Unit 4 Pharmacology: Intravenous Anesthetics Flashcards by Sydney Elmore

Chemical name of propofol

2,6-diisopropylphenol

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MOA of propofol

GABA-A agonist, chloride conductance and neuronal hyperpolarization

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clearance of propofol

liver (CYP450) and extra hepatic metabolism. clearance exceeds liver blood flow. extra hepatic clearance occurs in the lungs (mostly)

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CV effects of propofol

decreased BP (d/t decreased SNS tone, vasodilation, myocardial depression)
decreased SVR
decreased venous tone-> decreased preload
decreased myocardial contractility

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respiratory effects of propofol

shifts CO2 response curve down and to the right (less sensitive to CO2). respiratory depression/apnea
inhibits hypoxic ventilatory drive

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CNS effects of propofol

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

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risk factors of PRIS

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

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clinical presentation of PRIS

acute refractory bradycardia and at least one of the following:
metabolic acidosis (base deficit >10mmol/L
rhabdomyolysis
enlarged or fatty liver
renal failure
HLD
lipemia

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how to minimize or eliminate pain of propofol on injection

giving an opioid, giving lidocaine, injecting into a larger or more proximal vein

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how is fospropofol metabolized

via the enzyme alkaline phosphatase to propofol.

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chemical name of fospropofol

phosphono-O-methyl-2,6 diisopropylphenol

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onset and DOA of fospropofol as compared to propofol

slower onset and longer DOA

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initial dose and repeat bolus of fospropofol

initial dose 6.5mg/kg
repeat bolus 1.6mg/kg not more than 4 min

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chemical name of ketamine

2-(o cholphenyl)-2(methylamino) cyclohexanone hydrochloride

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MOA of ketamine

NMDA antagonist (antagonizes glutamate).
secondary receptor targets: opioid, MAO, serotonin, NE, muscarinic, Na+ channels.
dissociates the thalamus (sensory) from the limbic system (awareness)

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DOA of ketamine

10-20 minutes (may require 60-90 minutes to return to full orientation

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clearance of ketamine

liver (P450 enzymes).

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active metabolite of ketamine

norketamine. 1/3-1/5 the potency of ketamine. renal excretion

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CV effects of ketamine

increase in SNS tone, CO, HR, SVR, PVR (caution if severe RV failure). will act as a cardiac depressant in someone with catecholamine depletion (sepsis)

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respiratory effects of ketamine

bronchodilator, intact airway reflexes, maintains respiratory drive, does not significantly shift CO2 response curve, increase in PO and pulmonary secretions

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CNS effects of ketamine

increase in CMRO2, CBF, ICP, EEG activity. nystagmus, emergence delirium.

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risk factors of ketamine induced emergence delirium

age >15 years, female gender, ketamine dose >2mg/kg, hx personality DO

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describe analgesic effects of ketamine

relieves somatic pain better than visceral pain
blocks central sensitization and wind up in dorsal horn of spinal cord
prevents opioid induced hyperalgesia (ex after remi infusion)
analgesic properties make it good for burn patients or pre existing chronic pain patients

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ketamine and etomidate should be avoided in patients with a hx of

acute intermittent porphyria

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when compared to other induction agents, which drug undergoes the smallest amount of plasma protein binding?

ketamine (12%)

chemical name of etomidate

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

DOA of etomidate

5-15 minutes

clearance of etomidate

CYP450 and plasma esterases. rapid awakening due to redistribution (not metabolism)

MOA of etomidate

GABA-A agonist

CV effects of etomidate

hemodynamic stability (minimal change in HR, SV, CO) SVR decreased, which accounts for small reduction in BP does not block SNS response to laryngoscopy. opioid or esmolol would help

respiratory effects of etomidate

mild resp depression (less than propofol or barbiturates)

CNS effects of etomidate

decreased CMRO2, CBF, ICP. CPP remains stable

does etomidate provide analgesia

etomidate decreases cortisol and aldosterone synthesis via inhibition of

11 beta hydroxylase (located in the adrenal medulla)

relationship between etomidate and seizures

if the patient has a hx of seizures then it decreases the seizure threshold. if they do not have a hx of seizures then it has no effect.

chemical make up of thiobarbiturates

sulfur molecule in the second position ex) thiopental, thiamylal

chemical make up of oxybarbiturates

theres an oxygen molecule in the second position ex)methohexital, pentobarbital

chemical name of thiopental

5-ethyl-5-(1-methylbutyl)-2-thiobarbituric acid

is there pain on IV administration of thiopental

MOA of thiopental

GABA-A agonist. depresses reticular activating system in the brainstem. low/normal dose increases affinity of gaba for its binding site while high dose directly stimulates the GABA-A receptor

thiopental dose for adult and children

adult 2.5-5mg/kg children 5-6mg/kg

OOA thiopental

30-60 seconds

DOA of thiopental

5-10 minutes

clearance of thiopental

CYP450

active metabolite after high dose of thiopental

pentobarbital

CV effects of thiopental

HoTN is primarily the result of ventilation and decreased preload. myocardial depression is secondary cause. causes non immunogenic histamine response. baroreceptor reflex is preserved

respiratory effects of thiopental

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

CNS effects of thiopental

decrease in CMRO2, CBF, ICP, EEG activity.

does thiopental have neuroprotection for focal or global ischemia

yes for focal ischemia (ex carotid endarterectomy), no for global ischemia

what is acute intermittent porphyria caused by

defect in heme synthesis that promotes accumulation of heme precursors

s/sx of acute intermittent porphyria

severe abdominal pain, n/v anxiety, confusion, seizures, psychosis, coma, skeletal muscle weakness

anesthetic management of acute intermittent porphyria

liberal hydration, glucose supplementation, heme arginate, prevention of Hothermia.

gold standard for electroconvulsive therapy and dose

methohexital (induction dose 1-1.5mg/kg)

dexmedetomidine class

imidazole

dexmedetomidine MOA

alpha 2 agonist, decreases cAMP and inhibits the locus coeruleus in the pons (sedation)

dose of dexmedetomidine (loading, maintenance)

1mcg/kg over 10 min maintenance infusion .4-.7mcg/kg/h

onset and DOA of dexmedetomidine

with loading dose: 10-20 min after infusion is stopped: 10-30 min

clearance of dexmedetomidine

liver (p450)

describe the dexmedetomidine modulated alpha 2 negative feedback loop

acts on pre synaptic alpha 2 receptors which produces a negative feedback loop by decreasing NE release from pre synaptic nerve terminal. reduces SNS tone and produces sedation

CNS effects of dexmedetomiding (CBF, CMRO2, ICP)

decreases CBF but no change in CMRO2 and ICP

describe the MOA of dexmedetomidine as it relates to analgesia

alpha 2 stimulation in the dorsal horn of the spinal cord (decreases substance p and glutamate release)

how can you administer precedex to a kid without an IV

nasal or buccal (3-4mcg/kg 1 hour before surgery)

formulation of midazolam (and what happens in bottle versus body)

imidazole ring. in the vial (low pH), ring is open and hydrophilic. when it enters the body, ring closes and it becomes more lipophilic so it can cross the BBB more easily

MOA of midazolam

gaba a agonist. increases frequency of channel opening- neuronal hyper polarization.

dose of midazolam for sedation, induction, PO in kids

iv sedation: .01-.1mg/kg iv induction .1-.4mg/kg PO sedation .5-1mg/kg

OOA and DOA of midazolam

IV 30-60 seconds IV DOA 20-60 min

active metabolite of midazolam

1 hydroxymidazolam (.5x potency of midazolam)

CV effects of midazolam

decreases BP and SVR

respiratory effects of midazolam

induction dose cases respiratory depression

CNS effects of midazolam

induction dose (not sedation dose) decreases CMRO2 and CBF. anterograde amnesia anticonvulsant anxiolysis spinally mediated skeletal muscle relaxation (antispasmodic) no analgesia

why does diazepam take forever to metabolize

undergoes enterohepatic recirculation

half life of diazepam

43 hours

onset of lorazepam

slow

greatest to least potency of diazepam, midazolam, lorazepam

lorazepam>midazolam>diazepam

describe a time when remimazolam would be a good option

indicated for induction and maintenance for adults undergoing procedural sedation lasting 30 minutes or less

flumazenil initial dose

.2 (titrated in increments until desired response is achieved)

flumazenil DOA

30-60 min (for this reason, repeat dosing is necessary)

Unit 4 Pharmacology: Intravenous Anesthetics Flashcards

(77 cards)