IV anesthetics Flashcards
ID this drug
popofol
2, 6 diisopropylphenol
Propofol
chemical name
class
formulation
MOA
dose
onset
DOA
clearance
active metabolites
awakening from propofol is due to redistribution from
the brain
CV effects of propofol
decreased BP, SVR, venous tone, preload, myocardial contractility
respiratory effects of propofol
shifts CO2 response curve down and to the right (less sensitive to CO2)
inhibits hypoxic ventilatory drive
CNS effects of propofol
decreased CMRO2, CBF, ICP, IOP, no analgesia, anticonvulsant properties, myoclonus may occur
PRIS presentation
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
egg lecithin is derived from
yolk
PRIS risk factors
propofol dose >4mg/kg/h
infusion duration >48h
sepsis
continuous catecholamine infusions
high dose steroids
significant cerebral injury
PRIS tx
d/c propofol
maximize gas exchange
cardiac pacing
PDE inhibitors
glucagon
ecmo
RRT
ID this drug
phosphono-o-methyl-2,6 diisopropylphenol aka fospropofol
fospropofol
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite
SE’s of fospropofol that are unique
genital and anal burning lol do not sign me up for this
fospropofol is metabolized by alkaline phosphatase into
propofol, formaldehyde, phosphate
ID this drug
2-(o-chlorophenyl)-2(methylamino) cyclohexanone hydrochloride aka ketamine
ketamine
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite
CV effects of ketamine
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
respiratory effects of ketamine
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
CNS effects of ketamine
increased CMRO2, CBF, ICP, EEG activity, nystagmus, blepharospasm (avoid during eye surgery)
presentation of ketamine induced emergence delirium and risk factors
hallucinations (up to 24h)
benzos most effective
risk factors >15y, female, ketamine dose >2mg/kg, hx personality DO
ketamine and analgesia
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
ketamine should be avoided in patients with a history of
acute intermittent porphyria
ketamine plasma protein binding
12% (smallest of all induction agents)
plasma protein binding of propofol
98%
plasma protein binding of diazepam
98%
plasma protein binding of midaz
94%
plasma protein binding of lorazepam
90%
plasma protein binding of etomidate
75%
name this drug
R-1-methyl-1-(a-methylbenzyl) imidazole 5 carboxylate (etomidate)
etomidate
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite
CV effects of etomidate
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
respiratory effects of etomidate
respiratory depression
CNS effects of etomidate
decreased CMRO2, decreased CBF, decreased ICP, stable CPP, no analgesia
etomidate inhibits
11 beta hydroxylate and
17 alpha hydroxylase
ponv is most common with which induction agent
etomidate
etomidate should be avoided in patients with a hx of
acute intermittent porphyria
is this an oxybarbiturate or a thiobarbiturate?
oxybarbiturate (O2 molecule in 2nd position)
thiobarbiturate (sulfur molecule in 2nd positon, increases lipid solubility and potency)
ID this drug
5 ethyl 5 (1 methyl butyl)-2-thiobarbituric acid
aka thiopental
thiopental
class
formulation
MOA
dose
onset
DOA
clearance
active metabolite
CV effects of thiopental
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
respiratory effects of thiopental
resp depression (shifts CO2 response curve to the right)
histamine release can cause bronchoconstriction (caution with asthma)
CNS effects of thiopental
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)
define acute intermittent porphyria
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
s/sx of acute intermittent porphyria
GI: severe abdominal pain (most common and typically first), n/v
CNS: anxiety, seizures, confusion, psychosis, coma
PNS: skeletal muscle weakness, bulbar weakness
drugs to avoid with acute intermittent porphyria
any drug that induces ALA synthase can potentially accelerate production of heme precursors
barbiturates
etomidate
ketamine
ketorolac
amiodarone
many CCB’s
BC pills
anesthetic management of acute intermittent porphyria
liberal hydration
glucose supplementation (reduces ALA synthase activity)
heme arginine (reduces ALA synthase activity)
prevention of hypothermia
tx of inta arterial injection of thiopental
injection of vasodilator: phentolamine or phenoxybenzamine
sympathectomy: stellate ganglion block or brachial plexus block
metabolism of phenobarbital
excreted unchanged in the urine (while p450 metabolizes all other barbiturates)
drugs to avoid with acute intermittent porphyria
barbiturates
etomidate
ketamine
ketorolac
amiodarone
CCB
BC
