Watershed phenomena during extracorporeal life support and their clinical impact: a systematic in vitro investigation

Abstract

Aims Extracorporeal life support (ECLS) during acute cardiac failure restores haemodynamic stability and provides life-saving cardiopulmonary support. Unfortunately, all common cannulation strategies and remaining pulmonary blood flow increase left-ventricular afterload and may favour pulmonary congestion. The resulting disturbed pulmonary gas exchange and a residual left-ventricular action can contribute to an inhomogeneous distribution of oxygenated blood into end organs. These complex flow interactions between native and artificial circulation cannot be investigated at the bedside: only an in vitro simulation can reveal the underlying activities. Using an in vitro mock circulation loop, we systematically investigated the impact of heart failure, extracorporeal support, and cannulation routes on the formation of flow phenomena and flow distribution in the arterial tree. Methods and results The mock circulation loop consisted of two flexible life-sized vascular models (aorta and vena cava) driven by two paracorporeal assist devices, resistance elements, and compliance reservoirs to mimic the circulatory system. Several large-bore antegrade and retrograde access ports allowed connection to an ECLS system for extracorporeal support. With four degrees of extracorporeal support-that for cardiac failure, early recovery, late recovery, and weaning-we investigated aortic blood flow velocity, blood flow, and mixing zones using colour-coded Doppler ultrasound in the aorta and its corresponding branches. Full retrograde extracorporeal support (3-4 L/min) perfused major portions of the aorta but did not reach the supra-aortic branches and ascending aorta, resulting in an area in the thoracic aorta demonstrating nearly stagnant blood flow velocities during cardiogenic shock and early recovery (0 ± 4 cm/s; À10 ± 15 cm/s, respectively) confined by two watersheds at the aortic isthmus and renal artery origin. Even increased ECLS flow was unable to shift the watershed towards the aortic arch. Antegrade support resulted in homogeneous flow distribution during all stages of cardiac failure but created a markedly negative flow vector in the ascending aorta during cardiogenic shock and early recovery with increased afterload. Conclusions Our systematic fluid-mechanical analysis confirms the clinical assumption that despite restoring haemodynamic stability, extracorporeal support generates an inhomogeneous distribution of oxygenated blood with an inadequate supply to end organs and increased left-ventricular afterload with absent ventricular unloading. End-organ supply may be monitored by near-infrared spectroscopy, but an obviously non-controllable watershed emphasizes the need for additional measures: pre-pulmonary oxygenation with a veno-arterial-venous ECLS configuration can allow a transpulmonary passage of oxygenated blood, providing improved end-organ supply.

Microcirculatory Response to Changes in Venoarterial Extracorporeal Membrane Oxygenation Pump Flow: A Prospective Observational Study

“…The decreased preload and increased afterload may reduce the patient's own cardiac output. In patients with VA-ECMO, head and brain perfusions are determined according to the balance between VA-ECMO pump flow and the patient's own cardiac output (34,35). Further studies are required to investigate whether sublingual microcirculation is correlated with cerebral blood flow in patients with VA-ECMO.…”

Simulation of Fluid-Structure Interaction in Extracorporeal Membrane Oxygenation Circulatory Support Systems

“…In this cannulation approach, ECMO provides continuous retrograde perfusion into the distal aorta which then collides with pulsatile antegrade perfusion from the heart to create a dynamic watershed region with mixing of the colliding flows 17,18 . The complex hybrid circulation generated by dual perfusion from the ECMO circuit and the heart, termed here as the ECMO:failing heart circulation 18 , differs significantly from physiologic ventriculo-vascular interactions as the left ventricle ejects against continuous retrograde filling of the aorta.…”

Impact of the inspiratory oxygen fraction on the cardiac output during jugulo-femoral venoarterial extracorporeal membrane oxygenation in the rat

“…Furthermore, the LVEDV did not differ between the experimental groups, implying that the ECMO-induced watershed has not increased the afterload or moved towards the heart. Moreover, experiments with an in-vitro mock circulation loop demonstrated that an increased ECMO flow was unable to shift the watershed towards the aortic arch [ 30 ]. In summary, this study underlines the importance to avoid apnea during awake V-A ECMO with femoral cannulation in order to lower the risk for pulmonary and coronary hypoxia.…”