Physiological Rhythms Unit, Department of Surgery and Anaesthesia, University of Otago, 23A Mein Street, Newtown, Wellington 6021, New Zealand.
Am J Physiol Heart Circ Physiol. 2010 May;298(5):H1588-99. doi: 10.1152/ajpheart.00036.2010. Epub 2010 Mar 12.
Respiratory sinus arrhythmia (RSA) is classically described as a vagally mediated increase and decrease in heart rate concurrent with inspiration and expiration, respectively. However, although breathing frequency is known to alter this temporal relationship, the precise nature of this phase dependency and its relationship to blood pressure remains unclear. In 16 subjects we systematically examined the temporal relationships between respiration, RSA, and blood pressure by graphically portraying cardiac interval (R-R) and systolic blood pressure (SBP) variations as a function of the respiratory cycle (pattern analysis), during incremental stepwise paced breathing. The principal findings were 1) the time interval between R-R maximum and expiration onset remained the same ( approximately 2.5-3.0 s) irrespective of breathing frequency (P = 0.10), whereas R-R minimum progressively shifted from expiratory onset into midinspiration with slower breathing (P < 0.0001); 2) there is a clear qualitative distinction between pre- versus postinspiratory cardiac acceleration during slow (0.10 Hz) but not fast (0.20 Hz) breathing; 3) the time interval from inspiration onset to SBP minimum (P = 0.16) and from expiration onset to SBP maximum (P = 0.26) remained unchanged across breathing frequencies; 4) SBP maximum and R-R maximum maintained an unchanged temporal alignment of approximately 1.1 s irrespective of breathing frequency (P = 0.84), whereas the alignment between SBP minimum and R-R minimum was inconstant (P > 0.0001); and 5) beta(1)-adrenergic blockade did not influence the respiration-RSA relationships or distinct RSA patterns observed during slow breathing, suggesting that temporal dependencies associated with alterations in breathing frequency are unrelated to cardiac sympathetic modulation. Collectively, these results illustrate nonlinear respiration-RSA-blood pressure relationships that may yield new insights to the fundamental mechanism of RSA in humans.
呼吸窦性心律失常（RSA）经典地描述为迷走神经介导的心率增加和减少，分别与吸气和呼气同时发生。然而，尽管呼吸频率已知会改变这种时间关系，但这种相位依赖性的确切性质及其与血压的关系仍不清楚。在 16 名受试者中，我们通过图形描绘心脏间隔（R-R）和收缩压（SBP）变化作为呼吸周期的函数（模式分析），系统地检查了呼吸、RSA 和血压之间的时间关系，在递增的逐步有节奏的呼吸中。主要发现是：1）R-R 最大值和呼气开始之间的时间间隔保持不变（约 2.5-3.0 秒），而与呼吸频率无关（P = 0.10），而 R-R 最小值随着呼吸变慢而从呼气开始逐渐转移到吸气中期（P < 0.0001）；2）在慢呼吸（0.10 Hz）但不是快呼吸（0.20 Hz）期间，心脏加速存在明显的预吸气和后吸气之间的定性区别；3）从吸气开始到 SBP 最小值（P = 0.16）和从呼气开始到 SBP 最大值（P = 0.26）的时间间隔在整个呼吸频率下保持不变；4）SBP 最大值和 R-R 最大值保持不变的时间对准约 1.1 秒，而与呼吸频率无关（P = 0.84），而 SBP 最小值和 R-R 最小值之间的对准是不稳定的（P > 0.0001）；5）β1-肾上腺素能阻断不会影响慢呼吸期间观察到的呼吸-RSA 关系或不同的 RSA 模式，表明与呼吸频率变化相关的时间依赖性与心脏交感神经调节无关。总的来说，这些结果说明了非线性呼吸-RSA-血压关系，这可能为人类 RSA 的基本机制提供新的见解。
