Anesthetics Flashcards

1
Q

Definition of clinical anesthesia

A

no mvmt in the presence of painful stimuli

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2
Q

How is anesthetic potency measured?

A

the dose that prevents mvmt with painful stimuli in 50% of pts

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3
Q

Define minimal alveolar concentration

A

the concentration of anesthetic in end tidal expired air that prevents movement with painful stimuli in 50% of pts

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4
Q

general anesthetic mechanism

A

increase inhibitory or decrease excitatory neurotransmission

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5
Q

where do anesthetics likely target?

A

GABA(A) receptors
NMDA receptors
or membrane associated proteins are influenced

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6
Q

Stages of general anesthesia

A

premedication (anti-anxiety drugs)
induction (usually IV, use of inhalational anesthetic is limited to emergencies)
Maintenance (inhalational anesth have short half lives)

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7
Q

Common properties of parenterally administered gen anesthetics

A

hydrophobic

IV bolus

pass into brain and sp cord in one pass of circulation–significance: rapid induction

as blood levels decrease, come back out of the brain

Duration of action in brain is shorter than half life. (think how it also gets stored in adipose tissue) So multiple doses get complicated

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8
Q

Properties of inhalational anesthetics

A

very low therapetic index (LD50/ED50)

gaseous or readiy vaporized

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9
Q

What should the blood:gas partition coefficient be if used for anesthesia? and why?

A

low

b/c induction is quick (equilibrium quickly reached) and recovery is quick

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10
Q

what affects induction with a gaseous anes?

A

anesthetic concentration in inspired air
pulmonary ventilation (more promient for gas with moderate blood:gas partition coeffic than for gas with low)
pulmonary blood flow (more prominent for gas with moderate blood:gas PC than for gas with low)
arteriovenous concentration gradient (determined by PC btwn blood and tissue, rate of blood flow to organ, concen gradient)

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11
Q

When is equilibration for inhaled anesthetic fast? slow?

A

fast for gases w low blood:gas PC

slow for gases w high fat: blood PC

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12
Q

what determines the half life of an inhaled anesthetic?

A

blood:fat PC

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13
Q

What results in rapid recovery from an inhaled anesthetic?

A

low solubility in blood and fat

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14
Q

What do ALL anesthetics have in common for respiration?

A

depress respiration via effects in the CNS, increase paCO2

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15
Q

How do local anesthetics work?

A

bind reversibly to inside of pore of voltage gated Na channels

cause sensory loss, motor paralysis

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16
Q

What types of local anesthesia

A

topical anesthesia
local infiltration
nerve block
spinal and epidural

17
Q

What form is the local anesthetic in as it penetrates the neuronal membrane?

A

unionized form

18
Q

What form is the local anes in at its site of action?

A

ionized form

19
Q

What property do all local anesthetics have in common?

A

weak bases

20
Q

What effect do local anes have on resting membr potential?

A

no effect

21
Q

What kinds of nerves are more sensitive to local anes?

A

those with positive membrane potential

those that are more frequently stimulated

22
Q

What effect does decreasing tissue pH have on local anes’action?

A

efficacy is decreased

23
Q

What are local anes often co administered w?

A

vasoconstrictors (epinephrine, phenylephrine)

24
Q

What neurons are sensitive to the local anes block first?

A

small unmyelinated neurons (pain first, posture/touch/pressure/motor last)

this is reversed in coming out of anesthesia

25
Q

toxicity and side effects of local anes

A

interfere w/ fxn of all organs in which conduction of impulses occurs

systemic toxic reactions–high conc in circulation

intraneuronal injection causes damage

26
Q

local anes toxicity at first in the CNS?

A

CNS–stimulation, restlessness

27
Q

Local anes severe toxicity with CNS?

A

higher doses–drowsiness, respiratory depression

can cause death, usually by respiratory depression

28
Q

local anes’ CV toxicity

A

depression occurs after CNS effects

effects: myocardial contractility decreases–decreases BP
decreases rate of conduction–AV block, arrhythmia
arteriolar vasodilation

can lead to cardiac arrest

29
Q

Toxicity of local anes determined by

A

balance btwn rate of absoprtion into the systemic circulation and elmination

30
Q

how are local anes metabolized

A

ester local anes–inactivated by plasma esterases

amide local anes–metabolized in the liver–CAUTION: liver disease

31
Q

effects of vasocontrisctors for local anes

A

increase duration of action

decrease toxicity

32
Q

Which kind of local anes are not associated with allergic rxns

A

amides