SVV and GEDV significantly correlated with volume induced percentage change in SV. This significant correlation was reversed after NE administration for SVV and persisted for GEDV. In conclusion, NE administration significantly affected PPV and SVV, whereas the volumetric variable GEDV remained unchanged.

Impact of epinephrine and norepinephrine on two dynamic indices in a porcine hemorrhagic shock model

“…In this regard, physicians should consider the present physiologic concept when interpreting PPV and SVV values in patients who receive vasopressors because usual thresholds (13%) 9 could be too high in this setting. 25,37,38 For instance, a truly hypovolemic patient may decrease PPV and SVV with the administration of NE; the physician could either inaccurately pursue vasopressor administration or interpret PPV and SVV decreases as an autotransfusion from unstressed to stressed blood volume, thus confirming the need for VE to restore unstressed blood volume. Giving fluids to these types of patients even if the PPV value is less than 13% would decrease vasopressor IV doses.…”

Dynamic Arterial Elastance as a Ventriculo-Arterial Coupling Index: An Experimental Animal Study

“…However, significant changes in contractility and arterial load may occur over longer periods of time. Moreover, clinical conditions such as the use of vasoactive therapy (Kubitz et al, 2008;Renner et al, 2009;Hadian et al, 2011;Monge Garcia et al, 2017a;de Courson et al, 2019;Wodack et al, 2019), acute hemorrhage (Berkenstadt et al, 2005;Renner et al, 2009), fluid administration (Kim and Pinsky, 2008;Monge Garcia et al, 2011;Cecconi et al, 2014;Monge Garcia et al, 2014;Seo et al, 2015), sepsis (Cherpanath et al, 2014) or pharmacological changes in contractility (Mesquida et al, 2011), may alter the interaction between PPV and SVV and therefore modify the eventual value of Ea dyn . In our study, PPV was significantly associated with changes in Ea and related to both TPR and C art , acting mostly as a peripheral factor, while SVV was associated with Ees, representing more as the central component of Ea dyn .…”

Effects of arterial load variations on dynamic arterial elastance: an experimental study

“…Considering both experimental groups, haemorrhage decreased SV from 2.9 (0.7) to 2.4 (0.5) ml (P<0.001), but did not affect CO [from 0.36 (0.11) to 0.34 (0.08) litre min À1 ; P¼0.59], because of a compensatory increase in HR [from 123 (28) to 143 (15) beats min À1 ; P<0.05]. Bleeding increased Ea dyn from 0.78 (0.23) to 0.95 (0.26) (P¼0.03).…”