Blood Pressure Modulation by Central Venous Pressure and Respiration: Buffering Effects of the Heart Rate Reflexes

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Despite 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 Results

Random 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.


Both 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.

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