Pharm Lecture 2 Inhaled Agents

Front 1

poppy
introduced into these countries

Back 1

India and China 600-1200 BC

Front 2

Prior to poppy pioneered the use of

Back 2

cannabis
incense and aconitum

Front 3

Chinese performed abdominal surgery using

Back 3

boiled cannabis mixed in wine

Front 4

Europe through the 18th century
Variety of Solanum species of herbs
combined with

Back 4

wine or opium

Front 5

13th century_________ used the above mixtures
with opiates to induce unconsciousness

Back 5

Italy

Front 6

Opium used directly in a wound acts on

Back 6

peripheral opioid receptors

Front 7

Medicine containing willow leaves
(salicylate, the predecessor of aspirin)
were applied directly to

Back 7

the source of
inflammation.

Front 8

Crucial drawback to herbal anesthetics
2 points

Back 8

 “When soporifics are weak they are useless, and
when strong, they kill.”
 Led to the drying and packing of opium in standard
chests

Front 9

developed of Morphine 1803

Back 9

German pharmacist Friedrich Serturner

Front 10

Morphine named after

Back 10

Greek god of Dreams

Front 11

1853 use of morphine spread following

Back 11

Following the development of the hypodermic needle

Front 12

Used for pain relief and “cure” for opium and alcohol

Back 12

Morphine

Front 13

more addictive
than alcohol or opium

Back 13

Morphine

Front 14

Extensively used during the civil war resulting
in

Back 14

400,000 sufferers of “soldierʼs disease” of
morphine additions.

Front 15

Became the most abused narcotic analgesic
in the world

Back 15

morphine

Front 16

Morphine Became a controlled substance under

Back 16

Harrison Narcotics Tax Act of 1914

Front 17

Synthesized from morphine in 1874 and brought to the market in 1898 by Bayer

Back 17

Diacetylmorphine or Heroin

Front 18

1.5-2 times more potent

Back 18

Diacetylmorphine or Heroin

Front 19

Surpassed morphine as the most commonly
abused narcotic in the world in the 1920s

Back 19

Diacetylmorphine or Heroin

Front 20

CO2 experiments in the 1820

Back 20

Henry Hill Hickman
would nearly suffocate farm
animals and amputate body parts

Front 21

Recognized as one of the Fathers of Anesthesia by the British

Back 21

Henry Hill Hickman

Front 22

Isolated oxygen 1776

Back 22

Joseph Priestly
philosopher, scientist
and nonconformist

Front 23

Developed soda water

Back 23

Joseph Priestly
philosopher, scientist
and nonconformist

Front 24

Experimented with
electricity

Back 24

Joseph Priestly
philosopher, scientist
and nonconformist

Front 25

Discovered Nitrous
Oxide 1773

Back 25

Joseph Priestly
philosopher, scientist
and nonconformist

Front 26

The anesthetic
qualities of Nitrous
Oxide discovered

Back 26

British chemist
Humphrey Davy in
1799.

Front 27

1845 demonstrated
N2O for the Mass
Gen Hosp

Back 27

Horace Wells
traveling dentist

Front 28

Dentist who demonstrated
the use of ether at the
Mass Gen Hosp 1846

Back 28

William Thomas Green
Morton

Front 29

Became embroiled in a
legal battle over his
“discovery”
Died penniless in 1863 in
New York

Back 29

William Thomas Green
Morton

Front 30

First general
anesthetic in 1842
three years prior to
Mortonʼs
demonstration.

Using ether

Back 30

Crawford W Long

Didnʼt publish his
findings until 1848.

Front 31

Discovered the
anesthetic properties of
Chloroform anesthesia
1848

Back 31

James Young Simpson

Front 32

British obstetrician who
delivered Queen Victoriaʼs
2 children

Back 32

British obstetrician who
delivered Queen Victoriaʼs
2 children

His anesthesiologist was
John Snow

Front 33

Ether
 Known as

Back 33

Diethyl Ether

Front 34

Ether
physical properties

Back 34

Clear,
colorless,
highly flammable liquid with a low boiling
point and a characteristic odor.

Front 35

Has a higher therapeutic index than chloroform: as a result
still in widespread use in developing nations

Back 35

Ether

Front 36

Ether Metabolized by

Back 36

cytochrome P450

Front 37

Ether inhibits

Back 37

alcohol dehydrogenase. Was often mixed with
alcohol for recreational use in late 18 and early 1900s

Front 38

Ether Strong association with (3)

Back 38

with post-op nausea and vomiting when
used as an anesthetic.
Enhanced airway secretions.
Slow onset and slow recovery

Front 39

Ether Other uses:

Back 39

common laboratory solvent. Used as starting
fluid for gasoline and diesel engines.

Front 40

Chloroform
 Discovered in 1831 by

Back 40

by American physician Samuel
Guthrie.

Front 41

Began to replace ether until its toxicity was
discovered.

Back 41

chloroform

Front 42

Chloroform Major uses today:

Back 42

production of R-22

Front 43

Labeled as a human carcinogen and has been
banned as a consumer product in the US since 1976

Back 43

chloroform

Front 44

year anesthetic property of N2O discovered.

Back 44

1800

Front 45

year first ether anesthetic

Back 45

1842-

Front 46

N2O, ether, and chloroform were
the only anesthetic in use year

Back 46

1840s - 1930s

Front 47

1930s -1950s few agents added: all were

Back 47

flammable or hepatotoxic

1930 Cyclopropane: explosive w/ O2 and N2O
 1951 Fluoxene: extremely nephrotoxic, flammable

Front 48

birth of fluorine chemistry year

Back 48

1940s

Front 49

saw the development of hydrogenated
hydrocarbons. Halothane

Back 49

1950

Front 50

1960 Methoxyflurane

Back 50

renal toxicity, slow induction
and recovery. Brand name Penthrane

Front 51

1973 Enflurane related cases of

Back 51

hepatotoxicity
similar to halothane rapid onset and recovery

Front 52

Desflurane

Back 52

1993

Front 53

Sevoflurane

Back 53

1995

Front 54

The Unitary Theory of Anesthesia

Back 54

No structure/activity relationships for inhaled
anesthetics. All gases produce anesthesia by a
common mechanism of action at the molecular level.

Front 55

The Meyer-Oveton rule states that

Back 55

the potency of an IA correlates directly with lipid solubility.

Front 56

Mechanism of Action IA

Back 56

This increased lipid solubility causes the I/
A to enter the cell bio-membrane.
 Causes structural distortion of the membrane
 Distortion reduces nerve impulses along a
nerve cell

Front 57

Problems w/ Unitary Theory

FYI

Back 57

 Not all lipid soluble molecules are anesthetics
• Some are convulsants
 Correlation between anesthetic potency and lipid
solubility is only approximate.
 Change of 1o C can similarly change lipid bilayer
without producing anesthesia
 There does not appear to be a single macroscopic
site of action that is shared by all I/As.

Front 58

Molecular and cellular mechanism
I/A bind to

Back 58

I/A bind to specific binding sites on membrane
proteins. Not the lipid bilayer.

Front 59

may be important
site of action for IA

Back 59

Evidence that GABA and glycine

Front 60

Evidence that GABA and glycine cause 2X

Back 60

• Leads to increased chloride permeability and CNS
depression
• Enhance the effects of GABA or augments chloride
conductance.

Front 61

I/A do not appear to 4X

Back 61

to effect excitatory
neurotransmitters
• Glutamate, AMPA, NMDA and Kainate

Front 62

The two universal effects of I/A

Back 62

 Immobility in response to noxious stimuli - Occurs by action on the spinal cord

 Unconsciousness: achieved by action on brain

Front 63

Result from actions at separate molecular and
anatomic sites and are produced by different mechanisms.

Enhance GABA in

Back 63

Reticular Activating System

Front 64

Result from actions at separate molecular and
anatomic sites and are produced by different
mechanisms.

Potentiate glycine in

Back 64

brain-stem and spinal
cord.

Front 65

interest in the NMDA

IA induce anesthesia by

Back 65

acting as a NMDA
receptor antagonist, blocking NMDA.

Bind to Calcium channels on the outer surface of
the neuron, providing a high level of NMDA
receptor blockade. Normally activated by
glutamate.

Front 66

NMDA responsible for

Back 66

memory and cognitive
brain processes.

Front 67

Ketamine NMDA receptor antagonist.

Back 67

Acts similarly as IA but bind at regulatory sites on the
NMDA sensitive calcium transporter complex, which
provides slightly lower levels of NMDA receptor
blockade.

Front 68

NMDA receptor is

Back 68

a complex structure activated by a
number of ligand and electrical channels.
• Current research aimed at discovering the role of the NMDA
receptor in the treatment of schizophrenia, Huntingtonʼs
Disease, depression, ADHD, and other brain dementias.


• The Journal of Neuroscience, Journal of Physiology, Journal
of Anesthesia & Analgesia

Front 69

Pharmacokinetics of I/A

Describes their:

Back 69

 Absorption or uptake from the alveoli into
pulmonary capillary blood
 Distribution in the body
 Metabolism
 Elimination principally via the lungs.

Front 70

8 Influenced by or Factors affecting MAC
both inease or decrease

Back 70

 Aging: reflected in decreases in lean body mass and
increases in body fat. Increases the Vd for fat soluble
agents.
 Decreased hepatic function and
 Decreased pulmonary gas exchange decreases
anesthetic clearance with age.
 Decreased cardiac output in the elderly increase
uptake

Front 71

Factors Affecting Mac:Age: Max at

Back 71

6-18 months and decreases by
6% per decade

Front 72

Factors Affecting Mac: CNS catecholamine

Back 72

increases MAC

Front 73

Factors Affecting Mac:Hypernatremia:

Back 73

increases MAC

Front 74

Factors Affecting Mac:Chronic ETOH

Back 74

increases MAC

Front 75

Factors Affecting MAC Temp

Back 75

decreases MAC 2-5% or each one 1o
C change.

Front 76

Factors Affecting MAC - Pregnancy:

Back 76

decreases MAC

Front 77

Factors Affecting MAC - Acute ETOH

Back 77

use decreases MAC

Front 78

Factors Affecting MAC also affected by 3 areas
decreased by 3 physical states

Back 78

Metabolic acidosis, hypoxia, hypotension

Front 79

The alveolar partial pressure (PA) is in
equilibrium with

Back 79

the arterial blood (Pa) and brain
(Pbr). As a result, the PA is an indirect
measurement of anesthetic partial pressure in
the brain.

Front 80

FI (inspired gas concentration) affects delivery to the
alveoli
• Determined by 3 factors

Back 80

Determined by fresh gas flow
• Vaporizer settings
• Breathing circuit volume and circuit absorption

Front 81

PA determined by

Back 81

PA determined by delivery (input) to the alveoli minus
uptake or loss of blood into the arterial blood
• Concentration effect
• Second gas effect

Front 82

Alveolar partial pressure is important because it determines the

Back 82

partial pressure of anesthetic in
the blood and ultimately, in the brain.

Front 83

Partial pressure of the anesthetic in the brain is directly proportional to its

Back 83

brain tissue
concentrations, which determines clinical effect.

Front 84

Three factors that affect the anesthetic
uptake:

Back 84

Solubility in the blood of the agent
Alveolar blood flow
Partial pressure difference between alveolar
gas and venous blood.

Front 85

Insoluble agents are taken up by the blood less readily thus

Back 85

alveolar concentrations rise
faster and induction is faster.

Front 86

The higher the blood/gas coefficient, the
greater the

Back 86

solubility and the greater its
uptake by the pulmonary circulation.

Front 87

Rise of alveolar concentration toward
inspired concentration most rapid with

Back 87

least blood soluble agent (N2O) and least
rapid with the most blood soluble agents.

Front 88

How does alveolar blood flow affect uptake and
distribution of IA?

Back 88

Alveolar blood flow is essentially equal to cardiac output.

As CO increases, anesthetic uptake increases,
the rise in alveolar pressure slows, and induction is slowed.

Low output states predispose patients to overdosage
with soluble agents.

Front 89

Low output states predispose patients to

Back 89

Low output states predispose patients to overdosage
with soluble agents.

Front 90

Higher than anticipated levels of IA may lower CO even further due to its

Back 90

myocardial
depressant effect.

Front 91

Alveolar gas to venous blood partial
pressure difference:
 This gradient depends

Back 91

on tissue uptake

Front 92

The transfer of blood to tissue is determined by:

Back 92

 Tissue solubility of agent
 Tissue blood flow
 Partial pressure difference between arterial blood and tissue.

Front 93

The concentration effect

Back 93

The higher the FI the more readily the the PA
approaches the FI

Front 94

Second-Gas Effect

Back 94

The second gas effect reflects the ability of
high-volume uptake of one gas (first gas) to
accelerate the rate of increase of the PA of a

Front 95

Pharmacokinetics of I/A

Back 95

Four Tissue groups based on their solubility.

Front 96

Vessel Rich Group

Back 96

Brain, Heart, Liver, Kidney, and endocrine organs.
• Equilibrates with blood in 4-8 minutes

Front 97

Muscle Group

Back 97

 Skin and muscle
• Equilibrates with blood in 2-4 hours

Front 98

Fat Group

Back 98

Equilibrates w/blood 70-80 minutes for N2O, 30 hrs for Sevo

Front 99

Vessel-poor Group

Back 99

Bone, ligaments, teeth, hair, and cartilage
• No uptake

Front 100

Pa (arterial gas concentration) is affected
by: 3x

Back 100

 Blood gas partition coefficient
 Cardiac output
 Ventilation perfusion mismatching

Front 101

Blood Gas Partition Coefficient
 An indicator

Back 101

of speed of uptake and
elimination.

Front 102

When the BG Partition coefficient is high,

Back 102

a
large amount of anesthetic must be dissolved
in the blood before the Pa equilibrates with
the PA.

Front 103

Increased CO results in

Back 103

more rapid uptake
slowing the rise in PA and induction is slowed

Front 104

A decreased cardiac output

Back 104

speeds the rate of
increase of the PA because there is less uptake to
oppose input.

Front 105

 Alveolar-to-venous Partial Pressure
Differences fyi

Back 105

Vessel rich group (brain, heart, liver, kidneys)
• These tissues rapidly equilibrate with the Pa due
to small mass and high blood flow.
• After 5-15 minutes (depending on blood solubility)
the returning venous blood is the same partial
pressure as the PA.

Front 106

Transfer from the arterial blood to the
brain is dependent upon 3x

Back 106

 Brain/Blood partition coefficient
 Cerebral blood flow
 Arterial to venous pp difference

Front 107

5 Factors affecting the arterial
concentration of IA

Back 107

 V/Q abnormalities
 Emphysema
 Endobronchial intubation
 Congenital Heart Disease
 All increase the alveolar-arterial difference

Front 108

Elimination of Inhaled Anesthetic or
Recovery
 Depends on

Back 108

lowering the concentration of
anesthetic in brain tissue.
• Eliminated by biotransformation- is greatest on
agents that undergo extensive metabolism such
as methoxyflurane.
• Transcutaneous loss: is insignificant
• Exhalation via the lungs: most important route.

Front 109

Biotransformation of Inhalational Agents

Back 109

 Halothane
20%
 Enflurane
2%
 Sevoflurane
2-5%
 Isoflurane
.2%
 Desflurane
.02%

Front 110

8 Recovery speeded by many of same factors that speed induction.

Back 110

 Elimination of rebreathing
 High fresh gas flows
 Low anesthetic circuit volume
 Low absorption by the anesthetic circuit
 Decreased blood gas solubility
 High cerebral blood flow
 Increased ventilation
 Elimination of nitrous oxide can lead to diffusion
hypoxia

Front 111

Diffusion Hypoxia
 Occurs when

Back 111

N2O is discontinued

Front 112

Diffusion Hypoxia law

Back 112

 Follows Ficks Law of Diffusion

Front 113

MAC is

Back 113

The alveolar concentration of inhaled anesthetic that
prevents movement in 50% of patients to a noxious
stimulus

Front 114

MAC

Back 114

The alveolar concentration of inhaled anesthetic that
prevents movement in 50% of patients to a noxious
stimulus

Front 115

MAC is rather consistent varying only

Back 115

10-15% among
individuals

Front 116

5 Factors that increase MAC

Back 116

 Hypernatremia
 Hyperthermia
 Drug induced elevations in catecholamine stores
 Women with natural red hair
 Tracheal intubation requires the highest MAC to prevent skeletal muscle responses.

Front 117

7 Factors that decrease MAC

Back 117

 Hypothermia
 Hyponatremia
 Pregnancy: decreases MAC by 30% by term
 Lithium
 Lidocaine
 Neuraxial Opioids
 PaO2 < 38 mm Hg
 B/P < 40 mm HG

 Pre-op meds
 Drug induced decreases in CNS catecholamine
stores
 Alpha-2 agonist
 Acute ETOH intoxication
 Cardio pulmonary bypass

Front 118

Factors that decrease MAC
 Increase in age

Back 118

Results in a progressive decrease in MAC of 6% per
decade after age 40.

Front 119

MAC unaffected by: FYI

Back 119

 Duration of anesthesia
 Hyper or hypokalemia
 Anesthetic metabolism
 Chronic ETOH abuse
 Thyroid gland dysfunction
 Gender
 PaCO2 15-95mm Hg: PaO2 > 38mm Hg
 B/P > 40 mmHg

Front 120

MAC Awake- is

Back 120

the MAC of anesthetic that abolishes
response to verbal command in 50% of patients. 20
to 50% of MAC depending on the agent.

Front 121

MAC BAR-

Back 121

the Mac at which autonomic responses
are blocked. About 2 MAC

Front 122

ED 95:

Back 122

1.3% MAC

Front 123

Upon emergence, at 10% of MAC there is a
response to

Back 123

“open your eyes”.

Front 124

Cardiovascular effects of Inhalation Agents 5x

Back 124

 Myocardial protection against reversible and
irreversible ischemia. Reduces infarct size and
myocardial reperfusion injury following global
ischemia. Clinical significance still unknown.
 Direct CNS depression
 Direct cardiac depression
 Lower SVR
 Block baroreceptor response

Front 125

Coronary circulation
 Ischemia caused by

Back 125

vasodilating coronary arteries
and redistributing coronary blood flow from areas
that depend on collateral circulation

Front 126

Cardiac Dysrhythmias
 Alter

Back 126

electrical activity in the heart
 Slowing of SA discharge
 AV junctional rhythms are not uncommon
 Sensitizes the heart to catecholamine
• Especially halothane
 Heart rate increases
• Iso and Des

Front 127

Pulmonary Effects
 Respiratory depression leading decrease in

Back 127

Minute
Volume with increase in pCO2

Front 128

Depress ventilatory responses to

Back 128

hypercarbia and
hypoxia in dose dependent manner

Front 129

probably the most potent b.dilator

Back 129

Halothane

Front 130

not cause bronchodilation

Back 130

Nitrous does

Front 131

Preferential dilation of distal airways as compared to

Back 131

proximal

Front 132

 Pulmonary Effects
 Depresses mucociliary clearance

Back 132

of type II
alveolar cells.

Front 133

Pulmonary Effects
Depresses mucociliary clearance of

Back 133

type II alveolar cells.
Modest inhibitory effects on hypoxic
pulmonary vasoconstriction, leading to
shunting and decreased oxygenation.
 All except N2O decrease airway resistance in
patients with COPD.

Front 134

Central Nervous System eeg

Back 134

Decreased wave frequency and increases amplitude.
 Higher concentrations greater than 2 MAC yields
isoelectric EEG and burst suppression.

Front 135

Protects against ischemia by

Back 135

decreasing CMRO2

Front 136

Causes cerebral vasodilation at

Back 136

or above 1 MAC
leading to increased ICP

Front 137

can cause
convulsions

Back 137

Enflurane and to a lesser extent, Sevo,

Front 138

Dose dependent relaxation of uterus at

Back 138

at or
grater than 1 MAC

Front 139

Uterine and Fetal effects 4x

Back 139

Dose dependent relaxation of uterus at or
grater than 1 MAC
 Associated with increased blood loss during
C/S
 Inhaled anesthetics cross placenta
 Dose related effect evidenced by fetal
cardiovascular depression, reduction of CBF
and O2 delivery to brain.

Front 140

muscle relaxation.

Back 140

 Dose dependent muscle relaxation.
• At spinal level or centrally mediated
• May desensitize the NMJ to ACTH

Front 141

Allows sufficient relaxation to permit ET intubation
and facilitate intra-abdominal procedures.
• Potentiates the the action of

Back 141

muscle relaxants.

Front 142

Hepatotoxicty: correlates with extent of

Back 142

oxidative metabolism
• Halothane> Enflurane> Isoflurane> Desflurane
• 50 cases reported with enflurane, fewer cases
with isoflurane
• One case report with desflurane.

Front 143

GI and Renal Effects
 GI 2x

Back 143

• Can delay gastric emptying
• Associated with nausea and vomiting

Front 144

Renal Effects

Back 144

• All can cause a dose dependent decrease in GFR and renal
blood.
• Best avoided by adequate fluid replacement and avoiding
hypotension. Then
• Sevo associated with Compound A.

Front 145

Sevoflurane and Compound A
 Sevo degrades to

Back 145

compound A in the presence of
alkali CO2 absorbents (soda lime and baralyme) but
not calcium hydroxide.
 Associated factors leading to higher Compound A
formation.

Front 146

6 Associated factors leading to higher Compound A
formation.

Back 146

• Low fresh gas flow
• Higher absorbent temperatures
• High CO2 production
• Greater Sevo concentrations
• Baralyme more implicated than soda lime.
• Dose and time dependent.

Front 147

ways to Avoiding Compound A

Back 147

 Use des!
 Toxic threshold reached after prolonged sevo
anesthesia
 More of a theoretical concern
 Avoid sevo in pre-existing renal disease
 Avoid fresh gas flows < 1L/min
 For anticipated exposure greater than 2 MAC hrs,
increase FGF to 2L/min or greater.

Front 148

Carbon Monoxide
 CO forms in the presence of

Back 148

desiccated (dried out)
CO2 absorbents.
 Desflurane> Isoflurane> enflurane
 Common scenario first case Monday morning, fresh
gas flows left on.
 Intraoperative detection difficult
 Pulse oxymeters canʼt distinguish between
carboxyhemoglobin and oxyhemoglobin
 CO2 toxicity undetected in great proportion of cases.

Front 149

The “oldest” IA still in use today.

Back 149

Nitrous Oxide

Front 150

Nitrous Oxide
 Enters a closed gas space quicker than
nitrogen diffuses out of the space so that

Back 150

any
space in the body that contains air (nitrogen)
will expand.

Due to difference in blood gas solubility
between nitrogen (BGSC = .014) and nitrous
(BGSC = .47) Moves faster into spaces than
nitrogen can move out.

Front 151

Nitrous Oxide Potential bone marrow depression d/t

Back 151

Leads to Methylation Deficiency resulting in:
• Bone marrow suppression
• Myeloneuropathy in adults
• Neurotoxicity in childhood

A non-scavenged environment may promote more
spontaneous abortions and decreased fertility.
Occupational exposure may increase the incidence
of low birth weight infants.

Front 152

Nitrous exposure can increase

Back 152

homocysteine levels and may not return
to normal for a week or more.
 Elevated level of Homocysteine can increase
platelet aggregation
 Is cytotoxic to cells and oxidizes low density
lipoproteins
 Inhibits flow mediated vasodilatation of
vascular smooth muscle

Front 153

Halothane YI

Back 153

 Halogenated alkane
 Highly potent, highly soluble
 Sensitizes the heart to catecholamines
 Mild hepatic reactions seen in up to 20% of patients
receiving halothane. Not seen in children.
 Susceptible to decomposition therefore stored in
amber colored bottles and thymol is added as a
preservative.

Front 154

Halothane hepatitis occurs

Back 154

Halothane hepatitis occurs in 1 in 6000 to
35,00 patients exposed, leading to massive
necrosis.
 Doesnʼt occur in children
 Halothane hepatitis usually occurs after
repeat exposure through a immune mediated
response. Specific antibodies against
halothane induced antigens

Front 155

Enflurane FYI

Back 155

Halogenated methyl ethyl ether
 May cause seizure activity
 Risk for fluoride induced nephrotoxicity not
substantiated
 Increased risk of seizure activity especially in
combination with hyperventilation.
 Enhances action of paralytics more than any
other IA.

Front 156

Isoflurane FYI

Back 156

 Halogenated methyl ethyl ether
 Preserves baroreceptor reflex: may see a HR
increase.
 Heart friendly but does decrease SVR at high
doses
 Coronary steal no greater than other agents.
 Resistant to degradation by absorbers, can
be used with low fresh gas flows.

Front 157

Desflurane FYI

Back 157

Desflurane
 Requires heated vaporizer
 Fluorinated methyl ethyl ether
 Low solubility, low potency by comparison
 Pungent, irritating to airways
 Tachycardia when concentrations increased quickly
 Resistant to degradation, can be used with low fresh
gas flow. Manufacture recommends .35 L/min or
greater.

Front 158

Sevoflurane FYI

Back 158

Sevoflurane
 Fluorinated methyl isopropyl ether
 Carbon dioxide absorbents degrade to
compound A
 Transient biochemical abnormalities found
after prolonged Sevo exposure are not
associated with clinical signs of sustained
nephrotoxicity

Front 159

Sevoflurane class

Back 159

Fluorinated methyl isopropyl ether

Front 160

Desflurane class

Back 160

Fluorinated methyl ethyl ether

Front 161

Isoflurane class

Back 161

Halogenated methyl ethyl ether

Front 162

Enflurane class

Back 162

Halogenated methyl ethyl ether

Front 163

Halothane class

Back 163

Halogenated alkane