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Anesthesia Pharm > Inhalation Agents > Flashcards

Inhalation Agents Flashcards

1
Q

High Solubility means

A

Blood acts as a reservoir and it stays in the blood and will not get to the brain

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2
Q

what does uptake do?

A

it counters the pressure from the alveoli – creating a huge reservoir

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3
Q

what will decrease in CO do to your IA?

A

pt with poor EF perfusing much less will have higher alveolar concentration of IA = then it will have higher brain concentration BUT will get delivered slower

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4
Q

Name the Inhalation agents

A
  • Isoflurane
  • sevoflurane
  • desflurane
  • nitrous oxide
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5
Q

What is the ideal inhalation anesthetic

A
  • Poorly soluble
  • nonpunget
  • non-flammable
  • inexpensive
  • easy to produce
  • potent
  • environmentally safe
  • no hepatic metabolism
  • not a trigger for MH
  • not emetogenic
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6
Q

MAC is defines as

A

minimal alveolar concentration

  • alveolar concentration at which 50 % of subjects move in response to noxious stimulus
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7
Q

Factors Increasing Anesthetic Requirements: Drugs give 4 samples

A
  1. Amphetamine (acute use)
  2. Cocaine
  3. Ephedrine
  4. Ethanol
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8
Q

Factors Increasing Anesthetic Requirements is highest at age ______

A

age 6 months

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9
Q

Factors Increasing Anesthetic Requirements: Electrolytes and Temperature

A
  1. Hypernatremia
  2. Hyperthermia
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10
Q

Factors Increasing Anesthetic Requirements: Genetics

A

Red Hair

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11
Q

Factors Decreasing Anesthetic Requirements 12 DRUGS

A
  1. Propofol
  2. Etomidate
  3. Barbiturates
  4. Benzodiazepines
  5. Ketamine

. Alpha 2 agonist (clonidine, dex)

  1. Ethanol
  2. Opioids
  3. Amphetamines (chronic use)
  4. Lithium
  5. Verapamil
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12
Q

MAC fractions / multiple of inhalation agents are roughly ______

A

additive

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13
Q

MAC that prevents movement in 95% of patients in incision. with no other medications administered concurrently

A

1.3 MAC

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14
Q

What is the MAC of Isoflurane

A

1.17%*

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15
Q

What is the MAC of Sevoflurane

A

1.80%

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16
Q

What is the Mac of Desflurane

A

6.6%

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17
Q

What is the MAC of Nitrous Oxide

A

104%

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18
Q

The average alveolar concentration permitting voluntary response to command. “ Open your eyes, breathe”

A

MAC awake

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19
Q

MAC awake for most modern IA

A

1/3 MAC

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20
Q

The concentration at which a patient can remember events; This is the point at which patient loses ability to learn

A

MAC aware –> generally patient will move and follow commands before they can make a memory

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21
Q

MAC- BAR: Average alveolar concentration which (autonomic response)

A

BLUNTS AUTONOMIC response

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22
Q

Addition of fentanyl 1.5-3 mcg/kg reduces MAC-BAR by approx _____ %

A

50

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23
Q

MACaware is related to 1._____ not 2.______

A
  1. amnesia 2. consciousness
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24
Q

Sevo MAC aware

A

<0.6%

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25
Q

Sevo MAC awake

A

0.6%

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26
Q

Sevo MAC

A

1.80%

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27
Q

Sevo MAC - BAR

A

2.88%

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28
Q

N20 MAC aware

A

<60%??

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29
Q

N20 MAC awake

A

60%

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30
Q

N20 MAC- BAR

A

Not possible

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31
Q

Indirect but reliable measure of PBr

A

Alveolar Partial Pressure

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32
Q

is the setting of the dial of the partial pressure of the alveolar the same as inspired concentration?

A

NO

The setting of the dial of the Partial pressure of the alveolar is NOT the same as the inspired CONCENTRATION

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33
Q

The FI is NOT the same as the ______ ______

A

alveolar concentration

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34
Q

What is the our most distal (exhaled concentration by gas alveolar) measurement of partial pressure?

A

Alveolar Partial pressure

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35
Q

Metabolism of IA is _____

A

minimal

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36
Q

At equilibrium, between 2 phases, the partial pressure is _____ in both phases

A

equal

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37
Q

The principal objective of inhalation anesthesia

A

is to achieve a constant and optimal brain partial pressure (as reflected by the PA …or really the ET concentration by gas analyzer).

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38
Q

PA is used as an index of:

A
  • Depth of anesthesia
  • Recovery from anesthesia
  • Anesthetic equal potency (MAC)
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39
Q

The depth of anes induced by IA depends primarily on the ____

A

partial pressure

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40
Q

What determines Alveolar Partial Pressure?

A

delivery into the alveoli minus loss of drug into blood uptake

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41
Q

Input depends on:

A
  • The inhaled partial pressure
  • Alveolar ventilation and FRC
  • Characteristics of the anesthetic breathing system
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42
Q

Uptake depends on:

A
  1. Solubility of the anesthetic in body tissues of the anesthetic in the body
  2. Cardiac output

3.Alveolar to venous PP differences (A-vD)

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43
Q

Initial administration of an anesthetic to offset the impact of uptake requires

A

A high PI is required during INITIAL administration of an anesthetic to offset the impact of uptake

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44
Q

Higher PIs will help you achieve the desired PA more quickly—accelerating the rate of rise of the PA PBr This is called _______ and is related to the concentration effect

A

OVERPRESSURE

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45
Q

As the A-vD decreases, the rate of uptake into blood ______ and the PI should be ______ to avoid overdose

A
  1. decreases 2.decreased
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46
Q

If you use the overpressure technique, keep your hand on the ______ until you have dialed the concentration back down to avoid problems

A

vaporizer

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47
Q

Increasing alveolar ventilation ↑ the rate of rise of the ____ toward the ___

A

1. PA

2.PI - Agents taken up by the blood is rapidly replaced with fresh gas mixture

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48
Q

What IA causes nausea?

A

ALL OF THEM

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49
Q

It is defined as the concentration at 1 atm that prevents skeletal muscle movement to a painful stimulus

is it a form of ED50?

A

MAC

Minimal Alveolar Concentration

–> Alveolar concentration at which 50% of subjects move in response to a noxious stimulus

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50
Q

T/F

The prevention of movement in MAC is cerebral mediated

A

False

The prevention of movement with MAC is SPINALLY MEDIATED.

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51
Q

What happens to anesthetic requirements if you are a chronic ETOH use?

A

you will increase your amount of anesthetic requirement if for a chronic ETOH

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52
Q

0.5 MAC N20 + 0.5 MAC ISO = 1 MAC

What is the relationship of combining two inhalation agents?

What is the MAC where 95% of patients are prevented from moving on incision?

A

MAC fractions/ multiple of inhalation agents are roughly additive

1.3 MAC prevents movement in 95% of patients on incision

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53
Q

Does N20 contribute more or less to MAC in advanced age?

A

N20 contributes MORE to MAC in advanced age

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54
Q

What is the relationship of opioids with VA?

A

Synergistically decreases requirements

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55
Q

What are these numbers?

A

% is equal to 1 MAC being dialed in the vaporizer

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56
Q

When you awaken your patient and you started asking them to squeeze their hands or open their eyes – and they were able to what level is this of MAC?

A

MACawake

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57
Q

Does your patient that just followed commands [MACawake] able to remember?

A

NO. They are not yet MACaware

They really do not know whats going on

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58
Q

This is the point where patients start remembering events

A

MACaware

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59
Q

Why do patients in PACU keep asking the nurse the same thing over and over again but are able to follow commands

A

Generally, the patient will move and follow commands before they can make a memory

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60
Q

This is the MAC level in which the autonomic system effect is blunted to a noxious stimuli

A

MAC -BAR

Average alveolar concentration Blunts Autonomic Response to a noxious stimulus (incision)

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61
Q

If a patient is in MAC -BAR what will you no longer see?

A

Patient on MAC -BAR will NOT have a change in

Blood Pressure

Heart Rate

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62
Q

How is Nitrous delivered?

A

Nitrous is delivered in

L/ MIN

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63
Q

How much is the MAC-BAR50 for Sevo when combined with 66% of N2O?

A

2.2 MAC- BAR50 for Sevo combined with 66% of Nitrous

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64
Q

is it possible to have a MAC-BAR with Nitrous?

A

It is not possible to have a MAC-BAR from Nitrous

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65
Q

How many TIMES of your MAC to achieve MAC-BAR?

A

MAC - BAR is usually 1.6X your MAC

i.e Sevoflurane 1.8% MAC X 1.6 = 2.88%

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66
Q
A
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67
Q

What is PA?

A

Partial Pressure in the alveoli

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68
Q

IA from the vaporizer to the alveoli is called?

is it the same as the alveolar concentration?

A

FI = inspired concentration

IA FROM THE VAPORIZER TO THE ALVEOLI

it is not the same as the setting on the dial

it is not the same as the alveolar concentration (FA)

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69
Q

What equilibrates?

A

Partial Pressure

is what equilibrates

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70
Q

What determines the depth of anesthesia?

volume percent or partial pressure?

A

Partial Pressure

it is the equilibriation of Partial pressure

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71
Q

What is UPTAKE?

A

Abrosption (UPTAKE)

from the alveoli into pulmonary capillary blood

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72
Q

What is PA used as an index of ?

A

Depth of Anesthesia

Recovery from anesthesia

Anesthetic equal potency

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73
Q

What are the tissue compartments?

74
Q

Determinants of PA

A

Delivery into the alveoli (INPUT) minus loss of drug into the blood (UPTAKE)

FA= INPUT - UPTAKE

75
Q

INPUT depends on

C.A.T

A
  • Characteristics of the anesthetic breathing system (tubing, loss in the atmosphere)
  • Alveolar ventilation or Functional Residual Capacity (FRC)
  • The inhaled pressure (PI)
76
Q

How can you induce anesthesia at the rate that you want?

A
  1. Increase the administered amount [alveoli can fill up faster]
  2. Slow down the leak [the less soluble the drug the faster the alveoli can fill up]
77
Q

What is “OVERPRESSURE”

A

delivering a higher percentage –> the higher the faster the alveolar concentration shall be

78
Q

What will happen if you increase alveolar ventilation?

A

Î the rate of rise of the PA towards PI

Agent taken up by blood is rapidly replaced with fresh gas mixture

79
Q

What happens to PBr during hyperventilation?

(hypocapnia)

A

decrease CBF and may delay the rate of rise of PBr

80
Q

What is the ventilatory pattern of change in patients receiving IA?

on Spontaneous Ventilation?

A

IA produces DD depression of ventilation

–> pt takes lower TV and increased RR

–> protective mechanism, as the body start taking IA the body starts decreasing TV on Spont ONLY

81
Q

Interpret this chart.

What are the minute ventilations?

A
  1. Opiods = increase in TV, decrease in RR
  2. Breathing IA = decrease TV, increase RR

NORMAL BREATHING MV: 5000ml/mim

Opiods: 4750 ml/min

IA: 5000 ml/min

82
Q

What is this?

A

CO2 response curve

83
Q

Anesthetic Breathing System affects input

what are the characteristics of the breathing system which increase the rate of rise of PA?

A

–Volume of the external breathing system

–Solubility of the inhaled anesthetic into the components of the breathing system

–Gas inflow (FGF) from the anestheticmachine

84
Q

T/F

Gas flows is directly proportional to PA?

A

•High fresh gas flows will ↑ the rate of rise of the PA

  • Faster filling of the volume of the anesthetic circuit (soda lime canister,breathing bag…)
  • Greater amount of drug per unit of time to replace gases that are taken up at the alveoli
85
Q

How can solubility affect the rate of rise of PA?

A

Anything that gets absorbed in the system can affect the rate of rise in the PA

–This slows the rate of rise of the PA

–At the conclusion of the procedure, reverse gradients will delay the rate of the fall of the PA (delay recovery)

87
Q

What denotes solubilities of IA in the blood and tisses?

A

Ostwald partition coefficient

  • These distribution ratios describe how anesthetics distribute between 2 phases (PPs, not concentrations) equilibrate! at 37°C at atmospheric pressure.
88
Q

Blood: Gas partition coefficient of Iso is?

what does this mean?

A

Blood:Gas partition coefficient, 1.46(Iso)

  • At equal partial pressures, the amount of drug/volume in the blood is ~1.5 times that in the alveolar gas

Isoflurane is highly soluble

89
Q

What is is the Blood:Gas partition coefficient of

Halothane

Isoflurane

Sevoflurane

Desflurane

Nitrous Oxide

90
Q

What is the best IA to use for a patient with a large body habitus?

A

Desflurane

“fast on fast off” as compared to a drug that has higher solubility and has a possibility of depot build-up

91
Q

Work hoarse for most cases?

A

Sevoflurane

92
Q

T/F

Increased solubility is inversely proportional to the rate and rise of the PA towards the PI

93
Q

Classify the following IAs according to solubuluty

Soluble

Intermediately

Poorly soluble

A

Soluble- none of the modern inhaled agents

Intermediately soluble – Iso

Poorly soluble - Sevo, Des, N20

94
Q

FA/ FI Curves

95
Q

How long does it take for 95% equilibration of PP between blood and tissue phases?

A

3 TIMES CONSTANT

96
Q

What does fat do to anesthetics?

A

FAT has an enormous capacity to uptake anesthetics and can take up to 24- 48 hours to equilibriate

97
Q

What is the relationship of CO and anesthetics?

what will it do to the rate of rise of PA

How about induction?

A

↑CO results in ↑ uptake of anesthetic into blood from the alveoli

–The rate of rise of PA will slow

•Inhalation induction is slow

↓CO results in ↓ uptake of anesthetic into blood from the alveoli

–The rate of rise of PA is fast

•Inhalation induction is rapid

98
Q

What is the reason behind this statement?

•Changes in CO influence the rate of rise of PA toward the PI of soluble anesthetics more than poorly soluble anesthetics

A

N2O has a rapid rise in PA regardless of CO

•This is due to its lack of potency and the high inspired concentrations delivered (70% for N2O vs. 1.15% for Iso)

  • N20 will have a rapid rise because of the higher volume of anesthetics being delivered
99
Q

What is the effect of VA to CO?

What may occur?

A

VA can depress CO

  • when CO is depressed, there will be a decrease in uptake leading to an increase in PA

POSITIVE FEEDBACK

–As the Pa rises, increasing cardiac depression results in more rapid rise in PA

•Excessive depth of anesthesia may result, especially if combined with mechanical ventilation!

101
Q

What affects delivery into the alveoli?

102
Q

What affects the lost of the drug in to the blood?

103
Q

What is the concentration effect?

A
  • We are looking at the rate of rise of the PI and how to can impact the rise of PA
  • The higher the PI, the more rapidly the PA approaches the PI (overpressure)
  • concentrating effect; overpressure and augmentation of gas inflow
  • temporary phenomenon
104
Q

Second Gas Effect

A

The use of nitrous during the induction to hasten the effects of sevo [drug of choice]

105
Q

If the second gas is O2, the result is

A

Alveolar Hyperoxygentaion

106
Q

What happens if the second gas is a volatile anesthetic?

A

results in a more rapid rise in PA toward the PI (more rapid inhalation induction)

107
Q

T/F

Metabolism is desirable

108
Q

What is the rule of 2

A

Desflurane 0.02%

Isoflurane 0.2%

Sevo 2%

  • undergoes hepatic biotransformation -
109
Q

How do we eliminate IA from the body?

A

MAJORITY through exhalation

- Percutaneous loss (and loss from open wound) of IAs (like CO2) is minimal (<1%) and does not influence the rate of rise or recovery from IAs

110
Q

What is the amount of metabolism of inhaled anesthetics?

Halothane

Sevolflurane

Isoflurane

Desflurane

Nitrous Oxide

111
Q

During recovery from anesthesia, what do you want to see?

What is the difference between induction and recovery?

A

The rate of decrease in the brain as reflected by the PA

– You can overpressure to speed induction, but you cannot under pressure (deliver <0%) to speed recovery--

– you cant make a negative pressure –

112
Q

When can you achieve equilibrium in all tissues?

A

Equilibrium MAY NOT BE achieved in all tissues at the conclusion of surgery (muscle, fat)

113
Q

When does fat continue to take up anesthetic?

what is the effect of that in recovery?

A

Fat may continue to take up anesthetic as long as Pa is greater than the tissue partial pressure

- it initially speeds the decrease in PA

115
Q

Which patient will recovery faster?

The patient Iso or the one given sevo?

A

The patient is given Sevo

– Time to recovery is much longer for the more soluble anesthetics compared to poorly soluble anesthetics –

116
Q

What will happen to the absorbed components of the breathing system?

What will it do to the rate of decrease of PA?

A

Anesthetics that has been absorbed into the components of the breathing system will return to the gases in the breathing circuit and SLOW the rate of decrease of the PA

= slower recovery=

117
Q

How can you blow off the gas?

How can you hasten the gas being blown off the absorbed breathing system?

A

Increase fresh gas flows (FGF) to (>5L/min)

  • this will dilute the agents returning into the inspired gases from components of the breathing system and speed the rate of decrease of the PA
118
Q

We know that anesthesia is not ON and OFF

Adjustments (titration) are made based on

(3)

A
  • The patient response to the drug
  • Interactions with other medications
  • The degree of stimulation (surgical, ETT)
119
Q

What do you want to do at the conclusion of surgery?

A
  • Gradually decrease the percentage
  • Sx done: suturing, putting dressing –> less stimulating
  • just waiting for the patient to wake up –> least amount of stimulation
120
Q

Elimination of IAs depends on:

(2)

A

Elimination of IAs depends on

- Length of administration

- Blood: Gas Solubility of the agent

121
Q

In less than 5 minutes how much would be the initial decrease of IA Iso, Enf, Sevo and Des?

A

The initial decrease (50% decrement time) for Iso, Enf, Sevo, and Des in <5 mins and does not vary considerably with the duration of the anesthetic

122
Q

The initial phase of elimination is a function of?

A

The initial phase of elimination is a function of alveolar ventilation

123
Q

What is the 90% decrement time for Iso, Sevo, Desflurane

after 6 hours of anesthesia?

124
Q

When is the major differences in elimination among these agents?

A

The major differences in elimination among these agents is during the final 20% of the elimination process

125
Q

What is the Meyer -Overton Hypothesis?

A

The MAC of a volatile substance is inversely proportional to its lipid solubility

-POTENCY CORRELATES WITH LIPOPHILICITY -

126
Q

What is 5 Angstrom Theory?

128
Q

Which receptors do volatiles act on?

129
Q

Amnesia is mediated by?

A

Probably NOT spinal cord mediated

memory is lost at concentrations less than MACawake

– always anetrograde amnesia–

130
Q

Belief that inhaled anesthetics act by effects at multiple sites

A

Multisite Theory of Narcosis

131
Q

Belief that anesthetics act on no more than 2 - 3 sites to produce a specific effect

A

Unitary Theory of Narcosis

132
Q

What is the Protein Based Mechanism?

A

Current consensus for MOA

  • GA is produced by membrane bound protein interactions in the brain and spinal cord

Brain: GABA -A

VA will stimulate inhibitory receptors and inhibit stimulatory receptors

Spinal Cord: Glycine, NMDA inhibition, Na Channel inhibition–> produces immobility mostly in the ventral horn

133
Q

MOA of N20?

A

N20: NMDA antagonism, Potassium 2P- channel stimulation

DOES NOT STIMULATE GABA -A RECEPTORS

134
Q

Effects on Systems amongs VA?

A

Similar effects among different agents at equipotent concentrations

  • especially during the maintenance phase of anesthesia
  • Co- existing diseases, differences in age, degrees of surgical stimulation, concurrent drug therapy, etc. may cause variations in responses
135
Q

how is MAP changed?

What is the reason the decrease in MAP

How does N20 change the map?

A

decrease in MAP is mainly affected( d/t) the the decrease in SVR

136
Q

Which IA will you see an increase in HR?

A

Iso and Des are a little more irritating

137
Q

Which IA will cause a decrease in HR?

is it mac related?

A

Sevo greater than MAC > 1.5 you will see an increase in HR comparable to Des and Iso

138
Q

How is Cardiac Output/ Index affected by VA?

139
Q

How can you lessen the cardiac effects of the VA?

A

By using N20 as an additive

140
Q

When do you see this most?

A

Desflurane

– when mac was abruptly increased you can see a rapid rise in HR

  • rise in HR is expected but more exaggerated with an increase in concentration of Des .

- this is related to SNS activity

141
Q

Myocardial Conduction effects of VA

A

NO sensitization as compared to Halothane

142
Q

Which drug do you generally avoid in patients with congenital prolonged QT syndrome?

why?

A

Dr. Cansino generally do not consider this with avoiding Sevo

“all drugs will prolong QT “

143
Q

What VA may induce Coronary Steal?

A

Coronary steal; as the myocardial demand increases healthy vessels will dilate.

“stealing away blood from ischemic areas and directing it to healthy issues”

All VA produces anesthetic preconditioning

144
Q

how does minute ventilation correlate with VA?

A

Similar Minute Ventilation does not mean similar VA

145
Q

How is the response to CO2 affected?

How is the response to O2 affected?

146
Q

Which IA decrease bronchial constriction?

A

ALL potent IAs decrease bronchial constriction

147
Q

What do Iso and Des do to the bronchioles? why?

How can it be attenuated?

148
Q

What do IAs do to HPV?

A

HPV decreases V/Q mismatch.

IAs inhibit HPV especially at greater than 1-2 MAC

149
Q

What kind of chest wall changes do you see?

150
Q

N20 effects on CBF and CMRO2

A

mildly excitatory

151
Q

Effects of VA to CNS

152
Q

You are doing a crainy how do we decrease the ICP if we are using VA?

A

We do not like that

– hyperventilate make the patient hypocarbic to make the cerebral vessels constrict –> decrease in blood flow –> decrease in icp

all VA increase ICP exceeding 1 mac

153
Q

How does VA affect autoregulation?

A

Autoregulation is impaired at concentrations more than A MAC [50 - 150 MAP]

- However cerebrovascular response to PaCO2 is maintained

155
Q

IAs effects on Evoke Potentials?

156
Q

Remember this EEG changes !

A

possible that this VA can cause epileptic properties

157
Q

Neuromuscular Effects

A

VA will potentiate the muscle relaxant effects

158
Q

What triggers MH?

A

ALL VA!

Hal and SUCCS

159
Q

Which VA can potentiate a more severe hepatic injury?

A

* all VA agents produce dose-dependent reductions in hepatic blood flow and mild elevations in LFTs

Hal, Iso , Des

—> mostly due to hepatic necrosis.

–> TRIFLUOROACETATE BAD!– binds to hepatocytes

–> hepatic injury was what caused problems

160
Q

What causes immunologic response that results in hepatic necrosis?

A

TRIFLUOROACETATE BINDS COVALENTLY TO HEPATOCYTES

TRIFLUOROACETATE-HEPATOCYTE COMPLEX triggers immune response

162
Q

Effects on System - Renal

A

decrease SVR decrease renal perfusion

163
Q

Sevo is metabolized to ____?

A

Sevo is metabolized to inorganic F

164
Q

What does Sevo do to renal function

A

prolonged Sevo anesthesia does not impair renal function

– not so much of an issue because SEVO is only 2% metabolized by the liver –

165
Q

This toxin causes nephrotoxicity?

what are the signs of nephrotoxicity

A

Inorganic F greater than 50 mmol/L

167
Q

another by-product by Sevo that may cause nephrotoxicity

168
Q

What produces more relaxation as compared to Halothane?

A

Ether derivatives produces more skeletal muscle relaxation than Hal

169
Q

Effects of N2O at skeletal muscles

A

N2O produces skeletal muscle rigidity at high concentrations

170
Q

Will N20 enhance NMBAS?

A

N20 DOES NOT ENHANCE NMBAS

171
Q

Des MH can manifest until?

A

MH may not manifest immediately

Post Des MH reported to manifest 3 hours post anesthetic

172
Q

Effects on Obstetrics

A

ALL

TOCOLYTICS

dose-dependent decreases in uterine contractility and blood flow

modest: 0.5 mac

Substantial effect at >1.0 MAC

n20 does not produce tocolytic effects

173
Q

Effects on Immune System

What does N2O do?

VAs and measles?

whats the cause?

174
Q

What IA is teratogenic and best avoided in pregnancy esp. on the 1st semester

A

N2O

due to inhibition of DNA synthesis

175
Q

N20 effects on Bone Marrow

A

not relevant since you don’t give N2O for more than 24 hours.

176
Q

N20 and Peripheral Neuropathy

A

ability of N2O to oxidize irreversibly the cobalt atom of the vitamin B12 such that the activity of B12 enzyme is decreased

–> knowledge thing than clinical implications

177
Q

Which organ has the most decreased O2 requirement?

A

O2 requirements decrease similarly among the VA

- HEART -

requirements are decreased more than other organs

178
Q

How much is metabolized depends on the agent

179
Q

IMPORTANT!

CARBON MONOXIDE

what produces more?

what can increase Carbon monoxide production?

A

when delivering VA and it interacts with CO2 absorbent

Carbon monoxide is produced during degradation by CO2 absorbens

Des>Enf>Iso

  1. Carbonmonoxide will bind to iron and pulse Ox will look normal–> if the CO2 absorbent in the system is dry that can accelerate the production
  2. if temp of CO2 absorbent is high
  3. low gas flows and increased metabolic production of CO2
  4. or high FGF for a long period of time and that causes desecration of the carbon dioxide absorbent
  5. type of CO2 absorbent
180
Q

Pharmacoeconomics

What are the cost considerations?

Anesthesia Pharm (25 decks)

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