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APEX Pharmacology > PHARMACOLOGY-IV anesthetics > Flashcards

PHARMACOLOGY-IV anesthetics Flashcards

1
Q 
Propofol
MOA=
Onset=
Duration=
pKa=
A

MOA= GABA-A agonist increasing Cl- conductance and neuron hyperpolarization. Prevents AP
Onset= 30-60 seconds
Duration= 5-10 minutes
pKa=11

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2
Q 
Propofol
Clearance=
Active metabolite=
Induction dose=
Maintenance dose=
A

Clearance= liver + extra hepatic metabolism (lungs)
Active metabolite= none
Induction dose= 1.5-2.5 mg/kg IV
Maintenance dose= 25-200 ,cg/kg/min

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3
Q

Propofol
Respiratory effects=
CV effects=
CNS effects=

A

Respiratory effects= decreased respiratory drive

CV effects= decreased BP, SVR, preload, and contractility

CNS effects= Decreased ICP and IOP, NO analgesia +/- SZ activity

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4
Q

What is the chemical name and class for propofol

A 
Name = 2,6- diisopropylphenol
Class = Isopropylphenol
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5
Q

How do GABA-A receptors react when stimulated

A

Cl- conductance is increased, hyperpolarizing the neuron. This reduces the resting membrane potential making an action potential less likely

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6
Q

What causes the respiratory depressant effect when propofol is administered

A

A shift in the CO2 response curve down and to the right means there is less sensitivity for CO2 to drive respirations

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7
Q

What specific respiratory drive does propofol inhibit

A

hypoxic ventilatory drive

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8
Q

How are cerebral blood flow and oxygen consumption affected by propofol

A

Both are decreased

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9
Q

What miscellaneous properties does propofol have

A

Antioxidant properties = free radical scavenger

Altered urine color d/t phenol excretion (green) or increased uric acid excretion (cloudy)

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10
Q

What are 2 preservatives that may be added to propofol

A
  1. Disodium edetate (Diprivan)

2. sodium metabisulfate (generic)

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11
Q

Can patients with allergies to soy, peanuts, and egg receive propofol

A

Yes

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12
Q

What part of an egg is used in propofol production.

How does this relate to people with egg allergies

A

Egg lecithin found in propofol is derived from the yolk

People are usually allergic to the albumin in the egg white

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13
Q

What are clinical presentations of propofol infusion syndrome

A 
Metabolic acidosis (base deficit > 10 mmol)
Rhabdomyolysis
Renal failure
Hyperlipidemia
Enlarge fatty liver
Lipemia
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14
Q

What is the treatment for propofol infusion syndrome

A 
D/C propofol
Initiate cardiac pacing
Start PDE inhibitors
ECMO
Glucagon
CRRT
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15
Q

What is the discard time for infusion and syringes of propofol

A 
Infusion = 12 hours
Syringes = 6 hours
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16
Q

How do the additives in propofol cause possible complications

A

Metabisulfite = bronchospasm in asthmatic patients

Benzyl alcohol = should be avoided in infants

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17
Q

Other than sedative properties, what properties does propofol contain

A

Antipruritic
Antiemetic
Antioxidant

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18
Q

D/t the long-chain triglycerides in propofol what can be impaired?
Why is this significant?

A

Oxidative phosphorylation
Fatty acid metabolism

Significance = cells are starved of O2, especially in cardiac and skeletal muscle

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19
Q

What are risk factors for propofol infusion syndrome (6)

A
  1. Propofol dose >4 mg/kg/hr
  2. Infusion duration > 48 hrs
  3. Sepsis (inadequate O2 delivery)
  4. Continuous catecholamine infusions
  5. High-dose steroids
  6. Significant cerebral injury
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20
Q

Why is contamination concerning with propofol infusion or syringes

A

It supports bacterial and fungal growth

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21
Q

How is propofol injection pain minimized (3)

A

Inject into larger more proximal vein
Giving opioid before propofol
Giving lidocaine before propofol

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22
Q

What dose of propofol can be an effective antipruritic

A

10 mg IV

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23
Q

What dose of propofol can be an effective antiemetic

A

10 - 20 mg IV

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24
Q 
Fospropofol 
MOA=
Onset=
Duration=
pKa=
A

MOA= GABA-A agonist
Onset= 5 - 13 minutes
Duration= 15 - 45 minutes
pKa=

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25
Q 
Fospropofol 
Clearance=
Active metabolite=
Induction dose=
Repeat dose=
A

Clearance= liver + extrahepatic metabolism
Active metabolite= propofol
Induction dose= 6.5 mg/kg IV
Repeat dose= Max 1.6 mg/kg q4min

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26
Q 
Fospropofol
Respiratory effects=
CV effects=
CNS effects=
Other=
A

Respiratory effects= similar to propofol
CV effects= similar to propofol
CNS effects= similar to propofol
Other= genital and anal burning

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27
Q

Class of fospropofol

A

isopropylphenol

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28
Q

How is the formulation for fospropofol different from propofol

A

It’s an aqueous solution which prevents burning on injection and doesn’t support microbial growth

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29
Q

What is the MOA of fospropofol

A

It’s metabolized to propofol by the enzyme alkaline phosphatase which prolongs onset. It binds to GABA-A increasing Cl- conductance

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30
Q

Which receptor does ketamine antagonize

A

NMDA

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31
Q 
Ketamine
MOA= primary and secondary
Onset= (IV, IM)
Duration=
pKa=
A 
MOA=
-Primary = NMDA antagonist
-Secondary = binds to secondary receptors i.e. opioid, MAO, serotonin, NE, muscarinic, Na+ channel
Onset
-IV= 30-60 sec
-IM= 2 - 4 min
Duration= 10-20 minutes
pKa= 7.5
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32
Q 
Ketamine
Clearance=
Active metabolite=
Induction dose= (IV, IM)
Opioid sparing dose=
A 
Clearance= liver
Active metabolite= Norketamine
Induction dose= 
-IV = 1-2 mg/kg
-IM = 4-8 mg/kg
-PO=10 mg/kg
Opioid sparing dose= 0.1-0.5 mg/kg
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33
Q 
Ketamine
Respiratory effects=
CV effects=
CNS effects=
Other=
A

Respiratory effects= maintains respiratory drive, increased oral secretions
CV effects= Increased SNS tone, SVR, HR, CO
CNS effects= Increased ICP, IOP, nystagmus, analgesia. Emergence delirium, lowers SZ threshold.
Other= Avoid with acute intermittent porphyria

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34
Q

Chemical name and class of ketamine

A

Name = 1-(o-Cholophenyl)-2(methylamino) cyclohexanone hydrochloride

Class = Arylcyclohexylamine; phencyclidine derivative

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35
Q

What is the formulation or ketamine

A

Aqueous solution available as 1%, 5%, and 10% solutions

Racemic mixture

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36
Q

Ketamine MOA

A

NMDA receptor antagonist. Antagonizes glutamate

Dissociates the thalamus (sensory) from the limbic system (awareness)

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37
Q

Describe the clearance of ketamine

A

Liver (P450 enzymes)

-Chronic ketamine use induces the enzymes that metabolize it

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38
Q

How does chronic ketamine use affect the enzymes that metabolize it.
Why is this significant?

A

It’s an enzyme inducer

This causes rapid escalation in tolerance

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39
Q

What is the metabolite for ketamine?

Describe the potency of the metabolite

A

Active metabolite = norketamine

potency = 1/3 - 1/5 the potency of ketamine

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40
Q

How is ketamine excreted

A

Renal

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41
Q

How does ketamine affect the myocardium if SNS isn’t intact

A

It is a myocardial depressant
If catecholamines are depleted or SNS isn’t intact, then myocardial depression will be prominent. Can cause severe bradycardia d/t muscarinic action

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42
Q

What are respiratory effects of ketamine

A
  • Bronchodilation
  • Airway reflexes remain intact
  • Respiratory drive remains intact
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43
Q

How does ketamine affect the CO2 response curve

A

Does not significantly shift CO2 response curve

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44
Q

What are CNS effects of ketamine

A
  • increased CMRO2
  • increased cerebral BF
  • increased ICP
  • increased IOP
  • increased EEG activity
  • Emergence delirium
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45
Q

How does emergence delirium present with ketamine use?

What is helpful

A

Nightmares and hallucinations

Benzodiazepines are effective in preventing emergence delirium

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46
Q

How does ketamine affect pain

A
  • Good analgesia with opioid-sparing effects
  • Relieve somatic pain > visceral pain
  • Blocks central sensitization and effects in the dorsal horn of the SC
  • prevents hyperalgesia following remifentanil infusion
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47
Q

What conditions should ketamine use be avoided in

A

CAD

Acute intermittent porphyria

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48
Q

What is an off-label use for ketamine

A

sub-hypnotic doses can treat MDD resistant to treatment

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49
Q

What is the plasma protein binding for ketamine?

How does this relate to other IV anesthetics?

A

12%

MUCH lower

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50
Q 
Etomidate
MOA= 
Onset= 
Duration=
pKa=
A

MOA= GABA-A agonist
Onset= 30-60 seconds
Duration= 5-15 minutes
pKa=

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51
Q

Etomidate
Clearance=
Active metabolite=
Induction dose=

A

Clearance= Liver + plasma esterases
Active metabolite= none
Induction dose= 0.2-0.4 mg/kg

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52
Q

Etomidate
Respiratory effects=
CV effects=
CNS effects=

A

Respiratory effects= mild respiratory depression
CV effects= minimal
CNS effects= decreased ICP, no analgesia

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53
Q

Chemical name and class of etomidate

A

Chemical name= R-1-methyl-1-(a-methylbenzyl) imidazole-5-carboxylate

Class=Imidazole

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54
Q

How does the imidazole etomidate function in different pH’s

A

Acidic pH = imidazole ring opens = INCREASED H2O solubility

Physiologic pH = imidazole ring closes = INCREASED lipid solubility

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55
Q

Describe the clearance of etomidate

A

Liver P450 enzymes and plasma esterases

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56
Q

Why does rapid awakening occur with etomidate?

A

Due to redistribution NOT metabolism

57
Q

What are CV effects and benefits of etomidate

A
  • Hemodynamic stability with minimal change to HR, SV, and CO
  • SVR is decreased lowering BP minimally
  • Doesn’t blunt SNS response to laryngoscopy
58
Q

What are respiratory effects of etomidate

A

Mild respiratory depression but less than propofol and barbs

59
Q

What are 5 CNS effects of etomidate

A
  1. decreased CMRO2
  2. decreased CBF d/t cerebral vasoconstriction
  3. decreased ICP
  4. Stable cerebral perfusion
  5. No analgesia
60
Q

Does etomidate provide analgesia

A

No

61
Q

Which IV anesthetic can increase mortality in patients with Addisonian crisis?
Why?

A

Etomidate

It is an 11-beta-hydroxylase and 17-alpha-hydroxylase inhibitor which is what cortisol and aldosterone synthesis is dependent on

A single dose of etomidate suppresses adrenocortical function for 5-8 hours

Avoid etomidate in patients reliant on intrinsic stress response because they need alllllll the cortisol (i.e. addison’s crisis, severe sepsis)

62
Q

What are 4 undesirable effects of etomidate

A
  1. myoclonus
  2. Suppression of adrenocortical function for up to 24 hrs
  3. Nausea and vomiting
  4. Acute intermittent porphyria
63
Q

What conditions should etomidate use be avoided and why

A
  1. Addison’s crisis
  2. Severe sepsis
  3. Acute adrenal failure
  4. Acute intermittent porphyria

d/t depletion of intrinsic cortisol stress response. Don’t want to inhibit cortisol production

64
Q

How does myoclonus present following etomidate use

A

Involuntary skeletal muscle contractions, dystonia, or tremor

65
Q

What effect can etomidate have in patients with a history of seizures

A

It can increase epileptiform activity and risk of seizures

66
Q

Thiopental
MOA=
Onset=
Duration=

A 
MOA= GABA-A agonist
Onset= 30-60 seconds
Duration= 5-10 minutes
67
Q

Thiopental
Clearance=
Active metabolite=
Induction dose=

A

Clearance= Liver
Active metabolite= None
Induction dose= 2.5-5 mg/kg IV

68
Q

Thiopental
Respiratory effects=
CV effects=
CNS effects=

A

Respiratory effects= decreased drive, bronchoconstriction d/t histamine release
CV effects= HoTN, myocardial depression, baroreceptor reflex preserved
CNS effects= Decreased ICP, hyperalgesia possible

69
Q

What conditions should thiopental use be avoided

A

Acute intermittent porphyria

70
Q

What can occur with intra-arterial thiopental injection?

Treatment?

A

Intense vasoconstriction and crystal formation leading to tissue necrosis

Tx: vasodilator like phentolamine or phenoxybenzamine. Stellate ganglion nerve block for sympathectomy of UE

71
Q

What medication is used for electroconvulsive therapy and why

A

Methohexital

Decreases seizure threshold and produces better-quality seizure

72
Q

What chemical are barbiturates derived.

How is PK/PD altered

A

Derived from barbituric acid

Substitutions on the barbituric acid ring can modify PK/PD

73
Q

What molecule is added to barbituric acid to form thiobarbiturates

A

Sulfur molecules in the 2nd position

74
Q

What is an example of a thiobarbiturate

A

Thiopental

75
Q

What molecule is added to barbituric acid to form oxybarbiturate

A

Oxygen molecule in the 2nd position

76
Q

Give an example of an oxybarbiturate

A

Methohexital

Pentobarbital

77
Q

What chemical substitution on barbituric acid can lower seizure threshold and increase potency.
Name medication

A

Adding methyl group on nitrogen

Methohexital

78
Q

What chemical substitution on barbituric acid can increase anticonvulsant effects.
Name medication

A

Adding a phenyl group to the carbon in the fifth position

Phenobarbital

79
Q

How do each of the following drugs affect seizures
Methohexital
Phenobarbital

A

Methohexital = lower seizure threshold

Phenobarbital = increased anticonvulsant effect

80
Q

Chemical name and class for thiopental

A

name= 5-ethyl-5-(1-methylbutyl)-2-thiobarbituric acid

Class=barbiturate

81
Q

What is the solubility and pH for thiopental

A 
Solubility = water soluble
pH = 9
82
Q

Describe the MOA for thiopental

A

GABA-A agonist depresses the reticular activating system in the brain stem

83
Q

How are the GABA receptors affected by thiopental dosing

A

Low/normal= increases affinity of GABA for its binding site

High dose= directly stimulates GABA-A receptor

84
Q

Describe the clearance mechanism for thiopental.

How does repeated dosing affect clearance

A

Liver P450

Repeated dosing causes tissue accumulation leading to longer wake-up time and hangover effect

85
Q

What determines awakening following thiopental administration

A

Determined by redistribution NOT metabolism

86
Q

What is the active metabolite for thiopental

A

Normal dose = NO active metabolite

High dose= pentobarbital

87
Q

BP effect btween propofol and thiopental

A

thiopental produces less HoTN than propofol

88
Q

Describe 4 CV effects of thiopental

A
  1. HoTN is d/t venodilation which decreases preload
  2. Myocardial depression
  3. Non-immunogenic histamine release
  4. Baroreceptor reflex preserved cause reflexive tachycardia with HoTN to maintain CO
89
Q

What is the mechanism that causes HoTN with thiopental administration

A
  1. Venodilation causes decreased preload
  2. Myocardial depression
  3. non-immunogenic histamine release (short-lived)
90
Q

Respiratory effects of thiopental

A
  1. Respiratory depression d/t CO2 response curve shifting right
  2. bronchoconstriction d/t histamine release
91
Q

What respiratory condition should thiopental be used with caution and why

A

Asthma

d/t bronchoconstriction from histamine release

92
Q

Which direction does the CO2 response curve shift with thiopental use?
How does this affect respiratory drive?

A

Curve shifts RIGHT

Causes respiratory depression

93
Q

CNS effects of thiopental (6)

A
  1. Decreased CMRO2
  2. Decreased CBF from vasoconstriction
  3. Decreased ICP
  4. Decreased EEG activity
  5. No analgesia
  6. Neuroprotection with focal ischemia
94
Q

How can thiopental be useful when performing an EEG

A

It can cause burst suppression or isoelectric EEG

95
Q

How can thiopental affect acute intermittent porphyria

A

By inducing ALA synthase which accelerates the production of heme precursors and their accumulation

96
Q

What are the symptoms of acute intermittent porphyria
GI
CNS
PNS

A 
GI= severe abd pain, N/V
CNS= Anxiety, confusion, seizures, psychosis, coma
PNS= skeletal muscle weakness, bulbar weakness (both can lead to respiratory failure)
97
Q

List medications that should be avoided with acute intermittent porphyria (7)

A
  1. Barbiturates
  2. Etomidate
  3. Ketamine
  4. Ketorolac
  5. Amiodarone
  6. CCBs
  7. BCPs
98
Q

Anesthetic management for acute intermittent porphyria (6)

A
  1. Liberal hydration
  2. glucose supplementation reduces ALA synthase activity
  3. Heme arginate reduces ALA synthase activity
  4. Prevent hypothermia
  5. Administer ALP safe medications
  6. Avoid regional anesthesia
99
Q

Methohexital induction dose

A

1-1.5 mg/kg

100
Q 
Dexmedetomidine
MOA= 
Onset= 
Duration=
pKa=
A 
MOA= alpha-2 agonist
Onset= 10-20 minutes
Duration= 10-30 minutes
pKa= 7.1
101
Q 
Dexmedetomidine
Clearance=
Active metabolite=
Loading dose=
Maintenance dose=
A

Clearance= Liver
Active metabolite= None
Loading dose= 1 mcg/kg over 10 minutes
Maintenance dose= 0.4-0.7 mcg/kg/hr

102
Q 
Dexmedetomidine
Respiratory effects=
CV effects=
CNS effects=
Other=
A

Respiratory effects= Respiratory drive preserved
CV effects= Bradycardia, HoTN, HTN w/ rapid administration
CNS effects= Sedation, analgesia, no ICP effects, limited effects on evokes
Other= Antishivering, decreased emergence delirium

103
Q

Chemical name and class for dexmedetomidine

A

Chemical name = (S)-4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole monohydrochloride

Class = imidazole

104
Q

Is dexmedetomidine lipid or water soluble

A

Water

105
Q

Describe the MOA of dexmedetomidine

A

Alpha-2 agonist
Binds to presynaptic alpha-2 receptors decreasing cAMP which inhibits the locus coeruleus in the pons leading to sedation

106
Q

Describe the mechanism that produces HTN with rapid dexmedetomidine administration

A

Rapid administration produces peripheral alpha-2 effects before the central effects that reduce SNS tone. Peripheral effects include alpha-2 stimulation in vasculature causing vasoconstriction.

107
Q

How does dexmedetomidine affect the CO2 response curve

A

It doesn’t!

108
Q

Describe the CNS effects of dexmedetomidine

A
  1. decreased CBF
  2. No change in CMRO2
  3. No change in ICP
  4. Sedation d/t decreased SNS tone and reduced arousal
109
Q

How does dexmedetomidine affect shivering

A

It impairs the thermoregulatory response producing antishiver effects

110
Q

How is analgesia produced with dexmedetomidine

A

The alpha-2 receptors are stimulated in the dorsal horn of the spinal cord. This decreases substance P and glutamate release (excitatory NT)

111
Q

Pediatric nasal or buccal dose of dexmedetomidine

A

3-4 mcg/kg

112
Q

Compare the elimination half-lives of midazolam, diazepam and lorazepam

A

Diazepam > lorazepam > midazolam

113
Q

Why is the elimination half-life of diazepam so long

A

It undergoes enterohepatic recirculation

t1/2 = 43 hours

114
Q 
Midazolam
MOA= 
Onset= 
Duration=
pKa=
A

MOA= GABA-A agonist
Onset= 30-60 seconds
Duration= 20-60 minutes
pKa=

115
Q 
Midazolam
Clearance=
Active metabolite=
Sedation dose
IV=
PO=
A 
Clearance= Liver
Active metabolite= 1-hydroxymidazolam
Sedation dose
IV= 0.01-0.1 mg/kg
PO= 0.5-1 mg/kg
116
Q

Midazolam
Respiratory effects=
CV effects=
CNS effects=

A

Respiratory effects= Minimal but synergistic respiratory depression with other sedatives
CV effects= Minimal
CNS effects= Anterograde amnesia, anticonvulsant properties, anxiolysis, antispasmodic

117
Q

Midazolam class

A

Class = benzodiazepine

118
Q

What is the formulation for midazolam and how is affected by pH

A

Formulation = imidazole ring

Acidic pH= imidazole ring OPENS and increases WATER solubility
Physiologic pH= imidazole ring CLOSES

119
Q

Describe the MOA of midazolam

A

GABA-A agonist increases the frequency of channel opening. This increases chloride conductance and neuronal hyperpolarization

120
Q

Describe the active metabolite for midazolam.

A

1-hydroxymidazolam

0.5x potency
Rapidly conjugated to inactive compound
Renal failure prolongs effects of active metabolite

121
Q

CV effects of midazolam

A

Minimal effects with sedation dose

HoTN and decreased SVR with induction dose

122
Q

Respiratory effects of midazolam

A

minimal effects with sedation dose

Respiratory depression with induction dose

Opioids potentiate respiratory depressant effects

COPD pts are more sensitive to the respiratory depressant effects

123
Q

CNS effects of midazolam (6)

A
  1. Minimal effect on CMRO2 and CBF with sedation dose
  2. Decreased CMRO2 and CBF with induction dose
  3. Anterograde amnesia
  4. Anticonvulsant
  5. Anxiolysis
  6. Spinally mediated skeletal muscle relaxation (antispasmodic)
124
Q

CNS effects of diazepam

A
  1. Antispasmodic agent by reducing skeletal muscle tone at the level of the spinal neurons
  2. Anticonvulsant
125
Q

CNS effects of lorazepam

A
  1. Amnestic effects last up to six hours

2. Anticonvulsant properties with slow onset

126
Q

Compare the relative potency of midazolam, lorazepam, and diazepam from greatest to least potent

A

Lorazepam > midazolam > diazepam

127
Q

Why do diazepam and lorazepam cause irritation with injection

A

The additive to enhance water solubility, propylene glycol, causes venous irritation

128
Q

Indications, induction dose, and maintenance dose for remimazolam

A 
Indications = Procedural sedation <30 minutes
Induction= 5 mg IV over 1 minute
Maintenance= 2.5 mg IV over 15 seconds q2 minutes
129
Q

Remimazolam
Peak sedation=
t1/2=

A

Peak sedation= 3-3.5 minutes after administration

t1/2 = 0.5-2 minutes

130
Q

Metabolism of remimazolam

A

non-specific plasma esterases

131
Q

Excretion of remimazolam

A

Urine

132
Q

Benefits of remimazolam in procedural sedation

A

Faster onset of action, deeper sedation, and faster recover

133
Q

How does remimazolam compare to propofol for procedural sedation

A

Less respiratory depression and better cardiopulmonary stability

134
Q

What patients should not received remimazolam

A

Patients with a history of severe hypersensitivity to dextran 40

135
Q

MOA of flumazenil

A

GABA-A receptor competitive antagonist

Higher affinity for receptor but shorter duration

136
Q

Initial flumazenil dose

Repeat dose

A 
Initial = 0.2 mg IV
Repeat = 0.1 mg q1 minute
137
Q

Duration of flumazenil and significance for dosing

A

30-60 minutes

Repeat doses may be required d/t longer benzo half-life

138
Q

Flumazenil side effects and cautions

A
  1. benzo-dependent patients may have signs of withdrawal or sz with administration
  2. Does not increases SNS tone, anxiety, or neuroendocrine stress
  3. Tends to reverse sedative effects over amnestic ones

APEX Pharmacology (8 decks)

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