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Mo and Mik > m and m 8 - inhal agts > Flashcards

m and m 8 - inhal agts Flashcards

1
Q

Methoxyflurane and enflurane are 2 of oldest anesthetics. Why isn’t methoxyflurane used any more?

A

Methoxyflurane is highly soluble, causing long induction and emergence (high solubility, low vapor pressure). Also highly metabolized by CYP enzymes to free fluoride, oxalic acid (both nephrotoxic). Lastly, caused vasopressin resistant high output renal failure

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2
Q

Methoxyflurane and enflurane are 2 of oldest anesthetics. Why isn’t Enflurane used any more?

A

Depressed cardiac contractility, decreased secretion of CSF and could cause tonic clonic seizures

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3
Q

Of the main inhalation anesthetics used in clinical practice today, which 2 are useful for induction?

A

Halothane and sevoflurane

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4
Q

What are 3 factors that will affect The composition of the gas inspired by the patient?

A

Fresh gas flow rate, volume of breathing system and absorption by the circuit

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5
Q

During induction, which is higher: alveolar gas concentration or inspired gas concentration? Why?

A

Alveolar gas concentration is lower because the body takes up the gas. If there was no uptake, The alveolar gas and inspired gas concentrations would be close to equal

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6
Q

True or false, gas partial pressure is directly proportional to the gas concentration in a given tissue

A

True

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7
Q

True or false, The greater the uptake of an anesthetic gas, the greater the difference between inspired and alveolar gas, therefore the slower the rate of induction

A

True, you want low uptake so that equilibrium is reached quickly

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8
Q

Nitrous oxide has a blood / gas coefficient of 0.47, one of the lowest of any anesthetic agent. What does this mean in words?

A

At equilibrium i.e. steady state, the same volume of blood will have 0.47% of nitrous oxide comparred to the same volume of alveolar gas

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9
Q

The higher a gas’ blood/gas coefficient, the more soluble the gas is. True or false?

A

True, e.g. halothane has a blood gas coefficient of 2.4 percent, one of the highest of the currently available anesthetics

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10
Q

What is the effect of cardiac out put on anesthetic uptake? Think of uptake as solubility

A

As CO increases, uptake increases (more unsaturated blood), Therefore Induction will slow down

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11
Q

What is the danger of having a low output state re: soluble inhalation anesthetics?

A

The rate of rise of alveolar concentrations will Increase in low output states, predisposing patients to overdose of soluble anesthetic agents

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12
Q

What are the 5 organs considered vessel rich?

A

Brain, kidneys, endocrine, heart and liver

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13
Q

During induction, Increasing ventilation is more significant for soluble or Insoluble gases?

A

More significant for soluble gases. Insoluble gases will quickly reach steady state. Soluble gas has a larger Vd, therefore needs to saturate more tissue, so increasing ventilation (i.e. delivery) is important to help soluble gases reach steady state faster

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14
Q

Ether and halothane are associated with a negative feedback loop during induction, Explain.

A

Both these anesthetics will depress spontaneous ventilation. As levels in tissues rise, the patient breathes less, meaning uptake is decreased. That is the negative feedback loop

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15
Q

During induction which is usually higher, arterial or alveolar partial pressures?

A

Alveolar is higher. Reasons include venous admixture, alveolar dead space and non-uniform alveolar gas distribution

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16
Q

What is the effect of vQ mismatch on arterial and alveolar partial pressures?

A

VQ mismatch will have a net effect of increased alveolar partial pressures and decreased arterial partial pressures

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17
Q

Which one has faster elimination, halothane or isoflurane? Why?

A

Halothane, because it undergoes more biotransformation by CPY enzymes than isoflurane

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18
Q

What is the CYP enzymes associated with gas anesthetic biotransformation?

A

CYP 2E1

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19
Q

What is diffusion hypoxia? What agent is involved? How is this prevented?

A

Nitrous oxide diffuses so fast that it dilutes the concentrations of O2 and CO2, causing transient hypoxia. Prevent by administering 100 % oxygen for 5-10 minutes after stopping nitrous

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20
Q

What is the proposed mechanism of nitrous oxide anesthesia? What other inhaled anesthetic shares the same mechanism?

A

NMDA-R antagonism

Xenon

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21
Q

What is the Meyer Overton rule?

A

Re: Inhalation anesthetics, potency correlates with lipid solubility. Thought to be currently incorrect

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22
Q

What are 2 proposed mechanisms of general anesthetics?

A
  • Potentiation of GABA-A at GABA receptor
  • Potentiation of glycine at strychnine sensitive glycine receptor
  • Activation of inwardly rectifying potassium current (TREK-1 and TASK receptors)
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23
Q

True or false, current evidence supports notion that early exposure to anesthetics causes developmental delays?

A

False - evidence is not conclusive at this time

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24
Q

Identify the anesthetic agents associated with the following MAC values 0.75, 1.2, 2.0, 6.0 and 105

A

Halothane, isoflurane, sevoflurane, desflurane and nitrous oxide

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25
Q

How much MAC would cause 95% of population to not respond to surgical stimulus?

A

1.3

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26
Q

By what percent does MAC requirement decrease each decade?

A

About 6%

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27
Q

Nitrous oxide [stimulates/depresses] the sympathetic NS.

A

Stimulates.

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28
Q

Under what situations may nitrous oxide be associated with myocardial depression? (2)

A

Coronary artery disease

Hypovolemia

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29
Q

Why might nitrous oxide cause increase in RVEDP?

A

It can cause vvasocontricion of the pulmonary smooth muscles

30
Q

What is effect of nitrous oxide of

  • RR
  • tidal volume
  • Hypoxic drive
A

Increases RR, Decreases Tv and also inhibits/depresses hypoxic drive (FYI, same patter for all the inhalational anesthetics)

31
Q

What is the effect of nitrous oxide on

  • Cerebral blood flow
  • Intracranial pressure
  • Cerebral metabolic rate
A

Increases blood flow, increases intracranial pressure and increases cerebral metabolic rate (effect on CMRO2 is unique to nitrous)

32
Q

True or false, inhalation agents generally increase cerebral blood flow and pressure while IV anesthetics will decrease cerebral blood flow and pressure.

A

True

33
Q

Under what conditions can nitrous oxide cause skeletal muscle rigidity?

A

In high concentrations in Hyperbaric chambers

34
Q

What is the effect of nutrous oxide of

  • Renal blood flow
  • GFR
  • UOP
A

Decreased renal blood flow by increasing renal vascular resistance, decreases GFR and UOP

35
Q

Nitrous oxide is associated with peripheral neuropathies and megaloblastic anemia with prolonged exposure to anesthetic concentrations. Why?

A

it irreversibly oxidises cobalt atom in Vit B12, and inhibits enzymes that are B12 dependent, most notable methionine synthetase and thymidylate synthetase. These enzymes are needed for myelin formation and DNA synthesis, respectively

36
Q

There is a single general class of contra-indication for using nitrous. What is this and what are some examples?

A

Any body cavity that contains air because nitrous oxide will diffuse into this cavity

  • Arterial air embolism
  • Pneumothorax
  • Intestinal obstruction
  • Intracranial air
  • Intraoccular air bubbles
37
Q

Among inhalation agents, which is a DIRECT MYOCARDIAL DEPRESSANT? Mechanism?

A

Halothane - at 2.0 MAC it will cause a 50% decrease in CO and BP, It interferes with sodium-calicum exchange and Intracellular calcium utilization

38
Q

How does halothane cause bradycardia?

A

Blunts the baroreceptor reflex to hypotension that would ordinarily decrease vagal stimulation to the Heart

39
Q

How does halothane affect response to epinephrine

A

It sensitizes the heart to epinephrine induces arrythmias

40
Q

What is the effect of halothane on apneic threshold? Hypoxic drive?

A

Increases apneic threshold (the PaCO2 at which patient remain apneic) and depresses hypoxic drive

41
Q

What is the effect of halothane on asthma? Mucus clearance?

A

Good for asthma as it relaxes smooth muscles. Bad for mucus clearance as it diminishes clearance, leading to post op hypoxia and atelectasis

42
Q

What is the effect of halothane on

  • Cerebral blood flow
  • Cerebral vascular resistance
  • Cerebral blood flow autoregulation
A

Will cause decreased vascular resistance, Increasing cerebral blood flow and can therefire cause increased intracranial pressure.

43
Q

How can you prevent halothane induced rise in intracranial pressure?

A

Hyperventilate the patient BEFORE induction with halothane

44
Q

WHat is the effect of halothane on

  • Renal blood flow
  • GFR
  • UOP
A

Decrease all three. Specifically for halothane, the decrease in renal blood flow may also be attributed to its depression of CO

45
Q

What is the effect of halothane oN hepatic blood flow?

A

Decreases blood flow to liver

46
Q

What is the principal metabolite of halothane? What is the enzyme primarily responsible for producing?

A

Trifluoroacetic acid, CYP2E1

47
Q

What are 3 risk factors for halothane hepatitis?

A
  • Recent repeated exposure to halothane
  • Middle aged obese woman
  • Personal or family hx of halothane hepatitis
48
Q

What is the liver pathological pattern associated with halothane hepatitis?

A

Centrilobular necrosis

49
Q

What drug is specifically associated with increasing suceptibility to halothane hepatitis?

A

Phenobarbital, It is an inducer

50
Q

What is the current predominant hypothesis re: mechanism of halothane hepatitis?

A

Immune mediated. Repeated exposure causes antibodies that react to the trifluoroacetic acid protein adducts, leading to an immune response

51
Q

Three contraindications to halothane are:

A
  • Unexplained / known hepatic dysfunction
  • Avoid in intracranial mass lesions (as with other inhalation agents)
  • Avoid In pts with decreased LVEF or hypovolemia
52
Q

Generally speaking, inhalation agents will not change or decrease HR. What is the 2 exceptions that will cause tachycardia and increase in catecholamines?

A

Isoflurane and desflurane

53
Q

Isoflurane can cause dilation of coronary arteries. What is the clinical significance of this?

A

This can cause coronary steal, as it will decrease flow to areas with fixed coronary lesions

54
Q

Like other gas anesthetics, what is the effect of isoflurane on RR and TV? Response to hypoxia and hypercapnia?

A

Decreases both RR and TV, also decreases response to hypoxia and hypercapnia

55
Q

What is the effect of Isoflurane on cerebral blood flow and intracranial pressure? How is this prevented (different from halothane?)

A

Isoflurane will increase CBF and increase intracranial pressure. Can reverse increased intracranial pressure with hyperventilation during the increase in Intracranial pressure, unlike with halothane where hyperventilation can to occur before exposure to halothane

56
Q

What is the major metabolite of isoflurane? How is it similar and different from halothane?

A

Trifluoroacetic acid, same as halothane. However, there is minimal hepatic metabolism of isoflurane, thus, not as much of the metabolite forms

57
Q

Desflurane is unique because it has a [high/low] vapor pressure and relatively [high/low] potency. It is relatively [fast/slow] on and off

A

High vapor pressure - boils at room temp
Relatively low potency
Relatively fast on/off

58
Q

Why is desflurane vaporizer heated?

A

Heated to increase the pressure in the vaporizer to 1300 mmHg, which will ensure that despite changes in temperature, the desflurane won’t boil

59
Q

How is desflurane addition to fresh gas flow different from other gases?

A

Other gases will have fresh gas pass through the vaporizing chamber. Desflurane is added directly into the fresh gas flow

60
Q

What is the effect of desflurane on
BP
SVR
HR

A

Will decrease BP and SVR, Increase HR

61
Q

What is the significance of using desflurane in patient with CAD? What are three agents that can prevent this effect?

A

Rapid rise in concentrations will cause increase in HR, blood pressure and catecholamine levels. Can block with fentanyl, esmolol or clonidine?

62
Q

Like other gas anesthetics, what is the effect of Desflurane on RR and TV? Response to hypoxia and hypercapnia?

A

Decreases both RR and TV, also decreases response to hypoxia and hypercapnia

63
Q

Desflurane will increase cerebral blood flow and intracranial pressure, like other inhalation agents. What is the effect on cerebral metabolic rate?

A

Will decrease CMRO2

64
Q

Which inhalation agent is most likely associated with clinically significant carbon monoxide poisoning? Mechanism? How is this prevented

A

Desflurane - it is degraded by the CO2 absorbent to carbon monoxide, which may be detected ABG. It can be prevented with calcium hydroxide absorbent

65
Q

A combination of which 2 inhalational agents can be used for masked induction?

A

Sevo + nitrous oxide

66
Q

Sevoflurane, desflurane and isoflurane - which is most likely to be associated with a fall in cardiac output?

A

Sevo

67
Q

Sevoflurane, desflurane and isoflurane - which is most likely associated with long QT syndrome?

A

Sevo

68
Q

True or false, sevoflurane will cause enough muscle relaxation to allow for intubation?

A

True

69
Q

Sevoflurane, desflurane and isoflurane - which is most metabolized? By which CYP? Significance?

A

Sevoflurane is most metabolized by CYP2E1. Unlike the other 2, there is enough metabolism to note a rise n serum fluoride. Theoretically, but not clinically, this can inpair renal concentrating ability

70
Q

What is the significance of compound A? It is associated with which of the following Sevoflurane, desflurane and isoflurane ? How to prevent? (2)

A

Compound A is potentially nephrotoxic degradation product of sevoflurane interaction with alkali (CO2 absorber). Prevent with

  • Fresh gas flow at least 2L per minute
  • Use calcium hydroxide
71
Q

Xenon is an anesthetic that has a MAC of 0.71, has little cardiac, hepatic or renal side effects. Why is it not widely used?

A

Expensive, scavenged from atmosphere by expensive distillation process

Mo and Mik (9 decks)

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