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IV Anesthetics Flashcards

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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
Propofol protein binding
98 %
26
Does Propofol have analgesia properties
NO!
27
Neuro effects of Propofol
Decrease everything CMRO2 CBF ICP IOP BIG DROP IN CPP Burst surpression in EEG
28
How much does propofol decrease blood pressure by? What parameters go down (CO SVR SNS CI SV)
roughly 25-45 % Decreases everything!
29
Respiratory effects of PROP
Dose dependant decrease in RR Decrease Vt Increase apnea time Decrease sensitivity to CO2 Small Bronchodilation
30
What does prop do to urine and why
Turns urine green (Phenols) and Cloudy (uric Acid)
31
What does propofol not do?
Does not Enhance NMBAs cause MH Affect Corticosteroid synthesis Affect hepatic or renal function
32
What are people allergic to in propofol?
Diisopropyl side change and phenyl nuclei Preservatives
33
What are key clinical characteristics of PRIS
EKG changes (widening QRS and arrythmias)** Refractory Bradycardia** Severe metabolic Acidosis Rhabdo Fever Hyper K Hypotension** HLD Hypoxia Cardiac Failure Hepatic Problems RF
34
Risk Factors for PRIS
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
35
Management of PRIS
D/c Prop Supportive measures (50% mortality) Pacing glucogon CRRT Phosphodiesterase inhibitor increase gas exchange
36
Fospropofol MOA Dose Onset Duration
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
Benefits and drawbacks of Fosprop
No burning. Less allergic reaction. No bacterial growth concern
38
Benefits of Etomidate
minimal hemodynamic effects d/t Alpha2B adrenoceptors mediates compensatory increase in BP Unless severe aortic or mitral valve disease Minimal Cardiorespiratory depression
39
Propblems with Etomidate
Burn on injection Supresssion of adrenocortical function Contributes to Acute porphyries increase post op NV Involentary Myoclonus
40
MOA of Etomidate
R isomer is a selective modulator of GABAa
41
Etomidate onset duration Dose
0.2-0.4 mg/kg onset 30-60s Duration 5-15 minutes
42
Metabolism of Etomidate
Hepatic transformation by ESTER HYDROLYSIS to inactive metabolites small amount excreted unchange in urine highly protein bound 77%
43
Etomidate CNS effects
Dose dependant CNS depressions within one arm-brain circulation NO ANALGESIA CBF CMRO2 IOP decreased Excitatory muscle contraction
44
Adrenocortical effects of Etomidate
Inhibition of 11BHydroxylase-->stops formation of cortisol from cholesterol Lasts for 24 hours after first dose
45
CNS Effects of Benzodiazepines (5)
Anxiolysis Antegrade Amnesia Sedation Hypnosis Anticonvulsant Dose dependant CNS depression
46
Benzo MOA
GABAa Agonist at the benzodiazapine receptor site
47
Midaz effects compared to other benzos
More Amnesia than sedation
48
Midaz Pregnancy
Crosses the placenta
49
Midaz Metabolism And metabolite, Acitve or inactive
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
What effects microsomal oxidation? Midaz (5)
Age liver disease Obesity Gender Renal status
51
Half life of Midazolam Diazepam Lorazepam
Midaz- 1.9 hours Diaz- 43 hours Loraz- 14 hours
52
1-Hydroxmedazolan
Metabolite of midaz 1/2 the potency is rapidly conjugated, but can have longer lasting effects in renal impairment
53
Cardiovascular effects of benzos
Sedation-> minimal unless paired with opioids or geriatrics Induction dose decreasees SBP and SVR
54
Resp Effects of Benzos
Dose dependant respiratory depression (Midaz the most) Synergistic Resp depression with opioids
55
When are Benzos Contraindicated
Acute Porphyria
56
Midaz Dosing Onset Duration Sedation- IV / Oral Induction
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
58
Remimazolam offset and half life
11-14 minutes Following last dose half life of 37-53 minutes
59
Remimazolam metabolism
No active metabolites,
60
Remimazolam Doseing initial and maintanance Adult ASA III-IV
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
Flumenizil dosing
0.2 mg IV Additional 0.1 mg to total of 1 mg may be given in 60 second intervals
62
Flumenizil Onset
2 minutes
63
MOA flumenizil
Competative antagonist of benzodiazepines receptor
64
Flumenizil duration
30-60 minutes
65
Flumenizil contraindications
Antiepileptic Drug use Neuro patients (head bleed)
66
Ketamine effects
Amnesia, dissociative, Analgesia Nystagmus
67
Ketamine MOA
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
NMDA receptor
Subtype of glutamate receptor involved in transfer of signal from brain and spinal cord Channel must be open to work
69
Metabolism of ketamine and metabolites
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
Ketamine dosing IV Induction IM Sedation Infusion chronic pain depression
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
Ketamine Protein bound
12 % protein
72
Ketamine Onset
2-5 minutes
73
Ketamine elimnation
2-3 hours
74
Ketamine Hepatic extraction
High so elimination is depednatnt on flow to the liver
75
CNS effects of ketamine
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
CV effects of ketamine
Circulatory Stim Increase Myocardial O2 consumption DONT GIVE WITH MI or HEART DISEASE Increase BP HR Cardiac contractility and CVP
77
Respiratory effects of ketamine
Short duration bronchodilation Reflexes (vomit) and respiratory tone intact Does NOT release histamine Increase pulmonary compliance Increase in secretions!
78
Dexmedetomidine Class
Imidazolines
79
Dex MOA
Alpha 2 agonist (in CV and CNS) Stimulation decreases catacholamine relsease activates sleep Analgesia d/t receptors in the anterior horn
80
Dex Metabolism Metabolites and elimination
Rapid hepatic metabolism involving conjugation of N-methylation and hydroxylation NO ACTIVE METABOLITES Secerted in urine and bile
81
Dex half life
6 minutes
82
Onset of Dex
10-20 minutes
83
protein binding of dex
94 %
84
Loading dose for Dex and Maintanence dose
1mcg/kg over 10 minutes 0.2-0.7 mcg/kg/hr
85
CNS effects of dex
dose dependatnt sedation that resemblees sleep Good Wake up test Dose not interfere with Electrophys monitoring NO change in CMRO2 ICP Decreased CBF
86
CV effects of Dex
Hypotension and bradycardia due to alpha stim and systemic vasodilation
87
Dex Resp effects
small decrease in reflex Normal CO2 response Refelexes maintained Decrease airway reactivity in COPD

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