A study on the effects of acute sleep deprivation on pulse pressure
Currently a great proportion of our population experiences sleep deprivation. There has been research carried out previously and depicted an increase in diastolic blood pressure due to sleep deprivation. This leads to greater risk for diseases and even death in sleep deprived individuals. For any given level of mean arterial blood pressure, a high or low pulse pressure is by itself an accurate indicator of an individual’s risk for cardiovascular diseases and even death. Low and high pulse pressure have been separately linked to increased mortality rates. There is no available data on any physiological influence of lack of sleep on an individual’s pulse pressure. Thus this study set out to determine effects of chronic sleep deprivation on pulse pressure as an independent physiological variable of blood pressure in healthy adults between ages 20 and 40 years. This study set out to assess any relationship between chronic sleep deprivation and pulse pressure in healthy subjects aged between 20 and 40 years. It was a randomized control trial done at The Karen Hospital involving healthy human subjects working at the hospital aged between 20 and 40 years. All subjects who volunteered for the study underwent physical examination. Sociodemographic characteristics, medical history and sleeping pattern were obtained using the study questionnaire. A sample size of 56 human subjects was used. An inclusion and exclusion criteria was used to form a test group of 28 subjects and a control group of 28 subjects. Test group comprised fourteen males and fourteen females who were sleep deprived. The control group comprised fourteen males and fourteen females who were non- sleep deprived. The study was conducted over a period of one month. On a daily basis, at 7.30 a.m every day, blood pressure readings were taken using a manual sphygmomanometer for both the test group and the control group. A sleep deprived subject must have had less than four hours of sleep for the last 24 hours whereas a non- sleep deprived subject must have had more than 6 hrs of sleep in the last 24 hrs. Data was collected by the principal investigator using predesigned data collection sheets. Pulse pressure and fractional pulse pressure were derived using their respective formulae. Data was then entered into Microsoft Excel sheets and data cleaning was done before analysis. These were coded then analysis done using IBM SPSS software. All the fifty six subjects who had been recruited were studied. The mean pulse pressure at recruitment of the control group was 48.09 mmHg while that of the test group was 47.22 mmHg. Both groups at recruitment had an equal mean fractional pulse pressure of 0.54 with mean age of control group at 28.42 years and that of test group at 27.86 years. By the fourth week of the study, the control group had a mean 50.0 mmHg and a mean fractional pulse pressure of 0.58; the test group had a mean pulse pressure of 44.43 mmHg and a mean fractional pulse pressure of 0.54. A person chi-square test revealed no relationship between pulse pressure and number of hours slept (Chi square value =165.99 df= 190 p= 0.895). There was also no relationship between fractional pulse pressure and number of hours slept (Chi- square value=- 454.98, df= 460, p=0.557). Pearson’s correlation analysis between pulse pressure and number of hours slept in both groups revealed a non-significant and positive relationship (p= 0.686). The correlation was weak in strength(r= 0.055). There was an association between sleeping more hours and having an increased pulse pressure. Correlation analysis between fractional pulse pressure and number of hours slept revealed a non- significant and negative relationship (r=-0.046 p=0.739). Multiple regression was also conducted on overall effect of gender, both the two groups and number of hours slept on predictors had no relationship with pulse pressure. It was deducted from the study that the relationship between sleep deprivation and pulse pressure or fractional pulse pressure in healthy young adults aged between 20 and 40 years is not statistically significant. This was observed in both the test group and control group throughout the period of the study.