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2-Anesthesia Pharm > Wk 1-Inductions & Benzos > Flashcards

Wk 1-Inductions & Benzos Flashcards

1
Q

Define: Sedative

A

a drug that induces a state of calm or sleep, still arousable

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2
Q

What is an example of a sedative procedure?

A

MAC

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3
Q

Define: Hypnotic

A

a drug that induces hypnosis or sleep, form of disassociation from the environment

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4
Q

Define anxiolytic.

A

any drug that reduces anxiety

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5
Q

What is is sedative-hypnotics?

A

collective term, drugs that reversibly depress the activity of the CNS. This class of drugs play an important role in every aspect of anesthesia delivery from conscious sedation to general anesthesia

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6
Q

Define general anesthesia.

A

drug-induced unconsciousness that abolishes conscious memory as one component

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7
Q

What is the triad of general anesthesia?

A

amnesia, muscle relaxation, analgesia

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8
Q

The ______ have greater potency then the sedative effects.

A

Amnestic potency

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9
Q

What drug is important in the recall of events during general anesthesia and child birth? Why?

A

Benzodiazepines, Important consideration when concerned with “recall” of events (conscious memory) during anesthesia, especially during procedures that require general anesthesia.
But also an important consideration for events (as childbirth) where a patient’s memory of the event is warranted.

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10
Q

Define anterograde amnesia.

A

After receiving a drug

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11
Q

Define retrograde.

A

Before giving the drug

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12
Q

Benzos will _______ the GABA (A) receptor’s affinity for GABA

A

increase

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13
Q

Define an allosteric modulator

A

the binding of a substance(called an allosteric modulator) to a certain site on a receptor in a way that alters the conformation of other sites on the receptor, thereby increasing or decreasing the affinity of the receptor for other molecules.

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14
Q

γ-Aminobutyric acid type A (GABAA) receptors are inhibitory or excitatory

A

inhibitory CNS receptors in neurons, and major targets of general anesthetics such as etomidate and propofol.

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15
Q

What do GABAa receptors contain?

A

five subunits arranged around a chloride-conducting pore

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16
Q

_____ subunits account for the anxiolysis, whereas _______ account for the sedative, amnestic and anticonvulsive

A

α2; a1

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17
Q

States of _______ and ______ can increase bioavailability.

A

Hypoalbumenia/liver disease

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18
Q

What are the common side effects of benzos?

A

Fatigue, drowsiness (most common)

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19
Q

What is of concern with elderly taking benzos?

A

Concern with cognitive disturbances postoperative in the elderly.

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20
Q

What are some physiological changes that make the elderly more sensitive to benzos (6)?

A

aging brain with memory impairment and age related changes in CNS receptors. Decreased metabolism and clearance of drugs. Also increase in body fat and age-related decreases in serum albumin (more unbound drug available)

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21
Q

What other agents can produced synergistic sedative effects in combo with benzos?

A

ETOH, inhaled and injected anesthetics, opioids, and alpha2 agonists

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22
Q

What can happen with benzos and ETOH?

A

Life threatening CNS depression when used in conjunction with ETOH (they have cross tolerance).

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23
Q

What meds are used to treat alcohol withdrawal?

A

Lorazepam (Ativan) and valium

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24
Q

Do you have a burning sensation with midazolam?

A

No, easily well tolerated

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25
Q

What is true regarding midazolam and pregnancy?

A

Teratogenic concerns (cleft palate): Pregnancy test on all childbearing woman before administering (or waiver)

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26
Q

What is the pKa of midazolam?

A

6.2

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27
Q

What is the metabolite produced by midazolam biotransformation?

A

1-hydroxymidazolam: ½ activity of parent

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28
Q

What is an imidazole ring?

A

Imidazole ring: midazolam exists with both an “open structure” that is protonated to allow for aqueous suspension and the “closed structure” that is physiologic active, highly lipophilic. Structure changes with pH of environment (gastric or IV) favoring the more “closed” form

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29
Q

What effect dose increased vd have on infusion rate?

A

Increased Vd may require a higher initial infusion rate at initiation

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30
Q

Where is midazolam metabolized?

A

CYP 3A4

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31
Q

What dose of midazolam can cause transient apnea, especially in the presence of opioid?

A

> 0.05 mg/kg

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32
Q

What phases of biotransformation will midazolam undergo?

A

Glucuronamide conjugation and oxidative hydroxylation

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33
Q

What is the pediatric dosing of midazolam?

A

0.25-0.5mg/kg

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34
Q

How often before induction should midazolam be given prior to induction, in pediatrics?

A

20-30 minutes

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35
Q

What is the IV sedation adult dose of midazolam ?

A

1.0-2.5mg IV

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36
Q

What is the half-time peak effect of midazolam?

A

5.6 minutes

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37
Q

What is the duration of IV sedation midazolam?

A

15-80 minutes

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38
Q

What is the anesthesia induction dose of midazolam?

A

0.1-0.2mg/kg IV

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39
Q

What is the loading and maintenance dose of postop midazolam sedation?

A
  • 0.5-4.0 mg IV loading dose

- Maintenance 1-7 mg/hour IV (for postop intubated patients)

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40
Q

What is the adult dosing range of paradoxical vocal cord motion (postop stridor)?

A

0.5-1 mg IV

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41
Q

Onset IV (min of midazolam)

A

0.5-1 min

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42
Q

Onset IV (min of Diazepam)

A

1-5 min

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43
Q

Onset IV (min of lorazepam)

A

1-3 min

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44
Q

pKa (midazolam)

A

6.57

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45
Q

pKa (diazepam)

A

3.4

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46
Q

pKa (Lorazepam)

A

11.5

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47
Q

vD (midazolam)

A

1.1 L/Kg

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48
Q

vD (Diazepam) L/Kg

A

1.1 L/Kg

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49
Q

vD (Lorazepam) L/Kg

A

1.3 L/Kg

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50
Q

Clearance (midazolam) mL/kg/min

A

1.6 mL/kg/min

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51
Q

Clearance (Diazepam) mL/kg/min

A

0.38 mL/kg/min

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52
Q

Clearance (Lorazepam) mL/kg/min

A

1.1 mL/kg/min

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53
Q

Midazolam (Elimination 1/2 time)

A

1.9 hours

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54
Q

Diazepam (Elimination 1/2 time)

A

43 hours

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55
Q

Lorazepam (Elimination 1/2 time)

A

14 hours

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56
Q

Define elimination half-life

A

isthe length of time required for the concentration of a drug to decrease to half of its starting dose in the body

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57
Q

What is produced from the metabolism of Diazepam? What clinical significance does this have?

A
  • Prolonged duration of action

- Active metabolite: desmethyldiazepam

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58
Q

What is the elimination half-time in healthy patients for diazepam?

A

40 hours

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59
Q

What is the MOA of flumazenil?

A

Specific BZO GABAA receptor antagonist (competitive)

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60
Q

What is the initial dose of flumanezil?

A

Recommended initial dose 0.2mg IV (8-15mcg/kg IV)

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61
Q

What is the recommended additional dose of flumazenil?

A

If needed, additional doses of 0.1mg IV (total dose of 1 mg) at 60 second intervals

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62
Q

What is the duration of action of Flumazenil?

A

30-60 minutes

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63
Q

Peak effects of Flumazenil can be seen in ______ minutes. What is the approximate half life?

A

1-3 minutes; 1 hr

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64
Q

What is the drug classification for demedetomidine?

A

Potent, highly selective alpha 2-adrenergic receptor agonist

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65
Q

What is the site of action that dexmedtomidine exerts its effects?

A

Pontine Locus Coeruleus (brainstem)

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66
Q

What is clonidine?

A

Clonidine is partial agonist with less selectivity for alpha 2 as compared to Dex which is a full agonist with much higher selectively

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67
Q

What is the elimination half-time of dexmedetomidine?

A

2-3 hours

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68
Q

How is dexmedetomidine metabolized?

A

Undergoes extensive hepatic metabolism (slightly inhibits enzymes): N-glucuronidation
& P450 Hydroxylation

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69
Q

Does dexmedetomidine suppress respiratory function?

A

No

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70
Q

What are the major cardiovascular side effects of dexmedetomidine?

A

Bradycardia and hypotension

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71
Q

What is formed through the biotransformation of Flumazenil?

A

Inactive metabolites

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72
Q

What is the main goal of induction agents?

A

IV medications that lead to rapid loss of consciousness

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73
Q

What is TIVA?

A

TIVA: total intravenous anesthesia- a technique for providing anesthesia

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74
Q

What is the steps to induction?

A

Provide sedation, Induce (start) general anesthesia - usually in combination w/ other drugs, Used as the sole anesthetic drug for some procedures, Maintain a state of anesthesia for longer procedures via infusion.

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75
Q

What are some examples of induction agents?

A

Etomidate, Propofol, Ketamine, Dexmedetomidine

76
Q

What induction agents have Non-GABA MOA?

A

Ketamine and Dexmedetomidine

77
Q

What is in the aqueous solution with Propofol?

A

10% soybean oil, 2.25% glycerol, and 1.2% purified egg phosphatide

78
Q

Can you comix propofol?

A

No, This formulation supports bacterial growth, use aseptic technique and do not comix

79
Q

What is the difference between generic and propofol?

A

Formulations differ between Propofol and generic: Generic uses metabisulfite as preservative

80
Q

What is the MOA of propofol (2)?

A

Selective modulator of Y-aminobutyric acid (GABAA) receptors & ↓ dissociation of GABA/potentiates GABA (again - CNS inhibitory neurotransmitter)

81
Q

Describe the clearance of propofol.

A

Clearance of propofol from the plasma exceeds hepatic blood flow - tissue uptake (pulmonary uptake) as well as hepatic oxidative metabolism by cytochrome P450 important in the removal of this drug from the plasma

82
Q

What is the onset of propofol ?

83
Q

What is duration of propofol?

A

5-10 minutes

84
Q

What is the elimination half-life of propofol?

A

0.5-1.5 hours

85
Q

What is special about the elimination of propofol?

A

Context-sensitive half-time for infusions lasting up to 8 hours is less 40 minutes

86
Q

What is the induction dose of propofol?

A

1.5-2.5mg/kg IV

87
Q

Why does pediatric patients require a higher induction dose of propofol?

A

Pediatric patients require a higher induction dose on a mg/kg basis (reflects a larger central distribution volume and higher clearance rate)

88
Q

Why does elderly patients require a lower induction dose of propofol?

A

Elderly patients require a lower induction dose (25-50%) due to a smaller central distribution volume and decreased clearance rate

89
Q

What is a favorable property specific to propofol?

A

Prompt recovery with minimal to low incidence of N&V; antiemetic properties

90
Q

What is the maintenance dose of propofol for anesthesia?

A

100-300mcg/kg/min

91
Q

What are some non-hypnotic applications of propofol?

A

Antiemetic effects, antipruritic effects, anticonvulsant activity, attenuation of bronchoconstriction, analgesia

92
Q

What dose can decrease the seizure duration? When will this not be indicated?

A

In doses >1mg/kg decreases seizure duration in patients undergoing ECT therapy

93
Q

How is propofol useful for asthmatic pts?

A

Attenuation of bronchoconstriction:

  • Decreases wheezing in asthmatic patients
  • Caution with metabisulfite formulation
94
Q

What type of pain will propofol not relieve?

A

Does NOT relieve acute nociceptive pain

95
Q

Cerebrovascular autoregulation not affected by ___________.

A

propofol induced hypotension

96
Q

What EEF changes can high dose propofol produce?

A

burst suppression on EEG

97
Q

What effect on bp does propofol produce?

A

decrease systemic BP (exaggerated in pts w/ hypovolemia, the elderly, and pts with left ventricular dysfunction)

98
Q

What is the negative inotropic effects associated with propofol?

A

Negative inotropic effect results from a decrease in intracellular calcium availability secondary to inhibition of trans-sarcolemmal calcium influx

99
Q

What profound side effects can be associated with propofol?

A

Profound bradycardia and asystole can occur despite prophylactic anticholinergics (1.4 in 100,000)

100
Q

What effect dose propofol have on ventilation during induction?

A

Dose-dependent depression of ventilation, with apnea occurring in 25-35% of pts following induction (opioids enhance ventilatory depression)

101
Q

What respiratory effect can be seen with propofol maintenance infusion?

A
  • Propofol maintenance infusion decreases tidal volume and RR
  • Ventilatory response to arterial hypoxemia decreased due to effects at the central chemoreceptors
102
Q

What hepatic effects can be caused by prolonged infusion of propofol?

A

Prolonged infusions can cause hepatocellular injury, lactic acidosis, bradyarrhythmias, and rhabdomyolysis secondary to propofol infusion syndrome

103
Q

What is important to known about propofol and urine output?

A

Prolonged infusion can cause urine to turn green due to phenols in the urine

104
Q

What effect does propofol have on IOP?

A

Propofol ↓ IOP that occurs immediately following induction and intubation

105
Q

What can propofol do to platelets aggregation?

A

Can inhibit platelet aggregation induced by proinflammatory lipid mediators (thromboxane A2 and platelet activating factor)

106
Q

What are common side effects of propofol?

A

Pain on injection, allergic reactions, lactate acidosis, prodconvulsant activity, abuse potential, antioxidant properties and bacterial growth

107
Q

What is a metabisulfite sensitivity?

A

The metabisulfite formulation can be an issue for those with reactive airways (sensitivity to sulfites)

108
Q

What is at risk of developing if you comix propofol?

A

Common to comix Propofol with lidocaine to decrease pain on injection: may cause oil droplets to coalescence (risk pulmonary embolism)

109
Q

What is the practice regarding administration of propofol to pt with egg and soy allergies?

A

Concerns with egg allergies or soy allergies and propofol - considered safe as the allergies are due to proteins not oils or lecithin

110
Q

With propofol, unexplained tachycardia could be indicative of ________.

A

may be sign of lactic acidosis (measure ABGs and serum lactate concentration)

111
Q

__________ is associated with propofol

A

Prolonged myoclonus

112
Q

What effect can propofol infusion syndrome have on fatty acid metabolism?

A

Propofol infusion syndrome results from either direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism

113
Q

What are some predisposing factors to propofol infusion syndrome?

A

Predisposing factors include young age, severe critical illness of central nervous system or respiratory origin, exogenous catecholamine or glucocorticoid administration, inadequate carbohydrate intake and subclinical mitochondrial disease. Treatment options are limited.

114
Q

What two bacteria does propofol support growth of?

A

E. coli and Pseudomonas aeruginosa

115
Q

What is unique about the administration of etomidate?

A

Administered only as a single isomer (R+ isomer)

116
Q

What is the pKa of etomidate? What does this mean?

A

pKa 4.2 - very hydrophobic at physiologic pH

117
Q

What is the moa of Etomidate?

A

Gated modulating effects of GABAa, agonists at central alpha2-receptors, thereby maintaining vascular tone and mycoardial contractility following induction

118
Q

99% of etomidate is in the _______ form at physiologic pH

119
Q

What effect does low albumin have on etomidate?

A

low albumin concentration causes an increase in the unbound pharmacologically active fraction of etomidate in the plasma

120
Q

What is the elimination half-life of etomidate?

121
Q

What is the induction dose of etomidate?

A

standard induction dose of 0.2-0.4mg/kg IV

122
Q

Is etomidate an analgesic?

A

No, Does NOT produce analgesia

123
Q

Principal limiting factor of etomidate is transient depression of __________

A

adrenocortical function

124
Q

What pt population should you use caution in prescribing etomidate?

A

Use caution when administering to patients with a history of seizures and epilepsy (can activate seizure foci on EEG)

125
Q

What is the induction dose for cardiac pts of etomidate?

A

0.3 mg/kg IV

126
Q

Etomidate in acutely hypovolemic patients can result in ________

A

hypotension

127
Q

What can occur if the induction dose is 0.45 mg/kg IV?

A

significant decreases in BP and CO

128
Q

What is important about the administration of etomidate?

A

Apnea can accompany rapid IV injection (slow push)

129
Q

What is the relationship of minute ventilation and etomidate induction?

A

Etomidate-induced decreases in minute ventilation are offset by compensatory increases in RR

130
Q

What is the relationship to anesthetics and anticonvulsant activity?

A

Many of the anesthetics produce anticonvulsant activity at high doses (including etomidate). However, etomidate decreases seizure threshold (reason to use with caution with seizure patients).

131
Q

What is the relationship of etomidate and myoclonus?

A

Occurs in 50-80% of patients (without a premedication) and is dose-related

132
Q

What is the etiology of etomidate and myoclonus?

A

Etiology for myoclonus is subcortical disinhibition. Can be an issue at it raises intraocular pressure and may increase risk of aspiration for patients with a full stomach

133
Q

What is the relation of etomidate and adrenocortical suppresion?

A

Inhibition of the enzyme II B-hydroxylase lasts hours after an induction dose of etomidate (can lower cortisol up to 72 hrs)

134
Q

What medication is known to have a “hangover” feeling and unpleasant taste during induction?

A

Sodium Pentothal (STP)

135
Q

What is the relationship between Sodium Pentothal (STP) and analgesia?

A

Thiopental (STP): no analgesic properties - may actually increase sensitivity to pain

136
Q

What is the MOA of Sodium Thiopental (STP)?

A

Mimics the action of GABA by directly activating GABAa receptors at higher doses

137
Q

What is the onset and awakening of Sodium Thiopental (STP)?

A

Ultra-rapid onset; rapid awakening (30-45 sec

138
Q

How long before consciousness returns with Sodium Thiopental (STP)?

139
Q

What is the resulting active metabolite of Sodium Thiopental (STP)?

A

pentobarbital

140
Q

How is the elimination half-life of Sodium Thiopental (STP) affected by pediatric patients?

A

Elimination ½-time shorter in pediatrics: ↑ hepatic clearance

141
Q

How is the elimination half-life of Sodium Thiopental (STP) affected by pregnant patients?

A

Prolonged in pregnancy: serum albumin levels decrease with pregnancy and STP highly protein bound

142
Q

Sodium Thiopental (STP): Laryngeal and cough reflexes are not abolished until large doses of _________ have been administered

A

barbiturates

143
Q

What is a contraindication to sodium thiopental?

A

Exacerbate heme enzyme defect responsible for disease porphyria (contraindicated)

-Induces δ-aminolevulinic acid (ALA) synthetase (porphyria)

144
Q

What is porphyria?

A

cells fail to change chemicals in your body (porphyrins and porphyrin precursors) into heme

145
Q

What is the IV induction dose of Methohexital?

A

1-2 mg/kg IV

146
Q

What is the elimination half-life of Methohexital?

147
Q

What type of anesthesia does ketamine produce?

A

dissociative anesthesia

148
Q

What are two major characteristics of ketamine? (2)

A

Amnesia and intense analgesia

149
Q

What can cause emergence delirium with ketamine?

A

Emergence delirium if sole anesthetic

150
Q

What form of ketamine is most frequently used? Which isomer produced more desired effects?

A

Racemic, S (+) isomer produces more desired effects

151
Q

What is the R (isomer) of ketamine?

A

R (-) isomer specific in blocking adenosine triphosphate-regulated potassium channels thus limiting racemic mixture of ketamine for any cardiac protective effects in limiting infarct size with an MI patient.

152
Q

What is the primary MOA of ketamine?

A

NMDA - noncompetitive antagonist

153
Q

What does the stimulation of the limbic system by ketamine mean?

A

Although the cortical region is depressed: the limbic system is stimulated (excitatory behavior: emotions, memories, arousal)

154
Q

What other medication works similarly to ketamine?

A

noncompetitive antagonist - binds within an open channel at phencyclidine site (so does Mg++)

155
Q

Which ketamine isomer has the greater affinity?

A

S (+) isomer

156
Q

What is the NMDA receptor?

A

NMDA is an excitatory CNS receptor (one of 3 types of Glutamate Receptors). It is both a ligand-gated receptor and voltage ion receptor

157
Q

Glutamate: __________ neurotransmitter

A

excitatory

158
Q

Glycine: _________ neurotransmitter

A

inhibitory

159
Q

Where are NMDA receptors found?

A

NMDA receptors are found in excitatory neurons in the CNS: very important controlling synaptic plasticity and memory function

160
Q

What is the pKA of ketamine?

A

7.5 at physiologic pH

161
Q

When are peak plasma concentrations of IM and IV ketamine achieved?

A

Peak plasma concentrations after 1 minute IV & 5 minutes IM

162
Q

How does late psychodynamic effect result during a ketamine administration?

A

Late psychodynamic effects result from redistribution back into plasma from vessel-poor tissues

163
Q

What is the elimination half time of ketamine?

164
Q

What is form from the demethylation of ketamine?

A

active metabolite (80%): norketamine, Contributes to prolonged effects of ketamine (analgesia)

165
Q

What can be administer to assist with the hypersalivation associated with ketamine?

A

Coadminister antisialagogue (glycopyrrolate > atropine)

166
Q

What is atropine?

A

As a lipid soluble tertiary amine compound: atropine will cross the blood brain barrier so can get central effects as miosis and altered mental status along with its desired antimuscarinic effects of increased HR and decreased salivation

167
Q

What is scopolamine?

A

also a tertiary amine (used more for sedation and antinausea medication

168
Q

What is glycopyrrolate?

A

Glycopyrrolate is a hydrophilic quaternary amine and crosses the blood brain barrier poorly

169
Q

What is the dose for analgesia of ketamine?

A

0.2-0.5 mg/kg

170
Q

What is the action of ketamine at the spinal NMDA receptor?

A

postoperative pain

171
Q

What can be used for pediatric cardiac surgery?

A

Continuous infusions of ketamine for postoperative sedation and analgesia (E.g.: pediatric cardiac surgery): 1-2 mg/kg/hour

172
Q

What is the dose of ketamine used for opioid tolerance reversal?

A

0.3 mg/kg/hour

173
Q

What is the induction dose for ketamine IV and IM?

A

1-2 mg/kg IV or 4-8 mg/kg IM

174
Q

When does LOC occur with ketamine?

A

Loss of consciousness in 30-60 seconds after IV administration and 2-4 minutes after IM injection

175
Q

How long will amnesia persist with ketamine?

A

Amnesia persists for 60-90 min after return to consciousness (no retrograde amnesia)

176
Q

What is the difference between IM or IV ketamine?

A

bioavailability high and rapid after IV, IM doses- first pass hepatic effect affect PO

177
Q

What patient population should ketamine be avoided in?

A

Avoid in patients with systemic or pulmonary hypertension or increased ICP

178
Q

What are the CNS clinical effects of ketamine?

A

ICP, neuroprotective, EEG and Somatosensory evoked potentials

179
Q

What will increase within the plasma concentration after ketamine administration?

A

↑ plasma concentrations of epi and NE occur after administration

180
Q

What does ketamine need?

A

Ketamine needs an intact and normally functionally CNS

181
Q

What can happen if ketamine is rapidly administered or given with opioid?

A

Apnea can occur if administered rapidly or in conjunction with an opioid

182
Q

What increase risk factors of emergence delirium?

A

Increased incidence with age >15 years, female gender, doses >2mg/kg IV, and a history of personality disorders

183
Q

What can be administer before ketamine to help prevent emergence delirium?

A

BZO (versed) administered 5 min prior to induction with ketamine most effective in prevention

184
Q

What drug interaction with ketamine will cause hypotension?

A

Volatile anesthetics

185
Q

What effect does beta blockade have on ketamine?

A

Beta blockade reduces increases in HR and BP

186
Q

What effect does ketamine have on have on nondepolarizing muscle relaxants?

A

Enhances nondepolarizing muscle relaxants: interferes with calcium ion binding or its

187
Q

ketamine affects intracellular ________

2-Anesthesia Pharm (4 decks)

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