VExUS: common misconceptions, clinical use and future directions

Figures

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  Fig. 1. 1a: Intravascular volume is composed of unstressed volume that does not distend the vascular walls and stressed volume that distends the walls resulting in elastic recoil of the walls generating the MSFP. MSFP increases with increased stressed volume (where the walls are further distended) and decreased compliance (where the vessels become stiffer and unstressed volume is converted to stressed volume). 1b: The CVP depends on the cardiac efficiency and the MSFP. Venous return is driven by the difference in MSFP and the CVP. When CVP = MSFP venous return will be zero. Increases in the MSFP or decreases in the cardiac efficiency will increase CVP, but the CVP and cardiac output depends on the operating point where the venous return line and Frank-Starling curves intersect. V0= unstressed volume, Ve=stressed volume, Cs=systemic vascular compliance, Vr=resistance to venous return, VR= Venous Return

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  Fig. 2. 2a: A normovolemic person is infused with repeated boluses of crystalloid, thus raising the MSFP. Initially the response is to increase the VR with only small increases in the CVP. However, once the limit of RV compliance is reached the CVP and MSFP rapidly rise with little increase in VR. The rise in MSFP results in venous congestion of the organs and limits perfusion. 2b: Relationship of venous compliance. Initially, additional stressed volume raises the venous pressures minimally until the limits of compliance is reached. At that point the venous pressures rapidly rise with addition of even small amounts of volume

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  Fig. 3. An acute rise in RV afterload due to a pulmonary embolism causes a significant decrease in RV efficiency. The VR drops whilst the CVP rises. Any attempt at a volume challenge will most likely result in an increase in the CVP and MSFP without a significant increase in the VR

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  Fig. 4. An acute rise in systemic vascular compliance (without a change in volume) results in a decrease in MSFP, CVP, and VR. Administration of either a vasopressor or a crystalloid bolus will shift the MSFP toward normal. However, note that the original drop in MSFP was independent of actual volume, and was instead a result of a change in vascular compliance alone