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Anes 516: Pharmacology > Lecture 5: Non-barbiturates > Flashcards

Lecture 5: Non-barbiturates Flashcards

1
Q

What is the drug name of propofol? Where does that abbreviation come from?

A

Diprivan

2,6 diisopropynlphenol

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2
Q

In an aqueous solution, propofol is:

A

insoluble

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3
Q

What percentage of the white solution that you inject into your patient is actually propofol?

A

1%

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4
Q

Mechanism of action for propofol?

A

It works similarly to barbiturates; it decreases dissociation of GABA to its receptor, so keeps Cl- channels open to hyperpolarize cell and decrease neurotransmission.

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5
Q

Distribution half-life of propofol?

A

2-8 minutes

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6
Q

Why must you stop propofol infusions after three days?

A

Lipids build up in circulation to cause hyperlipidemia

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7
Q

Why can propofol cause green urine?

A

Thiol ring

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8
Q

Why don’t patients wake up feeling hungover on propofol like they do on thiopental?

A

The half life of propofol is so short, meaning that by the time the drug as redistributed in the tissues, prompting the patient to wake up, the vast majority of the drug has already been excreted from the body.

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9
Q

Although propofol is principally metabolized by the liver, what proportion of a dose is metabolized in the lung via first-pass metabolism?

A

30%

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10
Q

Why do patients wake up so quickly on propofol?

A

Redistribution to tissues with no GABA receptors

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11
Q

How should you adjust your propofol doses in patients with liver or kidney failure?

A

No need to adjust; effect is redistribution-dependent, not metabolism-dependent

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12
Q

How much less propofol do elderly patients require? Why?

A

25-50% less because they have a smaller central distribution volume and decreased clearance

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13
Q

Does propofol have any effect on the fetus of a pregnant mother?

A

While propofol does cross the placenta, it doesn’t have any effect on the fetus d/t its mechanism of metabolism.

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14
Q

Ideally, propofol induces a decrease in CBF and CMRO2, but it doesn’t affect ICP. However, at what point are we concerned propofol’s effect on ICP?

A

If ICP increases too high, our brains will compensate by decreasing CBF and decreasing MAP; therefore, there will be a decrease in CPP.

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15
Q

What is an appropriate dose for a GA TIVA? How can we ensure that TIVA level is sufficient

A

100-200 mcg/kg/min

Use a BIS to ensure sufficiency

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16
Q

What are some less common uses of propofol?

A

1) Antiemetic effect
2) Antipruritic effect
3) Anticonvulsant effect
4) Attenuation of bronchoconstriction

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17
Q

In what way does proprofol have an anticonvulsant effect?

A

It decreases dissociation of GABA, an inhibitory neurotransmitter–therefore, it decreases excitatory activity that brings about seizures

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18
Q

Etomidate is like midazolam in solution in that:

A

it is water soluble, but when it sees physiological pH, it becomes lipid soluble

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19
Q

Why is etomidate so painful upon injection?

A

Its composition is 35% glycerol–burns when it hits the blood.

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20
Q

How much more glycerol does etomidate contain than propofol?

A

17x more in etomidate than in propofol

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21
Q

Of the racemic mixture that etomidate exists as, how many isomers are active?

A

Only one

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22
Q

What is the reticular activating system and how does etomidate affect it?

A

It’s the part of the brainstem that mediates awareness, and etomidate suppresses it, causing you to go to sleep.

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23
Q

In addition to affecting the RAS, etomidate also works on:

A

GABA and GABA receptors

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24
Q

Onset, peak, and duration of etomidate?

A

Onset: 30 sec
Peak: 1 minute
Duration: 3-5 minutes

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25
Q

What proportion of etomidate will be bound to protein within the body?

A

78%

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26
Q

What is the half-life of etomidate?

A

2.6 hours

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27
Q

What type of metabolism does etomidate undergo? Where? By what enzymes?

A

Hydrolysis in the liver by plasma esterase and cyt P450

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28
Q

How is etomidate eliminated?

A

Via the kidneys

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29
Q

By what percent does etomidate decrease CBF and CMRO2?

A

35-45%

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30
Q

Why do we not use etomidate on seizure patients while we are mapping seizures out?

A

Etomidate causes excitatory spikes in EEG that resemble those that a seizure would produce. May ruin data.

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31
Q

What do we mean when we claim that etomidate is cardiovascular stable?

A

We mean that it produces minimal cardiovascular effects; while there are still effects, they are not nearly as severe as those of propofol.

32
Q

Does etomidate suppress ventilation?

A

Yes.

33
Q

Which induction drug produces myoclonus? What is myoclonus?

A

Etomidate; myoclonus is brief, involuntary twitching of a muscle or a group of muscles–larger movement than fasiculations

34
Q

By what mechanism does etomidate suppress adrenocortical activity?

A

It inhibits 11-beta hydroxylase enzyme, which is integral to corticoid synthesis

35
Q

How many doses of etomidate required to suppress adrenocortical activity?

A

One dose

36
Q

Why is etomidate a good choice for septic patients?

A

They are already so vasodilated that propofol would only potentiate the cardiovascular issues they have.

37
Q

Which induction drug is a derivative of PCP?

A

Ketamine

38
Q

What class of drug is ketamine?

A

Phencylclidine

39
Q

What receptors are ketamine’s main targets?

A

1) NMDA
2) Opioid receptors (analgesic effect)
3) MAO
4) Muscarinic (causes salivation)

40
Q

How do we avoid emergence delirium in our patients who receive ketamine?

A

Administer a sub-anesthetic dose and use in conjunction with other drugs, like propofol

41
Q

What kind of receptor is an NMDA receptor? How does ketamine affect it?

A

NMDA receptor = glutamate receptor

Ketamine prevents receptor from binding to glutamate.

42
Q

Which induction agent is most beneficial in post-thoracotomy phase?

A

Ketamine

43
Q

Unlike all other induction drugs, ketamine does not:

A

act on GABA receptors

44
Q

Ketamine inhibits MAO, which causes:

A

increased levels of serotonin and dopamine in the brain.

45
Q

Onset and duration of IV ketamine?

A

Onset: 30 seconds
Duration: 5 - 10 minutes

46
Q

Onset and duration of IM ketamine?

A

Onset: 3 - 4 minutes
Duration: 12 - 25 minutes

47
Q

Elimination time of ketamine:

A

2.5 hours

48
Q

Where is ketamine metabolized? By?

A

In the liver by cyt P450

49
Q

What is the metabolite of ketamine? Active or inactive?

A

Norketamine; active

50
Q

How is ketamine eliminated from the body?

A

Renal

51
Q

How does low-dose ketamine affect somatic vs. visceral receptors?
Why the difference?

A

While low-dose ketamine seems to relieve both pain and intensity in visercal receptors (located in thorax, abdomen, etc.), it seems to only alleviate pain–not intensity–in somatic areas of the body (musculoskeletal areas). This is likely because NMDA receptors play different roles in these tissues.

52
Q

How does low-dose ketamine compare to morphine in epidural/spinal situations?

A

10,000x less potent than morphine

53
Q

When used for epidurals and spinals, what receptors does ketamine target?

A

Mu receptors

54
Q

How long does it take for a patient to lose consciousness with IV ketamine?
What about IM?

A

IV ketamine: 30 seconds

IM ketamine: 2-4 minutes

55
Q

What is ketamine’s effect on CMRO2 and CBF?

A

Increases them both

56
Q

What is ketamine’s effect on ICP?

A

Increases ICP

57
Q

In terms of EEG, what effect does ketamine produce?

A

Excitatory

58
Q

What induction drug can be used for somatosensory evoked potential (SSEP) monitoring?

A

ketamine

59
Q

In what way does ketamine increase secretions?

A

Increases activity of salivary and tracheobronchial mucus glands

60
Q

Ketamine can have antagonistic effects on muscarinic receptors. How does this effect blood pressure, heart rate, and cardiac output?

A

It increases them

61
Q

Why shouldn’t you use ketamine unopposed in a bad heart?

A

It is a myocardial depressant

62
Q

How do you prevent emergence delirium in patients?

A

Use benzos w/ ketamine

63
Q

Who are most likely to develop emergence delirium?

A

1) Kids
2) Women
3) Pyschiatric patients

64
Q

In what patients would ketamine be a good choice?

A

1) Children
2) Asthmatics
3) Patients w/ chronic pain

65
Q

In what patients would ketamine be a poor choice?

A

1) Patients w/ increased ICP
2) Patients w/ increased IOP
3) Patients w/ ischemic heart disease (as sole agent)
4) Patients w/ vascular aneurysm
5) Psychotic patients

66
Q

What percent of a dose of ketamine is bound to protein?

A

27%

67
Q

Duration of ketamine?

A

10-15 min

68
Q

Duration of propofol?

A

4-8 min

69
Q

Duration of etomidate?

A

4-8 min

70
Q

What class of drug is dexmedetomidine?

A

short-acting alpha-2 agonist (sympathomimetic)

71
Q

Which non-barbiturate possesses anxiolytic, anesthetic, analgesic, and hypnotic properties?

A

Dexmedetomidine

72
Q

Why isn’t dexmedetomidine often used for MACs?

A

Slow onset

73
Q

Bolus dose of dexmedetomidine?

A

1 mcg/kg over 10 minutes

74
Q

Why must we dose slowly when dosing dexmedetomidine?

A

Can cause bradycardia and hypotension

75
Q

What is the infusion rate of dexmedetomidine?

A

0.2 - 0.7 mcg/kg/hr

76
Q

If patient presents with Addison’s disease, which non-barbiturate is contraindicated?

A

Etomidate b/c patient already has low levels of steroids

Anes 516: Pharmacology (5 decks)

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