Sedative/Hypnotics

Question 1

deprival edta has

Answer 1

preservative in it. hence edta

Question 2

propofol generic preservative =

Answer 2

sodium metabisulfite. Which can cause bronchospasm

Question 3

ampofol-low preservative

Answer 3

has no preservative r/t Lower lipid concentration

Question 4

aqua-van prodrug

Answer 4

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

Question 5

propofol MOA

Answer 5

Acts at GABAa (major)
glycine (minor)

reduces rate of dissociation of GABA from GABAa

NO SPINAL CORD DEPRESSION (despite glycine)

Question 6

volume of distribution of propofol is

Answer 6

HUGE

Vd 3.5 - 4.5 L/Kg

Question 7

metabolism of propofol is

Answer 7

CAPACITANCE dependent

because clearance exceeds hepatic blood flow. -

Relies on enzyme activity

Question 8

elimination half time of propofol

Answer 8

0.5 to 1.5 hours

Question 9

CNS effects of propofol

Answer 9

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

EEG burst suppression

antioxidant effects (vitamin E)

Question 10

highest dose of propofol is usually in

Answer 10

toddlers r/t increasing circulation

Question 11

must reduce propofol dose in

Answer 11

elderly, neonates

Question 12

propofol + bronchodilation

Answer 12

in COPD Patients, except when using generic with sodium bisulfate

Question 13

hypercarbia and hypocarbia respones in propofol

Answer 13

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

potential for bronchodilator in COPD

Question 14

CV effects of propofol

Answer 14

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?

Question 15

antipruritic and anti-emetic at

Answer 15

sub hypnotic doses

mechanism unknown.

Question 16

doses of propofol:

Answer 16

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

Question 17

metabolites of propofol

Answer 17

4-hydroxypropofol is 1/3 as potent

Question 18

Etomidate/Amidate is

Answer 18

carboxylated imidazole derivative

Question 19

Etomidate is ____ Lipid soluble

Answer 19

HIGHLY LIPID SOLUBLE.

pKa = 6.9

at physiological pH becomes highly lipid soluble hence fast onset.

Question 20

MOA etomidate:

Answer 20

binds to a specific site on the receptor

increases the affinity of GABA to GABAa

Question 21

onset of etomidate:

Answer 21

rapid, one arm to brain

Question 22

etomidate redistribution:

Answer 22

terminates hypnotic effect

Question 23

elimination half time of etomidate is

Answer 23

3-5 hours

Question 24

metabolism of etomidate is

Answer 24

PERFUSION dependent

Question 25

etomidate is a weak

Answer 25

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

Question 26

etomidate dose:

Answer 26

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

Question 27

CNS effects of etomidate

Answer 27

decrease IOP, ICP, CMRO2, CBF. Can INCREASE EEG at epileptic foci. Good in ECT, may cause seizure. MYOCLONUS

Question 28

CV effects of etomidate

Answer 28

MINIMAL! distinguishing feature

Question 29

Resp effects of etomidate

Answer 29

minimal decrease in response to Co2. minimal decrease in TV. INCREASE IN RR. hiccups/coughing.

Question 30

metabolism of etomidate

Answer 30

perfusion decedent liver. CYP 450 also some ester hydrolysis

Question 31

notable features of etomidate outside of CV/CNS/RESP

Answer 31

depression of synthesis of cortisol and aldosterone. 4-8 hours corticosuppresion C/I in PROPHYERIA PONV 30-40% highest incidence

Question 32

ketamine MOA

Answer 32

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.

Question 33

ketamine CNS:

Answer 33

``` dissociative. nystagmus pupil dilation salvation myoclonus ``` INCREASED CMRO2, CBF, IOP, ICP

Question 34

ketamine RESP:

Answer 34

minimal effects, bronchodilator! increased secretions

Question 35

ketamine: CV

Answer 35

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

Question 36

ketamine metabolism:

Answer 36

CYP 450 perfusion depedent INDUCES ENZYME METABOLISM, so tolerance develops

Question 37

ketamine metabolites:

Answer 37

NORKETAMINE | 1/3 to 1/5 as potent

Question 38

ketamine doses:

Answer 38

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

Question 39

precedex MOA:

Answer 39

potent alpha 2 agonist

Question 40

large density of alpha 2 at

Answer 40

pontine locus cerealus -> does sleep

Question 41

precedex CNS:

Answer 41

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

Question 42

precedex thermoregulation:

Answer 42

depresses thermoregulation and also inhibits shivering.

Question 43

precedex CV

Answer 43

bolus = initial hypertension then! decrease HR, SVR, BP, Bradycardia, risk for heart block asystole. ATTENUATES CV responses -> sympatholytic, decrease catecholamines

Question 44

precedex resp:

Answer 44

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

Question 45

metabolism of precedex

Answer 45

RAPID metabolism, but also inhibits CYP450. MAY INTERFERE WITH METABOLISM OF OTHER DRUGS

Question 46

specific antagonist for precedex =

Answer 46

atipamezol

Question 47

precedex dose

Answer 47

bolus: 1 mcg/kg over 10 min | infusion 0.2 - 1 mcg/kg/hr