Document Type

Thesis

Date of Award

Spring 5-31-2004

Degree Name

Master of Science in Biomedical Engineering - (M.S.)

Department

Biomedical Engineering

First Advisor

Stanley S. Reisman

Second Advisor

David S. Kristol

Third Advisor

Ronald H. Rockland

Abstract

Sleep deprivation (SD) has been thought a potential factor to trigger cardiovascular events by increasing the sympathetic nervous system activity. The aim of the present study was to evaluate the relationship between sleep deprivation and the autonomic nervous system activity by means of heart rate variability (HRV) and blood pressure variability (BPV). All data were acquired in the sleep lab of Columbia University.

Data were acquired from the two groups, SD and control. Subjects in the SD group did not sleep for thirty-six hours but subjects in the control group slept at night as usual. There were five different data acquisition stages; baseline (stage 0 and stage 1), twelve hours of sleep deprivation (stage 2), twenty-four hours of sleep deprivation (stage 3) and thirty-six hours of sleep deprivation (stage 4). ECG and blood pressure were measured for one hour in each stage. Data were acquired in the supine and sitting positions and volunteers were then asked to use a computer to study the SD effects on cognitive performance. Sleep deprivation produces negative effects on cognitive performance. Cognitive performance deficits involved reduced ability to pay attention and impairment of the ability to think quickly and not make mistakes. In this study, we tested whether the negative effects reflect on the autonomic nervous system (ANS).

The low frequency (LF) area and the high frequency (HF) area were calculated using the Power Spectrum Analysis of HRV and BPV. The LF area of HRV is associated with the sympathetic nervous system activity plus the parasympathetic nervous system activity but the HF area of HRV is associated with only the parasympathetic nervous system activity. The LF area of BPV is believed to be related purely only to the sympathetic nervous system activity, rather than to a mixture of sympathetic and parasympathetic nervous system activities. In this study, the LF and HF areas were timenormalized and the normalized LF and HF areas were averaged for a mean value analysis.

In addition to the mean value analysis, One Factor ANOVA and Two-Factor ANOVA were conducted for the significance comparison tests. In One Factor ANOVA and the mean value analysis, after thirty-six hours of sleep deprivation, the LF area of HRV increased significantly in the sitting position and when subjects began the cognitive task. No significant increase in the LF area was observed in the supine position and after ten minutes of the cognitive task. The significantly increased LF area could reflect an increased stress level and acts as a predictor of cardiovascular events. Sleep deprivation can cause negative effects on cognitive performance especially at the beginning state of the cognitive task. The LF area of BPV did not change significantly in the supine and sitting positions during thirty-six hours of sleep deprivation. After thirty-six hours of sleep deprivation, the LF area of BPV increased significantly when people began the cognitive task as did the LF area of HRV. Significant changes were observed after thirty-six hours of sleep deprivation in One Factor ANOVA but a significant change was observed after twelve hours of SD in Two-Factor ANOVA. Although there was a significant change in the LF area, no significant HF change was observed in the control and SD groups.

The negative effect of sleep deprivation reflects on the autonomic nervous system. Sleep deprivation did not affect the HF area significantly but significant LF area changes occurred due to sleep deprivation. HRV responses to SD were different according to positions. Subjects experienced more negative effects in the sitting position then in the supine position. The LF area of HRV and BPV increased significantly at the beginning state of the cognitive task after thirty-six hours. Sleep deprivation may induce the LF area to increase and people can experience a mental stress and cognitive performance deficit at the beginning of cognitive performance.

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