Module 4-Induction Flashcards

1
Q

Identify the MAC level when the patient responds to repeated painful stimuli, airway intervention is needed, ventilation possibly inadequate & CV function is maintained

A

Deep Sedation

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2
Q

Identify the MAC level where the patient responds to verbal/tactile stimulation, no airway intervention needed, ventilation is adequate & CV is usually maintained

A

Moderate Sedation

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3
Q

Pseudocholinesterase is inhibited by what drugs?

A

Esmolol, Neostigmine, Regland, in burn patients, renal & liver disease

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4
Q

Sugammadex is effective against

A

Vecuronium & Rocuronium

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5
Q

What ventilation mode is used with ETT placement?

A

Volume Control

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6
Q

MOA of Lidocaine

A

Inactivates Na+ channel & is concentration dependent

Prevents action potential

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7
Q

What is the onset of Succinylcholine?

A

30 seconds

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8
Q

What is the duration of Succinylcholine?

A

7-12 min

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9
Q

What is the IV does of Succinylcholine?

A

1-1.5mg/kg IV

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10
Q

What is the IM does of Succinylcholine?

A

3-4mg/kg IM

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11
Q

When are the effects of Succinylcholine increased?

A

When an anticholinesterase reversal is given

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12
Q

How much should you increase Succinylcholine by to give a defasciculating dose?

A

Increase dose by 1.5-2mg/kg or give NDMR 3-5 min prior

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13
Q

Non-depolarizers MOA

A

They are competitive antagonists

Prevents initiation of an Action Potential

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14
Q

Intubating dose of Atracurium

A

0.5mg/kg

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15
Q

Onset of Atracurium

A

3-5 min

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16
Q

Duration of Atracurium

A

30-45min

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17
Q

How is Atracurium metabolized?

A

Ester Hydrolysis

Non-specific plasma esteraase

Hofmann elimination (pH & temp dependent)

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18
Q

Atracurium can cause a

A

Histamine release

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19
Q

Onset of Mivacurium

A

3-4min

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20
Q

Mivacurium causes this at low doses

A

Histamine release

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21
Q

What is the intubating does of Mivacurium?

A

0.2mg/kg

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22
Q

What is the duration of Mivacurium

A

15-20min

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23
Q

How is Mivacurium metabolized?

A

Pseudocholinesterase

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24
Q

Intubating dose of Cis

A

0.1-0.2mg/kg

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25
Q

What is the onset of Cis

A

4-7 min

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26
Q

What is the duration of Cis

A

35-50min

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27
Q

How is Cis metabolized?

A

Hofmann Elimination

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28
Q

What is the intubating dose of Vecuronium

A

0.1mg/kg

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29
Q

What is the onset of Vecuronium?

A

3-4min

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30
Q

What is the duration of Vecuronium

A

25-50min

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31
Q

Which NDMR is the fastest?

A

Rocuronium

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32
Q

What is the onset of rocuronium?

A

1.5-3min

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33
Q

What is the duration of Rocuronium?

A

30-70min

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34
Q

What is the standard intubating dose of Rocuronium

A

0.6mg/kg

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35
Q

What is the RSI dose of Rocuronium

A

1.2mg/kg

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36
Q

What are the vent settings when using an LMA?

A

VC or PSV

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37
Q

How much Fentanyl can you administer for induction?

A

100-200mcg

2-3mcg/kg

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38
Q

MAC is a measure of

A

Potency

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39
Q

Propofol lasts for

A

10 min

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40
Q

What is the MAC dose of Propofol?

A

20-100mcg/kg/min

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41
Q

What is the MAC dose of a Ketamine infusion?

A

0.1-0.3mg/kg/hr

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42
Q

What is the bolus dose of Precedex

A

0.25-0.75 mcg/kg

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43
Q

% of Ketamine Pro Binding

A

12%

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44
Q

What is the elimination half life of ketamine?

A

2-3 hours

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45
Q

Distribution half life of Ketamine

A

11-17

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46
Q

What is the distribution half life of propofol

A

2-4

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47
Q

Elimination half life of Propofol

A

1-5

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48
Q

Pro binding % of Propofol

A

98

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49
Q

Distribution half life of Etomidate

A

2-4

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50
Q

Elimination half life of Etomidate

A

2-5

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51
Q

Pro binding of Etomidate

A

75

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52
Q

Propofol, Etomidate & Barbiturates cause

A

An extension of Cl- opening, causing hyperpolarization

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53
Q

What is the percentage makeup of Propofol

A

10% soybean

2.25% glycerol

1.2% egg lecithin

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54
Q

What makes propofol susceptible to bacterial contamination?

A

The emulsion

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55
Q

What is in Propofol that can cause an allergy & also prevents bacterial & fungal growth

A

0.005% disodium edetate

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56
Q

Generic Propofol contains

A

Sodium Metabisulfite or benzyl alcohol as a preservative

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57
Q

What technique should you use when drawing up propofol?

A

Aseptic

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58
Q

When should Propofol be discarded?

A

After 6 hours

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59
Q

Propofol binds to what sub-unit?

A

Beta 2

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60
Q

With Propofol administration, the influx of Cl- hyper polarizes which synaptic membrane?

A

The post-synaptic membrane

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61
Q

Propofol is a ______stimulant

A

Direct stimulant

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62
Q

What causes burning for Propofol

A

2.25% glycerol

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63
Q

What is the dwelling dose of Lidocaine?

A

20-40mg

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64
Q

Propofol has what effects?

A

Antiseizure
Antiemetic

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65
Q

What can help with Propofol burn

A

Lidocaine
Large bore IV

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66
Q

Why dose Propofol cause cloudy urine?

A

Uric Acid Crystals

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67
Q

What are the side effects of Etomidate?

A

Pain on injection
Myoclonia
N/V
Adrenocortical Suppression

68
Q

There will be a decrease if plasma cortisol for how many hours after Etomidate is given

A

8-24 hours

69
Q

What enzyme is inhibited with Etomidate administration

A

11 beta-hydroxylase

70
Q

What is the induction dose of Etomidate

A

0.2-0.3mg/kg

71
Q

Etomidate will decrease

72
Q

What do we give with Ketamine & why?

A

Benzos to help with the dissociative, unpleasant feeling

73
Q

Ketamine effects on BIS monitoring

A

Will increase it due to increased cerebral blood flow

74
Q

What is the onset of Ketamine

75
Q

What is the duration of Ketamine

76
Q

What is the MOA of Mg+

A

NMDA antagonist

77
Q

Which medications can be given for pain control

A

Mg
Ketamine
Precedex

78
Q

What is the Ketamine dose for pain

A

0.25-0.5mg/kg IV

79
Q

Why is an antisialagogue given with Ketamine?

A

Because Ketamine causes increased oral secretions

80
Q

Does Ketamine increase IOP?

A

Yes, usually at high doses of 6mg/kg, but not with 3mg/kg

81
Q

Benzos will increase

A

The Cl- channel opening frequency

82
Q

What is the onset of Benzos

83
Q

What is the duration of Benzo

84
Q

Midazolam produces what effects

A

Anxiolytic
Sedative
Hypnotic
Amnestic
Anticonvulsant

85
Q

How are Benzos classified?

A

Elimination half life

86
Q

Elimination of Diazepam

A

Greater than 24 hours

87
Q

Elimination 1/2 time of lorazepam

A

6-24 hours

88
Q

Elimination 1/2 time of Midazolam

A

Less than 6 hours

89
Q

Benzos provide what type of amnesia?

A

Anterograde

90
Q

Is Remimazolam organ independent?

A

Yes, just like Remifentanil

91
Q

What makes Remimazolam susceptible to non-specific tissue esterases

A

Carboxylic ester moiety

92
Q

Presynaptic effects of Precedex

93
Q

Post synaptic effects of Precedex

A

CV effects

94
Q

MOA of Precedex

A

Negative feedback

Decreases release of NE

Hyperpolarization

95
Q

What is often seen with Precedex

A

HOTN
Bradycardia

96
Q

Precedex resembles

A

Natural Sleep

97
Q

Fentanyl MOA

A

Mu opioid agonist

98
Q

Celebrex MOA

A

COX-2 inhibitor

99
Q

Gabapentin MOA

A

Blockage of Ca+ voltage gated channels

100
Q

Acetaminophen MOA

A

COX 1 & 2 inhibitors

101
Q

IV onset of Fentanyl

102
Q

Peak time of Fentanyl

103
Q

Duration of Fentanyl

104
Q

Fentanyl goes through

A

1st pass pulmonary uptake

105
Q

Scopolamine causes antagonism of

A

Muscarinic acetylcholine (M1) receptors

Blocks impulse from inner ear to medulla

Apply 2-4 hours pre-stimulus

106
Q

What are anticholinergic side effects?

A

Dry mouth, blurred vision, tachycardia, dry skin, rash

107
Q

How do you treat central anticholinergic syndrome?

A

Tx with Physostigmine since it crosses the BBB

108
Q

Tylenol has no effect on

A

PLTs & has no anti-inflammatory effects

109
Q

Tylenol can cause

A

GI bleed, CV events & hepatic toxicity

110
Q

Celecoxib has the highest risk for

A

Thrombosis due to COX 2 inhibition

111
Q

Celecoxib increases the risk for

112
Q

Celecoxib decreases the risk of

A

GI effects

113
Q

Which 2 neuromuscular blockers are likely to cause anaphylaxis

A

Succinylcholine
Rocuronium

114
Q

When does the dose of Sch need to be increased?

A

When given to an MG patient

115
Q

Sch has a higher affinity for

116
Q

What are some characteristics of Sch (dosage wise)?

A

Faster onset 30sec

Duration 7-12 min

1-1.5mg/kg IV

117
Q

Make up of Sch drug

A

2 Ach molecules are fused together

Competitive agonist of Ach

118
Q

What complaint is often associated with Sch

A

Muscle weakness

119
Q

What complication can potentate Sch

A

Pseudocholinesterasae deficiency

120
Q

Sch binds what receptors?

A

Nicotinic, which blocks Na+ channels from opening & enter the cell

121
Q

Non depolarizers like Rocuronium are

A

Competitive antagonist to Ach

Prevent initiation of action potential

122
Q

What is the onset of Roc

123
Q

What is the duration of Roc

124
Q

What is the intubating & RSI dose of Roc

A

Intubating: 0.6mg/kg

RSI: 1.2mg/kg

125
Q

Phenylephrine is a

A

Synthetic non-catecholamine

126
Q

Phenylephrine mimics

A

NE effects, but is less potent & last longer

127
Q

Phenylephrine causes

A

DIRECT alpha 1 effects

Bradycardia

128
Q

What is the bolus dose of Phenylephrine

129
Q

Esmolol is a selective

A

Beta 1 antagonist

130
Q

Characteristics of Esmolol

A

Decreases SNS response

Short acting

Decreases anesthetic response

Opioid sparing

Masks light anesthesia

131
Q

What is the bolus dose of Esmolol

A

0.5-1mg/kg vs 0.2-0.5mg/kg??

132
Q

How is esmolol metabolized?

A

Ester hydrolysis in the plasma

133
Q

When in clindamycin given?

A

With Ancef allergy

134
Q

What is the dose of Clindamycin?

A

600-900 mg Q6H

135
Q

Clindamycini & NMB

A

Clindamycin will potentiate the effects of NMB

136
Q

When is Vanc given?

A

PNC allergy 10-15mg/kg

MAX 2g

137
Q

When should vans be infused?

A

60 min to 2 hours

138
Q

Ephedrine is an

A

Indirect acting non catecholamine

139
Q

Characteristics of Ephedrine

A

Alpha & beta effects

Increases HR & BP, CO & contractility

140
Q

When is Ephedrine not effective

A

Catecholamine depletion

141
Q

What is the bolus dose of ephedrine?

A

2.5-10mg bolus

142
Q

B:G of Sevo

143
Q

B:G Des

144
Q

B:G Iso

145
Q

B:G N2O

146
Q

Iso MAC

147
Q

Sevo MAC

148
Q

Des MAC

149
Q

N2O MAC

150
Q

What is MAC awake

A

The alveolar concentration where patient opens eyes

151
Q

MAC awake during induction

152
Q

MAC awake during emergence

153
Q

MAC bar is the

A

Alveolar concentration required to block autonomic response following painful stimuli

154
Q

Movement is prevented in

A

95% of the population at 1.3 MAC

155
Q

Awareness & recall are prevented at

A

0.4-0.5 MAC

156
Q

MAC bar is equal to

157
Q

What factors increase MAC?

A

Red head

Chronic ETOH

INcreased CNS NT activity

Increased Na+

Infants 1-6 months

Hyperthermia

158
Q

What factors decrease MAC

A

Acute ETOH

Sedation drugs

Hyponatremia

Old age (decreased by 6%/decade after 40)

Extremes of age

Pregnancy

159
Q

What factors have no effect on MAC

A

Thyroid issues
Potassium
Gender

160
Q

Which drugs are metabolized by Pseudocholinesterase

A

Ester Locals

Succinylcholine

161
Q

Which drugs are metabolized by non-specific esterases

A

Remifentanil
Esmolol
Clevidipine
Atracurium

162
Q

Which drugs are metabolized by Hofmann elimination

A

Cisatracurium
Atracurium

163
Q

Flagyl is what type of drug?

A

Prodrug that causes a concentration gradient

164
Q

What is the dose of Flagyl

A

500-1000mg given within 60 min

165
Q

When should Flagyl be avoided/

A

ETOH patients

166
Q

What is the MOA of Vanc

A

Inhibits cell wall synthesis

167
Q

Vance can cause what syndrome?

A

Red man syndrome