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Inhalants Flashcards

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1
Q

% Anesthetic = ?

A

% anesthetic = flow of anesthetic from vaporizing chamber/total gas flow

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2
Q

Anesthetic Uptake = ?

A

Anesthetic Uptake = S x CO x (PA-Pv/Pbar) where Pv = mixed venous blood, PA = alveolar concentration, Pbar = atmospheric pressure in mm Hg

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3
Q

Clearance

A

% clearance = 100 x VA /(agent blood/gas PC x CO + VA)

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4
Q

Panes ?

A

Panes = fractional anesthetic concentration x total ambient pressure

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5
Q

STP

A

0*C (273K), 760mm Hg (1atm)

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6
Q

1 atm = barr, mm Hg, Torr?

A

1 atm = 1 barr, 760mm Hg, 760 Torr

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7
Q

1 atm = psi, kPa, cmH20?

A

1atm = 14.7psi, 101.325kPa, 1030 cmH2O

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8
Q

1atm = ? dynes/cm^2

A

1atm = 1.013x10^6 dynes/cm^2

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9
Q

Saturated vapor concentration of a gas

A

= SVP/barometric pressure x 100%

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10
Q

Gas

A

agent that in gaseous form at room temp/ambient pressure (ambient conditions)

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11
Q

Vapor

A

gaseous state of an agent that is a LIQUID at ambient temperature

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12
Q

Critical Temperature

A

temperature above which substance cannot be liquified no matter how much pressure applied

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13
Q

Pseudocritical temperature

A

specific critical temperature at which a mixture will split into components

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14
Q

Vapor Pressure

A

pressure that vapor molecules exert when liquid/vapor phases in equilibrium

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15
Q

SVP

A

maximum concentration of molecules in vapor state for each liquid at each temperature, depends only on temperature

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16
Q

Saturated Vapor Concentration

A

max concentration of inhalant you can obtain at ambient conditions
o Calculation: SVP/Pressure of air x 100%

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17
Q

Boiling Point

A

temperature at which vapor pressure = atm pressure

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18
Q

Solubility

A

ability of an agent to dissolve in liquids, solids; application of Henry’s Law S=V*P

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19
Q

Partition Coefficient

A

concentration ratio that describes how inhalant ax will partition itself btw two phases at equilibrium

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20
Q

Avogardo’s Principle

A

equal vol of gas under same temp/pressure contain 6.02x10*23 molecules

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21
Q

Partial Pressure

A

individual pressure that each gas exerts in mixture of gases, application of Dalton’s Law

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22
Q

Blood Gas Partition Coefficient

A

predicts speed of induction, recovery, change in depth

Lower BG PC: less soluble in blood, faster induction/recovery/depth change

Higher BG PC: blood acts like a sink, increased solubility in blood, slower induction/recovery/depth change

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23
Q

Oil Gas Partition Coefficient

A

predicts potency
o Higher number  potency, lower MAC

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24
Q

Which agents contain preservatives?

A

Sevo, halothane, methyoxyflurane

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25
Q

MW - desflurane

A

168g

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26
Q

MW - enflurane

A

185g

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27
Q

MW - Halothane

A

197g

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28
Q

MW - isoflurane

A

Same as enflur, 185g

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29
Q

MW - methyoxyflurane

A

165g

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30
Q

MW - N2O

A

44g

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31
Q

MW - sevo

A

200g

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32
Q

Specific gravity (20*C) (g/mL)- des

A

1.47

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33
Q

Specific gravity (20*C) (g/mL) - enflurane

A

1.52

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34
Q

Specific gravity (20*C) (g/mL) - halothane

A

1.86g/mL

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35
Q

Specific gravity (20*C) (g/mL) - isoflurane

A

1.49

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36
Q

Specific gravity (20*C) (g/mL) - methyoxyflurane

A

1.42

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37
Q

Specific gravity (20*C) (g/mL) - N2O

A

1.42

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38
Q

Specific gravity (20*C) (g/mL) - sevo

A

1.52

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39
Q

BP (*C) - des

A

23

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40
Q

BP (*C) - enflur

A

57

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41
Q

BP (*C) - halothane

A

50

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42
Q

BP (*C) - iso

A

48.5

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43
Q

BP (*C) - Methyoxyflurane

A

105

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44
Q

BP (*C) - N2O

A

-89

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45
Q

BP (*C) - sevo

A

59

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46
Q

VP mmHg at 20*C - des

A

700

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47
Q

VP mmHg at 20*C - enflur

A

172

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48
Q

VP mmHg at 20*C - halo

A

243

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49
Q

VP mmHg at 20*C - iso

A

240

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50
Q

VP mmHg at 20*C - methoxyflurane

A

23

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51
Q

VP mmHg at 20*C - sevo

A

160

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52
Q

VP mmHg at 24*C - des

A

804

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53
Q

VP mmHg at 24*C - enf

A

207

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54
Q

VP mmHg at 24*C - halo

A

288

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55
Q

VP mmHg at 24*C - iso

A

286

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56
Q

VP mmHg at 24*C - methoxyflurane

A

28

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57
Q

VP mmHg at 24*C - sevo

A

183

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58
Q

mL vapor/mL liquid at 20*C - des

A

209.7

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59
Q

mL vapor/mL liquid at 20*C - enflur

A

197.5

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60
Q

mL vapor/mL liquid at 20*C - halo

A

227

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61
Q

mL vapor/mL liquid at 20*C - iso

A

194.7

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62
Q

mL vapor/mL liquid at 20*C - methoxy

A

206.9

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63
Q

mL vapor/mL liquid at 20*C - sevo

A

182.7

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64
Q

Which agents are unstable in Sodalime?

A

Halo, sevo, methoxy

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65
Q

General MAC - des

A

6.5-8.5

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66
Q

General MAC - N2O

A

> 200

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67
Q

General MAC - Enf

A

1.6

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68
Q

General MAC - iso

A

1.3-1.6

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69
Q

General MAC - halothane

A

0.9-1.2

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70
Q

General MAC - methoxy

A

0.16-0.2

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71
Q

General MAC - ether

A

3-3.2

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72
Q

General MAC - sevo

A

2.3-2.6

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73
Q

VP Ether

A

425

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74
Q

BP ether

A

34.5

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75
Q

% metabolized - des

A

0.02

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76
Q

% metabolized - N2O

A

0.004

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77
Q

% metabolized - enfl

A

2-8

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78
Q

% metabolized - sevo

A

2-5

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79
Q

% metabolized - iso

A

0.2

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80
Q

% metabolized - methoxy

A

50

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81
Q

% metabolized - halothane

A

40-45

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82
Q

Inorganic inhalants

A

N2O, cyclopropane, xenon

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83
Q

Structure of most inhalants

A

= organic compounds
o Aliphatic – straight or branch chained hydrocarbons or ethers - 2 organic radicals attached to atom of oxygen with general structure ROR’

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84
Q

Why halogenation?

A

Addition of halogens - gas at room temp, R side of periodic table - Fl, Br, Cl

Less reactive, more potent, nonflammable

Cl, Br convert many compounds of low potency into more potent drugs

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85
Q

Fluorine

A

atomic # 9, weight 19

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86
Q

Bromine

A

atomic #35, weight 80

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87
Q

Chlorine

A

atomic # 17, weight 35

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88
Q

Atomic # vs atomic weight

A

Atomic # = # of protons
Atomic weight = # protons + # neutrons

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89
Q

Challenges with addition of fluorine atom

A

improves stability, but lowers potency, solubility
* Reduced solubility = lower potency, rapid equilibration

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90
Q

Halothane Structure

A

halogenated aliphatic ethane
o Halothane + catecholamines increased cardiac arrhythmias
o Incidence of arrhythmias reduced by ester linkage – chemical structure preserved across all inhalants developed since

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91
Q

Halothane Decomposition

A

decomposition, addition of thymol
 Problem: thymol less volatile, accumulated in vaporizers, malfunction
 Fl now used in place of Br, Cl - +shelf life, stability, can go without thymol
 Fluorine ion: toxic to organs (kidneys) – only problematic if metabolized

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92
Q

Density

A

amt of matter or mass percent per unit vol

d=m/V

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93
Q

Dalton’s law

A

Partial pressure exerted by a gas is proportional to its fractional contents

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94
Q

Henry’s Law

A

Amt of gas dissolved in a liquid proportional to partial pressure of that gas at equilibrium with that liquid (blood gases)

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95
Q

Rauolt’s Law

A

Partial vapor pressure of each component in an ideal mixture of liquids = vapor pressure of each component x mole fraction in the liquid

96
Q

Ideal Gas Law, principles

A
  1. Ideal gas molecules do not attract, repel each other - only interaction is elastic collision upon impact with each other or an elastic collision within walls of container
  2. Ideal gas molecules themselves take up no vol - gas takes up vol since molecules expand into a large space, but ideal gas molecules approximated as point particles that have no vol in and of themselves
97
Q

Ideal Gas Law

A

PV = nRT

98
Q

Boyle’s Law

A

At constant temp, vol of fixed amount of gas varies inversely with its pressure

PV=K –> P1V1=P2V2

99
Q

Charle’s Law

A

At constant pressure, the vol of fixed gas varies directly with its absolute temperature

V/T = K –> V1/T1=V2/T2
TEMP IS IN KELVIN!!!

100
Q

Gay Lussac’s Law

A

At constant vol, pressure of fixed amt of gas varies in proportion with absolute temperature

P/T = K –> P1/T1 = P2/T2

101
Q

Partial Pressure

A

Individual pressure of each gas in a mixture of gas, absolute value
* Partial pressure of agent same in different compartments that in equilibrium with each other

102
Q

Mole

A

relates number of molecules, quantity of a substance containing same number of particles as there are atoms in 0.012kg of carbon 12, Avogardo’s number 6.0226x1023 per gram molecular weight

103
Q

Under STP…

A

number of gas molecules in 1gm of molecular weight = 22.4L

104
Q

Specific Gravity

A

relative value, ratio of weight of unit vol of one substance to similar vol of water for liquids, vol of air for gases/vapors under similar conditions

105
Q

Vapor Pressure

A

pressure exerted by vapor molecules when liquid, vapor phases in equilibrium

 Some in surface layer gain sufficient velocity to overcome attractive forces btw neighboring molecules, escape from surface  enter gas phase
 Vaporization/evaporation: change in state from liquid to gas
 Dynamic, in closed container at constant temp will reach equilibrium: # of molecules leaving = # of molecules entering
* Gas phase saturated

106
Q

Saturated VP Concentration

A

Relates VP to ambient pressure

  • Example: iso – max concentration at 20*C at sea level= 240/760 * 100 = 32%, 760 is sea level pressure
  • If in Denver at 20*C, 635mm Hg: 240/635 = 37.8%
107
Q

Saturated VP

A

maximum concentration of molecules in vapor state that exist for a given liquid at each temperature

unique to each agent, depends only on temperature – not ambient pressure

108
Q

MOA Temperature Changes within a Vaporizer

A

o If temp of liquid increases: more molecules escape, enter gas phase–> greater number of molecules in vapor phase = greater VP, concentration
o If temp of liquid decrease: fewer molecules escape/more return to liquid phase = less VP, concentration
o Liquid cooling = natural consequence of vaporization process
 ‘Fastest molecules escape first, avg kinetic energy of those left behind decrease so temp decreases
 As temp decreases, VP and vapor concentration decreases

109
Q

Latent Heat of Vaporization

A

amount of energy consumed for a liquid to be converted to vapor, calories to convert 1g liquid to vapor without change in temperature

110
Q

Specific Heat

A

calories required to increase 1g of liquid 1oC

111
Q

Thermal Conductivity

A

measure of ability to conduct heat
o Copper, aluminum, brass&raquo_space;> steel

112
Q

Boiling Point

A

temperature of liquid at which VP = Patm (760 mmHg)
o Boiling point decreases at increased altitude, no change in vapor pressure but have change in barometric pressure

113
Q

Critical Temperature

A

temperature above which substance cannot be liquefied no matter how much pressure applied

114
Q

Molecular Weight

A

(aka molecular mass): mass of a molecule of a substance based on 12 as the atomic weight of carbon, summing anatomic weights of atoms in molecular formula
o Ex: H2O = H – atomic weight of 1, oxygen = 16 so MW of oxygen = 16

115
Q

Triple Point

A

temperature, pressure at which solid, liquid, vapor phase all coexist in equilibrium

116
Q

Ax solubility in blood, tissues

A

primary factor for rate of uptake, distribution within body –> primary determinant of speed of ax induction, recovery

Also influences how they dissolve in rubber goods on machine

117
Q

Henry’s Law

A

total number of molecules of given gas dissolving in solvent depends on chemical nature of gas, partial pressure of gas, nature of solvent, temperature

Vol of gas (V) = partial pressure of gas (P) x Solubility coefficient (S)
* S = solubility coefficient for gas in solvent at given T(temperature)
* Applies to gases that do not combine with solvents to form compounds

118
Q

Solubility in lipid

A

relationship to anesthetic potency
 Low solubility = more rapid equilibration – determines speed of induction

Uptake = solubility x CO x [(PA-Pv)/Pbar]

119
Q

solvent made up of mixture of gases

A

each gas dissolves in solvent in proportion to partial pressure of individual gases
o Total pressure exerted by all molecules

120
Q

Three compartment model

A

Passive gradient from gas phase to oil: gas molecules move into oil compartment  gradient develops for gas molecules in oil to move into water

At given temperature, when no more gas dissolves into oil (solvent) = fully saturated (equilibrium)

At equilibrium, pressures of gas in all three compartments will be the same

BUT # of molecules or volume of gas partitioned between two liquids will vary with nature of liquid and gas

121
Q

What is the key about the three compartment model?

A

at equilibrium at given temperature, PRESSURE of gas in all compartments the same but actual # of molecules in compartments different

Less gas dissolves in a solvent as temp increases, more gas taken up as solvent temp decreases
* Ex: Gases become more soluble in blood when patient hypothermic

122
Q

Solubility Coefficient

A

extent to which gas will dissolve in a solvent
 Inhalants: usually expressed as partition coefficient (PC), concentration ratio of anesthetic in solvent and gas phases or btw two tissue solvents
* Describes capacity of given solvent to dissolve anesthetic gas
* Eg how anesthetic will partition itself btw gas and liquid solvent phases after equilibrium established

123
Q

Movement of anesthetic gas

A

occurs bc partial pressure difference in gas, liquid solvent phases –> no partial pressure difference (equilibrium), no net movement

124
Q

Blood Gas Coefficients Order

A

Nice dogs serve icy enchiladas (every) holiday meal BUT since blooD, des is actually first then nitrous - order of increasing BG coefficients

125
Q

BG PC

A

predicts speed of anesthetic induction, recovery, change of ax depth
o Lower BG, faster onset

SOLUBILITY: inversely proportional to BG
Sevo is LESS soluble in blood than iso

126
Q

OG PC

A

predicts potency
o Lower OG, higher potency

Nice dogs serve icy enchiladas (every) holiday meal

127
Q

removal of ax from blood/tissues and solubility

A
  • Solubility of tissue determines in part quantity of anesthetic removed from blood by tissue to which exposed
    o Higher tissue solubility, longer it will take to saturate tissues with anesthetic
    o All things equal: anesthetics that are very soluble in tissues require LONGER period for induction, recovery
128
Q

Coefficients of Rubber, Plastic

A
  • If amt of rubber goods used in apparatus used to deliver ax to patient is substantial/anesthetic agent very soluble in rubber, amt of uptake of agent by rubber may be significant  less important with current equipment
129
Q

What does ax depth directly vary with?

A

with Panes in brain tissue

130
Q

Pharmacokinetics of anesthetics

A

o Move down a series of pp gradients from higher to lower tension until equilibrium
 Vapor pressure in vaporizer  patient breathing circuit –> lungs –> arterial blood –> tissues
* At induction, Panes at vaporizer is high, progressively decreases as go down chain

131
Q

PA(anes)

A

is pivotal: usually GE at alveolar level efficient such that PAanes = Paanes
 Brain = highly vascular, rapidly equilibrates with Pa anes
* By controlling PAanes, reliable indirect control of Pbrain anes
 Essentially: PAanes = Paanes = Pbrainanes
 Panes = fractional anesthetic concentration x total ambient pressure with fractional anesthetic concentration Canes/100
* In blood or tissues, actual quantity of anesthetic depends on: Panes, anesthetic solubility as determined by PC within solvent (blood or oil)
* At equilibrium, partial pressure of gas in alveoli and among tissue compartments will be equal BUT concentrations will vary among tissues

132
Q

Factors that Determine PA of anesthetic

A
  1. Increased alveolar delivery via increased ax concentration, increased alveolar ventilation
  2. Decreased removal from alveoli
133
Q

Ax: uptake - increased alveolar delivery from increased inspired ax concentration

A
  • increased vaporization of agent
  • increased vaporizer dial setting
  • increased FGF
  • Decreased gas vol of patient BC
134
Q

Ax update - increased alveolar ventilation

A
  1. increased minute ventilation
  2. decreased dead space ventilation
135
Q

Ax update - decreased removal from alveoli

A
  • decreased blood solubility of ax
  • decreased CO
  • decreased alveolar-venous ax gradient
136
Q

Delivery to alveoli

A

Balance btw anesthetic input (alveolar delivery), loss (uptake by blood/tissue)

137
Q

Inspired Concentration

A

 Upper limit dictated by SVP, dependent on temperature
 Characteristics of patient BS also important: volume, amt of rubber/plastic, position of vaporizer (VIC vs VOC), FGI
 Characteristics of patient breathing system (volume, material (i.e. rubber, plastic etc), position of vaporizer (inside or outside of circuit), fresh gas inflow

138
Q

Vol of Circuit and Effect on Inspired Concentration

A
  • BC contains gas vol that must be replaced with gas containing desired anesthetic concentration  buffer that delays rise of anesthetic concentration
    o Small animals with NRB: high FGF should not differ from vaporizer setting
    o Larger animals on circle – volume may be large compared to FGF – marked delays/must wash out, rebreathing expired gas with less anesthetic than FGF, expired gas contains less anesthetic than FG, inspired gas concentration will be less than FG leaving the vaporizer
     Horses, cattle, closed circuit FGF (FGI low vs circuit vol)
139
Q

Equipment

A

 High solubility of some anesthetics (methoxyflurane) in rubber, plastic delays development of appropriate inspired anesthetic concentration
* Loss of anesthetic to these equipment ‘sinks’ s apparent vol of circuit, clinically important
* No longer relevant with current inhalants used

140
Q

VIC, Inspired Concentration of Inhalants

A

VIC: increased FGF into circuit decreases Fi (no flow compensation, decreased SA

141
Q

VOC, Inspired concentration of inhalants

A

increased FGF will increase Fi (technically increases RATE of delivery) so reaches equilibrium with FA faster

142
Q

Effect of hypoventilation on ax induction

A

decreased rate at which alveolar concentration changess over time vs Fi – slower induction, slower changes

143
Q

Second Gas Effect

A

administration of potent inhalant eg N2O can speed uptake of concurrently administered inhalant agent
Increases rate of rise of alveolar concentration

144
Q

Removal from alveoli/uptake by blood

A

Eger: anesthetic uptake product of 3 factors – solubility (S; BG PC), cardiac output (CO), difference in anesthetic partial pressure btw alveolus, venous blood returning to lungs (PA-Pv/Pbar) where Pbar = barometric pressure (mm Hg)

145
Q

Effect of Solubility on removal

A

 Solubility of inhalation anesthetic in blood, tissues characterized by partition coefficient (PC)
* How inhalation agent distributes btw two phases or two solvents eg quantity of agent in blood and alveoli, or btw blood and muscle once equilibrium established

146
Q

Agents with low blood solubility…

A

more rapid equilibration, smaller amount of anesthetic must be dissolved in blood before equilibrium reached with gas phase

147
Q

Agents with high blood solubility…

A

blood acts like large sink into which anesthetic is poured, reluctant to give up to other tissues including brain
* Pharmacologically inactive reservoir interposed btw lungs, brain

148
Q

Effect of CO

A

 Greater CO more blood passing through lungs carrying anesthetic away from alveoli  delays rise of PA anes
* With greater CO, such as with excitement, delay onset
* Inhalant cleared away faster
 Decreased CO, PA anes will rise more quickly
 Remember, gas movement is all about pressure gradients

149
Q

Alveolar to venous anesthetic partial pressure difference

A

Magnitude of difference in anesthetic partial pressure btw alveoli, mixed venous blood returning to lungs related to amt of uptake of ax by tissues
Largest gradient during induction
Once equilibrium reached, tissues no longer absorb anesthetic/no longer tissue uptake from lungs  mixed venous blood returning to lungs contains as much anesthetic as when left lungs - Pv=PA

150
Q

Distribution of CO

A
  • Brain, heart, hepatoportal system, kidneys receive ~75% total blood flow per minute –> rapidly equilibrate with Pa anes compared to other body tissues
  • Skin, muscle = 50% body in humans, at rest receive 15-20% CO – saturation of tissues takes hours to accomplish
  • Fat = poorly perfused, saturation is slow, anesthetics more soluble in fat than other tissues
151
Q

Clearance

A

% clearance = 100 x VA (agent blood/gas PC x CO + VA)
o Affected by alveolar ventilation, CO, agent sol***
 Wash out of less solub agents high at first DT lung FRC then rapidly declines to lower output level, continues to decrease but at slower rate
 Wash out of more solub agents also high at first but magnitude of decrease less, decreases more gradually with time

152
Q

Other Important Factors in Elimination

A

Percutaneous loss
Intertissue diffusion of agents
* Limited clinical important
Metabolism
* Methoxy, maybe halothane
Transcutaneous movement of inhalation agent
* Small amt

153
Q

What is the most important factor in wash out?

A

DURATION OF AX

o Rebreathing circuits: circuit may reduce rate of recovery bc need to wash out inhalant, can reduce via high FGF of O2 only
 Essentially use RBC as NRB

154
Q

Other names for diffusion hypoxia?

A

Fink Effect, Third Gas Effect

155
Q

Diffusion Hypoxia

A

at end of giving N2O, patient goes to room air – lrg vols N2O return from blood to lung, displace other gases in lung esp oxygen
 If on room air (21% oxygen), N2O will dilute alveolar oxygen: decreased PaO2 from levels found in room air  life threatening hypoxia
 Mitigate by 100% oxygen for 5-10min after discontinuation if N2O

156
Q

Biotransformation

A

o Most inhalation anesthetics not chemically inert, varying degrees of metabolism
 Primarily liver, lesser in lung, kidney, GIT
o Metabolism: may facilitate in recovery of anesthesia, may result in acute/chronic toxicities from intermediate or end metabolites
 Magnitude: by chemical structure, hepatic enzyme activity (cytochrome P450 in ER of hepatocyte), blood concentration of anesthetic, disease states, genetic factors.

157
Q

Metabolism

A

Least N2O, most methoxy

Never deny iguanas sunny eateries (that) have mangos.

158
Q

Factors that Favor Elimination

A
  • Increased alveolar ventilation
  • Decreased CO
  • Decreased BG PC
  • Decreased Duration of GA
159
Q

Factors that Increase Ax Uptake

A

Agent Vaporization
Vaporizer Setting
Increased FGF
Increased MV

160
Q

Factors that Decrease Ax Uptake

A

Increased vol of breathing circuit
Increased dead space volume
Lower BG PC
Lower CO
Lower arterial-venous anesthetic gradient

161
Q

MAC

A
  • 1963 Merkel and Eger made the standard index of anesthetic potency: MAC
    o Minimum alveolar concentration of an anesthetic at 1 atm that produces immobility in 50% of subjects exposed to a supramaximal noxious stimuli
    o Corresponds to the effective dose50 (ED50)
    o ED95 (humans) 20-40% > MAC
162
Q

How is MAC related to potency?

A
  • Anesthetic potency = 1 / MAC
    o MAC is inversely related to oil/gas PC
    o Very potent anesthetic like methoxy (high oil/gas PC) has a low MAC
    o Agent with low oil/gas PS = high MAC
163
Q

How MAC determined?

A

Healthy patients without any other influence of drugs

164
Q

MAC determination - people

A

initial noxious stimulus = skin incision

165
Q

MAC determination - SA

A

o SA (mice to dogs, pigs): forceps or other surgical instrument to tail base or base of dewclaw
 In dogs, ovarian/ovarian ligament traction  sevoflurane MAC vs tail clamp

166
Q

MAC(awake)

A

humans on emergence, MAC in which humans open eyes after verbal stimulus (coined by Stoelting)
o Verbal stimulus less intense than surgical incision, response occurs at lower concentration of ax than movement following incision

167
Q

MAC - BAR

A

MAC required to not have increases in catecholamines when skin incision made

168
Q

MAC of N2O

A

o Because nitrous MAC > 100%, cannot be used by itself at one atmosphere pressure in any species and still provide adequate amounts of O2
o Usually administered with another mower potent agent to reduce concentration of that more potent agent necessary for anesthesia

169
Q

MAC Reduction of dogs vs humans

A

o Significantly less MAC reduction in dogs vs humans: 60% N2O with halothane = 55% decrease in healthy humans vs 20-30% in dogs

170
Q

ED50

A

1MAC, light plane of ax

171
Q

MAC-awake

A

voluntary responses, awareness
MAC 0.3-0.5

172
Q

MAC 1

A

Prevent movement to sx stimulus in 50% of population, ED50

173
Q

MAC1.3

A

Prevents movement in 95% of individuals, prevents response to tracheal intubation - ED95

174
Q

MAC1.7-2.0

A

MAC-BAR: blunts autonomic response to sx stimulus

175
Q

MAC and Apneic Index

A

Apneic Index = 1.5-3MAC

176
Q

CV collapse

A

2.7-3MAC

177
Q

Factors that Increase MAC

A

Drugs that cause MAC: amphetamine, ephedrine, morphine (horses), laudanosine, physostigmine

Hyperthermia

Hypernatremia

178
Q

No change in MAC

A

ABP >50mmHg
Atropine, glycol, scopolamine
Duration of ax
Gender
Hyper/hypokalemia
Metabolic AB change
PaO2 >40mmHg
PaCO2 15-95mmHg

179
Q

CNS

A

o Reversible, dose-related state of CNS depression (somatic, motor)
o Hemodynamic, endocrine unresponsiveness to noxious stimuli
o Exact MOA unknown
 Influence electrical activity of brain, cerebral metabolism, cerebral perfusion, ICP, analgesia

180
Q

Molecular Mechanism

A
  1. Meyer-Overton
  2. Cantor
181
Q

Meyer-Overton/Critical Vol Hypothesis

A

strength of inhalants based on lipid vs water affinity: oil:water partition coefficient
 Cell lipid membrane = site of action
 Limitations: does not explain effect of differences btw stereoisomers, ax cut off effect or non-immobilizers

182
Q

Cantor Hypothesis

A

may alter molecular composition, forces within bilayer plane –> change within lateral pressure profile exerted upon proteins in lipid membrane
 Non-immobilizers: may not access interfacial regions of membrane critical to modulation of embedded protein R
 Ion channels/membrane lipids: chiral centers that may interact differently with anesthetic stereoisomers
 Fills in gaps of Meyer-Overton

183
Q

protein theories

A

Inhaled anesthetics bind proteins, modulate function in absence of lipid environment

Potentiate inhibitory target cells: GABAA, glycine, two pore domain K channels

Inhibit excitatory cell targets: NMDA, AMPA, nicotinic R, VG Na channels

Inability to identify R for anesthetic action –> multiple cell R, ion channel target modulation

184
Q

Site of action in brain

A

cerebral cortex, amygdala, and hippocampus  hypnosis, amnesia
* Amnesia= amygdala and hippocampus
* EEG: hippocampal-dependent -rhythm frequency slows  to amnestic effects with subanesthetic doses of iso
* alpha4, beta3 subunits of GABA partly responsible for iso depression
* Mice: antagonism of 5 subunit-containing GABAA R restores hippocampal-dependent memory during sevo
* GABAA vs TREK-1 K+ channels

185
Q

Spinal Cord

A

critical site for suppressing noxious-evoked movement (immobility)
* Principally responsible for preventing movement during surgery with inhaled anesthetics
* NMDA, glycine receptor antagonism
* Depression of locomotor neuronal networks located in ventral horn

186
Q

Analgesia assoc with xenon, n2O:

A

Supraspinally DH of SC

analgesia via glutamatergic R inhibition, inhibit NMDA receptors and K2P/TREK1 receptors
o Additional modulation of noradrenergic opioid R pathways
o Ca channels: decrease Ca available and responsiveness – BP and negative inotropic effects (not true with xenon

187
Q

N2O, xenon: 0.8-1MAC…

A

decreased but do NOT prevent wind-up/central sensitization
o No benefit of higher concentrations

188
Q

N2O, Xenon: 0.4-0.8MAC…

A

decreases withdrawal responses to noxious stimuli, but can actually cause hyperalgesia
o Peak effect at 0.1MAC
o Potent nicotinic cholinergic R inhibition

189
Q

5HT3

A

Autonomic effects

190
Q

EEG Effects

A

No parameter has sensitivity/specificity to justify use of EEG alone as reliable index of ax depth
* Improvements in technology: Bispectral index

As depth of ax increases, cerebral cortex becomes desynchronized - decreased in frequency, increase in EEG activity

191
Q

EEG Effects and MAC

A

increased frequency of EEG activity ~0.4MAC
wave amplitude increases then progressively declines ~1MAC
Burst suppression ~1.5MAC
Isoelectric activity (flat late) at ~2.0MAC iso, servo, des; 3.5 halothane

192
Q

Enflurane and EEG

A

spontaneous or noise-initiated sz in dogs, people
o Substantial increases in cerebral blood flow, CMO2

193
Q

Cerebral Metabolism

A

all decrease cerebral metabolic rate (CMR), least with halo

194
Q

CBF

A

–Either no change or increase - dose-related VD from ax, decreased CMO2

Halothane (greatest) > N2O > enf, iso, des > sevo (least)
* N2O: severe vasodilation
* increased CBF –> increase blood brain vol, ICP
* Most likely DT time-dependent increase in NO synthase inhibition

Horses: regional CBF constant over wide range of CPPs despite changes in ICP

195
Q

Loss of Cerebrovascular Autogregulation

A

uncoupling of CP from CMO2
o 0.5MAC: diminished, obtunded
o High MACs: cerebrovascular autoregulation very diminished –> CBF simply function of CPP
o Effects on CBF = duration-dependent

Sevo: best at maintaining cerebral autoregulation

196
Q

CO2 Tension and Autoregulation

A
  • Autoregulation lost, CBF increases at lower MAC when patients hypoventilate
  • Interaction greater with iso + CO2 than sevo + CO2
197
Q

ICP

A

Increases DT increased CBF
* Regardless of species, cerebrovascular autoregulation better preserved at MAC-multiple of halothane ax when hyperventilation maintained, PaCO2 decreased

198
Q

Respiratory Effects

A

–Decreased SpV as dose increases: VT>RR

–Decreased minute ventilation, increased dead space ventilation (increased VD/VT >0.3-0.5)

–Hypercapnia DT depression of alveolar minute ventilation, stimulation of ventilation by central and chemoR blunted

–Bronchospasm

–Respiratory depression worsened with concurrent drugs

199
Q

Bronchospasm and Inhalants

A

–BD DT decreased cholinergic transmission
–iso, +/- enflurane, sevo, des: relaxation of constricted bronchial SmM least equal to or exceeds that caused by halothane via inhibition of M3

–Airway irritation: desflurane at >7%, lesser extent with iso

200
Q

Factors Influencing Respiratory Effects

A
  1. Ventilation - assisted not usually effective in substantially lowering PaCO2, CMV best
  2. Duration of ax: higher MAC for prolonged periods = significant temporal increase in PaCO2
  3. Respiratory depression blunted by sx, noxious stimulus - effect diminishes at increased deoth
201
Q

Cardiac Effects

A

Myocardial depression (interference with Ca), decreased symapthoadrenal activity

Decreased CO = dose dependent, DT decrease in SV from decreased myocardial contraction HALOTHANE
–Also affected ABP

Variable effects on HR

202
Q

Cardiac Dysrhythmias, Catecholamines

A

Increased automaticity of myocardium, increased likelihood of propagated impulses from ectopic sites (especially ventricle)
* Newer ether-derived agents: do not predispose heart to extrasysoles

Spontaneous dysrhythmias- halothane
* Markedly decreases amount of epi necessary to cause VPCs

Halothane > Enflurane, methoxy > des, sevo iso
 ALL agents exaggerate adrenergic agonist associated dysrhythmias

203
Q

Factors Influencing Circulatory Effects

A
  1. Mode of Ventilation/PaCO2 - CV usually depressed during IPPV
  2. Noxious Stimulation - blocked at MACbar/MAC1.5-2.0
204
Q

How IPPV Depresses CV Activity

A

Direct mechanical action (increase intrathoracic pressure, resultant decrease in venous return to heart)

Indirect (pharmacologic action of PaCO2)
o Increase PaCO2 = direct depression of heart, SmM of peripheral blood vessels (dilation)

Indirect (via sympathetic activity) stimulation of circulatory function

205
Q

CV Effects of Other Drugs

A

MAC reduction –> decreased CV effects

N2O may directly depress myocardium, counterbalanced by sympathomimetic effect - net improvement of CV function

206
Q

Kidneys

A

All useful agents: similar, mild, reversible dose-related decrease in renal BF, GFR –> anesthesia-related decrease in CO
 Smaller vol concentrated urine vs awake
 increased BUN, creatinine, inorganic phosphate may accompany prolonged ax

Renal function reduction highly influenced by hydration, hemodynamics during GA
 Mitigated by IVF, prevention of marked reduction in renal BF

207
Q

Methoyxflurane and Nephrotoxicity

A

Renal failure characterized by polyuria unresponsive to VP n
MOA: biotransformation of methoxyflurane, large release of free fluoride ions
* Peak levels, prolonged exposure DT high adipose accumulation during ax

Free fluoride ions cause direct damage to renal tubules
 Reported in dogs in conjunction with tetracycline, banamine

Enflurane: also able to produce fluoride ions, above nephrotoxic threshold in humans but not seen

208
Q

Sevoflurane and Fluorine Ion Induced Nephrotoxicity

A

–Production of FI ions in humans > nephrotoxic threshold

–Histological, clinical, biochemical evidence of injury rare

209
Q

Why Sevoflurane Lacks Nephrotoxicity vs Methoxy

A

Area under serum fluoride concentration vs time curve may more important determinant of nephrotoxicity than peak serum fluoride concentrations
o Sevo = poorly soluble, rapidly eliminated by lungs
o Duration of availability for biotransformation limited

Hepatic metabolism vs methoxy = hepatic, renal
o Lack of intrarenal ax defluorination may markedly reduce nephrotoxic potential
o Horse: increase serum fluorine, magnitude/time course of increase similar to humans, no evidence untoward renal effects

210
Q

Compound A Production

A

degradation of sevoflurane by CO2 absorbents

Nephrotoxic = renal injury, death in rats

Proposed MOA: species-specific metabolic degradation to directly nephrotoxic compounds

most commercially available absorbents in US no longer contain KOH, NaOH
 Baralyme>Sodalime, not Amsorb

211
Q

Hepatic Effects of Inhalant

A

–hepatocellular injury DT decreased HBF, DO2
Isoflurane better maintains O2 delivery, agent less likely to cause hepatocellular injury

–Iso >/~ Sevo, Des&raquo_space;> Halothane
 Cofounding factors: N2O, concurrent hypoxia, prior induction of hepatic drug-metabolizing enzymes, mode of ventilation, PEEP
* May worsen conditions,  likelihood of hepatocellular damage

212
Q

Halothane Hepatic Effects

A
  1. Inhibition of drug metabolizing capacity
  2. Mild, self-limiting hepatocellular damage
  3. Halothane hepatitis - fatal immune-meditated toxicity
213
Q

Malignant Hyperthermia

A

Pharmacogenetic myopathy via activation of RYR1 – swine, horses, dogs, humans

Halothane = most potent triggering agent, can be any volatile anesthetic
o Rapid rise in cellular metabolic activity, death if not treated quickly
o Monitoring of temp, CO2 production, other signs of metabolic imbalance IE ABG warranted and susceptible, suspected patients
 Avoid triggering agents, prophylactic tx with dantrolene

214
Q

Pigs Most Susceptible to MH

A

Pietrain, Landrace, Poland China Pigs

215
Q

Clinical Signs MH

A

muscle rigidity, hyperthermia with 1*C increase Q5min, tachyarrhythmias, tachypnea

216
Q

ABG Changes Assoc with MH

A

metabolic acidosis, hypercapnia, base deficit >8mEq/L, hyperlactatemia, hyperkalemia

217
Q

Treatment for MH

A

active cooling, CMV, TURN OFF VAPORIZER, HCO3 PRN (0.3kgsdesired change), switch circuits, TIVA or xenon, dantrolene 5mg/kg IV or 10mg/kg PO via stomach tube

218
Q

N2O

A

low blood solubility, limited CV/resp system depression, minimal toxicity
o Not potent – MAC humans 100%, dogs 188%, cats 255%- will not anesthetize healthy individual as solo agent

Main benefit: allow reduction of primary more potent inject/inhal

 As concentrations of N2O increases, change in proportion, partial pressure of other constituents of inspired breath esp O2
No more than 75% N2O to avoid hypoxemia (usually 66%)
>sea level, lower N2O to ensure adequate PIO2

219
Q

Nitrous Second Gas Effect

A

Very low blood solubility = rapid onset

Large vol of N2O leaves alveoli, allowing for concentrating effect of second gas to create faster induction

High concentration of N2O administered concurrently in mixture with inhalation agent, alveolar concentration of simultaneously administered anesthetic increases more rapidly than when ‘second’ gas administered without N2O

220
Q

Contraindications for N2O Use

A

ruminants/horses, pneumothorax, GDV, FB, air embolism, cavotomy , esophageal FBs

221
Q

Systemic Effects of Nitrous

A

-Direct myocardial depression, counteracted by SNS stimulation - increased BP, arrhythmias
-Little effects on resp, kidney, liver

222
Q

Elimination N2O

A

rapid, exhaled breath
 Biotransformation to molecule N2 very small, mainly by intestinal flora

223
Q

Effect of Inhalants on Uterine Tissue

A

o Decreases uterine SmM contractility, BF

224
Q

SE N2O

A
  1. Prolonged exposure = megaloblastic hematopoiesis DT interference with RBC/WBC production by BM
  2. Polyneuropathy
  3. Vascular inflammation
  4. Induced inactivation of vit B12-dependent enzyme methionine synthase via oxidation of cobalt from B12 - interruptions of folic acid metabolism
  5. Abuse potential
  6. Interference with some respiratory monitoring
225
Q

N2O Transfer to Closed Spaces

A

When N2O introduced into inspired breath, re-equilibration of gases in gas spaces

N2O quickly enters, N2 slowly leaves
–N2O = 30x more soluble in blood (BG PC 0.47): vol of N2O that can be transported to closed gas space many times vol of N2 can be carried away (BG PC 0.015)

Result: net transfer of gas to gas space as increased in vol with gut, pneumothorax, blood embolus; increased pressure; pneumocephalogram,

226
Q

Where does N2O go in the body?

A

ETT
Gut
Middle Ear
Sinuses

227
Q

Diffusion Hypoxia

A

Lrg vol N2O stored in body during ax, unequal exchange of N2O for N2, deficiency in blood oxygenation may occur at end of ax if abrupt substitution of air for N2O

Rapid outpouring of N2O from blood into lung = transient but marked decrease in PAO2

227
Q

Diffusion Hypoxia

A

Lrg vol N2O stored in body during ax, unequal exchange of N2O for N2, deficiency in blood oxygenation may occur at end of ax if abrupt substitution of air for N2O

Rapid outpouring of N2O from blood into lung = transient but marked decrease in PAO2

228
Q

What is the NIOSH limit for inhalant exposure?

A

2.0ppm

229
Q

What is the NIOSH limit for N2O?

A

25ppm

230
Q

Role of Contemporary volatile anesthetics as green house gases

A

Stratospheric ozone layer known to be damaged by rapid, widespread global usage and subsequent atmosphere presence of volatile, synthetic, long lived organochlorine and bromine containing compounds = chlorofluorohydrocarbons, CFCs

All contemporary volatile anesthetics = potentially destructive to ozone layer as halogenated compounds

In effect only chlorine containing halothane, isoflurane (less so)
* Relative contribution of these two volatile agents estimated at most 0.01% of annual global release of CFC’s

Substances that contain only fluorine do not harm the ozone layer

231
Q

N2O Environmental Effects

A

 Emission highlighted as single most important ozone depleting emission, expected to remain largest throughout 21st century
 Long atmospheric lifetime so contributes to warming as well as ozone depletion

232
Q

Which two inhalants have the most significant environmental effects?

A

Des, N2O

233
Q

Desflurane Environmental Effects

A

has highest heat trapping effects, now removed from markets in some countries
 MAC Basis: desflurane&raquo_space;> iso > sevo

234
Q

Ozone depleting potential of inhalants

A

o Iso, halothane = chloroflurocarbon, ozone depleting capacity
 Des, sevo = hydrofluorocarbons, no ozone depleting potential

N2O: ozone depleting potential

235
Q

Xenon

A

–Inert noble gas, MAC 71%

–No compounds, no biotransformation - requires prolonged denitrogenation

–BG PC 0.14 –> rapid induction

–CV safe, no potential to induce MH

–Used for contrast imaging, neuroprotectivity

–Not FDA approved - research only

236
Q

Xenon MOA

A

post synaptic NMDA R blockade at K2P - decreases in excitatory neurotransmission

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