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Hypertension. 1993;21:236-247

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Hypertension, Vol 21, 236-247, Copyright © 1993 by American Heart Association


ARTICLES

Mild hypovolemic stress alters autonomic modulation of heart rate

JK Triedman, RJ Cohen and JP Saul
Department of Cardiology, Children's Hospital, Boston.

In response to changes in central venous volume, changes in vagal efferent cardiac outflow have been demonstrated in animals but not in humans. In this study, frequency domains analysis was used to quantify modulation of heart rate by respiration and blood pressure in normal human adults undergoing mild central hypovolemic stress induced by blood donation and postural change. In supine subjects, blood donation caused no change in mean heart rate, pulse pressure, or in the variance of heart rate or blood pressure. There were small decreases in mean and systolic blood pressure. A significant decrease in vagal modulation of heart rate was seen in the 0.12-0.5-Hz frequency band, as measured by the change in the relation of lung volume to heart rate in this frequency band (-4.49 beats per minute [pbm] per liter [1], p < 0.001). Comparison of supine and tilt positions revealed marked changes in heart rate and blood pressure means and variances consistent with more pronounced decreases in intracardiac filling pressures and unloading of the arterial baroreceptors. A further progressive decrease in the vagal modulation of heart rate by lung volume was observed in the 0.12-0.5-Hz band, with a near-linear response of magnitude of respiratory sinus arrhythmia over a range of estimated central venous volume. Transfer function analysis can detect changes in autonomic response to mild degrees of central hypovolemia, which are insufficient to cause changes in mean heart rate or heart rate variance. This represents evidence for modulation of heart rate control by cardiopulmonary baroreceptors. A near-linear relation between magnitude of respiratory sinus arrhythmia and central venous volume suggests that this may have clinical relevance in patient monitoring.


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