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Anesthesia MM/TL > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

What is th MOA of ketamine?

A

NMDA receptor antagonist
Inhibits post synaptic receptors in the spinal cord
Dissociates the thalamus (sensory impulses) from the limbic system (awareness)

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2
Q

When are peak plasma levels of ketamine achieved when injected IM?

A

10-15 minutes

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3
Q

How lipid soluble is ketamine?

A

More so than thiopental and less protein bound so very fast brain uptake

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4
Q

What is distribution half life of ketamine?

A

10-15 minutes

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5
Q

How is ketamine biotransformed?

A

In the liver

It has a high elimination half-life

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6
Q

How are the end products of ketamine excreted?

A

Renally

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7
Q

What are the CV effects of ketamine?

A

Increase Bp, CO, HR, PAP, myocardial work

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8
Q

How does it cause the CV effects it causes?

A

By inhibiting the reputable of norepinephrine

By stimulating the central sympathetic nervous system

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9
Q

What does ketamine do to the heart at high doses?

A

It is a direct myocardial depressant by inhibition calcium

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10
Q

How is ventilatory drive affected with ketamine?

A

Minimal unless administered with opioids

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11
Q

What are the respiratory effects of ketamine?

A

Potent bronchodilator

Increased secretions

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12
Q

What are the cerebral effects of ketamine?

A

It increases CBF, CMRO2, and ICP except with BZDs

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13
Q

What does diazepam do to ketamine?

A

Prolongs it’s half-life

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14
Q

What does diazepam and midazolam due to ketamine’s cardiovascular effects?

A

it attenuated the cardio stimulators effects

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15
Q

What anesthetics does ketamine act synergistically?

A

Volatile anesthetics

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16
Q

What anesthetics is ketamine additive with?

A

Propofol, BZDs, GABA agents

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17
Q

What happens when using alpha and beta antagonists with ketamine?

A

The myocardial depressant effects are unmasked

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18
Q

What is the MOA of etomidate?

A

Depresses the RAS and mimics GABA

Disinhibition of the extra pyramidal tract

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19
Q

What are the side effects of etomidate?

A

Adrenal insufficiency
Myoclonus
PONV

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20
Q

What is unique about the structure of etomidate?

A

It has an imidazole ring like midazolam that gives it water solubility in acidic solutions?

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21
Q

What does etomidate have to be injected with?

A

Propylene glycol because it is water soluble in acidic solutions

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22
Q

What is the consequence of injecting with propylene glycol?

A

It burns

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23
Q

How is etomidate rapid onset?

A

Highly lipid soluble at physiologic ph

Large nonionized fraction

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24
Q

How is etomidate biotransformed?

A

Hepatic enzymes and plasma esterases

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25
Q

How is etomidate excreted?

A

In the urine

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26
Q

What are the CV effects of etomidate?

A

Mild reduction in peripheral vascular resistance

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27
Q

What are the cerebral effects of etomidate?

A

Decreases CMR, CBF, ICP

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28
Q

What are the endocrine effects of etomidate?

A

Inhibition of the synthesis of cortisol and aldosterone

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29
Q

What does fentanyl do to etomidate?

A

It increases the plasma level and prolongs the elimination half-life of etomidate

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30
Q

What drugs decrease the myoclonus caused by etomidate?

A

Opioids

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31
Q

What is the MOA of Propofol?

A

It facilitates the inhibitory signals of GABA and increases the binding affinity for GABAa receptor.

32
Q

Why must Propofol bottles be used in 6 hours?

A

Because the formulation can grow bacteria

33
Q

How quickly do people wake up from Propofol and why?

A

2-8 minutes due to short initial distribution half-life

34
Q

What is a determining factor in the amount of Propofol to use in a TIVA?

A

Age

35
Q

How is Propofol biotransformed?

A

In the liver and other sites

Excreted in Urine

36
Q

What is Propofol infusion syndrome?

A

Metabolic acidosis
Lipemia
Death
Green urine

37
Q

What are the CV effects of Propofol?

A

Decreased BP
Impaired barorerceptor response
Increase coronary sinus lactate

38
Q

What are the factors associated with Propofol induced hypotension?

A

Age
Large doses
Rapid injection

39
Q

What are the respiratory effects of Propofol?

A

Apnea
Histamine release (but less bronchospasm than etomidate or barbs)
Inhibits hypoxia vent drive

40
Q

What are the cerebral effects of Propofol?

A

Decrease CBF and ICP

Also, decreases CPP due to its effect on BP

41
Q

What does Propofol do to intraocular pressure?

A

Decreases it

42
Q

What is the loading dose of dexmedetomidine

A

0.5-1mcg/kg over 10 minutes

70 kg person = 35-70 mcg

43
Q

What is the infusion rate of dexmedetomidine

A

0.4-1.2 mcg/kg/HR

44
Q

What is the terminal half life of dex?

A

2 hours

45
Q

What are the side effects of dex?

A

Hypotension
Bradycardia
Heart block

46
Q

What properties does dex have?

A

Hypnotic
Analgesic
Opioid sparing
Minimal respiratory depression

47
Q

What is the mechanism of action of dexmedetomidine?

A

Alpha 2 agonist

Imidazoline agonist

48
Q

How does dexmedetomidine differ from clonidine?

A

It is 8 times more specific at the alpha 2 receptors

49
Q

How much time until onset of action of dexmedetomidine?

A

15 minutes (due to redistribution)

50
Q

How long does it take for peak concentration to be achieved?

A

1 hour

51
Q

What is the elimination half-life of dexmedetomidine at 0.2-0.7 mcg/kg/hr?

A

2-2.5 hours

52
Q

What are the routes of administration of dexmedetomidine?

A

IV, oral, transdermal, IM

53
Q

How is dexmedetomidine metabolized?

A

P450 enzymes via glucuronide conjugation and biorransformation
Metabolites are excreted in urine

54
Q

What is the major site by which dexmedetomidine causes analgesia?

A

Th spinal cord

55
Q

What other sites produce the analgesic effect of dexmedetomidine?

A

Decreased conduction through A and C fibers
Release of encephalin
Alpha 2

56
Q

What happens first with Propofol?

A

Hypnosis

Cardiovascular effects are delayed

57
Q

How is ketamine metabolized?

A

P450

58
Q

What kind of pain is ketamine effective for?

A

Nociceptive

Neuropathic

59
Q

When is ketamine contraindicated?

A 
ischemic heart disease
Chronic heart failure 
Intracranial mass and spontaneous ventilation 
Open eye injury
Vascular aneurysms
Psychiatric disease
60
Q

What does etomidate do to CPP?

A

Maintains it because it does not affect MAP

61
Q

What drugs are painful on injection?

A

Etomidate
Rocuronium
Propofol

62
Q

What does 11-betahydroxylase do?

A

It converts deoxycorticosterone to corticosterone and 11-deoxycorticosterone cortisol to cortisol

Therefore blocking this enzyme inhibits cortisol and aldosterone production

63
Q

How is dexmedetomidine metabolized?

A

Extensively in the liver

64
Q

What is preserved with dexmedetomidine

A

Hypercapnic ventilatory response so causes limited respiratory at high doses

65
Q

Why doesn’t liver disease affect Propofol metabolism?

A

Due to the high extraction ratio of Propofol (all of Propofol that reaches the liver will be metabolized, regardless of enzyme induction

66
Q

Which drugs depend on liver blood flow?

A 
Propofol
Ketamine
Lidocaine
Metoprolol 
Diltiazem 
Propanolol
Fentanyl
67
Q

What is unique about Propofol metabolism?

A

Some of it is extra hepatic because the extraction ratio is more than the cardiac output that the liver sees

68
Q

How should Propofol be dosed for induction?

A

Based on lean body weight

69
Q

How should Propofol be dosed on infusion?

A

TBW

70
Q

What are the risk factors for Propofol infusion syndrome?

A

Kid
4-5mg/kg/hr or 65-80 mg/kg/min greater than 24 hours
Concurrent catecholamines or corticosteroid administration
Concurrent neurological or inflammatory disease
Concurrent lipid metabolism disorders

71
Q

What is the pathophysiology of Propofol. Infusion syndrome?

A

Impaired fatty acid metabolism and utilization leading to anaerobic metabolism

Causes cardiac and skeletal muscle damage, renal failure, rhabdo, pancreatitis

72
Q

What is fospropofol?

A

A prodrug that must be first metabolized to Propofol

73
Q

What is the onset of action of fospropofol?

A

4-10 minutes

74
Q

What is the principal pathway of metabolism of Propofol?

A

Glucoronidation

75
Q

What happens to the rate of induction in a left to right cardiac shunt?

A

It would decrease because there is recirculating of blood in the pulmonary system

76
Q

What happens to rate of induction in a right to left cardiac shunt?

A

It would increase because more blood is bypassing the pulmonary circulation and going straight to the brain

77
Q

What are the risk factors for ketamine emergence delirium?

A 
Older age 
Female
Neurotic
Outgoing
Larger bolus dose
Has dreams at home

Anesthesia MM/TL (36 decks)

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