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Sleep and Sedation in Icu 2

The document discusses the critical importance of sleep and sedation in the Intensive Care Unit (ICU), highlighting how sleep deprivation affects critically ill patients and the role of sedation in managing anxiety and facilitating care. It details the physiological aspects of normal sleep, the disturbances caused by ICU environments, and the implications of various sedatives on sleep architecture. Strategies for promoting better sleep in the ICU setting are also presented, emphasizing the need for careful sedation management to improve patient outcomes.

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Ananya Chaturvedi
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12 views26 pages

Sleep and Sedation in Icu 2

The document discusses the critical importance of sleep and sedation in the Intensive Care Unit (ICU), highlighting how sleep deprivation affects critically ill patients and the role of sedation in managing anxiety and facilitating care. It details the physiological aspects of normal sleep, the disturbances caused by ICU environments, and the implications of various sedatives on sleep architecture. Strategies for promoting better sleep in the ICU setting are also presented, emphasizing the need for careful sedation management to improve patient outcomes.

Uploaded by

Ananya Chaturvedi
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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SLEEP AND SEDATION IN

INTENSIVE CARE UNIT

PRESENTOR : Dr.Abhishek Patel


MODERATOR : Dr.Astha mam
INTRODUCTION

● Sleep is an essential physiologic function with restorative effects on cognition,


immunity, and metabolism.
● Critically ill patients in the ICU commonly experience sleep deprivation and
disruption of circadian rhythms.
● Sedation is often used to reduce anxiety and facilitate ventilation—but it can
further alter natural sleep architecture.
● Understanding the relationship between sleep and sedation can help improve
outcomes in critically ill patients.
Normal Sleep Physiology
Non-Rapid Eye Movement (NREM): ~75–80%
of total sleep

Stage N1 (Light sleep): Transition from


wakefulness; easily arousable.

Stage N2: Sleep spindles and K-complexes


appear; memory consolidation begins.

Stage N3 (Slow-Wave Sleep, SWS): Deepest


stage; physical restoration, growth hormone
release.
Rapid Eye Movement (REM) Sleep: ~20–25% of total sleep

High brain activity, vivid dreaming, muscle atonia.

Important for memory consolidation, emotional regulation.

● A full sleep cycle = 90–110 minutes.

● 4–6 cycles per night in healthy individuals.

● Circadian rhythm regulated by suprachiasmatic nucleus (SCN) and melatonin.

Melatonin: Melatonin level decrease with increasing age making older icu patient more
sensitive to circadian rhythm disruption.

Opioids increase melatonin level throughout 24 hr period


Sleep Disturbance in the ICU

● ICU sleep is fragmented, with frequent arousals and altered architecture.


● Loss of circadian rhythm, reduced SWS and REM sleep.

Causes:

● Environmental: 24/7 Light exposure, noise >50 dB, staff interactions, alarms
● Patient-related: Pain, dyspnea, delirium, mechanical ventilation
● Pharmacological:benzodiazepines (decrease slow-wave sleep),
opioids(suppress REM), inotropes, corticosteroids (disrupt circadian rhythm).
● Illness severity: Sepsis, inflammation affect sleep via cytokines (e.g. IL-1,
TNF)
Consequences of Sleep Deprivation
Neurocognitive effects:

Delirium, hallucinations, poor memory, anxiety

Physiological effects:

Immune dysfunction, insulin resistance, altered HPA axis response

Respiratory & Cardiovascular:

Respiratory muscle fatigue, poor weaning from ventilation

Increased sympathetic tone → tachycardia, hypertension

Mortality association:

Sleep disruption correlates with increased ICU length of stay and worse outcomes
Sedation in ICU
Indications:

1.Reduce anxiety, agitation

2.Promote synchrony with mechanical ventilation

3.Facilitate procedures

4.Prevent self-harm or device removal

5.Improve comfort in palliative or end-of-life care

However, sedation does not restore physiologic sleep.

Many sedatives suppress REM and SWS, which are essential for restorative
sleep.
Sedation vs. Sleep – Key Differences
Sedatives Used in ICU and Their Effect on Sleep
1. Benzodiazepines (e.g., Midazolam, Lorazepam)
Mechanism:

GABA-A receptor agonists.


Increase total sleep time, but suppress deep and REM sleep.

Effects on Sleep:

↓ Slow-wave sleep (Stage N3)


↓ REM sleep
↑ Light sleep (N1, N2)
Disrupts normal sleep architecture
Promotes non-physiological sedation rather than restorative sleep
Clinical Implications:

Associated with increased ICU delirium

Poor sleep quality may lead to psychological sequelae post-ICU


2. Propofol
Mechanism:

Potentiates GABA-A receptor activity.

Effects on Sleep:

EEG pattern mimics non-REM sleep, but it is not physiologic sleep.


↓ REM and SWS
Disrupts circadian rhythm
Induces unconsciousness, not true sleep
Clinical Implications:

Promotes immobility and amnesia, but not sleep restoration


Associated with sleep fragmentation upon emergence
PROPOFOL INFUSION SYNDROME (PRIS)

Occurs with high-dose (>4 mg/kg/hr) infusions >48 hrs, mainly in ICU.

Characterized by:

Metabolic acidosis

Rhabdomyolysis

Hyperkalemia

Cardiac failure

Renal failure

Avoid high-dose infusions in ICU unless clearly indicated.


3. Opioids (Fentanyl, Morphine, Remifentanil)
Mechanism:

μ-opioid receptor agonists

Effects on Sleep:

↓ REM and SWS


↑ Arousals and sleep fragmentation
Alter sleep-wake cycles
Suppress circadian melatonin secretion

Clinical Implications:

Poor sleep quality, contributes to delirium


Tolerance and hyperalgesia may worsen sleep over time
4. Ketamine
Mechanism:

NMDA receptor antagonist

Effects on Sleep:

Increases REM sleep at low doses


High doses disrupt sleep architecture
May produce vivid dreams, hallucinations

Clinical Implications:

Adjunct role in preserving REM, especially when used intermittently


May induce psychotropic effects that interfere with restful sleep
5. Dexmedetomidine
Mechanism:

Selective alpha-2 adrenergic agonist, acts on the locus coeruleus (a natural sleep-
promoting center). Activation of the receptors in the brain and spinal cord inhibits
neuronal firing, causing hypotension, bradycardia, sedation and analgesia.

Dosage:
Loading dose : 0.5 - 1 microgrm / kg
Infusion dose : 0.1 - 1 ug/kg/hr

Effects on Sleep:

Most sleep-like sedation among ICU drugs


Preserves N2 and N3 sleep, partially restores REM
Mimics natural non-REM sleep more closely than other agents
Clinical Implications:

Associated with lower delirium risk


Enhances sleep continuity and sleep architecture
Often used for overnight sedation in ventilated patients to promote sleep

Advantages:

EEG features resemble natural NREM sleep

Minimal respiratory depression


Preserves sleep architecture better than other agents

Ideal for weaning, delirium prevention, or neuro exams

Limitations:

Bradycardia, hypotension, cost


SEDATION ASSESSMENT TOOLS
1. Importance of Monitoring Sedation:

Avoid oversedation and undersedation.

Ensure patient comfort, safety, and facilitate clinical goals.

Necessary for titrating sedatives and assessing readiness for weaning/extubation.

2. Common Sedation Scales:

a. Richmond Agitation-Sedation Scale (RASS)


b. Sedation-Agitation Scale (SAS)
C.Ramsay sedation scale
Prolonged deep
section(RASS<= -3)
Associated with
increase icu , hospital
stay & delirium.

Target in ICU:
-2 to 0
(Light sedation)
2. Sedation-Agitation Scale (SAS)
3.Ramsay Sedation Scale(Older, Less Used Now)
BIS – Bispectral Index Monitoring
Sleep-Promoting Strategies in ICU
Environmental interventions:

Noise reduction (<40 dB), earplugs, eye masks

Light control: simulate day-night cycle

Bundle care to minimize night-time disruptions

Chronotherapy:

Melatonin supplementation

Pharmacologic:

Use sedatives like dexmedetomidine which support sleep physiology

Music therapy
“A calm, cooperative ICU patient is
safer and heals faster than a deeply
sedated one.” — Miller’s Anesthesia
THANK YOU !!

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