Lecture 6 (Exam 2)- Induction Drugs (Part 2) Flashcards

1
Q

Which induction agent has the highest analgesic properties?

A

Ketamine
(Slide 40)

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2
Q

What is Ketafol?

A

Ketamine + Propofol in one syringe… Risky.
(Slide 41)

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3
Q

Compounding, combining, admixing, diluting, pooling, reconstituting, repackaging, or otherwise altering a drug or bulk drug substance to create a sterile preparation is…

A

Sterile Compounding
(Slide 42)

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4
Q

If your patient is tachycardic and hypertensive, would you give Ketamine or Propofol?

A

🌶️ Propofol. Remember it has bradycardia and HOTN results.

Ketamine would worsen tachycardia and HTN.

-Example at end of lecture

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5
Q

What is Ketamine’s (Ketalar) onset IV?

IM? Why would we give it this route?

A

IV: RAPID! ⚡️ 30-60 secs
IM: 2-5mins - better for pediatrics w/ no IV. 👶🏽

Slide 25 & 28

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6
Q

What is Ketamine’s duration of action?
What cases would it be good for?

A

10-20 mins; good for short cases and/or outpatient procedures.

Slide 25

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7
Q

Ketamine is highly lipid soluble (5x -10x more potent > Thiopental) & not plasma bound.

What does this mean for it’s Vd and E 1/2 time?

A

It would have a very high Vd (3L/kg) but a lower E1/2 time (2-3hrs).

Slide 25

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8
Q

Ketamine’s Vd is 3L/kg (large), what does this mean for its clearance?

What is it metabolized by?

A

It is fast! Hepatic clearance 1L/min!

Metabolized: CYP450! 😃

Slide 26

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9
Q

What is Norketamine?

A

The active metabolite of Ketamine.
It is 1/3 as potent

Slide 26

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10
Q

What is the induction dosage of Etomidate?

A

0.3 mg/kg

(0.2-0.4 mg/kg as per book –> for the exam, the answers will be in this range.)

Slide 10

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11
Q

_______ is alternative to propofol or barbiturates for IV induction of anesthesia and does not have hangover or cumulative drug effect.

A

Etomidate
( unlike barbiturates, it does not stay in fat and redistribute itself; etomidate clearance is faster than barbiturates.)
Slide 10

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12
Q

Which induction drug is best with unstable cardiovascular system especially with low EF?

A

Etomidate
Slide 10

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13
Q

What patient population is susceptible to Ketamine tolerance?

What can we do to adjunct this?

A

Burn patients :(

We can use Multi-Modal anesthesia
(Gabapentin, Motrin, Mg, IV Tylenol, Lidocaine gtt)

Slide 26

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14
Q

List the following doses for Ketamine:

  1. Induction dose, IV & IM
  2. Maintenance dose, IV & IM
    (*HINT: IM is the same dose)
A

Slide 27

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15
Q

You decided to pick up an ICU BEDSIDE contract during your online semester of CRNA school & asked to give an IV Ketamine bolus to your wild’n’out patient. 🤪

1) Your doc orders a measly 0.1mg/kg and you look at him with disgust & bluntly tell him the normal range for Ketamine is ___ - ___ here in the ICU.

2) Your patient rips out her IV seconds before you can administer the IV dose.
Looks like she is getting it IM…what is your dose range?

A

IV: 0.2 - 0.5 mg/kg
*This is the same amount of our IV maintenance dose.

IM: 4 - 8mg/kg

Slide 27

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16
Q

You are a saint of a CRNA and decide to go into Pediatric Cardiac surgery. ❤️‍🩹

What is the gtt range of a Ketamine infusion?
This is also the same dose for post-op sedation & analgesia.

A

Slide 27

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17
Q

who do you give etomidate to: 45 y/o patient with EF <40% and with a lot of other comorbidities or 70 y/o patient with EF>65% and runs 5 miles a day?

A

45 y/o patient with EF <40%
Slide 10

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18
Q

Do you need to give analgesia if you give etomidate to the patient?

A

Yes, Etomidate does not have an analgesic effect.
(Acc. to Dr. Castillo, remember you have to use analgesic when you perform direct laryngoscopy and tracheal intubation because they need to be in stage 3.)
Slide 10

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19
Q

How does Etomidate cause an involuntary myoclonic movement?

A

Alters in the balance of inhibitory and excitatory influences on the thalamocortical tract.
Slide 11

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20
Q

What percentage is the myoclonic activity of etomidate?

A

50% to 80%
(17% thiopental, 13% methohexital and 6% propofol)
Slide 11

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21
Q

How can involuntary myoclonic movements be attenuated?

A

By administration of opioids or benzos prior to administration of etomidate.
Slide 11

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22
Q

We need to be cautious when giving etomidate to what type of patient?

A

Patient with seizure disorder
Slide 11

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23
Q

Fentanyl 50mcg/ml is available. The Patient is 75 kg. Administer Fentanyl 1 mcg/kg to attenuate myoclonus. How many mls will you administer?

A

1.5 mls
(Desired/Available = Quantity; Desired = 75 Kg * 1 mcg/kg = 75 mcg)
Slide 12

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24
Q

Etomidate causes ______________ ___________ to stress response.

A

Adrenocortical suppression
(During stress, SNS is activated; ↑HR, ↑ BP)
slide 13

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25
Q

What happens when you do not respond to normal stress responses due to etomidate administration?

A

Severe hypotension and longer mechanical ventilation hours.

Slide 13

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26
Q

With Ketamine, Is the ventilatory response to CO2 maintained?

A

Yes!

(but could increase no more than 3mmHg CO2)

(slide 35)

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27
Q

With Ketamine, IF the PaCo2 were to increase, how much would it increase by?

A

no more than 3mmHg

(slide 35)

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28
Q

With Ketamine, are the upper airway skeletal muscle tone and reflexes maintained and intact?

A

Yes!

(slide 35)

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29
Q

Your prego patient needs a one shot dose of Ketamine into her epidural space. 🤰What is the range?

What is the Intrathecal dose range?

A

Epidural: 30mg (one time dose)

IT: 5 - 50mg in 1ml NS (I am checking with Castillo bc the book contradicts this stating it should be in 3 mls)

pg. 343, PDF Stoeltings Pharm book
Slide 27

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30
Q

How long does inhibition of enzyme required to convert cholesterol to cortisol lasts following the administration of etomidate?

A

4 to 8 hours
(Make sure you look at graph on slide 14)
Slide 13

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31
Q

Why is Ketamine called “angel dust”?

A

Because it is a Phencyclidine derivative. 🍦
(Slide 20)

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32
Q

Will we see an increase or decrease in the amount of salivary and tracheobronchial mucous gland secretions with Ketamine?

A

Increase!

(so it is important to give something to subdue or decrease the amount of secretions- Dr. C said “Glycopyrrolate”

(slide 35)

33
Q

T/F:
Ketamine has amnestic and intense analgesic properties.

A

True
(Slide 20)

34
Q

Does Ketamine induce histamine release?
What does it do to the Bronchioles?

A

No histamine release and it is a GREAT Bronchodilator

(slide 35)

35
Q

Referring to Ketamine, what is meant by dissociative anesthesia?

A

It resembles a cataleptic state (a trancelike state marked by loss of voluntary motion in which the limbs remain in whatever position they are placed) in which the eyes remain open with a slow nystagmic gaze (an involuntary eye movement which may cause the eye to rapidly move from side to side, up and down, or in a circle, and may slightly blur vision.)
“It is like talking to a sloth, or in slow motion. The eyes are open but when you know no one is home. They are in their own little world; it disconnects them from reality.”

(Slide 20)

36
Q

Is Ketamine good to use in a smoker or patients with COPD/asthma?

A

Yes!
It is a great bronchodilator and does not release histamine

(slide 35)

37
Q

What is an antisialagogue?

Why would we give one with Ketamine?

How many syllables does it have?

What is the example med and dose Castillo gave us in lecture?

A

Antisialagogues are anticholinergic drugs. (Scopolamine, atropine, etc.)

https://youtu.be/UnOfb3E812g
Lolz, I think it has 5.

Glycopyrrolate, 0.2mg > atropine/scopalamine

Slide 28
pg. 342 PDF Stoletings Pharm book

38
Q

You give your patient Ketamine, what are some signs and symptoms that they are experiencing dissociative amnesia?

A

They are non-communicative, or they do not answer questions appropriately, but wakefulness is present.
Hypertonus, muscle overactivity that occurs when communication between the brain and spinal cord is affected by injury or illness.
Purposeful skeletal muscle movements. (Soft restraints might be needed sometimes)

39
Q

What is a major side-effect we worry about with Ketamine?
What causes this?

A

Emergence Delirium
Due to its Psychedelic Effects

(slide 36)

40
Q

What are some advantages Ketamine has over Propofol and Etomidate?

A
  1. Lipid emulsion vehicle is not required which means there is no pain @ injection site.
  2. Profound analgesia at sub-anesthetic doses (0.25-0.35 mcg/Kg -Castillo)
  3. Can be used for withdrawals
    (Slide 21)
41
Q

The “Psychedelic Effects” seen with the admin of Ketamine affects what percentage of patients?
And how long can these effects last up to?

A

5-30% of patients
Last up to 24 hours

(slide 36)

42
Q

When would you expect your patient to return to consciousness after giving a bolus of IV Ketamine?

Full consciousness?

A

You got 10 - 20 mins to party while they out. 🕺🏻💃🏾

Full consciousness 60-90mins (they have amnesia during this time)

Slide 28

43
Q

What are the s/sx of the “Psychedelic Effects” seen with the admin of Ketamine?

A

visual, auditory, proprioceptive, and confusional illusions = delirium.
Morbid & vivid dreams (in color) and hallucinations

(slide 36)

44
Q

What are two disadvantages of using Ketamine?

A
  1. Frequency of emergence delirium
  2. Abuse potential
    (Slide 21)
45
Q

What is the MOA of the Psychedelic Effects seen with Ketamine?

A

due to the depression of the inferior colliculus and medial geniculate nucleus that is responsible for separating fantasy from reality.

(slide 36)

46
Q
A

5mls total! You add 4mls…to the 1ml.

47
Q

Ketamine uses the preservative Benzethonium Chloride. What is the effect of this preservative in the human body?

A

it causes inhibition of the nicotinic ACh receptors!
It causes sympathetic nervous system stimulation!
Not a stable idea CV wise… ☠️
(Slide 21)

48
Q

Is S-Ketamine (+) or R-Ketamine (-) preferred?
Why?

A

S-Ketamine the left handed optical isomer is preferred over R-Ketamine the right handed optical isomer because:
1. It has more intense analgesia
- 2x greater than racemic
- 4x greater than R-Ketamine
2. More rapid metabolism and recovery
3. Lower incidence of emergence reactions
4. Less salivation 👅💦
(Slide 23)

49
Q

To prevent the Psychedelic Effects seen with Ketamine Administration, what do we do/give?

A

Admin Benzodiazepine IV 5 min prior to Ketamine admin.

(slide 36)

50
Q

What 2 Medications do we always give prior to giving Ketamine?

A

Benzodiazepine (to prevent psychedelic effects
Glycopyrrolate (to decrease secretions)

(slide 36)

51
Q

What are 4 things to consider when using racemic Ketamine?

A
  1. Inhibit uptake of catecholamines back into the postganglionic sympathetic nerve endings
    -Cocaine-like effect
    -Avoid in patients with: CAD, A-fib, SVT, Hx of V-fib, or ST/NST MI.
  2. Less fatigue
  3. Less cognitive impairment
  4. Part of the multimodal technique
    (Slide 23)
52
Q

What receptors does Ketamine bind to?

A

It binds non-competitively to N-methyl-D-aspartate (NMDA) receptors.
(Slide 24)

53
Q

What is glutamate?

A

It is the most excitatory neurotransmitter in the CNS!
Glycine is an obligated co-agonist!
(Slide 24)

54
Q

Ketamine _______ activation of the NMDA receptors by glutamate and _______ the presynaptic release of glutamate.

A

Inhibits, decreases
(slide 24)

55
Q

Does Ketamine have a strong or weak action on the GABA-A receptor?

A

Weak!
(Slide 24)

56
Q

What other receptor sites, besides NMDA, does Ketamine work on?!

A

Opioid (µ, δ, and κ; weak σ)
monoaminergic, voltage-sensitive sodium, L-type Ca++ channels,
muscarinic & neuronal nicotinic acetylcholine.

*Think about what else Ketamine does…
(Slide 24)

57
Q

What 3 things does Ketamine inhibit?
And what are the results from these inhibitions with consideration to our muscle relaxants?

A
  • Inhibits platelet aggregation (results in increased bleeding)
  • Inhibits cytosolic free calcium concentrations (results in enhanced non-depolarizing neuromuscular blocking drugs (NMBDs)
  • Inhibits plasma cholinesterase (results in increase of Succinylcholine which will prolong paralyzation and apnea)

(slide 37)

58
Q

Can you administer Ketamine in patients with asthma and pulmonary hypertension?

A

(Trick question)
Yes for asthma- great bronchodilator
but NO for Pulmonary Hypertension (pg. 344)

59
Q

What are 3 drug that react with Ketamine?
And what are the interactions?

A
  • Volatile anesthetics- causes hypotension
  • NDNMB drugs “ronium”- enhances these drugs effects
  • Succinylcholine- prolongs its effects.

(slide 38)

60
Q

_________ is a potent direct cerebral _______________, as it _________ ICP.
HINT: Similar to Thiopental

A

Etomidate; vasoconstrictor; decreases

(slide 15)

61
Q

Etomidate decreases CBF to __% and CMRO2 to __%.

CMRO2 (Cerebral Metabolic Rate of Oxygen) can also be referred to as CMRG which stands for?

A

35%; 45%

Cerebral Metabolic Rate of Glucose

(slide 15)

62
Q

_________ produces similar EEG changes as Thiopental, except more frequent __________ spikes.

This med also ______ seizure threshold so that means seizure foci may be __________.

This med may augment amplitude of _____________ ______ _________ monitoring, therefore this drug is not ideal with this type of monitoring.
What med would be a better alternative?

A

Etomidate; excitatory

lower; activated

Somatosensory Evoked Potential (SSEP)

Propofol is a better alternative for this type of monitoring

(slide 15)

63
Q

Etomidate is the most _____ stable induction agent with minimal changes to which factors?
(This means Etomidate is ideal for pts with an EF of < 40-50%.)

However, we could still see a mild ⬇️ to ____ with normovolema..

We would see sudden hypotension w/ _________, especially at what induction dose?

A

cardiovascular;
HR, SV, CO, and contractility

SVR

hypovolemia; We see this at an induction dose of 0.45 mg/kg IV (higher than normal)

(slide 16)

64
Q

True or False:

Etomidate causes intra-arterial damage.

Etomidate causes vein irritation and/or pain upon injection.

Etomidate does NOT release histamine

A

FALSE - Etomidate does NOT cause intra-arterial damage

TRUE - per Castillo

TRUE - no histamine release

(slide 16)

65
Q

Which induction med causes LESS ventilation depressant than barbiturates?
Why is this?

Just remember though, RAPID IV injection will still cause a little _____.
So start LOW and give SLOW

A

Etomidate because it has RAPID clearance (think Etomidate as the speed dating induction med - exciting at first but that excitement rapidly wears off)

APNEA
(Jerry from speed dating took your breath away…until he said he still lived with his mom)

(slide 17)

66
Q

What is the Minute Ventilation formula?

Etomidate causes our _____ ______ to ⬇️ which is then offset by compensatory _________ in frequency of ___________ ____. (Transient 3-5 mins)

This reflex is all d/t the stimulation of CO2 _________ _______. (might not start breathing until EtCO2 hits 50 mmHg)

A

Minute Ventilation formula = Vt x RR

tidal volume (Vt); ⬆️ ; respiratory rate (RR)

medullary centers

(slide 17)

67
Q

What lesson was Dr. Castillo teaching us when comparing Brevital and Pentothal?

A

That there are other factors in play other than lipid solubility.
Brevital has a lower lipid solubility than Pentothal but it is more non-ionized than Pentothal.

Anesthesia can have grey areas.

Slide 5

68
Q

What are the Cardiac Output percentages for the 4 groups of the body?

A

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

Slide 6

69
Q

Adipose tissue has a _______ vascular supply

A

decreased

Slide 6

70
Q

Etomidate is _______ at physiologic pH and ______ at an acidic pH.

A

lipid soluble
water soluble

slide 8

71
Q

T/F Etomidate contains 15% propylene glycol and causes pain and irritation in the injected vein.

A

False.
Its 35% :)

slide 8

72
Q

Etomidate causes a high incidence of _________.

A

Myoclonus

slide 8

73
Q

What is the only drug with direct systemic absorption in oral mucosa that bypasses hepatic metabolism?

A

Etomidate

slide 8

74
Q

What is the MOA of Etomidate?

A

Selective modulator of GABAa receptors

Will probably be a test question

Slide 9

75
Q

What is the onset of Etomidate and what is the amount bound to albumin?

A

1 minute s/p IV injection
76% albumin bound

Slide 9

76
Q

How much faster is the clearance of Etomidate compared to Thiopental?

A

5x

Faster clearance offsets the large Vd.
Faster clearance = more prompt awakening

Slide 9

77
Q

Elimination half-time of Etomidate

A

2-5 hours

Slide 9

78
Q

Etomidate is metabolized by what?

A

hydrolysis by hepatic microsomal enzymes and plasma esterases.

Slide 9

79
Q

Areas and percentages of elimination of Etomidate.

A

85% in urine
10%-13% in bile

Slide 9