Division of Physiology, Institute of Basic Medical Sciences, University of Oslo, Blindern, P.O. Box 1113, 0317, Oslo, Norway.
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Eur J Appl Physiol. 2017 Nov;117(11):2237-2249. doi: 10.1007/s00421-017-3711-0. Epub 2017 Sep 12.
Increased variability in cerebral blood flow (CBF) predisposes to adverse cerebrovascular events. Oscillations in arterial blood pressure and PaCO induce CBF variability. Less is known about how heart rate (HR) variability affects CBF. We experimentally reduced respiration-induced HR variability in healthy subjects, hypothesizing that CBF variability would increase.
Internal carotid artery (ICA) blood velocity was recorded by Doppler ultrasound in ten healthy subjects during baseline, control-mode, non-invasive mechanical ventilation (NIV), i.e., with fixed respiratory rate, hypovolemia induced by lower body negative pressure, and combinations of these. ICA beat volume (ICABV) and ICA blood flow (ICABF) were calculated. HR, mean arterial blood pressure (MAP), respiratory frequency (RF), and end-tidal CO were recorded. Integrals of power spectra at each subject's RF ± 0.03 Hz were used to measure variability. Phase angle/coherence measured coupling between cardiovascular variables.
Control-mode NIV reduced HR variability (-56%, p = 0.002) and ICABV variability (-64%, p = 0.006) and increased ICABF variability (+140%, p = 0.002) around RF. NIV + hypovolemia reduced variability in HR and ICABV by 70-80% (p = 0.002) and doubled ICABF variability (p = 0.03). MAP variability was unchanged in either condition. Respiration-induced HR and ICABV oscillations were in inverse phase and highly coherent (coherence >0.9) during baseline, but this coherence decreased during NIV, in normovolemia and hypovolemia (p = 0.01).
Controlling respiration in awake healthy humans reduced HR variability and increased CBF variability in hypovolemia and normovolemia. We suggest respiration-induced HR variability to be a mechanism in CBF regulation. Maintaining spontaneous respiration in patients receiving ventilatory support may be beneficial also for cerebral circulatory purposes.
脑血流（CBF）的变异性增加易导致不良的脑血管事件。动脉血压和 PaCO 的波动会引起 CBF 的变异性。关于心率（HR）变异性如何影响 CBF 的了解较少。我们在健康受试者中实验性地降低了呼吸引起的 HR 变异性，假设 CBF 变异性会增加。
在基线、控制模式、无创机械通气（NIV）期间，通过多普勒超声记录 10 名健康受试者的颈内动脉（ICA）血流速度，即采用固定呼吸频率、下体负压诱导的低血容量以及这些方法的组合。计算 ICA 搏动容积（ICABV）和 ICA 血流（ICABF）。记录心率（HR）、平均动脉血压（MAP）、呼吸频率（RF）和呼气末 CO。使用每个受试者 RF±0.03 Hz 的功率谱积分来测量变异性。相位角/相干性测量心血管变量之间的耦合。
控制模式 NIV 降低了 HR 变异性（-56%，p=0.002）和 ICABV 变异性（-64%，p=0.006），并增加了 RF 周围的 ICABF 变异性（+140%，p=0.002）。NIV+低血容量使 HR 和 ICABV 的变异性降低了 70-80%（p=0.002），并使 ICABF 变异性增加了一倍（p=0.03）。两种情况下 MAP 变异性均无变化。在基线时，呼吸引起的 HR 和 ICABV 振荡呈反相且高度相干（相干性>0.9），但在 NIV 期间，在正常血容量和低血容量下，这种相干性降低（p=0.01）。
在清醒的健康人中控制呼吸可降低低血容量和正常血容量时的 HR 变异性并增加 CBF 变异性。我们认为呼吸引起的 HR 变异性是 CBF 调节的一种机制。为了脑循环的目的，在接受通气支持的患者中维持自主呼吸可能也有益。
