INHALED ANESTHETICS I Flashcards Preview

ANESTHESIA PHARM 2 > INHALED ANESTHETICS I > Flashcards

Flashcards in INHALED ANESTHETICS I Deck (40):
1

what the body does to the drug

pharmacokinetics

2

pharmacokinetics ADME

Absorption
Distribution
Metabolism
Elimination

3

the depth of general anesthesia depends on what?

the partial pressure (or gas fraction) exerted by the inhalational agent in the pt's brain.

4

describe how arterial blood partial pressure, alveolar partial pressure, and inspired gas affect brain partial pressure

partial pressure of inspired gas (I) affects alveolar (A) partial pressure affects arterial (a) blood partial pressure affects brain (br) partial pressure
VAPORIZER –> CIRCIUT (PI) LUNGS (PA) BLOOD (Pa) BRAIN (Pbr)

5

define time constants for inhalational anesthetics

TC = volume (capacity)/ flow

6

why do we turn flows way up in the beginning of the case?

reduce time constants
* if volume of the circuit it 6L, and we crank flows up to 12L/min, 1TC = 30sec, so 1.5min to get 95% change in sevo concentration in lungs

7

define solubility

relative affinity of an anesthetic for two phases (and therefore the partitioning of that anesthetic between the two phases) at equilibrium

8

is solubility for inhaled anesthetics good or bad? why?

bad. slows things down

9

define equilibrium for inhaled anesthetics

no difference in partial pressures – partial pressure of two phases is the same between alveoli and lungs (not concentration)

10

define partial pressure in a mixture of gases

in a mixture of gases, each gas has a partial pressure which is the pressure which the gas would have if it alone occupied the volume

11

how can we increase the partial pressure of inspired agent?

increase concentration, increase fresh gas flows (or both), decrease the volume of the circuit (fixed volume), decrease the absorption by the machine/plastics (again, fixed), or wait.

12

define alveolar partial pressure (PA)

actual pressure inside the lungs

13

what is the goal of agent delivery?

drive the alveolar partial pressure (PA) into equilibrium with the inspired partial pressure (PI) (PA/PI = 1)

14

why is alveolar partial pressure (PA) not static?

agent is constantly being absorbed into pulmonary blood flow
*PA = input into the alveoli – uptake into the blood

15

how do we increase alveolar partial pressure?

increase the amount of agent that is taken into the lungs/ partial pressure of inspired agent
* increase ventilation (minute ventilation)
* increase concentration of gas inspired

16

define minute ventilation

the volume of gas inhaled or exhaled per minute

17

what number do we use to measure partial pressure of agent in the brain?

ET gas concentration as a measure of PA (at equilibrium, the alveolar partial pressure should measure the partial pressure of the brain)

18

what are the two ways to increase initial concentration and uptake?

1) concentration effect (increase ventilation/ increase concentration)
2) 2nd gas effect

19

define concentration effect

impact of the inspired partial pressure of the agent (PI) to increase the rate of rise of the partial pressure of the alveolus (PA)

20

demonstrate concentration effect

* start with 20% gas concentration delivered (20ml gas in a total of 100ml)
* 50% of gas absorbed into pulmonary circulation
* concentration of gas remaining in alveoli is 11% (10ml gas in a total of 90ml)
* by increasing initial concentration to 80%, remaining concentration increases to 67% (40ml of 100ml absorbed, leaving 40ml gas in 60ml total

21

define 2nd gas effect

high volume of uptake of one gas accelerates the rate of increase of the PA of the companion gas
* if the uptake of gas A > uptake of gas B, when delivered together, gas A increases the rate of uptake of gas B

22

when is the 2nd gas effect most/ least effective?

2nd gas effect is most effective in the first couple of breaths; after that, the effect is negligible

23

on an everyday basis, in what situations is the 2nd gas effect most effective/ most used?

inhalational induction of kids

24

PA = ?

PA = PI – uptake

25

what affects the uptake of anesthetic agent?

solubility, cardiac output, alveolar – venous difference
* UPTAKE = SOLUBILITY * CO * (PA – PV)
(gas dissolved in blood; does not affect PA)

26

define solubility

relative affinity of inhaled anesthetic for two phases at equilibrium

27

how does solubility of agent affect PA/PI?

* increasing solubility of agent increases uptake, decreases PA/PI rise, therefore slowing down induction
* decreasing solubility of agent decreases uptake, increases PA/PI rise, therefore speeding up induction
** UPTAKE = SOLUBILITY * CO * (PA – PV)
*** if PA = PI – uptake, and solubility increases uptake, PA decreases as uptake increases, therefore PA/PI rise is slowed

28

which agent has high solubility (blood/gas partition coefficient) and thus slower induction rate?

halothane (2.4), isoflurane (1.4)

29

which agents have low solubility (blood/gas partition coefficient) and thus faster induction rate?

desflurane (0.42), nitrous oxide (0.47), sevflurane (0.65)

30

describe how the blood/gas partition coefficient relates to induction

the blood/gas coefficient describes how much more agent is needed in the blood to force equilibrium between blood and alveolus. the less soluble a substance is in the blood, the less is necessary in the circulation to force equilibrium in the alveolus because the undissolved gas is taken up by the alveoli more quickly and you're loosing less to the blood

31

how does cardiac output affect PA/PI?

(just the same as solubility) – * increasing cardiac output introduces more "clean" blood (no dissolved agent) to alveolar/vessel interface, thus decreasing the concentration of dissolved agent, requiring more agent to reach partial pressure equilibrium
**UPTAKE = SOLUBILITY * CO * (PA – PV)
*** if PA = PI – uptake, and CO increases uptake, PA decreases as uptake increases, therefore PA/PI rise is slowed

32

does cardiac output have a greater effect on soluble or insoluble agents?

soluble agents

33

what affects tissue uptake of anesthetic gases?

TISSUE UPTAKE = TISSUE SOLUBILITY * TISSUE BLOOD FLOW * (PARTIAL PRESSURE OF BLOOD – PARTIAL PRESSURE OF SPECIFIC TISSUE)

34

why do we use end-tidal agent volumes as a measurement of how much agent is being exposed to the brain?

because not only are you loosing agent to dissolution in blood, but fat and muscle also on the way to the brain.

35

why do (alveoli and) vessel-rich groups experience such quick agent upload/offload times?

vessel-rich groups receive 75% of total cardiac output.
* tissue uptake is directly proportional to cardiac output.
** therefore, VRGs upload and offload agent (equilibriate) faster

36

why does muscle experience such slow agent upload/offload times?

although muscle comprises 50% of body mass, it only receives 19% of CO
* tissue uptake is directly proportional to cardiac output.

37

why does fat experience such slow agent upload/offload times?

fat (20% body mass) only receives 6% of cardiac output.
* tissue uptake is directly proportional to cardiac output.
** therefore, fat tends to not absorb an excessive amount of agent (could never reach equilibrium)

38

how do we get rid of anesthetic gases?

* EXHALATION
** hepatic biotransformation (mostly halothane)
*** transcutaneous loss (to the skin)

39

what is the difference in tissue partial pressures during induction vs recovery?

* induction – all tissues have zero partial pressure
* recovery – varying tissue partial pressures (dependent on muscle mass, obesity – thus the art in emergence)

40

what physical/physiologic factors can change agent pharmacokinetics?

* age
* lean muscle
* body fat
* hepatic function (not so much)
* pulmonary gas exchange
* cardiac output