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General Principles > Exam 2- Induction Agents > Flashcards

Exam 2- Induction Agents Flashcards

1
Q

Low dose IV anesthetics produce __________ and high doses produce __________________

A

sedation; unconsciousness

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2
Q

T/F: All IV anesthetics are sedative-hypnotics and produce dose-dependent CNS depression

A

true

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3
Q

what modeling map does propofol follow?

A

three-compartment model

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4
Q

half-life

A

the time it takes for the plasma concentration of a drug to decrease to 50% of its original concentration

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5
Q

what is the best example of a drug with context-sensitive half-time?

A

remifentanil

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6
Q

which drug is an ultrashort opioid agonist?

A

remifentanil

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7
Q

which drug has an ester component structure and is eliminated rapidly due to metabolism by plasma esterased?

A

remifentanil

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8
Q

The context-sensitive half-life is independent of

A

the infusion duration

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9
Q

propofol primary mechanism of action

A

GABA-A receptor agonist (enhancement of GABA inhibition)

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10
Q

propofol CNS effects

A

CNS depressant, neuroprotective, anticonvulsant, decreases CMRO2, CBF, and ICP

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11
Q

propofol CV effects

A

significant decrease in SVR, stroke volume and cardiac output

drop in systolic and diastolic without increasing HR

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12
Q

propofol pulmonary effects

A

respiratory depressant in higher doses and potent bronchodilator (due to direct effect on intracellular calcium)

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13
Q

propofol misc. effects

A

Major side-effects: pain with injection and propofol infusion syndrome

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14
Q

which agent treats and prevents PONV?

A

propofol

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15
Q

is propofol safe for use in patients with MH?

A

yes

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16
Q

key clinical use of propofol

A

General anesthesia induction and maintenance

Good for TIVA

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17
Q

where is propofol primarily metabolized?

A

by the liver

inactive and water-soluble metabolites are excreted by the kidneys

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18
Q

how does propofol produce an unconscious state?

A

by enhancement of GABA inhibitory pathways and perhaps central cholinergic transmission, NMDA or alpha-adrenergic sites

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19
Q

what does a low dose of propofol produce

A

sedation and possible paradoxical excitation

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20
Q

higher doses of propofol produce

A

loss of consciousness and apnea, relaxation of muscles, need for airway support

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21
Q

propofol neuroprotective effects

A

lowers cerebral metabolic oxygen consumption (CMRO2), decreased ICP by lowering CBF

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22
Q

propofol and cerebral perfusion

A

cerebral perfusion pressure lowered

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23
Q

what does propofol do in patients with seizures?

A

treat status epilepticus, shorten seizure duration

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24
Q

propofol vascular effects

A

vasodilation and venodilation

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25
Q

is apnea present w propofol?

A

yes in higher doses

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26
Q

maintenance doses of propofol causes what respiratory effects?

A

diminished TV and increased RR

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27
Q

how can PONV be treated?

A

propofol 10-15 mg IV

or infusion 10 ug/kg/min

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28
Q

propofol pruritus effects

A

can treat opioid-induced pruritus in a dosage of 10 mg IV

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29
Q

propofol IV induction dose

A

1-2.5 mg/kg (2mg/kg) produces unconsciousness in 30s.

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30
Q

propofol IV continuous infusion

A

25-75 mcg/kg/min

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31
Q

propofol anesthesia maintenance

A

100-200 mcg/kg/min

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32
Q

what is propofol usualy concentration

A

10mg/mL

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33
Q

propofol issues

A

Allergic potential related to its phenyl nucleus and di-isopropyl side chain

Anaphylaxis has been reported

Egg lecithin (fatty part of yolk), proteins from eggs cause allergy

Generic propofol contains sodium metabisulfite, which is contraindicated in patients with sulfite sensitivity

pain on injection in 60-70% of population

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34
Q

propofol doses in children

A

Children have larger volumes of distribution and faster clearance so may need more

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35
Q

which population requires larger dose requirements?

A

chronic alcoholics

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36
Q

which population has prolonged effects from propofol?

A

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

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37
Q

which populations should propofol not be used in?

A

CV disease, trauma, hypotension, bleeding

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38
Q

how long is propofol good in an opened vial

A

up to 12 hours

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39
Q

how long is propofol good for after being drawn into a syringe

A

6 hours

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40
Q

propofol infusion syndrome (PRIS) symptoms

A

acute refractory bradycardia potentially leading to asystole

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

can also be seen in cardiomyopathies, skeletal myopathy, or hyperkalemia

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41
Q

when is PRIS usually seen

A

in critically ill adults

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42
Q

PRIS hepatic effects

A

Can cause green urine. Increased extrahepatic metabolism of propofol and excretion of these metabolites in urine, also with longer infusions urine may become milky colored

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43
Q

etomidate site of action

A

GABA-A receptor agonist

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44
Q

which induction agent is hemodynamically stable?

A

etomidate

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45
Q

which induction agent can cause adrenocortical suppression in critically ill patients

A

etomidate

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45
Q

which induction agent can cause PONV

A

etomidate

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45
Q

which population is etomidate good for?

A

cardiac, trauma, elderly

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45
Q

which induction agent is a carboxylated imidazole derivative

A

etomidate

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46
Q

will etomidate result in vaso-irritation?

A

yes from solvents in the propylene glycol formation

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47
Q

can etomidate be given via continuous infusion

A

not really; limited due to possible adrenal suppression

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48
Q

where is etomidate metabolized?

A

by the liver and plasma esterases

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49
Q

where is etomidate excreted?

A

80% by kidneys; 20% by the bile

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50
Q

what % of etomidate is protein bound?

A

75%, highly protein bound

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51
Q

what is etomidate elimination half life

A

3-6 hours

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52
Q

what is etomidate initial distribution half-life

A

2.7 minutes

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53
Q

what is etomidate redistribution of half life

A

29 min

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54
Q

what is etomidate volume of distribution

A

2.5-4.5 L/kg

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55
Q

what is etomidate induction dose

A

0.2-0.3 mg/kg

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56
Q

what is etomidate usual concentration

A

2 mg/cc

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57
Q

etomidate mechanism

A

binds as an agonist to the GABA-A

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58
Q

etomidate CNS effects

A

vasoconstrictor that reduces CBF, ICP, and CMRO2

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59
Q

what can etomidate cause on induction

A

seizure-like myoclonic movements; treat with versed/opioid

60
Q

which induction agent is hemodynamically stable on induction

A

etomidate

61
Q

etomidate cardiovascular effects

A

minimal to no effect on MAP, PA pressure, PCWP, CVP, SV, CI, SVR and PVR

62
Q

etomidate risks

A

adrenocortical suppression

Inhibits the activity of 11 β-hydroxylase and prevents conversion of cholesterol to cortisol

63
Q

which induction agent is a PCP derivative

A

ketamine

64
Q

what kind of CNS effects does ketamine have

A

analgesia and anesthetic, dissociation, emergence delirium & hallucinations

65
Q

which induction agent is a racemic mixture?

A

ketamine

66
Q

which induction agent has high lipid solubility and low protein binding

A

ketamine

67
Q

ketamine bioavailability

A

IM, transnasal, rectal, and oral

68
Q

ketamine lipid solubility

A

high lipid solubility and low protein binding

69
Q

which induction agent has rapid redistribution

A

ketamine

70
Q

what is ketamine mostly metabolized by

A

the liver CYP450 enzymes

71
Q

how does the liver metabolize ketamine

A

demethylation to norketamine

72
Q

ketamine onset of IV

A

30-60 seconds

73
Q

ketamine duration

A

10-20 min

74
Q

ketamine induction dose IV and IM

A

0.5-2 mg/kg IV

4-5 mg/kg IM

75
Q

ketamine usual concentration

A

10 mg/cc

76
Q

ketamine produces functional dissociation between

A

thalamocortical and limbic systems

77
Q

ketamine CNS effects are primarily related to its

A

antagonistic activity at the N-methyl-D-aspartate (NMDA) receptor

78
Q

what other receptors does ketamine bind to

A

Non-NMDA glutamate receptors
Nicotinic receptors
Cholinergic receptors
Monoaminergic receptors
Mu, delta and kappa-opioid receptors
It also inhibits neuronal Na+ channels (Local anesthetic action) and Ca+ channels (Cerebral vasodilation)

79
Q

ketamine clinical state

A

dissociative

unconscious with eyes open (nystagmus)

maintain spontaneous respiration

no reaction to painful stimuli

80
Q

ketamine induction dose side effects

A

associated with increased hr and bp

81
Q

what drug is a good choice for hemodynamically unstable

A

ketamine

82
Q

what is a good drug choice for OB

A

ketamine

83
Q

when should ketamine be used with caution

A

cardiac patients with sever right heard dysfunction because it increases PVR

84
Q

ketamine can also be used for

A

management of acute pain and depression

85
Q

which induction agent can be used in opioid abuse patients

A

ketamine

86
Q

ketamine CNS effects

A

potent cerebral vasodilator

increase in CBF of 60-80% during normocapnia that can be attenuated with hyperventilation

87
Q

when is ketamine contraindicated

A

patients with elevated ICP

88
Q

ketamine airway effects

A

does not produce significant depression of ventilation

maintains airway reflexes

can increase secretions d/t its effect on muscarinic receptors

89
Q

does ketamine bronchodilate?

A

yes

90
Q

ketamine cardiovascular effects

A

SNS stimulation

everything goes up (MAP, CO, myocardial oxygen requirements, SVR)

91
Q

what is the ideal induction agent for a patient with hypovolemia

A

ketamine

however, in a shock patient →
profound hypotension

92
Q

emergence delirium

A

A phenomenon associated during the postoperative period in patients who have received ketamine anesthesia

Visual, auditory illusions
Confusion
Delirium

93
Q

incidence of emergence delirium

A

5-30%

94
Q

how to prevent emergence delirium

A

preop midazolam

recover patient in calm and quiet environment

95
Q

how does dexmedetomidine work

A

It is a highly selective, specific, and potent α-2 adrenergic agonist

96
Q

what does dexmedetomidine inhibit

A

norepi release in locus coeruleus

97
Q

which induction agent mimics natural sleep like state

A

dexmedetomidine

98
Q

what does dexmedetomidine produce

A

dose-dependent sedation and analgesia with mild respiratory depression

99
Q

dexmedetomidine protein binding

A

highly protein bound, 94%

100
Q

dexmedetomidine metabolism

A

rapid hepatic metabolism involving conjugation, N-methylation, and hydroxylation

101
Q

how is dexmedetomidine excreted

A

urine and feces

102
Q

dexmedetomidine relation to CYP enzymes

A

weak inhibitory effects that could cause increased plasma concentrations of opioids

103
Q

dexmedetomidine CNS effects

A

It has sedative, anxiolytic, and analgesic effects (spinal cord and brain)

Patients are sedated but easily arousable, and able to follow commands

The analgesic effects reduce postsurgical opioid requirements

104
Q

dexmedetomidine ventilatory depression?

A

yes, less than other sedative-hypnotic and opioid anesthetics

105
Q

what kind of dexmedetomidine administration reduces minute ventilation

A

bolus administration

106
Q

dexmedetomidine cardiovascular effects

A

increased potential for hypotension and bradycardia because of high α- 2- adrenoreceptor activity

107
Q

what induction agent blunts hemodynamic effects of direct laryngoscopy and improves hemodynamic stability when given as an adjuvant

A

dexmedetomidine

108
Q

in which population may dexmedetomidine cause severe bradycardia

A

children –> best to titrate

109
Q

When is dexmedetomidine used

A

critical care environment when controlled ventilation is required

after extubation

adjuvant during induction or maintenance

blunts SNS response to laryngoscopy

110
Q

which induction agent is good for procedural sedation

A

dexmedetomidine

111
Q

dexmedetomidine sedation dose

A

0.5-1 mcg/kg over 10 min

followed by infusion of 0.2-0.7 mcg/kg/hr

112
Q

dexmedetomidine usual syringe concentration

A

4 mcg/mL

113
Q

dexmedetomidine side effects

A

hypotension

bradycardia (40%)

dry mouth and nausea

hypertension

114
Q

how can dexmedetomidine bradycardia be treated

A

Can be treated with atropine, ephedrine or volume

Omitting the loading dose can decrease incidence of bradycardia

115
Q

which induction agent has anticonvulsant properties

A

benzodiazepines

116
Q

benzodiazepines effects

A

amnesia

minimal cardiovascular or resp depression

central skeletal muscle relaxant

anxiolysis and sedation

117
Q

benzodiazepines mechanism of action

A

GABA-A

118
Q

what do benzodiazepines increase

A

chloride conductance causing hyperpolarization of the membrane increasing nerve resistance to stimulation

119
Q

do benzodiazepines burn on injection

A

usually not because they are more water soluble (versed)

120
Q

how can benzodiazepines be administered

A

PO, IV, IM, rectally, intranasally, infusion

121
Q

benzodiazepine absorption

A

rapid absorption from the gut >50% undergo first pass hepatic excretion

122
Q

benzodiazepine protein binding

A

highly protein bound, high lipid solubility

123
Q

benzodiazepine ICP effect

A

can decrease CMRO2 and CBF with little effect on ICP

124
Q

what do benzodiazepines do to upper airway reflexes

A

may be decreased as well as central respiratory drive

125
Q

what do benzodiazepines do cardiovascularly

A

can decrease SVR and BP

126
Q

which drug class produces anterograde amnesia

A

benzodiazepines

127
Q

how to reverse benzodiazepine administration?

A

flumazenil

128
Q

flumazenil dose

A

0.15 mg IV over 15 seconds

if after 45 seconds no response give 0.2 mg

repeat at 1 min intervals (do not exceed 4 doses)

129
Q

children common midazolam dose before OR

A

0.5 mg/kg 30 min prior to OR

130
Q

adult midazolam dose

A

1-2 mg in preop

131
Q

which benzodiazepine is water soluble

A

midazolam

undergoes conformational change in the bloodstream before becoming more lipophilic

132
Q

which benzodiazepines are not water soluble

A

lorazepam and diazepam (often cause vein irritation)

133
Q

what kind of barbiturate is methohexital

A

oxybarbiturate

134
Q

barbiturate metabolizm

A

primarily hepatic

inactive metabolites are excreted in urine and bile

135
Q

barbiturate mechanism of action

A

cortical and brainstem GABA inhibitory pathways

136
Q

barbiturate effects

A

loss of consciousness, respiratory and cardiovascular depression

hypnotic effects from inhibition of central excitatory pathways

137
Q

thiopental elimination half-life

A

12 hours

138
Q

anticonvulsant to treat status epilepticus

A

thiopental

139
Q

which induction agent may be used for induction of anesthesia in patients with ↑ ICP, as well as the treatment of ↑ ICP that is resistant to hyperventilation alone

A

thiopental

140
Q

how does thiopental protect the brain

A

Cerebrovascular vasoconstriction

This leads to ↓ cerebral blood flow

Subsequent ↓ in intracranial pressure

Decreased cerebral metabolic O2 consumption

141
Q

what does thiopental stimulate

A

release of histamine from mast cells

142
Q

what precipitates with thiopental

A

succinylcholine, rocuronium, and lidocaine

143
Q

acute intermittent porphyria

A

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

all barbiturates can precipitate an attack and must be avoided in patients with a hx of this disorder

144
Q

5 P’s of AIP

A

pain in abdomen

polyneuropathy

psychological abnormalities

pink urine

precipitated by medicines (sulfur containing drugs)

145
Q

methohexital elimination half life

A

4 hours

146
Q

which agent can cause proconvulsant activity

A

methohexital

147
Q

which is the agent of choice in electroconvulsive therapy

A

methohexital

148
Q

methohexital pain on injection?

A

yes.

149
Q

methohexital induction dose

A

1-2 mg/kg IV

20-30 mg/kg rectally

150
Q

thiopental induction dose

A

2.5-5 mg/kg IV

reduce dose by 30-35% in elderly

General Principles (6 decks)

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