Department of Mathematics and Statistics, Georgia State University, Atlanta, Georgia.
Neuroscience Institute, Georgia State University, Atlanta, Georgia.
J Appl Physiol (1985). 2020 Nov 1;129(5):1193-1202. doi: 10.1152/japplphysiol.00452.2020. Epub 2020 Sep 17.
Excessive blood pressure variation is linked to the development of hypertension and other diseases. This study assesses the relative role of respiratory sinus arrhythmia (RSA) and pulse pressure (PP) on the amplitude and timing of blood pressure variability with respiration [Traube-Hering (TH) waves]. We analyzed respiratory, electrocardiogram, and blood pressure traces from healthy, supine male subjects ( = 10, mean age = 26.7 ± 1.4) during 20-min epochs of resting, slow deep breathing (SDB), and recovery. Across all epochs, blood pressure and heart rate (HR) were modulated with respiration and the magnitude of RSA; TH waves increased during SDB. The data were deconstructed using a simple mathematical model of blood pressure to dissect the relative roles of RSA and PP on TH waves. We constructed the time series of the R-wave peaks and compared the recorded TH waves with that predicted by the model. Given that cardiac output is determined by both heart rate and stroke volume, it was surprising that the magnitude of the TH waves could be captured by only HR modulation. However, RSA alone did not accurately predict the timing of TH waves relative to the respiratory cycle. Adding respiratory modulation of PP to the model corrected the phase shift showing the expected pattern of BP rising during inspiration with the peak of the TH wave during early expiration. We conclude that short-term variability of blood pressure referred to as TH waves has at least two independent mechanisms whose interaction forms their pattern: RSA and respiratory-driven changes in PP. Variability in blood pressure has become an important metric to consider as more is learned about the link between excessive blood pressure variability and adverse health outcomes. In this study using slow deep breathing in human subjects, we found that heart rate and pulse pressure variations have comparable effects on the amplitude of blood pressure waves, and it is the common action of the two that defines the phase relationship between respiration and blood pressure oscillations.
血压变异性过大与高血压和其他疾病的发生有关。本研究评估了呼吸窦性心律失常（RSA）和脉压（PP）在血压变异性随呼吸[Traube-Hering（TH）波]的幅度和时间变化中的相对作用。我们分析了健康、仰卧男性受试者在休息、缓慢深呼吸（SDB）和恢复 20 分钟期间的呼吸、心电图和血压轨迹[Traube-Hering（TH）波]。在所有的阶段，血压和心率（HR）都随呼吸和 RSA 的幅度而变化；在 SDB 期间，TH 波增加。使用血压的简单数学模型对数据进行了分解，以剖析 RSA 和 PP 对 TH 波的相对作用。我们构建了 R 波峰的时间序列，并将记录的 TH 波与模型预测的波进行了比较。由于心输出量取决于心率和每搏输出量，因此令人惊讶的是，TH 波的幅度仅可通过 HR 调制来捕获。但是，仅 RSA 并不能准确预测 TH 波相对于呼吸周期的时间。将 PP 的呼吸调制添加到模型中，纠正了相位偏移，显示出血压在吸气期间上升的预期模式，TH 波的峰值出现在早期呼气期间。我们得出结论，血压的短期变异性（称为 TH 波）至少有两个独立的机制，它们的相互作用形成了其模式：RSA 和呼吸驱动的 PP 变化。随着人们对血压变异性过大与不良健康结果之间的联系了解的增加，血压变异性已成为一个重要的考虑因素。在这项使用人类受试者缓慢深呼吸的研究中，我们发现心率和脉压变化对血压波幅度有相当的影响，正是这两个因素的共同作用定义了呼吸和血压波动之间的相位关系。
