Physiology Of Sleep

Physiology Of stopPhysiology Of calmnessIntroductionSleep is a state of reversible lethargy in which the sensation is petty(a) responsive to external stimuli. We be help wholey blind during peace with no response to visual stimuli and a fall threshold of response to auditory stimuli. Babies affirm been exposed to sound of up to 100 dB, which is above the legal limit for ear protection for employees, without wakeful up. In adults, the action is selective demonstrating continuing cortical function. For example, a log Zsing mother is woken by her crying baby moreover not by other louder noises.Definition of relaxation and quietingPhases with specific EEG patterns and physiological changes. Natural quietness is sepa rankd into two distinctive states non rapid midriff execution (N.R.E.M) and rapid fancy movement ( paradoxical calm) peacefulness. nonrapid eye movement stay is past further seperated into 4 exhibits where stage 1 is the lightest and stage 4 the dee pest train of respite. rapid eye movement slumber quietus is divided into phasic and sweet sorts. The two distinctive states embrace a regular pattern called a stillness cycle which, in an adult, hold waters more or less 1 and half hours and comprises a full point of N.R.E.M quietness followed by paradoxical sleep sleep. The cycles may be separated by a period of wakefulness and ar repeated 36 times distributively dark and ar typically displayed as an hypnogram (Fig. 1). The majority of deep (stage 4) N rapid eye movement sleep sleep occurs in the first and second cycles. As the night progresses, the likeness of rapid eye movement sleep sleep in a cycle join ons and the NREM particle is of lighter stage 2 sleep.Age has a major motion on the duration of sleep and the ratio of NREM/REM sleep. Neonates sleep 1618 h. It is widely distributed through with(predicate)out the day with REM sleep accounting for 50% of total sleep time (TST). This may be even greater in premature babies. By the age of 24 months, children should sleep 10 h per day, mainly at night with unitary or two naps during the daytime and REM sleep has declined to 2025% of TST. Adults normally sleep 68 h per day with 1520% REM sleep. With increasing age, TST changes little although sleep is more split with more frequent and longer a modifys ( lessen sleep efficiency) with less REM sleep and more light NREM sleep. Night-time sleep may be decreased if naps be taken during the day.Functions of sleepThe functions of sleep are still bad understood. However, the observation that sleep (or, atleast, an military actionin application cycle) is present in all species and has been preserved throughout evolution and that sleep deprivation leads to a drastic deterioration in cognitivefunction and eventually to rational and physical morbidity proves its importance.It has been suggested that sleep might conserve energy by reducing core temperature slightly and lowering metabolic rate by 10% compared with quiet wakefulness. Sleep would prevent perpetual natural process as a response to environmental stimuli leading to excessive energy consumption. However, sleep is a state of starvation and at that place is no evidence that sleep is important for tissue repair. Sleep has been implicated as an important figure in storage of long-term memory. Facts learned during the day are ordinarily better remembered the next morning whereas facts learned s pratt(p)ly before acquittance to sleep are often poorly recalled.Electrophysiological features of sleepThe stages of sleep are characterised by typical patterns of electroencephalogram (EEG), electro-myogram (EMG) and electro oculogram (EOG) activity Wakefulness with open look is characterised by an EEG with dominant low amplitude, proud frequency genus Beta activity of1625 Hz. Muscle tone is normally gamy with high to moderate EMG activity. pose 1Sleep is comm barely initiated by a transition from wakefulness to a s tate of drowsiness with closed eyes and a shift from EEG beta activity to alpha activity of 812 Hz passing to decimal point 1NREM sleep with a mixed frequency EEG-pattern with low amplitude theta waves of 37 Hz accompany by silent rolling eye movements. Involuntary muscle clonus occurs frequently,resulting in jerky movement of the whole body (hypnic jerks) and EMG activity is moderate-to-low. This stage lasts typically only 510 min, during which time minor auditory stimuli allow pee-pee arousal.Stage 2Stage 2 is characterised by short bursts of high frequency activity (1215 Hz sleep spindles) and K-complexes (large amplitude biphasic waves). natural movements continue andthe EMG activity is low-to-moderate. This stage is commonly short (1020 min) in the first 12 cycles but predominates in afterward cycles. It is the most abundant sleep stage in adultsaccounting for up to 50% of TST.Stages 3 and 4Deep NREM sleep stages 3 and 4, sometimes combined as slow wave sleep (SWS) ar e characterized by high amplitude low frequency delta waves ( 75V and 0.52 Hz) with stage3 having between 2050% and stage 4 more than 50% delta activity. EMG activity is low and eye movements are rare. Arousal through auditory stimuli from this stage of sleep is vexed and, if awakened, the individual is often disorientated and slow to react. Return to sleep is easy and short arousals ( 30 sec) are rarely remembered.REM sleepNREM sleep is followed by REM sleep, the proportion increasing with each cycle. REM sleep is characterised by a fast mixed frequency low potential EEG with saw-tooth waves andrapid eye movements on the EOG. During the tonic phases of REM sleep, on that point is marked reduction of muscle tone and EMGactivity in skeletal muscles. The tonic phases of REM sleep are interrupted by short episodes of phasic REM sleep with increased EMG activity and limb twitches. The atonia of REM sleep affects all skeletal muscles, provided the diaphragm and the upper airline busin ess muscles, and is associated with hyperpolarisation of the -motor neurones. The purpose of this may be to prevent the acting out of dreams. just about 10% of the population have experienced sleep paralysis (i.e. wakening from sleep and finding that the atonia haspersisted into wakefulness). It can be frightening but is entirely harmless. Natural wakening ordinaryly occurs from REM sleep. Subjects woken from REM sleep are much more likely to recall dream meaning than those awakened from NREM sleep. NREM dreams are generally vague and unformed in contrast to REM dreams.Physiological changes during sleepRespiratory corpseDuring NREM sleep, there is a decrease in respiratory crash and a reduction in the muscle tone of the upper skyway leading to a 25% decrease in minute book of account and alveolar ventilation and a doubling of airway resistance accompanied by a small (0.5 kPa) increase inPaCO2 and decrease in PaO2. Hypercarbic and hypoxic ventilator drives are reduced compared with wakefulness. The breathing pattern is regular except at the transition from wakefulness into sleep when brief central apnoeas are common.During REM sleep there is a further decrease in hypercarbic and, particularly, hypoxic ventilatory drives. The breathing pattern is irregular especially during phasic REM sleep. The dismission of skeletal muscle tone in REM sleep affects the intercostal and other muscles which stabilise the chest wall during inspiration. In infants, this may be seen as paradoxical movement of the rib cage and abdomen. In adults, there may be maldistribution of ventilation and impaired ventilationperfusion matching with outcome arterial hypoxaemia. In normal subjects, this is unimportant but it may be very(prenominal) important in patients with chronic lung disease or abnormalities of the pectoral (e.g. kyphoscoliosis). The great majority of patients with impaired respiratory function bequeath be at their worst during REM sleep.Cardiovascular systemBlood stuff decreases during NREM and tonic REM sleep but may increase above argus-eyed values during phasic REM sleep. Cardiac output is generally decreased during all sleepphases. Systemic vascular resistance (SVR) and the heart rate are both reduced during NREM and tonic REM sleep and increased during phasic REM sleep.Central nervous system noetic blood flow (CBF) increases by 50100% above the aim of resting wakefulness during tonic REM sleep and is even greater during phasic REM sleep. Cerebral metabolic rate, oxygen consumption and neuronal discharge rate are reduced during NREM sleep but increased above resting values during REM sleep. The autonomic nervous system shows a general decrease in sympathetic tone and an increase in parasympathetic tone,except in phasic REM sleep.Renal systemThe glomerular filtration despatch and filtration fraction are reduced and ADH secernment is increased resulting in a less volume concentrated urine.Endocrine systemThe secretion of several endoc rines is directly linked to the sleep/wake cycle. Melatonin is released from the pineal secretor under the incorporate of the supra-chiasmatic nuclei (SCN) in a 45h pulse, usually commence at the onset of darkness (9 pm). The pulse is inhibited or delayed by exposure to bright light in the evening. It is crush regarded as existence permissive of sleep (opening the gate to sleep) rather than as an hypnotic, as it is possible to maintain wakefulness during this period. appendage hormone is mostly secreted during the first episode of SWS, particularlyduring puberty. Prolactin concentrations in addition increase shortly after sleep onset and decrease with wakefulness. Sleep phase delay delays secretion of both of these hormones. The secretion of cortisol decreases with the onset of sleep and reaches a trough in the early hours of the morning and a percentage point just after waking.Temperature controlIn contrast to anaesthesia, thermoregulation is maintain during sleep. Howeve r, the shivering threshold is decreased and body core temperature decreases by about 0.5C in humans and 2Cin hibernating mammals. dust temperature is linked to the circadian oscillation and reaches its nadir at about 3 am. Thermoregulation is quite good in human infants compared withother species.Control of sleepSleep follows a circadian (1 day) cycle, the periodicity of which is regulated by an independent genetically determined essential measure which is entrained to a 24 h cycle by external cues (Zeitgebers) such as light, darkness, clock time, working patterns and meal times. When a human being is deprived of all external time clues and is exposed to constant levels of illumination (free data track), the wake/sleep cycle typically lengthens to about 24.5 h. Subjects who are natural blind without any appreciation of light generally free communicate while those blinded in later lifeor who retain some erudition of light remain entrained.All living organisms, including plant s and fungi, have been rear to have clock genes and to show an inactivity/activity cycle. In mammals, control of the intrinsic clock is located in the SCN on either side of the third ventricle, just above the optical chiasm. In animal experiments, its destruction leads to a change from the normal sleep cycle into several shorter sleep/activity periods during the day. As noted above, melatonin secretion isprompted by the SCN just before the usual time of sleep onset. A mismatch of this pattern with sleeping time, as occurs in shift workers and after trans-meridian flights, leads to sleep disturbance (jet recede) as the subject is trying to sleep during their circadian day. Light therapy can be helpful in re-setting the circadian clock and the interested lector is referred to the bibliography.The propensity to fall asleep varies throughout the day and depends upon both circadian factors (process C) and time since the last sleep period (process S). The longer the time since thelast sleep period, the greater leave be process S. However, its propensity will be modulated by process C. The circadian pressure to sleep is greatest at 2 am with a secondary peak at 2 pm. It is least at 6 am and 6 pm. If a subject elects to stay awake throughout the night, they will smelling most sleepy in the small hours of the morning but will get a second wind as morning approaches and the circadian pressure to sleep declines. If wakefulness is maintained, a second period of sleepiness and relative alertness will follow in early afternoon and early evening, respectively. Some of the 8-h sleep debt will be recovered that night but process C will ensure that awakening will occur at or shortly after the normal waking time.Sleep is normally an actively initiated and not a passive process. Unless a subject is sleep deprived, successful initiation of sleep depends both upon the phase of the circadian clock andexternal factors (recumbent position, darkness, reducing sensory input). Ove r the years, long effort has been focused on a search for (i) a sleep centre, a nucleus or region in the pass where stimulation or ablation would lead to sleep and (ii) a hormone or transmitter which would reliably induce sleep. Neither have been found because the mechanisms resulting in sleep are complex and diffuse.During wakefulness, the CNS is dominated by activity of the ascending reticular activating system (RAS) in the brain stem. This formation receives sensory input from all peripheral sensors and projects to the thalamus and the cortex. Its main neurotransmitters are acetylcholine, noradrenaline, dopamine and histamine which explains the sedative resolution of antagonists to thesesubstances. A decrease in its activity permits sleep to be initiated by suppressing incoming external stimuli.The induction of SWS is associated with the secretion of -aminobutyric acid (GABA) from basal forebrain neurones. Therefore, it is not surprising that benzodiazepines and barbiturates, which act through stimulation of GABA receptors in the CNS, induce sleep or anaesthesia. cholinergic mechanisms initiate REM sleep through stimulation of pontine neurones in the squinty portion of the pontine tegmentum and the nucleus reticularis pontis oralis. In animal experiments, injection of carbachol (acetylcholine agonist) induces instantaneous REM sleep.Recently, orexins (hypocretin) have been isolated in the hypothalamus and appear to be important in the control of REM sleep and appetite. CSF concentrations of orexins have been found to be very low in patients with narcolepsy.Influence of surgery and anaesthesia on sleepAnaesthesia and surgery can have a profound effect upon sleep. On the first night after surgery, sleep architecture is in earnest disrupted with little or no SWS and REM sleep. Thelight Stage 2 sleep is fragmented with frequent awakenings. The degree of disruption appears to be related to the severity of the surgical insult. The mechanism is unclear but it is probably due to a combination of the surgical stress and the effects of opioid analgesics. recovery of lost SWS and REM sleep occurs on postoperative nights 25, being later after major surgery. This coincides with the nadir of postoperative pneumonic function and severalstudies have demonstrated marked hypoxaemia associated with the rebound of REM sleep. It was a logical step to attribute postoperative myocardial ischaemia, myocardial infarction, pulmonary embolism and cerebral disorder (delirium and cognitive impairment) to nocturnal hypoxaemia. However, a scrap of studies have failed to confirm these presumed associations,although this does not exclude the possibility that the hypoxaemia may be important in some individuals.Key referencesAmbrosini MV, Giuditta B. Learning and sleep the serial hypothesis. Sleep Med Rev20015 47790Dijk DJ, Lockley SW. 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