Abstract
OBJECTIVES
Limb ischaemia during extracorporeal life support (ECLS) using femoral artery cannulation is frequently observed even in patients with regular vessel diameters and without peripheral arterial occlusive disease. We investigated underlying pathomechanisms using a virtual fluid-mechanical simulation of the human circulation.
METHODS
A life-sized model of the human aorta and major vascular branches was virtualized using 3-dimensional segmentation software (Mimics, Materialise). Steady-state simulation of different grades of cardiac output (0–100%) was performed using Computational Fluid Dynamics (CFX, ANSYS). A straight cannula [virtualized 16 Fr (5.3 mm)] was inserted into the model via the left common femoral artery. The ECLS flow was varied between 1 and 5 l/min. The pressure boundary conditions at the arterial outlets were selected to demonstrate the downstream vascular system. Qualitative and quantitative analyses concerning flow velocity and direction were carried out in various regions of the model.
RESULTS
During all simulated stages of reduced cardiac output and subsequently adapted ECLS support, retrograde blood flow originating from the ECLS cannula was observed from the cannulation site up to the aortic bifurcation. Analysis of pressure showed induction of zones of negative pressure close to the cannula tip, consistent with the Bernoulli principle. Depending on cannula position and ECLS flow rate, this resulted in negative flow from the ipsilateral superficial femoral artery or the contralateral internal iliac artery. The antegrade flow to the non-cannulated side was generally greater than that to the cannulated side.
CONCLUSIONS
The cannula position and ECLS flow rate both influence lower limb perfusion during femoral ECLS. Therefore, efforts to optimize the cannula position and to avoid limb malperfusion, including placement of a distal perfusion cannula, should be undertaken in patients treated with ECLS.
Femoral artery cannulation combined with axillary artery cannulation is safe for Stanford type A aortic dissection
