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2022 Drug Deck > Sedative/Hypnotics > Flashcards

Sedative/Hypnotics Flashcards

not barbs not Benzes

1
Q

deprival edta has

A

preservative in it. hence edta

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2
Q

propofol generic preservative =

A

sodium metabisulfite. Which can cause bronchospasm

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3
Q

ampofol-low preservative

A

has no preservative r/t Lower lipid concentration

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4
Q

aqua-van prodrug

A

hydrolysis in plasma
can be unpredictable
slower onset, higher VD, higher potency

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5
Q

propofol MOA

A

Acts at GABAa (major)
glycine (minor)

reduces rate of dissociation of GABA from GABAa

NO SPINAL CORD DEPRESSION (despite glycine)

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6
Q

volume of distribution of propofol is

A

HUGE

Vd 3.5 - 4.5 L/Kg

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7
Q

metabolism of propofol is

A

CAPACITANCE dependent

because clearance exceeds hepatic blood flow. -

Relies on enzyme activity

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8
Q

elimination half time of propofol

A

0.5 to 1.5 hours

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9
Q

CNS effects of propofol

A

cerebroprotective
(decreses CBF, ICP, CMRO2, and CPP)

EEG burst suppression

antioxidant effects (vitamin E)

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10
Q

highest dose of propofol is usually in

A

toddlers r/t increasing circulation

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11
Q

must reduce propofol dose in

A

elderly, neonates

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12
Q

propofol + bronchodilation

A

in COPD Patients, except when using generic with sodium bisulfate

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13
Q

hypercarbia and hypocarbia respones in propofol

A

decreased ventilatory response to arterial hypoxemia /hypercarbia, intact ventilatory response to hypoxic pulmonary vasoconstriction

potential for bronchodilator in COPD

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14
Q

CV effects of propofol

A

25 - 40 % decrease in BP up to 40%
dose dependent myocardial depression and vasodilation

decrease in SV, CO, SVR

heart rate unchanged - inhibition of baroreceptors?

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15
Q

antipruritic and anti-emetic at

A

sub hypnotic doses

mechanism unknown.

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16
Q

doses of propofol:

A

induction 1 to 2.5 mg/kg or to 3 mg/kg in toddlers

GA maintenance: 100-300 mcg/kg/min
sedation infusion: 25 - 100 mcg/kg/min

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17
Q

metabolites of propofol

A

4-hydroxypropofol is 1/3 as potent

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18
Q

Etomidate/Amidate is

A

carboxylated imidazole derivative

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19
Q

Etomidate is ____ Lipid soluble

A

HIGHLY LIPID SOLUBLE.

pKa = 6.9

at physiological pH becomes highly lipid soluble hence fast onset.

20
Q

MOA etomidate:

A

binds to a specific site on the receptor

increases the affinity of GABA to GABAa

21
Q

onset of etomidate:

A

rapid, one arm to brain

22
Q

etomidate redistribution:

A

terminates hypnotic effect

23
Q

elimination half time of etomidate is

A

3-5 hours

24
Q

metabolism of etomidate is

A

PERFUSION dependent

25
Q

etomidate is a weak

A

base

but is water soluble in bottle. which is why we cant give it with a barb cause precipitates

26
Q

etomidate dose:

A

induction: 0.2 to 0.6 mg/kg (0.3 mg/kg)
maintenance: 10 mcg/kg/min c opined and n2o
sedation: 5-8 mcg/kg/min
rectal: 6.5 mg/kg

27
Q

CNS effects of etomidate

A

decrease IOP, ICP, CMRO2, CBF.

Can INCREASE EEG at epileptic foci. Good in ECT, may cause seizure.

MYOCLONUS

28
Q

CV effects of etomidate

A

MINIMAL! distinguishing feature

29
Q

Resp effects of etomidate

A

minimal decrease in response to Co2.

minimal decrease in TV.

INCREASE IN RR.

hiccups/coughing.

30
Q

metabolism of etomidate

A

perfusion decedent liver. CYP 450

also some ester hydrolysis

31
Q

notable features of etomidate outside of CV/CNS/RESP

A

depression of synthesis of cortisol and aldosterone.
4-8 hours corticosuppresion

C/I in PROPHYERIA

PONV 30-40% highest incidence

32
Q

ketamine MOA

A
  1. glutamate antagonist at NMDA
  2. Muscarinic agonsit?
  3. weak actions at GABA
  4. agonist at opiod (Mu, sigma, kappa, delta)
  5. inhibition at Ca++ channel, vgNa like LA.
33
Q

ketamine CNS:

A 
dissociative. 
nystagmus
pupil dilation
salvation
myoclonus

INCREASED CMRO2, CBF, IOP, ICP

34
Q

ketamine RESP:

A

minimal effects, bronchodilator!

increased secretions

35
Q

ketamine: CV

A

inhibits reuptake of NE so increased BP, SVR, HR, CO but directly is a cardiac depressant.

36
Q

ketamine metabolism:

A

CYP 450
perfusion depedent
INDUCES ENZYME METABOLISM, so tolerance develops

37
Q

ketamine metabolites:

A

NORKETAMINE

1/3 to 1/5 as potent

38
Q

ketamine doses:

A

spinal: 0.2 to 0.5 mg/k
sedation/analgesia: 0.2 to 0.5 mg/kg
induction: 1-2 mg/kg IV
4-8 mg/kg IM

PO/intranasal: 60 mg/kg

39
Q

precedex MOA:

A

potent alpha 2 agonist

40
Q

large density of alpha 2 at

A

pontine locus cerealus -> does sleep

41
Q

precedex CNS:

A

uncoupling!!! decrease CBF with no effect on ICP or CMRO2

42
Q

precedex thermoregulation:

A

depresses thermoregulation and also inhibits shivering.

43
Q

precedex CV

A

bolus = initial hypertension
then! decrease HR, SVR, BP, Bradycardia, risk for heart block asystole.

ATTENUATES CV responses -> sympatholytic, decrease catecholamines

44
Q

precedex resp:

A

minimal changes in RR, mod decrease in TV.
No change in Co2 response.
UPPER AIRWAY OBSTRUCTION POSSIBLE.

45
Q

metabolism of precedex

A

RAPID metabolism, but also inhibits CYP450.

MAY INTERFERE WITH METABOLISM OF OTHER DRUGS

46
Q

specific antagonist for precedex =

A

atipamezol

47
Q

precedex dose

A

bolus: 1 mcg/kg over 10 min

infusion 0.2 - 1 mcg/kg/hr

2022 Drug Deck (12 decks)

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