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week 7 neuro > General anesthetics > Flashcards

General anesthetics Flashcards

1
Q

What is MAC?

A

This is the minimum alveolar conc. that prevents movement in response to surgical stimulation in 50% of subjects

  • it is an indicator of gas potency
  • indicated by how lipophillic it is as well as how fast the mechanism of action works in the brain
  • Faster mechanism of action and high lipophillicy would have the lowest MAC and considered the most potent drug!
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2
Q

Would a smaller MAC be more lipophilic or less?

A

More lipophilic

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3
Q

What does 1.04 MAC mean?

A

It means you need 104% of the drug in the body to get it to knock you out. Thus you would need another drug to get you knocked out.

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4
Q

What are the 5 general effects of GA?

A

Amnesia
SKM relaxation
inhibition of autonomic reflexes
Analgesia
Unconsciousness
- none of the currently available GA’s can cause all 5 and only 5 alone.
- we rely on IV and inhaled drugs- a balance between to the two

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5
Q

What is an ideal drug?

A

rapid, smooth loss of consciousness, rapidly reversible upon discontinuation and a wide margin of safety (LARGE Therapeutic index)

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6
Q

What is conscious sedation?

A

Drug induced alleviation of anxiety and pain and….
smaller doses of sedative medication (altered level of consciousness)
- patient will maintain patent airway and is responsive to verbal commands

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7
Q

Name some common drugs that can cause conscious sedation?

A 
Diazepam
Midazolam
Propofol 
Benzos and opioids 
- benefit is there are rapidly reversible
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8
Q

What drug would you use to reverse opioids?

A

Naloxone

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9
Q

What drug would you give to reverse benzos?

A

Flumazenil

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10
Q

What is deep sedation?

A

Similar to light state general anesthesia

  • There is a gray medium between deep sedation and GA
  • may be even indistinguishable from GA
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11
Q

What are two ways which GA works?

A
  1. Enhance inhibitory activity

2. inhibition of excitatory activity

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12
Q

How does GA target and act on enhancing inhibitory activity?

A
  1. Either through chloride channels
    - pump Cl- into cell to make it stay at resting membrane potential
    - do so through GABAa and glycine
  2. or through K+ channels
    - Postsynaptically it hyper-polarizes
    - pre it hyperpolarizes and thus no NT’s are released
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13
Q

How does GA target and act on inhibition of excitatory activity?

A
  1. inhibits release of glutamate via AMPA and NMDA
    - how ketamine and NO works
  2. via Nicotinic and muscarinic receptors
    - through ACh
    - nicotine can modulate amnesia and analgesia
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14
Q

What are the volatile anesthetics?

A

Halothane, enflurane, isoflurane, desflurane and sevoflurane
- low VP and high BP

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15
Q

What are the gaseous anethetics?

A

NO

- high VP and low BP

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16
Q

What are the factors controlling uptake of inhaled anesthetics?

A
  1. Inspired conc and ventilation
  2. Solubility
  3. Alveolar-venous partial pressure difference
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17
Q

What 2 parameters determine how quickly the alveolar conc changes?

A
  1. inspired conc or partial pressure (how much is given)

2. Alveolar ventilation (how big the breath is)

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18
Q

What is the partial pressure alveoli ratio?

A 
Alveolar conc (FA)/(FI) inspired conc.
- significance being that the closer this number is the one the faster anesthesia will occur during inhaled induction
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19
Q

What is the partioning coefficient?

A

Blood:gas (Otsward coefficient)

  • basically how fast the drug can pass from the gas of lungs to the blood
  • the higher solubility in the blood would indicated a higher B:G ratio and would cross the blood/gas barrier easier.
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20
Q

How would you compare solubility to B:G to FA/FI?

A

The higher the solubility the faster it crosses the B:G barrier and the greater number of B:G

  • This means it will take longer to reach FA/FI to reach equilibrium because so much is lost to the blood right away.
  • So higher solubility means higher B:G and means longer time to reach high conc. in the blood and the anesthetic agent is the brain can rise no faster than it does in the blood.
  • Lower B:G thus means faster onset of anesthetics
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21
Q

What does a B:G of 1.7 mean?

A

Means that at equilibrium there is 1.7x more drugs in the blood than in the gas. Since B:G is high its soluble and would take longer to have its effects.

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22
Q

What is henry’s law?

A

Number of gas molecules that enter a liquid equilibrium is reached is determined by the solubility of the gas in the liquid.
- as pressure decreases the amount of gas dissolved in a liquid decreases

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23
Q

What is the alveolar venous partial pressure difference?

A

Dependent mainly on the uptake of the anesthetic by the tissues, even non neuronal tissues
- influences by tissue:blood coefficients

24
Q

How does tissue:blood coefficient affect induction of anesthesia?

A

The more soluble the drug is in tissues, the highly perfused tissues will take that drug and will have less venous partial pressure of the drug.
- thus the longer it will take to reach FA/FI

25
Q

How would elimination of a drug be faster?

A

Have a smaller B:G and be less soluble. Exact opposite of onset.

  • most inhaled anesthetics are exhaled through the lungs rather than excreted by the kidneys
  • metabolized at a very small extent
26
Q

What is the only way to speed recovery?

A

To hyper ventilate

27
Q

At what levels of MAC is amnesia evident?

A

0.2-0.4

28
Q

What are some of the cerebral effects of GA?

A
  • decreased metabolic rate which decreases blood flow
  • The net effect depends on conc of anesthetic because some GA’s are vasodilators which would increased cerebral blood flow
  • at 0.5 MAC reduction of CMR is greater than vasodilation for example
  • keep in mind an increased in cerebral blood flow is not desired for ICP pts
29
Q

What are the 4 levels of CNS depression

A
  1. Analgesia
  2. Excitement (bad)
  3. Surgical anesthesia
  4. Medullary depression (bad)
30
Q

How is volatility related to vapor pressure?

A

They are directly related

- the higher the vp and more volatile a drug is.

31
Q

What are some highly volatile GA’s?

A

Desflurane> halothane>isoflurane>enflurane

32
Q

What do inhaled anesthetics do the blood pressure?

A

They all decrease it

33
Q

What GA’s preserve CO?

A

Isoflurane and desflurane and sevoflurane

- cause vasodilation but minmially effect CO

34
Q

What drugs have minimal effect on arterial resistance?

A

Halothan and enflurane

35
Q

What are some respiratory effects of GA’s?

A

All volatile drugs are respiratory depressants

- all drugs except NO cause dose dependent decrease in tidal volume and increased RR

36
Q

What GA’s seem to be nephrotoxic?

A

Enflurane and sevoflurane due to fluoride iones

37
Q

What is a rare but significant cause of anesthesia?

A

Malignant hyperthemia

  • Muscle ragidity, tacy, hyperthermia, hyperkalemia, metabolic acidosis
  • Caused mainly by succinylcholine
  • treat with Dantrolene- released Ca from SR
38
Q

what is the mechanism of action of Propofol?

A
  • chloride channel current mediated through GABAa.
  • Very poor solubility in water
  • less of a hangover effect after due to high plasma clearance
39
Q

Where is propofol metabolized?

A

The liver

40
Q

How does propofol affect the CNS?

A

Hypnotic not a analgesic

- decreased CMR=Decreased Flow=Decreased ICP

41
Q

what does propofol do the the CV and respiratory system?

A

CV: vasodilation and inhibits the baroreflex response that should come there after of hypotention
- thus inhibition from 10 and 9 stay the same so no compensatory increased in BP

Res: depressant

  • also an antiemetic
  • pain at injection is also common
42
Q

what are some barbiturates?

A

Theopental and methohexital
which ct to activated GABAa which acts on chloride channels
- of not they have a high toxicity

43
Q

What is the CNS effects of barbs?

A

Vasoconstrictors and thus decreased cerebral flow, then volume then ICP
- no analgesia

44
Q

CV and respiratory effects of Barbs?

A

Vasodilation in the periphery and allows for compensatory increase in HR

  • RR- depressant
  • good for the induction of anesthesia
45
Q

What are some benzos?

A

Midazolam, Loraxepam and diazepam

46
Q

what is the mechanism of action of benzos?

A

Facilitates GABAa

highly lipid soluble and thus has a rapid CNS onset

47
Q

What is the only benzo that is suitable for IV infusion and why?

A

Midazolam because of its short sensitive half time

aka Versed

48
Q

What are the effects of Benzos on the CNS?

A

Decreased CMRo2 via decreased blood flow

- smaller extent than Prop and barbs

49
Q

What are some of the CV and RR effects of Benzos?

A

CV: no CO change bu decreased in BP peripherally

RR: minimal depression

50
Q

what is the mechanism of action of Etomidate?

A

GABAa mediated but often chosen for it minimal hemodynamic effects.

  • example patient with blood loss
  • very good for pts with myocardial contractibility compromise
51
Q

what is the effect of etomidate on the CNS?

A

It is a potent cerebral vasoconstrictor

  • decrease in blood flow and decrease in ICP
  • CV stable
  • RR depressant
52
Q

What does etomidate do to the endocrine system?

A

It is a adrenocortical suppressant

- it inhibits the action of 11b- hydroxylate which is the enzyme needed to convert cholesterol to cortisol

53
Q

what is the mechanism of action of Ketamine?

A

Inhibition of the NMDA receptor complex

- high lipid solubility

54
Q

What are the effects of ketamine on the CNS?

A

Upleasant emergence reactions
cerebral vasodilatory that increases cerebral blood flow as well as CMRO2
-not given to people with ICP
- vivid dreams, out of body experiences and hallucinations
- fear and confusion
- no as many of these affects on kids

55
Q

What are the effects of ketamine on Cv and RR?

A

increases BP, HR and CO by mediation of sympathetic stimulation

56
Q

what can be added to opioids to cause GA?

A

benzos

- hemodynamic stabilty- good for pts with compromised myocardial functoin

week 7 neuro (12 decks)

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