Sleep and ICU

Reviewed and revised 9 June 2014

OVERVIEW

  • Sleep is a  naturally occurring periodic, reversible state of cognitive and sensory disengagement from the external environment, from which a person can be aroused by sensory stimulation
  • Sleep is essential for physiologic rest and emotional well-being
  • Chemically-induced sedation is physiologically different to normal sleep and lacks restorative effects
  • Sleep patterns and architecture in the critically ill is usually abnormal
  • There are multiple causes of disrupted sleep in ICU

NORMAL SLEEP

Normal sleep architecture

  • Normal sleep consists of rapid eye movement (REM) sleep and non-rapid eye movement (Non-REM) sleep
  • a total of 7-8 hours per night is usual
  • normal human sleep period consists of four to six 90- to 100-minute periods during which NREM and REM alternate in a cyclical fashion
  • Non-REM sleep involves decreased activity of reticular activating system
  • involves increased activity in pre-optic region of hypothalamus and suprachiasmatic area

Nonrapid eye movement sleep is divided into three stages—N1, N2 and N3—which account for , , and  of the total sleep period

  • N1 (2% to 5% of total sleep period) — marks the entry into sleep from the waking state and is characterized by low-voltage theta waves (4–8 Hz) on EEG; aka  “light sleep”
  • N2(45% to 55%) — slower, higher amplitude waves with K-complexes and sleep-spindles on EEG
  • N3 (15% to 20%) — there is a particularly high threshold for arousal with high amplitude delta waves (0.5–2 Hz) on EEG; importatnt for restorative processes such as memory consolidation; aka  “slow wave” or “deep” sleep (and formerly known as stages 3 and 4 under the Rechtschaffen and Kales system)

Rapid eye movement (REM) sleep (20% to 25% of the total sleep period)

  • Tonic REM occurs throughout the REM period with intermittent bursts of phasic REM, during which the brain is highly active and dreaming and perceptual learning occur
  • Tonic REM is characterized by skeletal muscle atonia and low voltage, high amplitude, mixed frequency beta and “saw-tooth” theta waves on EEG
  • Phasic REM is characterized by rapid eye movements, along with autonomic variability and somatic muscle twitches

CIRCADIAN RHYTHMS

The sleep-wake cycle is regulated by two opposing processes:

  • Process S (sleep homeostat)
    • regulates the drive for sleep (including sleepiness, sleep onset, and sleep promotion)
    • primary neurotransmitter is adenosine,produced by  ATP metabolism which increases as a function of wakefulness
    •  Diurnal secretion of melatonin by the pineal gland also plays a role in sleep promotion
  • Process C (circadian pacemaker)
    • drives wakefulness
    •  suprachiasmatic nucleus is modulated by neural pathways that inhibit melatonin release via exposure to bright light
    •  neurotransmitters that promote wakefulness include orexin, acetylcholine, serotonin, norepinephrine, dopamine, and histamine

PHYSIOLOGICAL EFFECTS OF SLEEP

Temperature

  • core body temperature peaks late in the day and declines before sleep onset
  • Temperature sensitivity decreases during NREM
  • REM is characterized by poikilothermia and lose of compensatory mechanisms such as shivering and sweating

Metabolic

  • metabolic rate decreases by 10%
  • O2 consumption highest in REM sleep and lowest in stages 3 and 4 on non-REM sleep

Respiratory

  • loss of voluntary control of respiration
  • hypoxic and hypercapnic ventilatory drives are reduced, with responsiveness lowest during REM compared to NREM sleep
  • transition from wakefulness to N1 is marked by a decrease in minute ventilation  tidal volume and respiratory rate
  • As NREM sleep progresses, hypoventilation and a 3 to 7 mm Hg increase in arterial PCO2 levels
    (due to relaxation of upper respiratory muscles, increased airway resistance, and diminished central respiratory drive)
  • During REM sleep, respiratory rate and tidal volume vary widely especially during bursts of phasic REM

 Cardiovascular

  •  NREM has increased parasympathetic tone with decreased HR, BP and SVR; HR rises with increased venous during inspiration, and falls with decreased venous return during expiration
  • tonic REM is characterised by bursts of vagal activity on the background of decreased sympathetic tone lead to bradyarrhythmias and sinus pauses.
  • phasic REM has increased sympathetic activity with transient increases in HR and BP by up to 35%

 Gastrointestinal

  • During sleep, esophageal motility is reduced and rectal tone is preserved, while gastrointestinal motility remains relatively unchanged. A decrease in swallowing and saliva production also occurs, and the tonic contraction of upper esophageal sphincter prevents aspiration. Gastric acid secretion follows a circadian rhythm, peaking during early sleep.

Endocrine

  • Growth hormone (GH) peaks during the early stages of N3
  • Prolactin (PRL) peaks during the second half of the sleep period
  • Cortisol levels follow the circadian rhythm and rise in the early morning, peak in the late morning, and decline toward nighttime, reaching a nadir after sleep onset
  • Thyroid stimulating hormone (TSH) follows a similar circadian rhythm, peaking before sleep onset and declining slowly during sleep; secretion is inhibited by N3 sleep and increases with sleep deprivation

SLEEP DISRUPTION IN ICU PATIENTS

Sleep disruption in ICU patients typically includes:

  • difficulty with sleep initiation
  • sleep fragmentation
  • early morning awakenings and frequent arousals
  • decreased total sleep time
  • most sleep happens during the day
  •  predominance of wakefulness and light sleep (sleep stages I and II)
  • relative lack of rapid eye movement (REM) and deep sleep (delta sleep, formerly referred to as non-REM sleep stages III/IV)

Causes (often multi-factorial, and specific causes may not be known)

  • Critical illness (e.g. sepsis leads to disruption of normal melatonin secretion cycle)
  • Environment
    • noise level, spectrum and reverberation time  (staff conversation and alarms are most important)
    • light
    • patient care activities (monitoring, positioning, suction)
  • Mechanical ventilation (e.g. discomfort of the endotracheal tube, ineffective respiratory efforts, inudction of central apnoea events if not properly adjusted for the patient’s needs)
  • Pre-existing cause of sleep disturbance (e.g. end-stage renal failure, obstructive sleep apnoea, dementia)
  • Patient care activities (only accounts for ~30% of arousals and awakenings)
  • Pain
  • Anxiety and stress
  • Drugs
    • Sedatives (decrease sleep latency but cause a decrease in slow wave sleep and REM sleep so that sleep in non-restorative)
    • Substance abuse/ withdrawal
    • Numerous other medications may alter sleep architecture (e.g. antibiotics, gastric protectants)

Effects of sleep disruption and deprivation

  • delirium (adversely effects long term outcome; results from sleep deprivation and sedatives)
  • other neuropsychiatric sequelae (e.g. PTSD, anxiety, cognitive impairment)
  • increased sympathetic and decreased parasympathetic tone
  • BP and HR lability and increased risk of acute myocardial infarction in normal subjects
  • impaired immune function
  • increased cortisol and catecholamine levels
  • increased oxygen consumption and CO2 production
  • negative nitrogen balance
  • delayed weaning from mechanical ventilation (reduction in ventilatory response to hypoxia and hypercapnia)
  • increased T3 and T4 (though these are suppressed by critical illness)
  • GH and PRL suppression may impact on muscle wasting and immune function
  • hyperglycaemia (insulin hyposecretion and resistance)
  • fatigue may impair early mobilisation and physiotherapy

ASSESSMENT AND MANAGEMENT OF SLEEP IN ICU

Assessment of sleep quality (often difficult or infeasible in clinical practice)

  • Daily sleep diaries, visual analog scales (VAS), questionnaires, and symptom or quality of life questionnaires with sleep items (subject to recall bias and other problems)
  • Direct observation of arousals and motor activity (under-estimates sleep disruption)
  • Actigraphy (movement detector, under-estimates sleep disruption)
  • Bispectral index  (detects sleep, not reliable for depth of sleep)
  • polysomnography (gold stand, usually not feasible)

Management

  • treat underlying cause
  • noise reduction (earplugs, behavioural modification, sound masking, and acoustic absorption)
  • provide appropriate light exposure (maintain a quiet, dark room during the nigh, and reduce sleep interruptions during the nocturnal hours)
  • coordinate patient activities and interventions with sleep cycle
  • optimise ventilatory support  to avoid non-triggering breaths, apnoea and desaturation episodes
  • consider short-acting hypnotics (e.g. zolpidem, which maintains deep sleep stages better than benzodiazepines), sedating antipsychotics and antidepressant medications if still unable to sleep (but these risk causing delirium)
  • if sedation needed for sleep, propofol may be better for restorative sleep than benzodiazepines or opiates
  • role for melatonin is uncertain
  • role for complementary measures (such as relaxation techniques and massage) is uncertain
  • consider consulting a sleep specialist in refractory or problematic cases

References and Links

Journal articles

  • Bellapart J, Boots R. Potential use of melatonin in sleep and delirium in the critically ill. Br J Anaesth. 2012 Apr;108(4):572-80. PMID: 22419624. [Free Full Text]
  • Kamdar BB, Needham DM, Collop NA. Sleep deprivation in critical illness: its role in physical and psychological recovery. J Intensive Care Med. 2012 Mar-Apr;27(2):97-111. PMC3299928.
  • Matthews EE. Sleep disturbances and fatigue in critically ill patients. AACN Adv Crit Care. 2011 Jul-Sep;22(3):204-24. PMC3149788.
  • Mistraletti G, Carloni E, Cigada M, Zambrelli E, Taverna M, Sabbatici G, Ombrello M, Elia G, Destrebecq AL, Iapichino G. Sleep and delirium in the intensive care unit. Minerva Anestesiol. 2008 Jun;74(6):329-33. PMID: 18500209. [Free Full Text]
  • Shapiro CM, Devins GM, Hussain MR. ABC of sleep disorders. Sleep problems in patients with medical illness. BMJ. 1993 Jun 5;306(6891):1532-5. PMC1677972.
  • Watson PL, Ceriana P, Fanfulla F. Delirium: is sleep important? Best Pract Res Clin Anaesthesiol. 2012 Sep;26(3):355-66. doi: 10.1016/j.bpa.2012.08.005. PMC3808245.
  • Weinhouse GL, Schwab RJ, Watson PL, Patil N, Vaccaro B, Pandharipande P, Ely EW. Bench-to-bedside review: delirium in ICU patients – importance of sleep deprivation. Crit Care. 2009;13(6):234. PMC2811939.
  • Xie H, Kang J, Mills GH. Clinical review: The impact of noise on patients’ sleep and the effectiveness of noise reduction strategies in intensive care units. Crit Care. 2009;13(2):208. PMC2689451.

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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