Improving ICU experience by appropriate use of Sedatives & Analgesics in ICU

1. PHARMACOTHERAPY of SEDATIVES &
ANALGESICS in ICU
DR SUBHANKAR PAUL
EMERGENCY MEDICINE & CRITICAL CARE
Gauhati Medical College & Hospital

2. “Pain is perfect misery, the worst of evils . . .”
John Milton
Paradise Lost

3. CONTENTS
• INTRODUCTION
• DEFINITIONS
• STRESS RESPONSE
• PAIN PATHWAY
• MODALITIES OF PAIN CONTROL
• DRUGS
• CONCLUSION

4. INTRODUCTION
• “Contrary to popular perception, our principal function in
patient care is not to save lives (since this is impossible on a
consistent basis), but to relieve pain and suffering, the patients
that experience the greatest pain and suffering are the ones in
the ICU” ........................ [Marino]
• most patients who are discharged from the ICU remember
discomfort and unrelieved pain as a dominant experience
during their ICU stay

5. Stressful Experiences in the ICU
(a) unrelieved pain,
(b) inadequate sedation,
(c) inability to communicate (in intubated patients),
(d) difficulty sleeping, and
(e) hallucinations and nightmares
• The most frequently cited source of stress is painful procedures
• Stressful experiences during the ICU stay can have prolonged
neuropsychiatric effects INCLUDING post-traumatic stress disorder

6. STRESS RESPONSE

7. Stress Response

9. Pain in Critically Ill Patients
• the prevalence of pain is the same in surgical ICUs and medical
ICUs
• Concept of Hypernociception
Critically ill patients experience pain more readily than healthy
subjects (hypernociception). For example, the most painful
experiences for ICU patients are endotracheal suctioning, and
being turned in bed. In addition, 30–50% of critically ill patients
experience pain while at rest, without a noxious stimulus. This
type of pain typically involves the back and lower extremities

10. • The heightened pain experience in critically ill patients is
attributed to immobility and systemic inflammation. (The rest
pain experienced by ICU patients is similar to the myalgias
experienced during a systemic infection.) Failure to recognize
this heightened nociceptive state is a major source of
inadequate pain relief in the ICU. Frequent pain assessments
using pain intensity scales (described next) can help to correct
problems with inadequate pain control in the ICU

11. Pain has a number of adverse consequences
• provoking anxiety
• contributing to lack of sleep
• worsening delirium
• increasing the stress response
• causing respiratory embarrassment due to atelectasis
and sputum retention
• causing immobility with venous and gut stasis.

13. Pain pathway
Pain pathway

14. Monitoring Pain
• The pain sensation can be described in terms of intensity,
duration, location, and quality, but pain intensity is the
parameter most often monitored because it reflects the
“unpleasantness” of pain.
• Pain Intensity Scales
• Pain intensity scales are used to determine the need for, and
evaluate the effectiveness of, analgesic therapy. There are 6
different pain intensity scales, but only a few are needed to
assess pain intensity in most ICU patients

15. Scale Method Comments
Adjective rating
scale
Easy to administer.
Visual analog
scale
Pain intensity measured in millimeters from one
end.
Numeric rating
scale
Can be used in patients with visual, speech, or
manual dexterity difficulties.
5-Point global
scale
Patient rates pain as: A decrease of one point is a large change; other
scales allow monitoring of small changes in pain and
may be more sensitive.
0 = none
1 = a little
2 = some
3 = a lot
4 = worst possible
Verbal
quantitative
scale
The patient is asked to self-report pain on a scale of 0 to 10
without descriptors.
Most commonly used scale, easy to administer.

16. Behavioral Pain Scale (BPS)

17. Role of Vital Signs ??
• Vital signs (e.g., heart rate) show a poor correlation with patients’
reports of pain intensity (the gold standard), and they can remain
unchanged in the presence of pain .
As a result,
VITAL SIGNS ARE NOT RECOMMENDED FOR PAIN ASSESSMENTS

18. Modalities of Pain management
• a caring and supportive ICU team, whom the patient can trust
• warm and comfortable surroundings
• attention to pressure areas
• bowel and bladder care
• adequate hydration and amelioration of thirst (e.g. moistening the mouth)
• early tracheostomy where indicated to reduce the discomfort of
endotracheal intubation
• Analgesics &/or sedatives
• Local/Regional Anaesthesia
• supplemental treatments such as acupuncture, acupressure, massage and
transcutaneous electrical nerve stimulation (TENS).

19. Drugs
OPIOID ANALGESIA
NON-OPIOID ANALGESIA
Nsaids
Drugs for neuropathic pain
 Local Anaesthetics

20. LOCAL ANAESTHETICS – REGIONAL ANALGESIA
• femoral nerve block for hip and femur injuries
• intercostal or paravertebral nerve blocks or catheters for thoracic
and upper abdominal injuries or wounds;
• brachial plexus or intravenous regional anaesthesia for isolated
upper limb injuries or procedures (e.g. fracture manipulation)
• epidural analgesia for thoracic and abdominal pain (e.g. flail chest,
pancreatitis
• intrapleural analgesia/anaesthesia, applied either via a catheter
placed for this purpose or via inter-costal drains

21. OPIOID ANALGESIA
• The natural chemical derivatives of opium are called opiates.
Opiates and other substances that produce their effects by
stimulating discrete opioid receptors in the central nervous
system are called opioids (eg.Morphine/Pethidine/Tramadol)
• The term narcotic refers to a general class of drugs that blunt
sensation and depress consciousness (i.e., narcotize).

22. CLASSIFICATION OF OPIOIDS
• 1. Natural opium alkaloids: Morphine, Codeine
• 2. Semisynthetic opiates: Diacetylmorphine
• (Heroin), Pholcodeine.
• Many others like—Hydromorphone, Oxymorphone,
• Hydrocodone, Oxycodone, are not used in India.
• 3. Synthetic opioids: Pethidine (Meperidine),
• Fentanyl, Methadone, Dextropropoxyphene,
• Tramadol.

24. Opioid receptor transducer mechanisms

25. BRAIN
periaqueductal gray,
locus ceruleus, and the rostral ventral medulla
spinal cord
interneurons and primary afferent neurons in the dorsal horn
Sensory neurons
immune cells (recruited to sites of inflammation)

26. CNS ACTIONS of MORPHINE
depressant actions stimulatORY ACtions
• CTZ : Nausea and vomiting
• Edinger Westphal nucleus of III nerve :
miosis , decrease in intraocular
tension.
• Vagal centre : bradycardia
• Certain cortical areas and hippocampal
cells : Excitation, Muscular rigidity and
Immobility , Convulsions
• Analgesia
• Sedation
• Mood and subjective effects
• Respiratory centre
• dose dependent DEPRESSION
• Cough centre
• Temperature regulating centre
• vasomotor centre

27. Neuro-endocrine FSH, LH, ACTH levels are lowered,
while prolactin and GH levels are
raised
Hypothalamic
influence on pituitary is reduced
CVS Vasodilatation
shift of blood from pulmonary to
systemic circuit
(a) histamine release.
(b) depression of vasomotor centre.
(c) direct action decreasing tone of blood vessels
GIT Constipation Action directly on intestines and in CNS
Spasm of pyloric, ileocaecal and anal
sphincters.
Decrease in all gastrointestinal secretions
Central action causing inattention to
defecation reflex
Biliary tract may cause biliary colic spasm of
sphincter of Oddi
Urinary bladder urinary urgency and
difficulty in micturition
Tone of both detrusor and
sphincter is increased
Bronchi can cause bronchoconstriction releases histamine

29. Morphine 0.1 milligram/kg IV Onset: 1–2 min
(IV) and 10–15 min
(IM/SC)
10 milligrams IM Peak effect: 3–5
min (IV) and 15–30
min (IM)
0.3 milligram/kg
PO
Duration: 1–2 h
(IV) and 3–4 h
(IM/SC)
Meperidine
(pethidine)
1.0–1.5
milligrams/kg
IV/IM
Onset: 5 min (IV) Contraindicated
when patient
taking a
monoamine
oxidase inhibitor;
neurotoxicity may
occur when
multiple doses
given in the
presence of renal
failure
Peak effect: 5–10
min (IV)
Duration: 2–3 h
(IV)
Fentanyl 1.0 microgram/kg
IV
Onset: <1 min (IV) High doses can
cause chest wallPeak effect: 2–5

30. Drugs and Dosing Regimens
• given intravenously as intermittent bolus doses or continuous
infusions
• It is important to emphasize that opioid dose requirements can
vary widely in individual patients, and that the effective dose of
an opioid is determined by each patient’s response, not by the
recommended dose range of the drug

31. Drug EquiAnalges
ic Dose (mg)
Typical Adult Dose Infusion(dose
/kg/hr
Onset Peak effect duration
Morphine 10 0.03-0.1mg/kg 0.02-
0.07mg/kg/hr
1–2 min (IV) and
10–15 min
(IM/SC)
3–5 min (IV) and
15–30 min (IM)
1–2 h (IV) and
3–4 h (IM/SC)
Meperidine
(pethidine
75mg 1.0–1.5 milligrams/kg
IV/IM
5 min (IV) 5–10 min (IV 2–3 h (IV)
Fentanyl 200 0.3-1.5 microgram/kg
IV
0.7-
10microg/kg/hr
<1 min (IV 2–5 min (IV 30–60 minutes
(IV)
Pentazocine 50 0.5-1mg/kg
Buprenorphine 0.3 milligram IV/IM
every 6 h
0.01mg/kg/hr
Tramadol 350

32. TRAMADOL
MOA
centrally acting analgesic relieves pain by opioid as well as additional
mechanisms.
• affinity for μ opioid receptor is low, while that for κ and δ is very
low.
• it inhibits reuptake of NA and 5-HT, and thus activates
monoaminergic spinal inhibition of pain
• Its analgesic action is only partially reversed by the opioid
antagonist naloxone.

33. • Pharmacokinetics : oral bioavailability is good (oral: parenteral
dose ratio is 1.4). The t½ is 5 hours and effects last for 4–6 hrs
• Dose :Dose: 50–100 mg oral/i.m./slow i.v. infusion (children
• 1–2 mg/kg) 4–6 hourly.Injected i.v. 100 mg tramadol is
equianalgesic to 10 mg i.m. morphine;
• USES ; Tramadol is indicated for mild-to-moderate short-lasting
pain due to diagnostic procedures, injury, surgery, etc, as well as
for chronic pain including cancer pain, but is not effective in
severe pain
• Tramadol causes less respiratory depression, sedation,
constipation, urinary retention and rise in intrabiliary pressure
than morphine

34. Patient-Controlled Analgesia
• For patients who are awake and capable of drug self-administration,
patient-controlled analgesia (PCA) can be an effective method of
pain control, and may be superior to intermittent opioid dosing. The
PCA method uses an electronic infusion pump that can be activated
by the patient. When pain is sensed, the patient presses a button
connected to the pump to receive a small intravenous bolus of drug.
After each bolus, the pump is disabled for a mandatory time period
called the “lockout interval,” to prevent overdosing.
• When writing orders for PCA, you must specify the initial loading
dose (if any), the lockout interval, and the repeat bolus dose. PCA
can be used alone or in conjunction with a low-dose opioid infusion

35. Commonly Used Intravenous Opioids

36. Adverse Effects of Opioids
1. Respiratory Depression
2. Cardiovascular Effects (decreases in blood pressure and heart rate)
3. Decreased Intestinal Motility (a risk for aspiration pneumonia)
4. Nausea and Vomiting (stimulation of the chemoreceptor trigger zone )
5. Other smooth muscles
• Biliary tract ( spasm of sphincter of Oddi )
• Urinary bladder ( urinary urgency and difficulty in micturition )
• Bronchi (bronchoconstriction mediated by histamine )
• The triad of miosis, hypoventilation, and coma should suggest
overdose with an opioid

37. PRECAUTIONS AND CONTRAINDICATIONS
1. Infants and the elderly are more susceptible to the respiratory
depressant action of morphine.
2. It is dangerous in patients with respiratory insufficiency
(emphysema, pulmonary fibrosis, cor pulmonale), sudden
deaths have occurred.
3. Bronchial asthma: Morphine can precipitate an attack by its
histamine releasing action.
4. Head injury: morphine is contraindicated in patients with head
injury

38. PRECAUTIONS AND CONTRAINDICATIONS…… cont
5. Hypotensive states and hypovolaemia exaggerate fall in BP due to
morphine.
6. Undiagnosed acute abdominal pain: morphine can aggravate certain
conditions, e.g.
diverticulitis, biliary colic, pancreatitis. Inflamed Appendix may rupture
7. Elderly male: chances of urinary retention are
high.
8. Hypothyroidism, liver and kidney disease patients are more sensitive to
morphine
9. Unstable personalities: are liable to continue with its use and become
addicted.

39. NON-OPIOID ANALGESIA
NSAIDS DRUGS FOR NEUROPATHIC PAIN

40. CLASSIFICATION
OF
NSAIDS

41. intravenous non-opioid analgesics
• acetaminophen,
• ketorolac,
• Diclofenac sodium

43. Adverse effects

44. DRUGS for Neuropathic Pain
• recommended drugs for neuropathic pain (e.g., from diabetic
are
• Gabapentin ( 600 mg every 8 hrs for gabapentin)
• Pregabalin (75-150 mg PO OD )
• carbamazepine(100 mg every 6 hours for carbamazepine),
• amitryptyline (10-25 mg OD )

45. Sedation in ICU

46. ANXIETY IN THE ICU
• Anxiety and related disorders (agitation and delirium) are observed
in as many as 85% of patients in the ICU
• 1. Anxiety is characterized by exaggerated feelings of fear or
apprehension that are sustained by internal mechanisms more
than external events.
• 2. Agitation is a state of anxiety that is accompanied by increased
motor activity.
• 3. Delirium is an acute confusional state that may, or may not, have
agitation as a component. Although delirium is often equated with
agitation, there is a hypoactive form of delirium that is
characterized by lethargy

47. Sedation
• Sedation is the process of relieving anxiety and establishing a
state of calm
1. general supportive measures
2. drug therapy

48. Monitoring Sedation
• The routine use of sedation scales is instrumental in achieving
effective sedation
• The sedation scales that are most reliable in ICU patients are
the the Richmond Agitation-Sedation Scale (RASS) & Sedation-
Agitation Scale (SAS)

49. Richmond
Agitation
Sedation Scale
(RASS)

50. SEDATIVES in ICU
 GABA-A RECEPTOR AGONISTS
• Benzodiazepines
• Propofol
• Barbiturates
 MAJOR TRANQUILLISERS
 α2-AGONISTS

51. BENZODIAZEPINES
• MOA : BZDs act by enhancing
presynaptic/postsynaptic
inhibition through a specific
BZD receptor which is an
integral part of the GABA A
receptor–Cl¯ channel
complex

52. BENZODIAZEPINES

53. ADVERSE EFFECTS
• Side effects of hypnotic doses are dizziness, vertigo,ataxia,
disorientation, amnesia, prolongation of reaction time—
impairment of psychomotor skills
• can aggravate sleep apnoea.
• BZDs synergise with alcohol and other CNS depressants leading
to excessive impairment
• Concurrent use with sod. valproate has provoked psychotic
symptoms

54. BENZODIAZEPINES
Advantages
• dose-dependent amnestic effect that is
distinct from the sedative effect. The
amnesia extends beyond the sedation
period (antegrade amnesia),
• anticonvulsant effects
• sedatives of choice for drug
withdrawal syndromes, including
alcohol, opiate, and benzodiazepine
withdrawal
Disadvantages
• (a) drug accumulation with prolonged
sedation, and
• (b) the apparent tendency for
benzodiazepines to promote delirium.
• Propylene Glycol Toxicity
• Abrupt termination of prolonged
benzodiazepine infusions can produce
a withdrawal syndrome, characterized
by agitation, disorientation,
hallucinations, and seizures

55. PROPOFOL

56. PROPOFOL
CHEMICAL NATURE 2,6diisopropylphenol , Propofol is highly lipophilic, and is suspended in a 10% lipid emulsion to
enhance solubility in plasma
Commercial Preparation 1% solution in an aqueous solution of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg
phosphatide
MOA selective modulator OF GABAA-Cl Channel complex
DOSE •Propofol dosing is based on ideal rather than actual body weight,
•Loading : 5μg/kg/min
•Maintenance : 5-50 μg/kg/min
•Loading doses are not advised in patients who are hemodynamically unstable (because of the
risk of hypotension
• no dose adjustment is required for renal failure or moderate hepatic insufficiency
ONSET a rapid IV injection (<15 seconds), produces unconsciousness within about 30 seconds
DURATION A single intravenous bolus of propofol produces sedation within 1–2 minutes, and the drug
effect lasts 5–8 minutes
METABOLISM +
ELIMINATION
Hepatic metabolism ,+ with extrahepatic clearance (pulmonary uptake and firstpass
elimination, renal excretion)
elimination halftime : 0.5 to 1.5 hours

57. CNS CEREBRO PROTECTIIVE EFFECT
1. decreases cerebral metabolic rate for oxygen (CMRO2), cerebral blood
flow, and intracranial pressure (ICP).
DECREASE IOP
CVS 1. decreases in systemic blood pressure (relaxation of vascular smooth muscle
produced by propofol is primarily due to inhibition of sympathetic
vasoconstrictor nerve activity) : exaggerated in hypovolemic patients, elderly patients,
and patients with compromised left ventricular function. Adequate hydration
before rapid IV administration of propofol is recommended
2. negative inotropic effect : BradycardiaRelated Death
RESPI Dosedependent depression of ventilation, with apnea
HEPATIC does not normally affect , Prolonged infusions of propofol have been associated with hepatocellular
injury
RENAL •does not normally affect,
•Urinary uric acid excretion is increased (may manifest as cloudy urine when the uric acid crystallizes in
the urine under conditions of low pH and temperature ) : no adverse renal effects
Prolonged infusions of propofol > excretion of green urine (presence of phenols in the urine.) : does
not alter renal function

58. OTHER EFFECTS
(Nonhypnotic Therapeutic
Applications)
1. Antiemetic Effects (10 to 15 mg IV) followed by 10 μg/kg/minute
More effective than ondansetron in preventing postoperative nausea and vomiting, effective
against chemotherapyinduced
Nausea and vomiting
2. Antipruritic Effects ((10 mg IV, is effective in the treatment of pruritus associated with neuraxial
opioids or cholestasis)
3. Anticonvulsant Activity :
4. Attenuation of Bronchoconstriction
5. Analgesia : does not relieve acute nociceptive pain.
6. Coagulation : does not alter tests of coagulation or platelet function
7. Allergic Reactions (phenyl nucleus and diisopropyl
side chain )
8. potent antioxidant properties resemble endogenous
antioxidant vitamin E
SIDE EFFECTS respiratory depression
and hypotension
Anaphylactoid re-actions to propofol are uncommon but can be severe
 green urine is observed occasionally from harmless phenolic metabolites
lipid emulsion in propofol preparations can promote hypertriglyceridemia
Propofol Infusion Syndrome (abrupt onset of bradycardic heart failure, lactic acidosis,
rhabdomyolysis, and acute renal failure )

59. Propofol
• Uses
• Propofol has sedative and amnestic effects, but no analgesic effects
• A single intravenous bolus of propofol produces sedation within 1–
2 minutes, and the drug effect lasts 5–8 minutes
• Because of the short duration of action, propofol is given as a
continuous infusion. When the infusion is stopped, awakening
occurs within 10–15 minutes, even with prolonged infusions
• Propofol was originally intended for short-term sedation when
rapid awakening is desired (e.g., during brief procedures), but it is
being used for longer periods of time in ventilator-dependent
patients, to avoid delays in weaning from ventilatory support

60. • Propofol was originally intended for short-term sedation when
rapid awakening is desired (e.g., during brief procedures), but
it is being used for longer periods of time in ventilator-
dependent patients, to avoid delays in weaning from
ventilatory support
• Propofol can be useful in neurosurgical patients and patients
with head injuries because it reduces intracranial pressure and
the rapid arousal allows for frequent evaluations of mental
status

61. Dexmedetomidine
• MOA = alpha-2 receptor agonist
• has sedative, amnestic, and mild analgesic effects and does not
depress ventilation
• The most distinguishing feature of dexmedetomidine is the
type of the sedation it produces

62. • Cooperative Sedation
• The sedation produced by dexmedetomidine is unique
because arousal is maintained, despite deep levels of sedation.
Patients can be aroused from sedation without discontinuing
the drug infusion, and when awake, patients are able to
communicate and follow commands. When arousal is no
longer required, the patient is allowed to return to the prior
state of sedation
• similar to temporary awakening from sleep. In fact, the EEG
changes in this type of sedation are similar to the EEG changes
in natural sleep

63. • Delirium
• Clinical studies have shown a lower prevalence of delirium in
patients who are sedated with dexmedetomidine instead of
midazolam and based on these studies, dexmedetomidine is
recommended over benzodiazepines for the sedation of
patients with ICU-acquired delirium

64. [MIDEX trial] & propofol [PRODEX trial])
Conclusions: Among ICU patients receiving prolonged mechanical ventilation,
dexmedetomidine was not inferior to midazolam and propofol in maintaining light
to moderate sedation. Dexmedetomidine reduced duration of mechanical
ventilation compared with midazolam and improved patients’ ability to
communicate pain compared with midazolam and propofol.

65. Conclusion In mechanically ventilated ICU patients managed with
individualized targeted sedation, use of a dexmedetomidine infusion
resulted in more days alive without delirium or coma and more time at
the targeted level of sedation than with a lorazepam infusion

66. Conclusions: From an economic point of view, dexmedetomidine
appears to be a preferable option compared
with standard sedatives for providing light to moderate ICU sedation
exceeding 24 hours. The savings potential
results primarily from shorter time to extubation

67. •

68. Adverse Effects of DEXMEDETOMIDINE
• dose-dependent decreases in heart rate, blood pressure, and
circulating norepinephrine levels (sympatholytic effect)
• Life-threatening bradycardia has been reported, primarily in
patients treated with high infusion rates of dexmedetomidine
(>0.7 µg/kg/min) together with a loading dose
• Patients with cardiac conduction defects should not receive
dexmedetomidine, and patients with heart failure or
hemodynamic instability should not receive a loading dose of
the drug

69. Haloperidol
• MOA : first-generation antipsychotic agent
• ACTIONS :
• sedative and antipsychotic effects by blocking dopamine receptors
in the central nervous system
• no respiratory depression, and
• hypotension is unusual in the absence of hypovolemia
• Because haloperidol has a delayed onset of action, midazolam can
be given with the first dose of haloperidol to achieve more rapid
sedation

70. Intravenous Haloperidol for the Agitated Patient

71. Adverse Effects
• (a) extrapyramidal reactions : (e.g., rigidity, spasmodic
movements) are dose-related side effects of oral haloperidol
therapy, but these reactions are uncommon when haloperidol
is given intravenously (for unclear reasons)
• (b) ventricular tachycardia : prolongation of the QT interval on
the electrocardiogram, which can trigger a polymorphic
ventricular tachycardia (torsade de pointes,) reported in up to
3.5% of patients receiving intravenous haloperidol
• (c) neuroleptic malignant syndrome : idiosyncratic reaction to
neuroleptic agents that consists of hyperpyrexia, severe
muscle rigidity, and rhabdomyolysis

72. NMDA RECEPTOR ANTAGONIST : Ketamine
• It produces a sedative state known as ‘dissociative anaesthesia’,
with the following characteristics:
• mild sedation
• amnesia
• analgesia
• reduced motor activity
Limitations:
• Hallucinations, and delirium during the recovery/withdrawal Phase
• Whole body catatonic state
• Sudden shooting of BP

73. • Uses : LIMITED
• sedation in severe asthmatics (for its bronchodilator effect),
• In patients following head injury (for its effect at the NMDA
receptor)
• in patients where analgesia is difficult (e.g. extensive burns)
• DOSE
• 0.2-0.8 mg/kg IV over 2-3 min
• 2-4 mg/kg IM

75. SEDATION STRATEGIES : Recent Aspects
• Goal-directed sedation
sedatives are freely adjusted (usually by the bedside nurse) to attain a
prescribed level of sedation from a sedation scoring system
• Patient-targeted sedation protocols
a structured approach to the assessment of patient pain and distress,
coupled with an algorithm that directs drug escalation and de-escalation
based on the assessments
• Daily interruption of sedation
daily interruption of both sedative and analgesic infusions until the patient
awakens or exhibits distress that mandates resumed drug administration

76. • Intermittent sedation
Involves use of longer-acting sedative agents, typically
lorazepam, given by intermittent bolus titrated via a sedation
Scoring system
• ‘analgosedation’ or analgesia-based sedation
• Patient-controlled sedation

77. THE FUTURE
• patient-controlled sedation
• target-controlled infusions (TCI) in intensive care
• automated/semiautomated sedation delivery systems
• melatonergic agents for nocturnal sleep (e.g. ramelteon,
valdoxane).

78. TAKE HOME MESSAGES : Improving the ICU
Experience
• Critically ill patients experience pain in situations that are not normally
painful
• Unrelieved pain can be a source of agitation, so make sure that pain is
relieved before considering a sedative drug for agitation
• When a benzodiazepine is used for prolonged (>48 hrs) sedation, attention
to preventing drug accumulation and prolonged sedation can result in a
shorter time in the ICU
• Consider using dexmedetomidine for sedation, PARTICULARLY in ventilator
dependant patients because this drug allows the patient to be aroused
while still sedated (more like sleep than a drug-induced stupor)
• Finally, communicate with patients (e.g., tell them what you are going to
do before doing it), and allow some “down time” for patients to sleep

79. REFERENCES
• Stoelting’s Pharmacology And Physiology In Anesthetic Practice -
5th Edition
• Marino's The ICU Book, Fourth Edition - Marino, Paul L
• Miller's Anesthesia 8TH EDITION
• KD Tripathi - Essentials of Medical Pharmacology, 6th Edition
• Tintinalli’s
• Clinical Practice Guidelines for the Management of Pain, Agitation,
and Delirium in Adult Patients in the Intensive Care Unit

80. THANK YOU