Induction Agents Flashcards

1
Q

Low dose IV anesthetics produce ____ and high doses produce ___

A

low dose = sedation
high dose = unconsunessness

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2
Q

T/F
We do not witness stage 2 with IV induction.

A

True
No outward presentation of stage 2; goes thru stage 2 in ~2 seconds
EEG can show tho

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3
Q

TIVA

A

total IV anesthesia

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4
Q

Uses for induction agents

A

Induction of anesthesia
TIVA (Total intravenous anesthesia)
MAC (Monitored anesthesia care)
Sedation during local and regional anesthesia

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5
Q

All IV anesthetics are ____ and produce…

A

sedative-hypnotics
dose-dependent CNS depression

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6
Q

Ideal induction agent criteria

A

-Hypnosis and amnesia
-Rapid onset (time of one arm–brain circulation)
-Rapid metabolism to inactive metabolites
-Minimal CV and resp depression
-No histamine release/hypersensitivity reactions
-nonmutagenic, noncarcinogenic
-No untoward neurologic effects (seizures, myoclonus, neurotoxicity)
-beneficial effects: analgesia, antiemetic, neuroprotection, cardioprotection
-P.kinetic models for accurate dosing
-Ability to continuously monitor delivery

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7
Q

mutagenic

A

inducing or capable of inducing genetic mutation

we want our indxn agents to be nonmutagenic

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8
Q

ideal induction agent should be ___ soluble

A

water

however, a balance of water and lipid solubility is important

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9
Q

____ support microbial support

A

Lipids

Propofol has a preservative in it

also why we want water-soluble preparations for indxn agents

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10
Q

IV anesthetics have a ___ onset

A

rapid

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11
Q

IV anesthetics distribute rapidly to…

A

higher perfused and vessel-rich tissues

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12
Q

allows for rapid crossing of the blood-brain barrier

A

lipophilicity

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13
Q

Three-phase process that occurs after a bolus of propofol

A

-Rapid distribution phase(A): plasma –> peripheral tissues

-Slow distribution phase(B): into other tissues while the drug in rapid distribution tissue —> back to plasma

-Terminal phase or elimination phase(C): removed from the body

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14
Q

the branch of pharmacology concerned with the movement of drugs within the body

A

Pharmacokinetics

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15
Q

Used to describe the behavior in IV agents (propofol) during infusion via a pump

A

Three-Compartment Model

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16
Q

Central compartment

A

(CA1, blood)

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17
Q

Peripheral compartments

A

(CA2 and CA3)

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18
Q

Elimination

A

(G1)

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19
Q

Three compartment model steps

A
  1. Propofol is injected into the blood and fills the central compartment
  2. Redistributes to peripheral compartments (one rapid and one slow)
  3. Elimination
  4. Accumulation over time in peripheral compartments (infusion), less drug is removed from the central compartment by redistribution and less drug is needed to be infused
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20
Q

Elimination half-time (t1/2)

A

The time it takes for the plasma concentration of a drug to decrease to 50% of its original concentration (after one bolus dose)

1 compartment model

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21
Q

T/F
Context-sensitive half-time applies to IV boluses

A

false
applies to infusions!

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22
Q

In order to use Elimination half-time (t1/2), we must follow a ___ compartment model.

A

1

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23
Q

In order to use Elimination half-time (t1/2), the drug must be…

A

only in the blood phase or a drug administered only once (bolus)

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24
Q

Context-sensitive half-time

A

The time to achieve a 50% reduction in concentration after stopping a continuous infusion.

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25
Q

What does this graph tell us about fentanyl and propofol?

A

fentanyl has a much higher CSHT than propofol

will keep patient asleep for much longer

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26
Q

What does this graph tell us?

A

CSHT of opioids

note how remifent drops to 50% extremely quickly & how fentanyl takes very long

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27
Q

T/F
Remifentanil is distributed to tissue

A

False
broken down via ester hydrolysis rapidly
does not redistribute well

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28
Q

T/F
the ability to distribute into tissues and redistribute into the plasma compartment increases the half-life of a drug

A

True

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29
Q

Which opioid has a context-sensitive half-time that is essentially independent of the duration of the infusion?

A

remifentanil

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30
Q

Context-Sensitive half-time(3-compartment model)

A

Describes the transfer of drug:

plasma –> peripheral compartments –> (once the infusion is stopped) back into the central compartment

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31
Q

Propofol (Diprivan)

A

2,6-diisopropylphenol

Rapid onset, predictable context-sensitive half-time

Rapid emergence, rapid redistribution

Antiemetic properties

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32
Q

you must know this table in its entirety

A
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33
Q

How much of propofol is protein bound?

A

98%

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34
Q

⭐️
Propofol
primary mechanism

A

GABA-A receptor agonist
enhancement of GABA inhibition

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35
Q

⭐️
Propofol
CV effects

A

significant decreases in
SVR, SV, & CO

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36
Q

⭐️
Propofol
pulmonary effects

A

respiratory depressant
potent bronchodilator

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37
Q

⭐️
T/F
Unlike opioids, Propofol does not exhibit potential for addiction.

A

False
Addiction potential: may elicit feelings of well-being or euphoria during emergence

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38
Q

⭐️
Propofol
Key Clinical Uses

A

-General anesthesia: induction & maintenance

-TIVA
-Conscious & deep sedation

-ICU sedation

-PONV prophylaxis & rescue!

-Safe with malignant hyperthermia

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39
Q

⭐️
T/F
When used for surgical procedures, propofol can only be used in the OR.

A

False
Used for conscious and deep sedation, including out-of-operative-room settings

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40
Q

⭐️
Is propofol safe to use in malig.hyperthemia?

A

yes

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41
Q

⭐️
Propofol
CNS effects

A

-CNS depressant
-neuroprotective
-anticonvulsant
-decreases CerebPerfPrsr, CMRO2, CBF, & ICP

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42
Q

What happens when the GABA receptor allows Cl- to flow in?

A

-hyperpolarized
-does not allow electrical conductivity

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43
Q

Propofol is primarily metabolized by the ____. The kidneys excrete …

A

liver
inactive and water-soluble metabolites

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44
Q

Most common extrahepatic sites of propofol metabolism are ….
They account for ___% of metabolism.

A

kidneys and lungs
30%

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45
Q

Which model explains the elimination of propofol?

A

3 compartment

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46
Q

How does propofol induce an unconscious state

A

enhances GABA’s inhibitory pathways
~central cholinergic transmission, NMDA or alpha-adrenergic sites

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47
Q

paradoxical excitation

A

unpredictable movement, not easily arousable

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48
Q

T/F
Higher doses of propofol will always create deeper sedation/anesthesia

A

False
possible paradoxical excitation (unpredictable movement, not easily arousable) at higher doses

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49
Q

T/F
Propofol is an anticonvulsant and can treat status epilepticus

A

True

also shortens seizure duration

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50
Q

T/F
Propofol can be used for electroconvulsive therapy (ECT)

A

False
ECT requires inducing a seizure & propofol is an anticonvulsant

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51
Q

⭐️
Why are the CV effects of propofol more significant after induction than gtt?

A

CV effects are dose dependent

Smooth muscle relaxant & impair SNS

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52
Q

T/F
Propofol affects the SNS.

A

True
decreases sympathetic activity
indirect effects on arterial vasodilation and venodilation

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53
Q

With larger doses of propofol, what changes are you likely to see in the BP and HR?

A

Drop in SBP & DBP without the increased HR

(decreased CO, SV, SVR)

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54
Q

What makes propofol a good bronchodilator?

A

direct effect on intracellular calcium

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55
Q

Maintenance doses of propofol can result in which resp effects?

A

diminished tidal volume and increased RR

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56
Q

An induction dose of propofol will create apnea how quickly?

A

within 30 seconds

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57
Q

T/F
Propofol can only exhibit its antiemetic effects when used with certain adjuncts.

A

False
PONV is decreased with propofol administration regardless of the type of anesthetic

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58
Q

Propofol dose for PONV

A

10-15mg IV

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59
Q

Propofol infusion rate for PONV prophylaxis

A

Background infusions of 10 ug/kg/min

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60
Q

How does Propofol prevent PONV?

A

possible direct effect on the vomiting center (Chemoreceptor trigger zone)

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61
Q

Propofol dose for opioid-induced pruritus

A

10 mg IV

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62
Q

How does Propofol treat opioid-induced pruritus?

A

Mechanism is related to spinal cord suppression

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63
Q

What makes propofol the induction agent of choice?

A

rapid, predictable awakening

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64
Q

What makes propofol easily titratable?

A

quick recovery (very short elimination half-life)

predictable clearance

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65
Q

Induction dose of Propofol

A

1-2.5 mg/kg
(2 mg/kg)

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66
Q

IV sedation/MAC propofol dose

A

25-75 mcg/kg/min (variable)

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67
Q

Maintenance of anesthesia (GA) dose of propofol

A

100-200 mcg/kg/min (variable)

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68
Q

Propofol usual concentration

A

10mg/mL (200mg/20mL)

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69
Q

Which pt population typically requires lower doses of propofol?

A

old ppl
small ppl

(note: peds need more b/c high Vd & Cl)

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70
Q

What gives Propofol its allergic potential?

A

its phenyl nucleus and di-isopropyl side chain

egg LECITHIN
most egg allergies are actually to egg proteins; prop = lecithin (fatty part of yolk)

Generic contains sodium metabisulfite = contraindicated in patients with sulfite sensitivity

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71
Q

Why is propofol painful on injection?

A

thick, glycerol-based emulsion

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72
Q

How common in pain on injection from propofol?

A

60-70% of pts complain

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73
Q

Children need (higher/lower) doses of prop bc…

A

higher doses

higher Vd and faster clearance

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74
Q

Why do elderly people need lower doses of prop?

A

prolonged effects and increased sensitivity due to decreased cardiac output and clearance

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75
Q

Would prop be okay to use in a pt with CV Dz?

A

probably not
decreases CO, SV, SVR and BP

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76
Q

Opened propofol vials are good for ____ & ___ for syringes.

A

vial (infusion) = 12 H
syringe = 6 H

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77
Q

Propofol Infusion Syndrome (PRIS)

A

-Doses of 4 mg/kg/hr for > 48 hours (67 ucg/kg/min)

-brady; possible into asystole

-unexplained: metabolic acidosis, hyperkalemia, rhabdomyolysis, hyperlipidemia, and/or enlarged liver, renal failure, EKG changes, arrhythmias

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78
Q

Green urine with prop use is a sign of…

A

Increased extrahepatic metabolism

excretion of these metabolites in urine

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79
Q

Which conditions may contribute to Propofol Infusion Syndrome (PRIS)?

A

cardiomyopathies, skeletal myopathy, or hyperkalemia

Highly dependent on infusion dose and duration

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80
Q

with longer propofol infusions urine may become…

A

milky colored

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81
Q

Etomidate (Amidate)

A

GABA-A receptor agonist

A carboxylated imidazole derivative

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82
Q

T/F
Avoid use of etomidate in patients prone to hypotension.

A

False
Etomidate is hemodynamically stable

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83
Q

Etomidate
adverse effects

A

Adrenocortical suppression (critically ill)

Postoperative nausea and vomiting possible

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84
Q

Etomidate is good for which pts?

A

cardiac, trauma, and elderly

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85
Q

⭐️
Why do we not use etomidate infusions?

A

Continuous infusion limited due to possible adrenal suppression

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86
Q

Etomidate follows with compartment model?

A

3

87
Q

Etomidate metabolism

A

liver & plasma esterases
excreted by kidneys (80%) and in bile (20%)

88
Q

Is Etomidate highly protein bound?

A

Yes
75%

89
Q

Etomidate has a (fast/slow) onset. This is due to…

A

fast
redistribution

90
Q

Is etomidate irritating to veins? Why or why not?

A

yes
Solvent (propylene glycol) contribute to veno-irritation and phlebitis

91
Q

⭐️
How long does etomidate’s adrenal suppression last?

A

up to 72 H

92
Q

Etomidate Induction dose:

A

0.2-0.3 mg/kg

93
Q

T/F
Etomidate is considered a proconvulsant

A

true
lowers seizure threshold

94
Q

Etomidate MoA

A

GABA-A agonist

95
Q

Etomidate
CNS effects

A

potent vasoconstrictor that reduces CBF, ICP and CMRO2

96
Q

When giving etomidate as an induction agent, we should watch for ____. If that happens, we give ____.

A

seizure-like, myoclonic movements

versed/opioids

97
Q

Etomidate
CV effects

A

Minimal/no effect on MAP, PA pressure, PCWP, CVP, SV, CI, SVR and PVR

98
Q

How does etomidate cause adrenocortical suppression?

A

Inhibits 11β- hydroxylase
prevents conversion of cholesterol –> cortisol

99
Q

If prolonged, adrenocortical suppression will cause…

A

hypoTN

100
Q

Ketamine (Ketalar) is a derivative of…

A

Phencyclidine (PCP)

-chiral compound
-racemic: S and R enantiomers

101
Q

When emerging from Ketamine, what may the pt experience?

A

Emergence delirium & hallucinations

102
Q

⭐️
T/F
The Ketamine compound is achiral.

A

False
-PCP analog
-chiral compound
-racemic mix: S and R enantiomers

103
Q

Of all induction agents, which is metabolized into a clinically significant metabolite?

A

Ketamine
Liver: demethylation = norketamine (biologically active, 1/3 - 1/5 as active)

104
Q

What is Ketamine’s metabolite?
Is it active or inactive?

A

norketamine

active (1/3-1/5 as active)

105
Q

Ketamine metabolism

A

-mostly liver
-cytochrome P-450 enzymes
-demethylation to norketamine

106
Q

Ketamine has (high/low) lipid solubility & (high/low) protein binding.

A

high lipid sol.
low protein binding

107
Q

T/F
Ketamine can only be given IV.

A

False
Bioavailable by multiple routes: IM (93%)
transnasal (25-50%)
rectal/oral (16%)

108
Q

T/F
Ketamine rapidly redistributes

A

True

109
Q

Ketamine
induction dose

A

0.5-2 mg/kg IV
4-5 mg/kg IM

110
Q

Ketamine onset (IV)

A

30-60 seconds

111
Q

Ketamine duration

A

10-20 mins

112
Q

Ketamine MoA

A

It produces a functional dissociation between thalamocortical & limbic systems

NMDA antagonist

113
Q

What’s the benefit of using Ketamine with opioids/propofol?

A

Inhibit 2 different pain pathways

114
Q

Ketamine acts as a (agonist/antagonist) at the ___ receptor

A

antagonist
NMDA

115
Q

T/F
SNS stimulation is expected with Ketamine.

A

True

MAP, CO, SVR, and myocardial oxygen requirements increase

116
Q

Aside from the NMDA receptor, where does Ketamine act?

A

-Non-NMDA glutamate receptors

-Nicotinic receptors
-Cholinergic receptors
-Monoaminergic receptors

-Mu, delta and kappa-opioid receptors

-inhibits neuronal Na+ channels (Local anesthetic action)
& Ca+ channels (Cerebral vasodil8)

117
Q

T/F
Ketamine exerts effects similar to local anesthetics.

A

True
ketamine inhibits neuronal Na+ channels (Local anesthetic action)

118
Q

Ketamine’s antagonist activity at the NMDA receptor causes…

A

pain relief

119
Q

Ketamine is a NMDA receptor (agonist/antagonist).

A

antagonist

120
Q

Dissociative amnestic state
is seen with which drug?

A

Ketamine

121
Q

Dissociative amnestic state

A

(ketamine)
-unconscious; eyes open (nystagmus)
-spontaneous respiration
-do not react to painful stimuli

122
Q

Induction doses of ____ are associated with increased HR and BP

A

Ketamine

123
Q

Can we give ketamine to a hemodynamically unstable pt?

A

Yes!

124
Q

T/F
Ketamine can be given to OB pts

A

True

125
Q

Ketamine should be used with caution in pts with which cardiac condition?

A

severe right heart dysfunction (Ketamine increases PVR)

126
Q

T/F
Ketamine can be used for depression

A

True

127
Q

What causes Ketamine’s profound analgesia?

A

probably due to prevention of developing hyperalgesia

128
Q

T/F
It’s okay to give ketamine to opioid abuse patients.

A

True

129
Q

Emergence
Benefits of using ketamine

A

Using less opioid and adding ketamine can produce faster wake up.

130
Q

T/F
Ketamine is not indicated for use in chronic pain.

A

False
treats acute and chronic pain

131
Q

T/F
Ketamine causes significant respiratory depression.

A

False

132
Q

Ketamine (increases/decreases) ICP. This is due to…

A

-increases ICP
-Potent cerebral vasodilator
-increases CBF of 60-80% during normocapnia

133
Q

How can we can attenuate ketamine’s effect on ICP?

A

raises ICP
attenuate with hyperventilation

134
Q

T/F
Increased ICP is an absolute contraindication to ketamine.

A

False
relatively contraindicated
research in progress

135
Q

Due to its effect on muscarinic receptors, ketamine increases _____ _____.

A

airway secretions

136
Q

How does Ketamine affect the airways (2)?

A

good bronchodilator

maintains protective airway reflexes

137
Q

Ketamine’s CV effects resemble…

A

SNS stimulation

MAP, CO, SVR, & myocardial oxygen requirements increase

138
Q

The mechanism for ketamine-induced CV effects

A

direct SNS stimulation

139
Q

T/F
Ketamine can be used in pts w/ mild to severe hypovolemia.

A

False

ideal for induction in a hypovolemic patient

HOWEVER, use in critically-ill or shock-like patient = profound hypoTN

d/t catecholamine depletion in these patients, leading to unopposed direct myocardial depression

140
Q

Emergence Delirium

A

phenomenon associated w/ postop ketamine anesthesia

-Visual, auditory illusions
-Confusion
-Delirium

141
Q

Ketamine
Emergence Delirium usually occurs at doses higher than…

A

> 2 mg/kg

dose-dependent occurrence

142
Q

Emergence Delirium Prevention

A

-preop midazolam
-Recover in calm/quiet environment

143
Q

Dexmedetomidine (Precedex)

A

alpha 2-adrenergic agonist

highly selective, specific, and potent

144
Q

Which is more selective of alpha 2 receptors?
Precedex
Clonidine

A

Precedex (7-8x more)

145
Q

How does Precedex induce sedation?

A

activation of α2-receptors in the locus coeruleus
& induces a state mimicking natural sleep.

146
Q

T/F
Precedex has analgesic properties.

A

True

147
Q

T/F
Precedex does not cause respiratory depression.

A

False
can produce mild resp. depression

148
Q

How does Precedex affect norepinephrine?

A

Inhibits Norepi release in locus coeruleus

149
Q

How does Precedex affect opioid metabolism?

A

Dexmedetomidine: weakly inhibits CYP-450 system

could cause increased plasma [ ] of opioids administered during anesthesia

150
Q

What % of Precedex is protein bound?

A

94%

151
Q

Precedex faces (rapid/slow) (hepatic/renal) metabolism involving which reactions?

A

rapid
hepatic

conjugation
N-methylation
hydroxylation

152
Q

Precedex CNS effects

A

-sedative, anxiolytic, & analgesic effects (spinal cord and brain)

153
Q

T/F
Analgesic effects of Precedex do not alter the amount of opioid needed.

A

False
decreases opioid requirement

154
Q

Precedex respiratory effects

A

-less ventilatory depression vs. other sedative-hypnotic/opioid anesthetics

-Bolus will reduce minute ventilation

155
Q

If we give a bolus of Precedex, we should expect a decrease in which respiratory parameter?

A

minute ventilation

(amount of air that enters the lungs per minute)

156
Q

How does Precedex cause hypoTN and bradycardia?

A

high alpha-2-adrenereceptor activity

157
Q

Which pt population is esp at risk for bradycardia from precedex?

A

Children

158
Q

Benefits of using Precedex as anesthetic adjuvant

A

blunt the hemodynamic effects of direct laryngoscopy

improves hemodynamic stability

159
Q

Precedex uses

A

-sedation: procedural, postop, ICU, when controlled ventilation is required

-extubation: breathe spontaneously and appear calm (pediatrics)

-IV adjuvant: induction or maintenance of GA, local/regional

-blunt acute SNS response to laryngoscopy

160
Q

Precedex sedation dose (initial)

A

0.5 - 1 mcg/kg given over 10 minutes

161
Q

Precedex sedation dose (drip)

A

0.2-.7 mcg/kg/hr

162
Q

Treating Precedex bradycardia

A

atropine, ephedrine or volume

Omitting the loading dose

163
Q

Precedex side effects

A

hypoTN
bradycardia
dry mouth
nausea
hyperTN

164
Q

The CV and resp effects of benzos are considered to be…

A

minimal

but be cautious

165
Q

benzos produce…

A

amnesia

166
Q

Benzos relax which muscles?

A

skeletal (centrally)

167
Q

Benzos MoA

A
  1. bind to alpha subunits of GABA receptor
  2. increasing Cl- conductance
  3. hyperpolarization of the membrane
  4. nerve resists stimulation
168
Q

Effects of Benzos are primarily d/t…

A

their effect on the central inhibitory neurotransmitter, GABA-A

169
Q

GABA is an (excitatory/inhibitory) ____.

A

inhibitory neurotransmitter

170
Q

Which benzo usually doesn’t burn on injection?

A

versed

other benzos typically burn

171
Q

Which benzo is water soluble in its bottle?

A

versed

172
Q

Versed’s first pass extraction is over ___%

A

50%

173
Q

Which benzo has shortest duration of action?

A

Versed/midazolam

174
Q

What contributes to Versed’s short duration?

A

rapid redistribution, hepatic metabolism and renal clearance

175
Q

T/F
Versed dosage should be adjusted in pts with renal/liver Dz

A

true

Versed = hepatic metabolism and renal clearance

176
Q

Benzos
CNS effects

A

Can decrease CMRO2, CBF with little effect on ICP

177
Q

Benzos
Resp effects

A

may decrease upper airway reflexes & central respiratory drive

178
Q

Benzos
CV effects

A

Can decrease the SVR and BP

179
Q

Do Benzos cross the placenta?

A

yes
avoid in OB if possible

180
Q

Benzos create amnesia in which timeframe?

A

remember everything up until the point you gave them versed

181
Q

What type of amnesia do benzos create?

A

Anterograde amnesia

a loss of memory for events occurring forward in time

182
Q

Benzo reversal

A

Flumazenil (Romazicon)

0.2 mg IV over 15 seconds

no reponse after 45 secs: give 0.2 mg

repeat at 1 min intervals (max: 4 doses)

183
Q

Flumazenil (Romazicon)
dosing

A

0.2 mg IV over 15 seconds

no reponse after 45 secs: give 0.2 mg

repeat at 1 min intervals (max: 4 doses)

184
Q

Benzo dosing
Versed
(Preop)

A

orally, nasally, rectally, IM, IV

peds preop: 0.5 mg/kg 30 mins b4 OR

adult preop: 1-2 mg

185
Q

Which benzo(s) are not water soluble?

A

Lorazepam and Diazepam

Don’t Like water”

186
Q

Which benzo(s) usually cause injection pain? Why?

A

Lorazepam and Diazepam

propylene glycol (like etomidate!)

Damn, Lady! That shit hurts!”

187
Q

induction drugs that contain propylene glycol

A

Lorazepam
Diazepam
Etomidate

188
Q

Versed
solubility changes upon administration

A
  1. water-soluble
  2. conformational change in bloodstream
  3. more lipophilic

Ring on its structure breaks once in blood and becomes lipophilic

189
Q

Barbiturate Classes

A

Oxybarbiturates
O2 atom on the #2 carbon atom

Thiobarbiturates
Replacement O2 atom w/ sulfur on the #2 carbon atom

BOTH: pyrimidine center

190
Q

Which barbiturate class contains sulfur?

A

Thiobarbiturates (pyrimidine center)

(O2 atom –> sulfur on carbon #2)

191
Q

Oxybarbiturates

A

Methohexital (used in ECTs)
Phenobarbital
Pentobarbital
Secobarbital

192
Q

Thiobarbiturates

A

Thiopental
Thiamylal

193
Q

What do the two barbiturate classes have in common?

A

pyrimidine center

194
Q

Barbiturate metabolism

A

Primary: hepatic

inactive metabolites excreted in urine and bile

195
Q

Barbiturate redistribution

A

Rapid redistribution into highly perfused compartments

rapid termination after a single dose

196
Q

Barbiturate extended infusion

A

(Thiopental)

accumulates in poorly perfused compartments

slow elimination (prolonged context-sensitive half-time and delayed recovery)

197
Q

Barbiturate
Sites of action

A

cortical and brainstem GABA inhibitory pathways

198
Q

Barbiturates will cause…

A

Loss of consciousness, respiratory and CV depression

199
Q

Hypnotic effects of barbiturates are likely enhanced by…

A

inhibits central excitatory pathways
(glutamate via NMDA receptors & acetylcholine)

200
Q

Thiopental elimination 1/2 life

A

12 H (long)

201
Q

Does thiopental induce or treat seizures?

A

anticonvulsant
used to treat status epilepticus

202
Q

How does thiopental affect ICP?

A

it decreases ICP!

-induction for pts with ↑ ICP

-treat ↑ ICP resistant to hyperventilation alone

203
Q

Thiopental protects the brain by…(4)

A

-cerebrovascular vasoconstriction
↓ cerebral blood flow
↓ intracranial pressure
-Decreased cerebral metabolic O2 consumption

204
Q

Thiopental stimulates the release of ___ from ___.

A

histamine
mast cells

205
Q

Thiopental precipitates with…

A

succinylcholine
rocuronium
lidocaine

(Pharm class: pancuronium)

206
Q

T/F
We cannot give succinylcholine, rocuronium, or lidocaine if we have already given the pt thiopental.

A

False
flush IV line thoroughly before giving after Thiopental

207
Q

Acute Intermittent Porphyria (AIP)

A

disorder of porphyrin enzyme metabolism, either in the liver or the bone marrow

208
Q

Porphyrins are involved in ___ production.

A

heme

209
Q

_____ can precipitate an attack of AIP, and must be avoided in patients with a history of this disorder

A

all barbiturates

210
Q

Acute Intermittent Porphyria (AIP)
5 P’s

A
211
Q

Methohexital (Brevital)

A

Oxybarbiturate

Proconvulsant activity

212
Q

Agent of choice in Electroconvulsive Therapy (ECT)

A

Methohexital (Brevital)

213
Q

Methohexital
Induction dose

A

1-2 mg/kg (IV)
20-30 mg/kg (Rectal)

214
Q

Thiopental
Induction dose

A

2.5-5 mg/kg (IV)

In the elderly reduce the dose by 30-35%