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Anesthesia Pharmacology > Lecture 5 (Exam 2) - Induction Drugs (Part 1) > Flashcards

Lecture 5 (Exam 2) - Induction Drugs (Part 1) Flashcards

1
Q

Does propofol have more clearance via hepatic or lungs?

Does it have more tissue uptake or CYP450?

A

Lungs!
This is d/t rapid redistribution

Slide 40

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2
Q

Propofol’s main metabolism is in the ______ by ______ enzymes.

What are the two metabolites produced?

How are they excreted?

A

liver, CYP450

Metabolites: Water-soluble sulfate and glucuronic acid

excreted by kidneys 🫘

Slide 40 & 41

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3
Q

Why do you warn patients to not operate heavy machinery 🚜 after receiving Propofol?
(Hint: What’s the E 1/2 life?)

A

E 1/2 life: 30-90mins
Castillo explains this as ‘variable’ and to warn patients to be safe!

Slide 40

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4
Q

Does Propofol have a longer or shorter Context-Sensitive half-time compared to Thiopental?
Why?

What is Propofol’s CSHT?

A

Shorter! (another reason to love prop)
Bc it is not as lipid soluble vs barbs.

CSHT: 40 mins (8hr infusions)

Slide 40

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5
Q

With Propofol: A cardiovascular side-effect is bradycardia or tachycardia?
And why?

A
  • Bradycardia. (profound bradycardia and asystole even in healthy pts)
  • Due to: A decrease in SNS response, and depression of baroreceptor reflexes

(slide 52)

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6
Q

Propofol has a Vd of _______L/kg with a clearance of ______mL/kg/min.

Why do patients wake up quicker with propofol vs other induction drugs?

A

Vd: 3.5 - 4.5 L/kg
Clearance: 30-60 mL/kg/min

They wake up faster bc of the faster clearance!
*Faster Vd = faster clearance (per Castillo - I think he meant larger Vd?!)

Slide 42

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7
Q

Propofol increases BP and HR.
True or False?

A

False.
It decreases both.

Slide 42

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8
Q

What is a Pulmonary side-effect seen with Propofol?
And what additional med causes a synergistic effect?

A
  • (dose dependent) depression of ventilation - Apnea
  • Opioids

(slide 53)

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9
Q

Thiopental is the Gold Standard when comparing induction drugs.

It decreases BP but does is increase or decrease HR???

A

Increases HR - in reflex of HOTN (hypotension).

Verbal on Slide 42

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10
Q

Your patient is a chronic alcoholic, ESRD and pregnant. 🤰
Are you at all concerned about her waking up after giving Propofol to her?

A

Nope. Crazy, I know.
-Propofol could be metabolized through psuedocholinesterases, via the lungs, or by the liver…
-Clearance is good, excretion by psuedocholinesterases.
-It will cross the placenta but is RAPIDLY cleared by the neonate circulation thanks to pseudocholinesterase metabolism.

Slide 43

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11
Q

What is the DOC for induction?

A

Propofol

Slide 44

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12
Q

What Pulmonary response remains intact with Propofol.
And is this response good or bad and why?

A
  • Intact hypoxic pulmonary vasoconstriction.
  • GOOD! “Intrapulmonary arteries constrict in response to alveolar hypoxia, diverting blood to better-oxygenated lung segments, thereby optimizing ventilation/perfusion matching and systemic oxygen delivery.”
    (Pg. 299 in book)

(slide 53)

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13
Q

List the two clinical uses of Propofol discussed.

A
  1. Induction
  2. Cont gtt

Slide 44

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14
Q

Can Painful surgical stimulation counteract the ventilatory depressant effect from Propofol?

A

YES!

(slide 53)

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15
Q

Does Propofol affect the liver?

A

No not normally. - Liver transaminase enzymes are normal.
(BUT prolonged infusion can cause Hepatocellular injury)

(slide 54)

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16
Q

For a Propofol gtt, what is the % used in ICU and why?

What is TIVA or ‘Balanced’ anesthesia? and what does TIVA stand for?

A

ICU gtt is 2% to reduce the amount of lipid emulsion administered. 🥛

Total IV Anesthesia - used in conjunction with other anesthetic drugs (fentanyl, versed gtts).

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17
Q

Does Propofol affect the Kidneys?

A

NO!
Renal creatinine concentrations are normal

(slide 54)

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18
Q

What are 4 side-effects that can develop with prolonged infusion of Propofol?

A
  • Hepatocellular injury
  • “Propofol infusion syndrome”
  • Green urine
  • Cloudy urine

(slide 54)

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19
Q

What is the induction dose of Propofol for:
1) Adults
2) Children (Black Box warning for Propofol Infusion Syndrome)
3) Elderly

A

1) 1.5 - 2.5 mg/kg IV

2) “~3 - 3.5mg/kg IV” (⬆️ doses); the BB warning exists but apparently we still give it. (I never gave it to kids unless they were teens)

3) ≤ 1mg/kg” (25-50% ⬇️ doses)

Slide 45

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20
Q

What 2 characteristics in the urine are seen with prolonged Propofol infusions?
And what causes these?

A
  • Green urine- from Phenols
  • Cloudy urine- from uric acid crystallization
    (remember even with these signs, there is no alteration in renal function)

(slide 54)

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21
Q

Onset of Barbiturates is _____ and _____ awakening due to _____ uptake

A

30 seconds
rapid awakening
rapid uptake
Slide 19

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22
Q

What is “Propofol Infusion Syndrome”?
What causes it?
What are the signs and symptoms?
How is is diagnosed?
Is is treatable?

A
  • Due to: High dose Infusions of >75mcg/kg/min for longer than 24hrs
  • S/S: Lactic acidosis, Brady-arrythmias, Rhabdomylosis
  • Dx: ABG and Serum lactate concentrations
  • IS reversible in early stages by d/c of infusion but can cause Cardiogenic Shock and pt may need accelerated care towards ECMO support.
    (Pg. 302 in book)
    (slide 55)
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23
Q

Distribution of barbiturates from brain to other tissues is _______

A

rapid
Slide 19

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24
Q

Does Propofol cause pain on injection?
If so, what are 2 things to help prevent this?

A
  • Yes (seen in <10% of pts)
  • Give Lidocaine prior, Or inject in a larger vein

(slide 56)

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25
Q

How many doses of barbiturates are available at 5 minutes and 30 minutes?

A

At 5 minutes: 1/2 total dose
At 30 minutes: 10% of the total dose
Slide 19

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26
Q

What are 6 other side effects in other organs from Propofol infusion?

A
  1. Pain on injection
  2. Decreased intraocular pressure (IOP)
  3. Inhibits platelet aggregation (can promote bleeding)
  4. Allergic reactions (egg yolk/Lecithin)
  5. Prolonged myoclonus
  6. Abuse & misuse

(Also found on pg. 301: “Hypertriglyceridemia with prolonged administration, potential for pulmonary embolism) are believed to be due in large part to the lipid emulsion formulation.”)

(slide 56)

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27
Q

Context sensitive half-time with prolonged infusion of barbiturates is _________.

A

Long
(The longer you infuse, the more it distributes to fats, muscles, and non-vessel-rich groups, and prolongs the recovery from sedation even after you stop the drip –> know the graph in the slide figure 5-19)
Slide 19

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28
Q

Where does the drug distribute first during induction?

A

Vessel-rich groups like the brain, heart, kidney, and liver
(then, the drug gets distributed to the muscle group and at last the fat group.)
slide 20

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29
Q

During emergence the drug from ____ and _____ group will reinfuse into ______ .

A

fat and muscle group
brain and viscera
(that’s why pt’s go from stage 3 to stage 2 and finally after metabolism and excretion, we will able to extubate patient)
Slide 20

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30
Q

Reservoir for barbiturates is _____. So, redosing or using larger doses can cause a _____ effect.

A

Fat
Cumulative effect.
( That is why the context-sensitive half-time is prolonged with barbiturates.)
Slide 21

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31
Q

Barbiturates are dosed according to ?

A

Lean body weight
Slide 21

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32
Q

Equilibrium of barbiturates to plasma occurs at _____?

A

15 minutes
( Muscle group is the site of initial redistribution aside from brain and vessel rich group)
Slide 21

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33
Q

If patient is in shock, what happens to the redistribution of barbiturates to muscle group?

A

Decreases
Slide 21

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34
Q

Muscle mass is decreased in what population?

A

Elderly and women
Slide 21

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35
Q

How are Barbiturates metabolized and excreted?

A

Metabolism is 99% via hepatocytes
Excretion via renal
Slide 22

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36
Q

Why do pediatric patients have shorter half-time elimination than adults?

A

Higher clearance aka higher metabolism (according to DR. Castillo)
Slide 22

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37
Q

What is the percentage protein binding of Barbiturates?

A

Albumin 70% to 85%
Slide 22

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38
Q

70% to 85% of the albumin-bound barbiturates are active or inactive drug?

A

Inactive drug
(In order for the drug to be active and reach to effector site, it needs to be unbound or free from plasma albumin/protein)
Slide 22

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39
Q

Lipid soluble form of barbiturates favors ______.
Less lipid soluble form of barbiturates favors ______.

A

Acidosis and are in Non-ionized form
Alkalosis and are in ionized form.
( so Barbiturates are acidic drug. Barbiturates tend to stay in non-ionized forms and likes to stay in fat and muscle reservoir.)
Slide 23

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40
Q

What are the clinic implications of Barbiturates?

A

Previously used for hangover
Treat grand mal seizures ( now benzos used)
Rectal administration with uncooperative /young patients ( now we have PO versed or intranasal spray of precedex.)
Increased ICP, cerebral protection, and induction ( barbiturates causes vasoconstriction, ↓CBF,↓CMRO2)
Slide 23

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41
Q

Which isomers of barbiturates are more potent?

A

S-isomers are more potent than R-isomers of barbiturates
(marketed only as racemic mixture)
Slide 24

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42
Q

Barbiturates are divided into two groups:

A

Oxybarbiturates
Thiobarbiturates
( we don’t use these drugs anymore in US.)
Slide 24

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43
Q

Name some examples of oxybarbiturates.

A

Methohexital
phenobarbital
pentobarbital
Slide 24

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44
Q

Name some examples of Thiobarbiturates:

A

Thiopental
Thiamylal
Slide 24

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45
Q

What is the dose of Thiopental (Sodium Pentothal) and elimination half time?

A

4mg/kg IV and elimination half-time is longer than methohexital
(longer than propofol and etomidate combined)
Slide 25

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46
Q

In 30 minutes, how much of thiopental stays in the brain?

A

10% ; causes rapid distribution to skeletal muscles and fat. So need to supplement with inhaled anesthetic quickly so that pt does not wake up after 30 minutes.
Slide 25

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47
Q

Do we increase or decrease thiopental dose in elderly/ shock patients?

A

Decrease
( Thiopental favors acidic environment)
Slide 25

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48
Q

What is Fat/blood partition coefficient of Thiopental?

A

11
(which is really high, so the dose is calculated on IBW.)
Slide 25

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49
Q

Do barbiturates cause an induction in enzymes?

A

Yes
(Slide 33)

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50
Q

With prolonged continuous infusion of barbiturates, how long does it take for there to be an induction of enzymes?

A

2-7 days
(Slide 33)

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51
Q

With the induction of enzymes by barbiturates, what are some drugs that can be affected?

Would you have to increase their dose or decrease their dose?

A

Anticoagulants
Phenytoin
Tricyclic Anti-Depressants
Digoxin
Corticosteroids
Bile Salts
Vitamin K

You would have to increase the dose!

(Slide 33)

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52
Q
  1. What is SSEP?
  2. When do we use it?
  3. Why are barbiturates used with SSEP?
A
  1. Somato Sensory Evoked Potential!
  2. SSEP is the sensory level we monitor with scoliosis surgery because we do not want the surgeon to cut the nerves in the spine that can affect the upper and lower extremities!
  3. They are the desired drugs because they do not affect the neuron transmission component!
    (Slide 33)
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53
Q

With barbiturates there is a moderate transient decrease in _____ and _____.

A

Renal Blood Flow
GFR
(Slide 33)

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54
Q

Is propofol a GABA agonist?

A

Yes!
(Slide 35)

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55
Q

What is the propofol induction dose for a healthy adult?

A

1.5 to 2.5 mg/kg IV
(Slide 35)

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56
Q

For the elderly would we increase or decrease the propofol induction dose?

A

Decrease
(Dr Castillo)

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57
Q

For children, would we increase or decrease the propofol induction dose?

A

Increase
(Dr Castillo)

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58
Q

What is the conscious sedation dose of propofol for an adult?

A

25 to 100 mcg/kg/min
(Slide 35)

59
Q

What is the maintenance dose of propofol for an adult?

A

100 to 300 mcg/kg/min
(Slide 35)

60
Q

Rapid injection of propofol (<15 seconds) produces unconsciousness within how many seconds?

A

30 seconds
(Slide 35)

61
Q

A constitution of 1% solution of propofol is how many mg/mL?

A

10 mg/mL
(Slide 37)

62
Q

A constitution of 2% solution of propofol is how many mg/mL?

A

20 mg/mL
(Dr Castillo)

63
Q

A 1% constitution of propofol is made up of ____ soybean oil, _______ glycerol and _______ purified egg phosphatide (Lecithin).

A

10% soybean oil, 2.25% glycerol and 1.2% purified egg phosphate
(Slide 37)

64
Q

Your patient says they are allergic to eggs before their colonoscopy, what do you do next? You planning on giving them propofol?

A

You ask them what component of the egg they are allergic too. Propofol has lecithin in it, which comes from the egg yolk. If they are allergic to the egg whites you are good administer propofol!
(Dr Castillo)

65
Q

What are 3 disadvantages of using propofol?

A
  1. It supports bacterial growth!
  2. Causes increased triglyceride concentration (in prolonged IV infusions)
  3. Pain on injection
    (Slide 37)
66
Q

What is the generic component of propofol we use now?

A

Diprivan
(Dr Castillo)

67
Q

Ampofol is a commercial preparation of propofol, what two things did Castillo want us to know about it?

A
  1. Low lipid emulsion with no preservatives
  2. Higher incidence of pain on injection
    (Slide 38)
68
Q

Aquavan is a commercial preparation of propofol, what three things did Castillo want us to know about it?

A
  1. It is a prodrug that obviates pain on injection
  2. Its byproducts can cause unpleasant dysesthia! (An impulse from an ordinary stimulus can be unpleasant or painful)
  3. It has a slower onset, larger Vd, and higher potency!
    (Slide 38)
69
Q

What GABA receptors does propofol work on?

A

Alpha
(Slide 39)

70
Q

Is GABA the primary inhibitor NT in the brain?

A

Yes
(Slide 39)

71
Q

When propofol binds to GABA-A, what occurs?

A

There is a transmembrane chloride conductance increase! Which then causes hyper polarization of the postsynaptic cell membrane and functional inhibition of the postsynaptic neuron!
(Slide 39)

72
Q

T/F:
Immobility from propofol anesthesia is not caused by drug-induced spinal cord depression?

A

True!
(Slide 39)

73
Q

What is the conscious sedation dose for propofol?

A

25 - 100 mcg/kg/min
(slide 46)

74
Q

This GABA agonist is the drug of choice for brief GI endoscopy procedures.

A

Propofol
Also good to keep pts intubated/sedated in ICU.
(Slide 46)

75
Q

You use propofol as your choice for conscious sedation. What other kinds of meds will you give as adjuncts?

A

Versed, Opioids
(Slide 46)

76
Q

You use propofol as your drug of choice for conscious sedation. Besides the sleepiness, what are some additional effects of propofol?

A

Minimal analgesic and amnestic effects.
Prompt recovery without residual sedation.
Low risk of PONV.
Anticonvulsant.
Antiemetic.
Antipruritic.
Bronchodilator.
(Truly a wonder drug - slide 46)

77
Q

You thought zofran was good for PONV, well the real top dollar stuff is propofol! At what dose is propofol an antiemetic?

A

10 - 15 mg IV followed by a 10 mcg/kg/min infusion. This is also called the “sub hypnotic” dose.
(Slide 47)

78
Q

What is the MOA for the antiemetic effect of propofol?

A

Propofol depresses subcortical pathways and directly inhibits the vomiting center. (Slide 47)

79
Q

At what dose will wonder drug propofol cure your itchiness?

A

Antipruritic dose = 10 mg IV (slide 48)

80
Q

At what dose will Dr. Castillo’s favorite drug propofol stop your seizures?

A

Anticonvulsant dose = 1 mg/kg IV (slide 48)

81
Q

Will knocking yourself out with propofol help you breathe better?

A

Propofol is a bronchodilator! So it will help your airways open up, meaning it’s a good drug for COPD pts.

HOWEVER, if you give yourself a heaping dose, you will have depression of ventilation leading to apnea.

But hey, at least your airways are nice and open even if you forget to breathe in.
(Slide 48, 53)

82
Q

Things that red wine has in common with propofol: GABA agonist and potent anti_______.

A

Antioxidant (slide 48)

83
Q

Desflurane, isoflurane, sevoflurane, and succinylcholine can all do this one thing that propofol cannot.

A

Inhaled anesthetics and Succ can all trigger MH!! But propofol is a perfect angel of a drug and would NEVER do something so ratchet. (Slide 48)

84
Q

What is stage 2 of anesthesia known as and why?

A

Delirium stage and the most dangerous stage.
It is characterized by excitement, CV instability, dysconjugate ocular movements (exorcism), laryngospasm, and emesis. Response to stimulation is exagerrated and they be waking up choosing VIOLENCE

Slide 12

85
Q

What are the 5 components of Stage 3 of Anesthesia? Depression in all elements of nervous system function.

Im not really sure of a great way to ask this so feel free to change it but he said we need to memorize these

A

Stage 3 “Surgical Anesthesia”
Hypnosis
Analgesia
Muscle Relaxation
Sympatholysis
Amnesia

Slide 13

86
Q

Propofol’s effect on our CBF, CMRO2, ICP?

A

⬇️ CBF, CMRO2, ICP
(Slide 49)

87
Q

When would autoregulation of CBF and PaCO2 be affected by propofol?

A

Normally propofol maintains autoregulation, however if you give a giant dose this can cause a systemic drop in BP. Large enough drop in BP can cause a decrease in cerebral perfusion pressure and loss of autoregulation.

Anyways, keep MAP > 60 like you’ve been doing all your ICU career. (Slide 49)

88
Q

What EEG changes might be seen with propofol?

A

Per book…cortical EEG changes, same as thiopental. (Slide 49)

89
Q

Does propofol cause SSEP suppression?

A

No! Unless you add inhaled anesthetics or nitrous. (Slide 49)

90
Q

What sort of movement might you see with propofol going during induction/emergence?

A

Myoclonus (slide 49)

91
Q

What are the components of Stage 4 Anesthesia?

A

Stage 4 “Medullary Paralysis”
-Cessation of spontaneous respiration
-Cessation of Medullary cardiac reflexes
-All reflexes are absent
-Flaccid paralysis
-Marked hypotension with weak, irregular pulse
-May lead to death

*Too much anesthesia! Back er down a notch. *

Slide 14

92
Q

No question here but more of an FYI to go look at slide 50 of the induction ppt.

A

It’s a graph/table and readings of EEG. SO FUN. Enjoy 😊 (slide 50)

93
Q

What is important that the patient be able to perform for us to be able to extubate them?

A

-Follow commands
-Achieve appropriate respiratory goals (TV and rate)

Slide 15

94
Q

What is the usual pathway with emergence of anesthesia?

A

We go back the way we came. Stage 3 to Stage 1 to extubation and awake-fullness.

Slide 15

95
Q

What are the 4 induction drugs mentioned in lecture?

A

Barbiturates
Propofol
Etomidate
Ketamine
Slide 16

96
Q

What category of drugs are the GOLD STANDARD and we compare the properties of these to all of the other induction drugs?

A

Barbiturates

Slide 17

97
Q

How does propofol decrease your BP and SVR? In which conditions would this be much worse in?

A

Propofol will ⬇️ BP more than thiopental could. Propofol does this through inhibition of SNS and by decreasing intracellular Ca. No SNS or intracellular Ca —> no smooth muscle contraction —> vascular smooth muscle relaxation —> ⬇️ SVR.

This is especially worse in hypovolemia, elderly, LV compromise. (Slide 51)

98
Q

What are Barbiturates derived from and why are they not used anymore in anesthesia practice?

A

Derived from barbituric acid.

Used in lethal injection cocktail for capital punishment.

Slide 17

99
Q

When was Thiopental introduced?

A

1934

Slide 17

100
Q

Describe the mechanism of action of Barbiturates.

A

-Potentiate GABAa channel activity
-Directly mimics GABA
-Acts on gluatamate, adenosine, and neuronal nicotinic ACh receptors
-Cerebral vasoconstrictor
-Decreases CBF
-Decreases CMRO2 by 55%
-No analgesia (does have muscle relaxation and hypnosis per lecture)

Slide 18

-

101
Q

Why is it important for CBF and CMRO2 to be married and inseparable?

A

An increase in CMRO2 without increase in CBF = hypoxia

Increase in CBF without increase in CMRO2 = edema, increased ICP.

(important concept with any drugs we give in the OR per Castillo)

Slide 18

102
Q

A drug that induces a state of calm or sleep

A

Sedative
(slide 5)

103
Q

A drug that induces hypnosis or sleep

A

Hypnotic
(Slide 5)

104
Q

An anxiolytic is a drug that reduces ___________ and has sedation as a side effect

A

Anxiety
(Slide 5)

105
Q

Do sedative-hypnotics reversibly or irreversibly depress the activity of the CNS?

A

Reversibly
(Slide 5)

106
Q

State of drug-induced unconsciousness

A

General anesthesia
(Slide 5)

107
Q

What are the three main types of anesthesia?

A

General Anesthesia
Spinal/Local Anesthesia
Procedural Sedation/Conscious Sedation/Monitor Anesthesia Care (MAC)
(Slide 6)

108
Q

The administration of a combination of sedatives and analgesics to induce a depressed level of consciousness, allowing patients to tolerate unpleasant procedures and enabling clinicians to perform procedures effectively

A

Procedural Sedation or Conscious Sedation or MAC (monitored anesthesia care)
(Slide 6)

109
Q

What four organs are in the vessel-rich group?

A

Brain
Heart
Kidney
Liver
(Slide 7)

110
Q

True or False:
All medications that are given, no matter the route, can enter systemic circulation

A

True
(Slide 7)

111
Q

What four groups are drugs distributed to after administration?

A

Vessel-Rich Group (75% CO)
Muscle Group (18% CO)
Fat (5% CO)
Vessel-Poor Group (2% CO)
Slide 7

112
Q

What are the five components of general anesthesia?

A

Hypnosis
Analgesia
Muscle Relaxation
Sympatholysis
Amnesia
(Slide 8)

113
Q

In which stage of anesthesia do patients suffer from delirium?

A

Stage 2
(Slide 9)

114
Q

In stage 4 of anesthesia, ___________ paralysis can cause death

A

Medullary
(Slide 9)

115
Q

Which stage of anesthesia begins with the initiation of an anesthetic agent and ends with the loss of consciousness

A

Stage 1- Analgesia
(Slide 11)

116
Q

True or False: During stage one of anesthesia, patients can maintain protective reflexes, open their eyes, and breathe normally

A

True
(Slide 11)

117
Q

What are the three most significant airway reflexes?

A

Coughing, swallowing, gagging
(Slide 11)

118
Q

Define Partition Coefficient

A

the distribution of a given agent at equilibrium between two substances at a given temperature, pressure, and volume

Ex. 50% of sodium thiopentol is available in the arterial blood and 50% is available in the vessel rich poor group. Simply means they are at equilibrium

(slide 26)

119
Q

Describes the distribution of an anesthetic between blood and gas at the same partial pressure

A

Blood-gas coefficient

(slide 26)

120
Q

True or False
A higher blood-gas coef. (coefficient) correlates with a higher solubility of an anesthetic in blood and thus SPEEDING the rate of induction

The blood can be considered a pharmacological reservoir

A

FALSE - higher B-G coef correlates w/ a higher solubility of an anesthetic in blood and thus SLOWING the rate of induction

TRUE

PS. another important partition coef. is the fat-blood

(slide 26)

121
Q

This barbiturate has a lower lipid solubility than Pentothal. Which drug is it?
HINT: At a normal pH, it’s 76% non-ionized and it’s very lipid soluble and is rapidly metabolized by hepatocytes with induction doses

A

Methohexital

(slide 27)

122
Q

Wanda the witch CRNA gave her pt some Methohexital and now the pt won’t sit still because they keep doing what?

HINT: Try scaring the pt
Additional hint: It won’t matter regardless because you’re about to make them ride the lightening

A

Hiccups (or as Castillo spells it, Hiccoughs)
Also will induce myoclonus

Wanda the witch Hexed the pt with Hiccups

Also remember that Methohexital is most commonly used for Electro Convulsive Therapy (ECT)

(slide 27)

123
Q

Methohexital’s dose is?

Per Rectum dose is?

A

1.5 mg/kg IV

PR dose is 20-30 mg/kg (Wanda better buy me a drink first)

(slide 28)

124
Q

Does Methohexital induce SZ’s or ⬇️ SZ duration?

SZ = seizure

A

Trick question, it does BOTH

However it’s worth noting with cont’d infusions it will cause SZ’s in
1 out of 3 pt’s

Also ⬇️ SZ duration 35-45% in ECT pts compared to Etomidate (shocking)

(slide 28)

125
Q

Barbiturates cause what type of CV effects in a normovolemic pt?

A

in lieu of a 5 mg/kg induction dose of Thiopental
- transient 10-20 mmHg ⬇️ in SBP
- transient 15-20 bpm ⬆️ in HR

(slide 29)
(pic is from slide 30)

126
Q

If we give Barbiturates to a hypovolemic, CHF, or pt taking beta blockers, then we can expect a ____ __ ____________ response

A

Lack of baroreceptor

Castillo instead prefers to use Propofol or Etomidate for these pt populations

(slide 29)

127
Q

With this type of med, we can expect to see some Histamine release which is usually asymptomatic.

__________ can cause an anaphylactoid response upon consecutive exposures

A

Barbiturates

Thiopental can cause an anaphylactoid response in a pt who has been exposed to thiopental in the past.

(slide 29)

128
Q

Clifford the big red CRNA made a boo-boo and gave Thiopental to a pt who has been exposed to the drug in the past and is now rapidly developing an anaphylactoid response. What drugs should Clifford prepare ASAP?

A

Epi and if not effective then Vasopressin

(slide 29)

129
Q

Barbiturates cause dose-dependent depression of our ventilatory centers, therefore we need ______ levels of CO2 to trigger our pts medullary and pontine center to make our pts breathe _____________.

A

higher; spontaneously

(slide 31)

130
Q

A ventilated pt that was recently given barbiturates while under anesthesia but now needs to be prepared for emergence. We would want our pt’s CO2 level to be in the _______ range, and we can do that by either ______ the frequency of breathes OR _______ the Vt.

A

50-55 mmHg;
⬇️;
⬇️

(slide 31)

131
Q

Long question, engage thinking caps:

Arthur, the hasty CRNA, decides to administer a Barb. (barbiturate) to his pt and decides to just inject it via hypodermic needle into what he believes to be the pt’s Left AC vein. The pt is vented and sedated so no big deal. Suddenly the pt’s Left radial arterial line appears damp and the pt’s BP drops rapidly per the monitor. He also notices the left hand begin to turn blue. What did Arthur just do?

A

The dadgum iggit injected the barb in the pt’s artery which caused intense vasoconstriction and subsequently obscured the pt’s arterial line reading.

(Oddly enough, Arthur has done this before and knew to quickly double check the BP via cuff on the opposite arm. He also quietly pressure wrapped the errored site and casually removed the arterial line since the event left it worthless anyway. Dr. Fuknutz won’t notice anyways)

But he forgot something!!!! Look out for the other notecard to find out what!

(slide 32)

132
Q

What’s the treatment in the event you let Arthur, the hasty CRNA, help you with a case and he injects a barb. into your pt’s artery?

A

Inject a vasodilator like Lidocaine or Papaverine (side note: Arthur likes to be called daddy - weeeeeiiiiirrrrddddooooo) to sustain adequate blood flow

(slide 32)

133
Q

You are called to emergently intubate a pt. The pt’s BP is crashing and they’re having a severe asthma attack. You choose ketamine to induce the pt. The med student asks why you chose ketamine. So, why did you choose ketamine?

A

Ketamine stimulates sympathetic activity and is an excellent bronchodilator! Therefore your pt’s BP will increase and their breathing will improve.

This is a great drug for acutely hypovolemic pts, will not worsen hypovolemia. (Slide 30)

134
Q

Papaw finally got that chest pain worked up, turns out he needs a quadruple bypass!! Now!! As the highly paid bartender of the OR, what cocktail are you gonna mix up for Papaw to put him to sleep for surgery?

A

Diazepam 0.5 mg/kg IV
Ketamine 0.5 mg/kg IV
continuous Ketamine drip 15 - 30 mcg/kg/min IV
(Slide 30)

135
Q

What type of patients would you consider IM Ketamine?

A

Pediatric pts, All age groups - uncooperative/difficult to manage pts (like with dementia). (Slide 30)

136
Q

Outside of the OR, what might you use Ketamine for? (4 uses, Dr Castillo’s friend in Jacksonville makes money treating some of these)

A

1) Sedation/analgesia for burn dressing changes, debridement, skin grafting
2) Wean off of opioids/reversal of opioid tolerance (ketamine clinic)
3) Trt psych disorders such as depression, PTSD, OCD (ketamine clinic)
4) Restless Leg syndrome - PO dose
(Slide 31)

137
Q

Giving Ketamine to a pt with pulmonary HTN can increase the pulmonary HTN by how much %?

A

44%!!! Gonna need some viagra stat after all that ketamine (Slide 31)

138
Q

You should double check yourself before you give Ketamine to patients with either of these 2 conditions.

A

Caution in pts with pulmonary HTN, Neuro pts with increased ICP. (Slide 31)

139
Q

Ketamine will do what to your CBF?

A

Ketamine is a cerebral vasodilator so CBF ⬆️ by 60% —> ⬆️ ICP.

This effect does have a limit…Once you reach doses of 0.5 - 2mg/kg IV, ICP will not increase further. (Slide 32)

140
Q

Ketamine has what effect on EEG and SSEP?

A

EEG: excitatory activity, does not alter seizure threshold. Myoclonus will occur.

SSEP: increases amplitude of signal, this is reduced with N2O.
(Slide 32)

141
Q

Ketamine leads to an increase in the plasma levels of what 2 NTs?

A

Epi, Norepinephrine (slide 33)

142
Q

Ketamine can stimulate SNS activity, so you will see an increase in which vitals? What type of anesthetic meds might negate this activity?

A

Sys BP, Pulm Art Pressures, HR, CO, MRO2

Benzos, inhaled anesthetics, and N2O can blunt the SNS response
(slide 33)

143
Q

Your pt has been snoozing on a ketamine infusion, but suddenly their BP and CO drops!! And it’s actually not the surgeon’s fault this time. WTF happened? Could you give ephedrine to fix the problem?

A

Ketamine stimulates SNS activity…which in turn can deplete your catecholamine stores if your body can’t replenish them. No catecholamines = No NE/EPI = no BP or CO.

An indirect acting vasoconstrictor like ephedrine would be terrible to give in this pt! Might as well spray holy water on them and hope for the best.

They need a direct acting vasoconstrictor like phenylephrine to help them out. (Slide 33)

Anesthesia Pharmacology (20 decks)

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