Anesthesia Flashcards
lidocaine dose
1mg/kg - using ideal
suppress airway reflexes, reduce the pain of injection of other induction agents, and supplement their anesthetic effects.
fentanyl dosage
0.5- 1 mcs/kg - body weight
ketamine dosing
.25 mg/kg - body weight
propofol dosing
2mg/kg - using ideal
3mg/kg if weed user
MAC of sevo
1.8
maintenance dose of propofol
50- 200 mcgs/kg / minute
dexmedetomidine
Precedex, Alpha2-Adrenergic Agonist; Sedative
0.5 to 1 mcg/kg
intraoperative administration of dexmedetomidine ameliorates or reduces the incidence of agitated emergence delirium
Ketorolac
Weight ≥50 kg and age <65 years: 15 to 30 mg IV every 6 to 8 hours
Weight <50 kg or age ≥65 years: 15 mg IV every 6 to 8 hours
first generation NSAID - COX inhibitor
Use with caution or avoid in patients with kidney dysfunction, cardiovascular disease, or peptic ulcer disease
Use with caution in those at high bleeding risk, especially those taking concomitant anticoagulants
how many mcs in one mg
1 mg = 1000 micrograms
glycopylorate MOA and dosage
0.2 mg/ml
.004-.007 mg/kg
muscarinic anticholinergic agents, inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine
neostigmine MOA and dose
1mg/ml
Inhibits the hydrolysis of acetylcholine (anti cholinesterase) by competing with acetylcholine for attachment to acetylcholinesterase at sites of cholinergic transmission. It enhances cholinergic action by facilitating the transmission of impulses across neuromuscular junctions.
phenylephrine MOA and dose
hydromorphine dialudid MOA and dosage
respiratory rate for peds?
HR for peds?
BP for peds?
anywhere between 24 - 40 is relatively normal
60-140 bpm
systolic ~70-106
diastolic ~25-65
MAP =?
MAP = DP + 1/3(SP-DP)
SVR X CO
where
SVR = 80 X(MAP-CVP)/CO
CO = HR X SV (ESV - EDV)
EF CALCULATION
EF=(SV/EDV)
SV=ESV-EDV
rocuronoum MOA
NON depolarizing competing for cholinergic receptors at the motor end-plate.
This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine and edrophonium.
Ephedrine MOA
stimulation of alpha-1-adrenergic smooth muscle receptors within vasculature results in a rise in systemic vascular resistance and, consequently, systolic and diastolic blood pressure. Direct stimulation of beta-1 receptors by ephedrine and norepinephrine increases cardiac chronotropy and inotropy. Finally, beta-2-adrenergic receptor stimulation in the lungs results in bronchodilation with ephedrine administration, though it is not as pronounced as its cardiovascular effects
Ephedrine, a stereoisomer to better-known pseudoephedrine, is a sympathomimetic amine with unique effects due to its indirect mechanism than other sympathomimetic agents like pseudoephedrine and phenylephrine.[12] Ephedrine acts as both a direct and indirect sympathomimetic. It binds directly to both alpha and beta receptors; however, its primary mode of action is indirectly achieved by inhibiting neuronal norepinephrine reuptake and displacing more norepinephrine from storage vesicles.[13] This action allows norepinephrine to remain in the synapse longer to bind postsynaptic alpha and beta receptors.[14]
Ephedrine’s indirect mechanism results in a sustained or even increased heart rate due to norepinephrine’s ability to bind alpha and beta receptors, whereas more direct sympathomimetics like phenylephrine results in reflex bradycardia
phenylephrine MOA ?
can cause?
can cause reflex bradycardia because it is a alpha 1 specific agonist
- baroreceptor reflex bradycardia
direction lungs go when inhale?
Outward - expands - increasing volume of lungs
