Inhaled Anesthetics Flashcards

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1
Q

describe 6 factors affecting equilibration (onset) times of inhaled anesthetics

A

distribution (Fa=Fi)

lung uptake

tissue uptake

solubility

cardiac output

arterio-venous concentration gradient

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2
Q

define potency (MAC) of inhaled anesthetics

A

equilibrium concentration required to prevent movement to skin incision at 1 ATM in 50% of px

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3
Q

list 3 factors that increase MAC requirements

A

hyperthermia

elevated CNS catecholamine NT release (anxiety)

chronic alcoholism

acute amphetamine use

hypernatremia

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4
Q

list 3 factors that decrease MAC requirements

A

hypothermia

pregnancy

shock

increasing age

acute alcohol ingestion

CNS depressant drugs

chronic amphetamine use

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5
Q

describe the probable mechanism of inhaled anesthetic action

A

ligand-gated ion channels are the most likely target

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6
Q

describe clinical effects of inhaled anesthetics on organ systems other than the CNS

A

decreased BP

decreased myocardial function

increased HR

decreased O2 consumption by muscles

faster respiratory rate

lower tidal volume of breath

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7
Q

when does equilibrium occur? what is the tissue conc at equilibrium?

A

when alveolar concentrations equal inspired concentrations (what is breathed in is what is breathed out - takes many hours, usually do not reach it)

max conc exists in the tissues

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8
Q

determinants of rate of rise of lung concentrations

A

inspired gas partial pressure

ventilation rate

functional residual capacity (FRC)

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9
Q

what happens when there is an increase in the inspired anesthetic concentration? What law is this?

A

increased rate of induction by increasing the rate of transfer into the blood

Fick’s law: flux = (C1-C2) x (area x permeability / thickness) - concentration gradient is proportional to diffusion across a membrane, which is inversely related to the thickness of the membrane

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10
Q

minute alveolar ventilation is another word for

A

ventilation rate

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11
Q

how does functional residual capacity affect induction time of inhaled anesthesia?

A

increased FRC slows the flow of agent into the lung, so induction time is increased (slowed)

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12
Q

why does increased FRC increase the induction time?

A

the increased volume of lung that must be filled to obtain the effect

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13
Q

although Fa rises by inspired conc, MAV, and FRC, the rise of concentration is slowed greatly by…

A

LARGE amount of TISSUE UPTAKE (including blood)

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14
Q

3 primary determinants of tissue uptake

A

solubility of the agent

pulmonary blood flow (i.e. cardiac output)

arterio-venous concentration gradient (in the lung)

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15
Q

a ratio that describes the solubility of an agent in the body

A

blood/gas partition coefficient (B/G)

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16
Q

a larger B/G partition coefficient…

A

increases blood uptake and decreases alveolar concentration, which SLOWS induction (due to greater tissue uptake)

17
Q

problems associated with more soluble agents dissolving easily in the blood

A

increased equilibration times

reduced ability to exit the blood (blood holds the agent)

reduced ability to enter the brain and other tissues

18
Q

halothane has a higher partition coefficient, so its induction time…

A

is slower than other drugs with lower B/G, and its slower to come off of

19
Q

describe pulmonary outflow (cardiac output) as it pertains to equilibration time

A

increases in cardiac output DECREASES rate of alveolar concentration rise, and SLOWS equilibration time

20
Q

clinical importance of cardiac output in an ER situation

A

low cardiac output of a victim combined with low blood volume could give tragic effects of regular anesthesia dose, due to preferential blood shunting to the brain!

21
Q

as cardiac output increases, induction time..

A

increases (is slowed)

22
Q

increased tissue uptake effect on blood concentrations

A

decreases blood concentrations, which increases blood uptake from the lungs

23
Q

increased solubility of an agent

increased CO

increased AV conc gradient

ALL have what effect on equilibration time?

A

increase equilibration time (slow induction)

24
Q

ligand-gated ion channel examples that are the most likely targets of MOA of inhaled anesthetics

A

nicotinic ACh recpetors

5HT receptors

amino acid receptors esp GABA

25
Q

most prevalent transmitter in mammal CNS

A

GABA - inhibitory function in central coordination of excitability, motor, and autonomic activity

26
Q

what happens at the GABA receptor when GABA binds?

A

Cl- influx, membrane hyperpolarizes, neuronal excitability is reduced

27
Q

how do drugs enhanve GABAa current?

A

increasing Cl- influx, channel open frequency, and channel open duration

28
Q

where do inhaled anesthetics bind to GABA receptors? So, are they agonists or antagonists?

A

bind at sites distinct from GABA binding sites, so they are GABA agonists

29
Q

problems with GABA theories

A

GABAa activity is inhibited at high anesthetic conc

other GABAa agonists give anxiolysis (inhaled agents do not)

GABAa ANtagonists have little effect on inhaled agents

30
Q

effect of hyper/hypo thyroidism on MAC

A

no effect

31
Q

inhaled anesthetics effect on renal blood flow, glomerular filtration rate, hepatic blood flow, uterine smooth muscle,

A

decreased consistently

32
Q

effect of N2O on nausea and vomiting

A

increased

33
Q

what affects potency?

A

disease state, other meds, etc

34
Q

list of inhaled anesthetics

A

desflurane

sevoflurane

isoflurane

halothane

nitrous oxide