Taylor K M
Department of Surgery, National Heart and Lung Institute, Hammersmith Hospital, London, England.
Ann Thorac Surg. 1998 Nov;66(5 Suppl):S20-4; discussion S25-8. doi: 10.1016/s0003-4975(98)00970-9.
The spectrum of approaches to the issue of brain injury in cardiac surgical practice ranges from refusal to acknowledge that the problem exists to an overemphasis on cerebral risks that can unduly frighten patients. An appropriate approach to therapeutic and preventive strategies requires a fitting sense of proportion and an understanding of the mechanisms of cerebral injury.
This article reviews the incidence and severity of cerebral injury during cardiopulmonary bypass, the identification of high-risk patients, and the mechanisms of injury, including hypoperfusion, microemboli, and inflammatory response. It discusses the influences of alpha-stat and pH-stat strategies on cerebral blood flow during cardiopulmonary bypass; the use of retinal angiography to image the retinal circulation, thus providing a window on the cerebral microcirculation during bypass; magnetic resonance imaging evidence of an inflammatory response in the brain during bypass; and current efforts to gain better understanding of the molecular mechanisms involved in the inflammatory response.
The current incidence of stroke during cardiopulmonary bypass is somewhat lower than in the 1980s but still remains a significant problem. Levels of cognitive impairment also are unacceptably high. Recognized predictors enable us to identify patients at particularly high risk of stroke. Hypertensive patients are particularly susceptible to ischemic injury during bypass and should be perfused at mean perfusion pressures higher than those for normotensive patients. Under conditions of hypothermia, a pH-stat strategy causes loss of cerebral blood flow autoregulation, and the cerebral blood flow becomes pressure-passive. With both the pH-stat and alpha-stat strategies, cooling of the patient greatly increases the flow to metabolism ratio of the cerebral blood flow; however, this luxury perfusion brings to the brain not just an excess supply of oxygen but also an increased quantity of microemboli. Current investigative efforts are focused on the endothelial cell-leukocyte adhesion cascade, attempting to characterize beta2 and beta1 adhesion molecule expression in patients undergoing cardiac surgery. Hammersmith Hospital is about to complete a study of the effects of high-dose aprotinin on the inflammatory response pattern and on cerebral infarction.
Further progress in the development of therapeutic and preventive strategies with respect to cerebral injury during cardiac bypass depends on an increase in the understanding of the mechanisms involved. Current strategies should include optimizing cerebral perfusion and minimizing macroembolic and microembolic damage. The possibility of modifying the systemic inflammatory response is the most interesting challenge of the next few years.
在心脏外科手术中，对于脑损伤问题的处理方式多种多样，从拒绝承认该问题的存在到过度强调脑风险，这可能会过度惊吓患者。制定合适的治疗和预防策略需要恰当的权衡意识以及对脑损伤机制的理解。
本文回顾了体外循环期间脑损伤的发生率和严重程度、高危患者的识别以及损伤机制，包括低灌注、微栓子和炎症反应。讨论了α-stat和pH-stat策略对体外循环期间脑血流量的影响；利用视网膜血管造影对视网膜循环成像，从而为体外循环期间的脑微循环提供一个窗口；体外循环期间大脑炎症反应的磁共振成像证据；以及目前为更好地理解炎症反应中涉及的分子机制所做的努力。
目前体外循环期间中风的发生率比20世纪80年代有所降低，但仍然是一个重大问题。认知障碍水平也高得令人难以接受。已确认的预测因素使我们能够识别出中风风险特别高的患者。高血压患者在体外循环期间特别容易受到缺血性损伤，应在高于正常血压患者的平均灌注压下进行灌注。在低温条件下，pH-stat策略会导致脑血流量自动调节功能丧失，脑血流量变为压力被动型。采用pH-stat和α-stat策略时，患者体温降低会大大增加脑血流量的流量与代谢率之比；然而，这种过度灌注不仅给大脑带来了过量的氧气供应，还增加了微栓子的数量。目前的研究工作集中在内皮细胞-白细胞黏附级联反应，试图确定心脏手术患者β2和β1黏附分子的表达特征。哈默史密斯医院即将完成一项关于大剂量抑肽酶对炎症反应模式和脑梗死影响的研究。
在心脏搭桥手术期间脑损伤的治疗和预防策略方面取得进一步进展取决于对相关机制的理解的增加。当前的策略应包括优化脑灌注并尽量减少大栓子和微栓子损伤。调节全身炎症反应的可能性是未来几年最有趣的挑战。
