Anesthetics

Question 1

IV anesthetics
kinetics
hypnosis/amnesia
analgesia (cat for ket, myo for eto)

Answer 1

thiopental, propofol, etomidate, ketamine
FAST (onset & offset)
yes, except ketamine produces “dissociative” amnesia

none for pro/etom; the may have enhanced response; really only for ketamine

no effect for thio/propo; myoclonus for etomidate; catalepsy for ketamine

Question 2

MOA of IV anesthetics

Answer 2

thio/propo/eto –> enhace GABAa receptor fxn –> hypnosis, amnesia

ketamine blocks NMDA –> analgesia

Question 3

thiopental chars

Answer 3

fast onset, short duration (IV)
mainly used for induction, but not maintenance b/c high fat storage

• IV agents mainly all used for induction, not main
  efx: cardioresp depression; cerebral protection; decr in CMRO2 and CBF (brain using less O2) good for incr ICP b/c decr brain volume
• ALL anesthetics are lipid soluble –> fast redistributions –> blood levels go down fast and you wake up quick

Question 4

propofol chars
upside compared to thiopental?
downside?

Answer 4

fast onset/short duration/rapid elim

induction and maintenance, and for CONSCIOUS sedation

CR depression/Cereb protection

less NV (antiemetic)
pain on injection

*#1 drug used for IV

Question 5

etomidate

3 SE’s?

Answer 5

fast onset/short dur/semi-rapid elim
used for induction

MINIMAL CR depression (GOOD for pts who you don’t want to decr BP much); cereb protection

myoclonus/adrenal suppression (w/prolonged admin)/pain on injection

Question 6

ketamine

Answer 6

fast onset/longer dur/semi-rapid elim
IV/IM induction of anesthesia/analgesia

CV STIMULANT (activates SNS)
maintains spontaneous ventilation; bronchodilator
NO celeb protection (incr CMRO2 and CBF) --> DON'T GIVE TO PT w/high ICP

dissoc anesthesia; catalepsy; incr secretions
analgesic
postop dysphoria (hallucinations for days after: one reason not to give to older pts)

Question 7

inhaled anesthetics
onset/offset
hypnosis/amnesia
analgesia
relaxation

Answer 7

isoflurane, sevoflurance, desflurane, N2O

all fast (N2O=Desflurane> sevoflurane> isoflurane); but slower kinetics than IV drugs

less fast ones have HIGHER blood solubility

good for kids, producing hypnosis/amnesia

N2O less good for hypnosis/amnesia bc EC50 is above ATM pressure; best for analgesia
*can use for skittish pts when placing an IV so it doesn’t hurt as much

all the same for relaxation

Question 8

inhaled anesthetic MOA?

Answer 8

volatile: enhance GABAa receptor fxn –> hypnosis/amnesia; Na/Ca/K –> analgesia, skel musc relaxation

N2O blocks NMDA’s –> analgesia; not as great for amnesia

Question 9

volatile anesthetics

Answer 9

onset/offset depd on uptake/solubility; little metal, pulm elim
used for induction/maint (after IV induction)

CV depresion; resp depr (rapid shallow breaths); can incr ICP (decr CMRO2 but incr CBF due to vasodilation)

“complete anesthetics”
bronchodilators=impaired mucociliary clearance
airway irritation: des>iso>sevo
des=desgusting

Question 10

malignant hyperthermia

tx? also worry about 3 other things?

Answer 10

rxn only w/VOLATILE anesthetics
due to pts having mutations to proteins inv in skeletal musc excitation-contraction coupling –> incr myoplasmic Ca

hypermetabolism –> RIGIDITY, HEAT, CO2 production, ACIDOSIS, RHABDO, HYPERkalemia

Rx: DC volatile anesthetic; give IV DANTROLENE; then treat acidosis and alkalinize urine to tx the myoglobinuria as well as hyperkalemia

Question 11

local anesthetics

Answer 11

analgesia
local admin near peripheral nerves –> sensory/motor/sympathetic block

not specific for pain fibers, so they block AP’s in ALL axons

they target the VGSC (thus AP’s don’t reach CNS from PNS)

takes time bc needs to cross cell membrane in order to bind the INNER side of the VGSC pore

Question 12

esters v amides local anesthetics

problem w/esters?

Answer 12

esters: plasma esterases
amides: metabolized in liver

esters turn into PABA –> allergy/anaphylaxis

*know it’s an ester if it only contains ONE i in the name

Question 13

local anesthetic use

Answer 13

amides: lido/mepi/bupi/ropi/EMLA
(lido only for topical; all else for sub Q, PN, Neuraxial)

esters: benzocaine/tetracaine/cocaine
* all primarily for topical (exc tetracaine also for neuraxial)

Question 14

fast onset short duration local?

longer dur?

Answer 14

lidocaine

bupivicaine/ropivacaine for longer dur

EMLA=lido+prilocaine –> hoped to penetrate keratinized skin (but takes like an hour)

Question 15

local anesthetic toxicity

2 drugs that cause MHb?

Answer 15

systemic: absorption; accidental intravascular injection (very high blood levels rapidly)

METHEMOGLOBINEMIA: prilocaine and benzocaine

Question 16

systemic toxicity of lidocaine

Answer 16

1st: CNS efx: tingling/NV/tremors/confusion
then: seizure, coma
finally: resp/cardiac arrest
unique: BUPIVICAINE can cause cardiac arrest before you see any CNS excitation

Question 17

how to avoid systemic toxicity?

Answer 17

1) safe doses:
lidocaine: decr blood flow and thus absorption –> longer anesthetic effect bc still sitting by the nerve but not absorbed

3) avoid intravascular injection: ASPIRATE before injection; give slowly in incremental doses

Question 18

tx systemic toxicity

Answer 18

1) supportive: airway/BZD’s for seizure/ACLS for arrhythmias and CV collapse
2) lipid emulsion: 1.5 mL/kg bolus

Question 19

methemoglobinemia
2 drugs that cause?
tx?

Answer 19

prilocaine/benzocaine
high levels oxidize Fe2–>Fe3 which then can’t carry O2

tx: METHYLENE BLUE (1-2mg/kg)