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Anesthesia Pharm I > Benzodiazepines, flumazenil, naloxone, doxapram > Flashcards

Benzodiazepines, flumazenil, naloxone, doxapram Flashcards

1
Q

what are the pharmacologic effects of benzodiazepines?

A
  • sedation
  • anxiolysis
  • anticonvulsants
  • skeletal muscle relaxation
  • antegrade amnesia (only remembers from that time forward) *good for kids in holding with separation anxiety
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2
Q

describe the MOA of benzodiazepines.

A

BZD receptors are part of the GABA receptor, when activated, causes increased binding of GABA to its receptor opening Cl- channel, hyperpolarizing the neuron inhibition of the neuron to excitation
-also have an attraction to the glycine receptors in the brainstem and the spinal

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3
Q

what results from the action of benzos on the GABA receptors?

A
  • sedation from GABA receptors at the cortex

- anticonvulsant from GABA receptors at motor circuits in brain

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4
Q

what results from the action of benzos on the glycine receptors?

A
  • muscle relaxation from glycine receptors at spinal cord motor neurons
  • antianxiety from inhibition of afferent conduction at glycine receptors at brainstem
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5
Q

describe the GABA receptor

A

has separate binding sites for benzodiazepines, barbiturates, and ETOH
*if receptor is activated at more than one site (benzo with propofol or with alcoholic) effect is synergistic

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6
Q

describe midazolam (Versed)

A
  • most commonly admin as premedication or IV sedation
  • water-soluble at pH 3.5
  • imidazole ring makes it water soluble except when pH > 4 (body pH), it is lipid soluble (no pain on injection)
  • compatible with opioids and LR (acidic solutions)
  • routes: po, IM, sublingual, intranasal (uncooperative patients, very rapid onset), IV
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7
Q

what are some uses of midazolam?

A
  • premedication
  • sedation
  • induction of anesthesia
  • maintenance of anesthesia (not best choice, infusion has longer duration)
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8
Q

what are some CV effects of midazolam?

A
  • decrease in BP r/t SVR decrease
  • increase in HR (more than diazepam)
  • no change in CO
  • hemodynamic effects exaggerated in hypovolemic patients (no big change with normovolemc)
  • synergistic effects with opioids
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9
Q

what are some respiratory effects of midazolam?

A
  • dose-dependent decreases in ventilation (similar to diazepam)
  • *exaggerated in COPD, esp elderly with COPD
  • apnea with rapid injection of dose > 0.15 mg/kg IV and with opioids (don’t give both in holding!)
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10
Q

what are the CNS effects of midazolam?

A
  • decreases CMRO2 (metabolic rate, O2 consumption in brain)
  • decreases cerebral blood flow similar to barbiturates
  • *cannot cause EEG to become isoelectric like with pentothal (ceiling effect)
  • treat seizures from local anesthetic toxicity
  • excitement occurs in < 1% (peds) (treat with flumazenil)
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11
Q

what is the onset of midazolam?

A

0.9-5.6 minutes

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12
Q

how much of the oral dose of midazolam reaches circulation after hepatic first pass?

A

50%

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13
Q

what is the elimination 1/2 time of midazolam?

A

1-4 hrs

  • short duration of action d/t redistribution
  • may be doubled in elderly (give smaller dose)
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14
Q

how is midazolam metabolized and excreted?

A
  • hydroxylation by hepatic microsomal oxidative mech (C-P450)
  • hepatic clearance rate is 5x faster than lorazepam and 10x faster than diazepam
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15
Q

describe emergence from midazolam

A
  • slower awakening than pentothal
  • no N/V
  • no emergence excitement
  • one hour later after awake, no difference in alertness
  • *not good for outpatients since slower emergence
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16
Q

describe diazepam (Valium)

A
  • insoluble in water, dissolved in propylene glycol
  • *pain on injection, not good IM
  • rapidly absorbed orally
  • *peak concentration in 1 hr
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17
Q

what are CV effect of diazepam?

A
  • minimal BP, CO, or SVR decrease
  • less effects than barbiturates and midazolam
  • synergistic decreases with fentanyl
  • decreases exaggerated with hypovolemic patients
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18
Q

what are respiratory effects of diazepam?

A
  • depresses the response to CO2
  • minimal depressant effects until 0.2 mg/kg IV
  • *decrease in TV
  • apnea rarely occurs with dosages < 10 mg IV
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19
Q

what are CNS effects of diazepam?

A
  • decreases in CMRO2, CBF, ICP (less than barbiturates)
  • relaxant effects on skeletal muscle tone
  • decreases MAC up to 30%
  • decreases induction dose of thiopental
  • anticonvulsant prophylaxis (effects last longer than elimination 1/2 life, metabolites have same effect)
  • anxiolysis, amnestic (less than midazolam)
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20
Q

how is diazepam absorbed?

A
  • lipid soluble

- quickly absorbed for GI tract and crosses placenta

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21
Q

how is diazepam metabolized?

A

hepatic microsomal enzymes to:

  • desmethyldiazepam
  • oxazepam
  • both active metabolites
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22
Q

describe desmethyldiazepam

A
  • only slightly less potent than diazepam
  • drowsiness returns 6-8 hrs after admin (redistribution)
  • causes prolonged effects of diazepam
  • elimination 1/2 life 48-96 hrs
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23
Q

what is the elimination 1/2 life of diazepam?

A

21-37 hrs

  • increases with age
  • increases up to 5x with cirrhosis of the liver
  • prolonged with Tagamet, which has inhibitory effect on hepatic enzymes
24
Q

what is the peak effect of diazepam?

A

55 minutes

25
Q

describe lorazepam

A
  • insoluble in water, dissolved in polyethylene glycol or propylene glycol
  • less painful than diazepam
  • absorbed orally and IM
  • *slow onset and prolonged duration of action (not useful for outpatient))
  • *most potent
  • *antegrade amnesia lasts up to 6 hrs
26
Q

how is lorazepam metabolize?

A

into inactive metabolites

27
Q

why is lorazepam’s clinical effect longer?

A

slower release from the GABA receptors

28
Q

what is the elimination 1/2 life of lorazepam?

A

10-20 hrs (not as slow as diazepam d/t inactive metabolites)

*good for cardiac cases of younger patients (<50)

29
Q

what is the peak concentration time of lorazepam?

A

2-4 hrs (slower onset)

30
Q

describe flumazenil

A

-benzodiazepine antagonist

31
Q

what is the MOA of flumazenil?

A

competes with benzodiazepines for the BZD receptor sites on GABA receptors
*reverses respiratory depression effect of benzos

32
Q

what reversal effects can be seen with flumazenil?

A

DO NOT SEE: acute anxiety, stress response, HTN, tachycardia

  • could see withdrawal seizures for those on seizure tx
  • reversal of benzo effects buffered by weak agonist effect
33
Q

what is the onset of flumazenil?

A

2 minutes

34
Q

what is the duration of flumazenil?

A

30-60 minutes
*may need to redose or start infusion since benzo effects are longer and may become sedated or respiratory depressed again with lorazepam or diazepam

35
Q

describe naloxone (Narcan)

A
  • opioid antagonist

- antagonizes mu receptors more than kappa

36
Q

what is the MOA of naloxone?

A

attraction of naloxone for the receptor displaces the opioid from the receptor; the antagonist binds and inactivates the receptor

37
Q

what are clinical indications for naloxone use?

A
  • opioid overdose
  • post op ventilatory depression d/t opioids
  • neonatal ventilatory depression d/t maternal opioids
  • adverse effects of spinal and epidural opioids
38
Q

what is the onset of naloxone?

A

1-3 minutes

39
Q

what is the duration of naloxone?

A

30-45 minutes d/t redistribution

*may need to redose for opioids with longer effects

40
Q

how is naloxone metabolized?

A

primarily in the liver

41
Q

what are the respiratory effects of naloxone?

A
  • primary goal is to reverse respiratory depression
  • if titrated properly, can reverse depression without weakening analgesic effect
  • acute pulmonary edema can be caused by an increase in pressure and increased permeability of pulmonary capillaries (give small, incremented doses
42
Q

what are the cardiovascular effects of naloxone?

A
  • sympathetic stimulation **PAIN
  • tachycardia, ventricular irritability (V fib)
  • HTN
  • r/t speed and extent of reversal
  • titrate in small doses or even better just avoid reversal if possible
43
Q

what are CNS effects of naloxone?

A
  • N/V (r/t speed and dose)

- return of airway reflexes (possible laryngospasm)

44
Q

how does naloxone affect the neonate?

A

crosses the placenta and may cause life threatening withdrawal symptoms if opioid abusing mother

45
Q

how does naloxone affect opioid dependency?

A

if patient normally on opioids, may precipitate abstinence syndrome
*too much narcan can cause life threatening withdrawals

46
Q

when should you avoid naloxone?

A
  • critically ill
  • CAD
  • preexisting drug disease
  • CHF
  • cardiac surgery
  • opioid dependence
47
Q

describe doxapram

A

-CNS stimulant

48
Q

what is the MOA of doxapram?

A
  • stimulates hypoxic drive via the activation of the chemoreceptors in the carotid bodies
  • 1 mg/kg = PaO2 of 38 mmHg
  • produces an increase in TV and small increase in RR
49
Q

what are clinical indications for doxapram?

A
  • COPD patients who breathe based on hypoxic drive, but need supplemental O2
  • ventilatory depression and CNS depression d/t drugs (helps blow off volatile agent)
  • may see with propofol infusion but surgeon wants spontaneous breathing
50
Q

what is the onset and duration of doxapram?

A

onset: 1 minute
duration: 5-10 minutes

51
Q

how is doxapram metabolized?

A

mostly liver

52
Q

what are the CNS effects of doxapram?

A
  • stimulates hypoxic drive d/t activation of chemoreceptors in the carotid
  • mental status changes like confusion, dizziness, seizures (20-40x dose)
  • increased sympathetic outflow
  • vomiting
  • increased body temperature
53
Q

what are respiratory effects of doxapram?

A
  • increased minute ventilation by increasing tidal volume and slightly increasing RR
  • increases O2 consumption
  • wheezing (not good for COPD)
  • tachypnea (not good for COPD)
54
Q

what are CV effects of doxapram?

A
  • increased sympathetic stimulation
  • HTN
  • tachycardia
  • cardiac dysrhythmias
55
Q

when should doxapram not be used?

A
  • seizure disorder
  • cerebrovascular disease
  • acute head injury
  • CAD
  • HTN
  • asthma
  • halothane (sensitized to catecholamines)

Anesthesia Pharm I (28 decks)

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