血管迷走神经性晕厥（part1）【每周一问】NO.54
发布日期：2006-08-02 15:03 文章来源：丁香园
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关键词： 血管迷走神经性晕厥
病理生理
贝-亚反射/贝-贾反射/Bezold-Jarisch反射
机制/机理
点击次数：
2. What is the pathophysiology of the vasovagal response?
3. What is the Bezold-Jarisch reflex?
4. What other mechanism may be responsible for vasovagal response?
1. 血管迷走神经性晕厥有什么共同点？
2. 血管迷走神经性晕厥的病理生理是什么？
3. 什么是Bezold-Jarisch反射（贝-亚反射或贝-贾反射）？
4. 血管迷走神经性晕厥的其他机制有哪些？
参考答案：
1.血管迷走神经性晕厥有什么共同点？
血管迷走神经性晕厥为晕厥的最常见类型，每年美国发生晕厥的患者大约有100万，其中40%为血管迷走神经性晕厥[1]。Calkins等[2]强调，虽然血管迷走性（也叫血管减压性）晕厥可临床诊断（后几周将讨论此问题），但是在该人群中不必要的诊断试验的费用达到了16，000美元[2]。
2.血管迷走神经性晕厥的病理生理是什么？
虽然不能充分理解，但是如Foster[3]在1888年提出，血管迷走神经性晕厥的机制被认为是由于复杂的心动过缓导致脑血流灌注不足以维持意识清楚。今天，用于解释和触发血管迷走神经性晕厥的模型是Bezold-Jarisch反射（命名于两位独立工作的生理学家，主要研究心室对容量的反应）[4]。
3.什么是Bezold-Jarisch反射（贝-亚反射或贝-贾反射）？
Bezold-Jarisch反射（BJR）是一种神经心源性反射，通过心脏机械感受器激活启动而发生作用[4]。BJR显示，心室容量减少激活位于心室下后壁的牵张感受器。心室这种矛盾的伸缩通过神经交通发送冲动到中枢神经系统。这种交通主要包括迷走神经活动度，导致副交感神经活性的显著增加，最终产生特定个体出现血管迷走神经性晕厥三联症：血管舒张、心动过缓、意识消失[1]。
当前关于这些机制的最流行理论来自于控制出血[5]或内脏传入神经受到刺激[6]的动物研究。
4.血管迷走神经性晕厥的其他机制有哪些？
虽然Bezold-Jarisch反射是血管迷走神经性晕厥的主要机制，但是很多中枢神经系统递质也极可能发挥作用。这些递质包括5-羟色胺、腺苷和阿片类物质（即麻醉中常给的药物）。有趣的是，纳洛酮，一种阿片受体拮抗剂，也有增强压力反射机制的作用[7]，这表明，阿片类物质可抑制这些压力反射介导的迷走反射。此外，在情绪紧张阶段（比如麻醉医生在静脉导管植入时静脉穿刺困难时导致），前脑和下丘脑也在BJR中发挥调节作用[1]。
How common is vasovagal syncope?
Representing the most common type of syncope, vasovagal syncope is believed responsible for 40% of the approximately one million patients evaluated annually in the United States for syncope (1). Calkins et al. (2) noted that although the diagnosis of vasovagal (also called vasodepressor) syncope can be established clinically (to be discussed later this week), up to $16,000 (in 1991 dollars) of diagnostic testing is often performed unnecessarily on this patient population (2).
What is the pathophysiology of the vasovagal response?
Although incompletely understood, the mechanism of the vasovagal response, as initially proposed by Foster in 1888 (3), is believed to be due to profound bradycardia leading to diminished cerebral perfusion inadequate to maintain consciousness. Today, the model utilized to explain and trigger vasovagal syncope is the Bezold-Jarisch reflex (named after the two notable physiologists who worked independently to understand ventricular responses to volume) (4).
What is the Bezold-Jarisch reflex?
The Bezold-Jarisch reflex (BJR) is a neurocardiogenic reflex initiated by activation of the cardiac mechanoreceptors (4). The BJR suggests that decreased ventricular volume activates stretch receptors in the inferoposterior ventricular wall. This (lack of) stretching paradoxically increases neural traffic to the central nervous system. This traffic, composed mostly of vagal nerve activity, leads to a marked increase in parasympathetic activity, ultimately resulting in certain individuals in the vasovagal syncope triad of vasodilation, bradycardia, and loss of consciousness (1).
Most of the current knowledge into these mechanisms have been derived from investigations in animals subjected to controlled hemorrhage (5) or stimulation of visceral afferent nerves .
What other mechanism may be responsible for vasovagal response?
Although the Bezold-Jarisch reflex is the leading mechanism sited for vasovagal syncope, a number of central nervous system modulators most likely play a role. These include serotonin, adenosine, and opioids (i.e. modulators commonly affected or given during anesthesia). Interestingly, naloxone, an opioid receptor antagonist, has been noted to enhance the baroreflex mechanism (7), suggesting that opioids can blunt these baroreflex-mediated vagal responses. In addition, during emotional stress, such as that induced by an anesthesiologist involved in zealous chase for an elusive vein with an intravenous catheter, the forebrain and hypothalamus may play modulating roles on the BJR (1).
Question Author: Lawrence Tsen, MD, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School
References:
1. Fenton AM, Hammill SC, Rea RF, Low PA, Shen WK. Vasovagal Syncope. Ann Intern Med. 2000;133(9):714-725.
2. Calkins H, Byrne M, el-Atassi R, et al. The economic burden of unrecognized vasodepressor syncope. Am J Med 1993;95(5):473-9.
3. Foster M. A text book of physiology. 5th ed. London; Macmilan, 1890.
4. Stienstra R. Mechanisms behind and treatment of sudden, unexpected circulatory collapse during central neuraxis blockade. Acta Anaesthesiol Scand. 2000;44:965-71.
5. White CM, Chow MS, Fan C, Kluger J, Bazunga M. Efficacy of intravenous granisetron in suppressing the bradycardia and hypotension associated with a rabbit model of the Bezold-Jarisch reflex. J Clin Pharmacol 1998;38(2):172-7.
6. O'Cain PA, Hletko SB, Ogden BA, Varner KJ. Cardiovascular and sympathetic responses and reflex changes elicited by MDMA. Physiol Behav. 2000;70(1-2):141-8.
7. Schobel HP, Oren RM, Mark AL, Ferguson DW. Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans. Circ Res 1992;70(1):172-83.
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