Propofol, Ketamine, NSAIDs, & ERAS Flashcards

1
Q

What class of drug is propofol?

A

A sedative/hypnotic

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2
Q

What is the induction dose of propofol?

A

1.5-2.5 mg/kg IV

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3
Q

How long does an induction dose of propofol take to render the patient unconscious?

A

30 seconds

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4
Q

Is phase II of consciousness desirable or undesirable? How does propofol interact with phase II?

A

Undesirable; it is the excitatory phase; propofol allows the induction of anesthesia with very little time spent in phase II.

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5
Q

What is a major advantage of propofol over other induction agents regarding recovery?

A

It allows for rapid awakening with minimal CNS effects

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6
Q

Describe the solution in which propofol is administered.

A

A 1% solution in soybean oil, glycerol, and egg lecithin (a long-chain triglyceride) which supports bacterial growth and can transiently increase plasma triglyceride levels.

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7
Q

Which preservative does Diprivan have?

A

Disodium edetate and NaOH

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8
Q

Which preservative does generic propofol have?

A

Metabisulfite

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9
Q

True or false? Different propofol preservatives have the same pH.

A

False

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10
Q

Why is mixing propofol and lidocaine not recommended?

A

Can cause pulmonary emboli through coalesced oil

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11
Q

What is the problem with Ampofol?

A

Even more severe injection site pain compared to Diprivan.

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12
Q

What is the problem with Aquavan?

A

While it causes less injection site pain than propofol, it will cause genital burning!!

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13
Q

With which receptor does propofol interact and how?

A

Propofol is a GABA-A receptor agonist (inhibitory neurotransmitter)

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14
Q

What effect does the stimulation of GABA-A have?

A

Hyperpolarization of cell membranes

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15
Q

Into what organs is propofol taken up during the first pass effect?

A

Lungs and liver

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16
Q

Abnormalities with which liver enzyme can alter the metabolism of propofol?

A

Cytochrome P-450

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17
Q

What is the elimination half time for propofol?

A

0.5-1.5 hours

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18
Q

What are the context sensitive half times for propofol (time to 50% drop in blood level after infusion is stopped) after less than 3 hours? Greater than 3 hours? Greater than 8 hours?

A

10 minutes; 25 minutes; 40 minutes

Minimal for most surgical times

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19
Q

In ____, most of propofol goes back into circulation after 1st pass effect.

A

Lungs

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20
Q

Propofol is metabolized by the ____ and excreted mostly through the _______, however _____ and/or _____ disease does NOT impair elimination.

A

liver; kidneys; liver; renal

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21
Q

How does propofol’s clearance impact cumulation? Placenta? CP bypass?

A

Rapid clearance –> no cumulation
Crosses placenta but rapidly cleared from neonatal circulation
Unpredictable with CP bypass

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22
Q

Is propofol a good drug for OB? Why or why not?

A

As long as mom is hemodynamically stable, yes! Because while it does cross the placenta, it is rapidly cleared from neonatal circulation.

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23
Q

What is the induction dose of propofol?

A

1.5-2.5 mg/kg IV

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24
Q

Pediatrics require _______ doses of propofol due to _______ volume of distribution and ________ clearance.

A

increased; larger; faster

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25
Q

Elderly patients require _______ doses of propofol due to _______ volume of distribution and ______ clearance.

A

decreased; smaller; slower

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26
Q

What is the sedation infusion dose range of propofol?

A

25-100 mcg/kg/min

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27
Q

Propofol provides good _______ but no ________.

A

amnesia; analgesia

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28
Q

What is GA maintenance infusion dose range for propofol?

A

100-300 mcg/kg/min (less with opioids and volatile)

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29
Q

What is an antiemetic dose of propofol?

A

10-15 mg

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30
Q

What is an antipruritic dose of propofol?

A

10 mg

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31
Q

What is an anticonvulsant dose of propofol?

A

Greater than 1 mg/kg; does NOT decrease the therapeutic effectiveness of ECTs

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32
Q

Which preservative in generic propofol can cause bronchoconstriction?

A

Metabisulfite (use with caution in asthma, smokers)

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33
Q

Propofol has better analgesia for _________ pain than for ________ pain.

A

neuropathic; nociceptive

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34
Q

What are the neurologic systemic effects of propofol?

A

Decreased CMRO2, cerebral blood flow, and ICP

Autoregulation with PaCO2 NOT impacted (GOOD :)

Allows robust SSEPs and MEPs without N2O or volatile

No evidence of tolerance

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35
Q

What are the cardiovascular effects of propofol?

A

Decreased HR, SVR, CO; can be offset by laryngoscopy/intubation/LMA

Extreme drop in BP with hypovolemia, LV dysfunction, elderly

Does NOT have SA or AV node effects or QTc prolongation

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36
Q

What are the characteristics of propofol related bradycardia?

A

Causes increased incidence of oculocardiac reflex (“5 and dime reflex”) especially in peds

You should pretreat/treat with anticholinergic, however profound bradycardia/asystole may persist; increased doses do not attenuate.

May require epinephrine (direct beta agonist)

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37
Q

What are the respiratory effects of propofol?

A

Dose-dependent respiratory depression (both rate and TV)

Enhanced by opioids but offset by surgical stimulation

Causes downward shift of hypoxic response curve BUT HPV maintained

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38
Q

While _____ and ______ are usually not effected by propofol, prolonged infusions can cause ______ injury and _______ _________ ________.

A

liver; kidneys; liver; propofol infusion syndrome

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39
Q

What causes benign green urine with propofol with no renal dysfunction?

A

Phenol

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40
Q

What causes benign cloudy urine with propofol?

A

Uric acid

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41
Q

What effect does propofol have on intraocular pressure?

A

Decreases

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42
Q

What effect does propofol have on coagulation?

A

NO change in coagulation factors or platelet function BUT inhibits platelet aggregation

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43
Q

What side effects are related to propofol’s lipid profile?

A

Risk of infection, injection site pain, hypertriglyceridemia, pulmonary embolus

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44
Q

What ingredient of propofol can cause anaphylaxis?

A

Phenol (often after first exposure with neuromuscular blockers)

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45
Q

What is an adverse respiratory allergic effect of propofol?

A

Bronchoconstriction

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46
Q

Propofol Infusion Syndrome is seen after doses of >__ mcg/kg/min for >__ hours

A

75; 24

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47
Q

Propofol Infusion Syndrome is most often seen in which population?

A

Children

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48
Q

What are signs and symptoms of Propofol Infusion Syndrome?

A

Lactic (metabolic) acidosis, profound refractory (lethal) bradycardia in peds

Tachycardia is an EARLY sign of PIS and usually reverses when infusion is stopped.

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49
Q

What are differential diagnoses for Propofol Infusion Syndrome?

A

Hyperchloremic metabolic acidosis (NS) and increased organic acids (DKA, tourniquet release)

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50
Q

What alarming but benign symptom can occur upon propofol injection?

A

Myoclonus (NOT cortical epileptic in origin; NO contraindications in epileptic patients/EEG)

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51
Q

Propofol accounts for __% of known substance abuse in anesthesia practitioners.

A

40

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52
Q

Describe the antioxidant effect of propofol.

A

It scavenges free radicals (similarly to Vitamin E) and attenuates reperfusion injury from oxygen free radicals (post-MI, CP bypass, cross-clamping, tourniquets)

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53
Q

Unused propofol should be discarded in _ hours due to supporting _ ___ and ________ growth.

A

6; E. coli; Pseudomonas

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54
Q

Propofol does/does not trigger MH?

A

Does not

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55
Q

Which is safe for porphyria? (propofol/thiopental)

A

Propofol

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56
Q

Which causes adrenocortical suppression? (propofol/etomidate)

A

Etomidate

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57
Q

How is ketamine classified?

A

PCP derivative for dissociative anesthesia

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58
Q

Ketamine acts on the __________ and ______ systems.

A

thalamocortical; limbic

59
Q

What two major disadvantages of ketamine?

A

Emergence delirium; abuse potential (“Special K”)

60
Q

How do the stereo and racemic isomers of ketamine compare?

A

Racemic ketamine is used more commonly due to its more intense analgesia and fewer side effects

61
Q

What is ketamine’s MOA?

A

Binds noncompetitively to NMDA receptors as an antagonist, inhibiting the binding of glutamate to glycine which prevents the NMDA receptor from activating and inhibiting catecholamine uptake into post-ganglion nerves.

Also binds to opioid, monoaminergic, muscarinic, sodium and calcium channels, and nicotinic acetylcholines.

62
Q

Ketamine binds with all _____ receptors and is synergistic with ______, __________ and ________ agonists to promote dissociation.

A

opioid; opioid; dopamine; serotonin

63
Q

What are the antimuscarinic effects of ketamine?

A

Bronchodilation, sympathomimetic, anti-erectile dysfunction

64
Q

Why does ketamine have mild local-anesthetic-like properties?

A

Sodium channel binding

65
Q

What is the onset of ketamine?

A

30 seconds

66
Q

What is the duration of ketamine?

A

DD 5-15 minutes

67
Q

Ketamine is/is not lipid soluble.

A

is

68
Q

Ketamine peaks at _ minute(s) IV and _ minute(s) IM.

A

1; 5

69
Q

What pharmacokinetic property causes psych effects after emergence from ketamine?

A

Redistribution from high to low perfusion tissue

70
Q

Ketamine is largely cleared by the ________.

A

Liver

71
Q

Ketamine has a large ________ of ________.

A

volume; distribution

72
Q

Ketamine elimination 1/2 time

A

2-3 hours (much longer than propofol!)

73
Q

What metabolic property of ketamine leads to prolonged analgesia?

A

Hepatic metabolism into norketamine :)

74
Q

How is norketamine eliminated?

A

It is metabolized into inactive water-soluble compounds and excreted through the kidneys

75
Q

What is the MOA of ketamine dependence?

A

Repeated doses lead to enzyme induction, analgesic tolerance, and then dependence.

Tolerance can be seen in burn patients after only 2 short-interval doses. :(

76
Q

What is the subanesthetic does of ketamine for opioid-sparing analgesia?

A

0.2-0.5 mg/kg IV

77
Q

How does ketamine treat chronic pain syndromes?

A

Antagonizes NMDA, decreasing spinal cord sensitization

78
Q

What induction agent should you choose for a hemorrhaging OB patient?

A

Ketamine - due to its good hemodynamic profile and because it does NOT cause neonatal depression

79
Q

What is the pediatric CV post-op ketamine infusion dose?

A

1-2 mg/kg/hr

80
Q

_____ receptors are involved in the pathophysiology of _________ supporting ketamine’s utility with _________, ____, and ___.

A

NMDA; depression; depression; PTSD; OCD

81
Q

What are the induction doses for ketamine: IV? IM?

A

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

82
Q

What is the onset of loss of consciousness for ketamine?

A

30-60 seconds IV; 2-5 minutes IM

83
Q

A patient will return to consciousness in ~__ minutes after an induction dose of ketamine and to full orientation after __-__ minutes.

A

15; 60; 90

84
Q

What is your induction drug of choice for autistic teenage boys? Burn patients?

A

Ketamine

85
Q

Ketamine is good for hypovolemic patients unless…

A

…catecholamine stores are depleted (as with critically ill patients)

86
Q

Ketamine should be used with caution in ___ patients due to…

A

CAD; increased O2 demand

87
Q

Ketamine can worsen which two conditions?

A

Pulmonary hypertension and increased intraocular pressure

88
Q

When used as an adjunct in ________ ____ cases, small doses of ketamine are more hemodynamically stable than _____ without the emergence delirium that results from large doses.

A

propofol TIVA; opioids

89
Q

____________ makes ketamine good for ______/_________ ________ patients

A

Bronchodilation; asthma; reactive airway

90
Q

Ketamine can cause _________ which can interfere with ___ procedures

A

nystagmus; eye

91
Q

Ketamine is a potent cerebral _________ during normo______. Therefore, use with caution with ___ concerns.

A

vasodilator; capnea; ICP

92
Q

Large ketamine doses may cause _____ suppression; an anti________.

A

burst; convulsant

93
Q

Ketamine has negative _____tropic effects which are offset by positive ___ effects.

A

chrono; CNS

94
Q

Does ketamine cause histamine release?

A

No; also, patients rarely allergic.

95
Q

Ketamine inhibits platelet _________.

A

aggregation

96
Q

What effect does ketamine have on hemodynamics?

A

Increases everything (BP, HR, CO, myocardial work and O2 demand)

97
Q

How can the nurse anesthetist offset the hemodynamic effects of ketamine?

A

Using benzos, opioids, and volatiles

98
Q

Why should ketamine be used with caution in critically ill patients?

A

Because if their catecholamines are depleted, ketamine cannot enhance/protect their hemodynamics leading to poor tissue perfusion with shock states.

99
Q

A patient’s CO2 response and spontaneous ventilation will be maintained after ketamine infusion except under what conditions?

A

Rapid dosing or dosing concurrent with opioids.

100
Q

While airway reflexes stay intact with ketamine, what population should be intubated?

A

Aspiration risk

101
Q

Ketamine increases ________, therefore use of an __________ is recommended.

A

secretions; antisialagogue

102
Q

The psychedelic effects of ketamine can contribute to what adverse effect?

A

Emergence delirium; hallucinations for up to 24 hours

103
Q

What are 4 risk factors for disturbing psychedelic effects from ketamine?

A

Greater than 15 years old; female; greater than 2 mg/kg IV; personality disorders

104
Q

Emergence delirium with ketamine is rare after ________ ____ _ ___________.

A

greater than 3 anesthetics

105
Q

What 2 medications are often used in a “cocktail” with ketamine and why?

A

IV midazolam to prevent ED and glycopyrrolate for its antisialagogue effects

106
Q

How do COX-1 non-selectives differ from COX-2 (“coxibs”) inhibitors?

A

COX-1s inhibit both COX-1 and COX-2 while selective COX-2 inhibitors only inhibit COX-2 leading the latter to have a smaller side effect profile.

107
Q

What are some COX-I inhibitors?

A

ketorolac, ibuprofen, indomethacin, meloxicam, piroxicam, ketoprofen, naproxen, aspirin

108
Q

What are the advantages of COX-1 nonselectives?

A

Decreases platelet aggregation

109
Q

What are the disadvantages of COX-1 nonselectives?

A

Inhibits renal function, causes GI toxicity, inhibits platelet aggregation

110
Q

What are the advantages of COX-2 selective inhibitors?

A

Decrease pain, inflammation, and fever; less GI toxicity; no platelet effects

111
Q

What is the disadvantage of COX-2 selective inhibitors?

A

Increased cardiac risk

112
Q

NSAIDs have a _____ volume of distribution.

A

low

113
Q

NSAIDs are highly _____ bound.

A

protein

114
Q

Due to metabolism and protein binding, disease of these organs prolong the half-life of NSAIDs and increase risk of toxicity.

A

Kidneys and liver

115
Q

What explains selective COX inhibitors’ lack of effect on platelets?

A

No COX-2 in platelets

116
Q

What factors increase risk for GI toxicity with NSAIDs?

A

High dose, older age, H. pylori/ulcers, combination with ASA, anticoagulants, or corticosteroids

117
Q

Which NSAID appears to have the lowest cardiac risk?

A

Naproxen

118
Q

What are potential cardiac side effects of NSAIDs?

A

MI, heart failure, hypertension

119
Q

NSAIDs can decrease GFR, especially with which diagnoses?

A

CHF, renal disease, diabetes mellitus, hypertension, atherosclerosis, and hypovolemia

120
Q

In addition to GI, renal, pulmonary, and CV effects of NSAIDs, what other organ system can be affected?

A

Liver - failure and increased LFTs

121
Q

What conditions place patients at increased risk for anaphylaxis with NSAIDs?

A

Allergic rhinitis, nasal polyps, and asthma (due to prostaglandin inhibition in tissues)

122
Q

ASA has been known to rarely cause what condition in pediatric patients?

A

Reye’s syndrome

123
Q

How can NSAIDs interact with digoxin?

A

Decreased renal clearance can cause digoxin toxicity

124
Q

_________ significantly increases risk of renal toxicity with NSAIDs.

A

Hypovolemia

125
Q

What are uses for ketorolac?

A

potent analgesic, moderate anti-inflammatory, anti-pyretic

126
Q

What dose of ketorolac = 10 mg of morphine minus the CV and respiratory depression and minimal N/V?

A

30 mg IM/IV

127
Q

Ketorolac should be used in caution in the very young and elderly due to what relative to opioids?

A

Less clearance

128
Q

__________ reduces risk of renal toxicity with ketorolac as well as other NSAIDs?

A

Hydration

129
Q

What is ketorolac’s onset?

A

DD 30 minutes - 1 hour

130
Q

IV/IM ketorolac peaks after how long?

A

2-3 hours

131
Q

Ketorolac should not be given to which patients without first asking the surgeon?

A

Ortho, due to the potential to delay bone healing

132
Q

What is the “A-OK” protocol?

A

Protocol for amniotic fluid embolism; includes 1 mg atropine (vagolysis), 8 mg ondansetron (block serotonin receptors and vagolysis), 30 mg ketorolac (block thromboxane production)

133
Q

What drug is the leading cause of acute liver failure in the US?

A

Acetaminophen

134
Q

Through what MOA does acetaminophen cause liver failure?

A

Metabolite NAPQI depletes antioxidant glutathione, directly damages liver cells

135
Q

What drug is the first-line treatment for arthritis?

A

Acetaminophen

136
Q

To decrease risk of liver toxicity, the FDA recommends less than ____ mg/day of acetaminophen and less than ___ mg in a single dose.

A

2600; 650

137
Q

Acetaminophen in conjunction with what drug class is a good combination?

A

NSAID

138
Q

What is the dose for an Ofirmev infusion in patients older than 13 years? 2-13 years old?

A

1 gm over 15 minutes; 15 mg/kg

139
Q

What COX-1 inhibitor is the oldest, most widely-used medicine in the world?

A

Aspirin

140
Q

What is unique about ASA’s action on platelets?

A

It irreversibly inactivates COX-1 on platelets, essentially “neutering” platelet function for the remaining life of the platelet (5-7 days)

141
Q

How is ASA metabolized?

A

In the liver, by erythrocytes, and plasma esterases

142
Q

Signs and symptoms of aspirin/NSAID toxicity?

A

N/V, abdominal pain, tinnitus, CNS depression, metabolic acidosis, renal failure, agitation, coma, hyperventilation (compensation)

143
Q

What is the antidote for aspirin/NSAID toxicity?

A

There is none. Supportive care. Treat symptoms, hydrate, alkalinize urine, consider charcoal, hemodialysis.

144
Q

What is the role of NSAIDs in an ERAS protocol?

A

Can be used preop with acetaminophen and gabapentanoid as well as post-op on a scheduled basis