Hopson J R, Rea R F, Kienzle M G
Department of Internal Medicine, University of Iowa, Iowa City.
Herz. 1993 Jun;18(3):164-74.
Orthostatic hypotension and related neurologic symptoms are frequently encountered in clinical practice. The maintenance of appropriate blood pressure and heart rate responses upon assuming the upright posture are dependent upon: 1. intact mechanical (venous valves) mechanisms, 2. functioning arterial and cardiopulmonary baroreceptors, 3. normal peripheral neural pathways, 4. normal central neural integration, and 5. appropriate neurohormonal secretion. Dysfunction at one or more of these loci may facilitate the occurrence of orthostatic hypotension and syncope. In general, the mechanisms of orthostatic hypotension may be divided into three categories. In the first category, processes interfere with normal compensatory responses to upright posture. Examples of this mechanism include age related autonomic changes, diabetic neuropathy and central nervous system disease such as Shy-Drager syndrome. The second principal mechanism involves overwhelming otherwise normal reflexes by an intense orthostatic stimulus. An obvious example of this mechanism is syncope related to hemorrhage. A final category of orthostatic hypotension relates to interference with reflex responses by drugs that may limit vasoconstriction, heart rate or cardiac output adjustments or exaggerate venous pooling. These are commonly used medications such as vasodilators, beta-adrenergic blockers and nitrates. The treatment of orthostatic hypotension revolves around the recognition of underlying causes or contributing factors amenable to correction or avoidance. Other helpful treatment options include nocturnal head-up tilting and mineralocorticoids, both of which help to expand blood volume. Many other therapeutic agents have been tried in small and selected patient populations, often with disappointing results. While many of the drugs available (phenylephrine, ephedrine, tyramine, dihydroergotamine) can improve upright blood pressure, side effects are common, and supine hypertension is problematic in many patients. Interventions of this type should be carefully initiated in a monitored setting. The carotid sinus is an important component of a neural control system responsible for heart rate and blood pressure homeostasis. Excessive heart rate and blood pressure responses to distortion of the carotid sinus are the basis for the carotid sinus syndrome (CSS). Patients with CSS tend to be elderly males and local pathology in the neck is frequently involved. Atherosclerotic coronary artery disease and hypertension are important clinical correlates. Two major categories of carotid sinus hypersensitivity (CSH) are recognized: cardioinhibitory and vasodepressor. Cardioinhibitory CSH is the most common, and in its purest form consists of sinus bradycardia or arrest, asystole or AV block during carotid sinus massage. This vagally-mediated response is eliminated by atropine. Cardiac pacing is nearly universally successful in preventing severe symptoms.(ABSTRACT TRUNCATED AT 400 WORDS)
直立性低血压及相关神经症状在临床实践中经常遇到。在采取直立姿势时维持适当的血压和心率反应取决于：1. 完整的机械（静脉瓣膜）机制；2. 正常运作的动脉和心肺压力感受器；3. 正常的外周神经通路；4. 正常的中枢神经整合；5. 适当的神经激素分泌。这些位点中一个或多个出现功能障碍可能会促使直立性低血压和晕厥的发生。一般来说，直立性低血压的机制可分为三类。在第一类中，一些过程会干扰对直立姿势的正常代偿反应。这种机制的例子包括与年龄相关的自主神经变化、糖尿病性神经病变以及中枢神经系统疾病，如夏伊 - 德雷格综合征。第二个主要机制涉及强烈的直立性刺激压倒原本正常的反射。这种机制的一个明显例子是与出血相关的晕厥。直立性低血压的最后一类与药物对反射反应的干扰有关，这些药物可能会限制血管收缩、心率或心输出量的调节，或加剧静脉淤血。这些通常是常用药物，如血管扩张剂、β - 肾上腺素能阻滞剂和硝酸盐。直立性低血压的治疗围绕识别可纠正或避免的潜在病因或促成因素展开。其他有用的治疗选择包括夜间头高位倾斜和使用盐皮质激素，两者都有助于扩充血容量。许多其他治疗药物已在小部分特定患者群体中试用，结果往往令人失望。虽然现有的许多药物（去氧肾上腺素、麻黄碱、酪胺、双氢麦角胺）可以改善直立位血压，但副作用很常见，而且许多患者存在仰卧位高血压问题。这类干预应在有监测的环境中谨慎启动。颈动脉窦是负责心率和血压稳态的神经控制系统的重要组成部分。对颈动脉窦扭曲的过度心率和血压反应是颈动脉窦综合征（CSS）的基础。CSS患者往往是老年男性，颈部局部病变经常累及。动脉粥样硬化性冠状动脉疾病和高血压是重要的临床相关因素。公认的颈动脉窦过敏（CSH）主要有两类：心脏抑制型和血管减压型。心脏抑制型CSH最为常见，其最纯粹的形式包括在颈动脉窦按摩期间出现窦性心动过缓或停搏、心搏停止或房室传导阻滞。这种由迷走神经介导的反应可被阿托品消除。心脏起搏在预防严重症状方面几乎普遍成功。（摘要截断于400字）
