Erin's Pharm EXAM 2 Flashcards
1
Q
General anesthesia is a state of drug induced _____
A
unconsciousness
2
Q
What does the vessel rich group include?
What % of our CO does it get?
A
Brain, heart, kidney, liver
75%
3
Q
What does the muscle group include?
What % of our CO does it get?
A
Skeletal muscle and skin
18%
4
Q
What % of our CO does fat get?
A
5%
5
Q
What does the vessel poor group include?
What % of our CO does it get?
A
Bone, tendon, cartilage, hair, nails
2%
6
Q
What are the 5 components of general anesthesia?
A
Hypnosis
Analgesia
Muscle relaxation
Sympatholysis
Amnesia
(A MASH)
7
Q
According to Doctor Castillo what is the first stage of general anesthesia called?
A
analgesia
8
Q
According to Doctor Castillo what is the second stage of general anesthesia called?
A
delirium
most dangerous stage
9
Q
According to Doctor Castillo what is the third stage of general anesthesia called?
A
surgical anesthesia
10
Q
According to Doctor Castillo what is the fourth stage of general anesthesia called?
A
medullary paralysis
*pt is over sedated**
11
Q
These are our 4 protective airway reflexes
A
Sneezing
Coughing
Swallowing
Gagging
12
Q
Stage 1 begins with _______ and ends with ______
A
initiation of an anesthetic agent and ends with the loss of consciousness
13
Q
What is the lightest level of anesthesia?
A
stage 1
14
Q
How are our 4 protective airway reflexes impacted in stage 1?
A
They’re still present! Not impacted
15
Q
How are our 4 protective airway reflexes impacted in stage 2?
A
They are diminished
16
Q
How are our 4 protective airway reflexes impacted in stage 3?
A
They are absent
17
Q
How is sensory and mentation impacted during stage 1?
A
Depression
18
Q
Patients pass through stage 2 within ___ to ___ seconds. Max of ___ seconds
A
5-15, 30 seconds max
19
Q
Why is it important to pay attention to the EKG/SPO2 monitor during stage 2? What does it tell you?
A
pulse ox or EKG tone – it will increase due to excitation!!!! then HR goes back down after stage 2 is done
20
Q
According to Castillo, Stage 2 starts with ______ to the onset of _______ _____ of vital signs
A
loss of consciousness, automatic rhythmicity
21
Q
In modern day, patients pass through stage 2 quicker than they used to. Why?
A
Anesthetic agents are more rapid than ether and the use of short acting barbiturates.
22
Q
What are dysconjugate ocular movements?
What stage do you see it in?
A
Eyes moving in different directions Stage 2
(in reality we won’t see it because their eyes are taped shut)
23
Q
Why do we not intubate in stage 2?
A
-Potential for passive or active emesis
-Laryngospasms can occur due to hyper-excitability to stimuli
24
Q
This stage is characterized by the absence of response to surgical incision and depression in all elements of nervous system function
A
Stage 3
25
In stage 4, what 2 things are absent?
-Spontaneous respiration
-All reflexes
(Importantly: Medullary cardiac reflexes)
26
What is the medullary cardiac reflex?
A series of autonomic responses that regulate the HR and BP in response to changes in blood pressure and oxygen levels from the medulla oblongata
27
Characteristics of the pulse during stage 4?
Weak and irregular
28
Stage 2 is more prolonged during _____ than _____
emergence than induction
29
Because Inhalation induction takes longer than total IV anesthesia (TIVA). Patients will be in stage 2 up to ___minutes
15
**all phases occur longer in inhalation induction compared to IV**
30
This barbiturate used to be the most common but is not used in the USA anymore because of _____
thiopental; it is used for lethal injection
31
What is the gold standard induction drug?
Barbiturates
**we do not use them anymore but it used for comparison**
32
Barbiturate mechanism of action
potentiate GABA a channel activity; directly mimics GABA
33
What receptors do barbiturates act on? (4 total)
-GABAa
-Glutamate
-Adenosine
-Neuronal nicotinic acetylcholine
34
How do barbiturates impact cerebral vessels?
They are cerebral vasoconstrictors
35
Do barbiturates have an analgesic component?
NO
36
How do barbiturates impact CBF and CMRO2? By what % are they affected?
They decrease it, 55%
37
Why are barbiturates good for reducing the incidence of CVA?
Barbiturates decreases CBF and CMRO2 up to 55% - this decreases the risk of CVA/stroke b/c we are reducing metabolism of brain
38
When using IV induction medications CBF and CMRO2 are ______ (coupled or non-coupled?).
When using **inhalation** agents CBF and CMRO2 are ______ (coupled or non-coupled?).
IV - Coupled
Inhalation - Uncoupled
39
Babiturate onset
Rapid; 30 seconds
40
With a prolonged infusion of barbiturates, there is a _____ context-sensitive half-time
lengthy
41
How many minutes does it take for barbiturates to be equal in the skeletal muscle and plasma?
15 minutes
42
Barbituates are dosed on _____ body weight
lean / ideal body weight
43
Why are barbiturates dosed on ideal body weight?
Fat acts as a reservoir for the drug and acts like an IV bag which will redose the patient and have a cumulative effect
44
Where are Barbiturates metabolized? What % metabolism occurs here?
hepatocytes, 99%
45
How are Barbiturates excreted?
Renally
46
How is elimination half time of Barbiturates impacted in pediatric patients?
elimination half time is shorter
47
What % of Barbiturates is bound to albumin?
Why do we care?
70-85%
This acts as another reservoir because the drug can detach and produce effects again
48
What is the effect on redistribution if the drug has a high protein binding capacity?
It has a longer duration of action
49
With Barbiturates, the non-ionized lipid soluble drug favors: acidosis or alkalosis?
acidosis
50
With Barbiturates, the ionized less lipid soluble drug favors: acidosis or alkalosis?
alkalosis
51
Although Barbiturates are only marketed as racemic mixtures, it is important to know the ___ isomer is more potent than the ____ isomer
S (-) is more potent than R (+)
52
Name the three oxybarbiturates
* Methohexital
* Phenobarbital
* Pentobarbital
53
Name the two thiobarbiturates
* Thiopental
* Thiamylal
54
Which Barbiturate is used in conjunction with electroconvulsive therapy?
Methohexital
55
This drug is also known as truth serum
Thiopental
56
With thiopental, after 30 minutes only ___% in brain because of _____
10%, rapid redistribution
57
Thiopental (sodium pentothal) dose
4-5 mg/kg IV
58
Which has a longer elimination half time: thiopental or methohexital?
Thiopental
59
What is the fat/blood partition coefficient of thiopental? Is this high or low?
11; HIGH
60
This describes the distribution of a given agent at equilibrium between two substances at the same temperature, pressure and volume
Partition coefficient
61
The blood is considered a pharmacologically ____ reservoir in regards to the blood-gas coefficient
inactive
62
This describes the distribution of an anesthetic between blood and gas at the same partial pressure
blood-gas coefficient
63
A _____ blood-gas coefficient correlates with higher solubility of anesthetic in blood and thus ____ the rate of induction
higher, slows
64
Why does methohextial have a shorter duration of action than Pentothal?
Because methohexital has a lower lipid solubility than Pentothal
65
Other name for methohextial
brevital
66
At a normal pH ___% of methohextial is non-ionized
76%
67
At a normal pH ___% of Pentothal is non-ionized
61%
68
In comparison to oxybarbiturates, thiobarbiturates are ___ lipid soluble and have greater ______ potency
more, hypnotic
69
Why is it that the greater the ratio of fat to body weight, the less is the blood volume (ml/kg)?
Adipose tissue has decreased blood supply (its a vessel poor group)
70
What is excitatory phenomena?
Myoclonus, hiccough (hiccups lol)
71
True or false: methohextial is associated with excitatory phenomena
true
72
Methohextital (breivital) dose IV
1.5 mg/kg IV
73
Methohextital (breivital) dose rectal
20-30 mg/kg
74
How does Methohextital (breivital) impact the seizure threshold.
What surgery is this relevant to?
It lowers the threshold; more prone to having seizures
Induces seizures in patients undergoing temporal lobe resection
75
Methohextital (breivital) decreased seizure duration ___ - ___ % in ECT patients compared to etomidate
35-45%
76
Since barbiturates cause histamine release, what 2 things do we worry about?
Hypotension
Anaphylactoid response
77
Which barbiturate may have an anaphylactic response with previous exposure?
Thiopental
78
Caution administering barbiturates to patients with a lack of this response?
Baroreceptor
79
What is the dose dependent ventilatory response to barbiturates?
* The more we give, the more depressed the ventilatory centers get.
* The medullary and pontine are LESS sensitive to CO2; this leads to slow frequency and decreased tidal volume.
* Takes longer to return to spontaneous ventilation.
80
What happens immediately if you give barbiturates through an arterial line?
* Immediate, intense vasoconstriction and excruciating pain that radiates down the artery
81
What are the consequences if you give barbiturates down an arterial line?
1. Pain
2. Obscure of distal arterial pulses
3. Blanching and cyanosis
4. Gangrene and permanent nerve damage
82
If you give barbiturates down an arterial line, how do you treat it?
Injecting vasodilators; lidocaine or papaverine
83
What is Somatosensory evoked potential (SSEP)?
SSEP monitoring is a neurophysiological technique that assesses the function of the nervous system. It's used during surgery to detect changes in nerve conduction and prevent neurological injury.
84
What is the desired drug for SSEP monitoring?
Barbiturates
85
Barbiturates induce enzymes after ___ to ___ days of infusion and may persist for __ days
2 to 7
persist for 30 days
86
How do barbiturates impact RBF and GFR? Why?
They can cause a modest, transient decrease. Probably due to hypotension!
*Try to infuse crystalloids to prevent this**
87
What class is propofol?
GABA agonist
88
Full name of GABA
Gamma aminobutyric acid
89
Induction dose of propofol
1.5-2.5 mg/kg IV
90
Conscious sedation dose of propofol (gtt)
25-100 mcg/kg/min
91
Maintenance dose of propofol
100-300 mcg/kg/min
92
How many mcg in 1 mg?
1000 mcg = 1 mg
93
How quickly does a rapid injection of propofol produce unconsciousness?
30 seconds
94
What 3 components make up 1% propofol
1. Soybean oil (10%)
2. Glycerol (2.25%)
3. Purified egg phosphatide (lecithin) - (1.2%)
95
Is lecithin egg yolk or egg white?
Egg yolk!
96
1% propofol concentration
10 mg/ml
97
2% propofol concentration
20 mg/mL
98
3 disadvantages of the propofol mixture
-supports bacterial growth
-increased plasma triglycerides
-pain on injection (because of soybean oil)
99
Which commercial preparation of propofol causes dyesthia?
Aquavan
This is the burning sensation in genitals, especially in females
100
Which component of propofol makes it isotonic like the blood?
Glycerol
101
What causes immobility from propofol anesthesia?
It's action on the brain! It is NOT caused by drug induced spinal cord depression
102
Does propofol cause drug induced spinal cord depression
NO
103
What receptor does propofol hit (besides GABA) to contribute to its hypnosis effect?
Glycine
104
With propofol, what occurs first: hepatic first pass or pulmonary first pass?
Pulmonary
105
What hepatic enzyme metabolizes propofol?
CP450
106
Propofol elimination half time
0.5 - 1.5 hours
107
Propofol context-sensitive half-time (8 hour infusions)
40 minutes
108
Propofol volume of distribution
3.5-4.5 L/kg
109
How does propofol impact systemic BP and HR?
decreases them
110
What organ mainly metabolizes propofol
Liver
111
Etomidate elimination half time
2-5 hours
112
Etomidate volume of distribution
2.2-4.5 L/kg
113
Etomidate clearance
10-20 mL/kg/min
114
Propofol clearance
30-60 ml/kg/min
115
How does etomidate impact systemic BP and HR?
No change or decreased BP
No change on HR
116
Ketamine elimination half time
2-3 hours
117
Ketamine volume of distribution
2.5-3.5 L/kg
118
Ketamine clearance
16-18 ml/kg/min
119
How does ketamine impact systemic BP and HR?
Both are increased
120
Does propofol cross the placenta?
Yes, worry about fetal ion trapping so be careful with pregnant patients
121
What is the blackbox warning for propofol pertaining to?
Caution with pediatric patients
122
What is the induction drug of choice?
Propofol
123
Why do children require a higher dose of propofol?
Presumably reflecting they have a larger central distribution volume and higher clearance rate
124
Why do the elderly require a lower dose of propofol?
As a result of them having a smaller central distribution volume and decreased clearance rate
125
At what propofol blood level is there unconsciousness upon induction?
2-6 mcg/mL
126
Awakening without CNS effects is characteristic of propofol. Awakening typically occurs at plasma propofol concentrations of ___ to ____
1.0 -1.5 mcg/mL
127
What two benefits of propofol make it suited for ambulatory conscious sedation?
-Prompt recovery without residual sedation
-Low incidence of PONV
128
Propofol has ____ and ____ and _____ properties. However, at low doses we may need to supplement with ____ or ____ medications.
Analgesic and amnestic and anticonvulsant
Opiods or midazolam
129
Propofol is more effective than zofran in these two types of N/V
CINV (chemo induced)
PONV
130
How does propofol help with nausea and vomiting (MOA)?
depresses subcortical pathways and has a direct depressant effect on the vomiting center.
131
Propofol sub hypnotic dose
What is this good for?
10 to 15 mg IV followed by 10 µg/kg/minute
CINV and PONV
132
Dose of propofol to get anti-pruritic effects.
Why may patients experience pruritic?
Anti-pruritic effects:
10 mg IV
D/T neuraxial opioids exciting spinal cord or cholestasis
133
Propofol anti-convulsant dose
Anti-convulsant: 1 mg/kg IV
134
Why is propofol good for asthmatic patients
It has bronchodilator abilities
135
Does propofol trigger malignant hyperthermia?
no
136
This induction drug has potent antioxidant properties
propofol
137
How does propofol impact:
CBF
CMRO2
ICP
Decreases CBF
Decreases CMRO2
Decreases ICP
138
What is the CMRG? What is it related to?
Cerebral metabolic rate of glucose
CMRO2 (basically the same thing)
139
How does propofol impact Autoregulation r/t CBF and PaCO2?
They are maintained
140
How does propofol impact SSEP? What is the exception to this?
It does not impact it. This makes it great for neuro cases.
Exception: Unless volatiles or nitrous added
141
What are the excitatory movements propofol can cause?
Myoclonus
142
On an EEG, what do delta waves indicate? Theta waves? Alpha waves?
Delta waves: deep sleep **what we want for surgical anesthesia**
Theta - light sleep
Alpha waves – awake
143
Which decreases SBP more: thiopental or propofol?
What is the MOA of this?
Propofol
1. Inhibition of SNS…vascular smooth muscle relaxation… ↓ SVR
2. Decreases intracellular calcium
144
Why does propofol cause bradycardia?
-Decreases SNS response by reducing vagal tone; has direct effect on muscarinic receptor
-May depress baroreceptor reflexes– so no compensatory increase in HR
145
With this drug, profound bradycardia and asystole can be found with healthy adult patients and children
Propofol
146
Explain what is happening in this image
The HR response to IV atropine is impacted in patients receiving propofol. The decreases in HR **cannot** be overcome by larger doses of atropine which suggests propofol may decrease SNS activity.
*You may have to give a beta agonist for propofol induced bradycardia!*
147
How does propofol impact veniltation?
It produces dose dependent depression of ventilation. Apnea can occur as well.
148
How is hypoxic pulmonary vasoconstriction response impacted by administration of propofol?
It remains intact
149
What can counteract the ventilatory depressant effects of propofol?
Painful surgical stimulation
150
Why does propofol cause green urine?
Does this mean renal function is impacted?
Due to the phenols
No impact on renal function
151
Why does propofol cause cloudy urine?
Does this mean renal function is impacted?
-uric acid crystallization
-No alteration in renal function.
152
How does propofol impact intraocular pressure (IOP)?
Platelet aggregation?
Decreases IOP
Inhibits platelet aggregation
153
What is another name for propofol infusion syndrome?
lactic acidosis
154
With what doses / time period do you see Propofol Infusion Syndrome (Lactic Acidosis)?
High dose infusions of >75 µg/kg/min longer than 24H
155
What do we see with pediatric patients who have Propofol Infusion Syndrome (Lactic Acidosis)?
Severe, refractory, and fatal bradycardia in children
156
Signs and symptoms of Propofol Infusion Syndrome?
Diagnosis?
- Lactic acidosis
-Brady-dysrhythmias
-Rhabdomyolysis
Dx: ABG and serum lactate concentrations
157
Can you reverse Propofol Infusion Syndrome (Lactic Acidosis)?
Yes, in the early stage
158
The only carboxylated imidazole-containing compound for induction
etomidate
159
Etomidate is water soluble at an ______ pH and lipid soluble at _____ pH; weak ____ (acid or base?)
acidic, physiologic
It is a weak base
160
Etomidate is made up of 35% ________. This is why it burns on injection.
Propylene glycol
161
Only induction drug with direct systemic absorption in oral mucosa that bypasses hepatic metabolism
Etomidate
162
Etomidate causes excitatory effects that manifest as _____
myoclonus
163
What is the biggest indicator of onset of action
Lipid solubility is biggest indicator of onset of action!!!!
More lipid soluble = faster onset of action
164
Why is etomidate great for pediatric patients?
Because it has direct systemic absorption in oral mucosa that bypasses hepatic metabolism
165
When drug is given orally, first pass from liver metabolism usually eliminates ___% of drug
50%
166
Etomidate MOA
In/directly open Cl- Channels of GABAA receptors
Cell Hyperpolarization
167
Etomidate onset
Onset: 1-minute s/p IV injection
168
Etomidate is __% albumin bound
76%
169
Etomidate clearance: __x faster than Thiopental
We experience prompt awakening due to what property of etomidate?
5x faster
It is highly lipid soluble!
*this is due to the redistribution from the brain to inactive tissue sites*
170
How is etomidate metabolized?
Hydrolysis through hepatic microsomal enzymes & plasma esterases
171
Etomidate Elimination: __% in urine & __% - ___% in bile.
85%
10-13%
172
Etomidate half time
T ½: 2 - 5 hours
173
Etomidate peak time
2 minutes
174
Standard induction dose of etomidate
Dose: 0.3 mg/kg IV
175
What type of patients is etomidate the best for?
Unstable Cardiovascular System
-Especially with little or no cardiac reserve
176
Do patients experience hangover or cumulative drug effect with etomidate?
No
177
True or false: Etomidate has analgesic effects
FALSE
We need to give opioids during induction (direct laryngoscopy and tracheal intubation)
178
The incidence of myoclonus from etomidate can be decreased by doing what?
Prior administration of an opioid (such as fentanyl) or benzos
179
How much fentanyl would you give prior to etomidate to prevent myoclonus
Fentanyl: 1 to 2 µg/kg IV
180
Involuntary myoclonic movements:
___ to ___% Etomidate > ____% after Thiopental, ___% after Methohexital, ___% after propofol
50% to 80% Etomidate > 17% after Thiopental, 13% after Methohexital, 6% after propofol
181
This is an alteration in balance of inhibitory and excitatory influences on the thalamocortical tract.
Involuntary Myoclonic Movements
182
Caution using etomidate in patients who have a history of ____. Why?
seizures
May activate seizure foci
183
Etomidate causes ______ ____ by producing a dose dependent inhibition of the conversion of cholesterol to cortisol
Adrenocortical Suppression
184
Etomidate enzyme inhibition of 11-B-hydroxylase last for __ to __ hours after induction dose
4-8
185
Explain why we care about this graph
Etomidate, but not thiopental is associated with decrease in the plasma concentrations of cortisol
186
Etomidate ______ CBF and CMRO2 ___ to ___%
Decreases, 35% to 45%
187
Etomidate is a potent direct cerebral _____
What does this mean for ICP?
vasoconstrictor
↓ ICP
188
Etomidate has similar EEG changes (Thiopental) except more frequent _____ spikes
excitatory
189
Why do you not use etomidate in nerve surgery?
May increase amplitude of SSEP, gives us false positives
190
With an induction dose of 0.3 mg/kg of etomidate, how is CO/HR/SV impacted?
What about with a dose of 0.45 mg/kg IV?
It is not impacted, however SVR drops.
0.45: Significant decreases in systemic blood pressure and CO occur
191
True or false: etomidate releases histamine
false
192
Rapid IV injection to etomidate will cause this impact on the respiratory rate
apnea
*all induction drugs besides ketamine do this by the way*
193
Which of the following has a greater impact on depressing ventilation: etomidate or propofol/barbiturates?
Propofol/barbiturates
194
Why do patients who receive etomidate come back breathing earlier?
Stimulates CO2 medullary centers– so they come back breathing earlier
195
Which induction drug may be useful when maintaining spontaneous ventilation is desirable
etomidate
196
What else is ketamine called?
Angel dust or PCP
197
What kind of anesthesia does ketamine provide?
Dissociative
198
You walk in the room, your patients eyes are open with a slow systemic gaze. They are non communicative but awake. What drug are they most likely on?
Are they amnesic? Analgesic?
Ketamine
Yes!
Yes! It is intense analgesia
199
When giving ketamine, hypertonus may occur. Why is this a concern?
It can lead to rhabdomylosis
200
2 advantages of ketamine over Propofol and Etomidate
-No pain @ injection.
-Profound analgesia at subanesthetic doses
201
2 disadvantages of ketamine
Disadvantages:
Emergence delirium
Abuse potential
202
What preservative is with ketamine?
Why is this good?
Preservative: Benzethonium Chloride
Communicative effects: increases analgesia
203
What isomer of ketamine is used for therapy resistant depression?
S(+) ketamine (esketamine)
204
Which form of ketamine has cocaine like effects: S isomer, R isomer, or racemic?
Racemic
205
Which isomer of ketamine has: More intense analgesia, lower incidence of emergence reactions, and less salivation?
S isomer
206
Ketamine receptors?
Binds noncompetitively to N-methyl-D-aspartate (NMDA) receptors.
Inhibits activation of NMDA receptors by glutamate and decreases the presynaptic release of glutamate.
207
Most abundant excitatory neurotransmitter in CNS
glutamate
208
____ is an obligatory co-agonist of glutamate
Glycine
209
What other receptor sites does ketamine impact?
-opioid (µ, δ, and κ; weak σ),
-monoaminergic
-muscarinic
-voltage-sensitive sodium
-L-type calcium channels
-Neuronal nicotinic acetylcholine receptors which helps produce analgesic effects
(LVN MOM)
210
Ketamine has a weak action at this type of receptor
GABA A
211
What opioid receptor is weak
Weak opioid site is sigma (σ)
212
Ketamine has a rapid onset of action (similar to Thiopental)
The peak plasma concentrations @ _ minute(s) after IV & __ min(s) (IM)
1 minute IV
5 minutes IM
213
Ketamine has a:
____ (Short or long) duration of action
Duration: __ to ___ mins
___ to ___ min to return to full orientation.
Short duration of action
10 – 20 mins
60-90 min to return to full orientation.
214
Is ketamine highly, moderate or minimally lipid soluble?
Compare it to thiopental
Highly
5-10x more
215
Is ketamine significantly plasma bound?
No
216
What is ketamines VD?
3L/min
217
Ketamine elimination half-time
2 to 3 hours
218
Ketamine has a ____ (high or low) hepatic clearance rate of ___ L/min
high, 1L / min
219
What enzyme metabolizes ketamine?
CYP450
220
Ketamine active metabolite?
How potent is it in comparison to ketamine?
Norketamine
1/3 – 1/5 potency
221
Ketamine excretion organ
Excretion: Kidneys
222
What patient population develops a tolerance to ketamine?
Burn patients
223
Ketamine dose for induction:
IV
IM
PO
0.5 - 1.5 mg/kg IV
4 - 8 mg/kg IM
10 mg/kg PO
224
Ketamine dose for maintenance
IV
IM
0.2 - 0.5 mg/kg IV analgesia
4 - 8 mg/kg IM
225
Ketamine subanesthetic (analgesic dose)
0.2 - 0.5 mg/kg IV
226
4 prong approach on pain for ketamine:
Voltage channels
Nicotinic receptors
Active metabolite
Preservative
^ These things contribute to analgesia
227
Ketamine infusion dose post Op Sedation and Analgesia (pediatric cardiac surgery)
1 - 2 mg/kg/hour
228
Ketamine dose Neuraxial Analgesia
Concentration in how much saline?
Where can I give?
30 mgs Epidural
5 - 50 mg in 3 mLs of saline Intrathecal/Spinal/Subarachnoid
229
Why do you give robinul before ketamine?
Ketamine induces salivary secretions
230
Ketamine induction LOC effect time IV and IM
30 secs – 1 min (IV)
2 to 5 mins (IM)
231
Why do we induce with ketamine in hypovolemic patients?
Ketamine stimulates the SNS
232
Why is ketamine good for patients with asthma?
Bronchodilator properties and no histamine release
233
Can I give ketamine to a patient who has a hx of MH?
Yes
234
Induction Coronary artery disease ‘cocktail’:
-Coronary artery disease ‘cocktail’:
-Diazepam 0.5 mg/kg IV
-Ketamine 0.5 mg/kg IV
Continuous Ketamine infusion: 15 to 30 µg/kg/minute IV
235
How does ketamine impact ICP?
Increases it
236
Caution in ketamine with patients who have pulmonary HTN. Why?
It may increase it up to 44%
237
Why would an eye surgeon look at you like you were an idiot after you gave ketamine to their patient?
It causes nystagmus which is not great for eye procedures
238
Ketamine is a potent cerebral _____
vasodilator
239
How does ketamine impact CBF and CMRO2
↑ CBF by 60% (because it is a potent vasodilator); also increases CMRO (glucose also)
240
How does ketamine impact the EEG? Seizure threshold?
Increases Excitatory activity in EEG
Does not alter seizure threshold.
241
Ketamine can cause increased amplitude with SSEP → this can be reduced by administering _____
can reduced by N20
242
How does ketamine impact the CV system?
-Resemble SNS stimulation: Increases …
sBP, PAP, HR, CO, MRO2
-Increases plasma Epi & Norepinephrine levels
243
How can you blunt the SNS CV effects of ketamine
Blunted by pre-med with benzos or inhaled anesthetics & N20
244
You have an unexpected drop in sBP and CO with ketamine. What can cause this?
Depeleted catecholamine stores
245
If you have a drop in HR / BP due to ketamine. What is the drug of choice, why?
Epinephrine
The bradycardia is due to depleted catecholamines. Atropine will not work.
246
How is ventilatory response to CO2 impacted by ketamine?
Ventilatory response to C02 is maintained
247
With ketamine PaCO2 is unlikely to increase more than __ mmHg.
3
248
Ketamine impact on: upper airway skeletal muscle tone and reflexes
They maintained & intact.
249
Is emergence delirium an adverse reaction?
No, just a side effect
250
What percentage of patients experience emergence delirium?
5% to 30% of patients
(Psychedelic effects)
251
How long do the Psychedelic effects last after ketamine?
Morbid & vivid dreams (in color) and hallucinations up to 24H
252
How to prevent emergence delirium? 2 options
**-Benzodiazepine IV (5 minutes prior)
**-Also could give alpha 2 agonist; Clonidine and Dexmedetomidine
253
How does ketamine effect non-depolarizing muscle relaxing drugs?
Enhances
How? InIhibits cytosolic free calcium concentration
254
How does ketamine impact succs?
Prolongs apnea from Succinylcholine by Inhibiting plasma cholinesterases
255
Drug interactions:
Ketamine + Volatile anesthetic (Iso/Sevo/Des):
Hypotension
256
Obstructive Sleep Apnea and Ketamine risks and benefits:
**Risks:**
Psychiatric Effects, SNS activation, hypersalivation
**Benefits:**
Upper airway preservation (if appropriate dose) and ventilatory function (as long as subanesthetic doses)
257
Which induction agent has the highest analgesic properties:
-Propofol
-Ketamine
-Thiopental
-Etomidate
Ketamine!
258
What is Ketafol?
Ketamine + Prop mixed in a syringe
259
Why is ketafol mixture bad?
Propofol is not a chiral compound and Ketamine is, **its not stable.**
260
Propofol + lidocaine mixed in a syringe can create ____
lipid bubbles which causes risk of PE’s
261
We used to only be able to draw up our drugs 1 hour before surgery, but now we can draw up our drugs __ hours before case
4
262
What are the two components of pain?
Sensory-discriminative and motivational affective
263
What two ascending tracts are involved with the sensory-discriminative component of pain?
Where are they located?
Spinothalamic
Trigeminothalamic tracts
Located in the cerebral cortex
264
What does the sensory-discriminative component of pain tell us?
Perception of the quality of pain (ex: pricking, burning, aching), the location and intensity as well as duration.
265
Motivational-affective responses to painful stimuli include (4 things)
* Attention and arousal
* Somatic and autonomic reflexes→ ex. Touching something hot
* Endocrine responses
* Emotional changes
266
Nociception definition
The experience of pain with a series of complex neurophysiologic processes
267
Four distinct components of nociception:
* Transduction
* Transmission
* Interpretation
* Modulation (PNS and CNS)
268
What is Increased pain sensations to normally painful stimuli?
Hyperalgesia
269
Most common reason for people to go to doctor
Pain
270
What are the steps (starting with trauma to tissue) to pain perception
Trauma, transduction, transmission, modulation and perception
271
What part of the spinal cord is in charge of modulation?
Dorsal horn
272
What part of pain perception involves: Nerve/electrical impulses/signals start at the nerve endings?
Transduction
273
What part of pain perception involves: Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.
Transmission
274
What part of pain perception involves: Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.
Modulation
275
What part of pain perception involves: Thalamus acting as the central relay station for incoming pain signals & the primary somatosensory cortex serving for interpretation/discrimination of specific sensory stimuli.
Perception
276
These types of anesthetic drugs work on peripheral nociceptors and impact transduction (transduction of mechanical, chemical and thermal stimuli into an action potential)
LA and NSAIDs
277
This type of anesthetic works on pain transmission of action potentials via A delta and C fibers
LA
278
These anesthetic drugs work at the level of the spinal cord and impact modulation of afferent signals in the dorsal horn and production of reflex reactions
LA, opiods, ketamine and alpha 2 agonists
279
These anesthetic drugs work at the level of the brain and affect perception (activation of descending inhibitory pain pathways and memory)
Opioids, alpha 2 agonists, general anesthetics
280
Where does the modulation of pain impulses occur?
A. Thalamus
B. Dorsal Horn
C. Cortex
D. CNS
B. Dorsal horn
281
C FIBERS:
Myelinated or unmyelinated?
Fast or Slow pain?
* Unmyelinated
* Slow pain
282
Which type of fibers transmit information about burning pain from heat and pain from sustained pressure.
C fibers
283
A FIBERS
myelinated or unmyelinated?
Fast or slow?
Myelinated
Fast
284
What are type II fibers?
A delta (Aδ) fibers with lower conduction velocity
285
What are type I fibers?
Aβ & Aδ fibers
286
This type of nociceptor is responsive to heat, mechanical and chemical stimuli
Type I: Aβ & Aδ fibers
287
What are our peptides?
* Substance P
* Calcitonin
* Bradykinin [1st released]
* CGRP
288
What are our chemical mediators?
* Peptides (Substance P, Calcitonin, Bradykinin [1st released], CGRP)
* Eicosanoids
* Lipids (Prostaglandins, Thromboxanes, Leukotrienes, Endocannabinoids)
* Neutrophins
* Cytokines
* Chemokines
* Extracellular proteases and protons
(PEEL CNC)
289
______ Hyperalgesia occurs at the original site of injury from heat and mechanical injury and ____ Hyperalgesia occurs at uninjured skin surrounding the injury (only from mechanical stimuli).
Primary, secondary
290
What are some examples of things that decrease pain threshold?
-Being an infant
-No sleep
-Anxiety
-Hangovers
-Stress
-Not eating
291
Relay center for nociceptive & other sensory activity.
Spinal dorsal horn
292
What part of the dorsal horn are the main target for afferent C fibers? What are their other names?
Lamina I (marginal layer) and Lamina II (substantia gelatinosa)
293
Myelinated fibers innervating muscles and viscera terminate in laminae ___, ____ to ___ and the ___ horn
Lamina I, IV to VII, ventral horn
Pg #689 of textbook
294
These two laminae express the neurokinin 1 receptor (NK1) and are heavily innervated by substance P containing afferents.
III and IV
This is important for spinal / epidural anesthesia
295
Gate theory: A neurologic “gate” in the spinal ___ horn.
dorsal
296
With the gate theory, when the gate is open: pain is projected to _________ regions via ____ and ___ fibers
supraspinal brain regions
A delta and C fibers
297
With the gate theory, when the gate is closed: pain is not felt with simultaneous ______ impulses via _____ fibers which deliver information about ___ and ___
inhibitory
**Aβ fibers** (large diameter, myelinated: faster) deliver information about **pressure** and **touch** (rubbing)
298
Which parts of the brain are involved with perception of motivational-affective pain components.
Limbic cortex and thalamus
299
This part of the CNS depresses or facilitates the integration of pain info in the spinal dorsal horn.
Periaqueductal gray – rostral ventromedial medulla (PAG-RVM) system
300
Tissue injury and/or damaged cells release ____.
Give some examples
neuromdoulators
Substance P
Glutamate
CGRP
NMDA
AMPA
BDNF
Cytokines
301
An excitatory impulse mediator:
a. GABA
b. Glycine
c. Glutamate
d. Norepinephrine
Glutamate
302
These 5 neuromodulators deal with excitatory impulses
* Glutamate
* Calcitonin
* Aspartate
* Neuropeptide Y
* Substance P
(G CANS)
303
These 5 neuromodulators deal with inhibitory impulses
* Dopamine
* Enkephalin
* Norepinephrine
* GABA
* Glycine
304
Ascending Pathways of Nociceptive Information
1. Spinothalamic
2. Spinomedullary
3. Spinobulbar
4. Spinohypothalamic
305
Thalamus and cerebellum are a part of ___brain
hind
306
Somatosensory I and II are part of the ___ brain
forebrain
307
Where do the Supra-Spinal Modulation
Descending Inhibitory Tracts originate?
Periaqueductal gray
308
What are the three neurotransmitters involved with the descending inhibitory complex?
Neurotransmitters:
Endorphins, enkephalins, serotonin
309
PAG-RVM system works on these type of receptors
µ, κ, δ opioid receptors
310
Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?
PAG-RVM
311
Chronic pain: > ___ to ___ months: persists beyond tissue healing
3 to 6
312
This type of pain is characterized by a reduced nociceptive threshold and persists in the absence of a stimulis and is refractory to traditional anaglesics
Neuropathic
313
This type of pain is diffuse & poorly localized (referred to somatic sites: muscle & skin)
Visceral
314
A variety of painful conditions **following injury** in a region with impairment of sensory, motor, and autonomic systems
Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin & SQ tissues.
Complex Regional Pain Syndromes
315
Pain perception at ___ weeks of gestation
23
316
With patients in pain, they may have pulmonary effects such as splinting. What is this?
Respiratory splinting is defined as reduced inspiratory effort as a result of sharp pain upon inspiration. This can result in atelectasis post-operatively.
317
GI / GU resopnse to pain
-Enhanced sympathetic tone:↑ sphincter tone, and ↓ motility
-Ileus
-Urinary retention
-Hypersecretion of acid
-Stress ulceration
-Aspiration
**-N/V
**-Abdominal distention b/c of decreased peristalsis
318
In reponse to pain, your body _____ (increases or decreases) catabolic hormones and _____ (increases or decreases) anabolic hormones
Increases catabolic and decreases anabolic
319
Are the following catabolic or anabolic hormones:
Catecholamines
Cortisol
Glucagon
Catabolic
320
Are the following catabolic or anabolic hormones:
Insulin and testosterone
Anabolic
321
Pain / stress related hematologic Response
Hypercoagulability; increased risk for clots
322
When you are under pain / stress, you may have a negative nitrogen balance. What does this mean for your blood pH?
Acidosis may occur
323
Which opiod is the gold standard?
Morphine
324
What plant do opiods originate from?
Opiates from Papaver somniferum aka Opion aka poppy juice (350 BC)
325
Are opioids endogenous or exogenous?
ALL are Exogenous (synthethic and nonsynthetic)
326
What structure are: Morphine, Codeine, & Thebaine
Phenanthrenes
327
What structure catergory is: Papaverine & Noscapine
Benzylisoquinoline
328
Which Opioid receptor subtype is responsible for dysphoria?
Kappa
329
Which opioid receptor subtype is responsible for the hallucinogenic effects and decreased GI sensations?
Delta
330
Which opioid receptor subtype is responsible for majority of effects ex. Analgesia, euphoria, sedation, respiratory depression and constipation
Mu
331
Are opioids agonists or antagonists?
Agonists
332
How do opioids cause pre synpathic inhibition of acetylcholine, dopamine, norepinephrine, Substance P?
* Increased K+ conductance (hyperpolarization)
* Ca+ channel inactivation
* Decreased neurotransmission
* Pain modulators or anti-nociceptive
333
Where are opioid receptors located in the brain?
**Periaqueductal gray (PAG), rostral ventral medulla (RVM),** locus ceruleus & hypothalamus
334
Which receptor produces physical dependence?
Mu 1 or Mu 2
Mu2
335
What two opioid receptor subtypes deal with constipation, ventilatory depression and physical dependence?
Mu 2 and delta
336
These two opioid receptor subtypes deal with euphoria, low abuse potential and miosis
Mu 1 and kappa
337
These two opioid receptor subtypes deal with urinary retention
Mu1 and delta
338
Which opioid receptor subtype deals with bradycardia and hypothermia?
Mu 1
339
Which opioid receptor subtype deals with diuresis?
Kappa
340
Agonists of Mu1 and Mu2
-Endorphins
-Morphine
-Synthetic opioids
341
Agonists of kappa
Dynorphins
342
Agonists of delta
enkephalins
343
Antagonists of ALL opioid receptor subtypes
Naloxone, naltrexone and nalmefene
344
CV side effects of opioids
-Bradycardia
-Hypotension
-Decrease venous return and CO
-Possible histamine release
345
This drug class is cardioprotective from myocardial ischemia
Opioids
346
This drug can reverse antagonize ventilatory depression but not analgesia from opioids
Physostigmine
347
Normal deadspace
2 mL/ kg
348
Skeletal thoracic (chest wall) & abdominal muscle rigidity caused by opioids can be treated with
Narcan or muscle relaxants
349
True or false: large doses of opioids can cause myoclonus
True
350
Rank from least to greatest to prevelance of oddi spasm with the following meds:
Morphine, Demerol, Fentanyl
Least: Morphine 53%
Moderate: Demerol 61%
Greatest: Fentanyl 99%
351
How do you differentiate between a heart attack and a sphincter spasm caused by opioids?
Give naloxone; if pain persists it may be an MI!
352
Why do opioids cause vomiting?
Direct stimulation of CTZ (chemoreceptor trigger zone) and increased GI secretions and delayed GI emptying
353
Why do you avoid opioids in an ERCP?
Avoid opioids in ERCP b/c of sphincter spasm – if its spasms they can’t get in there to do procedure – fentanyl is biggest culprit, then meperidine then morphine
354
Why do you give glucagon to patients on opioids?
* glucagon increases gastric emptying (warning: diarrhea)
* Treatment for Oddi spasms
* 2 mg IV
355
GU effects opioids
Urinary urgency
356
Opioids side effects cutaneous
Cutaneous: histamine release → flushed face, neck, & upper chest.
357
Opioid effects on the neonate
Placenta: neonate depression; dependence (chronic)
358
How long does it take to develop a tolerance to morphine?
Morphine: 25 days
359
The development of the requirement for increased drug doses (usually 2 to 3 weeks).
Tolerance
360
Why do people develop a tolerance to opioids?
Downregulation: opioid receptors on the cell membrane surfaces become gradually desensitized by reduced transcription & subsequent decreases in numbers of opioid receptors.
361
Withdrawal from which of the following opioids has the longest onset and lasts the longest:
-Methadone
-Demerol and Fentanyl
-Morphine and Heroin
Methadone
362
Withdrawal from which of the following opioids has the quickest onset lasts the shortest:
-Methadone
-Demerol and Fentanyl
-Morphine and Heroin
Demerol and Fentanyl
363
True or false:
Higher doses of intra op opioids lead to less post op pain
False; they lead to greater post op pain
364
Morphine intra op dose
1-10 mg IV
365
Morphine post op dose
5-20 mg
366
Morphine onset
10-20 min
367
Morphine duration
4-5 hours
368
Fentanyl induction
1.5-3 mcg/kg IV 5 mins prior
369
Fentanyl onset
30-60 seconds
370
Fentanyl duration
1-1.5 hours
371
Sufentanil intraop
0.3-1 mcg/kg IV
372
Remifentanil duration
6-8 minutes
373
Sufentanil duration
1-1.5 hours
374
Sufentanil infusion
Infusion: 0.5 to 1 µg/kg/hr IV
375
Remifentanil intra op
Load: 0.5-1 mcg/kg over 1 minute
376
Remifentanil, Sufentanil and Fentanyl onset
30-60 seconds
377
Remifentanil infusion
0.125-0.375 mcg/kg/min
378
Meperidine post op dose for shivering
12.5 mg
379
Both meperidine and hydromorphone have an onset of ___ to ___ minutes and a duration of __ to __ hours
Onset: 5-15 minutes
Duration: 2-4 hours
380
Naloxone dose
1-4 mcg/kg
381
Naloxone onset and duration
Onset: 1-5
Duration: 30 minutes
382
Morphine active metabolites
Morphine-6-glucuronide: active analgesic
383
Morphine peak
IV:
IM:
IV: 15-30 minutes
IM: 45-90 min
384
Morphine onset for IV/IM
10-20 minutes
385
This agonist drug has a PO Hepatic 1st Pass: 25%.
No first pass uptake in lungs
Morphine
386
Demerol MOA
-Mu and kappa receptor agonist
-Alpha 2 agonist
387
What % of demerol is affected by Hepatic 1st pass?
80%
388
Where is meperidine metabolized?
Metabolites?
Hepatic
Normeperidine
389
How protein bound is meperidine?
60%
390
Meperidine E1/2 time
3 to 5 hours
*35 hours with renal failure* "
391
Other options besides demerol for post op shivering
Physostigmine and alpha 2 agonists (clonidine)
392
Side effects of demerol
tachycardia & mydriasis with dry mouth, (-) inotropy, serotonin syndrome (MAOIs & TCAs), impaired ventilation, crosses placenta
393
This opioid reaches its Blood:Brain Effect-Site Equilibration: 6.4 minutes→ very quick!
Fentanyl
394
Fentanyl lung first pass effect %
75%
395
This organs act as reservoirs and also have an effect on drug metabolism
Lungs
396
Principal metabolite of fentanyl
Metabolite: Norfentanyl
397
Fentanyl has a ____ volume of distribution
Large
398
How soon after you give a IV bolus dose of fentanyl is 80% gone?
IV bolus dose(<5 mins 80% is gone)
→ first goes to highly vascular tissues
399
Rank the context sensitive half time of the following drugs from longest to shortest:
-Fentanyl
-Remifentanil
-Sufentanil
-Alfentanil
Longest:
Fentanyl
Alfentanil
Sufentanil
Remifentanil (shortest)
400
Fentanyl dose for Analgesia:
1 to 2 µg/kg IV
401
Fentanyl dose for adjunct with inhaled anesthetics:
2 to 20 µg/kg IV
402
Fentanyl dose
Surgical Anesthesia (solo):
50 to 150 µg/kg IV
403
Fentanyl dose intrathecal
Intrathecal: 25 µg
404
Fentanyl dose transmucosal
Transmucosal (Oral): 5 to 20 µg/kg
405
Fentanyl dose pediatrics 2-8 years old
15 to 20 µg/kg PO 45 minutes prior
406
Fentanyl dose transdermal:
75 to 100 µg (18 hours steady delivery)
407
__ mg of PO fentanyl = __ mg of IV morphine
1 mg of PO Fentanyl = 5 mgs of IV Morphine
408
Fentanyl CV S/E
Large doses: no histamine release, depressed carotid sinus baroreceptor reflex
NO significant bradycardia
decreased BP & cardiac output
409
How does fentanyl impact the CNS?
-Seizure like activity
-Modest increase in ICP (6 to 9 mmHg)
410
This is 5-12x more potent than fentanyl
Sufentanil
411
Sufentanil has ___% lung first pass uptake
60%
412
Sufentanil ____% bound to alpha 1 acid glycoprotein
92.5
413
How is sufentanil excreted?
Excretion: renal and fecal (caution in chronic renal failure)
414
Does sufentanil bind to albumin or alpha 1 acid glycoprotein?
alpha 1 acid glycoprotein
415
Sufentanil analgesic dose
Analgesia: 0.1 to 0.4 µg/kg IV
416
Sufentanil induction dose
Induction: 18.9 µg/kg IV
417
Sufentanil CV effects
* Bradycardia
418
Alfentanil is ___ less potent than fentanyl (1976)
1/5th
419
Alfentanil onset
1.4 minutes > fentanyl & sufentanil
420
How does cirrhosis impact the E 1/2 time of alfentanil
Prolongs it
421
What is abnormal about alfentanil lipid solubility
90% nonionized at normal pH →so lower lipid solubility but has good Vd
422
Alfentanil metabolite
Noralfentanil
423
Alfentanil dose for Induction laryngoscopy:
15 to 30 µg/kg IV (90 seconds prior)
424
Alfentanil dose for induction alone:
Induction alone: 150 to 300 µg/kg IV
425
Maintenance dose of alfentanil with inhaled anesthethics
Maintenance: 25 to 150 µg/kg/hour IV with inhaled anesthetics
426
What happens if you give alfentanil to parkinsons patients
acute dystonia
427
Remifentanil
Selective ___ opioid agonist
µ(mu)
428
This opioid agonist is 15 to 20 times as potent as alfentanil (same as fentanyl)
Remifentanil
429
How is remifentanil metabolized?
Hydrolysis by nonspecific plasma and tissue esterases
430
Which opioid agonist has:
Brief action, rapid onset and offset (15 mins)
Precise and rapid titratable effect
Lack of accumulation
Rapid recovery when discontinued
Remifentanil
431
Do you dose remifentanil on actual body weight or IBW
IBW
432
Peak effect time of remifentanil
30-60 sec
433
Remifentnil clearance
Clearance: 3L/min (8x more rapid > alfentanil)
434
Remifentanil Elimination half-time
6.3 minutes (99.8%)
435
How long does it take to reach steady state with remifentanil infusion
10 minutes
436
Is remifentanil impacted by renal or hepatic disease?
No, metabolized by tissue esterases
437
remifentanil induction dose
0.5-1 mcg/kg over 30 to 60 seconds
438
Maintenance dose of remifentanil
0.25 to 1 µg/kg IV or 0.005 to 2 µg/kg/min IV
439
Before stopping remifentanil, you want to give ____________
longer-acting opioid
440
Diluadid is __x more potent than morphine
5x
441
Diluadid dose and how often to redose
Dose 0.5 mg IV → 1 to 4 mgs total
Re-dose every 4 hours
442
Why does codeine not have an IV form?
no IV b/c of histamine induced hypotension
443
Codeine e1/2 time
Elimination half time: 3 to 3.5 hours
444
Codeine dose for cough suppression:
Cough suppressant: 15 mgs
445
Codeine dose for analgesia
60 mgs
446
Codeine 120 mgs = __ mgs of Morphine
10
447
Which is more potent, codeine or morphine
Morphine
448
Tramadol information:
Potency:
Receptor:
PO dose:
Interaction:
Tramadol
5 -10x less (morphine)
µ with weak κ & δ
PO: 3 mg/kg
Interacts with Coumadin
449
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the greatest protein binding?
The least?
Greatest: Sufentanil
Lowest: Morphine
450
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the greatest clearance?
The least?
Greatest: Remifentanil
Lowest: Alfentanil
451
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the greatest VD?
The least?
Greatest: Fentanyl
Lowest: Alfentanil
452
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the longest E1/2 time?
The shortest?
Longest: Fentanyl
Shortest:Remifentanil
453
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the longest context sensitive half time?
The shortest?
Longest: Fentanyl
Shortest:Remifentanil
454
Of the following drugs:
Morphine
Meperidine
Fentanyl
Sufentanil
Alfentanil
Remifentanil
Which one has the longest effect side (blood brain) equilibirum time?
The shortest?
Longest: Fentanyl
Shortest:Remifentanil
455
Which of the following pharmacokinetic variables best describes onset of action?
A. Effect site equilibrium
B. Protein binding
C. Elimination half time
D. Pk
A
456
457
Which volatile and IV anesthetics favor bronchodilation the most?
A. Halothane and versed
B.Propofol and Isoflurance
C. Sevoflurane and ketamine
B. Propofol and iso
458
Which volatile and IV anesthetics favor bronchodilation the least:
A.Propofol and Isoflurance
B. Sevoflurane and ketamine
C. Halothane and versed
C
