The Effects of Vasoconstriction and Volume Expansion on Veno-Arterial ECMO Flow.

Werner Möller, Per; Hana, Anisa; Heinisch, Paul Philipp; Liu, Shengchen; Djafarzadeh, Siamak; Hänggi, Matthias; Bloch, Andreas; Takala, Jukka; Jakob, Stephan; Berger, David (2019). The Effects of Vasoconstriction and Volume Expansion on Veno-Arterial ECMO Flow. Shock, 51(5), pp. 650-658. Lippincott Williams & Wilkins 10.1097/SHK.0000000000001197

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BACKGROUND

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is gaining widespread use in the treatment of severe cardiorespiratory failure. Blood volume expansion is commonly used to increase ECMO flow (QECMO), with risk of positive fluid balance and worsening prognosis. We studied the effects of vasoconstriction on recruitment of blood volume as an alternative for increasing QECMO, based on the concepts of venous return.

METHODS

In a closed chest, centrally cannulated porcine preparation (n = 9) in ventricular fibrillation and VA-ECMO with vented left atrium, mean systemic filling pressure (MSFP) and venous return driving pressure (VRdP) were determined in Euvolemia, during Vasoconstriction (norepinephrine 0.05, 0.125 and 0.2 μg/kg/min) and following Volume Expansion (3 boluses of 10 mL/kg Ringer's lactate). Maximum achievable QECMO was examined.

RESULTS

Vasoconstriction and Volume Expansion both increased maximum achievable QECMO, delivery of oxygen (DO2) and MSFP, but right atrial pressure increased in parallel. VRdP did not change. The vascular elastance curve was shifted to the left by Vasoconstriction, with recruitment of stressed volume. It was shifted to the right by Volume Expansion with direct expansion of stressed volume. Volume Expansion decreased resistance to venous return and pump afterload.

CONCLUSIONS

In a circulation completely dependent on ECMO support, maximum achievable flow directly depended on the vascular factors governing venous return - i.e. closing conditions, stressed vascular volume and the elastance and resistive properties of the vasculature. Both treatments increased maximum achievable ECMO flow at stable DO2, via increases in stressed volume by different mechanisms. Vascular resistance and pump afterload decreased with Volume Expansion.

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