Abstract
Extracorporeal membrane oxygenation (ECMO) is a life-saving technique that is widely being used in centers throughout the world. However, there is a paucity of literature surrounding the mechanisms affecting cerebral physiology while on ECMO. Studies have shown alterations in cerebral blood flow characteristics and subsequently autoregulation. Furthermore, the mechanical aspects of the ECMO circuit itself may affect cerebral circulation. The nature of these physiological/pathophysiological changes can lead to profound neurological complications. This review aims at describing the changes to normal cerebral autoregulation during ECMO, illustrating the various neuromonitoring tools available to assess markers of cerebral autoregulation, and finally discussing potential neurological complications that are associated with ECMO.
Highlights
Introduction e purpose ofExtracorporeal membrane oxygenation (ECMO) is to provide adequate oxygenated blood to the tissues by bypassing either the pulmonary or cardiopulmonary system in severe respiratory failure and/or cardiac failure, respectively. e ECMO circuit essentially consists of 4 components: (1) an inflow cannula which drains blood from the venous system, (2) a pump which provides flow in the circuit, (3) an oxygenator, which is responsible for oxygenating the venous blood, and (4) an outflow cannula which delivers the warmed oxygenated blood back into the venous or arterial system [1, 2]
Cerebral autoregulation is the ability of cerebral arterioles to maintain steady cerebral blood flow (CBF) over a varying range of mean arterial pressures (MAP) [4]. is is termed as cerebral pressure autoregulation and can be classically described using the Lassen curve [5], where MAP on the x-axis is plotted against CBF on the y-axis (Figure 1)
A steady CBF is achieved by vasodilation and vasoconstriction of cerebral arterioles which in turn are influenced by neurogenic, myogenic, and metabolic mechanisms responding to changes in MAP [6]
Summary
Cerebral autoregulation is the ability of cerebral arterioles to maintain steady cerebral blood flow (CBF) over a varying range of mean arterial pressures (MAP) [4]. is is termed as cerebral pressure autoregulation and can be classically described using the Lassen curve [5], where MAP on the x-axis is plotted against CBF on the y-axis (Figure 1). A steady CBF is achieved by vasodilation and vasoconstriction of cerebral arterioles which in turn are influenced by neurogenic, myogenic, and metabolic mechanisms responding to changes in MAP [6]. Metabolic regulation is related to changes in perineuronal concentrations of CO2, O2, K+, Ca2+, H+, and adenosine [9,10,11,12,13] It should be kept in mind, that there is likely segmental and regional heterogeneity between the pial and parenchymal arteries and arterioles and their response to the above regulatory factors which can result in varying levels of CBF over the same range of CPP in different regions of the brain [8, 14,15,16]. Similar aberrations in cerebral autoregulation have been found in ischemic stroke [18, 25,26,27], intracerebral hemorrhage [28,29,30], and subarachnoid hemorrhage [31,32,33]
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