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Basic Principles > 2 - Anesthesia Mechanisms and Care > Flashcards

2 - Anesthesia Mechanisms and Care Flashcards

1
Q

What are the five components of anesthesia?

A

Unconsciousness

Amnesia

Analgesia

Immobility

Attenuation of Autonomic Responses

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2
Q

What is neural inertia?

A

It takes a much higher concentration of anesthetic to induce anesthesia than to maintain it

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3
Q

What is the definition of MAC?

A

Minimum Alveolar Concentration

The alveolar pressure of a gas at which 50% of humans do not respond to a surgical incision

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4
Q

MAC measurement only apply to _______ anesthetics, not to ______ anesthetics

A

gas

parenteral

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5
Q

What is the MAC equivalent in parenteral anesthetics?

A

The plasma concentration required to prevent a response to a noxious stimuli in 50% of subjects

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6
Q

What are three limitations of MAC?

A
  1. Quantal, not graded
  2. Not helpful with parenteral drugs
  3. highly dependent on the endpoint used to define it (verbal response, noxious stimuli)
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7
Q

Meyer-Overton Rule

A

Unitary Theory of Anesthetics

Strong correlation between lipid solubility and MAC

all anesthetics are likely to act at the same molecular site

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8
Q

Exceptions to Meyer-Overton Rule

A
  1. Many compounds that are structurally and chemically similar are not anesthetics (some halogenated compounds are anesthetics, some are anticonvulsants, some are neither)
  2. Anesthetic potency increases with chain length until a critical chain length is reached (cutoff effect), but their oil/gas partition does not exhibit this cutoff
  3. Enantiometers (mirror-image compounds) which have the exact same solubility do not have the same effect. Other properties like size and shape must also be important.
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9
Q

Lipid theories of anesthesia

A

Postulates that anesthetics dissolve in the lipid bilayers and produce anesthesia when they reach a critical concentration

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10
Q

Why is the lipid theory of anesthesia not considered the most likely?

A

No lipid theory can plausibly explain all anesthetic pharmacology

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11
Q

Aside from lipid solubility, the Meyer Overton Rule could also be explained by ___________

A

the direct interaction of anesthetics with hydrophobic sites on proteins!

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12
Q

Firefly Luciferase

A

purified water soluble protein that could be inhibited by general anesthetics

Strong evidence that anesthetics bind to proteins

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13
Q

What are four remaining mysteries concerning anesthesia binding?

A
  1. Do many anesthetic molecules interact with a single protein molecule or only a few?
  2. Do anesthetics compete with endogenous ligands?
  3. Do all anesthetics bind to the same protein pocket?
  4. How many proteins have hydrophobic pockets that anesthetics can bind to?
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14
Q

What is neuronal excitability?

A

the propensity of a neuron to generate and propogate action potentials

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15
Q

Is neuronal excitability effected by anesthetics?

A

Slightly hyperpolarizes, but may nevertheless contribute significantly to the action of anesthetics

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16
Q

What is the most likely subcellular site of general anesthetic action?

A

synaptic transmission

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17
Q

What is the difference between glutamatergic nuerons and GABAergic neurons?

A

Glutamatergic neurons rely on glial-secreted signals to establish synaptic transmission

GABAergic neurons establish functional synaptic transmission in the absence of glia

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18
Q

What are glial cells?

A

cells in the nervous system that support and protect neurons

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19
Q

What is GABA?

A

The chief inhibitory neurotransmitter in the brain

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20
Q

What is glutamate?

A

The primary precursor of GABA

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21
Q

How does GABA inhibit neurons?

A

It binds with ligand gated Cl ion channels and allows Cl to pour into the cell, hyperpolarizing the cell and preventing excitability

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22
Q

What is the MOA of volatile anesthetics at the presynaptic level?

A

Inhibit release of glutamate

Interfere with sodium channel activity

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23
Q

What is the MOA of volatile anesthetics at the postsynaptic level?

A

Potentiate GABA receptor activity

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24
Q

How do volatile anesthetics affect neurotransmission?

A

Inhibit excitatory neurotransmission

Enhance inhibitory neurotransmission

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25
Q

How are ion channels affected by volatile anesthetics?

A
  1. Voltage dependent calcium channels : minimal sensitivity to anesthetics
  2. Some Na channels are inhibited
  3. Tp/4TM K channels may be involved
  4. HCN channels may be involved
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26
Q

What are NMDA channels?

A

Glutamate-activated ion channels that conduct Na, K, and Ca

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27
Q

Which anesthetics inhibit NMDA-type glutamate receptors?

A

Ketamine

N20

Xenon

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28
Q

What is GABA potentiation?

Which drugs cause it?

A

Makes it easier for GABA to elicit a Cl current

Halothane, Enflurane

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29
Q

What is direct gating of GABA channels?

A

Ability of a gas to activate GABA(a) channels when GABA is absent

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30
Q

What is the main site of at which anesthetics inhibit motor response to noxious stimuli?

A

The spinal cord. Not the brain.

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31
Q

What is a plausible anesthetic target that accounts for amnesiac effect?

A

GABA(a) receptors in the Hippocampus and Amygdala

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32
Q

What is the difference between arousal and awareness?

A

Awareness is the ability to process and store information

Arousal is the state of receptivity to the external environment

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33
Q

What is the RAS?

A

Reticular Activating System

Diffuse collection of brainstem neurons that mediate arousal

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34
Q

What is the reticular formation?

A

Collection of neurons in the midbrain and pons responsible for arousal and sleep

Likely the site of arousal ablation under anesthesia

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35
Q

What does the thalamus regulate?

A

cortical excitability

likely a site of ablation of arousal and awareness

36
Q

What is the incidence of intraop awareness?

A

0.1-0.4%

37
Q

What is the Brice Questionnaire?

A

accepted tool for detecting awareness postop

  1. Last thing you remember before sleep
  2. First thing you remember waking up
  3. Did you remember anything in between
  4. Did you dream during your procedure
  5. What was the worst thing about your operation?
38
Q

When does awareness occur most?

Least?

A

Maintenance

Emergence

39
Q

What are risk factors for awareness?

A

Females

Young adults

obesity

after normal hours

Emergency procedure

obstetric, cardiac, thoracic sx

use of nondepolarizing relaxants

40
Q

Does BIS monitoring prevent awareness?

A

No

41
Q

Are children more or less likely to develop PTSD from awareness?

A

Less

42
Q

What is the difference between the elimination half life and the context-sensitive half-time?

A

C-S HT describes the time required for the plasma drug concentration to decrease by 50% after the termination of an infusion

43
Q

As infusion duration increases, the context-sensitive HT _________

A

also increases

44
Q

Fentanyl has a shorter half life than sufentanil, but after a two hour infusion fentanyl has double the context-sensitive HT. Why?

A

Fentanyl is stored in the compartments, so once the plasma concentration is cleared by the kidney, it is re-supplied by fentanyl returning from the periphery

45
Q

What is t1/2ke0?

A

the half time of equilibration between drug concentration in the blood and effect on the target

“lag time”

46
Q

Is t1/2ke0 more important with boluses or drips?

Why?

A

Boluses

Helps determine how far apart boluses should be given, and how big they should be

47
Q

How does a decrease in CO (either iatrogenic or disease related) effect redistribution?

How should that change administration?

A

Redistribution will likely be impaired 2/2 poor perfusion to normal distribution sites.

Give small, well spaced doses. The timing of onset and duration will be increased. Be careful.

48
Q

How does propofol interact with fentanyl?

Versed?

A

with fentanyl: reduces prop needed to suppress pain, but doesn’t effect amount needed for induction

versed: just the opposite

49
Q

What is Cpss50?

A

Mac equivalent for IV drugs

Plasma concentration of a drug at steady state that is required to abolish purposeful movement at skin incision in 50% of patients

50
Q

The effect of giving opiods and benzodiazepines together is not just _______, it is _________

A

additive

synergistic

51
Q

Versed does not have significant respiratory effects alone.

What happens when it’s given with fentanyl?

A

WAAAYYY more respiratory depression/hypoxia/apnea than either of them alone

52
Q

Why is propofol an ideal drug for MAC? (3)

A

context-sensitive HT short even with prolonged infusions

Short effect site equilibration (t1/2ke0)

Low incidence of PONV

53
Q

Propofol is a _____-_____,

while versed is a ________.

A

sedative-hypnotic

sedative

54
Q

How long does flumazenil effectively block benzos?

A

Up to 90 min, then symptoms may recur

55
Q

What are 3 common adverse effects of narcotics?

A
  1. Resp Depression
  2. Muscle rigidity
  3. PONV
56
Q

Are opiods significantly amnestic?

A

Nope

57
Q

Bolus admin of remifentanil is associated with _____ and ______

A

Respiratory depression

chest wall rigidity

58
Q

If respiratory depression develops and the remifentanil drip is decreased, how long will it take before you see a clinical change?

A

3 min

59
Q

What is the most logical mode of remifentanil adminstration during MAC?

A

Constant infusion without boluses

60
Q

Typical IV Dose:

Midazolam

A

1-2 mg prior to prop or remifent

61
Q

Typical IV Dose:

Fentanyl

A

0.5-2 mcg/kg bolus 2-4 min prior to stimulus

62
Q

Typical IV Dose:

Remifentanil

A

0.1 mcg/kg/min

63
Q

What is frequently given with ketamine?

Why?

A

Antisialagogue

Fear of laryngospasm

64
Q

Oral Ketamine

A

4-6 mg/kg

O 20-30 min

D 60-90 min

65
Q

IM Ketamine

A

2-4 mg/kg

O 5-10 min

D 30-120 min

66
Q

IV Ketamine

A

0.25-1 mg/kg increments

O 1-2 min

D 20-60 min

67
Q

Precedex is a _______ agonist that produces _______ and ______

A

Alpha2 receptor

sedation

analgesia

68
Q

Why is precedex useful in patients with OSA?

A

Hypercapnic arousal response remains intact

69
Q

Precedex

Initial Bolus Dose:

Infusion Rate:

A
  1. 5-1 mcg/kg over 10-20 min
  2. 2-0.7 mcg/kg/hr
70
Q

________ has amnestic properties at sub-hypnotic doses. _______ does not.

A

Propofol

Precedex

71
Q

Why does the upper airway collapse during anesthesia?

A

During inspiration, the pressure within the upper airway is subatmospheric, creating a tendency to collapse

In awake patients this is prevented by upper airway dilator muscle tone

72
Q

Why is airway obstruction a problem even when the patient has a normal respiratory drive?

A

The genioglossal mm and its counterparts are WAY more sensitive to sedatives than the diaphragm

73
Q

MAC related adverse respiratory outcomes were overrepresented in which groups?

A

Elderly

ASA 3&4

74
Q

Which MAC drug has a particularly suppressive effect on airway protective reflexes?

A

Propofol

75
Q

A patient is receiving supplemental O2 and has a normal SpO2. Is alveolar ventilation adequate?

A

Impossible to know. Supp O2 can easily mask alveolar hypoventilation

76
Q

What is the leading cause of death and severe injury during MAC?

A

Hypoxia d/t suppresion of spontaneous respiration by sedative-hypnotic drugs

77
Q

What is the second most common cause of injury in MAC?

A

Cautery fires, particularly head and neck

78
Q

How can fires in MAC be prevented?

A
  1. Don’t tent drapes
  2. Keep O2 as low as possible
  3. Use compressed air instead of O2
  4. Stop O2 flow 60 sec before cautery
  5. No alcohol prep
79
Q

Where should a precordial stethoscope be placed?

A

sternal notch

80
Q

When is respiratory depression more likely to be detected during MAC?

A

17.6x more likely to be identified when capnography is used

81
Q

Who is more at risk for hypothermia: MAC or general?

A

Both are at risk. Studies show no difference.

82
Q

Why does regional anesthesia tend to cause hypothermia?

A

Lower extremity vasodilation causes central cooling by moving blood into the periphery

83
Q

Why should you be vigilant if a patient says it’s too hot under the drapes?

A

Feeling of hyperthermia may occur with hypoxia, hypercarbia, cerebral ischemia, local anesthetic toxicity, and MI

84
Q

What are symtoms of low dose local anesthetic toxicity?

A

Sedation

Numbness of the Tongue and circumoral

Metallic taste

85
Q

What are symptoms of high dose local anesthetic toxicity?

A

slurred speech

skeletal mm twitching

restlessness

vertigo

tinnitus

86
Q

What MAC factors can increase local anesthetic toxicity?

A

Hypercarbia

Decrease hepatic blood flow

acidosis

hypoxia

87
Q
A

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