Center for Hypotension, 19 Bradhurst Ave, Suite 1600 S, Hawthorne, NY 10532.
Hypertension. 2014 Jun;63(6):1302-8. doi: 10.1161/HYPERTENSIONAHA.113.02824. Epub 2014 Apr 7.
Hyperventilation and reduced cerebral blood flow velocity can occur in postural tachycardia syndrome (POTS). We studied orthostatically intolerant patients, with suspected POTS, with a chief complaint of upright dyspnea. On the basis of our observations of an immediate reduction of cerebral blood flow velocity with orthostasis, we hypothesize that the resulting ischemic hypoxia of the carotid body causes chemoreflex activation, hypocapnic hyperpnea, sympathetic activation, and increased heart rate and blood pressure in this subset of POTS. We compared 11 dyspneic POTS subjects with 10 healthy controls during a 70° head-up tilt. In POTS subjects during initial orthostasis before blood pressure recovery; central blood volume and mean arterial pressure were reduced (P<0.025), resulting in a significant (P<0.001) decrease in cerebral blood flow velocity, which temporally preceded (17±6 s; P<0.025) a progressive increase in minute ventilation and decrease in end tidal CO2 (P<0.05) when compared with controls. Sympathoexcitation, measured by muscle sympathetic nerve activity, was increased in POTS (P<0.01) and inversely proportional to end tidal CO2 and resulted in an increase in heart rate (P<0.001), total peripheral resistance (P<0.025), and a decrease in cardiac output (P<0.025). The decrease in cerebral blood flow velocity and mean arterial pressure during initial orthostasis was greater (P<0.025) in POTS. Our data suggest that exaggerated initial central hypovolemia during initial orthostatic hypotension in POTS results in reduced cerebral blood flow velocity and postural hypocapnic hyperpnea that perpetuates cerebral ischemia. We hypothesize that sustained hypocapnia and cerebral ischemia produce sympathoexcitation, tachycardia, and a statistically significant increase in blood pressure.
直立性心动过速综合征（POTS）可出现过度通气和脑血流速度降低。我们研究了以直立呼吸困难为主诉、疑似 POTS 且不能耐受直立位的患者。基于我们观察到的直立位时脑血流速度即刻降低，我们假设由此导致的颈动脉体缺血缺氧引起化学感受器反射激活、低碳酸血症性过度通气、交感神经激活以及这部分 POTS 患者的心率和血压升高。我们比较了 11 例呼吸困难的 POTS 患者和 10 例健康对照在 70°头高位倾斜时的情况。在 POTS 患者血压恢复前的初始直立位期间，中心血容量和平均动脉压降低（P<0.025），导致脑血流速度显著降低（P<0.001），这先于分钟通气量的逐渐增加和呼气末二氧化碳分压的降低（P<0.05），与对照组相比。通过肌间神经活动测量的交感神经兴奋在 POTS 中增加（P<0.01），与呼气末二氧化碳分压呈反比，导致心率增加（P<0.001）、总外周阻力增加（P<0.025）和心输出量减少（P<0.025）。在 POTS 中，初始直立位期间脑血流速度和平均动脉压的降低更大（P<0.025）。我们的数据表明，在 POTS 中初始直立性低血压期间初始中枢血容量不足过度，导致脑血流速度降低和体位性低碳酸血症性过度通气，从而使脑缺血持续存在。我们假设持续的低碳酸血症和脑缺血引起交感神经兴奋、心动过速以及血压统计学显著升高。
