Non-rapid eye movement (NREM) sleep - Cardiovascular function
Even before the onset of NREM sleep the heart rate falls in parallel with the reduction in body temperature and is related to the fall in metabolic rate. Vasodilatation is due to reduced sympathetic activity and possibly accumulation of adenosine.
The cardiovascular system is more stable during NREM sleep than during REM sleep. The heart rate falls shortly after sleep onset, and there is then little further change between stages 2, 3 and 4 NREM sleep, although it continues to fall during the night because of a circadian rhythm.
The blood pressure is not under circadian control, but is more sleep-state dependent. It falls by 5–15% shortly after sleep onset due mainly to a reduction in cardiac output, but also to peripheral vasodilatation.
There is little difference between either the systolic or diastolic blood pressures in stages 2, 3 and 4 NREM sleep. This fall in blood pressure is absent if there is increased sympathetic activity, as in hypertension or obstructive sleep apnoeas, and in chronic renal failure and Cushing’s syndrome.
NREM sleep has been thought to be cardio-protective in that the coronary blood flow remains fairly constant during sleep, but there is a reduced perfusion pressure which may lead to ischaemia if there is coronary artery disease.
The cerebral blood flow is coupled to the metabolic rate of the central nervous system [6], and this autoregulation is both regional within the brain and independent of the autonomic nervous system. The cerebral blood flow falls by 10–20% in NREM sleep compared to wakefulness, and is less than during REM sleep. It is reduced particularly in the prefrontal cortex.
Cerebral blood flow increases if hypercapnia develops because this causes cerebral vasodilatation and an increase in cardiac output. It also increases during wakefulness in the presence of hypoxia, but this response is absent in stages 3 and 4 NREM sleep.
As a result there is a potential for reduction in oxygen delivery to the brain in hypoxic situations such as during obstructive and central sleep apnoeas. This may influence medullary function, and thereby modify upper airway and chest wall muscle control.
Cutaneous blood flow is increased due to vasodilatation, but there is probably little change in distribution of visceral blood flow during NREM sleep.