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Apex > Unit 4 Pharmacology: Volatile Anesthetics 2: Pharmacodynamics > Flashcards

Unit 4 Pharmacology: Volatile Anesthetics 2: Pharmacodynamics Flashcards

1
Q

N2O is ____ times more soluble than nitrogen. What does this mean?

A

34 x

For every 1 molecule of nitrogen that leaves a closed space, 34 molecules of N2O enter to take it’s place.

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2
Q

What is the nitrogen blood:gas partition coefficient?

What is the N2O blood:gas partition coefficient?

A

Nitrogen: 0.014
N2O: 0.46

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3
Q

How does N2O affect a compliant airspace? Fixed airspace?

A

Compliant: increase volume
Fixed: increase pressure

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4
Q

What are the compliant airspaces in the body that N2O can affect? At what rate are these affected?

A

Pulmonary blebs - fast equilibration between space and blood
Air bubbles in the blood - fast
Sulfa hexafluoride bubble in the eye - fast
Bowel - slow
Pneumoperitoneum - slow

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5
Q

What are the fixed airspaces that can be affected by N2O? At what speed?

A

Middle ear - fast equilabration between space and blood

Brain during intracranial procedures - fast

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6
Q

Discontinuation of N2O can do what to the ear?

A

Decrease middle ear pressure and result in serous otitis

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7
Q

When must N2O be discontinued if placing an SF6ocular gas bubble? How long should it be avoided?

A

D/C: 15 minutes before the SF6 bubble is placed

Avoid N2O for 7 - 10 days after the bubble is placed

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8
Q

There are 3 alternatives to SF6 for an intraocular bubble, what are they and how long should N2O be avoided?

A

Air: 5 days
Perfluoropropane: 30 days
Silicone oil: no contraindication to N2O

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9
Q

Is N2O flammable?

A

No, but it does suppose combustion

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10
Q

How does N2O affect the volume and pressure in anesthetic equipment?

A

It can increase the volume and pressure in:
ETT cuff
LMA cuff
Balloon-tipped pulmonary artery catheter

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11
Q

What is the deal with N2O and B12?

A

N2O irreversibly inhibits B12, which inhibits methionine synthase (enzyme required for folate metabolism and myelin production).

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12
Q

What are 7 potential side effects of N2O inhibiting B12?

A
  1. Megaloblasic anemia
  2. Neuropathy
  3. Immunocompromise
  4. Impaired DNA synthesis
  5. Concern of teratogenicity - clinical data lacking
  6. Possible risk of spontaneous abortion - many avoid in first 2 trimesters
  7. Homocysteine accumulation
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13
Q

What increases the risk of complications of N2O and B12 inhibition? Examples

A

Prolonged exposure: recreation use

Pre-existing B12 deficiency: pernicious anemia, alcoholism, strict vegan diet

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14
Q

Order the volatile agents from lowest to highest potency (4)

A

N2O
DES
SEVO
ISO

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15
Q

How is the potency of inhalation anesthetic measured?

A

MAC: this is the concentration of agent that prevents the nociceptive withdrawal reflex following a supramaximal painful stimulus is 50% of the population

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16
Q

What is the MAC for a 40 yr old in all 4 agents?

A

ISO: 1.2
SEVO: 2.0
DES: 6.6
N2O: 104

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17
Q

What is the essential triad of anesthetic actions?

What else may VAs do?

A
  1. Amnesia
  2. Loss of consciousness
  3. Immobility

VAs may also modulate autonomic function and provide some analgesia

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18
Q

What suggests that anesthetics exert their effects in different regions of the CNS?

A

The effects are dose dependent, Supra spinal effects (amnesia and LOC) occur at lower levels, while immobility requires a higher concentration

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19
Q

If you add 2 gases together (ie ISO and N2O) what happens to MAC?

A

MAC is additive

0.5 Mac ISO + 0.5 Mac N2O = 1 MAC

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20
Q

Define Mac awake. What is its value?

A

MAC-awake is the alveolar concentration at which a patient opens their eyes
~ 0.4 - 0.5 MAC during induction but as low as 0.15 MAC during recovery

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21
Q

Define MAC-bar? What is its value?

A

MAC-Bar is the alveolar concentration required to block the autonomic response following a supramaximal painful stimulus
~1.5 MAC

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22
Q

At what MAC can movement be prevented in 95% of the population?

A

1.3 MAC

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23
Q

Awareness and recall is generally assumed to be prevented at what MAC?

A

0.4 - 0.5 MAC

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24
Q

List 6 drugs that increase MAC

A 
Chronic alcohol consumption
(Increased CNS neurotranmitters:)
Acute amphetamine intoxication
Acute cocaine intoxication
MAOIs
Ephedrine
Levodopa
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25
Q

List 8 drugs/classes that decrease MAC

A 
Acute alcohol intoxication 
IV anesthetics
N2O
Opioids - IV and neuraxial
Alpha-2 agonists
Lithium
Lidocaine
Hydroxyzine
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26
Q

How does the electrolyte Na affect MAC?

A

Hypernatremia: increases MAC
Hyponatremia: decreases MAC

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27
Q

How does the electrolyte K affect MAC?

A

Hyper- and hypokalemia have no effect on MAC

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28
Q

How does the electrolyte Mg affect MAC?

A

Hyper- and hypomagnesemia have no affect on MAC

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29
Q

How does age affect MAC?

A

MAC is increased in infants from 1 - 6 months of age.
Prematurity decreases MAC.
Older age decreases MAC 6% per decade after the age of 40.

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30
Q

How does body temperature affect MAC?

A

Hyperthermia: increase MAC
Hypothermia: decreases MAC

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31
Q

How does red hair affect MAC? By what %?

A

Increases MAC by 19%

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32
Q

How does BP affect MAC?

A

Hypotension (MAP < 50 mmHg) decreases MAC

Hypertension has no affect on MAC

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33
Q

How does gender affect MAC?

A

No affect

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34
Q

How does thyroid disease affect MAC?

A

No direct effect

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35
Q

How does PaCO2 affect MAC?

A

PaCO2 > 95 mmHg decreases MAC

PaCO2 15 - 95 mmHg has no effect

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36
Q

How does hypoxia affect MAC?

A

Decreases MAC

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37
Q

How does anemia affect MAC?

A

Decreases MAC

<4.3 mL O2/dL blood

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38
Q

How does CPB affect MAC?

A

Decreases MAC

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39
Q

How does metabolic acidosis affect MAC?

A

Decreases MAC

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40
Q

How does Hypo-osmolarity affect MAC?

A

Decreases MAC

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41
Q

How does pregnancy affect MAC?

A

Pregnancy through 24-72 hours postpartum decreases MAC

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42
Q

They Meyer-Overton rule states:

A

Lipid solubility is directly proportional to the potency of an inhalation anesthetic

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43
Q

What is the Unitary hypothesis?

A

States that all anesthetics share a similar mechanism of action, but each may work at a different site

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44
Q

General anesthesia is produced by ________ in the _____ & ________.

A

Membrane bound protein interactions
Brain
Spinal cord

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45
Q

As a general rule the volatile anesthetics have what 2 effects on their target receptors?

A
  1. They stimulate inhibitory receptors

2. They inhibit stimulators receptors

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46
Q

What 3 inhibitory pathways are stimulated by VAs?

A

GABA-A receptors
Glycine channels
Potassium channels

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47
Q

What 4 stimulators pathways are inhibited by VAs?

A

NMDA receptors
Nicotinic receptors
Sodium channels
Dendritic spine function and motility

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48
Q

In the brain what is the most important site of volatile anesthetic action?

A

GABA-A receptor

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49
Q

The GABA-A receptor is what type of receptor?

A

Ligand gated chloride channel

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50
Q

Stimulation of the GABA-A receptor does what?

A

Increases chloride influx and hyperpolarizes neurons impairing their ability to fire.
They likely increase the duration the chloride channel remains open.

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51
Q

In the spinal cord where do VAs produce immobility?

A

In the ventral horn

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52
Q

What are the most important sites of VA action in the spinal cord (3)?

A

Glycine receptor stimulation
NMDA receptor inhibition
Na+ channel inhibition

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53
Q

Where is the site of action for gaseous anesthetics (N2O and Xenon)? (2)

A

NMDA antagonism
Potassium 2P-channel stimulation

They do not stimulate GABA-A receptor

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54
Q

What is the essential triad of general anesthesia?

A

Unconsciousness
Amnesia
Immobility

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55
Q

VAs causes unconsciousness in what 3 sites of action?

A

Cerebral cortex
Thalamus
Reticular Activating system

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56
Q

VAs cause amnesia in what 2 sites of action?

A

Amygdala

Hippocampus

57
Q

VAs cause immobility in what site of action?

A

Ventral horn

58
Q

VAs cause analgesia in what site of action?

A

Spinothalmic tract

59
Q

VAs cause autonomic modulation in what 2 sites of action?

A

Pons

Medulla

60
Q

In cardiac muscle and vascular smooth muscle, VAs decrease what ions influx?

A

Ca+2 - through the sarcolemma and reduce Ca+2 release from the sarcoplasmic reticulum

61
Q

How do halogenated agents affect BP? How?

A

Decrease MAP in a dose dependent fashion.
Primary cause: decreases intracellular Ca+2 in vascular smooth muscle -> systemic vasodilation -> decreased SVR and venous return
Secondary cause: decreases intracellular Ca+2 in the cardiac myocyte -> myocardial depression -> decreased inotropy

62
Q

How does N2O affect BP?

A

No change / possible increase
Hemodynamic effects can be explained by SNS activation. N2O + VA causes less BPP reduction when compared to the MAC equivalent of VA alone

63
Q

How do halogenated agents affect HR?

A

They directly affect cardiac conduction in a dose dependent fashion.

  • decrease SA node automaticity
  • decrease conduction velocity though AV node, His-purkinje system, and ventricular conduction pathways
  • increase duration of myocardial repolarization by impairing the outward K+ current, this increases action potential duration and prolongs the QT interval
  • altered baroreceptor function
64
Q

Do all of the halogenated agents increase HR? How much does it increase and why?

A

No. SEVO does not cause tachycardia.
DES and ISO increase HR from baseline by 5-10%. Most likely due to respiratory irritation. -> SNS activation -> increase NE release -> beta 1 stimulation

65
Q

How can the tachycardia from VAs be minimized/abolished?

A

It can be minimized by not abolished.

Opioids, alpha-2 agonists, beta-1 antagonists

66
Q

How does N2O affect HR?

A

N2O activates the SNS and increases HR

67
Q

How is contractility affected by halogenated agents?

A

There is a small decrease in baseline contractility, however the myocardium remains preload responsive.
Myocardial depression is dose dependent.

68
Q

N2O + _____ can cause myocardial depression

69
Q

How do VAs affect SVR?

A

Decrease.

Decreases intracellular Ca+2 in vascular smooth muscle -> systemic vasodilation -> decreased SVR

70
Q

Which VA causes the least reduction in SVR?

71
Q

How does N2O affect SVR?

72
Q

How do VAs affect coronary vascular resistance?

A

VAs increase coronary blood flow in excess of myocardial oxygen demand. They preferentially dilate the small cardiac vessels

73
Q

List the 3 VAs in order of potency of coronary artery vasodilation from greatest to least:

A

ISO > DES > SEVO

74
Q

What is the hearts oxygen extraction % ?

75
Q

As myocardial demand increases, health vessels dilate, the heart cannot significantly increase its )O2extraction ratio, so what does the heart do?

A

It increases its own blood flow to satisfy its O2 requirement.

76
Q

What is coronary steal?

A

Diseased coronary vessels are not able to dilate much more, so health ones do and blood flow is preferentially directed to healthy tissue

77
Q

Which VA is link to Coronary Steal, though current thinking is that this doesn’t really contribute to steal?

78
Q

The central chemoreceptors in the medulla monitor what value to determine minute ventilation?

79
Q

Every 1 mmHg in PaCO2 above baseline changes minute ventilation how?

A

Increases minute ventilation by 3 L/min

80
Q

What are VA pulmonary effects?

A

Dose dependent depression of the central chemoreceptors and the respiratory muscles

81
Q

What are the 3 mechanism by which VA contribute to hypercarbia?

A
  1. Altering the respiratory pattern
  2. Impair the response to CO2
  3. Impair motor neuron output and muscle tone to upper airway and thoracic muscles
82
Q

How do VAs alter the respiratory pattern?

A

Decrease Vt

Increase RR partially compensates fo the reduction in Vt, although not enough to prevent a rise is PaCO2

83
Q

What happens to the CO2 response curve with VAs?

A

It shifts down and to the right

84
Q

What other effect occurs when VAs impair the response to CO2?

A

Apneic threshold is increased: the PaCO2 at which a patient is stimulated to breathe.

85
Q

Where is the apneic threshold usually?

A

3 - 5 mmHg below the PaCO maintained during spontaneous ventilation

86
Q

What is the significance of the apneic threshold when considering assisted ventilation?

A

If ventilation is assisted to below the apneic threshold, the patient simply will not breathe. To reduce PaCO2 further one would need controlled ventilation.

87
Q

What does a right shift of the CO2 response curve imply? What does this create?

A

That for a given PaCO2 the minutes ventilation would be less than predicted?
This creates respiratory acidosis.

88
Q

What does a left shift of the CO2 response curve imply? What does this create?

A

That for a given PaCO2 the minute ventilation would be more than predicted.
This creates a respiratory alkalosis

89
Q

List 4 causes of a right shift of the CO2 response curve:

A 
(Depresses ventilation)
General anesthetics 
Opioids
Metabolism alkalosis 
Denervation of peripheral chemoreceptors
90
Q

List 7 causes of a left shift of the CO2 response curve:

A 
(Stimulates ventilation)
Anxiety
Surgical stimulation
Metabolic acidosis
Increased ICP
Salicylates
Aminophylline 
Doxapram
91
Q

Impairment of genioflossus or tensor palatine leads to what?

A

These are airway dilator muscles, impairment would lead to upper airway obstruction

92
Q

Impairment of the pulmonary muscles decreases _____ and the effectiveness of ______

A

FRC

ventilation

93
Q

What effect on the bronchi do halogenated agents have? What is the relationship with airway resistance?

A

Bronchodilation.

In the absence of increased airway resistance the effect is minimal.

94
Q

Which VA impairs the hypoxic ventilatory response the LEAST?

A

Desflurane

95
Q

Where is PaO2 monitored in the body?

A

Peripheral chemoreceptors in the carotid bodies monitor for hypoxemia and are important in the the hypoxic ventilatory drive, also in the aortic bodies

96
Q

The carotid bodies relay afferent input to the respiratory center via what nerve?

A

Glossopharyngeal nerve - CN IX

97
Q

The aortic bodies relay afferent traffic via what nerve?

A

The vagus nerve - CN X

98
Q

The carotid bodies are more sensitive to change is what?

Whereas the aortic bodies are more sensitive to changes in what?

A

Carotid bodies: changes in arterial gas tensions (PaO2, PaCO2) and H+ concentration
Aortic bodies: changes in BP

99
Q

VAs also depress ventilation by inhibiting muscles in the: (3)

A

Upper airway
Diaphragm
Intercostals

100
Q

How long after anesthesia are the peripheral chemoreceptors impaired after VAs?

A

Up to several hours after anesthesia

101
Q

The impaired response to acute hypoxia occurs at what MAC? But what does this NOT occur?

A

0.1 MAC

Response to PaCO2

102
Q

What cells in the carotid bodies provide the sensory arm of the hypoxic drive? Why are these important?

A

Glomus type I cells

It is hypothesized that VAs create a reactive oxygen species that impairs the Glomus type I cells

103
Q

Metabolism is the source of the reactive oxygen species that impairs the glomus type I cells, so those agents that undergo the ______ amount of biotransformation in the body inhibit the hypoxic drive the most. List the VA in the greatest to least hypoxic drive impairment.

A

Greatest.

SEVO > ISO > DES

104
Q

Does N2O impair the carotid bodies response to hypoxemia?

A

Yes, but likely for a different reason

105
Q

What type of patients is impairment of the hypoxic drive especially important?

A

This who rely on the hypoxic drive to breathe: emphysema, sleep apnea

106
Q

Do pain and surgical stimulation reverse the depression of the hypoxic ventilatory drive caused by VAs?

107
Q

What affect do VAs have on cerebral metabolic rate? (CMRO2)

A

VAs reduce CMRO2, but only to the extent that they reduce electrical activity, once isoelectric they can not reduce CMRO2 further.

108
Q

What MAC is required to produce isoelectric state?

A

1.5 - 2.0 MAC

109
Q

What 2 things is CMRO2 dependent on?

A
  1. Electrical activity - 60%

2. Cellular homeostasis - 40%

110
Q

SEVO at what MAC can produce seizure activity? What exacerbates this? Where is it more common?

A

2.0 MAC
Hypocapnia
Pediatric inhalation induction

111
Q

How does the brain match blood flow with metabolic requirement?

A

When metabolic demand increases, the blood vessels dilate - cerebrovascular resistance decreases.
When metabolic demand decreases, the blood vessels constrict - CVR increases.

112
Q

How do VAs affect cerebral vessel tone?

A

VAs are cerebral vasodilators, the decrease CVR

113
Q

What 2 competing factors occur in the cerebral vessels when using VAs? What is the net effect?

A

Vasoconstriction from the reduction in CMROs and vasodilation from the anesthetic agent.
The net effect is a dose dependent increase in CBF, cerebral blood volume, and ICP

114
Q

What 4 techniques can be used to partially offset the vasodilators effect of VAs?

A

Mild hyperventilation and/or concurrent administration of propofol, opioids, or barbiturates

115
Q

What affect does N2O have on CMRO2? Cerebral blood flow?

A

N2O increases CMRO2 and cerebral blood flow

116
Q

What is the equation for cerebral perfusion pressure?

A

CPP = DBP - LVEDP (or PAOP)

117
Q

What is cerebral autogregulation? What is its normal value?

A

Cerebral vasculature continuously adjusts vessel diameter to maintain a constant cerebral blood flow.
CPP: 50 -150 mmHg

118
Q

How do VAs affect cerebral autoregulation?

A

VAs disrupt cerebral autoregulation in a dose dependent fashion, CBF becomes increasingly dependent on blood pressure as the concentration of VA is increased.

119
Q

How do VAs affect CSF volume? (Production and absorption)

A

ISO: no effect on production, increases absorption

DES: increases/no effect on production, no effect on absorption

SEVO: decreases production, unknown about absorption

120
Q

The tendency of the VAs to affect CSF dynamics is greatly overshadowed by their ability to increase ______.

121
Q

What are evoked potentials used to monitor?

A

The integrity of neural pathways.

122
Q

What are the 4 types of EPs?

A

Somatosensory (SSEP)
Motor (MEP)
Visual (VEP)
Brainstem auditory (BAEP)

123
Q

What do SSEPs monitor?

A

The integrity of the dorsal column (medial lemniscus)

124
Q

What perfuses the dorsal column of the spinal cord?

A

Posterior spinal arteries

125
Q

What do MEPs monitor?

A

Integrity of the corticospinal tract

126
Q

What perfuses the corticospinal tract?

A

Anterior spinal artery

127
Q

Are SSEPs and MEP interchangable?

A

No. SSEPs do not monitor the anterior cord

128
Q

What are the 2 important components of EPs?

A

Amplitude - strength of nerve response

Latency - speed of nerve conduction

129
Q

VAs affect EPs by doing what to amplitude and latency? What affect does adding N2O have?

A

Decreasing amplitude and increasing latency.

N2O makes this worse

130
Q

Losing an EP signal, or recording a diminished response suggests what?

A

Ischemia to the neural pathway being monitored.

131
Q

As a general rule, you should be concerned about nerve ischemia when what occurs with amplitude and latency, and by how much?

A

Amplitude decreases by 50% or more

Latency increases by 10% or more

132
Q

What are 3 other confounding factors that affect amplitude and latency besides VAs?

A

Hypoxia
Hypercarbia
Hypothermia

133
Q

What is the best anesthetic technique to preserve EPs?

A

TIVA without N2O

134
Q

If you do use a VA while trying to monitor EPs, what is the recommended MAC to use and technique?

A

0.5 MAC or less

Supplement with IV agents - propofol, opioid

135
Q

During MEP monitoring what drug(s) should be avoided?

A

NMB - short acting is ok for induction

136
Q

What IV agent enhances the EP signals?

137
Q

What EPs are most resistant to the effects of anesthetics? Can any technique be used then?

A

BAEPs

Yes, any technique can be used.

138
Q

What EPs are the most sensitive to the effects of anesthetic agents?

139
Q

If EP signal dismisses or goes away during surgery, what are anesthetic goals to improve neural tissue perfusion?

A

Increase BP, volume expansion, transfusion (if anemic). Normalizing gas tensions may also help.

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