Orientation
Rapid review
What you should already have
Lesson 17 — consciousness and arousal; Lesson 18 — the electroencephalogram.
About 50 minutes
Plus the time it takes to redraw this lesson’s figures from memory, which is the fastest way to find out what you have not understood.
Where this shows up
Sleep physiology is the direct route into obstructive sleep apnoea, postoperative respiratory risk and delirium — three of the commonest perioperative problems in an ageing surgical population.
Learning outcomes
By the end of this lesson you should be able to:
- Describe the EEG signature of each non-REM stage and of REM sleep, and name the features unique to stage 2.
- Draw a normal adult hypnogram and state how cycle length and stage proportions change across the night.
- Compare non-REM and REM sleep across the cardiovascular, respiratory, thermoregulatory, muscular and endocrine systems.
- Explain the two-process model of sleep regulation and name the neural structures behind each process.
- State the similarities and the crucial differences between sleep and general anaesthesia.
- Explain why obstructive sleep apnoea worsens in REM sleep and in the postoperative period, and describe postoperative sleep architecture.
Together these settle one syllabus objective: Sleep architecture and its regulation. Tick it on the Physiology objective list once you can do all of the above without notes.
The minimum high-yield framework
- Two types. Non-REM in three stages (N1, N2, N3) and REM.
- Non-REM = quiet brain, movable body. EEG slows and grows, metabolism falls, tone is reduced but present.
- REM = active brain, paralysed body. Desynchronised EEG resembling wakefulness, dreaming, and near-complete skeletal muscle atonia.
- Cycle length about 90 minutes, four to six cycles a night. Slow-wave sleep dominates the first third; REM periods lengthen towards morning.
- Adult proportions — approximately N1 5%, N2 45%, N3 25%, REM 25%.
- Stage 2 signature: sleep spindles and K complexes.
- REM is autonomically unstable — irregular heart rate, blood pressure and respiration, and the loss of accessory and upper airway muscle tone that makes obstructive apnoea worst here.
- Two-process regulation: homeostatic sleep pressure (process S, adenosine) and circadian drive (process C, suprachiasmatic nucleus).
The state
Defining sleep
Architecture
The stages of sleep
| Stage | EEG | Eye movement | Muscle tone | Notes |
|---|---|---|---|---|
| Awake, eyes closed | Alpha (8-13 Hz), occipital | Slow roving | Normal | Alpha is abolished by opening the eyes |
| N1 | Low-voltage mixed frequency, theta (4-7 Hz); alpha disappears | Slow rolling | Slightly reduced | The transition to sleep. Around 5% of total sleep time; easily woken, and subjects often deny having slept |
| N2 | Theta background with sleep spindles (11-16 Hz bursts) and K complexes | Absent | Reduced | The largest single stage, around 45%. The spindles are generated by the thalamic reticular nucleus |
| N3 (slow-wave sleep) | High-voltage delta (0.5-4 Hz, over 75 µV) occupying more than 20% of the epoch | Absent | Reduced | Around 25%. The deepest stage, hardest to rouse from, and the stage of night terrors, sleepwalking and enuresis. Growth hormone is secreted here |
| REM | Low-voltage, desynchronised, fast — resembling wakefulness, hence 'paradoxical sleep' | Rapid, conjugate, bursts | Atonia, apart from diaphragm and extraocular muscles | Around 25%. Vivid dreaming, penile or clitoral tumescence, and autonomic instability |
The night
The hypnogram
A normal young-adult hypnogram
Four features to be able to draw. Sleep is entered through non-REM stage 1, never directly into REM. The first descent is the deepest, with the long block of slow-wave sleep in the first third of the night. The cycle repeats at roughly 90-minute intervals, giving four to six REM periods a night. And the balance shifts across the night: slow-wave sleep dominates early and REM periods lengthen towards morning, so the last REM period is the longest and often ends in waking.
Brief arousals are normal and are drawn. In an adult, REM occupies about a quarter of total sleep time — half in the full-term neonate, and falling again in old age. This is a representative night: no source publishes a per-minute trace, so the shape encodes the stated timings rather than measured data.
- Sleep is entered through non-REM, descending N1 → N2 → N3. Entering sleep directly into REM in an adult is abnormal and is a diagnostic feature of narcolepsy.
- The cycle is approximately 90 minutes, giving four to six cycles in a normal night.
- Slow-wave sleep is concentrated in the first third of the night and may be absent altogether from the last cycles.
- REM periods lengthen progressively, so the longest REM period is the last one before waking — which is why dreams are usually recalled from the early morning.
- Brief arousals to wakefulness are normal and are usually not remembered.
| Age | Total sleep | REM proportion | Slow-wave sleep |
|---|---|---|---|
| Neonate | 16-18 h | About 50%, and sleep may be entered through REM | Present, and cycles are shorter — about 50-60 minutes |
| Child | 10-12 h | Falling towards adult values | Abundant |
| Young adult | 7-8 h | About 25% | About 25% |
| Elderly | Reduced, and fragmented | Approximately preserved as a proportion | Markedly reduced, with more frequent nocturnal arousals |
Systems
Physiological changes in sleep
| System | Non-REM | REM |
|---|---|---|
| Cerebral | Metabolic rate and blood flow fall, by up to about 25% in slow-wave sleep. EEG synchronised | Metabolic rate and blood flow equal or exceed the awake value. EEG desynchronised |
| Cardiovascular | Heart rate, blood pressure and cardiac output fall steadily; vagal tone predominates. Stable | Marked variability — irregular heart rate and blood pressure, with surges. Sympathetic bursts. The period of greatest risk for myocardial ischaemia and arrhythmia |
| Respiratory | Rate and tidal volume fall; minute ventilation falls by around 10-15%; PaCO₂ rises by about 0.5-1 kPa (roughly 3-8 mmHg). Chemoreceptor sensitivity reduced. Breathing is regular | Breathing is irregular in rate and depth. Chemoreceptor and load responses are further blunted. Accessory and intercostal muscle contribution is lost — ventilation becomes diaphragm-dependent |
| Upper airway | Pharyngeal dilator tone reduced but present | Pharyngeal dilator tone markedly reduced or lost — obstructive events are longest and desaturation deepest |
| Muscle tone | Reduced; posture is maintained and movement occurs | Atonia, apart from diaphragm and extraocular muscles |
| Thermoregulation | Maintained, around a lower set point. Shivering and sweating both occur | Effectively suspended — poikilothermic. Neither shivering nor sweating occurs, so core temperature drifts with the environment |
| Endocrine | Growth hormone secretion peaks in slow-wave sleep, early in the night. Prolactin rises; cortisol is at its nadir | Cortisol rises towards the morning peak; testosterone peaks |
| Renal and gastrointestinal | Urine output falls; gastric acid secretion continues | Reduced gut motility; swallowing and salivation are reduced |
Control
The regulation of sleep
| Process S — homeostatic | Process C — circadian | |
|---|---|---|
| Drive | Sleep pressure accumulating with time awake | An intrinsic near-24-hour rhythm, independent of prior sleep |
| Substrate | Accumulation of adenosine in the basal forebrain during wakefulness, inhibiting arousal neurons | The suprachiasmatic nucleus of the hypothalamus, entrained to light by the retinohypothalamic tract |
| Behaviour | Rises during wakefulness, discharges during sleep — hence the rebound after deprivation | Oscillates regardless of sleep, producing the mid-afternoon dip and the early-morning trough |
| Pharmacology | Caffeine is an adenosine antagonist, which is precisely why it opposes sleep pressure | Melatonin from the pineal gland, secreted in darkness under suprachiasmatic control, is the output signal and can be given to shift the rhythm |
The two processes act on a switch. The ventrolateral preoptic nucleus of the hypothalamus is sleep-promoting and GABAergic; it inhibits the arousal nuclei of lesson 17 — tuberomammillary, locus coeruleus and raphe — and they inhibit it in return. Mutual inhibition of this kind behaves as a flip-flop switch, which is why transitions between sleep and wakefulness are rapid and complete rather than gradual. Orexin from the lateral hypothalamus stabilises the switch in the waking position, and its loss produces the abrupt, involuntary state transitions of narcolepsy and cataplexy.
Within sleep, the alternation between non-REM and REM is generated by a second reciprocal circuit in the pons: cholinergic REM-on neurons in the pedunculopontine and laterodorsal tegmental nuclei against monoaminergic REM-off neurons in the locus coeruleus and raphe. This explains a clinical observation — drugs that raise monoamine levels, such as antidepressants, suppress REM sleep.
The comparison
Sleep and anaesthesia
| Sleep | General anaesthesia | |
|---|---|---|
| Reversibility | By sensory stimulation — the defining feature | Not by stimulation. Only by elimination or reversal of the drug |
| Homeostatic drive | Present. Debt accumulates and is repaid | Absent. Anaesthesia does not discharge sleep debt, and may add to it |
| Architecture | Cyclical, with an orderly progression through defined stages | No cycles or stages; depth follows drug concentration |
| EEG | Alternates between synchronised non-REM and desynchronised REM | Progressive dose-dependent slowing to burst suppression and isoelectricity |
| Airway reflexes | Largely preserved | Progressively obtunded — the basis of the aspiration risk |
| Ventilatory response to CO₂ | Blunted | Markedly depressed, and abolished at depth |
| Memory | Preserved for events at arousal | Abolished — amnesia occurs at concentrations well below those causing unconsciousness |
| Shared machinery | The ventrolateral preoptic nucleus, the arousal nuclei and the thalamic gate | Anaesthetics recruit those same nuclei — the bottom-up account of lesson 17 |
Clinical application
Sleep-disordered breathing and the postoperative period
Obstructive sleep apnoea
Airway patency depends on the balance between the collapsing force of inspiratory negative pressure and the dilating force of the pharyngeal dilator muscles, chiefly genioglossus. Sleep reduces dilator tone; REM sleep reduces it most. That is why obstructive events in REM are the longest and produce the deepest desaturation, and why an overnight study that samples little REM sleep can underestimate severity.
The perioperative consequences are direct and worth stating as a chain rather than a list. Opioids and sedatives reduce dilator tone further and blunt the arousal response that terminates an obstructive event — so the patient obstructs for longer and rouses less readily. Repeated hypoxaemia and hypercapnia with large negative intrathoracic pressure swings drive sympathetic activation, systemic and pulmonary hypertension, right ventricular strain and arrhythmia. These patients are additionally likely to be difficult to mask-ventilate and to intubate.
Postoperative sleep architecture
Surgery disrupts sleep in a characteristic and clinically important pattern:
- On the first one to two postoperative nights, REM and slow-wave sleep are suppressed or abolished, by pain, opioids, the surgical stress response and environmental disturbance.
- From about the third to the fifth night there is a REM rebound, with more REM sleep than normal and longer REM periods.
- Because REM carries atonia, autonomic instability and the worst upper airway obstruction, the rebound is associated with episodic hypoxaemia, haemodynamic instability and myocardial ischaemia — and this is a recognised contributor to the delayed timing of postoperative cardiorespiratory events, which cluster on the second to fourth nights rather than immediately.
- Sleep disruption also contributes to postoperative delirium, along with the fragmentation caused by the intensive care environment.
The implications follow: opioid-sparing multimodal analgesia, caution with sedatives, continuation of home CPAP, extended monitoring in patients with severe obstructive sleep apnoea, and deliberate attention to the night-time environment.
Previously examinedOctober 2013 — the stages of sleep and the physiological changes accompanying them. Worked answers in the library
Consolidation
The lesson in one paragraph
Sleep is a reversible state of reduced awareness and responsiveness, distinguished from coma and anaesthesia by reversibility with sensory stimulation and by homeostatic regulation, and it is actively generated rather than a passive loss of arousal. It comprises non-REM sleep, in stages N1 with theta activity, N2 defined by sleep spindles and K complexes, and N3 slow-wave sleep with high-voltage delta; and REM sleep, with a desynchronised EEG resembling wakefulness, rapid conjugate eye movements, dreaming and skeletal muscle atonia sparing the diaphragm and extraocular muscles. Sleep is entered through non-REM, cycles about every 90 minutes over four to six cycles, with slow-wave sleep concentrated in the first third and REM periods lengthening towards morning; adult proportions are roughly N1 5%, N2 45%, N3 25% and REM 25%. Non-REM is a quiet brain in a movable body — cerebral metabolism falls, cardiovascular and respiratory variables fall steadily and regularly, and thermoregulation is maintained at a lower set point. REM is an active brain in a paralysed body — cerebral metabolism equals or exceeds the awake value, heart rate, blood pressure and breathing are irregular with sympathetic surges, ventilation becomes diaphragm-dependent, and thermoregulation is suspended so the subject is poikilothermic. Regulation is by two processes: homeostatic sleep pressure through adenosine accumulation, and the circadian rhythm of the suprachiasmatic nucleus entrained by light and expressed through melatonin. These act on a flip-flop switch of mutual inhibition between the GABAergic ventrolateral preoptic nucleus and the monoaminergic arousal nuclei, stabilised by orexin. Clinically, loss of pharyngeal dilator tone makes obstructive apnoea worst in REM, and the postoperative suppression of REM followed by rebound on nights two to four accounts for the delayed clustering of hypoxaemic and ischaemic events after surgery.