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Pharmacology for Anesthesia > 05 - Clinical Pharm of Inhalationals > Flashcards

05 - Clinical Pharm of Inhalationals Flashcards

0
Q

MAC is the concentration that prevent movement in ___ of patients in response to a certain stimulus

A

50%

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1
Q

Minimal alveolar concentration is really a

A

Median

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2
Q

MAC is best used to compare

A

Different agents

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3
Q

What are the other MACs?

A

MACawake (0.1 x MAC)
MACbar (1.7-2.0 x MAC)
MACrecall (0.3-0.5 x MAC)

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4
Q

T or F. MAC is additive.

A

True

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5
Q

Factors that increase MAC

A 
Younger age
Chronic alcoholism
Anxiety?
Acute sympathetic increase - COCAINE
Hyper metabolic state (thyroid? High fever)
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6
Q

Factors that decrease MAC

A 
Premedication
Older age
Pregnancy
Acute alcohol usage
Hypothermia
Hypercarbia/hypoxia
Sympathetic blockade
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7
Q

How much does MAC decrease with age?

A

Six percent per decade after age 40

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8
Q

Look at that chart

A

LOOK AT IT

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9
Q

Nitrous oxide is inorganic, _______, sweet smelling! and relatively insoluble

A

Non volatile

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10
Q

NO2 is non flammable but supports

A

Combustion

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11
Q

Nitrous cause CV _____ but stimulates

A

Depression

Catecholamines

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12
Q

Respiratory effects of NO2

A

Increased RR
Decreased TV
No change in MV
Very decreased hypoxic drive

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13
Q

Has analgesic properties but is not complete anesthesia?

A 
Nitrous
Increased ICP (CBF, CBV, CMRO2)
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14
Q

Which inhalational has no muscle relaxant properties?

A

Nitrous

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15
Q

T or F. NO2 can induce malignant hyperthermia.

A

False

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16
Q

Renal effects of NO2

A

Decreased GFR

Decreased urine output (due to decreased RBF)

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17
Q

Hepatic effects of NO2

A

Slightly decreased hepatic blood flow

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18
Q

GI effects of NO2

A

PONV (activates CTZ)

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19
Q

Elimination of NO2 is almost

A

100% exhalation

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20
Q

How does NO2 inactivate methionine synthetase?

A

It oxidizes the Co atom in B12

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21
Q

What are the toxicities of NO2?

A 
Inactivates methionine synthetase
Affects myelin formation
Homocysteine accumulation
Inhibits thymidylate synthetase (DNA synthesis)
Bone marrow depression
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22
Q

What effects are seen with disturbed myelin formation?

A

Peripheral neuropathies

Neurotoxicity

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23
Q

Teratogenicity is caused by

A

Inhibition of thymidylate synthetase (DNA synthesis) which is one of the effects of NO2

Teratogenicities are abnormalities of physiological development

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24
Q

What results from the bone marrow depression seen with NO2?

A

Megoloblastic anemia (anemia that results from DNA synthesis)

Specifically, pernicious anemia which causes alteration to the secretion of intrinsic factor, a protein essential for the absorption of B12 in the ileum

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25
Q

How long does it take to recover from NO2?

A

> 4 days

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26
Q

T or F. It is OK to harvest bone marrow from someone with megaloblastic anemia.

A

True???

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27
Q

_______ exposure to NO2 is particularly harmful

A

Serial

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28
Q

Other problems with NO2

A

Added cost of installation/management of pipeline
Added complexity to anesthesia machine
Concerns about exposure to workers
Risks of low FiO2 and catastrophic hypoxia

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29
Q

NO2 is ____ more soluble in the blood than N2

A

35x

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30
Q

NO2 diffuses out of blood and into ________ faster than air can diffuse into blood which can cause

A

Closed airspaces

Pneumothorax, trauma, venous air embolism, intracranial air, acute GI obstruction, intraocular air, tympanic membrane, blebs/bullae

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31
Q

Some other contraindications to NO2

A

Inborn errors of single carbon metabolism (and untested family members), antifolate chemotherapeutics, pernicious anemia, megaloblastic anemia, serial anesthetics

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32
Q

NO2 is recommended to be avoided for maintenance, especially in the ______ pregnancy and

A

First trimester
Extremes of age

Consider? Avoiding in patients with cardiac, vascular, neurogenerative disease

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33
Q

A halogenated alkane

A

Halothane

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34
Q

Halothane is cheap, safe, used worldwide. It is

A

Sweet

Non pungent odor

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35
Q

CV effects of halothane

A

Myocardial depression

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36
Q

By how much can halothane decrease blood pressure and cardiac output?

A

Up to 50%

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37
Q

Halothane ______ electrical conduction of the heart. It is sensitive to

A

Slows

catecholamines

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38
Q

Respiratory effects of halothane

A 
Increased RR
Very decreased TV
Decreased MV
Very decreased hypercapnic drive
Potent bronchodilator
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39
Q

Why does halothane cause blunted autoregulation?

A

It dilates vessels and increases cerebral blood flow but decreases CMRO2

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40
Q

What must be done before starting halothane?

A

Hyperventilate

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41
Q

Neuromuscular effects of halothane

A

Muscle relaxation
Potentiates NMB
Triggers MH

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42
Q

Renal effects of halothane

A

Decreased RBF, GFR, and UO (partially due to decreased CO)

43
Q

T or F. Halothane causes impaired hepatic clearance of drugs

A

True, it decreases hepatic blood flow

44
Q

Halothane is oxidized in the liver by CYP to

A

Trifluoroacetic acid (TFA)

45
Q

What percent of halothane is metabolized in the liver?

46
Q

1 in 5 adults develop ______ from halothane

A

Mild hepatotoxicity (lethargy, nausea, fever)

Likely related to changes in hepatic blood flow

47
Q

What is halothane hepatitis? Why?

A

A rare condition of massive hepatic necrosis/death

Likely an immune mechanism (eosinophilia, rash, fever); genetic?

48
Q

What causes centrilobar necrosis?

A

Hypoxia of reductive metabolites?

Associated with halothane

49
Q

Contraindications to halothane

A

Liver dysfunction after prior exposure
Intracranial HTN
Pheochromocytoma, severe cardiac disease
Beta blockers, Ca channel blockers, aminophylline

50
Q

Non pungent, low solubility - excellent for inhalation induction

A

Sevoflurane

51
Q

Sevoflurane and desflurane allow for fast emergence but it can lead to

A

Post op delirium, especially in peds

52
Q

CV effects of sevoflurane

A

Minimal changes in contractility and HR

53
Q

Respiratory effects of sevoflurane

A 
Increased RR
Very decreased TV
Decreased MV
Blunts hypercapnic drive
Bronchodilator
54
Q

Neuro effects of sevo fluorine

A

Increased CBF, ICP (responds to hyperventilation)

Decreases CMRO2

55
Q

Neuromuscular effects of sevoflurane

A

Muscle relaxation
Potentiates NMB
Triggers MH

56
Q

Allows for enough muscles relaxation for peds intubation

A

Sevoflurane

57
Q

Renal effects of sevo fluorine

A

Slightly decreases RBF

58
Q

Can cause the formation of compound A

A

Sevoflurane

59
Q

Hepatic effects of sevoflurane

A

No significant changes

60
Q

How much sevoflurane is metabolized in the liver?

61
Q

Inorganic fluoride ion of sevoflurane can lead to

A

Nephrotoxicity?

Not clinically seen

62
Q

BaOH or soda lime used with sevoflurane produces compound A which caused nephrotoxicity in rats. What is the recommendation to avoid this?

A

FGF at least 2 L/min if exposure will exceed 2 MAC-hr

Avoid flows <1 L/min

63
Q

What causes higher incidence of compound A?

A

Lower flow
Higher temp
Higher conc
Longer case

64
Q

Sevoflurane is unlikely to form

65
Q

Contraindications to sevoflurane

A

Nothing unique

66
Q

CV effects of isoflurane

A

Minimal cardiac depression (increased HR)

Some coronary artery dilation (?steal syndrome)

67
Q

Respiratory effects of isoflurane

A

Increased RR
Very decreased TV
Decreased MV
Blunts hypoxic/hypercapnic drives

68
Q

Isoflurane is an irritant, but

A

Bronchodilator

69
Q

Neuro effects of isoflurane

A

Increased CBF, ICP (>1 MAC)

Decreased CMRO2

70
Q

At 2 MAC, isoflurane can cause

A

EEG silence

71
Q

Renal effects of isoflurane

A

Decreased RBP, GFR, UOP

72
Q

Isoflurane decreases hepatic blood flow but has better _____ than with halothane

73
Q

Isoflurane is metabolized to

A

TFA

Increased fluoride levels but nephrotoxicity unlikely

74
Q

Contraindications to isoflurane

A

Nothing unique

75
Q

Desflurane is similar in structure to isoflurane but

A

Less soluble and potent

76
Q

Why does desflurane require a special vaporizer?

A

Des has a high vapor pressure and can boil at normal OR temps. Changes in temperature or altitude can change concentration of delivered gas.

77
Q

CV effects of desflurane

A

Increased HR
Decreased BP
No change in coronary blood flow

78
Q

Respiratory effects of desflurane

A

Increased RR
Very decreased TV
Decreased MV

79
Q

Which inhalants are irritants but bronchodilators?

A

Desflurane

Isoflurane

80
Q

Pungency of desflurane can cause

A

Salivation
Breath holding
Coughing
Laryngospasm

81
Q

Neuro effects of desflurane

A

Increased CBF, ICP (responds to hyperventilation)

Decreased CMRO2

82
Q

All inhalationals cause muscle relaxation, potentiate NMB, and trigger MH except

A

NO2 and xenon

83
Q

Renal and hepatic effects of desflurane

A

No effects

84
Q

Contraindications to desflurane

A

Nothing unique (maybe asthma)

85
Q

Elimination of desflurane

A

Minimal metabolism

86
Q

Advantages of xenon

A 
Inert
CV stability
Insoluble
Fast induction/recovery
No MH trigger
87
Q

Disadvantages to xenon

A 
Expensive
Low potency (MAC = 70%)
88
Q

Formula for cost of volatile agents

A

Cost = (conc x FGF x duration x MW x cost/mL) / ( 2412 x density)

89
Q

Where does malignant hyperthermia occur?

A

Skeletal muscles

90
Q

MH is a genetic defect with

A

Autosomal dominant inheritance

91
Q

MH related deaths have occurred even though patients have undergone

A

Multiple prior uneventful surgeries

92
Q

What is the gold standard for definitive diagnosis of MH?

A

Caffeine-halothane contracture test

Requires muscle biopsy at a specialized biopsy center

93
Q

There is a ______ association between heat stroke and susceptibility for MH

94
Q

Triggers of MH

A

All volatile agents and succinylcholine

95
Q

For prevention of MH, avoid triggers and

A

Flush anesthesia machine
STOP TRIGGERING AGENTS, CALL FOR HELP
Dantrolene
High flow O2, active cooling, treatment of acidosis and electrolytes, ICU mgmt

96
Q

What can be administered for MH and how does it work?

A

Dantrolene 2.5 mg/kg IV

It is a MR that reduces Ca release by muscle sarcoplasmic reticulum

97
Q

MH causes an abnormal release of calcium that causes

A

Sustained muscle contraction, including masseter muscle rigidity
Hypermetabolism - heat production, hypoxemia, acidosis, increased PaCO2, tachycardia
Rhabdomyolysis - increased serum K and creatinine kinase, arrhythmia, myoglobinuria, renal failure

98
Q

Rate of recurrence of MH

A

25% within 24-36 hours

99
Q

What’s the problem with using succinylcholine in young patients?

A

They could have undiagnosed muscular dystrophy an using sux can lead to hyperkalemic cardiac arrest.

100
Q

Does Neuroleptic Malignant Syndrome require MH precautions?

A

No/ It is related to the administration of antipsychotic drugs. It causes hyperthermia, muscular hypertonicity, autonomic instability, mental status changes

101
Q

What percent of children receiving halothane/sevo and sux develop MMR?

102
Q

What is MMR?

A

Masseter Muscle Rigidity - trismus making it difficult/impossible to open jaw
Mild MMR with sux is normal

103
Q

T or F? We do not assume that MMR or peripheral muscle rigidity is MH. Continue the surgery.

A

False. Assume it is MH and begin treatment. Postpone the surgery.

104
Q

Succinylcholine induced MMR can lead to _____. Patients should remain in the hospital for

A

rhabdomyolysis

12-24 hours

105
Q

What are signs of rhabdomyolysis?

A

myoglobinuria

myoglobinemia

106
Q

With sux induced MMR, CK and electrolyte levels should be checked every

Pharmacology for Anesthesia (9 decks)

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