Blood pressure modulation by central venous pressure and respiration. Buffering effects of the heart rate reflexes.
Blood pressure modulation by central venous pressure and respiration. Buffering effects of the heart rate reflexes.
复制标题
通过中心静脉压和呼吸调节血压。
DOI：
10.1161/01.cir.89.1.169
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发表时间：
1994
期刊：
影响因子：
37.8
通讯作者：
Saul,JP
中科院分区：
文献类型：
--
作者：
Triedman,JK;Saul,JP
背景技术尽管呼吸的影响和体位变化对静脉回流至心脏的影响导致心脏前负荷不断波动，但动脉血压仍保持显着恒定。通过使用频域技术来研究瞬时肺容量 (ILV) 和中心静脉压 (CVP) 变化对血压 (BP) 的影响，以量化心率 (HR) 反射对右心室前负荷变化对动脉压影响的减弱的贡献。方法和结果对 8 名仰卧位的人进行 ILV 的随机独立变化，然后进行 CVP（使用下半身负压获得）。在对照期间以及使用 0.04 mg/kg 阿托品和 0.2 mg/kg 普萘洛尔完全阻断后记录 HR、ILV、CVP 以及收缩压 (SBP) 和舒张压 (DBP)。通过互谱技术对成对关系进行频域分析。在自主神经阻滞期间，CVP 的波动高达 0.14 Hz，但引起的动脉压相应变化仅高达 0.08 Hz (P < .02)，表明心脏和肺血管系统的机械阻尼效应。血压波动也比 CVP 延迟 1.55 至 2.10 秒。在频率 < 0.1 Hz 时，CVP 与所有血压指数的关系随阻滞而增加（CVP-SBP，0.9 +/- 0.5 与 2.7 +/- 0.8 mm Hg/mm Hg，P < .01；CVP-DBP，1.3 +/- 0.4 与 4.3 +/- 1.4 mm Hg/mm Hg，P < .01；CVP 脉压[PP]，1.0 +/- 0.3 与 1.9 +/- 0.8 毫米汞柱/毫米汞柱，P < .05）。动脉血压的高频波动是呼吸活动相对纯粹的表现。在频率从 0.15 到 0.35 Hz 时，ILV 与 SBP 的关系在阻断时没有变化，而 ILV 与 DBP 和 PP 的关系下降（ILV-DBP，6.1 +/- 3.5 与 3.3 +/- 2.2 mm Hg/L，P < .02；ILV-PP，7.0 +/- 4.3 与 2.7 +/- 2.2 mm Hg/L，P < .01）。这些关系的相位相关变化表明，神经介导的 HR 变化可能抵消呼吸引起的机械效应。结论 CVP 变化引起的血压缓慢变化 (< 0.08 Hz) 和 ILV 引起的较快速变化均由心率反射主动缓冲。在封锁期间，插入的心肺结构的机械特性限制了 CVP 引起的血压波动。这些发现对于与心率控制受损相关的病理状况下的血压调节具有影响。
BACKGROUNDDespite constant fluctuations in cardiac preload caused by the effects of respiration and changes in posture on venous return to the heart, arterial blood pressure remains remarkably constant. The effects of instantaneous lung volume (ILV) and variations of central venous pressure (CVP) on blood pressure (BP) were studied by use of frequency domain techniques to quantify the contribution of heart rate (HR) reflexes to attenuation of the effects of changes in right ventricular preload on arterial pressure.METHODS AND RESULTSRandom independent variation of ILV, then CVP (obtained using lower-body negative pressure), was performed in eight humans in the supine position. HR, ILV, CVP, and systolic (SBP) and diastolic (DBP) BPs were recorded during control periods and after complete blockade obtained by use of 0.04 mg/kg atropine and 0.2 mg/kg propranolol. A frequency-domain analysis was performed on pairwise relations by the cross-spectral technique. During autonomic blockade, fluctuations in CVP were induced up to 0.14 Hz but caused corresponding changes in arterial pressure only up to 0.08 Hz (P < .02), indicating a mechanical damping effect of the heart and pulmonary vasculature. Fluctuations of BP were also delayed from CVP by 1.55 to 2.10 seconds. At frequencies < 0.1 Hz, relations of CVP to all indices of BP increased with blockade (CVP-SBP, 0.9 +/- 0.5 versus 2.7 +/- 0.8 mm Hg/mm Hg, P < .01; CVP-DBP, 1.3 +/- 0.4 versus 4.3 +/- 1.4 mm Hg/mm Hg, P < .01; CVP-pulse pressure [PP], 1.0 +/- 0.3 versus 1.9 +/- 0.8 mm Hg/mm Hg, P < .05). Higher-frequency fluctuations of arterial BP were a relatively pure manifestation of respiratory activity. At frequencies from 0.15 to 0.35 Hz, the relation of ILV to SBP was unchanged with blockade, whereas relations of ILV to DBP and PP decreased (ILV-DBP, 6.1 +/- 3.5 versus 3.3 +/- 2.2 mm Hg/L, P < .02; ILV-PP, 7.0 +/- 4.3 versus 2.7 +/- 2.2 mm Hg/L, P < .01). An associated change in phase of these relations suggested that neurally mediated changes in HR may offset mechanical effects caused by respiration.CONCLUSIONSBoth slow changes of BP (< 0.08 Hz) induced by variations of CVP and more rapid changes induced by ILV are actively buffered by heart rate reflexes. During blockade, the mechanical properties of interposed cardiopulmonary structures limit CVP-induced fluctuations of BP. These findings have implications for BP regulation in pathological conditions associated with impairment of HR control.