Skytioti Maria, Elstad Maja
Division of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Front Physiol. 2022 Jul 7;13:768465. doi: 10.3389/fphys.2022.768465. eCollection 2022.
Heart rate variability (HRV) has prognostic and diagnostic potential, however, the mechanisms behind respiratory sinus arrhythmia (RSA), a main short-term HRV, are still not well understood. We investigated if the central feedforward mechanism or pulmonary stretch reflex contributed most to RSA in healthy humans. Ventilatory support reduces the centrally mediated respiratory effort but remains the inspiratory stretch of the pulmonary receptors. We aimed to quantify the difference in RSA between spontaneous breathing and ventilatory support. Nineteen healthy, young subjects underwent spontaneous breathing and non-invasive intermittent positive pressure ventilation (NIV) while we recorded heart rate (HR, from ECG), mean arterial pressure (MAP) and stroke volume (SV) estimated from the non-invasive finger arterial pressure curve, end-tidal CO (capnograph), and respiratory frequency (RF) with a stretch band. Variability was quantified by an integral between 0.15-0.4 Hz calculated from the power spectra. Median and 95% confidence intervals (95%CI) were calculated as Hodges-Lehmann's one-sample estimator. Statistical difference was calculated by the Wilcoxon matched-pairs signed-rank test. RF and end-tidal CO were unchanged by NIV. NIV reduced HR by 2 bpm, while MAP and SV were unchanged in comparison to spontaneous breathing. Variability in both HR and SV was reduced by 60% and 75%, respectively, during NIV as compared to spontaneous breathing, but their interrelationship with respiration was maintained. NIV reduced RSA through a less central respiratory drive, and pulmonary stretch reflex contributed little to RSA. RSA is mainly driven by a central feedforward mechanism in healthy humans. Peripheral reflexes may contribute as modifiers of RSA.
心率变异性（HRV）具有预后和诊断潜力，然而，作为主要短期HRV的呼吸性窦性心律不齐（RSA）背后的机制仍未得到充分理解。我们研究了在健康人中，中枢前馈机制或肺牵张反射对RSA的贡献是否最大。通气支持减少了中枢介导的呼吸努力，但保留了肺感受器的吸气牵张。我们旨在量化自主呼吸和通气支持之间RSA的差异。19名健康的年轻受试者进行了自主呼吸和无创间歇性正压通气（NIV），同时我们记录了心率（HR，来自心电图）、平均动脉压（MAP）和通过无创手指动脉压曲线估计的每搏输出量（SV）、呼气末二氧化碳（二氧化碳分析仪）以及使用拉伸带记录的呼吸频率（RF）。变异性通过从功率谱计算的0.15 - 0.4 Hz之间的积分来量化。中位数和95%置信区间（95%CI）通过霍奇斯 - 莱曼单样本估计器计算。统计差异通过威尔科克森配对符号秩检验计算。NIV对RF和呼气末二氧化碳无影响。与自主呼吸相比，NIV使HR降低2次/分钟，而MAP和SV保持不变。与自主呼吸相比，NIV期间HR和SV的变异性分别降低了60%和75%，但它们与呼吸的相互关系得以维持。NIV通过减少中枢呼吸驱动降低了RSA，肺牵张反射对RSA的贡献很小。在健康人中，RSA主要由中枢前馈机制驱动。外周反射可能作为RSA的调节因素起作用。
