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Clinical Neuroscience 2 > Pharm- 16 > Flashcards

Pharm- 16 Flashcards

1
Q

What is P(CNS)?

A

CNS Partial pressure –> the level of the anesthetic in the CNS

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2
Q

Can you measure P(CNS) directly?

A

No

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3
Q

So how can you measure P(CNS)?

A

using P(Alv)

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4
Q

What is P(Alv)?

A

The partial pressure of the anesthetic in the lungs. basically the balance between the anesthetic delivered to the alveoli and the loss from the lungs (to blood + tissues)

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5
Q

So how does anesthetic get into the tissues from the alveoli space (generally)?

A

down a concentration gradient cuz theres a crap ton in the alvoli and nothing in the tissues

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6
Q

And how does the anesthetic get out of the tissues and back into the lungs?

A

remove the anesthetic from the lungs –> moves down its concentration gradient back ot to the lung space

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7
Q

WHat is the minimum alveolar concentration (MAC)?

A

It’s the P(alv) that results in the lightest possible anesthesia. basically the point in which anesthesia is induced.

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8
Q

True or false: a lower MAC means an lower potency of anesthesia.

A

FALSE. lower MAC = higher potency. takes less partial pressure to cause anesthesia.

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9
Q

What is AP50?

A

the partial pressure where analgesia (no pain) results in 50% of pts

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10
Q

Define: this is the partial pressure where movement is lost in 50% of pts when cut during surgery

A

MAC!

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11
Q

What is the analgesic index?

A

Ratio of MAC to AP50

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12
Q

If there is an increase in analgesic index, is there an increase or decrease in the partial pressure of anesthetic needed to gain anesthesia than that required for surgical anesthesia?

A

decreased

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13
Q

What is the therapeutic index?

A

LD50/MAC

MAC is the same as the ED50 for nongaseous things

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14
Q

Do you want the therapeutic index to be high or low? Why?

A

High because you want a high LD50 (only kills pts at a very high conc) and you want a low MAC (drug works at a lower conc)

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15
Q

What is the danger of some analgesics which have a lot therapeutic index?

A

Respiratory depression + cardiac arrest

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16
Q

Why must the dosing must be very accurate for analgesics?

A

There are no antagonists to their actions. To get rid of it if you OD you just need time and ventilation lol. Call an MD.

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17
Q

What exactly is the LD50?

A

lethal dose in 50% of subjects

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18
Q

What is the ED50/MAC?

A

the effective dose that gives desired effect in 50% of pt

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19
Q

What is the meyer overton rule?

A

Greater the lipid solubility (greater oil/gas coefficient) of anesthetic in olive oil = greater its potency

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20
Q

What is the oil/gas partition coefficient good at showing?

A

predictor of how soluble an anesthetic is in olive oil- essentially defines the potency (larger coefficient = more soluble = more potent).

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21
Q

What is the solvent/gas partition coefficent good at predicting?

A

predictor of how soluble an anesthetic is in a solvent (blood and plasma). High coefficient = more soluble

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22
Q

What is the diffusion of the anesthetic dependent on?

A

this is proportional to the tissue area as well as the partial pressure difference between the alveoli and the capillary beds

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23
Q

What is the role of perfusion of the anesthetic?

A

capillary beds then deliver the O2 + anesthesia to cells in body. THIS IS THE RATE LIMITING STEP.

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24
Q

What is the anesthetic flow rate?

A

the rate at which the blood perfuses the tissue and anesthetic reaches tissue

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25
Q

Why do you need do some changes for a fat person vs a muscular person as far as dosages of anesthetics?

A

i. Fat pt is going to have a lot of volume (fat) therefore he will store a more lipid soluble anesthetic MUCH more than a muscular patient.
ii. This means that the anesthetic will affect him much more as well as he will be MUCH slower to recovery and for the anesthetic to leave his body

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26
Q

What is the time constant for anesthetics?

A

If you increase the flow rate, you will decrease the time it takes to equilibrate between blood and tissue (faster) and vice versa

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27
Q

How well are anesthetics delivered to well-rich groups?

A
  • CNS + visceral organs

* Low capacity for anesthetic + high blood flow for delivery

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28
Q

How well are anesthetics delivered to muscle groups?

A
  • Muscle + skin

* High capacity + moderate blood flow = longer equilibrium time

29
Q

How well are anesthetics delivered to fat groups?

A

• High capacity for anesthetic + low flow for delivery = extremely long equilibrium time

30
Q

How well are anesthetics delivered to vessel-poor groups?

A
  • Bone, ligaments, cartilage

* Negligible flow + capacity

31
Q

What are the 4 factors that influence the equilibrium of alveolar with inspired partial pressure of anesthetics?

A

ventilation rate, perfusion rate, rate of anesthetic taken up by alveoli, chemical nature of the drug itself

32
Q

Nitrous oxide, desflurance, and sevoflurane are examples of what type of anesthetics?

A

perfusion limited

33
Q

What are the characteristics of perfusion-limited anesthetics?

A

o Induction + recovery quickly
o Smaller blood/gas coefficient = blood removes less anesthetic from alveoli –> alveolar partial pressure rises more quickly = induction quicker
o KEY: agents that are less soluble in blood induce anesthesia faster + recover faster

34
Q

Diethyl ether, enflurane, and isoflurane, halothane are examples of what type of anesthetics?

A

ventilation limited

35
Q

What are the characteristics of ventilation limited anesthetics?

A

o High blood/gas coeffient = high rate of uptake of anesthesia into blood  alveolar partial pressure rises slower = induction slower
o KEY: slow induction + slow recovery from anesthesia

36
Q

What happens to anesthetic delivery if thers hypoventilation?

A

decreases delivery of anesthesia to alveoli (breathe less, get less drugs there duh). SLOWER INDUCTION.

37
Q

And if there is hyperventialtion?

A

faster induction

38
Q

What does a decreased CO do to induction time?

A

blood removes anesthetics from alveoli slower –> alveolar pressure increases faster –> P(CNS) rises rapidly –> speed up induction

39
Q

What is the ventilation rate and CO in kids?

A

both are high

40
Q

What is the induction rate for kids vs adults?

A

since kids have a lot less fat and muscle, much more anesthesia gets to the brain and they are induced into anesthesia MUCH quicker (when compared to adults).

41
Q

What are the 3 factors that influence the speed of recovery and/or onset of induction?

A

1- amt of anesthesia in the mixed venous return (how much is in your system)
2- increased ventilation = removal faster
3- anesthetic can be eliminated from metabolism + ventialtion

42
Q

What happens in diffusion hypoxia?

A

in NO anesthesia, when you recover, if there is a large amt of NO that is coming out of the blood into the alveoli –> displaces O2 –> hypoxia.

43
Q

How can you prevent dissusion hypoxia?

A

Must deliver 100% O2 during the 1st 5-10 mins of recovery

44
Q

Halothane- use

A

good for peds due to nonirritating smell, slow induction + recovery

45
Q

Halothane- risk

A

Malignant hyperthermia

46
Q

What is malignant hyperthermia?

A

AD disease where ryanodine R is defective –> lots of Ca release in muscle –> tetanus –> hyperthermia.

47
Q

How can u treat malignant hyperthermia?

A

dantrolene

48
Q

What is the most widely used anesthetic?

A

isoflurane

49
Q

Enflurane- risk

A

renal toxicity, szrs

50
Q

Diethyl ether- use

A

not commonly used in US cuz of flammability + slow induction

51
Q

Desflurane + sevoflurane- use

A

quick induction b/c of high oil/gas coefficients

52
Q

Desflurane- adverse effects

A

irritating to airway –> cough/laryngospasm

53
Q

Sevolurane- characteristics

A

sweet tasting, can be unstable when exposed to CO2 absorbants –> nephrotoxic

54
Q

Thiopental- characteristics

A

rapid induction, cannot be removed via ventilation (u give it IV), removal is from VRG –> MG –> FG

55
Q

Propofol- characteristics

A

kills michael jackson lol, prepared intralipid (looks like milk), rapid metabolization, can be source of infection

56
Q

Etomidate- why it’s different than propofol

A

similiar to propofol but used for induction, there is also minimal cardiopulminary depression cuz of lack of effect on SANS

57
Q

KEtamine- use

A

produces dissociative anesthesia –> pt is awake but in analgesic amnesic state. can be used in emergencies

58
Q

Ketamine- adverse effect

A

hallucinations

I worked with this dude who used to go to raves and did a ton of drugs. he once snorted ketamine and said he was hallucinating that he was sitting on the back of his eyeball watching a movie through his pupil. he tripped for 3 days. hahaha

59
Q

Benzo’s (diazepam, lorazepam, midazolam)- used

A

Anxiolytic + anterograde amnesia, give to calm a pt

60
Q

How do u reverse benzo’s?

A

flumazenil (romazicon)

61
Q

Opioids (morphine, fentanyl)- use

A

poor amnesics but good analgesics, often used with general anesthetics

62
Q

Opioids- revesal

A

reversed with naltrexone

63
Q

Fentanyl + droperidol- use

A

analgesia + amnesia

64
Q

Fentanyl + droperidol + __???__ = neuroleptanesthesia

A

NO

65
Q

Tubocurarine + pancuronium- mech of action

A

block NmAchR –> muscle relaxation

66
Q

Succinylcholine- mech of action

A

depolarizing inhibitor –> muscle relaxation

67
Q

What is good about mixing only inhaled anesthetics?

A

potent + allows for rapid recovery

68
Q

Why is it good to use an IV agent + inhaled anesthetics?

A

 Short acting IV used to induce stage III anesthesia quickly, pt is able to pass stage II (excitement stage).
 Inhalation agent allows for depth of anesthesia to be maintained and is able to be removed quickly via ventilation
 When using opioids + inhaled = allows the amount of inhaled anesthesia to be much lower therefore reducing the risk of cardiovascular + respiratory depression

Clinical Neuroscience 2 (16 decks)

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