Volatile - Concepts Flashcards

1
Q

Concentration that will produce absence of movement in 99% of people in response to a noxious stimulus

A

1.3 MAC

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2
Q

B:G N2O

A

0.46

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3
Q

B:G desflurane

A

0.42

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4
Q

B:G sevoflurane

A

0.69

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5
Q

B:G Isoflurane

A

1.4

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6
Q

B:G enflurane

A

1.8

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7
Q

B:G halothane

A

2.4

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8
Q

B:G Diethyl ether

A

12

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9
Q

lower hematocrit will alter

A

the B:G coefficient

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10
Q

With a HCT of 21 (vs 43)

A

the B:G coefficient will be 20% less.

Effectively having a LOWER solubility and therefore increased induction

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11
Q

the faster FA = FI

A

the faster the onset

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12
Q

PAlveoli is used to estimate

A

aka Fa is used to estimate
depth of anesthesia
recovery from anesthesia
anesthesia potency or MAC

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13
Q

PAlveoli is determined by (4)

A
  1. Pi
  2. Alveolar ventilation
  3. Breathing Circuit
  4. FRC
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14
Q

The higher the alveolar ventilation

A

the faster the onset

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15
Q

first knee of Fa/Fi =

A

saturation of vessel rich group

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16
Q

second knee of Fa/Fi =

A

saturation of muscle group

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17
Q

terminal climb after second knee of Fa/Fi =

A

progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time

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18
Q

terminal climb after second knee of Fa/Fi =

A

progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time

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19
Q

uptake of a volatile agent is determined by

A
  1. solubility of agent
  2. cardiac output
  3. A-v [alveolar to venous] pressure differences
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20
Q

The higher the FRC

A

the SLOWER the induction

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21
Q

induction is faster in

A

children , smaller FRC

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22
Q

To achieve faster induction with agents that are more soluble

A

we over pressure.

high initial input (Fi) offsets impact (duration) of uptake

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23
Q

Increased Cardiac output =

A

INCREASED uptake, effect of increasing solubility, net = slower induction

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24
Q

Decreased CO =

A

decreased uptake, effect of decreasing solubility = faster induction

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25
Q

Pulmonary blood flow =

A

CO

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26
Q

Agents more affected by CO are

A

soluble agents

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27
Q

vessel rich group reach equilibrium within

A

5-15 minutes

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28
Q

after induction, the FI should be decreased as

A

the VRG equilibrates and again as the MRG equilibrates

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29
Q

For maintenance, due to decrease in uptake over time

A

the FI should be decreased otherwise overdose

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30
Q

increasing ventilation is a more effective strategy with

A

a more soluble agent , doesn’t make much of a difference for lower solubility drugs

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31
Q

negative feedback in the spontaneously breathing ventilating patient

A

in spontaneously ventilating patient, as the % inspired increase, ventilation is depressed (r/t drug effect) and the Fa/Fi will decrease (r/t decrease in alveolar ventilation)

this is protective against overdose

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32
Q

if you keep someone spontaneously breathing on volatile agents, the risk for overdose is

A

low

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33
Q

larger circuit volume will decrease

A

FA/FI slope will decrease , overcome with higher flow rates

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34
Q

with conditions of higher metabolism, you may have

A

increased minute ventilation and also increased cardiac output . This results in net Fa/Fi increase but only slightly

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35
Q

right to left shunt is more consequential for

A

agents with LOW solubility

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36
Q

V/Q mismatches will

A

generally SLOW induction, more pronounced in less soluble agents

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37
Q

the concentration effect states that the higher the PI

A

the more quickly the PA will approach the PI

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38
Q

N2O to nitrogen

A

N2O is 34x more soluble

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39
Q

blood gas solubility of nitrogen

A

b:g 0.014

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40
Q

emergency and recovery depends on [4]

A
  1. length of anesthesia
  2. depth of anesthesia
  3. solubility of the agent
  4. MAC awake
41
Q

sevoflurane’s biotransformation does result in

A

inorganic fluoride ions. Theoretical risk for fluoride induced high output renal failure.

[[unresponsive to ADH]]

42
Q

Soda lime + sevo =

A

compound A

accelerated when desiccated

43
Q

N2O irreversibly binds to

A

B12, which inhibits methionine synthase and thymidylate synthesis

44
Q

potential effects of prolonged exposure to N2O and B12

A
megaloblastic anemia [bone marrow suppression]
neuropathy 
immunocompromise
impaired DNA synthesis 
concern for teratogenicity? 
possible spontaneous abortion 
homocysteine accumulation 

previous history of alcoholism, pernicious anemia, strict vegan diet make these more likely

45
Q

amnesia and loss of consciousness occur at

A

LOWER MACs also these are SUPRASPINAL

46
Q

MAC awake =

A

alveolar concentration at which a patient opens his or her eyes,

47
Q

MAC bar =

A

alveolar concentration at which autonomic responses are blunted (1.5 MAC)

48
Q

HYPONATREMIA and MAC

A

hyponatremia will decrease MAC

49
Q

Older age and MAC

A

6% reduction in MAC for every decade after 40

50
Q

Hyperkalemia and MAC

A

no effect on MAC -
hyperkalemia, hypokalemia
hypermagnesemia, hypomagnesemia

51
Q

Hyperthermia and MAC

A

MAC will INCREASE.

52
Q

Hypothermia and MAC

A

MAC will DECREASE

53
Q

In red heads, MAC is generally

A

increased by 19%

“presumably due to mutations in the melanocyte stimulating hormone receptor and an increased production of pheomelanin”

54
Q

Meyer-Overton Rule

A

Meyer-overton rule states that lipid solubility is directly proportional to the potency of an inhaled anesthetic .

or, the greater the lipid solubility the lower the MAC value. [the greater the potency]

Implies the depth of anesthesia is determined by the number of anesthetic molecules that are dissolved in the brain and not necessarily the particular anesthetic agent that is used.

55
Q

unitary hypothesis

A

states that all anesthetics share a similar mechanism of action, but each may work at a different site.

56
Q

General rule, volatile anesthetics have the following effects on their target receptors

A

stimulate inhibitory pathways [GABA, GLYCINE, K channels]

Inhibit stimulatory pathways [NMDA, Nicotinic, sodium, dendritic spine function and motility ]

57
Q

In the brain, the most important site of volatile anesthetic action is the

A

GABA A receptor

spine -> glycine receptor
NMDA receptor
Na+ channel inhibition.

58
Q

Immobility is not due to GABA a in the spinal cord

A

ventral horn of spinal cord, glycine

59
Q

N2O + opioid =

A

can cause myocardial depression

60
Q

current theory on anesthetics

A

current potential sites of actions are modulating proteins:

  1. pre-synaptic voltaged gated sodium channels
  2. 2-pore potassium channels [trek + task}
  3. Inotropic and metabotropic receptors
    either inhibit stimulatory or stimulate inhibitory
61
Q

stage 1 of anesthesia

A

“analgesia or induction stage”

dizziness, a sense of unreality, and lessening sensitivity to touch and pain

Sense of hearing is INCREASED and responses to noises are INTENSIFIED

62
Q

stage 2 of anesthesia

A

is the stage of excitement. Vital signs show evidence of physiological stimulation, pt may respond violently to very little stimulation, MOST susceptible to laryngospasm

63
Q

stage 3 of anesthesia

A

Surgical anesthesia! Here we have 4 plans.

Each successive plane is achieved by increasing the concentrations of the anesthetic agent

64
Q

stage 4 of anesthesia

A

OVERDOSE! toxic or danger stage.

65
Q

fourth plane of anesthesia

A

demonstrated by cardiovascular impairment that results fro diaphragmatic paralysis, if this plane is not corrected immediately, stage 4 quickly ensues

66
Q

thymol is used in

A

Halothane as a preservative. Can cause sticky turnstiles or temperature compensating valves

67
Q

risk factors for halothane hepatitis

A

obese, female, multiple exposures to halothane

68
Q

classic presentation of halothane hepatitis

A

fever, anorexia, nausea, chills ,myalgia, rash, arthralgia, eosinophilia followed by jaundice 3-6 days later

69
Q

volatile not recommended during cardiac ablation

A

ISOFLURANE

it increases the refractoriness of accessory pathways and AV conduction so can interfere with interpretation of electrophysiological studies

70
Q

Isoflurane decrease in BP is because of

A

decrease in SVR

71
Q

CO in isoflurane is

A

maintained by HR, because partial preservation of baroreceptors

72
Q

tachypnea less pronounced at 1 MAC with

A

isoflurane

73
Q

electrically silent EEG at 2MAC with

A

isoflurane

74
Q

vasodilator of hepatic circulation

A

isoflurane

75
Q

isoflurane C/i

A

MH or maybe* extremely low CO -> r/t decrease in SVR

76
Q

Desflurane baroreceptors

A

INTACT

77
Q

isoflurane baroreceptors

A

partial preservation

78
Q

Decrease BP with desflurane is r/t

A

Decreased SVR

79
Q

When you give a higher concentration of desflurane [overpressure]

A

you will have a sympathomimetic effect, rapid transient increase in transient HR, blood pressure, catecholamine levels,

80
Q

desflurane C/I

A

malignant hyperthermia

kind of asthmatics

81
Q

CO not as well maintained with

A

sevoflurane

82
Q

Only common agent that does not increase R atrial pressure / CVP

A

sevoflurane

83
Q

best choice of a volatile for asthmatics is

A

sevoflurane because minimal airway irritation

84
Q

hepatic blood flow with sevo

A

is maintained

85
Q

sevoflurane C/I

A

MH and relative: renal impairment

86
Q

enflurane and hypoxic drive

A

ABOLISHED. Marked respiratory depression at 1 MAC

87
Q

Depresses mucociliary function

A

enflurance

88
Q

Increased secretion of CSF but decreased outflow

A

Enflurane

89
Q

EEG changes with enflurane are exacerbated by

A

high concentrations, hypocapnia, and repetitive auditory stim

90
Q

Hyperventilation with enflurane

A

IS NOT RECOMMENDED, can exacerbate EEG changes and lead to seizures

91
Q

enflurane C/I

A

avoid in patients with pre-existing kidney disease or impairment

avoid in patients with known or suspected seizure disorder

avoid in patients with increased ICP

MH

92
Q

OSHA and waste gas

A

no worked should be exposed to more than
2 ppm halogenated agents in o2
0.55 halogenated if used with n2o
25 ppm n2O

93
Q

no significant increase in MAC until

A

> 1.5 MAC

94
Q

increase risk of arrthymias with epi

A

Halothane
enflurane
N2O

95
Q

aminophylline is linked to serious

A

ventricular dysrthymias when used with halothane

96
Q

most potent MH trigger

A

halothane

97
Q

things that increase MAC (6)

A
1. chronic ETOH 
2 .Increased CNS neurotransmitters 
3. HYPERnatremia 
4. Increased in infants 1 -6 months 
5. HYPERthermia 
6. Red hair
98
Q

factors that decrease MAC (16)

A
  1. acute ETOH
  2. IV anesthetics
  3. N2O
  4. Opioids
  5. HYPONATREMIA
  6. Older age
  7. Prematurity
  8. HYPOthermia
  9. HYPOtensino
  10. HYPOxia
  11. Anemia
  12. Cardipulmonary by pass
  13. Metabolic Acidosis
  14. HYPOosmolarity
  15. Pregnancy through 72 hours post party
  16. PaCO2 >95 mmHg