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IC Part 2 > Drugs for Anesthesia > Flashcards

Drugs for Anesthesia Flashcards

1
Q

Stages of anesthesia

A

stage 1- analgesia stage- dec awareness of pain, may have some anmesia, decreased consciousness

stage 2- disinhibition. loss of consciousness to regular respiration, excitation and delirium may occur, amnesia occurs, vomiting and incontinence may occur

stage 3- surgical stage
regular respiration to respiratory arrest
unconscious, no reflexes. respiration and blood pressure maintained

stage 4- medullary paralysis stage- resp arrest to death. req’s mechanical and pharmacological support

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2
Q

conscious sedation

A

iv and/or local agents for brief procedures

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3
Q

balanced anesthesia

A

combination agents for major surgery

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4
Q

inhalable anesthetics

A

very controllable, readily reversible

disadvantage- not as fast or smooth as fixed agents

depress spontaneous and evoked neuronal activity
may involve actions at various ion channels- voltage gated K+ channels, GABAa receptor Cl- channel resulting in hyperpolarization

agents vary in potency, rate of induction, effect of cv fxn, degree of muscle relaxation produced

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5
Q

nitrous oxide

A

inhalable anesthetic, gaseous
insufficient potency for surgical anesthesia
analgesic activity
potential toxicity- chronic exposure can cause megaloblastic anemia

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6
Q

volatile inhalable anesthetic

A

halothane, enflurane, desflurane, isoflurane (most widely used), sevoflurane

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7
Q

pharmacokinetics of inhaled anesthetic

A

rate at which a given concentration of anesthetic in brain is reached depends on:
1) anesthetic concentration in inspired air- gasses flow from high pressure to low partial pressure–> high pp in lungs results in rapid achievement of anesthetic conc in blood
2) solubility- blood:gas partition coefficient (otswald coefficient)- solubility in blood
lower–> less soluble–> more rapid rise in pp in blood–> faster equilibration with brain
3) brain:blood partition coefficient- solubility in lipid- adequate for all agents, so doesn’t contribute to significant differences between clinically useful anesthetics

4) pulmonary ventilation- better ventilation=rapid onset of anesthetisa
5) pulmonary blood flow- partial pressure rises faster with low blood flow, slower with high blood flow

6) artereovenous concentration gradient- uptake into highly perfused tissue may decrease gas tension in mixed venous blood
7) elimination- reverse of process for uptake- less soluble–> faster elimination (based on blood:gas partition coefficient)

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8
Q

low solubility in blood

A

less soluble–> more rapid rise in pp in blood–> faster equilibration with brain–> reach anesthetic concentrations in brain more rapidly

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9
Q

elimination dependent on

A

blood:gas partition coefficient- less soluble–> faster elimination

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10
Q

minimum alveolar concentration (MAC)

A

concentration of anesthetic in inspired air at equilibrium when there is no response to skin inscision in 50% of pts
high MAC= less potent
nitrous oxide= highest MAC, never anesthetic

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11
Q

inhalable anesthetics that cause vasodilation and tachycardia

A

desflurane, isoflurane

causes decreased bp

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12
Q

inhalable anesthetic that causes vasodilation

A

sevoflurane

causes dec bp

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13
Q

inhalable anesthetic that depresses myocardium

A

nitrous oxide
halothane
enflurane
cause dec BP and dec CO

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14
Q

inhaled anesthetics with rapid rate of induction

A

nitrous oxide, sevoflurane, desflurane

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15
Q

lowest MAC

A

halothane

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16
Q

IV or fixed anesthetics

A

quick, easy, smooth induction

slow elimination

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17
Q

barbiturates

A

iv or fixed anesthetic
thiopental (redistributes to other tissues, can accumulate in adipose leading to long doa)
methohexital (used for ECT)
short and fast acting barbiturates
no analgesia
decrease in respiration at anesthetic doses
difficult to control level of anesthesia

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18
Q

propofol

A

iv or fixed anesthetic
actions at GABAa receptor (inc channel open time)
more rapid recovery than barbiturates due to faster hepatic metabolism
maintenance of anesthesia as well as induction
good for out patient because no hangover and those effects
less post op nausea and vomiting

can dec bp and blunts baroreceptor reflex

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19
Q

etomidate

A

iv
used for induction esp for pts at risk for hypotension
no analgesia
high incidence of nausea and vomiting, pain on injection, myoclonus

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20
Q

ketamine

A

iv anesthesia
dissociative anesthesia- noncompetitive antagonist at NMDA glutamate receptor ion channel
catatonia, analgesia, amnesia without loss of consciousness
short acting, pain on injection
cardiac stimulation

produces emergence phenomenon- hallucinations and disorientation, can be decreased by benzodiazepines so usually used with scmall children and pts at risk for hypotension or bronchospasm

experimental treatment for depression

21
Q

midazolam

A

benzo
shortest acting benzo and least irritating for iv
used for maintenance of anesthesia because induction too slow to induce anesthesia
good amnestic effects
rapid onset and recovery
antagonist flumazenil can accelerate recovery

22
Q

flumazenil

A

antagonist for midazolam

23
Q

fentanyl

A

opioid
cna achieve anesthesia with sufficient dose or in combo with benzos
-excellent post op analgesia
useful in pts with compromised CV fxn
can cause truncal rigidity and impair ventilation

24
Q

pre-anesthetic and adjunct medication reasons

A

inc rate of induction
decrease anxiety
decrease pre and postop pain
decrease side effects of general anesthetics
reduce amt of general anesthesia required

25
Q

scopolamine

A

anticholinergics to decrease salivation and gut motility and antiemetic

26
Q

neuromuscular blocking agents- paralytics

A

minimize anesthetic use
good for orthopedics
should not be used as a substitute for inadequate anesthesia

27
Q

competitive neuromuscular blocking agents

A

at nicotinic ach receptors- antagonists
inhaled anesthetics and certain antibiotics increase potency of agent

isoquinolines-
-d-tubocurarine causes large increase in histamine release- 80 min duration

mivacurium - 10 min duration

rocuronium- steroid derivative: 20 min duration

28
Q

depolarizing- nicotinic agonist

A

succinylcholine

stimulates motor end plate leading to persistent partial depolarization so that muscle cannot contract anymore

will cause initial fasciculation leading to muscle soreness

shortest duration of action

29
Q

d-tubocurarine

A

competitive antagonist neuromuscular blocking agent

cause histamine release leading to hypotension and bronchospasm

30
Q

drug interactions of neuromuscular blocking agents

A

mainly with aminoglycosides and isoflurane increase potency and duration of competitive antagonists

31
Q

local anesthetics

A

block sensory transmission from a local area of body to cns

use- infiltration, field block, spinal block, topical application

32
Q

local anesthetic mechanism

A

block nerve conduction by blocking voltage gated Na+ channels- preventing depolarization and conduction of cation potential
also blocks K+ channels at higher concentrations

higher frequency of stimualation- higher membrane potential-
higher anesthetic block

33
Q

clinical effects of local anesthetics

A
  • pain blocked first along pre and post ganglionic sym fibers (Adelta, B and C fibers)
  • then cold, warmth, touch, deep pressure (C fibers)
  • then muscle tone, proprioception, and motor fxn (Aalpha, Abeta, A y fibers)

(may be different experimentally)

34
Q

cocaine

A

esters, local anesthetics-
- vasoconstrictor, medium acting, used topically for nasal and ophthalmic procedures bc penetrates membranes- minimizes bleeding

35
Q

benzocaine

A

ester, local anesthetic
surface use only, lipophilic
used for burns, bites, hemorrhoids, catheter and endoscope palcement

36
Q

lidocaine

A

amides, local anesthetic
most widely used, medium acting
doa ~2 hrs, when administered with epinephrine (to vasoconstrict to minimize diffusion)

37
Q

Mepivicaine

A

medium acting, amide, local anesthetic

vasoconstricts, longer acting than lidocaine

38
Q

bupivicaine and ropivicaine

A 
longer acting (3-15 hrs)
ropivicaine- less cardiotoxic
39
Q

amides

A

local anesthetics

used for infiltration, peripheral nerve block, epidural block

40
Q

potency of local anesthetics affected by

A

pH
-local anesthetics are weak bases, and the cation interacts with Na+ channel, but unprotonated form is req’d to penetrate membrane to gain access to channel inside cell membrane
potency decreased at low pH

41
Q

duration of action of local anesthetic proportional to

A

time the drug is in contact with nerve

use vasoconstrictor (epinephrine) to increase duration and reduce systemic absorption

42
Q

CNS adverse effects for local anesthetics

A

low concentrations- sleepiness, light headedness, visual and auditory disturbance, metallic taste

high levels- nystagmus, myoclonus, leading to tonic-clonic seizures (esp esters)

direct neurotoxicity with spinal administration due to pooling in cauda equina

43
Q

CV adverse effects of local anesthetics

A

depression of myocardial conduction and peripheral vascular tone
hypotension
cocaine- hypertension, arrhythmias, myocardial failure

44
Q

allergic reaction of local anesthetics in

A

esters

due to p-aminobenzoic acid metabolites

45
Q

cauda equina syndrome

A

neural injury due to localized toxicity from continuous spinal anesthesia
most likely to occur with lidocaine

46
Q

transient neurologic symptoms

A

transient paina fter spinal and epidural anesthesia w/o loss of sensation, motor, or bowel fxn
most common with lidocaine

47
Q

pharmacokinetics for local anesthetic

A

readily diffuse for site of injxn and cause systemic effects

48
Q

metabolism of esters

A

rapidly hydrolyzed by pseudocholinesterases

49
Q

metabolism of amides

A

in liver and or blood followed by urinary excretion

IC Part 2 (27 decks)

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