Propofol, Ketamine, NSAIDs, & ERAS Flashcards
(144 cards)
1
Q
What class of drug is propofol?
A
A sedative/hypnotic
2
Q
What is the induction dose of propofol?
A
1.5-2.5 mg/kg IV
3
Q
How long does an induction dose of propofol take to render the patient unconscious?
A
30 seconds
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.
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
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.
7
Q
Which preservative does Diprivan have?
A
Disodium edetate and NaOH
8
Q
Which preservative does generic propofol have?
A
Metabisulfite
9
Q
True or false? Different propofol preservatives have the same pH.
A
False
10
Q
Why is mixing propofol and lidocaine not recommended?
A
Can cause pulmonary emboli through coalesced oil
11
Q
What is the problem with Ampofol?
A
Even more severe injection site pain compared to Diprivan.
12
Q
What is the problem with Aquavan?
A
While it causes less injection site pain than propofol, it will cause genital burning!!
13
Q
With which receptor does propofol interact and how?
A
Propofol is a GABA-A receptor agonist (inhibitory neurotransmitter)
14
Q
What effect does the stimulation of GABA-A have?
A
Hyperpolarization of cell membranes
15
Q
Into what organs is propofol taken up during the first pass effect?
A
Lungs and liver
16
Q
Abnormalities with which liver enzyme can alter the metabolism of propofol?
A
Cytochrome P-450
17
Q
What is the elimination half time for propofol?
A
0.5-1.5 hours
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
19
Q
In ____, most of propofol goes back into circulation after 1st pass effect.
A
Lungs
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
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
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.
23
Q
What is the induction dose of propofol?
A
1.5-2.5 mg/kg IV
24
Q
Pediatrics require _______ doses of propofol due to _______ volume of distribution and ________ clearance.
A
increased; larger; faster
25
Elderly patients require _______ doses of propofol due to _______ volume of distribution and ______ clearance.
decreased; smaller; slower
26
What is the sedation infusion dose range of propofol?
25-100 mcg/kg/min
27
Propofol provides good _______ but no ________.
amnesia; analgesia
28
What is GA maintenance infusion dose range for propofol?
100-300 mcg/kg/min (less with opioids and volatile)
29
What is an antiemetic dose of propofol?
10-15 mg
30
What is an antipruritic dose of propofol?
10 mg
31
What is an anticonvulsant dose of propofol?
Greater than 1 mg/kg; does NOT decrease the therapeutic effectiveness of ECTs
32
Which preservative in generic propofol can cause bronchoconstriction?
Metabisulfite (use with caution in asthma, smokers)
33
Propofol has better analgesia for _________ pain than for ________ pain.
neuropathic; nociceptive
34
What are the neurologic systemic effects of propofol?
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
35
What are the cardiovascular effects of propofol?
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
36
What are the characteristics of propofol related bradycardia?
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)
37
What are the respiratory effects of propofol?
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
38
While _____ and ______ are usually not effected by propofol, prolonged infusions can cause ______ injury and _______ _________ ________.
liver; kidneys; liver; propofol infusion syndrome
39
What causes benign green urine with propofol with no renal dysfunction?
Phenol
40
What causes benign cloudy urine with propofol?
Uric acid
41
What effect does propofol have on intraocular pressure?
Decreases
42
What effect does propofol have on coagulation?
NO change in coagulation factors or platelet function BUT inhibits platelet aggregation
43
What side effects are related to propofol's lipid profile?
Risk of infection, injection site pain, hypertriglyceridemia, pulmonary embolus
44
What ingredient of propofol can cause anaphylaxis?
Phenol (often after first exposure with neuromuscular blockers)
45
What is an adverse respiratory allergic effect of propofol?
Bronchoconstriction
46
Propofol Infusion Syndrome is seen after doses of >__ mcg/kg/min for >__ hours
75; 24
47
Propofol Infusion Syndrome is most often seen in which population?
Children
48
What are signs and symptoms of Propofol Infusion Syndrome?
Lactic (metabolic) acidosis, profound refractory (lethal) bradycardia in peds
Tachycardia is an EARLY sign of PIS and usually reverses when infusion is stopped.
49
What are differential diagnoses for Propofol Infusion Syndrome?
Hyperchloremic metabolic acidosis (NS) and increased organic acids (DKA, tourniquet release)
50
What alarming but benign symptom can occur upon propofol injection?
Myoclonus (NOT cortical epileptic in origin; NO contraindications in epileptic patients/EEG)
51
Propofol accounts for __% of known substance abuse in anesthesia practitioners.
40
52
Describe the antioxidant effect of propofol.
It scavenges free radicals (similarly to Vitamin E) and attenuates reperfusion injury from oxygen free radicals (post-MI, CP bypass, cross-clamping, tourniquets)
53
Unused propofol should be discarded in _ hours due to supporting _ ___ and ________ growth.
6; E. coli; Pseudomonas
54
Propofol does/does not trigger MH?
Does not
55
Which is safe for porphyria? (propofol/thiopental)
Propofol
56
Which causes adrenocortical suppression? (propofol/etomidate)
Etomidate
57
How is ketamine classified?
PCP derivative for dissociative anesthesia
58
Ketamine acts on the __________ and ______ systems.
thalamocortical; limbic
59
What two major disadvantages of ketamine?
Emergence delirium; abuse potential ("Special K")
60
How do the stereo and racemic isomers of ketamine compare?
Racemic ketamine is used more commonly due to its more intense analgesia and fewer side effects
61
What is ketamine's MOA?
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
Ketamine binds with all _____ receptors and is synergistic with ______, __________ and ________ agonists to promote dissociation.
opioid; opioid; dopamine; serotonin
63
What are the antimuscarinic effects of ketamine?
Bronchodilation, sympathomimetic, anti-erectile dysfunction
64
Why does ketamine have mild local-anesthetic-like properties?
Sodium channel binding
65
What is the onset of ketamine?
30 seconds
66
What is the duration of ketamine?
DD 5-15 minutes
67
Ketamine is/is not lipid soluble.
is
68
Ketamine peaks at _ minute(s) IV and _ minute(s) IM.
1; 5
69
What pharmacokinetic property causes psych effects after emergence from ketamine?
Redistribution from high to low perfusion tissue
70
Ketamine is largely cleared by the ________.
Liver
71
Ketamine has a large ________ of ________.
volume; distribution
72
Ketamine elimination 1/2 time
2-3 hours (much longer than propofol!)
73
What metabolic property of ketamine leads to prolonged analgesia?
Hepatic metabolism into norketamine :)
74
How is norketamine eliminated?
It is metabolized into inactive water-soluble compounds and excreted through the kidneys
75
What is the MOA of ketamine dependence?
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
What is the subanesthetic does of ketamine for opioid-sparing analgesia?
0.2-0.5 mg/kg IV
77
How does ketamine treat chronic pain syndromes?
Antagonizes NMDA, decreasing spinal cord sensitization
78
What induction agent should you choose for a hemorrhaging OB patient?
Ketamine - due to its good hemodynamic profile and because it does NOT cause neonatal depression
79
What is the pediatric CV post-op ketamine infusion dose?
1-2 mg/kg/hr
80
_____ receptors are involved in the pathophysiology of _________ supporting ketamine’s utility with _________, ____, and ___.
NMDA; depression; depression; PTSD; OCD
81
What are the induction doses for ketamine: IV? IM?
1-2 mg/kg IV; 4-8 mg/kg IM
82
What is the onset of loss of consciousness for ketamine?
30-60 seconds IV; 2-5 minutes IM
83
A patient will return to consciousness in ~__ minutes after an induction dose of ketamine and to full orientation after __-__ minutes.
15; 60; 90
84
What is your induction drug of choice for autistic teenage boys? Burn patients?
Ketamine
85
Ketamine is good for hypovolemic patients unless...
...catecholamine stores are depleted (as with critically ill patients)
86
Ketamine should be used with caution in ___ patients due to...
CAD; increased O2 demand
87
Ketamine can worsen which two conditions?
Pulmonary hypertension and increased intraocular pressure
88
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.
propofol TIVA; opioids
89
____________ makes ketamine good for ______/_________ ________ patients
Bronchodilation; asthma; reactive airway
90
Ketamine can cause _________ which can interfere with ___ procedures
nystagmus; eye
91
Ketamine is a potent cerebral _________ during normo______. Therefore, use with caution with ___ concerns.
vasodilator; capnea; ICP
92
Large ketamine doses may cause _____ suppression; an anti________.
burst; convulsant
93
Ketamine has negative _____tropic effects which are offset by positive ___ effects.
chrono; CNS
94
Does ketamine cause histamine release?
No; also, patients rarely allergic.
95
Ketamine inhibits platelet _________.
aggregation
96
What effect does ketamine have on hemodynamics?
Increases everything (BP, HR, CO, myocardial work and O2 demand)
97
How can the nurse anesthetist offset the hemodynamic effects of ketamine?
Using benzos, opioids, and volatiles
98
Why should ketamine be used with caution in critically ill patients?
Because if their catecholamines are depleted, ketamine cannot enhance/protect their hemodynamics leading to poor tissue perfusion with shock states.
99
A patient's CO2 response and spontaneous ventilation will be maintained after ketamine infusion except under what conditions?
Rapid dosing or dosing concurrent with opioids.
100
While airway reflexes stay intact with ketamine, what population should be intubated?
Aspiration risk
101
Ketamine increases ________, therefore use of an __________ is recommended.
secretions; antisialagogue
102
The psychedelic effects of ketamine can contribute to what adverse effect?
Emergence delirium; hallucinations for up to 24 hours
103
What are 4 risk factors for disturbing psychedelic effects from ketamine?
Greater than 15 years old; female; greater than 2 mg/kg IV; personality disorders
104
Emergence delirium with ketamine is rare after ________ ____ _ ___________.
greater than 3 anesthetics
105
What 2 medications are often used in a "cocktail" with ketamine and why?
IV midazolam to prevent ED and glycopyrrolate for its antisialagogue effects
106
How do COX-1 non-selectives differ from COX-2 ("coxibs") inhibitors?
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
What are some COX-I inhibitors?
ketorolac, ibuprofen, indomethacin, meloxicam, piroxicam, ketoprofen, naproxen, aspirin
108
What are the advantages of COX-1 nonselectives?
Decreases platelet aggregation
109
What are the disadvantages of COX-1 nonselectives?
Inhibits renal function, causes GI toxicity, inhibits platelet aggregation
110
What are the advantages of COX-2 selective inhibitors?
Decrease pain, inflammation, and fever; less GI toxicity; no platelet effects
111
What is the disadvantage of COX-2 selective inhibitors?
Increased cardiac risk
112
NSAIDs have a _____ volume of distribution.
low
113
NSAIDs are highly _____ bound.
protein
114
Due to metabolism and protein binding, disease of these organs prolong the half-life of NSAIDs and increase risk of toxicity.
Kidneys and liver
115
What explains selective COX inhibitors' lack of effect on platelets?
No COX-2 in platelets
116
What factors increase risk for GI toxicity with NSAIDs?
High dose, older age, H. pylori/ulcers, combination with ASA, anticoagulants, or corticosteroids
117
Which NSAID appears to have the lowest cardiac risk?
Naproxen
118
What are potential cardiac side effects of NSAIDs?
MI, heart failure, hypertension
119
NSAIDs can decrease GFR, especially with which diagnoses?
CHF, renal disease, diabetes mellitus, hypertension, atherosclerosis, and hypovolemia
120
In addition to GI, renal, pulmonary, and CV effects of NSAIDs, what other organ system can be affected?
Liver - failure and increased LFTs
121
What conditions place patients at increased risk for anaphylaxis with NSAIDs?
Allergic rhinitis, nasal polyps, and asthma (due to prostaglandin inhibition in tissues)
122
ASA has been known to rarely cause what condition in pediatric patients?
Reye's syndrome
123
How can NSAIDs interact with digoxin?
Decreased renal clearance can cause digoxin toxicity
124
_________ significantly increases risk of renal toxicity with NSAIDs.
Hypovolemia
125
What are uses for ketorolac?
potent analgesic, moderate anti-inflammatory, anti-pyretic
126
What dose of ketorolac = 10 mg of morphine minus the CV and respiratory depression and minimal N/V?
30 mg IM/IV
127
Ketorolac should be used in caution in the very young and elderly due to what relative to opioids?
Less clearance
128
__________ reduces risk of renal toxicity with ketorolac as well as other NSAIDs?
Hydration
129
What is ketorolac's onset?
DD 30 minutes - 1 hour
130
IV/IM ketorolac peaks after how long?
2-3 hours
131
Ketorolac should not be given to which patients without first asking the surgeon?
Ortho, due to the potential to delay bone healing
132
What is the "A-OK" protocol?
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
What drug is the leading cause of acute liver failure in the US?
Acetaminophen
134
Through what MOA does acetaminophen cause liver failure?
Metabolite NAPQI depletes antioxidant glutathione, directly damages liver cells
135
What drug is the first-line treatment for arthritis?
Acetaminophen
136
To decrease risk of liver toxicity, the FDA recommends less than ____ mg/day of acetaminophen and less than ___ mg in a single dose.
2600; 650
137
Acetaminophen in conjunction with what drug class is a good combination?
NSAID
138
What is the dose for an Ofirmev infusion in patients older than 13 years? 2-13 years old?
1 gm over 15 minutes; 15 mg/kg
139
What COX-1 inhibitor is the oldest, most widely-used medicine in the world?
Aspirin
140
What is unique about ASA's action on platelets?
It irreversibly inactivates COX-1 on platelets, essentially "neutering" platelet function for the remaining life of the platelet (5-7 days)
141
How is ASA metabolized?
In the liver, by erythrocytes, and plasma esterases
142
Signs and symptoms of aspirin/NSAID toxicity?
N/V, abdominal pain, tinnitus, CNS depression, metabolic acidosis, renal failure, agitation, coma, hyperventilation (compensation)
143
What is the antidote for aspirin/NSAID toxicity?
There is none. Supportive care. Treat symptoms, hydrate, alkalinize urine, consider charcoal, hemodialysis.
144
What is the role of NSAIDs in an ERAS protocol?
Can be used preop with acetaminophen and gabapentanoid as well as post-op on a scheduled basis
