Hypovolemia in Extracorporeal Life Support Can Lead to Arterial Gaseous Microemboli

Abstract

Next to severely decreased pump flow, hypovolemia in extracorporeal life support (ELS) can result in subatmospheric venous line pressure. Such pressure may lead to degassing and resultant gaseous microemboli (GME), with potential changes in neurological clinical outcome. CME activity resulting from degassing was investigated in relation to subatmospheric venous line pressure, partial oxygen pressure (pO2 ), and hematocrit in a model of a centrifugal pump-based circuit for long-term ELS. Additionally, a device that provides instantaneous volume buffer capacity during hypovolemia was evaluated in relation to GME appearance. An exponential relationship was found between decreasing venous line pressure and GME downstream of the centrifugal pump (P = 0.001). Arterial bubble activity appeared at subatmospheric venous line pressures of -200 mm Hg and less. A rising (pO2 ) increased formation of GME (P = 0.05). A rise in hematocrit, in contrast, did not affect embolic activity (P = 0.22). With simulated hypovolemia, volume buffer capacity added to the venous line dampened fluctuations of venous line pressure by approximately 40%, but a significant reduction in GME formation could not be found (P = 0.22). Moreover, the device enabled a 14% higher support flow. With ELS flow being related to patient volume status, hypovolemia can diminish support. A coherent decrease of venous line pressure triggers degassing of blood-dissolved gases and causes arterial GME, which can become massive during persistent conditions of limited venous return. Incorporation of a volume buffer capacity device into the extracorporeal support circuit enables a higher and more stable support flow in critically low patient filling.