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Pharm > IV Anesthetics > Flashcards

IV Anesthetics Flashcards

1
Q

pKa of Thiopental and methohexitla

A

10-11

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2
Q

MOA of Barbituates

A

Potentiates GABAa Channel activity
Increasing the duration of GABA is active opning Cl channels

But directly activates GABA at higher doses

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3
Q

How are Barbituates metabolized and what does their metabolism produce?

A

Hepatic Metabolism by Oxidation

Producing Porhyrins

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4
Q

What are theh two barbituates seen in Anesthesia

A

Methohexital (Brevital)
Thiopental

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5
Q

Which Barbituate is cleared faster?

A

Methohexital is cleared faster than Thiopental

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6
Q

What is Methohexital mostly used for ?

A

Methohexital is used for ECT therapy becasue it lowers the seizure threshold

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7
Q

What are barbituate consideration with induction using barbiturates?

A

Age weight and mostly Cardiac Output

Vd changes with age

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8
Q

CNS effects of Barbituates

A

Dose dependant CNS depression
Decrease everything
CMRO2
CPP
CBF
ICP
EEG

NO ANALGESIA

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9
Q

Respiratory effects of Barbituates*

A

Histamine release (Asthma concern)
Resp Depression
Dose dependant depression of medullary and pountine vent centers
(Decrease in CO2 response)

Lose reflexes at high doses

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10
Q

CV effects of barbituates
thiopental and how

A

Thiopental causes 5-10 decrease in BP

This is due to vasodilation and depression of medullary vasomotor centers and decrease SNS outflow to CNS

BUT compensated by 15-20 BPM HR increase

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11
Q

Dosing of Thiopental

A

3-5 mg/kg IV

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12
Q

Induction Dosing of Methohexital

A

1-1.5 mg/kg IV

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13
Q

Name the Structure

A

Propofol

2,6 Diisopropylphenol

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14
Q

What is propofol used for

A

Sedation induction maintenance of anesthesia

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15
Q

What are the lipid emulsion components in Propofol

and in genenric forms?

A

10 % soybean oil
2.25 % Glycerol
1.2 % purified Egg Lecithin

Generic–> Sodium Bisulfate

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16
Q

Ph and pKa of Propofol
Diprivan and generic

A

pH- 7-8.5 Generic- 4.5-6.4
pKa- 11

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17
Q

How often do you need to Change syringe and tubing for prop

A

syringe- 6 hours
Tubing- 12 hours

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18
Q

Propofol dosing
Induction
Maintanence
Sedation
Antiemetic
Antipuritic

A

Induction- 1-2.5 mg/kg bolus
Maintanence- 100-300 mcg/kg/min
Sedation- 25-75 mcg/kg/min or
10-20 mg bolus
Antiemetic- 10-15mcg/kg/min
Antipuritic- 10 mg

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19
Q

MOA of Propofol

A

Direct GABAa agonist
Changes conductance of Cl causing neuronal hyper polarization

Does not effect spinal motor neuron excitability

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20
Q

What IV anesthetic is ideal for spine/neuro cases?

A

Propofol does not effect spinal neuron excitability

Precedex. Can be woken up for test easily

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21
Q

Propofol kinetics time to awake and why

A

Time to awake is dose dependant but usually 5-15 minutes

Rapid distribution throughout VRG

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22
Q

Propofol distribution half life

A

2-4 minutes

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23
Q

Propofol Elimination half-life

A

1-5 hours

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24
Q

Propofol clearance

A

25 ml/kg/min

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25
Q

Propofol protein binding

A

98 %

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26
Q

Does Propofol have analgesia properties

A

NO!

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27
Q

Neuro effects of Propofol

A

Decrease everything
CMRO2
CBF
ICP
IOP
BIG DROP IN CPP

Burst surpression in EEG

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28
Q

How much does propofol decrease blood pressure by?

What parameters go down (CO SVR SNS CI SV)

A

roughly 25-45 %

Decreases everything!

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29
Q

Respiratory effects of PROP

A

Dose dependant decrease in RR
Decrease Vt
Increase apnea time
Decrease sensitivity to CO2
Small Bronchodilation

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30
Q

What does prop do to urine and why

A

Turns urine green (Phenols) and Cloudy (uric Acid)

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31
Q

What does propofol not do?

A

Does not

Enhance NMBAs
cause MH
Affect Corticosteroid synthesis
Affect hepatic or renal function

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32
Q

What are people allergic to in propofol?

A

Diisopropyl side change and phenyl nuclei
Preservatives

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33
Q

What are key clinical characteristics of PRIS

A

EKG changes (widening QRS and arrythmias)**
Refractory Bradycardia**
Severe metabolic Acidosis
Rhabdo
Fever
Hyper K
Hypotension**
HLD
Hypoxia
Cardiac Failure
Hepatic Problems
RF

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34
Q

Risk Factors for PRIS

A

High dose for long term
Dose >5mg/kg/hr
>48 hours of use
High-fat low-carb intake
Inborn errors of mitochondrial fatty acid oxydation
Concomitant Pressors or steroids

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35
Q

Management of PRIS

A

D/c Prop
Supportive measures (50% mortality)
Pacing

glucogon
CRRT
Phosphodiesterase inhibitor
increase gas exchange

36
Q

Fospropofol
MOA
Dose
Onset
Duration

A

Prodrug of Prop metabolized by Alkaline phosphate (lower onset and increase duration)
Dose- Bolus 6.5 mg/kg
Maintanence 1.6 mg/kg
onset- 5-13 minutes
duration 15-45 minutes

37
Q

Benefits and drawbacks of Fosprop

A

No burning. Less allergic reaction.
No bacterial growth concern

38
Q

Benefits of Etomidate

A

minimal hemodynamic effects
d/t Alpha2B adrenoceptors mediates compensatory increase in BP

Unless severe aortic or mitral valve disease

Minimal Cardiorespiratory depression

39
Q

Propblems with Etomidate

A

Burn on injection
Supresssion of adrenocortical function
Contributes to Acute porphyries
increase post op NV
Involentary Myoclonus

40
Q

MOA of Etomidate

A

R isomer is a selective modulator of GABAa

41
Q

Etomidate onset
duration
Dose

A

0.2-0.4 mg/kg
onset 30-60s
Duration 5-15 minutes

42
Q

Metabolism of Etomidate

A

Hepatic transformation by ESTER HYDROLYSIS to inactive metabolites

small amount excreted unchange in urine

highly protein bound 77%

43
Q

Etomidate CNS effects

A

Dose dependant CNS depressions within one arm-brain circulation

NO ANALGESIA
CBF CMRO2 IOP decreased
Excitatory muscle contraction

44
Q

Adrenocortical effects of Etomidate

A

Inhibition of 11BHydroxylase–>stops formation of cortisol from cholesterol

Lasts for 24 hours after first dose

45
Q

CNS Effects of Benzodiazepines (5)

A

Anxiolysis
Antegrade Amnesia
Sedation
Hypnosis
Anticonvulsant
Dose dependant CNS depression

46
Q

Benzo MOA

A

GABAa Agonist at the benzodiazapine receptor site

47
Q

Midaz effects compared to other benzos

A

More Amnesia than sedation

48
Q

Midaz Pregnancy

A

Crosses the placenta

49
Q

Midaz Metabolism
And metabolite, Acitve or inactive

A

Mostly in the liver by Microsomal oxidation and glucuronide conjugation

Metabolite–> l-hydroxymedazolam
Active 1/2 potency of midaz, but is rapidly conjugated. Renal imparement prolongs the effects

50
Q

What effects microsomal oxidation?
Midaz (5)

A

Age
liver disease
Obesity
Gender
Renal status

51
Q

Half life of Midazolam
Diazepam
Lorazepam

A

Midaz- 1.9 hours
Diaz- 43 hours
Loraz- 14 hours

52
Q

1-Hydroxmedazolan

A

Metabolite of midaz 1/2 the potency is rapidly conjugated, but can have longer lasting effects in renal impairment

53
Q

Cardiovascular effects of benzos

A

Sedation-> minimal unless paired with opioids or geriatrics

Induction dose decreasees SBP and SVR

54
Q

Resp Effects of Benzos

A

Dose dependant respiratory depression (Midaz the most)
Synergistic Resp depression with opioids

55
Q

When are Benzos Contraindicated

A

Acute Porphyria

56
Q

Midaz Dosing Onset Duration
Sedation- IV / Oral
Induction

A

Sedation Oral- 0.25-1mg/kg PO MAX 20 mg–> 20-30 min before surgery

IV- 0.25-2.5 mg onset 20-60 seconds
Duration- 15-80 minutes

Induction 0.1-0.2 mg/kg IV over 30-60 seconds

57
Q
A
58
Q

Remimazolam offset
and half life

A

11-14 minutes Following last dose
half life of 37-53 minutes

59
Q

Remimazolam metabolism

A

No active metabolites,

60
Q

Remimazolam Doseing initial and maintanance
Adult
ASA III-IV

A

Adult- 5 mg IV over 1 minute
Maintenance- 2.5 mg over 15 seconds

ASA III-IV- 5 mg IV over 1 minute
Maintenance- 1.25 mg-2.5 IV over 15 seconds

61
Q

Flumenizil dosing

A

0.2 mg IV
Additional 0.1 mg to total of 1 mg may be given in 60 second intervals

62
Q

Flumenizil Onset

A

2 minutes

63
Q

MOA flumenizil

A

Competative antagonist of benzodiazepines receptor

64
Q

Flumenizil duration

A

30-60 minutes

65
Q

Flumenizil contraindications

A

Antiepileptic Drug use
Neuro patients (head bleed)

66
Q

Ketamine effects

A

Amnesia, dissociative, Analgesia

Nystagmus

67
Q

Ketamine MOA

A

Antagonism of NMDA receptors (Kappa and Mu)
Dissociates the Thamlmus (sensory) from the limbic system (awareness)

Other effects on the Monoamine (MAO), Cholinergic, Opiate, Muscarinc, and adenosin receptors

Direct inhibition of cytokines in blood

inhibits TNF Alpha and IL-6 gene expression leading to anti-inflammatory and antihyperalgesia

68
Q

NMDA receptor

A

Subtype of glutamate receptor involved in transfer of signal from brain and spinal cord

Channel must be open to work

69
Q

Metabolism of ketamine

and metabolites

A

Extensive hepatic metabolism

Demethylation of ketamine by P450 to form Norketamine

Norketamine is 1/5-1/3 the potency

Chronic admin increases enzyme activity

70
Q

Ketamine dosing
IV Induction
IM
Sedation
Infusion chronic pain
depression

A

Inductions- 1.0-=4.5 mg/kg for 5-10 minutes surgical time
IM- 4-8 mg/kg for 12-25 min
sedation- 0.1-0.5 mg/kg IV
Infusion for chronic pain- 0.1-0.3 mg/kg/hr

Depression- 0.5mg/kg over 30-40 min

71
Q

Ketamine Protein bound

A

12 % protein

72
Q

Ketamine Onset

A

2-5 minutes

73
Q

Ketamine elimnation

A

2-3 hours

74
Q

Ketamine Hepatic extraction

A

High so elimination is depednatnt on flow to the liver

75
Q

CNS effects of ketamine

A

Increase CBF ICP CMRO2
Nystagmus
Increase EEG activity (seizure risk)
Drunk effects (decrease coordination slur speech)
Long term analgesia

Increases Blood flow by 60%

76
Q

CV effects of ketamine

A

Circulatory Stim
Increase Myocardial O2 consumption
DONT GIVE WITH MI or HEART DISEASE

Increase BP HR Cardiac contractility and CVP

77
Q

Respiratory effects of ketamine

A

Short duration bronchodilation
Reflexes (vomit) and respiratory tone intact
Does NOT release histamine
Increase pulmonary compliance

Increase in secretions!

78
Q

Dexmedetomidine Class

A

Imidazolines

79
Q

Dex MOA

A

Alpha 2 agonist (in CV and CNS)
Stimulation decreases catacholamine relsease
activates sleep
Analgesia d/t receptors in the anterior horn

80
Q

Dex Metabolism
Metabolites and elimination

A

Rapid hepatic metabolism involving conjugation of N-methylation and hydroxylation

NO ACTIVE METABOLITES

Secerted in urine and bile

81
Q

Dex half life

A

6 minutes

82
Q

Onset of Dex

A

10-20 minutes

83
Q

protein binding of dex

A

94 %

84
Q

Loading dose for Dex
and Maintanence dose

A

1mcg/kg over 10 minutes
0.2-0.7 mcg/kg/hr

85
Q

CNS effects of dex

A

dose dependatnt sedation that resemblees sleep
Good Wake up test
Dose not interfere with Electrophys monitoring

NO change in CMRO2 ICP
Decreased CBF

86
Q

CV effects of Dex

A

Hypotension and bradycardia
due to alpha stim and systemic vasodilation

87
Q

Dex Resp effects

A

small decrease in reflex
Normal CO2 response
Refelexes maintained
Decrease airway reactivity in COPD

Pharm (9 decks)

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