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GNURS625/Pharmacology for Anesthesia > Quiz 2 Intravenous Induction Agents > Flashcards

Quiz 2 Intravenous Induction Agents Flashcards

1
Q

Where is the synthesis and storage of neurotransmitter molecules?

A

The synaptic vesicle.

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2
Q

The reuptake of the neurotransmitter is sponged up by what?

A

Presynaptic neuron.

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3
Q

Where do the neurotransmitter molecules get released?

A

Synaptic cleft

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4
Q

Where does binding of a neurotransmitter occure?

A

Postsynaptic membrane.

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5
Q

What are some drug classes that interact with the GABA receptor?

A
  • GABA
  • Benzodiazepine
  • Propofol
  • Neurosteriods
  • Volatile Anesthetics
  • Ethanol
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6
Q

What receptor does Precedex work on?

A

Alpha 2

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7
Q

Is Precedex an agonist or antagonist?

A

Agonist

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8
Q

What are the advantages of anesthesia/induction agents?

A
  • Provide rapid onset of general anesthesia
  • Can be used for maintenance phase of general anesthesia
  • Can provide sedation for Monitored Anesthesia Care
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9
Q

What is the amount of time CRNAs have between induction agents to maintenance agents?

A

< 9 minutes

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10
Q

What is needed to have a balanced anesthesia?

A
  • Inhalation agents
  • IV induction agents
  • Sedative/hypnotic agents
  • Opioids
  • Neuromuscular blocking drugs
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11
Q

What is in common about all IV INDUCTION agents?

A

All are lipophilic

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12
Q

What is the one compartment model?

A

One compartment model describes the bolus of a drug to be rapidly distributed throughout the body evenly.

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13
Q

What is two compartment model?

A

Considers the body as a compartment with a central compartment with rapid mixing and a peripheral compartment with slower distribution. This means the central compartment has the drug shortly after drug administration and the peripheral compartment gets the drug more slowly.

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14
Q

What is three compartment model?

A
  1. Drug is injected and restricted to the central blood volume.
    2.Distribution is limited primarily to oxygen rich compartment at first (Brain, liver, kidneys, and gut).
  2. After this a two other phases take place.
    -The first is rapid redistribution to vessel poor group (shallow compartment).
    Primarily muscle tissues
    Phase lasts 2-4 minutes
    Patient would awaken from initial
    drug administration
    -Second is slow distribution phase occurs iwth redistribution into the peripheral compartments (deep compartment.
    Fat
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15
Q

What are some IV induction agents?

A
  • Barbiturates
  • Benzodiazepines
  • Propofol
  • Ketamine
  • Etomidate
  • Dexmedetomidine
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16
Q

Who was the first to introduce barbiturates?

A

Waters & Lundy introduced thiobarbiturate in 1935.

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17
Q

How many barbiturates have been developed since the 1930?

A

Over 2000.

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18
Q

What was the barbiturate of choice before it was removed from practice?

A

Thiopental

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19
Q

What is the description of a barbiturate?

A
  • Any drug derived from barbituric acid
  • Barbituric acid lacks CNS activity
  • Hypnotic, sedative and anticonvulsant effects occur through substitutions on the N1, C2, and C3 sites.
  • To make it lipophilic a substitution has to be placed on the barbituric.
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20
Q

What barbiturate drugs work by substitution at C2?

A
  1. -Sulfur-thiobarbiturate-thiopental-pentothal

2. Oxygen- methylated oxybarburate- methohexital-brevital

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21
Q

What is the mechanism of action for barbituates?

A
  • Post synaptic enhancement of GABA mediated inhibitory neurotransmitters
  • May also have GABA-mimetic effects
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22
Q

What does barbituates bind to?

A 
Protein binding
-Plasma albumin
-Whent the unbound faction of 
  barbiturate is increased the observed
  clinical effect is greater.
-Situations that increase unbound fraction of barbiturate.
      Decrease plasma protein 
      concentration
            Uremia
            Hepatic disease
            3rd trimester of pregnancy
      Competition of other drugs for
       protein binding sites
            Aspirin
            Naproxen
            Indomethacin
            Warfarin
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23
Q

What is the pharmacokinetics of barbituates?

A
  • 3 compartment model
  • redistribution has a major effecct on the duration of therapeutic action
  • Elimination occurs when inactive metabolites are excreted in the urine.
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24
Q

What is the metabolism of barbituates?

A 
-Hepatic metabolism
     Primarily  by oxidation 
     Second by N-dealkylation
     Desulfuration
     Destruction of barbituric acid ring
-Metabolite
     Inactive
     Excreted in urine
-P450 microsomal system
     Enxyme indution occures with chronic
     barbiturate use and increases rate of
     barbituate metabolism
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25
Q

What are the CNS effect of barbituates?

A

-Promply produces a 15-30 loss of LoC
-Produce mild to complete loss of consciousness
-post op drowsiness
-No analgesic properties and is not useful for maintenance of anesthesia
-dose dependent decrease in cerebral metabolic rate of oxygen consuption
-dose dependent decreases in cerebral blood flow
-Decrease in ICP and IOP
-Anesthetic doses have anticonvulsant
properties and can abruptly stop seizures

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26
Q

Do barbiturates cause a dose dependent histamine release?

A

Yes

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27
Q

What occurs with a barbiturate extravascular injection?

A

Irritation to surrounding tissue. (Mild vasospasm to sever tissue necrosis.

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28
Q

What occurs with intra arterial injection of a barbituate?

A

INJECTION

  • immediate vasospasm
  • severe vasoconstriction
  • intense pain
  • Blanching of entrire extremity
  • High risk for ischemic gangrene

Intervention

  • Dilute drug with NS
  • Papaverine 40-80 mcg (Vasospasm)
  • Stellate ganglion or bbrachial plexus block to increase circulation
  • Heparinization if not contraindicated
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29
Q

Benzodiazepines?

A
  • Librium
  • Diazepam
  • Serax
  • Lorazepam
  • Midazolam
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30
Q

What are benzodiazepines used for?

A
  • Anxiolytic (amygdala, hippocampus, limbic areas)
  • Sedation(brainstem and cortical recptors)
  • Anticonvulsant
  • Muscle relaxation (spinal cord)
  • Amnesia (forebrain and hippocampus)
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31
Q

Benzodiazepines VS. Barbiturates?

A
  • Less tolerance
  • Less abuse potential
  • Greater margin of safety against overdose
  • Fewer and less significant drug interaction
  • Do not induce hepatic microsomal enzymes
32
Q

Chemical structure of midazolam?

A
  • unique
  • Imidazole ring
  • Does not require a lipid vehicle
33
Q

What is the mechanism of action for Midazolem?

A

-Activation of GABAA receptor complex and enhancement of
GABA mediated chloride currents.
-Neurons become hyperpolarized and less excitable.
-Midazolam has greater potency and affinity for
benzodiazepine receptor site on GABAA.
*2-3 times the potency of diazepam

34
Q

What is the pharmacokinetics of Midazolam?

A

-Highly lipid soluble thus rapidly enter CNS.
-Highly protein bound
-Despite rapid passage into the brain, midazolam has a slower effect site
equilibrium. IV doses must be spaced to permit observation of peak clinical
effect prior to giving a repeat dose.
0.9 – 5.6 minutes
-CYP substrate
-Urinary excretion

35
Q

What affects do midazolam have on the CNS?

A
  • Decrease CMRO2 (to a lesser extent than barbiturates)
  • Decrease CBF (to a lesser extent than barbiturates)
  • Cannot produce an isoelectric EEG
  • Little to no change in ICP
  • Not neuroprotective
  • Potent anticonvulsant properties
  • Paradoxical excitement occurs in <1% of patients receiving versed
36
Q

What affect does midazolam on the cardiovascular?

A
  • Dose dependent decrease in systemic blood pressure.
  • Post-induction hypotension is greater after midazolam than diazepam.
  • Cardiac output is not changed.

-Blood pressure response is due to decrease in systemic vascular resistance.
Effects of vasodilation are exaggerated in the hypovolemic patient.
Midazolam does not prevent sympathetic response (increased HR & BP) to intubation of trachea.

37
Q

What effect does midazolam have on the respiratory system?

A

-Minimal, dose dependent decrease in ventilation.
-Decrease in ventilatory response to CO2.
-May observe a transient period of apnea after a rapid IV dose of drug.
Significant with midazolam
Synergistic and additive with opioids
-Depression of swallowing reflex.
-Decrease in upper airway activity

38
Q

What side effects do midazolam have?

A

-Allergic reactions – extremely rare
-Pain on injection
Diazepam – propylene glycol solvent
-Drowsiness, over sedation
-Anterograde amnesia

39
Q

What are the reversal agents for Benzodiazapines?

A

-Benzo antagonist- competitive
-200 mcg every 1–2 minutes until the effect is seen, to a
maximum of 3 mg per hour
-Some benzos have longer half lives than flumazemil (ex: midazolam)

40
Q

What is Propofol?

A
  • The most frequently administered drug for induction of anesthesia.
  • Provides excellent IV sedation in both the OR and ICU setting.
  • Can successfully be used for IV maintenance of general anesthesia
41
Q

What are the two reformulation of propofol?

A

-AstraZeneca
Diprivan
Disodiumedenate (EDTA)

-Propofol
Sodium metabisulfite
May cause sulfite related allergic reaction
Anaphylaxis
Asthmatic episodes in patient with known history of asthma

42
Q

What are the pharmacokinetics of propofol?

A
  • An IV induction dose of 1.5–2.5 mg/kg/IV causes rapid onset of unconsciousness. (30 seconds)
  • Rapid return of consciousness with minimal residual CNS effects is a significant benefit of propofol over other IV induction drugs. (Duration 3-10 min)

-Rapid clearance of propofol from the plasma exceeds hepatic blood flow.
Less “hangover” effect

  • Follows the three compartment model in a manner similar to the IV induction drugs.
  • CYP substrate and inhibitor (strong 3A4, mod 2C19)
43
Q

What is the mechanism of action for propofol?

A

-Propofol is a relatively selective modulator of gamma aminobutyric acid (GABAA) receptors.

44
Q

What effects do propofol have on the CNS?

A

-Decrease in CBF
-Decrease in CMRO2
-Decrease in ICP
-Decrease in IOP
-Neuroprotective during focal ischemia
-Possesses anti-epileptic properties
Not a good induction agent for ECT
Decreases seizure activity 35-45%
-May observe twitching or spontaneous movement of patient during induction.
-Not seizure activity

45
Q

What effects do propofol have on the Cardiovascular?

A

-Profound decrease in systemic blood pressure.
Significant peripheral vasodilation
Decrease in both afterload and preload
-This blood pressure effect is exaggerated in:
Elderly patients
Patient’s with hypovolemia or decrease intravascular volume
Rapid injection of drug

-Dramatic inhibition of normal baroreceptor reflex.
Small increase in heart rate with decrease in blood pressure
Exaggerated hypotensive response
Profound bradycardia and hypotension in healthy adults.

46
Q

What effect does propofol have on the respiratory system?

A

-Potent respiratory depressant.
-Typically produces apnea after induction dose.
-Maintenance infusion will decrease minute ventilation by
decreasing tidal volume and respiratory rate.
-Decrease ventilatory response to hypoxia.
-Decrease ventilatory response to hypercapnia.
-Significant reduction in upper airway reflexes:
Good intubating conditions
Good LMA conditions
Less laryngospasm, bronchospasm and wheezing after
airway instrumentation

47
Q

What are other effects propofol has?

A
  • Anti-emetic properties
  • Does not potentiate muscle relaxants
  • Pain on injection
  • Bradycardia
  • Risk of infection
  • Elevated serum triglycerides with prolonged administration
  • Potential for pulmonary embolism
  • Antipyretic activity
  • Antioxidant properties
48
Q

What is Propofol infusion syndrome?

A

-Lactic acidosis that occurs in patients who receive prolonged high-dose
infusions for greater than 24 hours.
75mcg/kg/min
-Lactic/metabolic acidosis has been documented after short term,
surgical infusions of propofol.
Kidney failure, rhabdomyolysis, cardiac arrest
-Unexpected tachycardia occuring during propofol anesthesia should
trigger evaluation for possible metabolic/lactic acidosis.
Serum lactate concentration
Arterial blood gas analysis
-Hypertrigyceridemia: hepatomegaly

49
Q

What is the treatment for propofol infusion syndrome?

A
  • Prompt discontinuation of propofol infusion
  • Treatment of lactic acidosis
  • Support of multi-system failure
50
Q

What is Fospropofol (Lusedra)?

A
  • Water soluble pro-drug of propofol
  • Same MOA
  • Similar side effects
  • No lipid vehicle
51
Q

What is Ketamine?

A

-Dissociative anesthesia
-EEG dissociation between thalamocortical and limbic system
-Patient is non-communicative
-Resembles a cataleptic state with eyes open and slow nystagmic gaze
-Varying degrees of hypertonicity or purposeful skeletal movement independent of
surgical stimulation
-Amnesia is not complete – !! give a benzodiazepine !!
-Intense analgesia
-Use is significantly limited by possibility of causing emergence delirium
Reduced by benzo use

52
Q

What is the chemical structure of ketamine?

A
  • Phencyclidine
  • 2-(O-chlorophenyl)-2-(methylamino)cyclo-hexanone
  • Partially water soluble
53
Q

What is the pharmacokinetics of ketamine?

A
  • Not significantly bound to plasma proteins
  • Leaves blood rapidly to be distributed to tissues
  • Extremely lipid soluble and crosses blood brain barrier
  • Recovery from a single bolus dose occurs primarily from redistribution
  • 3 compartment model of distribution
54
Q

What is the metabolism of ketamine?

A

-Extensive metabolism by hepatic microsomal enzymes.

-Demethylation of ketamine to norketamine.
Active metabolite with 1/3rd -1/5th potency of ketamine.
Norketamine may contribute to the prolonged effects of ketamine especially
with repeat doses or continuous infusion.
-Norketamine is hydroxylated and then conjugated into water soluble inactive
glucuronide metabolites which are excreted by the kidney.

55
Q

What is the mechanism of action of ketamine?

A 
-Binds noncompetitively to the phencyclidine recognition site on N-methyl-D-aspartate
  (NMDA) receptors.
       NMDA receptor antagonist
-Exerts weak action at GABAA receptor.
-May exert effects at other receptors:
      Opioid
      Monoaminergic
      muscarinic
-Inhibits nitric oxide synthase
      analgesic effects
-Inhibits reuptake of catecholamines
      Stimulates sympathetic nervous system
-Induces catecholamine release
      Beta 2 agonism- respiratory relaxation
56
Q

Does Ketamine attach to the N-methyl-D-aspartate (NMDA)?

A

Yes

57
Q

What effect does ketamine have on the CNS?

A

-Cerebral vasodilator
Increases cerebral blood flow
Increases CMRO2
-Not recommended for use in patient with intracranial pathology
-Is considered an anticonvulsant
-May be used for status epilepticus when other drugs fail
-May cause myoclonic movement on injection

58
Q

What effect does ketamine have on the cardiovascular?

A

-Direct myocardial depressant
Depressant effects are usually masked by stimulation of sympathetic nervous
system
May be significant in critically ill patient with limited reserve to increase
sympathetic activity
-Produces significant, transient increases in systemic BP, HR and CO
Centrally mediated sympathetic stimulation
Associated with increased cardiac work and increased cardiac metabolic
requirement for oxygen

59
Q

What effect does ketamine have on the respitory?

A

-No significant respiratory depression
-When used alone, respiratory response to hypercapnia is preserved
-Transient hypoventilation
-May cause short periods of apnea with rapid administration of drug
-Relaxes bronchial smooth muscle and thus may be helpful in patients with
reactive airways or bronchoconstriction

60
Q

What is etomidate?

A
  • Chemically unrelated to other IV induction agents
  • CNS effects result in hypnosis
  • No intrinsic analgesic properties
  • Minimal cardiovascular effects
61
Q

What is the chemical structure of etomidate?

A
  • Carboxylated imidazole derivative
  • Propylene glycol solvent
  • pH of 8.1
  • 2 isomers – R+ isomer is hypnotic
  • Only IV induction drug that is not a racemic mixture
62
Q

What is the pharmacokinetics of etomidate?

A

-Rapid distribution half-life
-Single IV bolus has extremely short duration of action (3-5 min, peak 1 min)
-76% plasma protein binding
-Follows a 3 compartment model
-Hepatic extraction ratio is near 60-70%
-Total body clearance is rapid
-Minimal drug accumulation makes it useful for repeat doses and continuous
infusions

63
Q

What is the metabolism of etomidate?

A

-78% metabolized by hepatic microsomal enzymes
Rapid hydrolysis of ethyl-ester side chain to its carboxylic acid ester
This metabolite is a water soluble, pharmacologically inactive compound

-3% of drug is recovered unchanged in the urine

64
Q

What is the limiting factors affecting use of etomidate?

A

-Transient depression of adrenocortical function.
Dose – dependent inhibition of adrenocortical enzymes
Reversible inhibition
Lasts 4-8 hours after single bolus induction dose
Greater if continuous IV infusion is used
Theoretically patients with sepsis/hemorrhage may be at a disadvantage
receiving Etomidate if the cortisol response is compromised
-Alternatively, thought to be beneficial suppression of adrenocortical stress
response and an advantage to provide “stress free” anesthetic

65
Q

What in the mechanism of action of etomidate?

A

-Potentiation of GABAA mediated chloride shift

66
Q

What effects does etomidate have on the CNS?

A
  • Decreased cerebral blood flow
  • Decreased CMRO2
  • Decreased ICP while maintaining CPP
  • Maintains cerebral blood vessel responsiveness to changes in CO2 level
  • Decrease IOP
67
Q

What effect does etomidate have on the cardiovascular?

A

-Provides cardiovascular stability and is drug of choice for patient with unstable
cardiac system.
-Minimal change in HR, BP, CVP.
-Myocardial oxygen supply and demand remains constant by balanced decrease in
both myocardial blood flow and decrease in oxygen consumption.
-Patient’s with aortic or mitral valvular disease may, however, have a significant
-decrease in systemic BP, PAP, PCWP.

68
Q

What effect does etomidate have on the respiratory?

A
  • Dose dependent decrease in minute volume with a compensatory increase in RR.
  • Decrease ventilatory response to CO2.
  • Brief periods of apnea followed by hyperventilation.
69
Q

What other consideration should be thought of for etomidate?

A

-Increased incidence of PONV
-Does not effect duration of induced seizure activity (good for electro-convulsive therapy)
-No analgesia properties
-Involuntary myoclonic movement is common during induction
Caused by alteration in balance of inhibitory/excitatory influences
on thalamocortical tract
May be decreased by prior opioid administration
-Standard induction dose: 0.2-0.4 mg/kg IV
-No histamine release
-Low incidence of allergic reaction

70
Q

What is Dexmedetomidine?

A

(Precedex)

  • Highly selective α2-adrenergic agonist
  • Active component is the D-isomer of medetomidine
  • Water soluble IV formulation
71
Q

What is the pharmacokinetics of precedex?

A
  • Highly protein bound
  • Rapidly metabolized by hepatic microsomal enzymes
  • Metabolites excreted in urine and bile
  • Clearance is high
  • Elimination half-time is short
72
Q

What is the metabolism for precedex?

A
  • active d-isomer of medetomidine
  • metabolized in liver
  • eliminated via kidney
73
Q

What is the mechanism of action for precedex?

A
  • Activates CNS α2 receptors and produces selective α2 agonist effects.
  • Hypnosis results from stimulation of α2 receptor at locus ceruleus.
  • Analgesia originates at the level of the spinal cord.
  • Sedative effect mimic a physiologic sleep state – activates endogenous sleep pathways.
  • Potential for tolerance.
74
Q

What effect does precedex have on the CNS?

A
  • Decrease in CBF
  • No change in ICP
  • No change in CMRO2
  • Decrease in plasma catecholamine concentration
  • Decrease in MAC requirement for inhaled anesthetics
  • Decrease in anesthetic requirement for opioid
75
Q

What effects does precedex have on the cardiovascular?

A
  • Moderate decrease in heart rate
  • Moderate decrease in systemic vascular resistance
  • Bolus of drug may cause brief increase in systemic blood pressure and pronounced bradycardia
76
Q

What effects does precedex have on the respiratory?

A
  • Small to modest decrease in tidal volume
  • No significant change in respiratory rate
  • Ventilatory response to CO2 does not change
  • May observe mild airway obstruction secondary to sedation
  • Synergistic effect with other sedative-hypnotics
77
Q

What are other consideration for precedex?

A

-Dose guidelines
0.5 – 1 mcg/kg load over 10-15 minutes
then infusion at 0.2 – 0.7 mcg/kg/hr
MUST decrease all concentrations of other anesthetic agents
-Current uses
Short term sedation in ICU
Sedation for fiber-optic intubation
Decrease post-operative delirium
Decreases arousal and produces a calm patient that can
easily be aroused to full consciousness.

GNURS625/Pharmacology for Anesthesia (13 decks)

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