Division of Neurology, Autonomic Neuro Lab, Scripps Clinic, 9898 Genesee Ave., La Jolla, CA, 92037, USA.
Appl Psychophysiol Biofeedback. 2024 Sep;49(3):383-393. doi: 10.1007/s10484-024-09646-1.
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 (CBF) during orthostatic stress are associated with a decrease in end-tidal CO (EtCO) 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, EtCO 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 CBF during HUT was associated with a larger reduction in ETCO and systolic BP during HUT. While deficits in cardiovascular autonomic control played a more important role in systolic OH, reduced EtCO was a major contributor to orthostatic cerebral hypoperfusion. These findings suggest that biofeedback treatments targeting both the autonomic nervous system and EtCO should be part of nonpharmacological interventions complementing the standard of care in OH patients with symptoms of cerebral hypoperfusion.
直立性低血压（OH）是一种直立不耐受（OI）形式，也是自主功能障碍的关键生理指标，与主要心脑血管事件风险增加相关。OH 患者报告有脑灌注不足的症状，这会使症状恶化并增加晕厥的风险。由于药物干预可独立于体位增加血压（BP），且无法恢复正常的压力反射控制，因此非药物治疗被认为是 OH 管理的基础。虽然在直立应激期间大脑血流速度（CBF）的降低与 OI 患者的终末潮气 CO（EtCO）和低碳酸血症的降低相关，但它们对 OH 严重程度的贡献尚不清楚。这些措施已成为各种生物反馈干预的生理目标。本研究探讨了心血管自主控制、EtCO 和脑灌注不足在因 OI 就诊的患者（N=72）中的关系。与无收缩期 OH 的患者相比，收缩期 OH 患者更可能为男性、年龄更大、表现出肾上腺和迷走神经压力反射敏感性降低以及直立倾斜试验（HUT）期间的心输出量控制降低。HUT 期间 CBF 的降低与 EtCO 和 HUT 期间收缩压的降低幅度更大相关。虽然心血管自主控制的缺陷在收缩期 OH 中发挥了更重要的作用，但 EtCO 的降低是导致直立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 EtCO 的生物反馈治疗应该是 OH 患者非药物干预的一部分，补充有脑灌注不足症状的 OH 患者的标准护理。
