Inhalational Anesthetics Flashcards

1
Q

What is the MOA of nitrous oxide?

A

NMDA receptor antagonist

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2
Q

What does NO do to myocardial contractility?

A

Depresses it

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3
Q

What does NO do to sympathetic nervous system?

A

Stimulates it so increases BP, CO, and HR because of the release of catecholamines.

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4
Q

What does NO do to the pulmonary vasculature?

A

Increases its resistance so causes increase in right ventricular end diastolic pressure

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5
Q

What does NO do to the respiratory system?

A

Increases the respiratory rate and decreases the tidal volume as a result of CNS stimulation.
It decreases hypoxia drive mediated by the carotid body chemoreceptors

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6
Q

What are the effects of NO in the CNS?

A

It increases CBF –> mild elevation in ICP

It increases CMRO2 (oxygen consumption in the brain)

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7
Q

What does NO do to muscle relaxation?

A

Actually causes skeletal muscle rigidity

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8
Q

What does NO do to renal system?

A

Decreases renal blood flow by increasing renal vascular resistance, decreasing GFR and UOP

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9
Q

What does the use of NO increase the risk of postoperatively?

A

PONV by activation of the CTZ

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10
Q

How is NO eliminated?

A

Thru exhalation

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11
Q

What enzyme does NO inhibit?

A

It irreversibly oxidizes the cobalt atom in vitamin B12 so it affects every vitamin b12 pathway.

  • myelin synthesis (methionine synthase), DNA synthesis (thymidylate synthase)

CAN CAUSE MEGALOBLASTIC ANEMIA AND PERIPHERAL NEUROPATHIES

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12
Q

Is NO teratogenic?

A

Yes

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13
Q

How does NO modulate the immune response?

A

It affects chemotasis and motility of PMNs

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14
Q

What are the contraindications to using NO

A

Pneumothorax, air embolism, SBO, pneumocephalus, tympanic membrane grafting (diffuses into air containing cavities due to solubility increasing the pressure within the cavity)
Pregnancy

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15
Q

What does NO do with other gases?

A

Decreases the MAC
Attenuated the circulatory and respiratory effects of volatile anesthetics
Potentials neuromuscular blockade

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16
Q

What are the effects on CV with isoflurane?

A

Increase in heart rate due to mild stimulation of beta receptors (no change in cardiac output)

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17
Q

What does isoflurane do to coronary arteries?

A

It dilates them

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18
Q

What are the respiratory effects of isoflurane?

A

Bronchodilates
Irritates the upper airway reflexes
Fall in minute ventilation

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19
Q

What does isoflurane do to the CNS?

A

Increases CBF and ICP at MAC greater than 1 (reversed by hyperventilation)

Reduces CMRO2

At MAC 2 it produces and electrically silent EEG

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20
Q

What does isoflurane do to muscles?

A

Relaxes them

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21
Q

What does isoflurane do to the renal system?

A

Decreases renal blood flow and therefore GFR and UOP

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22
Q

What is isoflurane metabolized to?

A

Trifluoroacetic acid

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23
Q

Can isoflurane trigger malignant hyperthermia?

A

Yes

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24
Q

What’s the difference between desflurane and isoflurane?

A

Desflurane has a fluorine atom instead of a chlorine atom

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25
Q

Why does desflurane cause rapid induction and emergence?

A

It’s low solubility

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26
Q

What is the blood/gas partition coefficient of desflurane?

A

0.42

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27
Q

What is the vapor pressure of desflurane?

A

High

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28
Q

What ar the cardiovascular effects of desflurane?

A

Cardiac output is maintained by mild beta stimulation
With increased dose it causes a decline in SVR
Increased CVP and pulmonary artery pressure

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29
Q

What do rapid increases in desflurane concentration lead to ?

A

Transient increases in heart rate, BP and catecholamines levels

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30
Q

What drugs attenuate the heart effect of desflurane with rapid increases in dosage?

A

Fentanyl
Clonidine
Esmolol

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31
Q

What does desflurane due to tidal volume?

A

Decreases it

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32
Q

What does desflurane do to respiratory rate?

A

Increases it

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33
Q

What do volatile anesthetics do to respiratory drive?

A

Decreases the ventilatory response to increasing PaCO2

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34
Q

Why is desflurane a poor choice as an induction agent?

A

It causes airway irritation

Can cause laryngospasm

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35
Q

What does desflurane do to the CNS.

A
Increases CBF
Increases CBV
Vasodilator cerebral vasculature 
Increases ICP
Decreases CMRO2
36
Q

What does desflurane do to an EEG?

A

Increases the activity initially and then as anesthesia depends the EEG slows.

37
Q

What is the neuromuscular effects of desflurane?

A

It is associated with dose-dependent decrease in the response to train of four and tetanus peripheral nerve stimulation

38
Q

What is desflurane degraded by and into

A

Barium hydroxide lime, Sodium hydroxide, Potassium hydroxide
Into carbon monoxide

39
Q

How do you minimize the risk of carbon monoxide poisoning in degraded desflurane?

A

Dispose of dried out absorbent or use calcium hydroxide instead

40
Q

What are the contraindications to using desflurane?

A

Severe hypovolemia
Malignant hyperthermia
Hypertension

41
Q

What does desflurane do to nondepolarizing neuromuscular blocking agents?

A

Potentiates them

42
Q

Can epinephrine be used with desflurane?

A

Yes, desflurane does not sensitize the myocardium to arrythmogenic effects of Epi

43
Q

How are sevoflurane and desflurane similar in structure?

A

They are both halogenated with fluorine

44
Q

What is the blood/gas coefficient of sevoflurane?

A

0.65

45
Q

Why is sevoflurane a better choice for induction than des?

A

No pungent, so not irritating to the upper airways and also reaches high alveolar concentration quickly

46
Q

What is desflurane associated with in the pediatric population?

A

Delirium

47
Q

What is the vapor pressure of sevo?

A

Modest

Can use a conventional variable bypass vaporizer

48
Q

What are the effects of sevo on the CV system?

A

Depresses myocardial contractility
SVR and arterial blood pressure declines, but less than with iOS and des
Decreases CO because it does not increase HR

49
Q

What does sevo do to the EKG?

A

Prolongs QT

50
Q

What does sevo do to the respiratory system?

A

Depresses respiration

51
Q

What does sevo do to the bronchioles?

A

Dilates them - can reverse bronchospasm

52
Q

What are the CNS effects of sevo?

A

Increase in CBF and ICP

Decrease in CMRO2

53
Q

What happens to auto regulation at high levels of sevo?

A

It is impaired, so CBF will decrease during hemorrhagic hypotension

54
Q

What does sevo do to the portal vein?

A

Decreases its flow

55
Q

What does sevo do to the hepatic artery?

A

Increases its flow

56
Q

Why should sevo be avoided in renal impairment?

A

It can be metabolized by the liver or degraded to fluoride or compound A which are nephrotoxic

57
Q

How does compound A accumulate?

A
With increases in respiratory gas temperature
Low flow anesthesia
Dry barium hydroxide
High sevo concentration
Long anesthetic duration
58
Q

What measures should you take to decrease the likelihood of renal injury by compound A?

A

Keep fresh gas flows at least 2L/min in long anesthetic cases

59
Q

What does sevo do to NMBA?

A

Potentials them

60
Q

What are the contraindications of sevo?

A

Severe hypovolemia
Malignant hyperthermia
high ICP

61
Q

What is Xenon?

A

An inert gas that does not form chemical bonds

62
Q

What is the MOA of Xenon?

A

It inhibits glycine binding at its receptor thereby inhibiting NMDA

63
Q

What are the effects of Xenon on the organ systems?

A

Nothing

64
Q

What does Xenon protect against?

A

Neuronal ischemia

65
Q

What is the MAC of isoflurane?

A

1.2

66
Q

What is the vapor pressure pf isoflurane?

A

240

67
Q

What is the MAC of sevoflurane?

A

2.0

68
Q

What is the vapor pressure of sevoflurane?

A

160

69
Q

What is the MAC of Des?

A

6

70
Q

How does renal failure occur from fluoride ions?

A

Direct fluoride ion toxicity to the collecting ducts which inhibits ADH effect so it is a high-output vasopressin resistant renal failure

71
Q

Why doesn’t sevoflurane cause fluoride associated renal failure?

A

The accumulation of fluoride ions decreases as soon as the gas is stopped due low blood and tissue solubility

72
Q

What do volatile anesthetics do to the heart?

A

Depress the SA node and cause junction all rhythm
Mild dose dependent decrease in myocardial contractility due to inhibition of L-type and T-type calcium channels and inhibition of sodium-calcium exchangers resulting in overall decrease of intracellularly calcium

73
Q

How does nitrous increase cardiac output?

A

By stimulation of the sympathetic nervous system

74
Q

How does isoflurane cause direct coronary vasodilation?

A

Activation of ATP-sensitive potassium channels
Inhibition of calcium influx through calcium channels –>
Reduction in calcium accumulation
Reduced calcium release by sarcoplasmic reticulum

75
Q

How much anesthetic vapor is in 1 ml of liquid volatile?

A

200 ml at room temperature

76
Q

What does nitric oxide do?

A

Decreases pulmonary vascular resistance and off loads the RH.
Inhibits platelet aggregation
Increases cGMP so causes smooth muscle relaxation

77
Q

Which vessels does nitric oxide primarily dilate?

A

Arterioles

78
Q

What is the MOA of sevo, iso, Des?

A

They potentiate GABA receptors and glycine
Produce immobility by effects in the spine
Amnesia by effects on hippocampus, amygdala, cerebral cortex
Block nociceptive info going up the afferents to cerebral cortex

79
Q

Which inhalational anesthetic potentiates NMBs the most?

A

Desflurane (by 60% in healthy patients)

80
Q

How do inhalational anesthetics potentiate NMB effect?

A

Directly: By relaxing skeletal muscle, especially when > 1 MAC
Indirectly: unknown mech, maybe central alpha adrenergics

81
Q

Which inhalational anesthetic does NOT provide skeletal relaxation?

A

NO

82
Q

Which class of NMBDs do inhalational anesthetics work more synergistically with?

A

The amino steroids: roc, vec, pan

83
Q

How much do isoflurane and sevoflurane augment NMBs?

A

40%

84
Q

Why does nitrous oxide have a faster rate of rise than desflurane?

A

Concentration effect

85
Q

What happens to the rate of inhalational induction in a right to left cardiac shunt?

A

It slows because there is less pulmonary blood flow and the anesthetic rich blood is mixing with the anesthetic poor blood

86
Q

What happens to the rate of inhalational induction with a left to right cardiac shunt?

A

Stays the same