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Neuroscience > Neuroscience Week 3: Anesthetics > Flashcards

Neuroscience Week 3: Anesthetics Flashcards

1
Q

Be able to explain the stages of inhalational anesthesia and the pharmacokinetics of inhaled anesthetics (alveolar wash-in, uptake from the lungs, solubility in blood, tissue uptake, and elimination), including the concept of minimum alveolar concentration.

A
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2
Q

Be able to describe the mechanisms of action (including analgesic properties) and organ system effects (including effects on intracranial pressure) of inhaled and intravenous anesthetics, the uses of these agents and their adverse effects, including malignant hyperthermia and its treatment.

A
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3
Q

Be able to list the key differences between amide and ester local anesthetics, as well as to explain in detail the mechanism of action of local anesthetics, the influence of pH on their actions, which nerve fibers are more or less sensitive to them (e.g., small unmyelinated fibers are the most sensitive to block), their uses and adverse effects.

A
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4
Q

Balanced Anesthesia Definition

A

Combination of inhaled anesthetics and IV medications

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5
Q

Monitored Anesthesia Definition

A

Oral or parenteral sedatives + local anesthetics

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6
Q

Conscious Sedation Definition

A

Alleviation of anxiety and pain + altered levels of consciousness produced by small doses of sedatives (in ICU, neuromuscular blockers may be also used)

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7
Q

Deep Sedation Definition

A

Light state of anesthesia (also used in ICU)

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8
Q

Depth of Anesthesia: Stage I

A

Analgesia and subsequent amnesia.

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9
Q

Depth of Anesthesia: Stage II

A

Excitement

  • delirium, combative behavior, increase in blood pressure and respiratory rate. To avoid, a shortacting I.V. anesthetic is given before.
  • in part due to inhibition of the function of inhibitory neurons in the brain, excitatory neurons are disinhibited
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10
Q

Depth of Anesthesia: Stage III

A

Surgical Anesthesia

regular respiration, skeletal muscle relaxation, decrease in eye reflexes and movements, fixed pupils. Loss of motor and autonomic responses to pain.

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11
Q

Depth of Anesthesia: Stage IV

A

Medullary Paralysis

depression of respiratory and vasomotor centers. can be followed by Death.

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12
Q

Neuron type sensitivity to anesthesia

A
  1. Dorsal horn = analgesia
  2. Frontal cortex = sedation
  3. Thalamic neurons and midbrain reticular formation = hypnosis
  4. Ventral horn = immobility
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13
Q

MAC

A
  • Potency of anesthetics is measured in minimum alveolar concentrations
  • Potency is an expression of the activity of a drug in terms of the concentration or amount of the drug required to produce a defined effect,
  • Efficacy. maximum effect that a drug can produce regardless of dose

In these examples NO is least potent and Isoflurane is the most potent example given on this slide

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14
Q

1 MAC

A

Alveolar concentration of anesthetic that renders immobile 50% of subjects exposed to a strong noxious stimulation

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15
Q

MAC examples

A
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16
Q

0.3 MAC

A

Analgesia

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17
Q

0.5 MAC

A

Amnesia

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18
Q

1.0 MAC

A

50% immobile

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19
Q

1.2 MAC

A

Sympathetically-mediated response to surgery is blunted

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20
Q

1.3 MAC

A

99% immobile

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21
Q

>/= 2.0 MAC

A

Potentially lethal

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22
Q

Most common Inhalational Anesthetics

A
  • Sevoflurane (Volatile)
  • Desflurane (Volatile)
  • Isoflurane (Volatile)
  • Nitrous Oxide (Gaseous)
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23
Q

Most common Intravenous Anesthetics

7 listed

A
  • Benzodiazepines (Midazolam)
  • Opioids (Fentanyl)
  • Barbiturates (Thiopental)
  • Propofol
  • Ketamine
  • Etomidate
  • Dexmedetomidine
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24
Q

Pharmacokinetics of anesthesia

A

*higher the ventilatory rate/depth = shorter induction time

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25
Q

Blood solubility of anesthesia

A
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26
Q

Anesthetic type high arterial pressures are reached rapidly and shorter induction time

A

with an anesthetic w/ Low blood solubility

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27
Q

Anesthetics Tissue Uptake

A

also remember Meyer-Overton rule

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28
Q

Meyer-Overton rule

A

the higher the lipid solubility the more potent the anesthetic

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29
Q

Anesthetic Elimination

A

clearance by the lungs is the main elimination route

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30
Q

the rate of recovey from anesthesia depends on

A

the rate of elimination of the brain

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31
Q

bronchospasm and anesthesia

A

avoid pungent agents in patients with bronchospasm

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32
Q

malignant hyperthermia

A
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33
Q

Malignant Hyperthermia Etiology

A
  • Autosomal dominant genetic disorder
  • Caused by mutations of muscle ryanodine receptor that are activated by inhaled anesthetics, leading to uncontrolled release of Ca2+ from the sarcoplasmic reticulum
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34
Q

Malignant Hyperthermia Clinical Presentation

A

Characterized by tachycardia, hypertension, severe muscle rigidity, hyperthermia, hyperkalemia and acidosis

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35
Q

Common when volatile anesthetics are combined with succinylcholine

A

Malignant hyperthermia

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36
Q

Malignant Hyperthermia common anesthesia cause

A

Common when volatile anesthetics are combined with succinylcholine

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37
Q

Malignant Hyperthermia Treatment

A
  • Treatment = dantrolene (blocks Ca2+ release via ryanodine receptor);
  • cooling;
  • oxygen;
  • correction of acid-base disturbances.
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38
Q

Example of Antagonist of Ryanodine Receptor

A

Dantrolene

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39
Q

How are different classes of anesthesia used in Balanced Anesthesia

A
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40
Q

Balanced Anesthesia Premedication

A

Midazolam (I.V. Benzodiazepine)

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41
Q

Balanced Anesthesia Induction reagents

A

Fentanyl IV opioid

Propofol IV anesthetic

Curare-like neuromuscular blocker (nondepolarizing blocker) (Pancuronium)

Tracheal intubation

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42
Q

Balanced Anesthesia Maintenance Reagents

A

Inhalational anesthetics

Sevoflurane 1-2% + Nitrous Oxide 66%

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43
Q

TIVA AKA

A

Total intravenous Anesthesia

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44
Q

Total Intravenous Anesthesia Premedication

A

Midazolam IV benzo

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45
Q

Total Intravenous Anesthesia Induction Reagents

A
  • Remifentanil (loading dose)
  • Propofol
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46
Q

Total Intravenous Anesthesia NMJ Blockade reagents

A

Rocuronium

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47
Q

Total Intravenous Anesthesia Maintenance Reagents

A
  • Remifentanil
  • Propofol
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48
Q

Total Intravenous Anesthesia complete procedure and reagents

A
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49
Q

After what reagent is a patient intubated?

A

NMJ Blockers

Rocuronium TIVA

Pancuronium Balanced Anesthesia

(Curare-like)

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50
Q

for what procedures can IV anesthetics used for?

A
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51
Q

Volatiles Mech. of Action

A

↑GABAAR, ↓NMDAR & CNS nAChRs

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52
Q

*N2O Mech. of Action

A

↑GABAAR, ↓NMDAR,

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53
Q

Midazolam Mech. of Action

A

↑ GABAAR

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54
Q

*Fentanyl Mech. of Action

A

R ↑ Opioid Rs

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55
Q

Thiopental Mech. of Action

A

↑ GABAAR

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56
Q

Propofol Mech. of Action

A

↑ GABAAR

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57
Q

Etomid. Mech. of Action

A

↑ GABAAR

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58
Q

Ketamine Mech. of Action

A

↓NMDAR

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59
Q

Dexmet Mech. of Action

A

α2 -adrenoceptor agonist

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60
Q

Volatiles Cardiovascular

A
  • ↓Peripheral resistance
  • ↓Myocardial O2 consumption
  • Dilate coronaries
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61
Q

N2O Cardiovascular

A

↓Myocardial function

↑Sympathetic (effects cancel out-minimal effect)

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62
Q

Midazolam Cardiovascular

A

↓Peripheral resistance

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63
Q

Fentanyl Cardiovascular

A

↓Heart rate

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64
Q

Thiopental Cardiovascular

A

↓Peripheral resistance and myocardial contractility

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65
Q

Propofol Cardiovascular

A

↓Peripheral resistance

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66
Q

Etomidate Cardiovascular

A

Stability

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67
Q

Ketamine Cardiovascular

A

↑Peripheral resistance and heart rate

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68
Q

Dexmedetomidine Cardiovascular

A

↓Peripheral resistance and heart rate

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69
Q

Volatiles Respiratory

A
  • Depression.
  • ↓Response to hypoxia.
  • ↓Mucociliary.
  • Bronchodilation
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70
Q

N2O Respiratory

A
  • Diffusional hypoxia.
  • Diffuse into cavities (pneumothorax; also bowel loop).

can lead to increased pressure of the thorax or intestines

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71
Q

Midazolam Respiratory

A

Depression (particularly when given with opioids)

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72
Q

Fentanyl Respiratory

A
  • Depression.
  • ↓Response to hypoxia.
  • Chest wall and laryngeal rigidity.
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73
Q

Thiopental Respiratory

A

Depression.

↓Response to hypoxia.

74
Q

Propofol Respiratory

A

Depression.

↓Response to hypoxia.

75
Q

Etomidate Respiratory

A

Less pronounced depression.

76
Q

Ketamine Respiratory

A

Stable but laryngospasm can occur

77
Q

Dexmet Respiratory

A

Little effect

78
Q

Volatiles GI

A

Nausea/vomiting

79
Q

N2O GI

A

Nausea/vomiting

80
Q

Midazolam GI

A

N/A

81
Q

Fentanyl GI

A

Nausea Constipation

82
Q

Thiopental GI

A

Nausea/ vomiting

83
Q

Propofol GI

A

Antiemetic

84
Q

Etomidate GI

A

N/A

85
Q

Ketamine GI

A

N/A

86
Q

Dexmedetomidine GI

A

N/A

87
Q

Volatiles CNS

A
  • ↓Metabolic rate
  • ↑Cerebral blood flow and intracranial pressure
    *
88
Q

N2O CNS

A

↑Cerebral blood flow and intracranial pressure via sympathetic

89
Q

Midazolam CNS

A

N/A

90
Q

Fentanyl CNS

A

↑ intracranial pressure in head trauma patients

91
Q

Thiopental CNS

A
  • ↓Metabolic rate
  • ↓Cerebral blood flow & intracranial pressure
  • decreases metabolic rate and decreases cerebral blood flow and intracranial pressure which can be neuroprotective
92
Q

Propofol CNS

A

↓Metabolic rate.

↓Cerebral blood flow & intracranial pressure.

93
Q

Etomidate CNS

A

↓Metabolic rate.

↓Cerebral blood flow & intracranial pressure.

94
Q

Ketamine CNS

A

↑Metabolic rate.

↑Cerebral blood flow & intracranial pressure.

95
Q

Dexmedetomidine CNS

A

↓Cerebral blood flow but little effect on intracranial pressure

96
Q

Volatiles Liver/ Kidneys

A

↓blood flow

97
Q

N2O Liver/ Kidneys

A

↓blood flow

98
Q

Midazolam Liver/ Kidneys

A

Failure slows elimination

99
Q

Fentanyl Liver/ Kidneys

A

Caution in liver failure

100
Q

Thiopental Liver/ Kidneys

A

N/A

101
Q

Propofol Liver/ Kidneys

A

N/A

102
Q

Propofol Liver/ Kidneys

A

Failure slows elimination

103
Q

Etomidate Liver/ Kidneys

A

(Adrenocortical suppression)

104
Q

Ketamine Liver/ Kidneys

A

N/A

105
Q

Dexmet Liver/ Kidneys

A

N/A

106
Q

Volatiles Uterus

A
  • ↓contraction
  • can be useful if you need to do an emergency C-section
107
Q

Anesthetics that increase intracranial pressure

A

have to be careful with patients with intracranial injuries

108
Q

decreases metabolic rate and decreases cerebral blood flow and intracranial pressure which can be neuroprotective

A
  • Thiopental
  • Propofol
  • Etomidate

DONT use Ketamine because it does the opposite

109
Q

Local Anesthetic classes

A

Esters (1 I)

Amides (2 I’s)

110
Q

Esters

A
111
Q

Amides

A
112
Q

Esters Medium Duration

A

Cocaine

113
Q

Amides Medium Duration

A

Lidocaine

114
Q

Esters Short Duration

A

Procaine

115
Q

Esters Long Duration

A

Tetracaine (2 a’s)

116
Q

Amides Long Duration

A

Bupivacaine (2 a’s)

117
Q

Local anesthetics lipophilic

A

Lipophilic agents are more potent and longer lasting for esters and amides alike

118
Q

Esters Metabolism

A

Hydrolized plasma esterases

119
Q

Amides Vs Esters

A

Amides are longer lasting

120
Q

Local Anesthetics Mechanism of Action

A
  • Mechanism of Action: open channel blockers of voltage-gated sodium channels
  • Local anesthetics block from the inside when channel is open; fibers with high firing frequency are blocked first (i.e. pain fibers)
  • Decrease action potential propagation. Cause nerve conduction to fail.
121
Q

Local Anesthetics are dependent upon?

A

pH

only the uncharged base can cross the membrane

the charged form will go and blocks the channel from the inside

122
Q

Local Anesthetics and Henderson Haselbach EQ

A
123
Q

Local Anesthetics Caveats

A

REMEMBER!!!!!!!!!!

In general, smaller fibers are blocked more easily than larger fibers, and myelinated fibers are blocked more easily than unmyelinated fibers.

  • Activated pain fibers fire rapidly; thus, pain sensation appears to be selectively blocked by local anesthetics.
  • Fibers located in the periphery of a thick nerve bundle are blocked sooner than those in the core because they are exposed earlier to higher concentrations of the anesthetic.

Order of blockade: Pain (fibers have high firing rate and long action potentials) →Other sensations → Motor

124
Q

Concurent injection of ________ with local anesthetics

A

Epinephrine

It causes vasoconstriction via activation of α1 adrenergic receptors, decreasing removal of the local anesthetic via absorption into circulation. This increases duration of the local anesthetic’s effect

  1. It activates presynaptic α2 adrenergic receptors, decreasing release of pain mediators such as Substance P
  2. It provides local bleeding control (vasoconstriction)
125
Q

Adverse Effects of Local Anesthetics

A

Restlessness and tremor. At high doses: convulsions (pre-medicate with benzodiazepine but could mask serious reactions), respiratory depression.

Neurotoxic injury. • Transient neurological symptoms (transient pain or dysesthesia) has been linked to lidocaine in spinal anesthesia.

Allergy - Especially, ester-type local anesthetics (very important)

126
Q

Cardiovascular Adverse Effects of Local Anesthetics

A

Lipid Emulsion can act as a sink and remove and sequester anesthetics

127
Q

Local Anesthetics Overview Table

A
128
Q

Question 1

A
129
Q

Question 2

A
130
Q

Question 3

A
131
Q

Question 4

A
132
Q

Question 5

A
133
Q

Question 6

A
134
Q

Question 7

A
135
Q

Question 8

A
136
Q

Question 9

A
137
Q

Question 10

A
138
Q

Question 11

A
139
Q

Question 12

A
140
Q

Question 13

A
141
Q

Question 14

A
142
Q

Question 15

A
143
Q

Question 16

A
144
Q

MAC to %anesthetic

A

1 MAC = 100% N2O so .3 MAC = 30% N2O

1 MAC = 1.4% Isoflurane so .3 MAC = .42% Isoflurane

145
Q

Alveolar Wash-in

A

↑Ventilatory rate/depth = shorter time to exchange lung gases with anesthetic mixture

increase the concentration and increase the depth of ventilation

146
Q

If you need to anesthetize quickly choose?

A

an anesthetic with a low blood solubility because high arterial pressures are reached rapidly and shorter induction

147
Q

Which tissues absorb Anesthetic most quickly

A
  • highly perfused tissues rapidly achieve a steady-state with the partial pressures in blood
  • muscles accumulate anesthetics more slowly due to lower perfusion rates and larger volume
  • Adipose tissue accumulates anesthetics more slowly due to lower perfusion rates but most anesthetics have high lipid solubility (patient will recover from anesthesia less quickly)
148
Q

the higher the lipid solubility of the anesthetic the more _______ is

A

Potency

so

the

lower

the

MAC

Potency is inversely related to MAC

149
Q

Major route of anesthetic clearance from the body

A

unchanged by the lungs

150
Q

Avoid pungent anesthetics in patients with

A

Bronchospasm

151
Q

Pungent

A

Very strong odor but sensitive

152
Q

Ach Antagonist Malignant Hypothermia

A

wont work because the Ca2+ release is from inside the cell

153
Q

Opioids

A

larynx rigidty preventing intubation, tracheostomy , naloxone antidote!

154
Q

Benzodiazepines

A
155
Q

Barbiturate anesthetics: Thiopental

A

rapid ultra short-acting

156
Q

Propofol

A

milk of amnesia

antiemetic (postoperative vomiting is uncommon)

157
Q

Propofol intracranial pressure

A

↓Intracranial pressure

158
Q

Propofol analgesic properties

A

not a good analgesic

159
Q

Ketamine

A
160
Q

Only IV anesthetic that produces cardiovascular stimulation (increases heart rate and cardiac output)

A

Ketamine

161
Q

Ketamine analgesic properties

A

good analgesic

162
Q

Ketamine respiratory effects

A

minimal effects on respiration

upper airway reflexes

163
Q

Don’t give ketamine to patients with?

A

patients with cardiovascular issues or vascular issues stroke, psychosis or schizophrenia

164
Q

Etomidate

A
165
Q

Etomidate Caveat

A

can use in anesthetic induction in patients at risk of hypotension because it produces minimal cardiovascular and respiratory depression

166
Q

Etomidate Side effects

A
  • Vomiting
  • pain on injection
  • Myoclonus
  • Decreases plasma levels of hydrocortisone
167
Q

Dexmedetomidine

A

used for short term sedation of intubated and ventilated ICU patients or during regional anesthesia

168
Q

For an opiod tolerant patient what type of anesthesia

A

propofol perhaps

169
Q

Two Is

A

Amide Local anesthetics

170
Q

Two As

A

long-acting local anesthetic

171
Q

How to treat arrhythymias from local anesthetics

A

lipid resuscitation

172
Q

pH has a major effect on?

A

Local anesthetic effect

173
Q

If patient has liver problems would an amide be appropriate

A

maybe not or decrease the dose

because amides are metabolized in the liver

174
Q

where do local anesthetics have their therapeutic effect

A

on the internal Na+ channels

175
Q

pH can block local anesthetics where?

A

intra and extracellularly because if it is charged it cannot get in

if it is not charged inside the cell then it cannot block the channel

176
Q

Actions of local anesthetics

A
177
Q

Why do you coinject with epinephrine

A

1 is extremely important

178
Q

aspirate before

A

putting in a local anesthetic

179
Q

Pre-medicate with ____________ to prevent convulsions but it could mask serious reactions

A

benzodiazepines

180
Q

Adverse effects of local anesthetics

A

IV Lipid Emulsion

181
Q

lidocaine is used to treat _____

A

ventricular arythmias maybe

Neuroscience (96 decks)

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