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Pharmacology for Anesthesia > 02 - IV Anesthetics > Flashcards

02 - IV Anesthetics Flashcards

0
Q

Mechanism of action - barbiturates

A

Depress Reticular Activating System
Suppress exciting neurotransmitters (Ach)
Enhance inhibitory neurotrans (GABA)

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1
Q

Ten criteria for the ideal IV anesthetic

A 
Water soluble and stable
Lack of pain on injection, no tissue damage with extravasation
Low incidence of histamine release or hypersensitivity
Rapid, smooth onset
Rapid metabolism to inactive metabolites
Steep dose-response curve
Minimal cardiac/respiratory depression
Decreases ICP/CMRO2
Rapid, smooth recovery
Minimal side effects
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2
Q

Solubility and acidity of barbiturates

A

Water soluble but alkaline (ph>10)

Weak acid with pka close to 7.4

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3
Q

Are barbiturates stable?

A

No, lasts only 2 to 6 weeks in the refrigerator

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4
Q

What does intra-arterial injection of thiopental cause? How is it treated?

A

Crystals that lead to thrombosis and necrosis

Papaverine, lidocaine, stellate ganglion block, heparin

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5
Q

Thiobarbiturates compared to oxybarbiturates?

A

Thiobarbiturates (thiopental, thiomylal) - higher lipid solubility -> greater potency, rapid onset, shorter duration

Oxybarbiturates (methohexital) - lower lipid solubility -> less potency, slower onset, longer duration

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6
Q

Which drug is used for lethal injection?

A

Thiobarbiturates

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7
Q

What causes methohexital to have a short duration of action unlike other oxybarbiturates?

A

The methyl group

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8
Q

Absorption of barbiturates

A

IV for general anesthesia

Rectal/IM for premedication

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9
Q

Onset and redistribution time of barbs

A 
Fast onset (30 sec) and rapid redistribution (10-20 min) after single dose
Due to lipid solubility
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10
Q

What causes higher plasma levels of barbiturates?

A

Hypovolemia
Hypoalbuminemia
Acidosis
Elderly

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11
Q

Why are barbiturates a poor choice for maintenance of anesthesia?

A

Multiple doses saturate peripheral compartments, meaning slower redistribution
Long elimination half life - 3 to 12 hours

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12
Q

Biotransformation of barbiturates

A

Almost complete hepatic oxidation

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13
Q

Difference in biotransformation between thiopental and methohexital?

A

Thiopental - low hepatic extraction -> capacity limited, longer elimination half life

Methohexital - high hepatic extraction -> perfusion limited capacity, shorter elimination half life

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14
Q

Liver disease is unlikely to cause prolonged effect of thiopental from

A

A single dose

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15
Q

Renal clearance is difficult for barbiturates because

A

They are protein bound and lipid soluble - biotransformation must occur first

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16
Q

Elimination half life of methohexital

A

3.9 hours

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17
Q

Elimination half life of thiopental

A

11.6 hours

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18
Q

Dosage of methohexital

A

1-1.5 mg/kg/hr

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19
Q

Dosage of thiopental

A

3-5 mg/kg

6-8 mg/kg for infants

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20
Q

2-4 mg/kg/hr of thiopental

A

Can treat intracranial hypertension or intractable seizures

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21
Q

CV effects of barbiturates

A

Decreased blood pressure, increased heart rate (central vagolytic effect)

Venous pooling

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22
Q

With barbs, CO is maintained except in pts with

A

Hypovolemia
CHF
Beta blockade (very decreased CO and BP)

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23
Q

Respiratory effects of barbiturates

A

Decreased hypoxic/hypercapnia drive
Airway obstruction
Bronchospasm/laryngospasm

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24
Q

Neuro effects of barbiturates

A 
Decreased CBF, ICP
Very decreased CMRO2 to burst suppression on EEG
Anti analgesic?
Anti epileptic
Tolerance/dependence
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25
Q

Why do barbs cause decreased renal blood flow?

A

Hypotension

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26
Q

Hepatic - barbs

A

Decreased hepatic blood flow
Induction of enzymes (CYP)
Porphyrin formation

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27
Q

What is porphyria and what can drug can cause it?

A

Disorder of enzyme in heme biosynthetic pathway

Caused by barbs

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28
Q

Acute porphyria

A

Overproduction and accumulation of porphyrin

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29
Q

Neuro effects of acute porphyria

A

Abdominal pain, Vomiting, Neuropathy, Weakness, Seizures, Hallucinations, Depression, Anxiety, Paranoia, cardiac arrhythmia, pain, diarrhea

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30
Q

May evoke histamine release

A

Sulfur (thio) containing compounds

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31
Q

Mechanism of propofol

A

Inhibitory transmission of GABA

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32
Q

What is intralipid?

A

Brand name of fat emulsion made from soybean oil, glycerol, and egg lecithin

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33
Q

Lecithin

A

In egg yolks while most allergies to eggs are from the white

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34
Q

Propofol supports bacterial growth

A

Opened vials should be discarded after six hours

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35
Q

Phospropofol (Aquavan)

A

A water soluble prodrug

Side effect of perineal burning

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36
Q

Absorption of propofol

A

IV

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37
Q

Distribution - propofol

A

Highly lipid soluble

Very fast redistribution

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38
Q

Redistribution time of propofol

A

Less than eight minutes

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39
Q

Why is propofol suggested to have extrahepatic metabolism?

A

Biotransformation exceeds HBF

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40
Q

Biotransformation of thiopental or propofol is faster?

A

Propofol is up to ten times faster than thiopental

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41
Q

Biotransformation - propofol

A

Liver conjunction (inactive metabolites) but not affected by moderate cirrhosis

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42
Q

What is propofol infusion syndrome and what causes it?

A

Lactic acidosis after prolonged (>24 hrs) of high dose infusion (>75 mcg/kg/min)

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43
Q

Symptoms of propofol infusion syndrome

A

Lipemia
Rhabdomyolysis
Metabolic acidosis
Death

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44
Q

Excretion of propofol

A

Renal, but not affected by chronic renal failure

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45
Q

Dosage - propofol

A

1.5-2.5 mg/kg
25-75 mcg/kg/min for sedation
100-200 mcg/kg/min for GA - target of 4-6 mcg/ml

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46
Q

Risks of using propofol as a sole agent for GA

A

Risk of awareness

Higher incidence of movement

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47
Q

CV effects - propofol

A

Very decreased SVR, contractility, and preload
Hypotension due to above
Potential for bradycardia
Coronary sinus lactate production

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48
Q

What can cause greater CV effects with propofol?

A

Rapid injection
Old age
LV failure

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49
Q

Respiratory effects of propofol

A

Profound depression of upper airway reflexes
Apnea
Decreased hypoxic/hypercapnia drive

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50
Q

Does thiopental or propofol produce less wheezing?

A

Propofol

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51
Q

Neuro effects of propofol

A

Decreased CBF, ICP, CMRO2
Antiemetic, antiepileptic
Occasional myoclonus, hiccough

52
Q

What is bradykinin?

A

Protein produced by propofol and its lipid solvent

Vasodilates and increases contact between aqueous phase of propofol and free nerve endings

53
Q

What part of propofol causes burning?

A

The phenol (present in aqueous phase)

54
Q

Ways to prevent propofol burn

A

Lidocaine and tourniquet (Bier block)
Pretreat with IV opioid (alfentanyl)
Mixing with lidocaine to acidify

55
Q

How might lidocaine help with propofol burn?

A

Inhibits bradykinin

56
Q

Why does propofol have potential for abuse and addiction?

A

Produces euphoria on emergence, intense dreaming, and amorous behavior

57
Q

Mechanism of etomidate

A

Depresses reticular activating system

Mimics GABA

58
Q

Reduces the effect of disinhibition of motor activity (myoclonus) from etomidate

A

Premedications (benzos, opioids)

59
Q

Solubility of etomidate

A

Highly lipid soluble
Dissolved in propylene glycol (burns)
Available in fat emulsion (no burn)

60
Q

Absorption of etomidate

61
Q

Distribution of etomidate

A

Highly protein bound, but highly lipid soluble

Rapid distribution

62
Q

Biotransformation - etomidate

A

Hepatic hydrolysis and plasma esterases

Impaired in severe liver disease

63
Q

Excretion - etomidate

64
Q

Dose of etomidate

A

0.2-0.3 mg/kg

65
Q

What medication is the first line induction agent in trauma or unstable patients? Why?

A

Etomidate

Minimal CV and respiratory effects

66
Q

Neuro effects - etomidate

A

Decreased CMRO2, ICP, CBF
Myoclonus
Antiepileptic
PONV

67
Q

Which drug can enhance EEG signal?

A

Etomidate

Ketamine

68
Q

What kind of EEG signals does etomidate produce in epileptic patients?

A

Seizure like signals

69
Q

Etomidate transiently inhibits

A

Cortisol/aldosterone synthesis (lasts 4-8 hours after one dose)

70
Q

Fentanyl ___________ of etomidate

A

Increases levels and prolongs action

71
Q

Produces dissociative analgesia

72
Q

Mechanism of ketamine

A

Dissociates thalamus from limbic cortex = “cataleptic state”
Inhibition + excitation
NMDA antagonist

73
Q

Produces hallucinations

A

Phencyclidine analogue (ketamine)

74
Q

Absorption of ketamine

75
Q

Solubility of ketamine

A

Water soluble

76
Q

Distribution of ketamine

A

Rapid uptake and redistribution

77
Q

Biotransformation - ketamine

A

Liver metabolism (some active) with high extraction (HBF dependent)

78
Q

Excretion of ketamine

79
Q

Dose of ketamine

A

Analgesia: 0.1-0.5 mg/kg
Induction: 1-2 mg/kg IV or 4-8 mg/kg IM
Mixed with propofol: 1 mg ketamine per 10 mg propofol

80
Q

CV effects of ketamine

A

Increased HR, BP, CO

81
Q

How does ketamine increase HR, BP, and CO?

A

By inhibiting the reuptake of norepinephrine

82
Q

Respiratory effects of ketamine

A

Bronchodilator

Salivation

83
Q

T or F. Ketamine decreases ventilation.

A

False. Minimal effect

84
Q

Neuro effects of ketamine

A

Increased CMRO2, CBF, ICP
Hallucination
Myoclonus, but probably anti epileptic

85
Q

Infusion of which drug can be used to treat chronic pain syndrome?

86
Q

Ketamine potentiates

A

Neuromuscular blockers

87
Q

Ketamine used with _________ can cause seizures?

A

Theophylline

88
Q

Ketamine with sympathetic antagonists

A

Unmasks cardiac depression

89
Q

Ketamine with _____________ inhibits norepinephrine uptake, causing

A

Tricyclic antidepressants

Hypotension
HF
Ischemia

90
Q

Mechanism of benzos

A

Enhance GABA in cerebral cortex

91
Q

Benzos soluble in water

92
Q

Benzos insoluble in water

A

Lorazepam (Ativan)

Diazepam (Valium)

93
Q

Absorption of benzos

A

IV/IM
PO
Nasally
SL

94
Q

Why are benzos a poor choice for GA?

A

IV required

Significant first pass hepatic effect

95
Q

Distribution of midazolam

A

Moderately lipid soluble
Rapid redistribution
Protein bound

96
Q

Duration of benzo effect

97
Q

Onset and peak effect of midazolam

A

30-60 sec onset

Pam effect in 5 min

98
Q

Biotransformation of benzos

A

Hepatic (CYP3A4)

99
Q

Which benzo has a long elimination half life, low hepatic extraction, and active metabolites?

100
Q

Which benzo has medium elimination?

A

Lorazepam due to lower lipid solubility

101
Q

Which benzo has the fastest elimination?

A

Midazolam, high hepatic extraction

102
Q

Excretion of benzos

103
Q

Dose of midazolam

A

Premed: 0.04-0.08 mg/kg IV, 0.4-0.8 mg/kg PO
Induction: 0.1-0.3 mg/kg IV (slow recovery)
Infusion: 0.02-01 mg/kg/hr

104
Q

Can reduce hallucinations from ketamine

105
Q

CV effects of benzos

A

Minimal depression

106
Q

Respiratory effects of benzos

A

Small decrease in hypercapnic drive

107
Q

Neuro effects of benzos

A 
Decreased CMRO2, CBF, ICP
Anterograde amnesia
Anxiolysis
Anti seizure
Muscle relaxation
108
Q

Barbs or benzos decrease ICP more?

A

Barbs

Benzos do not cause burst suppression

109
Q

Symptoms of benzo withdrawal

A

Irritability
Tremulousness
Insomnia
Death

110
Q

Slows diazepam clearance

A

Cimetidine

111
Q

Benzos and heparin

A

Displaces diazepam from protein binding

112
Q

Slows midazolam clearance

A

Erythromycin

113
Q

Benzos interact synergistically with

A

Volatiles, opioids, ethanol, barbs, CNS depressants

114
Q

Why is flumazenil used as a reversal for other benzos? Dose?

A

High affinity for receptor with minimal activity

0.01 mg/kg up to 0.2 M IV bolis

115
Q

Max dose of flumazenil

A

1 mg

0.2 mg repeated every minute up to five doses

Resedation likely - redoes at 20 min intervals

116
Q

T or F. Flumazenil decreases MAC.

A

False, no effect

117
Q

Mechanism of decmetetomidine (precedex)

A

Highly selective alpha 2 receptor agonist

118
Q

Which is more selective for the alpha 2 receptor? Dexmedetomidine or clonidine?

A

Dexmedetomidine

119
Q

Used for sedation of ventilated ICU patients

A

Dexmedetomidine

120
Q

Uses for dex

A

Anxiolysis
MAC
Anesthesia adjuvant
Awake intubations

121
Q

Dose of dex

A

0.2-0.7 mcg/kg/hr

TIVA 5-10 mcg/kg/hr (I’ve never seen it)

122
Q

CV effects of dex

A

Hypotension

Bradycardia

123
Q

Respiratory effects of dex

124
Q

At high doses, dex can reduce the MAC of volatiles by

125
Q

Why can dex be used for awake intubation?

A

Calm sedation with rousability

126
Q

Which induction agent can decrease CMRO2 to burst suppression on EEG?

127
Q

Which barb can cause neuro excitation?

A

Methohexital

Pharmacology for Anesthesia (9 decks)

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