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Pharmacology of Anesthesia > Intravenous Anesthetics > Flashcards

Intravenous Anesthetics Flashcards

0
Q

What is the induction dose of Propofol?

What is the duration of action of Propofol?

A

Induction: 1-2.5 mg/kg IV
Duration: 3-8 min

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1
Q

What is “balanced anesthesia”?

A

Using smaller doses of multiple drugs rather than using larger doses with one or two drugs

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2
Q

What is the induction dose of Thiopental?

What is the duration of action for Thiopental?

A

Induction: 3-5 mg/kg IV
Duration: 5-10 min

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3
Q

What is the induction dose of Methohexital?

What is the duration of action of Methohexital?

A

Induction: 1-1.5 mg/kg IV
Duration: 4-7 min

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4
Q

What is the induction dose of Midazolam?

What is the duration of action of Midazolam?

A

Induction: 0.1-0.3 mg/kg IV
Duration: 15-20 min

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5
Q

What is the induction dose of Diazepam?

What is the duration of action of Diazepam?

A

Induction: 0.3-0.6 mg/kg IV
Duration: 15-30 min

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6
Q

What is the induction dose for Lorazepam?

What is the duration of action of Lorazepam?

A

Induction: 0.03-0.1 mg/kg IV
Duration: 60-120 min

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7
Q

What is the induction dose for Ketamine?

What is the duration of action of Ketamine?

A

Induction: 1-3 mg/kg IV, 4-8 mg/kg IM (*can be given IM)
Duration: 5-10 min

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8
Q

What is the induction dose of Etomidate?

What is the duration of action of Etomidate?

A

Induction: 0.2-0.3 mg/kg IV
Duration: 3-8 min

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9
Q

What is the induction dose for Dexmedetomidine?

What is the duration of action of Dexmedetomidine?

A

Induction: N/A
Duration: N/A

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10
Q

What are the 4 components of General Anesthesia?

A

Anxiolysis
Hypnosis
Analgesia
Paralysis

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11
Q

What is the Meyer-Overeton rule?

A

The potency of an anesthetic is proportional to it’s lipid solubility - this suggests a lipophilic site of action

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12
Q

Most anesthesia agents work by…?

A

Increasing inhibitory neurotransmitters and decreasing excitatory neurotransmitters

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13
Q

What is Neostigmine?

A

A drug used to reverse muscle relaxants. One side effect is that it causes bradycardia - so we give glycopyrrolate to reverse those effects.

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14
Q

The central compartment of the body includes:?

A
  • The plasma and the vessel-rich group of tissues (Liver, brain, heart, and kidneys).
  • Elimination of the intravenous medications occurs through the central compartment - this is the area of action for the sedatives and narcotics
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15
Q

What is the peripheral compartment?

A

This is considered to be the vessel-poor group which includes muscle, bone, skin, and fat.

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16
Q

What is the distribution of cardiac output?

A

VRG - 75%
Muscle - 19%
Fat - 6%
VPG - 0.5%

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17
Q

What factors affect distribution?

A
  1. Protein binding decreases available drug
  2. Protein availability - affects bound and free fraction of the drug
  3. Lipid solubility
  4. Ionization
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18
Q

What is the volume of distribution?

A

Quantifies the distribution of a medication between plasma and the rest of the body after dosing
Equation - total amount of drug int he body divided by drug blood concentration

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19
Q

What is the mechanism of action of Propofol?

A
  • Presumed interaction with GABA
  • Delays the dissociation of GABA from receptors (1. increasing GABA activated openig of chloride ion channels, 2. Also acts as a sodium channel blocker)
  • Hyper-polarization of cell membranes
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20
Q

How is propofol metabolized?

A

Via glucoronidation in the liver (Clearance exceeds heaptic blood flow, 30% may occur in the lungs), renal excretion

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21
Q

Propofol Pharmacokinetics

A
  • 95-99% protein binding
  • Elimination half life 30-60 minutes
  • Tissue uptake & redistribution are important factors in termination of action
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22
Q

What is the therapeutic plasma concentration of propofol?

A

1.5 - 5

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23
Q

What is context sensitive half times for various IV anesthetics?

A
  • the time for plasma level to decrease 50% after stopping infusion
  • Time of infusion affects rate at which drug level decreases
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24
Q

What are the cardiovascular effects of propofol?

A
  • decreases SBP, MAP, SVR
  • No change to HR
  • Profound arterial and venous vasodilation decreases preload and afterload
  • Also blunts the baroreceptor response as well
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25
Q

What are the pulmonary/respiratory effects of propofol?

A
  • RR depressed dose dependent - apnea after bolus

- Reduces airway reflexes

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26
Q

What are the CNS effects of propofol?

A
  • Decreases CBF, ICP, CMRO2, IOP

- Beware of decreasing SBP and CBP because of decreased CPP

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27
Q

What are other considerations of Propofol?

A
  • Has hypnotic properties, but NOT analgesia
  • Allergic reactions - contraindicated with egg allergy
  • Bacteria formation in solution
  • Reduces PONV & PDNV
  • Burns upon rapid injection in small vein
  • Bronchodilator, decreases airway reflexes
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28
Q

What is Propofol infusion syndrome?

A
  • Acute refractory bradycardia (kids)
  • RBBB is an early sign
  • May lead to asystole if one or more: metabolic acidosis, rhabdomyolysis, hyperlipidemia, Enlarged or fatty liver
  • Associated with propofol infusion greater than 4 mg/kg for long duration (>48 hours)
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29
Q

What is the initial dose of Fospropofol?

A

Initial dose: 6.5 mg/kg

  • additional 1.6 mg/kg as needed
  • reduce dose 25% for >65 years and ASA 3-4
  • perianal paresthesia in 74%
  • not currently at UIHC
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30
Q

What is the mechanism of action of Etomidate?

A
  • rapid onset of sleep (30-60 sec)
  • assumed to enhance the effects of GABA
  • rapid awakening
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31
Q

What are the pharmacokinetics of Etomidate?

A
  • 75% protein bound
  • Hydrolyzed to inactive metabolites via ester hydrolysis
  • Elimination half life is 75 min
  • Excretion is 85% renal, 15% biliary
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32
Q

What are the CV effects of Etomidate?

A
  • typically does not affect SBP, HR, or SVR
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33
Q

What are the pulmonary effects of Etomidate?

A
  • minimal respiratory depression, increased with opioids
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34
Q

What are the CNS effects of Etomidate?

A
  • decreases CBF, ICP, and CMRO2
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35
Q

What are some other considerations for Etomidate?

A
  • burns on injection
  • myoclonus
  • ADRENAL SUPPRESSION - inhibits 11beta-hydroxylase and to a lesser extent 17alpha hydroxylase; inhibits the production of cortisol and aldosterone to cause hypotension
  • no analgesia
  • increases PONV vs NaP or Propofol
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36
Q

What is the mechanism of action for Ketamine?

A
  • NMDA, Opioid, Monoaminergic, Muscarinic receptors, and voltage gated Ca channels
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37
Q

What are the pharmacokinetics for Ketamine?

A
  • extremely lipid soluble
  • metabolized in the liver to norketamine (1/3 - 1/5 the potency of ketamine)
  • Norketamine is hydroxylated and conjugated to H2O soluble and excreted (90% renal)
  • elimination half life 2-3 hours
38
Q

What are the CV effects of Ketamine?

A
  • increases SBP, HR, and SVR
39
Q

What are the pulmonary effects of Ketamine?

A
  • No respiratory depression, but increased with the use of opioids
  • we can give Ketamine out in the holding area because it doesn’t cause respiratory depression
40
Q

What are the CNS effects of Ketamine?

A
  • Increased CBF, ICP, CMRO2
41
Q

What dose of Ketamine can provide profound adjunctive analgesia?

A

0.2-0.5 mg/kg can provide profound analgesia

42
Q

What do you have to beware of with Ketamine?

A
  • Emergence Delirium
  • Visual, auditory, proprioceptive, and confusion
  • Premedicating with Midazolam seems to help
43
Q

What are the Barbiturates?

A
  • Thiopental
  • Thiamylal
  • Methohexital
  • Barbituric Acid
44
Q

What is the mechanism of action of Barbiturates?

A
  • Interact with GABAa (alpha subunit) receptor
  • different from the GABA or the BZD site
  • directly activate CL ion channels, increase their opening - increases the efficacy of GABA
  • hyperpolarize postsynaptic cell membranes
  • Also block the AMPA receptors
45
Q

What are the pharmacokinetics of Barbiturates?

A
  • NaP 83% protein bound
  • Highly lipid soluble = rapidly into CNS
  • Achieve CNS uptake in 30 sec
  • Prompt awakening after a single dose
  • HEpatic metabolism (inactive) and eliminated by the kidneys
46
Q

What are the CV effects of the Barbiturates?

A
  • Decrease SBP and SVR

- Increase HR

47
Q

What are the pulmonary effects of Barbiturates?

A
  • Respiratory depression, APNEA, return with slow respers and decreased tidal volumes
48
Q

What are the CNS effects of Barbiturates?

A
  • Decreased CBF, ICP, CMRO2
49
Q

What are the renal effects of Barbiturates?

A
  • Modest decrease in blood flow and GFR
50
Q

What are the pH effects on Barbiturates?

A
  • Metabolic acidosis increases the effect of Barbiturates
  • Metabolic alkalosis decreases the effect of Barbiturates
  • Respiratory acidosis has much less effect
51
Q

What do you have to beware of with Barbiturates?

A
  • Extravasation causes tissue sloughing
  • NaP + SUX = concrete in IV line
  • Intrarterial injection causes severe vasoconstriction
  • Induce the P-450 system
  • Contraindicated in patients with Acute Intermittent Porphyria
52
Q

What are the Barbiturates Key Points?

A
  • Awakening due to redistribution
  • NaP causes dose dependent decrease in SBP, SVR, CO d/t myocardial depression and increased venous capacitance
  • Potent respiratory depressants
  • Poor analgesics - may cause hyperalgesia
  • Contraindicated in Acute Intermittent Porphyria
  • Can cause histamine release
  • Avoid SUBQ and Intra-arterial injection d/t tissue sloughing
53
Q

What are benzodiazepines used for?

A
  • Sedation, anxiolysis, anticonvulsant effects, spinal-cord mediated muscle relaxation, and anterograde amnesia and at high doses unconsciousness and respiratory depression
54
Q

What are some considerations for Benzodiazepines?

A
  • No analgesic properties
  • High therapeutic indexes
  • Benzodiazepine + Narcotic = T.I. less than 10
55
Q

What is the primary inhibitory neurotransmitter?

A

GABA

56
Q

What is the mechanism of action for Benzodiazepines?

A
  • They facilitate action of GABA at the alpha subunit
  • Enhanced opening of the Cl channels
  • Hyperpolarization of postsynaptic membrane
  • Postsynaptic neurons resistant to excitation
57
Q

What are the pharmacokinetics of Diazepam?

A
  • Very lipid soluble - rapid uptake by brain, rapid redistribution, large VD: 1-1.5 L/kg, 0.2-0.5 ml/kg/min clearance rate
  • Long Elimination half-life - 21-37 hrs in healthy volunteers, much longer in the elderly, duration of action is determined by metabolism and elimination
58
Q

How is Diazepam metabolized?

A
  • Primarily metabolized in the liver via oxidative N-demethylation
  • 3 active metabolites:
  • Desmethyldiazepam - slightly less active than diazepam, metabolized more slowly than diazepam
  • oxazepam
  • Temazepam
  • Hepatic clearance does not change as we age - bodily proportion of fatty tissue increases, which increases VD for lipid soluble drugs and takes longer to metabolize
  • Cimetidine delays hepatic clearance
59
Q

What are the anesthetic effects of Diazepam?

A
  • Reduces the dose of induction agent
  • Reduces the MAC of inhalation agent
  • 0.2 mg/kg IV diazepam reduces MAC of halothane from to 0.48% - increasing the dose dies not further reduce the MAC
60
Q

What are the pharmacokinetics of Midazolam?

A
  • 2-4 times as potent as diazepam
  • Imidazole ring (water soluble at pH <4, closes upon injection and becomes highly lipid soluble)
  • 96-98% protein bound
  • Very lipid soluble
  • Large volume of distribution - 1-1.5 L/Kg
  • High rate of clearance - 6-8 ml/kg/min
  • Short elimination half-life - 1-4 hrs in healthy volunteers
61
Q

What are other considerations of Midazolam?

A
  • oxidative hydroxylation in the liver
  • glucoronide conjugation in the kidneys
  • metabolism not affected by H2 receptor antagonists
  • Depressed ventilation with 0.15 mg/kg dose
  • dose related decrease in CBF and CMRO2
  • crosses the U-P (utero-placental) membrane - don’t give to pregnant women
62
Q

What drug is more potent than diazepam or midazolam?

A

Lorazepam

63
Q

What is the elimination T1/2 of Lorazepam?

A

10-20 hours

64
Q

How is Lorazepam metabolized?

A
  • metabolized to inactive metabolites via glucuronide conjugation in the liver
  • metabolism is not altered by age, liver dysfunction, or H2 receptor antagonists
65
Q

Why do the clinical effects of Lorazepam outlast that of diazepam?

A

Lorazepam dissociates from the GABAa slower

66
Q

What are some other considerations of Lorazepam?

A
  • Reliable GI and IM absorption - dissolved in propylene or polyethelyne glycol
  • Less lipid soluble than diazepam
  • Elderly pts are sensitive to BZDs
  • Slow onset limits usefulness as IV pre-med or intra-op sedative
67
Q

Lorazepam is an excellent PO pre-medication. What are the doses?

A
  • 0.5-2.0 mg @ HS and 0.5-2.0 mg PO @ 06-0700
  • 50 mcg/kg (max. 4 mg) gives maximal anterograde amnesia for up to 6 hours
  • Larger doses produce greater sedation without increased amnesia
68
Q

What drug is given to reverse BZDs?

A

Flumazenil - is a specific and exclusive BZD competitive antagonist with a high affinity for the BZD receptor

  • It reverses all BZD effects in a dose dependent manner
  • There is not an abrupt reversal of sedative/amnestic effects as with narcotic reversal with nalaxone
  • onset of action is 30 sec-2min
69
Q

What is the dosing for Flumazenil?

A
  • 0.2 mg IV over 15 seconds
  • Wait 45 sec
  • Re-dose 0.2 mg increments over 15 sec
  • DO NOT EXCEED 3.0 mg/hour
  • If no response after 1 mg Flumazenil consider other causes -
    1. Incomplete reversal of muscle relaxation
    2. residual anesthetic agents
    3. hypoxemia
    4. hypercarbia
    5. Surgical complication
70
Q

What are Physostigmine and Aminophylline?

A
  • Other agents used to reverse BZDs

- They are not recommended b/c they are nonspecific, unpredictable, and inconsistent

71
Q

What is Dexmedetomidine?

A

Alpha 2 - adrenergic agonist - sedation, anxiolysis, hypnosis, analgesia, sympatholysis

72
Q

What is the mechanism of action of dexmedetomidine?

A
  • Nonselective alpha 2 agonist
  • Alpha 2 adrenoreceptors are membrane spanning G proteins
  • -inhibition of adenylate cyclase
  • -modulation of ion channels
  • -alpha 2B & alpha 2C receptors in the brain and spinal cord and stimulation leads to sympatholysis, sedation, and antinociception
  • Sedation - receptors in the locus cereleus
  • Analgesia - receptors in LC and spinal cord
73
Q

What are the CV effects of Dexmedetomidine?

A
  • decreased HR and SVR

- indirectly decreases CO, SBP & contractility

74
Q

What are the pulmonary effects of Dexmedetomidine?

A
  • decreases minute ventilation but maintains CO2 response

- Similar to natural sleep

75
Q

What are the CNS effects of Dexmedetomidine?

A
  • not well defined

- some neuroprotection?

76
Q

What is the premedication dose of Dexmedetomidine?

A
  • 0.33-0.67 mcg/kg 15 min before surgery
  • decreases induction agent dose
  • decreases MAC
77
Q

What is the MAC dose of Dexmedetomidine?

A
  • 1 mcg/kg over 10 minutes
  • slower onset and offset than propofol
  • similar cardiorespiratory effects
  • 0.7 mcg/kg/min keeps BIS 70-80
78
Q

How is Dexmedetomidine used as maintenance of general anesthesia?

A
  • reduces MAC of inhaled agent
  • reduces postoperative opioid requirements
  • not useful as a solo general anesthetic
79
Q

What is the mechanism of action of Droperidol?

A
  • Acts centrally at sites where dopamine, norepinephrine, and serotonin act
  • Alters normal CNS signal transmission
  • Exerts antiemetic effect at red astrocytes in the Chemo-receptor trigger zone
  • Has moderate alpha-adrenergic blocking ability
  • May occupy GABA receptors on the postsynaptic membrane casuing a buildup of dopamine in the inter-synaptic cleft
  • Neuroleptic anesthesia - catatonic like state
80
Q

What are the CV effects of Droperidol?

A
  • decreases SVR, MAP
  • does not affect CO or contractility
  • Prolonged QT interval (delayed repolarization, torsades de pointes)
81
Q

What are the respiratory effects of Droperidol?

A

Minimal

82
Q

What are the CNS effects of Droperidol?

A

NO human data

  • may worsen extrapyramidal side effects
  • contraindicated in Parkinson Dz.
83
Q

What are the uses of Droperidol?

A

Antiemetic: 0.625-1.25 mg IM/IV in adults
Premedication: similar

84
Q

What is the onset of action of Droperidol?

What is the duration of action of Droperidol?

A

Onset: 5-8 min
Duration: 3-6 hours

85
Q

What are the pharmacokinetics of Droperidol?

A
  • elimination half-life 1.7-2.2 hours
  • Hepatic transformation - two metabolites
  • elimination liver and kidneys
86
Q

What is the most common IV anesthetic agent?

A

Propofol - provides rapid onset and offset, potentiates GABA induced Cl channels

87
Q

What IV induction agent is contraindicated in the porphyria patient?

A

NaP - rapid onset and offset with single dose

88
Q

What are BDZ primarily used for?

A
  • Anxiolysis, amnesia, and sedation

- Act through the GABA receptor

89
Q

What IV agent is a phencyclidine derivative?

A

Ketamine - produces dissociative anesthesia and also analgesia, works on the NMDA receptor

90
Q

What IV agent is an imidazole derivative that preserves cardiac function?

A

Etomidate - can suppress adrenocortical function and increases PONV

91
Q

What IV agent is an alpha 2 adrenergic agonist that produces sedation, hypnosis, and analgesia?

A

Dexmedetomidine - acts on alpha 2’s in the LC

92
Q

What IV agent is a butryphenone (Haloperidol derivative), major tranquilizer, rarely used for GA - BUT is a potent antiemetic?

A

Droperidol - may cause R on T and Torsades de Pointes

Pharmacology of Anesthesia (6 decks)

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