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NURA-661-01 Anesthesia Pharm > Inhaled Agents > Flashcards

Inhaled Agents Flashcards

1
Q

N2O synthesized by who?

When?

A

Priestly

1776

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2
Q

Diethyl ether effect similar to N2O, noted by who?

When?

A

Faraday

1796

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3
Q

Who tested effects on Prime minister noting euphora, analgesia and LOC?
When?

A

Humphrey David
1800

*Mainly used at carnival exhibitions or “ether frolics”, no medical use until mid-nineteenth century.

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4
Q

American Dentist ____________ decided to use N2O on his own tooth extraction in ______.

A

Horace Wells

1846

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5
Q

Who used Diethyl Ether, first, for cyst removal but did not report findings?
When?

A

Long

1842

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6
Q

Familiar with use of nitrous from dental partnership with Wells, _________________ Successfully demonstrated ether as an anesthetic at Mass General on what date?

A

William T.G. Morton (dentist)

OCT 16, 1846

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7
Q 
\_\_\_\_\_\_\_ first “ideal” anesthetic 
• Easy to make in pure form 
• Easy to administer 
• Liquid at room temp, but readily vaporized 
• Potent anesthetic, few drops needed, can produce anesthesia without diluting oxygen to hypoxic levels 
• Supports respiration and circulation 
• Not toxic to vital organs 
• Flammable!!
A

Ether

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8
Q

In what year did _____________, at Edinburgh University, use chloroform to treat pain during labor? The clergy was highly critical.

A

1846

James Simpson

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9
Q

In ____, Queen Victoria gave birth to her seventh child under the influence of chloroform popularizing the technique

A

1853

*procedure became known asanaesthésie à la reine

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10
Q 
Chloroform
• Pleasant odor 
• Nonflammable 
• (T or F) hepatotoxin 
• Severe cardiovascular depressant (T/F)
• High incidence of intra and postop deaths associated with its use 
• Difficult to administer
A
  • Pleasant odor
  • Nonflammable
  • Known hepatotoxin
  • Severe cardiovascular depressant
  • High incidence of intra and postop deaths associated with its use
  • Difficult to administer
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11
Q

Advances in fluorine chemistry in ____ allowed incorporation of fluorine into molecules were pivotal in development of modern anesthetics

A

1940

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12
Q

First halogenated hydrocarbon anesthetic?

• Withdrawn from market due to organ toxicity

A

Fluroxene

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13
Q

Methoxyflurane:

A

Halogenated methyl ethyl ether
Nonexplosive and nonflammable.
Most potent of volatile agents. MAC 0.16
Highly soluble B/G 12

70% metabolized (Oxidative metabolites include fluoride (F-) and oxalic acid, both nephrotoxic.
Flouride
vasopressin-resistant high-output renal failure

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14
Q

Theories of Anesthesia

Unitary theory-
Degenerated theory-
Some even suggest different targets for different effects (immobility VS unconsciousness)
•Immobility _________ mediated
•Hypnosis and amnesia ______
________ is the major inhibitory neurotransmitter in the spinal cord and may be the site of action of immobility effect.
2pore potassium channels membrane receptor ion channels that normally help maintain the cells RMP.

A

all GA act same mechanism
different classes = different mechanisms

spinal cord (MAC/GA)
brain

Glycine

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15
Q

Disproved: _______________ Theory
absorption of anesthetic molecules expands hydrophobic region– expansion of lipid bilayer beyond critical amount and alters membrane function

A

Meyer-Overton

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16
Q

Potential sites of action:

A

Pre-synaptic Voltage gated sodium channels

2-pore potassium channels

Ionotropic and metabotropic receptors
• GABAA and glycine
• Glutamate (NMDA, AMPA, Kainate)

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17
Q

Stages of Anesthesia- Guedel

A
  • Stage I = Amnesia/Analgesia
  • Stage II = Delirium/Excitement (troublesome stage ~ laryngospasm)
  • Stage III = Surgical Anesthesia 4 planes
  • Stage IV = overdose
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18
Q

Stages of Anesthesia- Guedel

Stage 1

A

called the stage of analgesia or induction
dizziness
sense of unreality
lessening sensitivity to touch and pain
sense of hearing is increased, and responses to noises are intensified

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19
Q

Stages of Anesthesia- Guedel

Stage 2

A

the stage of excitement
reactions involving muscular activity
delirium
vital signs show evidence of physiological stimulation the patient may respond violently to little stimulation

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20
Q

Stages of Anesthesia- Guedel

Stage 3

A

the surgical or operative stage
four levels of consciousness (planes)
anesthetist determines which plane is needed

Each successive plane is achieved by increasing the concentration of the anesthetic agent.

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21
Q

Stages of Anesthesia- Guedel

Stage 4

A

the toxic or danger stage
never desired
cardiopulmonary failure and death can occur

The fourth level of consciousness of stage 3 is demonstrated by cardiovascular impairment that results from diaphragmatic paralysis. If this plane is not corrected immediately, stage 4 quickly ensues.

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22
Q

Nitrous Oxide: MAC

A

104

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23
Q

Nitrous Oxide: Vp

A

38800

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24
Q

Nitrous Oxide: B/G

A

0.47

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25
Q

Nitrous Oxide is how many times more soluble than nitrogen in blood?

A

34

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26
Q

Nitrous Oxide:
Smell =
Color =

A

sweet/odorless

none

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27
Q

Nitrous Oxide: Flammability

A

None, but combustible?

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28
Q

Reduces MAC for Halothane, Enflurane, Isoflurane, Desflurane, and Sevoflurane by

A

30-50%

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29
Q

Nitrous Oxide: Cardiovascular Effects
• Direct action?
• May unmask what?

A

myocardial contractility depressant

undiagnosed myocardial depression in CAD, severe hypovolemia

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30
Q

Nitrous Oxide: Cardiovascular Effects

• Arterial BP, SVR, CO, & HR response?

A

unchanged or modestly elevated secondary to stimulation of catecholamines (sympathomimetic effect)

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31
Q

Nitrous Oxide: Cardiovascular Effects
• (Contracts or dilates) pulmonary vascular smooth muscle, and (increases or decreases) PVR and RA
pressure.
• So….dont use if?

A

Constricts, increases

PulmHTN, OSA

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32
Q

Nitrous Oxide: Cardiovascular Effects

• Associated with higher incidence of ____________ induced dysrhythmias

A

epinephrine

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33
Q

Nitrous Oxide: Pulmonary Effects
•Increases or decreases respiratory rate?
•Increases or decreases VT?
•Hypoxic drive markedly increased or decreased?
•Diffusion hypoxia!!!!!!!!!!

A

Increases
Decreases
Decreased
•depression of medullary ventilation center

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34
Q

Nitrous Oxide: Pulmonary Effects

•Change in VE and resting CO2 levels = ?

A

minimal

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35
Q

Nitrous Oxide: Cerebral Effects
•Increases or decreases CBF?
•Produces mild elevation or depression of ICP?
•Increases or decreases CMRO2?
*May increase motor activity – clonus and opisthotonos- a form of spasm in which?

A

Increases
Elevation
Increases
the head neck and spine are arched backwards

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36
Q

Nitrous Oxide: Neuromuscular Effects
•Does or does not provide significant muscle relaxation?
•May cause skeletal muscle rigidity or relaxation at > _ MAC?
•Is or is not an MH trigger according to MHAUS?

A
  • Does not provide significant muscle relaxation.
  • May cause skeletal muscle rigidity at >1 MAC (WE ARE NEVER NEAR 1 MAC)
  • Not an MH trigger according to MHAUS
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37
Q

Nitrous Oxide: Renal Effects
• Increases or decreases renal blood flow by increasing or decreasing renal vascular resistance?
• Increases or decreases GFR and urine output?

A
  • Decreases renal blood flow by increasing renal vascular resistance (sympathetic)
  • Decreases GFR and urine output (sympathetic)
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38
Q

Nitrous Oxide: Hepatic Effects

• Hepatic blood flow mildly increased or decreased?

A

• Hepatic blood flow mildly decreased (sympathetic)

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39
Q

Nitrous Oxide: GI Effects
• Meta-analysis 30 studies suggests postoperative nausea and vomiting risk increased or decreased?
• Causes ________ of the bowel

A

• Meta-analysis 30 studies suggests postoperative nausea and vomiting risk increased (activation of chemoreceptor trigger zone and vomiting centers in medulla and/or middle ear volume changes).
• Causes distention of the bowel
NOT indicated when pt. has bowel obstruction or most bowel surgeries

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40
Q

Nitrous Oxide: Biotransformation and Toxicity

•Almost exclusively eliminated by?

A

exhalation

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41
Q

Nitrous Oxide: Biotransformation and Toxicity
•Biotransformation limited to < ___%
•Irreversibly oxidizes cobalt atom in vitamin B12 and inhibits vitamin B12 dependent enzymes.
•Includes _________________, necessary for _______ formation and __________________, necessary for ______________.

A 
0.01
methionine synthetase
myelin
thymidylate synthetase
DNA synthesis
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42
Q

Nitrous Oxide: Biotransformation and Toxicity
•Almost exclusively eliminated by exhalation. •Biotransformation limited to < 0.01%
•Irreversibly oxidizes cobalt atom in vitamin B12 and inhibits vitamin B12 dependent enzymes.
•Includes methionine synthetase, necessary for myelin formation and thymidylate synthetase, necessary for DNA synthesis.
• Prolonged exposure (>__ hrs) and abuse can result in?

A

24
bone marrow depression (megaloblastic anemia)
peripheral neuropathies
pernicious anemia

***scavenging = important!!!

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43
Q

Nitrous Oxide: Biotransformation and Toxicity
• Avoid use in __________ patients
• May alter immune response to _______

A

pregnant

infection

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44
Q

Nitrous Oxide: Contraindications

A

● Diffuses rapidly into air containing cavities
• Air embolism (central line)
• Pneumothorax
• Acute intestinal obstruction
• Intracranial air
• Pulmonary air cysts
• Intraocular air bubbles (detached retina surgery w/ in 10 weeks)
• Tympanic membrane grafting or middle ear surgery
• Diffuses into ETT cuff

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45
Q

Nitrous Oxide: Contraindications
● Diffuses rapidly into?
• Avoid in patients with?
• Limited value in patients requiring?

A

air containing cavities
pulmonary HTN and OSA
high FIO2 (limitw max FiO2)

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46
Q

Nitrous Oxide: Drug Interactions

•Cannot be used as complete anesthetic (high MAC) •Decreases MAC requirements of other agents •Potentiates what?

A

neuromuscular blockade

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47
Q

Diffusion hypoxia:
occurs when inhalation of nitrous is discontinued abruptly, leading to a reversal of partial pressure gradients such that nitrous oxide leaves the blood to enter the alveoli.
High volume can dilute PAO2 = ?
as well as a dilution of PCO2 = ?
***Usually see it in first 5 minutes after dc so common practice to increase PaO2 to 100% as you turn it off.

A

hypoxia

reducing the respiratory drive

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48
Q

Isomer agents?

A

Enflurane

F F F
CCOC
ClF F

Isoflurane

F H F
CCOC
F Cl F

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49
Q

Volatile Agents
• Halogen substitutions increases or decreases anesthetic potency?
• Lower weight halogens (fluorine a.w.19) increased or decreased potency more than those of higher atomic weight (chlorine a.w.35.5)?

A

increases

decreased

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50
Q

Volatile Agents

• ________ substitution leads to most stable cpd. However it leads to?

A

Chloride

myocardial depression

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51
Q

Volatile Agents
• _____________ reduces flammability, and may produce potential for renal damage (flouride ions inhibit sodium reabsorption in ascending loop)

A

Fluorination

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52
Q

Halothane:
VP =
B/G =
MAC =

A

Halothane:
VP = 244
B/G = 2.3
MAC = 0.74

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53
Q

Enflurane:
VP =
B/G =
MAC =

A

Enflurane:
VP = 172
B/G = 1.8 (intermediate solubility)
MAC = 1.68 (high potency)

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54
Q

Isoflurane:
VP =
B/G =
MAC =

A

Isoflurane:
VP = 240
B/G = 1.4
MAC = 1.15

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55
Q

Desflurane:
VP =
B/G =
MAC =

A

Desflurane:
VP = 669
B/G = 0.42
MAC = 6

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56
Q

Sevoflurane:
VP =
B/G =
MAC =

A

Sevoflurane:
VP = 160
B/G = 0.69
MAC = 2

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57
Q

N2O:
VP =
B/G =
MAC =

A

N2O:
VP = 38,770
B/G = 0.47
MAC = 104

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58
Q

Pt temp:
Hypothermic =
Hyperthermic =

Liquid temp:
Warmer =
Colder =

A

Pt temp:
Hypothermic = decreases MAC
Hyperthermic = increases MAC

Liquid temp:
Warmer = less gas dissolved
Colder = more gas dissolved

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59
Q

Increase Altitude = Increased or decreased Barometric Pressure?

A

Decreased

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60
Q

Decreased Barometric Pressure = Underdosing or overdosing?

A

Underdosing?

240/760 = 1/3 = 33% < 240/500 = ½ = 50%

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61
Q

Minimum Alveolar Concentration =

A

The minimum alveolar concentration @ 1 ATM that produces immobility in 50% of patients exposed to noxious stimuli
• Inhalation equivalent of ED50

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62
Q

Factors Decreasing MAC

A
  • Increasing age
  • Hypothermia
  • Hyponatremia
  • Hypotension < 40mmhg
  • Pregnancy
  • Hypoxemia < 38 mmHg
  • Opioids
  • Ketamine
  • Benzodiazepines
  • Clonidine
  • A2 agonists
  • Local Anesthetics
  • ETOH (acute)
  • Lithium
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63
Q

Factors Increasing MAC

A
  • Hyperthermia
  • CNS stimulants
  • Youth- under one year of age
  • Increased pheomelanin production (red hair)
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64
Q

MAC values of different agents are _________

A

additive

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65
Q

To avoid movement when no muscle relaxant is on board in 95% of patients

A

requires 30% above 1 MAC or 1.3 MAC (similar to ED95)

Ex: Des ED95 = MAC of 6% x 1.3 MAC = MAC of 8%

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66
Q

MAC Awake =

Des/Sevo/Iso =
Halothane =
N2O =

A

the concentration that prevents consciousness in 50% of patients is approximately 1/2 - 1/3 MAC

1/3 MAC for Des, Sevo, Iso
½ for Halothane
60% for N2O

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67
Q

MAC memory =

A

the concentration of anesthetic associated with amnesia in 50% of of patients is significantly less than MAC Awake, thus NEVER go below MAC awake!

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68
Q

EEG burst suppression ~ _ MAC

A

2

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69
Q

Halothane: structure

A

Halogenated alkane derivative

_FCl
FCCH
_FBr

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70
Q

Halothane: VP

A

244

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71
Q

Halothane: B/G

A

2.3 (int. sol.)

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72
Q

Halothane: MAC

A

0.74 (high pot.)

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73
Q

Halothane: Odor

A

Sweet, Non-pungent (used to be go to for peds)

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74
Q

Halothane: Contains Thymol

A

Sticky, clogs up vaporizer

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75
Q

Halothane: Cardiovascular Effects

Direct =

A

Direct myocardial depressant = BP decrease

•Dose dependent decreases in CO (SV decrease 15-30%)

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76
Q

Halothane: Cardiovascular Effects

Does or does not decrease SVR?

A

Does not decrease SVR (iso, des, sevo do)

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77
Q

Halothane: Cardiovascular Effects

Coronary artery vasoconstrictor or vasodilator?

A

Coronary artery vasodilator, coronary blood flow decreased from drop in systemic BP, can cause ischemia.
•Yet…..Protection from decreased myocardial oxygen demands?

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78
Q

Halothane: Cardiovascular Effects

Blunts baroreceptor response to hypotension = ?

A

no increase in HR (iso, des, sevo increase HR)

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79
Q

Halothane: Cardiovascular Effects
•Increased or decreased right atrial pressure (CVP)?
•Increase or decrease cutaneous blood flow?

A
  • Increased right atrial pressure (CVP)

* Increase cutaneous blood flow (increase risk of bleeding and hypothermia)

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80
Q

Halothane: Arrhythmias
•Increased or decreased SA node depolarization- prone to?
•Increased or decreased conduction where?
•Caution when ___________ is injected!

A
  • Decreased SA node depolarization- prone to junctional rhythm
  • Decreased conduction AV node/His-Purkinje
  • Caution when epinephrine is injected!
81
Q 
Halothane: Respiratory Effects
• Increased or decreased RR? 
• Increased or decreased VT? 
• Increased or decreased VE?
• Increased or decreased resting PACO2? 
• Apneic threshold rises 
• Hypoxic drive severely depressed (even at low doses 0.1 MAC) 
• Potent bronchodilator can reverse asthma-induced bronchospasm
A

Increased
Decreased
Decreased
Increased

82
Q

Halothane: Respiratory Effects

• Apneic threshold rises or falls?

A

rises

83
Q

Halothane: Respiratory Effects

• Hypoxic drive severely elevated or depressed (even at low doses __ MAC) ?

A

depressed (even at low doses 0.1 MAC)

84
Q

Halothane: Respiratory Effects

• Potent broncho___________

A

dilator

*can reverse asthma-induced bronchospasm

85
Q

Halothane: Cerebral Effects
• “Uncouples cerebral blood flow and metabolism”
• *Stay well below __ MAC, but ideally avoid use

A

1/2

86
Q

Halothane: Cerebral Effects
• “Uncouples cerebral blood flow and metabolism”
• Increases or decreases CBF, ICP, IOP?

A

Increases

87
Q

Halothane: Cerebral Effects

• Modest increase or decrease in CMRO2?

A

decrease

88
Q

Halothane: Cerebral Effects
• Autoregulation is ___________
• Can prevent rise in ___ by hyperventilation prior to halothane administration

A

blunted

ICP

89
Q

Halothane: Cerebral Effects

• Cerebral activity increased or decreased?

A

decreased

90
Q

IA(s) that potentiate nondepolarizing NM blocking meds

A

Halothane, Sevo

91
Q

IA that evokes skeletal muscle relaxation 2X less than other volatile agents

A

Halothane (others are better choice)

92
Q

Halothane: Renal Effects

• Increases or decreases RBF, GFR and urine output?

A
  • Reduces RBF, GFR and urine output.

* Can limit by pre-op hydration

93
Q

Halothane: Hepatic Effects
• Increased or decreased hepatic blood flow?
• Hepatic artery vaso__________

A

Decreased

constriction

94
Q

Halothane: Hepatic Effects
• Anesthetic induced inhibition of ?
• Metabolism of what drugs may be impaired? Meaning they will….?

A

hepatic drug metabolizing enzymes

fentanyl, phenytoin, verapamil; stick around longer

95
Q

Halothane: Hepatic Effects

• Oxidized metabolite = ?, at __%

A

trifluroracetic acid

20%

96
Q

Halothane: Biotransformation and Toxicity

• Halothane produces _ types of hepatotoxicity in susceptible patients.

A

2

97
Q 
Halothane: General Toxicity
• \_\_% of adult patients develop mild, self-limited post-op hepatotoxicity. 
• Symptoms =  ?
• May be due to ?
*Pts generally recover?
A

20
Nausea, lethargy, fever, minor increases in transaminase enzymes
non-specific drug effect due to changes in hepatic blood flow that impairs hepatic oxygenation
Yes

98
Q

Halothane: Hepatitis
• Occurs in 1 in _0,000 to 1 in _0,000 adults
* 1:______ Extensive hepatic necrosis and death possible
• Most likely ________-mediated hepatotoxicity -__________ antibodies present in 70% of those diagnosed

A
  • Occurs in 1 in 10,000 to 1 in 30,000 adults
  • 1:35,000 Extensive hepatic necrosis and death possible
  • Most likely immune-mediated hepatotoxicity -Immunoglobulin G antibodies present in 70% of those diagnosed
99
Q

Volatile Agent Induced Hepatitis: National Halothane Study

•Classic presentation of VA associated hepatitis = ?

A

fever, anorexia, nausea, chills, myalgias, rash, fever, arthralgia, and eosinophilia followed by jaundice 36 days later

100
Q

Volatile Agent Induced Hepatitis: National Halothane Study

•Risk factors = ?

A 
PRIOR EXPOSURE!
age >40 years old
obesity 
female gender
Mexican ethnicity (chromosomal vulnerability)
genetic susceptibility
multiple brief procedures within brief duration of time
enzyme induction
101
Q

Volatile Agent Induced Hepatitis: Immune theory

A
  • Cytochrome P450 2EI oxidizes each anesthetic (except for sevoflurane) to yield highly reactive intermediates that bind covalently (acetylation) to a variety of hepatocellular macromolecules
  • Altered hepatic proteins may trigger an immunologic response that causes massive hepatic necrosis
102
Q

Volatile Agent Induced Hepatitis:

All IAs except? Because?

A

except for sevoflurane

103
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•Halothane _% metabolized

A

•Halothane 15-20% metabolized

104
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•Enflurane _% metabolized

A

•Enflurane 2.5-3% metabolized

105
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•Sevoflurane* _% metabolized
*chemical structure of sevoflurane prevents metabolism to a acetyl halide

A

•Sevoflurane* 2-5% metabolized

*chemical structure of sevoflurane prevents metabolism to a acetyl halide

106
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•Isoflurane _% metabolized

A

•Isoflurane 0.2-2% metabolized

107
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•Desflurane _% metabolized

A

•Desflurane 0.02% metabolized

108
Q

Volatile Agent Induced Hepatitis: Metabolism of Volatile Agents
•N2O _%

A

•N2O 0.004% (reductive metabolism GI tract)

109
Q

Halothane: Drug Interactions
• Myocardial depression exacerbated by ?
• What may cause BP instability?

A

Beta-adrenergic blockers and calcium channel blockers

Tricyclic antidepressants and MAO inhibitors

110
Q

Halothane: Drug Interactions

• _____________ use has resulted in serious ventricular dysrhythmias.

A

Aminophylline

*tx asthma

111
Q

Halothane: Contraindications =?

A
  • Patients with unexplained liver dysfunction, following halothane exposure
  • Pre-existing liver disease
  • Hypovolemia
  • Aortic stenosis
  • Patients with pheochromocytoma
  • Malignant Hyperthermia – Halothane the most potent trigger of all the volatile agents
112
Q

Most potent MH trigger of all the volatile agents =?

A

Halothane

113
Q

Mild myocardial depression (dose dependent) in what IAs?

A

Iso, Des, and Sevo

114
Q

What VAs can overdose result in CV collapse?

A

ALL

115
Q

Mild Beta Adrenergic stimulation cause by what IAs?
• lowers BP due to decreased SVR
• lowers left stroke volume by 15-30%

A

Iso, Des, and Sevo

116
Q

IAs causing increased right atrial pressure (CVP)?

A

Iso, Des, Halothane

117
Q

Rapid increases in concentration in what IAs => transient increase in HR, blood pressure and catecholamine levels?

A

Iso and Des

118
Q

Isoflurane: Structure

A

Halogenated methyl ethyl ether

Isoflurane

F H F
CCOC
F Cl F

119
Q

Isoflurane: Odor = ?

A

Pungent odor-NOT FOR PEDs INDUCTION!!!

120
Q

Isoflurane:
MAC =
BG partition coefficient =

A

MAC – 1.2 (high potency)

BG partition coefficient –1.4 (intermediate solubility)

121
Q

Isoflurane: Cardiovascular Effects

CO is maintained by what response?

A

Increased HR via partial preservation of baroreceptor reflex

122
Q

Isoflurane: Cardiovascular Effects

Elderly and neonates may experience what kind of response?

A

Decrease HR

123
Q

What IA increases cutaneous and skeletal muscle blood flow?

A

Isoflurane

124
Q

Overpressure results in ?

A

Initial increased HR and BP, followed by decreased SVR and BP?

125
Q

What IA is NOT recommended during cardiac ablation and why?

A

Isoflurane, because it increases the refractoriness of accessory pathways and AV conduction so can interfere with interpretation of electrophysiologic studies.

126
Q

Isoflurane: Cardiovascular Effects

• ________ coronary arteries

A

Dilates

127
Q

Anesthetic Pre-conditioning
• Brief exposure to what agents?
• Activate KATP channels - effect?

A

iso/des/sevo

hyperpolarizing effect (negative inotropic/relax vascular smooth muscle) which protects the tissue to subsequent ischemic episode

128
Q

Coronary steal syndrome
• In theory…may cause what and how?
• What IAs can cause this?

A

ischemia in patients with CAD by taking away from preferential dilation
ALL any that dilate coronary arteries

129
Q

Isoflurane: Respiratory Effects

• Tachypnea more or less pronounced at >1 MAC compared w/other agents

A

less

130
Q

What IAs blunt response to hypoxia and hypercarbia?

A

Halothane, Iso, Des, Sevo….well all of them really impact respiratory drive!?!

131
Q

What IAs are a bronchodilator?

A

Halo, Iso, Sevo

132
Q

What IAs decrease Vt and Mv, increasing PaCO2?

A

Halothane, Iso, Des, Sevo, En (N2O n/c to resting PaCO2)

133
Q

What IAs result in tachypnea?

A

N2O, Halothane, Iso, Des, Sevo….all of them really (Hal, Meth, En mostly according to the chart?)

134
Q

Isoflurane: Cerebral Effects
• Increased CBF and ICP at concentrations > _ MAC (effects greater/less than halothane and Enflurane?)
• Effects reversed by _________________

A

1, less

hyperventilation

135
Q

Isoflurane: Cerebral Effects
• Increases or decreases CMRO2?
• Electrically silent EEG at _ MAC (thought to provide cerebral protection during ischemic periods)

A

• Reduces CMRO2, electrically silent EEG at 2 MAC (thought to provide cerebral protection during ischemic periods)

136
Q

Isoflurane: Cerebral Effects

• Enhances/diminishes CSF reabsorption

A

• Enhances CSF reabsorption

137
Q

What IAs increase CBF and ICP?

A

N2O, Halothane, Iso, Des, Sevo, En ….. so all!

138
Q

What IAs increase IOP?

A

Halothane

139
Q

What IAs decrease CMRO2?

A

Iso, Des, Sevo the most, but also Halothane & En

140
Q

What IA maintains total hepatic blood flow – vasodilator of hepatic circulation
• Has beneficial effects on hepatic oxygen delivery
• This is a relatively new finding…some texts will still say that portal vein flow is reduced – 2003 study refutes

A

Isoflurane

141
Q

Renal Effects of IAs?

How can this be limited?

A

Decease in RBF, GFR, and urine output (r/t decreased CO and BP)

Can limit by pre-op hydration!

142
Q

Isoflurane-Forane: Metabolism & Toxicity
• Slowly metabolized __%
• Principal end product = ?

A 
0.2% 
Trifluroacetic acid (very small amount)
143
Q

Trifluroacetic acid is the end product of what IAs?

A

Halothane, Iso, En

144
Q

IAs with a CI of MH?

A

ALL!

145
Q

Isoflurane-Forane: Hepatotoxicity is common or rare?

• Does not produce fluoride ion at clinically significant levels

A

rare

146
Q

Isoflurane-Forane: Does or does not produce fluoride ion at clinically significant levels

A

does not

147
Q

Desflurane: Structure

A

Fluorinated methyl ethyl ether (Similar in structure to isoflurane)

Desflurane

F H F
CCOC
F F F

148
Q

Desflurane: Odor

A

Pungent odor

*caution with peds and stg II w/ asthmatics

149
Q 
Desflurane: 
 • Vapor pressure =
• MAC =
• Blood/gas partition coefficient =
• \_\_\_\_\_\_\_ wash-in (induction) and wash-out (emergence).
A
  • Vapor pressure close to atmospheric (669), need special vaporizer.
  • MAC 6.0 (low potency)
  • Blood/gas partition coefficient 0.42 (low solubility)
  • Rapid wash-in (induction) and wash-out (emergence).
150
Q

The TEC 6 Vaporizer:
• Electrically heated to ?
• Pressurized to

A 
39 degrees C
1520 mmHg (to keep it in the liquid phase)
151
Q

Desflurane: Cardiovascular Effects
• CO remains unchanged or slightly depressed at
_-_MAC

A

1-2 MAC

152
Q

Desflurane: Cardiovascular Effects

• Baroreceptor reflex ______, resulting in?

A

intact

rise in HR

153
Q

Desflurane: Cardiovascular Effects
• Rapid increases in concentration: transient increase in HR, blood pressure and catecholamine levels (greater or less than with isoflurane?)

A

greater

154
Q

Desflurane: Cardiovascular Effects

• Does or does not increase dilate coronary arterial blood flow

A

does not

155
Q

Desflurane: Respiratory Effects

Profound apnea at - MAC

A

1.5-2.0 MAC (i.e. assist)

156
Q

Desflurane: Respiratory Effects

>_% = Irritating to airways, salivation, breath-holding, coughing, and laryngospasm

A

6% (1 MAC)

157
Q

Desflurane Cerebral Effects
•Increases CBF and Cerebral oxygen consumption increased or decreased?
•Effect not usually seen until >_ MAC
•Neuro keep less than _ MAC (Can lower ICP with hyperventilation)

A

decreased
1 MAC
1 MAC
*Carrie -> 1 MAC and hypervent.

158
Q

Desflurane: Neuromuscular Effects

• Dose dependent decrease in response to ?

A

TOF and tetanic PNS

159
Q

Desflurane: Hepatic Effects =?

A

No evidence of hepatic injury following it use.

160
Q

IAs that potentiate NM blocking agents?

A

Des

161
Q

Desflurane: Biotransformation and Toxicity
• < _% metabolized
• Serum and urine inorganic fluoride levels (, =) preanesthetic levels?

A

0.1%

~=

162
Q

Desflurane: Biotransformation and Toxicity

• Carbon monoxide results from degradation of Des by ?

A

dried out CO2 absorbents

• high flows left on all weekend now 1st case on Monday morning

163
Q

Carbon Monoxide concentrations of all IAs relative to each other =

A

Des>Enf & Iso> Halo & Sevo

164
Q

Sevoflurane: structure

A

the only fluorinated methyl isopropyl ether

___C
COC
___C

165
Q

Sevoflurane: Odor

Good or bad for peds?

A

Non-pungent, sweet oder

*idea for peds

166
Q

Sevoflurane = fast on, fast off (T/F)

A

T

167
Q

Sevoflurane: Cardiovascular Effects

•SVR, and artBP decline more or less than isoflurane or Desflurane?

A

•SVR, and artBP decline slightly (less than isoflurane or Desflurane)

168
Q

Sevoflurane: Cardiovascular Effects

•HR, MAC, &CO?

A

•Little rise in HR (only significantly increases at >1.5 MAC), CO not as well maintained.

169
Q

Sevoflurane: Cardiovascular Effects

HR only significantly increases at >_ MAC), __ not as well maintained.

A

> 1.5 MAC

CO

170
Q

Sevoflurane: Cardiovascular Effects

•Coronary steal?

A

•No evidence of coronary steal

171
Q

Only common agent that does not increase CVP is?

A

Sevoflurane (halothane, des, iso increase)

172
Q

IA that does not cause SNS activation response with increases in concentration?

A

Sevoflurane

173
Q

IA with minimal airway irritation (best among all current anesthetics)?

A

Sevoflurane

*best choice for asthmatics

174
Q

Sevoflurane: Respiratory Effects

• Profound apnea at - MAC

A

1.5-2.0 MAC (i.e. assist)

175
Q

IAs causing profound apnea at 1.5-2.0 MAC (i.e. assist)?

A

Des, Sevo

176
Q

What is the best IA for neuro?

A

Sevoflurane

177
Q

Sevoflurane: CNS Effects
• Increases or decreases cerebral metabolism O2 consumption?
• Increases or decreases CBF < Halothane
• Inc. ICP
• Effect not usually seen until >1 MAC.
• Response to CO2 & autoregulation maintained at 1.5%

A
  • Dec. cerebral metabolism O2 consumption (> Halothane)
  • Inc. CBF (< Halothane)
  • Inc. ICP
  • Effect not usually seen until >1 MAC.
  • Response to CO2 & autoregulation maintained at 1.5%
178
Q

Sevoflurane: CNS Effects
Decrease in cerebral metabolism O2 consumption < or > Halothane?
Increase in CBF < or > Halothane?

A

Decrease in cerebral metabolism O2 consumption > Halothane

Increase in CBF < Halothane

179
Q

Sevoflurane: CNS Effects
• Effect not usually seen until >_ MAC.
• Response to CO2 & autoregulation maintained at __%

A

> 1 MAC

1.5%

180
Q

COMPOUND A mostly produced by degradation of what IA?

A

Sevo

181
Q

Sevoflurane: Metabolism & Toxicity
• Compound A is formed when Sevo interacts with?
• Cpd A not nephrotoxic alone but undergoes bioactivation thru glutathione conjugation and metabolism of its conjugates to produce reactive thiol may mediate renal toxicity

A

soda or baralyme (esp. at low flows) *not a metabolite

182
Q

Sevoflurane: Metabolism & Toxicity

Is Cpd A a metabolite of Sevo?

A

NO!

183
Q

Sevoflurane: Metabolism & Toxicity
• Cpd A is or is not nephrotoxic alone
• Undergoes bioactivation thru glutathione conjugation and metabolism of its conjugates to produce reactive _____ that MAY mediate renal toxicity

A

is not

thiol

184
Q

Sevoflurane: Metabolism & Toxicity

• Higher concentrations of compound A in presence of?

A 
Baralyme 
Soda lyme
Low flow anesthesia
High sevo concentrations 
Long duration
  • No clinical evidence of injury
  • Renal injury demonstrated in rats
  • Eger et al. demonstrated transient changes in renal function has not been reproduced by subsequent studies
185
Q

Sevoflurane: Metabolism & Toxicity
To minimize exposure to Compound A, sevoflurane exposure should not exceed _ MAC∙hours at flow rates of _ to < _ L/min. Fresh gas flow rates of

A

2 MAC∙hours
1 to < 2 L/min
<1 L/min

186
Q

Sevoflurane: Metabolism & Toxicity

As a rule of thumb, Carrie just keeps FGF > _ L/min when using Sevo!

A

2

187
Q

Sevoflurane: Metabolism & Toxicity
In addition to Cpd A, what is another renal concern?
What is the mechanism of action behind this concern?

A
  • Another concern is production of free fluoride ions = tubular injury and loss of concentrating ability – ARF.
  • Fluoride levels can rise close to levels associated with risk – although clinical evidence of injury does not exist
188
Q

Sevoflurane: Metabolism & Toxicity
• metabolized in liver P450
• -% undergoes biodegradation
• Can or cannot be metabolized to trifluroacetylated liver proteins? (= ___ risk of “halothane hepatitis”)

A

Sevoflurane: Metabolism & Toxicity
• metabolized in liver P450
• 3-5% undergoes biodegradation
• Cannot be metabolized to trifluroacetylated liver proteins – 0 risk of “halothane hepatitis”

189
Q

Sevoflurane: Contraindications = ?

A
  • Patients with impaired kidney function (relative contraindication)
  • Malignant Hyperthermia (absolute contraindication)
190
Q

Enflurane: structure

• Isomer of ?

A

Halogenated methyl ethyl ether

Enflurane

F F F
CCOC
ClF F

Isomer of Isoflurane

191
Q

Enflurane: Odor

A

• Mild, sweet, ethereal odor

192
Q

Enflurane: Adverse Effects
• Myocardial contractility depression
• Sensitizes heart to dysrhythmic effects of ?
• Hypoxic drive = ?
• Marked respiratory depression, at _ MAC, PACO2 60 mm Hg.

A

epinephrine
abolished
1 MAC

193
Q

Depressed mucociliary function caused by what IA?

A

Enflurane

194
Q

Enflurane effects on CSF?

A

Increases secretion of CSF and resistance to CSF outflow…….DO NOT USE FOR NEURO!

195
Q

Enflurane EEG effects?

A
  • EEG changes, tonic-clonic seizures.
  • Exacerbated by high concentration, hypocapnia, and repetitive auditory stim.
  • Hyperventilation not recommended.
196
Q

Enflurane: Biotransformation & Toxicity
• High or low metabolism (-%)?
• Fluoride production much more or less than Methoxyflurane?
• Detectable renal dysfunction likely or unlikely?

A

Enflurane: Biotransformation & Toxicity
• Low metabolism (2-5%).
• Fluoride production much less than Methoxyflurane.
• induces defluorination, may be clinically significant in rapid acetylators.
• Detectable renal dysfunction unlikely

197
Q

Enflurane: Contraindications?

A
  • Avoid in patients with preexisting kidney disease or impairment
  • Avoid in patients with known or suspected seizure disorders
  • Avoid in patients with increased intracranial pressure
  • Triggering agent for Malignant Hyperthermia
198
Q

OSHA & Waste Gases:
• No worker should be exposed to more than __ppm Halogenated agents in O2 or air
• No more than __ppm Halogenated agents if used with Nitrous Oxide
• No more than __ppm of N2O
• Highest levels found where?

A
  • No worker should be exposed to more than 2ppm Halogenated agents in O2 or air
  • No more than 0.55 ppm Halogenated agents if used with Nitrous Oxide
  • No more than 25ppm of N2O
  • Highest levels found between anesthesia machine and wall
199
Q

Xenon- FYI
•Inert gas, odorless, nonexplosive
•BG partition coefficient = 0.115
•MAC 63-71%
•Does expand closed air spaces < N2O though
•CV stability, blunt SNS response to pain, analgesia, hypnosis
•Costly
•Limited experience in patients at this time

A

FYI

NURA-661-01 Anesthesia Pharm (6 decks)

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