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Vicken Y. Totten MD, FACEP MS With help from Drs. David Cheng, Kelly Abbrescia, Tonya M. Thompson, and many others. Sedation. Historical notes. Alcohol probably the earliest analgesic Lousy analgesic, poor therapeutic window Opiates x 1000s years Highly valued, scarce

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Vicken Y. Totten MD, FACEP MS

With help from Drs. David Cheng, Kelly Abbrescia, Tonya M. Thompson, and many others

historical notes
Historical notes
  • Alcohol probably the earliest analgesic
    • Lousy analgesic, poor therapeutic window
  • Opiates x 1000s years
    • Highly valued, scarce
  • Chloroform / Ether / Nitrous Oxide
    • Major step towards anesthesia, analgesia

Review a few relevant definitions.

Review goals of procedural sedation

Review sedative agents


Pain: Noxious sensation transmitted by the nervous system to the brain; influenced by cognition and emotion.

Sedation: a spectrum of reduced responsiveness to one’s environment

Anesthesia: “no sensation” -- No response to environment, sometimes including own body needs

Analgesia: “No pain” - relief of pain without anesthesia.

more definitions
Dissociation (aka “dissociative sedation”). “The lights are on, and nobody’s home.”

Disruption of perception with maintenance of neural activity

Combines:i) sedation

ii) analgesia

iii) amnesia

iv) maintenance of muscle tone

More definitions
more definitions1
Anxiety: unpleasant emotional and physiological state of anticipating danger, pain, or distress.

“Anxiolysis” – breaking anxiety. Reducing anxiety without producing sedation (ie. without reducing LOC)

More definitions
controlled sedation
Controlled sedation

It’s a continuum!

Reassurance  general anesthesia.

To the extent that you take control away from the patient, be prepared to substitute for those functions

Sedation is NOT analgesia

levels of sedation
Levels of sedation

Minimal sedation / anxiolysis only

no depression of consciousness

Moderate sedation / moderately depressed LOC;

still responds purposefully to verbal commands or light touch

Deep sedation / markedly depressed LOC;

responds purposefully only to intense or painful stimuli

airway and respiratory function may be depressed

general anesthesia
General anesthesia

No purposeful response to any kind of stimuli. May have unconscious awareness of very painful stimuli (ie. HR RR BP ICP)

airway and respiratory function profoundly depressed; typically require airway and ventilation assistance

Autonomic & cardiovascular functions may be depressed

We don’t want to go here.

the ideal ed procedural agent
The Ideal ED Procedural Agent

No anxiety before event. (Anxiolysis)

No pain during event. (Analgesia)

No memory of event. (Amnesia)

And, complete function of all protective reflexes during the entire procedure

what other characteristics would ed procedural agents ideally possess
What Other Characteristics Would ED Procedural Agents Ideally Possess?

Rapid onset

Short duration of action.

Rapid offset (ie. zero residual action).

No hemodynamic effects.

Easy to use and administer

Wide therapeutic window

Minimal contraindications

Well tolerated (ie. minimal side-effects.)

doesn t exist so we settle for
Doesn’t exist. So we settle for…

Analgesia: Local or General

Sedation  Anxiolysis,

+/- amnesia for the event

Protective reflexes  usually diminished.

How much diminution of reflexes is tolerable?

the moderately sedated state includes
The moderately sedated state includes:

marked anxiolysis

full amnesia

maintenance of airway, respiratory function, and cardiovascular function

  • Easy to overshoot from moderate sedation to deep sedation or to the anesthetic state.
    • loss of airway protection
    • marked respiratory depression
    • possible cardiovascular / autonomic depression.
  • Sedation not always analgesic
ample pre sedation assessment
AMPLE Pre-Sedation Assessment-

A-Allergies- Foods, medications, latex, act.

M-Medications, including prior sedations

and how tolerated.

P-Past medical history

L-Last PO intake

E-Events leading to why patient is having sedation

asa classes
ASA classes
  • ASA 1: Healthy
  • ASA 2: Mild controlled disease, 1 system;
  • ASA 3: Poorly controlled disease 1 major system
  • ASA 4:≥ 1 system; severe disease, constant threat to life
  • ASA 5: Moribund, imminent death, not expected to live
get your team prepare
Get your team & Prepare
  • Additional person
  • “SOAP-ME”:
  • Suction
  • Oxygen
  • Airways (BVM, oral, LMA, ETT)
  • Pharmacy (meds)
  • Monitors
  • Equipment (defibrillator, airway supplies, etc)
reversal agents don t count on them
Reversal Agents-don’t count on them
  • Naloxone
    • Competitively binds all 3 opiate receptors
    • IV, IM, SC, SL, ETT
    • 0.1 mg/kg
  • Flumazenil
    • Can terminate paradoxical reactions
    • 0.02 mg/kg
    • Lowers seizure threshold
documentation monitoring
Documentation & Monitoring
  • Time out
  • Record q5 minutes
  • SPO2 & ETCO2 / HR / BP / LOC
  • O2 given
  • Medications
  • Interventions
remember for each drug
Remember for each drug…

The agent’s specific procedural role

Its onset / duration / offset

Hemodynamic effects


Potential side-effects


The standard: benzodiazepines

Benzos (BZP’s) bind to and potentiate GABA (CNS inhibitory neurotransmitter)

in smaller doses: 1) anxiolysis

in larger doses:

1) sedation

2) amnesia

3) respiratory and CV depression

midazolam versed the standard
Midazolam (Versed) the standard

Short acting, potent, reversible, safe. Hydroxylated by the liver. 1 active & 2 inactive metabolites.

Metabolites are conjugated and excreted in the urine.

Chronic alcoholics: potentiated metabolism,shortened duration of action

Cirrhosis or renal failure: decreased metabolism,prolonged duration of action


Highly lipid soluble at physiological pH  rapid CNS uptake

Peak effect within 1-5 minutes when given IV

Duration of effect variable 30-60 minutes…

Longer in the obese because of lipophilic distribution.

Activity sub-therapeutic after 7-15 mins.

midazolam the good
Midazolam, the good 

Has a wide therapeutic window.

1 mg -20 mg

Reliably produces




midazolam the bad
Midazolam, the bad 

In large doses, or with sedatives such as alcohol, opioids, can produce…

Profound sedation

Respiratory depression


idiot s guide to using midazolam versed
Idiot’s Guide to Using Midazolam (Versed)

Give initial dose & repeat q 3-5 minutes to desired effect

Healthy adults: 1- 2 mg IV

Drunk, high, elderly, cirrhotic, or RF pts: 0.5- 1 mg IV

Chronic alcoholics — not currently drunk: 2 – 4 mg IV initially, then 1 – 2 mg IV prn

side note
Side note:

Remember, a variable amount of analgesic is going to be added.

This may variably increase the level of sedation

increase the potential for airway, respiratory, and cardiovascular compromise

idiot s guide to midazolam
Idiot’s Guide to Midazolam

The role of midazolam is

Anxiolysis  Sedation & Amnesia

NOT Analgesia

Just because they aren’t kicking and screaming does not mean that they are pain free

diprivan propofol
Diprivan (Propofol)


Unique class of drug (structure is 1,6-diisopropylphenol)

Multifaceted mechanism of action:

GABA potentiation

reduced excitability of sensory and motor neurons

inhibition of the acetylcholine receptor channel

diprivan propofol1
Diprivan (Propofol)

Emulsified in Protein-free soybean oil with egg phosphatide

Painful on intravenous injection (mechanism unclear)

No preservatives — must be refrigerated, stored and handled properly

in theory, most egg-allergic patients should tolerate this protein-free emulsion

diprivan propofol metabolism
Diprivan (Propofol) metabolism

Liver  inactive conjugates.

Renal excretion

Interestingly, chronic hepatic or renal failure has minimal effect on diprivan kinetics

Propofol metabolism in the face of acute hepatic or renal failure has not been studied.

diprivan propofol the good
Diprivan (Propofol) the good 

anxiolytic/sedating effects

Profoundly relaxing

Amnestic properties

Anticonvulsant properties

Antiemetic properties

Very short half-life

diprivan propofol the bad
Diprivan (Propofol) the bad 

3-5 minutes for effect (we’re impatient!)

If dose overshoot  Profound sedation / respiratory depression and/or apnea

Frequent hypotension (pre-hydrate!)

Worse with alcohol, opioids, or other sedatives;

Caution: elderly or impaired hemodynamic status

diprivan propofol the ugly
Diprivan (Propofol) the Ugly 

Works better when injected slowly

Need to give with lidocaine

Has no analgesic properties

Sedation potentiated by analgesia

Amnesia somewhat inconsistent

idiot s guide to using diprivan
Idiot’s Guide to Using Diprivan

Infusion dosing: slower, but safer

0.3 mg / kg / min IV in adults (15 to 20 mg / min)

0.5 mg / kg / min IV in children

Infuse at this rate until patient is adequately sedated, and then continue at this rate until the procedure is nearing completion

idiot s guide to using propofol
Idiot’s Guide to Using Propofol

Bolus dosing: Faster. Greater risk of apnea, hypotension

Bolus of 0.75 mg / kg IV in adults (40 to 65 mg) and 1 mg / kg IV in children

If needed, give second ½ bolus in 2-3 mins

Q 2-4 min, give 10-20 mg in adults (0.5 mg / kg in children) to maintain sedation.


A derivative of PCP (animal tranquilizer / general anesthetic)

Drug of abuse (“Special K”)

Dissociative anesthetic

Decouples incoming sensation from neurologic processing

The patient has only internal or no stimuli to respond to.


neural discontinuity between the cortico-thalamic system…

responsible for higher-level functioning

and the limbic system.

responsible for emotions, motivations, and memory

Return of coupling can be variable. This is turn is responsible for “emergence phenomena”

dissociation effects include
Dissociation effects include:


Muscle tone and many reflexes maintained (eg. breathing, coughing, swallowing, corneal reflexes)

Analgesia. Possibly greater analgesia for somatic (ie. body wall) pain as opposed to visceral (ie. organ) pain


ketamine metabolism
Ketamine metabolism

P-450 cytochrome 3A4 to Norketamine

Mildly active 20-30% activity. Does not cross Brain-Blood Barrier sufficiently to cause dissociation

Metabolites conjugated and excreted in the urine

Because the conjugated metabolites have so little activity, Ketamine’s duration of action is not greatly increased in renal failure.

metabolic inducers
Metabolic inducers

Metabolism increased (duration reduced) with use of drugs that induce Cytochrome P-450 3A4:

chronic alcohol consumption

- chronic INH use

- dexamethasone

- rifampin

- St. John’s Wort

Anticonvulsants: Tegretol, Dilantin, Phenobarb

metabolic inhibitors
Metabolic inhibitors

Metabolism decreased (duration prolonged) by

acute alcohol consumption

macrolides (ie. erythromycin, Biaxin, azithromycin)




HIV protease inhibitors


grapefruit juice 

Ketamine  

Complex hemodynamic effects:

Direct myocardial depressant and systemic vasodilator

Indirectly stimulates the sympathetic system (possibly through inhibition of NE reuptake)

Overall, typically:

myocardial excitation   O2 use,  HR

systemic vasoconstriction   BP

Ketamine  

Typically indirect sympathetic stimulation predominates ( HR BP)

If decreased sympathetic reserve, direct effects predominate ( HR BP):

patients in toxic, septic, or hemodynamic shock

cocaine users

pts on prolonged catecholamine infusions

tyrosine-depleted patients

additional effects
Additional effects:  

bronchodilation  (use in asthmatics)

laryngospasm  (contraindicated in: children <3mo old & respiratory illnesses (?)

salivation and bronchorrhea  (pre-medicate with Atropine)

cerebral vasodilation (increased ICP) 

increased IOP 

emergence 

Emergence 

Emergence is not rare. TOTAL 7%

Confusion 3%

Bad dreams 2%

Hallucinations 1%

Excitement/irrational 1%

Patients <10yrs old less likely; >16yrs old more likely, to experience emergence.

Emergence 

Anecdotal evidence suggests that emergence reactions may be reduced by avoiding visual, verbal, or tactile stimulation during the recovery period (until the patient is fully conscious).

Therefore, have patients recover from Ketamine administration in a quiet, dark room whenever possible.

idiot s guide to using ketamine contraindications
Idiot’s guide to using Ketamine. Contraindications

Age < 3months

Upper respiratory infections

Procedures involving post. pharynx

Uncontrolled hypertension

Ischemic heart disease

CHF/pulmonary hypertension

Elevated ICP or IOP


Initial bolus below (peds & adults)

Highly lipid solubility  rapid CNS uptake (eg. peak effect in 1-5mins IV)

Second ½ bolus PRN to maintain desired level of sedation.

idiot s guide to using ketamine
Idiot’s guide to using Ketamine

Sedation + Analgesia + Amnesia

Can be sole agent for procedural sedation.

Typically, no need for additional analgesia.

½ procedural dose can be used to provide analgesia without sedation.

Consider theoretical need for additional analgesia in procedures involving predominantly visceral (as opposed to somatic) painful stimuli.

analgesia opiods
Analgesia. Opiods

5 major opioid receptors: mu, kappa, sigma, delta, epsilon

Opioid agonists (such as Morphine and Fentanyl) operate predominantly at the mu (u) receptors

perception of pain is mediated by u1- and u2-receptors, both:

centrally in the brain & supraspinally (by inhibiting sensory dorsal horn pathways in the spinal cord)


There are many different opioids (and many different ways of classifying them), but for the purposes of procedural sedation in the ED, one opioid in particular has emerged as the agent of choice.



fentanyl is
Fentanyl is

Semisynthetic, phenyl-piperidine derivative.

Highly lipid soluble  rapid CNS uptake

Rapidly redistributed from the CNS into the adipose tissue

Short duration of effect except… in Obese patients, large doses  significant drug-reservoir can be created in the adipose tissue, leading to a greatly prolonged (albeit mild) duration of effect.

fentanyl metabolism
Fentanyl metabolism

Dealkylated in the liver by our friend, Cytochrome P-450 3A4  Norfentanyl

Urine excretion.

Once again:

Drug activity will be reduced by Cyt P-450 3A4 inducers

Drug activity will be prolonged by Cyt P-450 3A4 inhibitors

Fentanyl 

Agent of choice for ED procedural sedation:

Rapid onset: peak activity in 2-5 mins IV

Short duration of action: sub-therapeutic within 10 mins

High potency (100 x Morphine)

Favourable cardiovascular profile

Low complication rate

fentanyl risks
Fentanyl Risks 

Itchy nose  quite common, quite inconsequential

Hypotension (low risk).

Fentanyl, unlike Morphine, does not release histamine; therefore the risk of  BP is low (unless combined with sedatives or alcohol)

Respiratory depression (low risk)

risk is once again low unless drug is combined with sedatives or alcohol

Chest wall rigidity

Rare <15 ug / kg (i.e. 7X the dose used for ED sedation)

idiot s guide to using fentanyl
Idiot’s guide to using Fentanyl

Only given IV (given over 30 secs)

1-2 ug / kg IV in adults, and 1-3 ug / kg IV in peds

Use higher doses if patient:

has an induced P-450 (eg. boozer)

Use lower doses if patient:

has an inhibited P-450 (eg. on Azithromycin)

If getting a sedative or is is <6 months old

pitfalls of ed sedation
Pitfalls of ED Sedation
  • Never should take more than 30 min
  • If ED is too crazy
  • Patient not a good sedation candidate
  • If you can’t stay in the room with the patient for the whole procedure
  • Remember this is elective!
discharge criteria ach
Discharge Criteria / ACH
  • Cardiovascular and Airway stability are assured
  • VS are baseline and pulse Ox >97%
  • Easily arouseable, protective reflexes intact
  • Talk, sit-up unaided, or ambulate with minimal assistance
  • Patient at pre-sedation level of responsiveness
discharge criteria uh
Discharge Criteria / UH
  • Back to baseline
  • VS baseline
  • Walk and Talk
  • Drink, eat & Pee