Assessment of Dynamic Changes in Stressed Volume and Venous Return during Hyperdynamic Septic Shock

Abstract

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).

Relationship of Effective Circulating Volume with Sublingual Red Blood Cell Velocity and Microvessel Pressure Difference: A Clinical Investigation and Computational Fluid Dynamics Modeling

“…In our study with patients in a dynamic hemodynamic equilibrium, a Pmca value < 14 mmHg was correlated with higher RBC velocity, probably due to an increase in vascular capacitance and sublingual vessel diameter and/or an increase in heart efficiency. However, there must always be a limit under which decreases in Pmca and venous return impair microcirculatory blood flow [ 11 , 12 , 16 , 17 , 18 , 20 , 51 ]. On the contrary, a higher Pmca (> 14 mmHg) may be the result of excessive vasoconstriction, eventually resulting in hemodynamic incoherence and tissue hypoperfusion.…”

“…The association between the Pmca and Δp ranges in our study further enhances the potential of Pmca to serve as a hemodynamic coherence monitoring tool. Bedside estimation of Pmca can track the effective circulating volume [ 12 , 16 , 18 , 59 , 60 ], while a Pmca value of 14 mmHg may indicate an adequate balance between the macro- and microcirculatory perfusion. The post-hoc bootstrapping metrics in the present study strongly encourage the evaluation of our findings in larger studies.…”

“…Decreases in Pmcf and effective circulating volume could affect microvascular red blood cell (RBC) velocity, resulting in insufficient oxygen extraction ratio (O 2 ER) [ 16 , 24 , 25 ]. On the other hand, fluid or vasopressor administration may increase stressed volume (Pmcf), eventually increasing CO and changing RBC velocity [ 18 , 26 , 27 ]. Considering that CO is determined by venous return, we hypothesized that the effective circulating volume, and thus Pmca, is associated with microcirculatory perfusion and tissue oxygenation.…”

“…Other elegant studies have shown that hypoxia and hypercapnia increase mean circulatory filling pressure (Pmcf) and vascular capacitance [ 11 , 12 ], enhancing microcirculatory flow through a physiological adaptation to match oxygen delivery to demand [ 13 , 14 ]. These data could explain, in part, the vessel cluster synchronization in the microcirculatory blood flow of some organs, which changes depending on the condition of the vascular network and the blood pressure (hemodynamic coupling) [ 15 ], suggesting an interplay between effective circulating volume and tissue perfusion [ 11 , 13 , 14 , 16 , 17 , 18 ].…”

The interplay between ‘rest volume’, mean circulatory filling pressure, and cardiac output that drives venous return

“…in hyperdynamic septic shock, fluid and/or vasopressor resuscitation may improve venous return but not the efficiency of the heart. 3 Also, progressive hypoxaemic hypercapnia and acidosis cause a marked decrease of the vascular capacitance system, which significantly increases MCFP via translocation of blood volume to the fast transit time peripheral systemic circuit. 6 Notably, following cardiac arrest, blood flow exponentially falls but continues for approximately 5 min without chest compressions.…”