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Anesthesia Pharmacology > Lecture 12 (Exam 3) - Inhaled Anesthetics II > Flashcards

Lecture 12 (Exam 3) - Inhaled Anesthetics II Flashcards

1
Q

In regards to CNS activity, volatile anesthetics decrease what two things?

A

CMRO2 and cerebral activity
Slide 15

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2
Q

The dose-dependent decrease in CMRO2 and cerebral activity associated with inhaled anesthetics begins at approximately what MAC value?

A

0.4 MAC
Slide 15

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3
Q

Burst suppression occurs at what MAC? What about electrical silence?

A

Burst Suppression = 1.5 MAC
Electrical Silence = 2 MAC
Slide 15

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4
Q

Which inhaled anesthetic decreases CMRO2 and cerebral activity the most?

A

Trick question
Isoflurane = Sevoflurane = Desflurane
Slide 15

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5
Q

Which inhaled anesthetic has proconvulsant activity?

A

Enflurane - Especially above 2 MAC or PaCO2 < 30 mmHg
Slide 16

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6
Q

What is it called when we stimulate the periphery and measure the response in the brain, evaluating transmission UP the spinal cord?

A

Somatosensory Evoked Potentials (SSEPs)
Slide 16

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7
Q

What is it called when we stimulate the brain and measuring the response in the periphery, evaluating transmission DOWN the spinal cord?

A

Motor Evoked Potentials (MEPs)
Slide 16

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8
Q

Inhaled anesthetics have a dose-related __________ in amplitude and ____________ latency of evoked potentials at values of 0.5-1.5 MAC

A

Decrease amplitude
Increase latency (Occur less frequently)
Slide 16

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9
Q

How do inhaled anesthetics affect cerebral blood flow?

A

Increase cerebral blood flow due to decreased cerebral vascular resistance - Leads to increased ICP
Slide 17

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10
Q

Dose-dependent increases in cerebral blood flow occur at what MAC value?

A

> 0.6 MAC
Slide 17

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11
Q

Which volatile has less vasodilatory effects, leading to less cerebral blood flow increases?

A

Sevoflurane
Slide 17

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12
Q

Which volatile has the worst increase in cerebral blood flow and should definitely NOT be used in patients with increased ICP?

A

Halothane
Slide 17

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13
Q

Per lecture, autoregulation is normally good between what values?

A

60-160 mmHg
Slide 18

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14
Q

Autoregulation is lost with the use of Halothane by what MAC value?

A

0.5 MAC
Slide 18

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15
Q

Sevo preserves autoregulation up until ____ MAC?

A

1 MAC
Slide 18

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16
Q

Increases in _____ parallels increases in CBF?

A

ICP
Slide 19

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17
Q

Increases in ICP are opposed by what?

A

Hyperventilation
Slide 19

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18
Q

Typically, ICP increases occur at MAC values > 0.8 MAC and increase by how much?

A

7 mmHg
Slide 19

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19
Q

Who is more at risk for increases in ICP when administering volatile anesthetics?

A

Patients with space-occupying lesions or tumors

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20
Q

Apnea occurs at _________ MAC

A

1.5-2.0 MAC
Slide 20

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21
Q

Volatile anesthetics produce a dose-dependent __________ in respiratory rate and ___________ in tidal volume

A

Increased rate
Decreased tidal volume
Slide 20

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22
Q

Inhaled anesthetics not only depress the medullary ventilatory center but also interfere with…

A

Intercostal muscles - They lose their coordination
Slide 20

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23
Q

True or False?
The rate change associated with inhaled anesthetics is insufficient to maintain minute ventilation or PaCO2

A

True
Slide 20

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24
Q

The price of anesthetics are based on what 3 things?

A
  • Cost of liquid/mL
  • Volume % of anesthetic delivered (based on potency)
  • FGF rate (high vs low rate of fresh gas flow)

(slide 8)

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25
Q

Is Desflurane 6.6% or Sevoflurane 1.8% more potent?

A

Sevo

(slide 8)

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26
Q

Is Ethrane used anymore in the US?

A

nope

(slide 9)

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27
Q

Volatile Anesthetics cause Bronchodilation by how?
And what is required for optimal bronchodilation?

A

By blocking voltage-gated Ca++ channels and depleting ca++ in SR
Requires intact epithelium (so any conditions with inflammatory processes or epithelial damages can alter the bronchodilation effects- i.e. Astham pts)

(slide 10)

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28
Q

To have bronchodilation with inhaled anesthetics without bronchospasms due to:

A
  • Baseline Pulmonary resistance unchanged by 1-2 MAC
  • Need histamine release or vagal afferent stimulation… (idk what this means and couldn’t find a good answer in the book)

(slide 10)

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29
Q

Risk factors for Bronchospasm with inhaled anesthetics include: (4)
And which anesthetic drug can cause bronchospasm?

A
  • COPD
  • cough response with ETT
  • Age <10
  • URI (upper resp infection)

Desflurane may worsen bronchospasm (esp. in smokers due to pungency/irritation)

(slide 10)

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30
Q

Is Sevoflurane or Isoflurane better at causing bronchodilation?

A

Sevoflurane

(slide 10)

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31
Q

Which inhaled anesthetic is BEST at bronchodilation but is not used anymore in US?

A

Halothane

(slide 10)

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32
Q

For respiratory resistance comparison, Which inhaled drug would be worst to give and which drug is best?

A

worst= Desflurane
best= sevoflurane > Isoflurane

(slide 11- diagram)

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33
Q

Neuromuscular wise, does inhaled anesthetics cause muscle relaxation? And what is it dependant upon?

A

Yes! But dose-dependant

(slide 12)

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34
Q

Inhaled Anesthetics potentiate depolarizing and nondepolarizing NMBDs how?

A

Through the nACh receptors at the NMJ
They enhance **glycine **(an inhibitory NT) at the spinal cord

(slide 12)

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35
Q

Does Nitrous Oxide have any relaxant effects on skeletal muscle?

A

NOPE!

(slide 12)

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36
Q

What is “ischemic preconditioning” with inhaled anesthetics?

A

“Brief episodes of myocardial ischemia occurring before a subsequent longer period of myocardial ischemia providing protection against myocardial dysfunction and necrosis”-pg. 273

Per Dr. Kane: “the heart recognizes brief periods of ischemia before it is subjected to a longer period of ischemia, it can set itself up for that long period to be less of an effect”

(slide 13)

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37
Q

What is the MOA towards “Ischemic preconditioning” with inhaled anesthetics?

A

Mediated by adenosine
- Increases protein kinase C activity
- Phosphorylates ATP sensitive K+ channels
- Production of reactive oxygen species (ROS)
end result: Better regulates vascular tone

(slide 13)

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38
Q

“Ischemic preconditioning” with inhaled anesthetics can occur as low as what MAC?
Also, this helps to prevent “reperfusion injury how?

A

0.25 MAC (so very low) - (So just a little exposure of the volatile anesthetic during this brief ischemic period, can help the heart be resistant (or not as susceptible) during those long ischemic periods)

(slide 13)

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39
Q

“Ischemic preconditioning” with inhaled anesthetics helps prevent “reperfusion Injury.” What would these be?
What procedures is this best used in?

A
  • Cardiac dysrhythmias
  • Contractile dysfunction

Clinically apparent in delaying MI for: PTCA, CABG
(giving the VA during these times can help pre-condition the heart)

(slide 13)

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40
Q

What kind of effect does VA have on Cardiac output?

A

Dose-dependent ↓ in CO offsets by mild ↑ in HR
(↓ CO is also due to ↓ SVR)
Slide 26

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41
Q

What kind of cardiac effect do you see in Nitrous?

A

Sympathomimetic, we will see mild increase in CO if we just give nitrous.
Slide 26

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42
Q

Some study suggests VA can cause _______ d/t coronary vasodilation.

A

Coronary steal
Slide 26

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43
Q

What kind of vessels does coronary steal occur?

A

Preferentially in 20-50 micrometer vessels
(not clinically significant)
Slide 26

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44
Q

What kind of cardiac dysrhythmias does VA cause?

A

Prolonged QT with potential risk of Torsades.
(with inhibition of K+ current)
Slide 27

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45
Q

Nitrous has ______proarrhythmic effect.

A

minimal
Slide 27

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46
Q

Which VA has increased refractoriness of accessory pathway and which does not?

A

Isoflurane has ↑ refractoriness of accessory pathway in ablation studies like vfib, vtach, and afib.

❤️Sevoflurane (surprise, surprise) does not have any effect.
(so choose sevoflurane for ablation cases)

Slide 27
**(Some of the cardiologist also thought propofol can cause increase refractoriness of accessory pathway, so we got away from GA and more to sedation cases.)

47
Q

What kind of immune effects does VA have?

A

Neuroendocrine stress response (↑ANS and HPA activation during GA, and we also see surge of catecholamines, ACTH, and cortisol)

  • We also suppress monocytes, macrophages, and T-cells.

Slide 28

48
Q

Why do we avoid GA in cancer cases and do sedation or regional cases?

A

Due to increase metastasis and increase mortality.
Slide 28

49
Q

Total hepatic blood flow and hepatic artery flow is _______ and Portal vein flow is ______ with VA.

A

Maintained and increased due to vasodilation
(This occurs at 1-1.5 MAC for isoflurane=desflurane=sevoflurane)
Slide 29

50
Q

Halothane is known to ______hepatic flow and ______oxygen delivery.

A

Decrease and Decrease
(Causes halothane hepatitis, and no longer use in US)
Slide 29

51
Q

When does hepatotoxicity occur and who are more prone to get hepatotoxicity?

A

When we have inadequate oxygenation of hepatocytes and concerns for preexisting liver disease.
(↓blood flow, ↓ oxygenation, and enzyme induction may produce centrilobular necrosis)
Slide 30

52
Q

Hepatotoxicity is divided into ______and _______.

A

Type I and Type II

53
Q

Type I hepatotoxicity occurs in ___ % of patients after _____weeks after exposure to VA.

A

20% and 1-2 weeks.
Slide 30

54
Q

What causes type I hepatotoxicity and what are the s&s of it?

A

Direct toxic effect or free radical effect and S&S includes Nausea, lethargy, fever.
Slide 30

55
Q

Type II is ____common and occurs ____ after VA exposure if they have prior exposure to VA.

A

less common and 1 month
Slide 30

56
Q

What is the cause of Type II hepatotoxicity?

A

Immune-mediated response against hepatocytes with prior exposure to VA and S&S of eosinophilia and fever.
(it has high mortality due to acute hepatitis and hepatic necrosis)
Slide 30

57
Q

What VA is worst mediator of Hepatotoxicity?

A

Halothane
Slide 30

58
Q

What is the compound that all our VA metabolized to except sevoflurane?

A

Acetyl Halide
Slide 31

59
Q

Where does metabolism of enflurane, isoflurane, and desflurane occur and what reaction does their metabolite produce?

A

Enflurane, desflurane, and isoflurane are oxidized by P450 enzyme to acetyl halides metabolites in the liver.
These metabolites are capable of causing antibody reaction.
Slide 31

60
Q

Which patients are we more like to see antibody reactions caused by acetyl halide?

A

Patients who are sensitized by Halothane or Enflurane (we don’t use them anymore, so we don’t see them either)
Slide 31

61
Q

What are the 4 functions of an anesthesia circuit?

A
  1. Delivers O2
  2. Delivers Inhaled anesthetics
  3. Maintain temperature and humidity
  4. Remove CO2 and exhaled anesthetics
    (Slide 2)
62
Q

What are 3 types of gas delivery systems?

A
  1. Rebreathing/Bain circuits
  2. Non rebreathing/Self inflating bag and bag/valve mask
  3. Circle system (what’s on our anesthesia machines)
    (Slide 2)
63
Q

What are some traits of Bain circuits?

A
  1. Portable - used for transport.
  2. Unable to attach a lot of monitoring equipment, at most ETCO2 & maybe PEEP.
  3. Has an adjustable APL valve
    (Slide 3)
64
Q

What are some traits of bag/valve mask system?

A
  1. Portable, ideal for transport
  2. Unable to deliver inhaled anesthetics.
    (Slide 4)
65
Q

What are some traits of circle breathing systems?

A
  1. This is what’s on the anesthesia machine.
  2. Very fancy, lots of different monitoring equipment can be attached. Can manually and mechanically ventilate.
  3. Able to absorb and remove CO2 and exhaled drugs.
    (Slide 5)
66
Q

What does FGF mean?

A

Fresh gas flow. (Slide 6)

67
Q

In high flow anesthesia, is FGF greater or lesser than minute ventilation?

A

Greater (slide 6)

68
Q

When would high flow anesthesia be used?

A

When you want RAPID changes in anesthesia, like during induction. (Slide 6)

69
Q

What are 2 reasons why you don’t want to use high flow anesthesia all the time?

A
  1. It’s very wasteful and it costs a lot of money to use.
  2. The fast flow can make the respiratory tracts very cold, which means your patient is cold too.
    (Slide 6)
70
Q

When would you use low flow anesthesia?

A

Low flow anesthesia is for slow delivery of anesthetic gases, so this would be used when you want slow changes in your anesthetic (after induction, maintenance). (Slide 7)

71
Q

In low flow anesthesia, is FGF greater or lesser than minute ventilations?

A

Lesser. (Slide 7)

72
Q

What are 2 benefits to using low flow anesthesia?

A
  1. Not as wasteful, so cheaper to use low flow.
  2. Pt stays warm.
    (Slide 7)
73
Q

Does sevoflurane lead to a build up of Compound A?

A

The old thought was that slow sevoflurane administration would lead to a build up of Compound A, which is made when the sevoflurane gets degraded by CO2 absorbers.
The thought was that compound A was nephrotoxic to humans, but we now know that is not true. <– bc not enought is produced in humans

(Slide 7)

74
Q

At what MAC dose does 50-70% depression of hypoxic response occur?

A

0.1 MAC

Slide 21

75
Q

At what MAC dose does 100% depression of hypoxic response occur?

A

1.1 MAC

Slide 21

76
Q

Which volatiles blunt hypoxic response?

A

all of them including nitrous.

Slide 21

77
Q

What would be a good gas to give if we wanted to limit depression of the hypercarbic response?

A

Nitrous. Can be substituted for part of MAC.

Slide 21

78
Q

Dr. Kane’s definition of hypoxic pulmonary vasconstriction.

A

A normal response of the body to divert blood away from the lung if it is not being ventilated. An attempt to optimize ventilation perfusion.

Slide 23

79
Q

How quickly does HPV kick in?
How much does regional blood flow decrease?

A

5 minutes.
Blood flow decreases by 1/2.

Slide 23

80
Q

Volatiles cause a dose-dependent increase or decrease in the HPV response?

A

decrease.

Up to 50% depression at 2 MAC.

Slide 23

81
Q

How do volatiles cause direct myocardial depression?

A

Alters calcium entry and SR function.

Slide 24

82
Q

Volatiles cause a dose dependent decrease in what cardiovascular parameters?

A

Contractility, Stroke volume, and CO
A decrease in MAP primarily due to a decrease in SVR.

Slide 24

83
Q

What volatile does not cause cardiovascular depression?

A

Nitrous.

Slide 24

84
Q

Overall, what do the volatiles do to heart rate?

A

Dose-dependent increase

Sevoflurane only in MAC >1.5

Significant increase with Desflurane overpressurization.

Slide 25

85
Q

Which one of our VA has the highest vapor pressure?

A

Desflurane (Soprane)

*remember it will evaporate in seconds after pouring it on a surface
*this is also why it used to have a special vaporizer for your circuit - it was heated to prevent it from boiling at room temp. 🥵

Slide 42

86
Q

Desflurane (Suprane)

  • Solubility & potency:
  • Pungency:
  • Over-pressurizing effect:
  • CO degradation if absorbent dehydrated:
A
  • Low solubility (0.42) - does not want to stay in blood, this is the reason for its fast on/off
  • The MOST pungent –> coughing, salivation, breath holding, laryngospasm
  • Over-pressurizing will cause SNS stimulation
  • The most likely to degrade into CO

Slide 42

87
Q

What would be your last choice VA for an inhalation induction and why? Which VA do we prefer?

A

Desflurane bc it is so pungent; we prefer Sevoflurane

Slide 42

88
Q

Sevoflurane (Ultane)

Solubility:
Pungency:
Metabolism & Degradation:
Cerebral vasodilation:

A
  • low solubility (0.69)
  • sweet smelling, NOT pungent - DOC for inhalation induction, least airway irritation of modern VA
  • inorganic Fluoride - vinyl halide, LEAST likely to form CO, Compound A
  • LEAST cerebral VD, DOC for neuro w/ ⬆ ICP
    🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠 🧠

Slide 43

89
Q

What is used in the 2nd gas effect?

A

Nitrous Oxide!

Slide 45

90
Q

Why cant we use N2O as a sole anesthetic?

A

Bc its MAC is 104…we cant give 1 MAC bc they highest we can give is 100.

Slide 44

91
Q

Does N2O cause skeletal muscle relaxation?
Does it have analgesic properties

A

No skeletal muscle relaxation but it does have analgesic properties!
This is why it’s great for dental procedures/minor procedures bc the patient maintains their airway and can serve as a short acting (~20 mins) to your pain meds if they are starting to wear off (epidural example Kane spoke about)

Slide 44

92
Q

What are some negatives to using Nitrous routinely?

A
  • can cause N/V @ 50% MAC mark
  • ⬆ PVR (can be bad for neonates – can cause a R –> L shunt & jeopardize arterial oxygenation)
  • diffuses easily into air-filled spaces (C/I in globe, bowel, inner ear & lung surgeries)

Slide 45

93
Q

Renal effects are ____-_________.

Inhaled anesthetics cause a ⬇️ in ___, ___, and __

This is r/t __, not vasopressin release.

A

dose-dependent

⬇️ in RBF, GFR, and UO

this is r/t ⬇️ in CO,…

(slide 32)

94
Q

How can we preoperatively prepare for any possible renal effects caused by inhaled anesthetics?

A

Preoperatively hydrate!!! This will abolish any unwanted ⬇️ to RBF, GFR, or UO. Also, intraoperative hydration is important too.

(slide 32)

95
Q

How can inhaled anesthetics be used to “precondition” the kidneys and enhance responses to ischemia?

A

By administering inhaled anesthetics early on intraoperatively, you actually provide ischemic preconditioning (IPC) by causing the activation of K-ATP channels, which allows them to activate sooner with subsequent periods of ischemia.

(slide 32)

96
Q

What component of IA causes nephrotoxicity?

What are 3 serum lab values that are ⬆️ in nephrotoxicity?

Worst IA to cause nephrotoxicity? Also was the first agent noticed to cause nephrotoxicity. (believed to have been removed from the market worldwide as a result)

A

fluoride metabolites or fluoride toxicity caused by our inhaled anesthetics (IA)

Hyperosmolarity, hypernatremia, ⬆️ creatinine

Methoxyflurane (70% metabolized)

(slide 33)

97
Q

True/False:

No data on whether other IA’s cause nephrotoxicity, but it is presumed

A

True

Newer volatiles have lower solubility = exhalation of gas before being metabolized and eliminated really

(slide 33)

98
Q

What is Fluoromethyl-2,2-difluro-1-vinyl ether also known as?

This molecule is a ______toxin.

What common IA causes compound A formation in low flow amounts? (in rats)

What about compound A makes it problematic?

A

“Compound A”

Nephrotoxin

Sevoflurane

Compound A causes ⬆️ amounts of potassium and sodium hydroxide
(slide 34)

99
Q

In the study with rats in response to IA, what was found in regard to compound A? At how many ppm did this occur?

A 400 ppm, rats ____.

A

Acute Tubular Necrosis (ATN)
ATN found to occur at a 100 ppm of compound A in rats

Rats died at 400 ppm

(slide 34)

100
Q

In human research, with FGF of _, _, and _ L/min respectively caused the breathing circuit to measure ___, ___, and ___ ppm of compound A.

In the human research, were any alterations noted in BUN, creatinine, or presence of protein-/glucosuria?

What does this mean for us?

A

In human research, with a FGF of 1, 3, and 6 L/min respectively caused the breathing circuit to measure 19.7, 8.1, and 2.1 ppm of compound A.

No

No clinical data to demonstrate compound A is a risk at low FGF

(slide 34)

101
Q

What is produced when ___________ reacts with baralyme (desiccated absorbent)?

What happens when these products are exposed to ⬆️ heat from exhaled gas?

What’s added to sevoflurane to mitigate this possible reaction?

What’s something you should do if you notice a climbing CO2 level?

A

sevoflurane; methanol and formaldehyde

Spontaneous combustion 💥🔥🔥

additional water (this helps inhibit and cool any possible reaction)

Reach down and touch CO2 absorber and check if its warm. If it is warm or beginning to “look” desiccated, then exchange for fresh CO2 absorber so you don’t go up in flames

(slide 35)

102
Q

uncommon, inherited genetic diagnosis seen after administering IA:

What test is commonly used to test if someone is predisposed to this dx?

What are triggers for this dx?

A

Malignant Hyperthermia

Caffeine contracture test

ALL VOLATILE ANESTETICS and SUCC’s

(slide 36)

103
Q

Malignant Hyperthermia is a ______________ state of ________ muscle.

MH causes what 3 s/s noted in lecture slide?

What are the 3 main s/s that WE will see intraop?

What’s the mortality rate if this dx is left untreated?

What med should we use in the event of MH?

What does this med do?

A

hypermetabolic, skeletal

3 s/s noted in lecture slide: Excessive release of Ca++, muscle rigidity, and rhabdomyolysis

⬆️ body temp, ⬆️ CO2 production that cannot be corrected with vent rate, ⬆️ O2 consumption

80% mortality if untreated

DANTROLENE - blocks intracellular Ca++ release

(also the slide mentions rhabdo supportive care)

(slide 36)

104
Q

All Volatile anesthetics are _______.

A

Emetogenic
(Slide 37)

105
Q

GA with two triggering agents (Volatile & opioid) have a _________ chance of PONV!

A

25-30%
(Slide 37)

106
Q

Nitrous given at above 50% MAC causes?

A

PONV!
This is why we do not give high doses of Nitrous and stay away from it if the patient has severe PONV. You would also want to avoid the use of volatile anesthetics and do TIVA!
(Slide 37)

107
Q

Why do we avoid Nitrous on pregnant moms during their first trimester?

A

Due to it causing B12 deficiency in the fetus!
Nitrous oxidizes cobalt ion in B12… which inhibits methionine synthase… which inhibits DNA synthesis!

Avoid the use of nitrous, and remember a scavenging systems should be used on moms during the first trimester.

(Slide 38)

108
Q

_____________ can happen if you are exposed to nitrous for 24 hours. (Can also happen with cumulative repeated exposure in intervals that are equal to or <3-days)

A

Megaloblastic bone marrow suppression.
(Slide 38)

109
Q

Nitrous exposure increases plasma homocysteine levels.
What are two drawbacks of this event?

A

Increased homocysteine levels are associated with low B vitamins and increased levels of atherosclerosis. This can then↑ peri-operative myocardial events!!!
(Slide 38)

110
Q

Dose-dependent (0.5- 1.0 MAC) VA can do what with OB patients?
(Hint: you give them a few sniffs)

A
  1. ↓ uterine smooth muscle contractility!
  2. Helpful with a retained placenta (Uterus relaxes and then releases the placenta)! This is usually done when other drugs like Pitocin are not working on the uterus.

******CAUTION****
With the use of VA, postpartum hemorrhage can occur because spiral arteries are uniquely devoid of musculature and dependent on uterine contractions to mechanically squeeze them into hemostasis!

(Slide 39)

111
Q

Nitrous has no effect on uterine contractility. Does it have analgesic properties?

A

It does! It can have analgesic properties without the use of opioid/BZD. It is given when an OB spinal is about to run out! If the patient starts to feel a painful stimuli and you are towards the end of the case, you can give them nitrous to help numb the pain while they finish closing.

(Slide 39)

112
Q

Flip this card to learn about the fun facts about Halothane!

A

The Fun Facts
1. It is a halogenated alkane.
2. It is compatible with inhalation induction
•It is sweet/non-pungent
•Has a high potency & intermediate solubility
3. Lower risk of N/V, non-flammable

THE CONCERNS!
1. Catecholamine-induced arrhythmias!
2. Occasional hepatic necrosis!
3. Pediatric brady-arrhythmias!
4. Decomposes to HCL acid unless thymol preservative is added!
(Slide 40)

113
Q

Flip this card to learn about the fun facts about Isoflurane (Forane)!

A
  1. An isomer of enflurane!
    •It is highly potent
  2. It is highly pungent (people do not like to breath it)!
  3. It has intermediate solubility & high potency (people do not go to sleep very quickly and are left laying on the table smelling the gas…)
  4. It is expensive to purify, distillation is complex and expensive!
  5. Resistant to metabolism so it is unlikely to cause organ toxicity!
  6. It is stable as it does not deteriorate after 5 years!
  7. It is helpful in patients you do not plan to extubate! Such as ICU patients!

(Slide 41)

Anesthesia Pharmacology (20 decks)

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