Abstract：
Orthostatic hypotension (OH) is a form of orthostatic intolerance (OI) and a key physiological indicator of autonomic dysfunction that is associated with an increased risk of major cerebrocardiovascular events. Symptoms of cerebral hypoperfusion have been reported in patients with OH, which worsens symptoms and increases the risk of syncope. Since pharmacological interventions increase blood pressure (BP) independent of posture and do not restore normal baroreflex control, nonpharmacological treatments are considered the foundation of OH management. While reductions in cerebral blood flow velocity (CBFv) during orthostatic stress are associated with a decrease in end-tidal CO2 (EtCO2) and hypocapnia in patients with OI, their contribution to the severity of OH is not well understood. These measures have been physiological targets in a wide variety of biofeedback interventions. This study explored the relationship between cardiovascular autonomic control, EtCO2 and cerebral hypoperfusion in patients (N = 72) referred for OI. Patients with systolic OH were more likely to be male, older, demonstrate reduced adrenal and vagal baroreflex sensitivity, and reduced cardiovagal control during head-up tilt (HUT) than patients without systolic OH. Greater reduction in CBFv during HUT was associated with a larger reduction in ETCO2 and systolic BP during HUT. While deficits in cardiovascular autonomic control played a more important role in systolic OH, reduced EtCO2 was a major contributor to orthostatic cerebral hypoperfusion. These findings suggest that biofeedback treatments targeting both the autonomic nervous system and EtCO2 should be part of nonpharmacological interventions complementing the standard of care in OH patients with symptoms of cerebral hypoperfusion.
摘要：
体位性低血压（OH）是体位性不耐受（OI）的一种形式，是自主神经功能障碍的关键生理指标，与主要脑血管事件的风险增加有关。已经报道了OH患者的脑低灌注症状，这会使症状恶化并增加晕厥的风险。由于药物干预增加血压（BP）与姿势无关，并且不能恢复正常的压力反射控制，非药物治疗被认为是OH管理的基础。虽然体位应激期间脑血流速度（CBFv）的降低与OI患者潮气末CO2（EtCO2）和低碳酸血症的降低有关，它们对OH严重程度的贡献还没有得到很好的理解。这些措施已成为各种生物反馈干预措施中的生理目标。这项研究探讨了心血管自主神经控制之间的关系，OI患者(N=72)的EtCO2和脑灌注不足。收缩期OH患者更可能是男性，年长的,显示肾上腺和迷走神经压力反射敏感性降低，与没有收缩期OH的患者相比，平头倾斜（HUT）期间的心迷走控制减少。HUT期间CBFv的更大减少与HUT期间ETCO2和收缩压的更大减少相关。虽然心血管自主神经控制缺陷在收缩期OH中起着更重要的作用，降低的EtCO2是体位性脑灌注不足的主要原因.这些发现表明，针对自主神经系统和EtCO2的生物反馈治疗应作为非药物干预措施的一部分，以补充具有脑灌注不足症状的OH患者的护理标准。
