The association between sleep deprivation and arterial pressure variations: a systematic literature review

Arterial hypertension is a cardiovascular disease defined as a sustained high blood pressure, constituting an important risk factor for the development of heart diseases, such as coronary heart disease and heart failure. At the same time, pathophysiological pathways underlying sleeping deprivation provides biological plausibility for a causation connection between sleep deprivation and acute or chronic blood pressure elevation, such as the mechanism behind blood pressure dipping at night, which strongly relies on reduced sympathetic activity provided by sleep, besides empirical and clinical evidence suggesting that sleep disorders incidence is correlate with posterior development of arterial hypertension. The aim of this study was to systematically review published studies analyzing the possible relationship between sleep deprivation and variations in blood pressure during nighttime and daytime.

The research was carried out in the second semester of 2020 following the PRISMA model and using the LILACS, MEDLINE and COCHRANE (CENTRAL) databases. The keywords used were associated using the Boolean method. Only trials and studies in humans unrelated to sleep apnea were included, in an attempt to answer the question proposed. Duplications and articles outside the topic were excluded.

After the selection processes, fourteen studies were left, which were classified, depending on the findings, in four categories: 1) blood pressure differences only in sleep deprivation's night; 2) blood pressure differences only in the following day after sleep deprivation's night; 3) blood pressure differences in both nights and 4) those that found no blood pressure differences.

It was found an increase in blood pressure on the night of sleep deprivation, suggesting a possible causality with an acute increase in blood pressure depending on the population studied. In general, sleep deprivation is acutely associated with blood pressure elevation or acute elevation of markers that suggest the role of compensatory mechanisms, such as increased natriuresis and increased parasympathetic activity.