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Apex Flashcards > IV anesthetics > Flashcards

IV anesthetics Flashcards

1
Q

ID this drug

A

popofol
2, 6 diisopropylphenol

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2
Q

Propofol
chemical name
class
formulation
MOA
dose
onset
DOA
clearance
active metabolites

A
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3
Q

awakening from propofol is due to redistribution from

A

the brain

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4
Q

CV effects of propofol

A

decreased BP, SVR, venous tone, preload, myocardial contractility

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5
Q

respiratory effects of propofol

A

shifts CO2 response curve down and to the right (less sensitive to CO2)
inhibits hypoxic ventilatory drive

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6
Q

CNS effects of propofol

A

decreased CMRO2, CBF, ICP, IOP, no analgesia, anticonvulsant properties, myoclonus may occur

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7
Q

PRIS presentation

A

presents with acute refractory bradycardia –> asystole and at least one of the following
metabolic acidosis (base deficit >10)
rhabdomyolysis
enlarged orr fatty liver
retail failure
HLD
lipemia (cloudy plasma or blood) may be an early sign

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8
Q

egg lecithin is derived from

A

yolk

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9
Q

PRIS risk factors

A

propofol dose >4mg/kg/h
infusion duration >48h
sepsis
continuous catecholamine infusions
high dose steroids
significant cerebral injury

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10
Q

PRIS tx

A

d/c propofol
maximize gas exchange
cardiac pacing
PDE inhibitors
glucagon
ecmo
RRT

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11
Q

ID this drug

A

phosphono-o-methyl-2,6 diisopropylphenol aka fospropofol

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12
Q

fospropofol
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite

A
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13
Q

SE’s of fospropofol that are unique

A

genital and anal burning lol do not sign me up for this

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14
Q

fospropofol is metabolized by alkaline phosphatase into

A

propofol, formaldehyde, phosphate

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15
Q

ID this drug

A

2-(o-chlorophenyl)-2(methylamino) cyclohexanone hydrochloride aka ketamine

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16
Q

ketamine
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite

A
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17
Q

CV effects of ketamine

A

increased SNS tone, CO, HR, SVR, PVR
sub hypnotic doses (<.5mg/kg) usually dont activate SNS

ketamine is a direct cardiac depressant which will be unmasked in patients who have catecholamine depression like sepsis

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18
Q

respiratory effects of ketamine

A

bronchodilation
upper aw muscle tone and reflexes remain intact
maintains respiratory drive although a brief period of apnea may occur after induction
does not significantly shift CO2 response curve
increased PO and pulmonary secretions

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19
Q

CNS effects of ketamine

A

increased CMRO2, CBF, ICP, EEG activity, nystagmus, blepharospasm (avoid during eye surgery)

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20
Q

presentation of ketamine induced emergence delirium and risk factors

A

hallucinations (up to 24h)
benzos most effective
risk factors >15y, female, ketamine dose >2mg/kg, hx personality DO

21
Q

ketamine and analgesia

A

relieves somatic pain > visceral pain
blocks central sensitization and wind up in dorsal horn of SC
prevents opioid induced hyperalgesia
analgesic properties make it good for burn patients (frequent dressing changes) and those with preexisting chronic pain issues

22
Q

ketamine should be avoided in patients with a history of

A

acute intermittent porphyria

23
Q

ketamine plasma protein binding

A

12% (smallest of all induction agents)

24
Q

plasma protein binding of propofol

A

98%

25
Q

plasma protein binding of diazepam

A

98%

26
Q

plasma protein binding of midaz

A

94%

27
Q

plasma protein binding of lorazepam

A

90%

28
Q

plasma protein binding of etomidate

A

75%

29
Q

name this drug

A

R-1-methyl-1-(a-methylbenzyl) imidazole 5 carboxylate (etomidate)

30
Q

etomidate
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite

A
31
Q

CV effects of etomidate

A

minimal change in HR SV CO
SVR is decreased which accounts for small reduction in BP
does not block SNS response to laryngoscopy. opioid or esmolol will help

32
Q

respiratory effects of etomidate

A

respiratory depression

33
Q

CNS effects of etomidate

A

decreased CMRO2, decreased CBF, decreased ICP, stable CPP, no analgesia

34
Q

etomidate inhibits

A

11 beta hydroxylate and
17 alpha hydroxylase

35
Q

ponv is most common with which induction agent

A

etomidate

36
Q

etomidate should be avoided in patients with a hx of

A

acute intermittent porphyria

37
Q

is this an oxybarbiturate or a thiobarbiturate?

A

oxybarbiturate (O2 molecule in 2nd position)
thiobarbiturate (sulfur molecule in 2nd positon, increases lipid solubility and potency)

38
Q

ID this drug

A

5 ethyl 5 (1 methyl butyl)-2-thiobarbituric acid
aka thiopental

39
Q

thiopental
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite

A
40
Q

CV effects of thiopental

A

HoTN r/t ventilation and decreased preload. myocardial depression is secondary cause
thiopental causes non immunogenic histamine release that also contributes to HoTN
baroreceptor reflex is reserved so reflex tachycardia helps preserve CO
produces less HoTN than propofol

41
Q

respiratory effects of thiopental

A

resp depression (shifts CO2 response curve to the right)
histamine release can cause bronchoconstriction (caution with asthma)

42
Q

CNS effects of thiopental

A

decreased CMRO2, CBF, ICP, EEG activity, no analgesia
focal ischemia protection: yes (CEA, temporary occlusion of cerebral arteries(
global ischemia protection: no (ex: cardiac arrest)

43
Q

define acute intermittent porphyria

A

defect in heme synthesis that promotes accumulation of heme precursors
key component of HGB, myoglobin, CYP450 enzymes
SuccinylCOA + glycine –> ALA synthase –>precursors –> heme
made worse by stimulation of ALA synthase, emotional stress, prolonged NPO status, CYP 450 induction

44
Q

s/sx of acute intermittent porphyria

A

GI: severe abdominal pain (most common and typically first), n/v
CNS: anxiety, seizures, confusion, psychosis, coma
PNS: skeletal muscle weakness, bulbar weakness

45
Q

drugs to avoid with acute intermittent porphyria

A

any drug that induces ALA synthase can potentially accelerate production of heme precursors
barbiturates
etomidate
ketamine
ketorolac
amiodarone
many CCB’s
BC pills

46
Q

anesthetic management of acute intermittent porphyria

A

liberal hydration
glucose supplementation (reduces ALA synthase activity)
heme arginine (reduces ALA synthase activity)
prevention of hypothermia

47
Q

tx of inta arterial injection of thiopental

A

injection of vasodilator: phentolamine or phenoxybenzamine
sympathectomy: stellate ganglion block or brachial plexus block

48
Q

metabolism of phenobarbital

A

excreted unchanged in the urine (while p450 metabolizes all other barbiturates)

49
Q

drugs to avoid with acute intermittent porphyria

A

barbiturates
etomidate
ketamine
ketorolac
amiodarone
CCB
BC

Apex Flashcards (71 decks)

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