Effects of epidural analgesia and atropine on heart rate and blood pressure variability: implications for the interpretation of beat-to-beat fluctuations.

Abstract

Cardiovascular variables such as heart rate, arterial blood pressure, stroke volume and the shape of electrocardiographic complexes all vary beat-by-beat. This variability occurs because of the dynamic response of cardiovascular regulatory systems to perturbations in cardiovascular function. We applied spectral analysis to the effects of sympathetic vasomotor blockade by epidural analgesia and parasympathetic blockade of the heart by atropine on the beat-to-beat variability of heart rate and blood pressure in humans. High-frequency fluctuations in heart rate (+/- 0.2 Hz) are caused by respiratory induced fluctuations of blood pressure, mediated by the vagus nerve. Low-frequency fluctuations (0.06-0.12 Hz) are related to sympathetic baroreflex control of vasomotor activity and heart rate. In our study, even partial parasympathetic blockade of the heart by atropine decreased the power in the high and low frequency heart rate fluctuations. There were no significant changes in blood pressure fluctuations in either frequency range. Sympathetic blockade by epidural analgesia decreased only low-frequency fluctuations of both heart rate and blood pressure. From a cardiovascular model and our experimental results we support the view that high frequency fluctuations in heart rate are due to the vagal response to blood pressure fluctuations caused by respiration and that the fluctuations around 0.1 Hz in both heart rate and blood pressure have their origin in the sympathetic baroreflex control loop of vasomotor activity.