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Pharmacology of Anesthesia > Volatile Anesthetics > Flashcards

Volatile Anesthetics Flashcards

0
Q

Theories of Inhaled Anesthetics: Explain the Meyer-Overton correlation

A
  • Chemically indifferent substances that are soluble in fat are anesthetics
  • The relative potency of inhaled anesthetics depends on their fat/water partition coefficient
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1
Q

How do the volatile anesthetics work?

A
  • We don’t really know!
  • We believe that they enhance the inhibitory effects more than they put a damper on the excitatory effects
  • Some how prevent normal neuronal signals from firing
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2
Q

Theories of Inhaled Anesthetics: Explain the Unitary Theory-

A
  • Cell membranes are mostly lipid, so the majority of anesthetic effects must come from the effects on the cell membranes
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3
Q

What is the concept of MAC?

A
  • MAC (minimum alveolar concentration): the concentration in non-paralyzed patients where 50% would not respond to surgical stimulation
  • Universal measure for inhaled anesthetic potency
  • MAC is analogous to plasma EC50
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4
Q

Who developed the concept of MAC?

A

Dr. Eger

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5
Q

1 MAC of any agent refers to?

A
  • Same thing for all agents, it’s a level of anesthesia at which 50% of the patients will not move upon surgical incision
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6
Q

Theories of Inhaled Anesthetics: Explain the Protein Centered Theory-

A
  • Signaling proteins (ion channels and receptors) are the molecular site of action
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7
Q

What is the effect of inhaled anesthetics on action potentials of the nervous system?

A
  • Small reduction in amplitude
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8
Q

What is the effect of inhaled anesthetics on action potentials of the cardiovascular system?

A
  • Reduced amplitude and duration
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9
Q

Inhaled anesthetics enhance inhibitory NT release and effects at what receptors?

A

Glycine, GABA receptors

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10
Q

Inhaled anesthetics decrease excitatory NT release and effects at what receptors?

A
  • Na channels, K2P channels, NMDA receptors, nicotinic acetylcholine receptors
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11
Q

What are the effects of inhaled anesthetics on the neocortex, hippocampus, amygdala?

A
  • Sedation, amnesia
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12
Q

What are the effects of inhaled anesthetics on the diencephalon (thalamus), brainstem (reticular formation)?

A
  • Unconsciousness
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13
Q

What are the effects of inhaled anesthetics on the spinal cord?

A
  • Immobility
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14
Q

What are the effects of inhaled anesthetics on the myocardium of the cardiovascular system?

A
  • Negative Inotropy through the excitation-contraction coupling
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15
Q

What are the effects of inhaled anesthetics on the conduction system of the cardiovascular system?

A
  • Dysrhythmias by targeting the reducing amplitude and duration of action potentials
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16
Q

What are the effects of inhaled anesthetics on the vasculature of the cardiovascular system?

A
  • Vasodilation through direct and indirect vasoregulation
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17
Q

Inhaled anesthetics hyperpolarize neurons to decrease what?

A
  • Neuronal Excitability, determined by resting membrane potential, threshold potential, and input resistance
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18
Q

What are the presynaptic effects of inhaled anesthetics?

A

They alter neurotransmitter release

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19
Q

What are the postsynaptic effects of inhaled anesthetics?

A

They affect neurotransmitter responses

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20
Q

General anesthetics act by binding directly to ______?

A
  • Amphiphilic cavities in proteins
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21
Q

The effects of inhaled anesthetics cannot be explained by a single molecular mechanism. Rather….?

A
  • Multiple targets contribute to the effects of each agent
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22
Q

The immobilizing effect of inhaled anesthetics involves a site of action in the ________?

A
  • Spinal Cord
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23
Q

The sedation/hypnosis and amnesia effects of inhaled anesthetics involve _______?

A
  • Supraspinal mechanisms
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24
Q

The immobility effect of inhalation agents is probably mediated by?

A
  • Spinal cord NMDA receptors
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25
Q

The immobility effect of inhaled anesthetics requires _____?

A
  • 2.5-4X MAC needed to produce amnesia and unconsciousness
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26
Q

The unconsciousness effects of inhalation anesthetics is caused by ____?

A
  • The hyperpolarization of thalamic sites, probably more of a dimmer switch than on/off
  • Depends on interrupting synchronicity between multiple neural networks
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27
Q

The lack of awareness and recall effects of inhaled anesthetics occur in what regions of the brain?

A
  • Hippocampal and amygdala
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28
Q

What is the last sense to go away and the first to return when using inhaled anesthetics?

A
  • Hearing
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29
Q

The sedation effects of inhalation anesthetics is caused by?

A
  • Potent agents: probably stimulate GABA

- N2O & Xenon: possibly antagonize NMDA

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30
Q

The neuroprotection effects of inhaled anesthetics _____?

A
  • Prevent apoptosis, decreased CMRO2 (increased inhibitory & decreased excitatory transmission)
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31
Q

N2O can cause?

A

Neurotoxcitiy (irreversible cell damage)

Potent agents - less so

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32
Q

What are the CV effects of inhaled agents?

A
  • Dose-dependent myocardial depression and hypotension ; decreased Ca availability and sensitivity in the heart
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33
Q

What are the respiratory effects of inhalation agents?

A
  • Significant respiratory depression via central depression (increased inhibitory, decreased excitatory transmission)
  • We will see decreased tidal volumes and an increase in RR in most of the inhalation agents, but the increased RR doesn’t compensate for the decreased tidal volume - so CO2 levels go up!
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34
Q

What are volatile anesthetics?

A
  • Small molecular weight compounds administered as gases or vapors via inhalation
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35
Q

Why are volatile anesthetics fluorinated?

A
  1. Reduce or eliminate toxicity (metabolism)
  2. Reduce or eliminate anesthetic flammability
  3. Allow increased speed of induction and recovery from anesthesia
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36
Q

The more fluorine molecules….?

A

The faster you go to sleep and the faster you wake up

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37
Q

All potent inhaled anesthetics ______ tidal volume, _____ RR, and _____ resting ETCO2.

A
  • Decrease tidal volume, increase RR, increase ETCO2

- Minute volume goes down, so your resting CO2 goes up

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38
Q

All potent inhaled anesthetics _____ the activity of laryngeal irritant receptors.

A

Increase

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39
Q

All potent inhaled anesthetics _____ the activity of pulmonary irritant receptors.

A

Decrease

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40
Q

All potent inhaled anesthetics _____ FRC. Why?

A
  • Decrease
  • Loss of intercostals
  • Altered respiratory pattern
  • Cephalad movement of the diaphragm
  • Altered thoracic blood volume
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41
Q

All potent inhaled anesthetics relax smooth muscle (bronchodilation) by….?

A
  • Directly depressing smooth muscle contractility
  • Direct effects on bronchial epithelium and airway smooth muscle cells
  • Indirect inhibition of reflex neural pathways
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42
Q

When is pulmonary vascular resistance the lowest?

A
  • At a lung volume equivalent to FRC
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43
Q

An increase in pulmonary vascular resistance causes a corresponding increase in pulmonary arterial pressure that promotes ….?

A

Interstitial fluid to fill the lungs due to hydrostatic pressure

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44
Q

What causes increased pulmonary vascular resistance?

A
  • PEEP
  • Alveolar hypoxia
  • Hypercapnia
  • critical closing pressure
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45
Q

Inhaled anesthetics tend to _______ and may therefore have indirect effects on pulmonary vascular resistance.

A
  • Reduce lung volume
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46
Q

Regional alterations in pulmonary vascular resistance affect: ?

A
  • Regional distribution of blood flow within the lung
  • Produce changes in ventilation-perfusion matching
  • and simultaneously affect gas exchange
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47
Q

What is Hypoxic Pulmonary Vasoconstriction?

A
  • It is unique to pulmonary circulation in that other vascular beds (coronary, cerebral) dilate in response to hypoxia
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48
Q

How do anesthetics interfere with Hypoxic Pulmonary Vasoconstriction to affect gas exchange?

A
  • All volatile anesthetics vasodilate the pulmonary vascular bed and cause dose dependent myocardial depression

(Pt that has an issue w/ oxygenation and one of the lungs has a tumor, if you give the patient an inhalation agent - you will be giving O2 to that area bc of vasodilation of the pulmonary vessels.)

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49
Q

All inhalation agents alter both the central and peripheral receptors, which …?

A
  • Shifts our CO2 response curves to the right, so we expect higher levels of CO2 when we have a patient breathing anesthetic agents
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50
Q

Oxygenation and O2 saturation is a function of….?

A
  • The amount of oxygen you are delivering into the patient
  • The amount of oxygen the blood is absorbing
  • How well they are perfusing the peripheral tissues
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51
Q

CO2 levels are a function of ….?

A
  • How much we are ventilating the patient and eliminating CO2 out of the lungs (if we give higher tidal volumes we will remove more CO2, if you give additional oxygen you don’t lower CO2 levels)
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52
Q

Where is the central Chemical Control of Respiration located?

A
  • Near the ventrolateral medulla and other brainstem sites
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53
Q

What does the central Chemical Control of Respiration respond to?

A
  • Changes in the hydrogen ion (H+) concentration in CSF, NOT arterial CO2 tension or pH
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54
Q

What affects central Chemical Control of Respiration more?

A
  • The central Chemical Control of Respiration is more profoundly affected by respiratory than by metabolic alterations in arterial carbon dioxide tension.
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55
Q

Where is the peripheral Chemical Control of Respiration located?

A
  • Carotid bodies
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56
Q

What does the peripheral Chemical Control of Respiration respond to?

A
  • Changes in arterial CO2 tension, pH, and arterial oxygen tension
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57
Q

In the post-operative phase, volatile anesthetics affect CO2 response curves in what way?

A
  • All volatile anesthetics depress the ventilatory response to hypercapnia in a dose-dependent fashion
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58
Q

What are the effects on CO2 response curves at less than 1 MAC of volatile anesthetics?

A
  • At less than 1 MAC, volatile agents markedly attenuate or entirely eliminate hypercapnia-induced increases in ventilatory drive
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59
Q

What are the effects of volatile anesthetics on CO2 response curves at less than 0.2 MAC?

A
  • At less than 0.2 MAC, volatile anesthetics may depress the peripheral chemoreflex loop and inhibit the ventilatory response to hypercapnia.
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60
Q

What effect do volatile agents have on the hypoxemia response?

A
  • Volatile anesthetics and nitrous oxide attenuate the ventilatory response to hypoxia in a dose-dependent manner - at concentrations as low as 0.1 MAC
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61
Q

What is closing capacity?

A
  • The lowest volume at which alveoli stay open and this is a function of the FRC
  • As the FRC decreases, the closing volume increases and eventually overtakes the FRC so some alveoli never open - this leads to atelectasis
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62
Q

Upon induction, what happens to the diaphragm?

A
  • It is shifted cephalad and decreases all lung volumes, especially the FRC
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63
Q

How does inhaled anesthetics and mechanical ventilation lead to altered blood gas homeostasis?

A
  • Mechanical ventilation affects venous return to the right side of the heart
  • Inhaled anesthetics are myocardial depressants
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64
Q

What can be caused by mechanical ventilation?

A
  • Barotrauma - may not be noticed immediately under general anesthesia
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65
Q

How do inhaled anesthetics affect both central and peripheral respiratory drives?

A
  • Inhaled anesthetics decrease the patients response to hypoxia and hypercarbia
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66
Q

All inhaled anesthetics cause respiratory depression in a dose dependent manner with an elevation in PaCO2 secondary to medullary depression. What does this lead to?

A
  • Right shift of the CO2 response curve
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67
Q

What are the effects of inhaled anesthetics on bronchial smooth muscle?

A
  • All inhaled anesthetics are bronchodilators and inhibit bronchoconstriction
  • Can assist bronchodilation in the reactive airway by deepening anesthetic
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68
Q

What is the apneic threshold during spontaneous respiration is only …?

A
  • 3-5 mmHg less than the PaCO2
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69
Q

How do all inhalation anesthetics blunt the hypoxic pulmonary vasoconstrictor response by…?

A
  • Nonselective vasodilation of pulmonary vasculature
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70
Q

What inhaled anesthetic causes the most depression of the ventilatory response to hypoxemia and hypercapnia?

A

Isoflurane

71
Q

What is the most important characteristics regarding Desflurane?

A
  • Desflurane is an extremely noxious pulmonary irritant

* Not recommended for inhalation induction and probably a poor choice for patients with reactive airway disease

72
Q

What are the effects of Desflurane on HR?

A
  • Causes very slight tachypnea
73
Q

What inhaled anesthetic is the least irritating of all the agents?

A

Sevoflurane - great for inhalation inductions

74
Q

What is the physiology for how inhaled anesthetics cause bronchodilation?

A
  • Involves both a decrease in intracellular calcium concentration and a reduction in calcium sensitivity
  • Inhaled anesthetics preferentially dilate the distal airways rather than the proximal airways
75
Q

How do inhaled anesthetics diminish the rate of mucus clearance?

A
  • They decrease ciliary beat frequency and alters the characteristics of mucus
76
Q

What is the main lipid component of surfactant?

A
  • Phosphatidylcholine
77
Q

How do volatile anesthetics decrease pulmonary surfactant?

A
  • They cause reversible reductions in phosphatidylcholine
78
Q

What is the Hypoxic pulmonary vasoconstriction mechanism?

A
  • important mechanism by which pulmonary blood is preferentially redistributed away from poorly ventilated lung regions to those with adequate alveolar ventilation
  • Most inhaled anesthetics attenuate HPV
79
Q

How do inhaled anesthetics affect the inspiratory and expiratory respiratory muscles?

A
  • Result of differential sensitivity of bulbospinal inspiratory and expiratory neurons
80
Q

What are the effects of volatile anesthetics on acute lung injury?

A
  • They may exhibit pro-inflammatory actions and worsen acute lung injury
  • They have been shown to reduce inflammation and improve both chemical and physiologic pulmonary function in acute lung injury
81
Q

What are the cardiovascular effects of inhaled anesthetics?

A
  • A dose dependent depression of myocardial contractility, decreased SBP, decreased SVR, and negative chronotropic effects
82
Q

Isoflurane, Desflurane, and Sevoflurane decrease arterial blood pressure by:?

A
  • Reductions in LV afterload
83
Q

Through what mechanisms do inhaled anesthetics have direct negative chronotropic effects?

A
  • Depress SA node

- Baroreceptor reflex activity

84
Q

Volatile anesthetics have the potential to produce bradycardia and atrioventricular conduction abnormalities via…?

A
  • Direct and indirect effects on sinoatrial node automaticity
85
Q

What 3 agents have been shown to be cardioprotective against ventricular fibrillation produced by coronary artery occlusion and reperfusion?

A

Halothane, enflurane, and isoflurane

86
Q

What inhaled anesthetics sensitize myocardium to the arrythmogenic effects of epinephrine?

A
  • Mainly Halothane

- The other agents do too, but to a lesser extent

87
Q

What gents do not sensitize the heart to ventricular extrasystoles?

A

Desflurane, Isoflurane, and Sevoflurane

88
Q

What is the major CV effect of Isoflurane?

A
  • Dose-dependent decrease in BP d/t decreased peripheral vascular resistance
89
Q

Even though Isoflurane has a mild negative chronotropic effect on the SA node, Isoflurane will likely result in an increased HR due to…?

A
  • Due to indirect activation of the sympathetic nervous system and activation of the autonomic nervous system and baroreceptor responses to hypotension
90
Q

What is the effect of Isoflurane on the coronary vessels?

A
  • Selectively causes coronary vasodilation and decreased coronary vascular resistance
91
Q

Does Isoflurane cause coronary steal?

92
Q

Abrupt increases in Desflurane concentrations causes…?

A
  • increased BP (30 mmHg)
  • increased HR (30 bpm)
  • Doubling of sympathetic nervous system activity
  • Increased plasma epinephrine levels
93
Q

Studies have shown no increased incidence of myocardial ischemia in patients receiving Desflurane compared to Isoflurane. What should be of concern with Desflurane?

A
  • Tachycardia, which greatly impacts coronary blood flow
94
Q

What are the CV effects of Sevoflurane?

A
  • Dose-dependent decrease in myocardial contractility, CO & SVR
95
Q

What is the most prominent CV effect of halothane?

A
  • Dose-dependent arterial hypotension
96
Q

Which inhaled anesthetic has the greatest negative inotropic effect among all the inhalation agents except Enflurane?

97
Q

What drug decreases the threshold at which catecholamines (natural or synthetic) will cause ventricular ectopy?

A
  • Halothane
  • It is recommended that no more than 100 mcg of Epi be injected in less than 10 minutes and no more than 5mcg/kg during the injection process. This response is worse with Hypercapnia. Children are less sensitive to this response.
98
Q

In a normal heart, volatile anesthetics produce..?

A
  • Dose-dependent myocardial depression

- Negative inotropic effects (d/t alterations in intracellular Ca homeostasis within the cardiac myocyte)

99
Q

Volatile anesthetics depress what reflex?

A
  • Baroreceptor reflex control of arterial pressure to varying degrees
100
Q

Do all inhalation anesthetics increase or decrease CBF?

A
  • Increase CBF by decreasing cerebrovascular resistance which leads to increased ICP.
  • We can compensate for this by hyperventilating the patient, but this only works for 6-8 hours
101
Q

What effects do inhalation anesthetics have on CMRO2?

A
  • They decrease CMRO2
102
Q

Which agent has slight cerebral protection properties?

A

Isoflurane

103
Q

What are the neuromuscular effects of inhaled anesthetics?

A
  • They have centrally mediated muscle relaxant properties, but need really high concentrations
104
Q

What is the only inhaled anesthetic that doesn’t have MH triggering properties?

A
  • Nitrous Oxide
105
Q

What are the hepatic effects of inhaled anesthetics?

A
  • All inhalation agents decrease hepatic blood flow
106
Q

What causes “Halothane Hepatitis”?

A
  • Reductive metabolism of halothane in the presence of hepatocyte hypoxia
107
Q

What agent is not metabolized in humans?

A
  • Nitrous Oxide
108
Q

What are the renal effects of inhaled anesthetics?

A
  • They cause decreases in renal blood flow, GFR, and urine output
109
Q

Metabolism that results in high __________ can cause renal failure?

A
  • high Fluoride levels can cause renal failure, but none has been reported with Sevoflurane
110
Q

Free fluoride concentration of _________ are nephrotoxic?

A
  • 40-50 uM/L
111
Q

What agents result in free fluoride ions in the blood?

A
  • Methoxyflurane, Ethrane, and Sevoflurane
112
Q

How do fluoride ions cause renal failure?

A
  • Directly inhibit renal tubular function including chloride transport in the ascending limb of the loop of Henle which leads to a concentrating defect
113
Q

What agent forms Compound A in desiccated soda lime?

A

Sevoflurane

114
Q

What are the obstetrical effects of inhaled anesthetics?

A
  • They decrease uterine blood flow and uterine contractility - we don’t want that because once the baby is born we want the uterus to contract
115
Q

What agent affects methionine synthetase and thymidylate synthetase?

A
  • Nitrous oxide decreases the activity of methionine synthetase and thymidylate synthetase, which is important in RNA/DNA replication patterns
116
Q

What agent is too impotent to provide anesthesia alone?

A
  • Nitrous oxide, MAC is 105%
117
Q

The effects of multiple agents are ______?

A
  • Additive, each 1Vol% N2O added to the inspired gases, 1Vol% less potent inhalation agent may be administered
118
Q

Describe the concentration effect?

A
  • As the N2O is taken up it leaves space in the FRC for fresh gas inflow to occur
  • As fresh gas saturated with anesthetic flows in, the concentration of anesthesia in the FRC increases faster
119
Q

Describe the Second Gas effect?

A
  • The 2nd gas (usually a potent inhalation agent) also rises to a higher concentration more quickly because of the concentration effect
120
Q

Which agent increases sympathetic nervous system tone?

A
  • Nitrous Oxide, this tends to counteract the hypotensive effects of ALL inhalation agents
121
Q

This agent has minimal respiratory effects such as decreased tidal volume and increased RR compared to other agents?

A

Nitrous Oxide

122
Q

This agent increases CBF, ICP, and CMRO2, but decreases seizure activity?

A
  • Nitrous Oxide
123
Q

N2O is 30 times more soluble in blood than _____ and will rapidly move into air spaces filler with ______ before the ____can move out?

A
  • Nitrogen, this is especially a problem with closed air spaces
124
Q

N2O is contra-indicated in what patients?

A
  • Tympanic membrane and ear surgeries
  • Pneumothoraces
  • Small bowel obstructions
  • Pneumocephalus
  • Concerns about Air Emboli
125
Q

NIOSH standards state less than ______ N2O in ambient OR air?

126
Q

What are Time Constants?

A
  • A way of describing the amount of change that occurs per unit of time for inhaled anesthetics in a dynamic system
127
Q

What percent does each time constant represent?

A
  • Each time constant represents a 63% change in the system
128
Q

What is the equation for figuring time constants?

A

Time Constant = Capacity of the System / Flow into the system

129
Q

What are the 3 components that make up the capacity within the system and their volumes?

A
  1. Ambu bag - 3000 cc
  2. FRC, exchange capacity in the lungs - 2500-3000 cc
  3. The tubing that connects back and forth - 500 cc
    - -> We have roughly 7 L in the system
130
Q

How many time constants are required to have a 98% change in the system?

131
Q

During induction and emergence, what are typical flow rates?

A
  • 8-10 L/min
132
Q

During maintenance, what are typical flow rates?

A

0.5-1 L/min

133
Q

What do we need higher flow rates during induction and emergence?

A
  • Because we want our gases to move in quickly and get the patient asleep, and on emergence we want to wake them up quickly
134
Q

Why is it okay to have lower flows during maintenance?

A
  • Because we are okay with slow changes, if we need to make fast changes we can turn our flow rates up
135
Q

How much oxygen does the average male consume per minute?

A
  • About 250 cc of oxygen per minute
    or. ..
  • 2-4 cc/kg/min
136
Q

Fe or alveolar concentration is…?

A
  • The closest we can get to measuring the brain concentration
137
Q

Time constants is more applicable to….?

A
  • Insoluble anesthetics agents (low Blood:gas coefficients)
138
Q

What does MAC generally refer to?

A
  • MAC incision or stimulus to the patient
139
Q

What is MAC Awake?

A
  • 1/3 to 1/4 MAC
  • The level of anesthesia that the patient can still be breathing some anesthesia and you can still talk to them and get them to wake up and respond to you
140
Q

What is MAC intubation?

A
  • Intubation is more stimulating than incision (MAC intubation > MAC)
  • This is higher than MAC b/c intubation is a very stimulating thing, this can be blunted with some fentanyl
141
Q

What is MAC Bar?

A
  • Blunt Autonomic Responses, 30-40% greater than MAC
  • If you have an anesthetic ongoing and you see “pure railroad tracks” absolutely no change in the vital signs to stimulations by the surgeons, you probably have the patient over anesthetized at that point
142
Q

How does advanced age decrease MAC?

A
  • MAC goes down about 6% per decade over 40 years of age
143
Q

Why are we concerned about MAC?

A
  • We want to make sure that our patients are not aware under anesthesia
  • If you know what MAC is and your shooting for MAC you will probably not have a patient that has awareness or recall during surgery
144
Q

Define Awareness?

A
  • Postoperative recall of events occurring during general anesthesia
145
Q

Define Amnesic wakefulness?

A
  • Responsiveness during general anesthesia without postoperative recall
146
Q

Define Dreaming?

A

Any experience (excluding awareness) that patients are able to recall postoperatively that they think occurred during general anesthesia and they believe is dreaming

147
Q

Define Explicit memory?

A
  • Conscious recollection of previous experiences (“awareness” is evidence of explicit memory)
148
Q

Define Implicit memory?

A
  • Changes in performance or behavior that are produced by previous experiences but without any conscious recollection of those experiences (“unconscious memory formation” during general anesthesia)
149
Q

What does low blood:gas solubility mean?

A
  • Means fast in and fast out
  • Low solubility means more for anesthesia - higher concentration in the brain faster than high solubility
  • N20, Desflurane, Sevoflurane
150
Q

What does high solubility mean?

A
  • Means slow on and slow off
  • More anesthetic in blood, muscle, fat and less for anesthesia in the brian
  • Halothane, Enflurane, ?Isoflurane
151
Q

What keeps the Fa/Fi from reaching 1.0?

A
  • Anesthetic being taken up
152
Q

What happens to uptake if the tissue is saturated?

A
  • There is no tissue gradient, so no uptake occurs
153
Q

If you have no cardiac output, what happens to uptake?

154
Q

What factors contribute to uptake?

A
  1. depends on anesthetic dissolved in blood and tissue
  2. Alveolar - Venous difference
  3. Cardiac Output
  4. Blood:Gas solubility
155
Q

What does not contribute to uptake?

A
  • Ventilation, if we ventilate more rapidly in the beginning we can get more into the lungs, but that doesn’t affect uptake
156
Q

When the partial pressure of agent in the blood and gas are in equilibrium, the coefficient tells you what?

A
  • How much agent is dissolved for each ml causing anesthesia
157
Q

What is Henry’s law?

A

The amount of gas that dissolves in liquid is directly proportional to the partial pressure of the gas over the liquid

158
Q

What is PA?

A
  • Fi of the agent, this is what is going into the lungs, not always what is set on the vaporizer
159
Q

A high PA equals what?

A
  • High delivered concentration, which means greater uptake because the PA to PV gradient will be higher
160
Q

The PV is equal to what?

A
  • Fe of the agent, this is the concentration coming back out of the patient, this is as close to the venous pressure that we can get
161
Q

A high PV equals what?

A

A high PV means high tissue concentration and less uptake because the PA minus PV is going to be smaller

162
Q

The greater the difference between PA and PV means what?

A
  • Greater the uptake
163
Q

How are agents delivered?

A
  • They are delivered in Vol% gas = partial pressure

- 6% Desflurane = 760 mmHg x 0.06= 46 mmHg

164
Q

What does an FA:FI of 1.0 represent?

A
  • This means that our lungs are fully saturated with the concentration of anesthetic gas that we want in the brain
165
Q

If 2/3 of inhaled anesthetic is taken up, what would the Fa/FI be?

A
  • 33% (high soluble agent)
166
Q

If 1/4 of the inhaled anesthetic is taken up, what would the FA/FI be?

A
  • 75% (low solubility)
167
Q

The FA is determined by?

A
  • how much is being taken up, it drops during induction bc a lot is being taken up
168
Q

Referencing the knees in the graph, what causes the initial rapid rise?

A
  • There is a sharp rise because the alveolus has no agent
169
Q

Referencing the knees in the graph, what does the first knee represent?

A
  • VRG taking up anesthetic - does not take long to saturate and satisfy this group because it receives most of the CO and it has a constant supply of anesthetic agent coming to it
170
Q

Referencing the knees in the graph, what does the third knee represent?

A
  • Muscle saturated, the fat group starts uptake around 2-4 hours depending on the agent
171
Q

Referencing the knees in the graph, the slope of line decreases because…?

A
  • Each compartment os saturated because FA/FI is rising more slowly as the rate of uptake is decreasing
172
Q

Why does a higher concentration of anesthetic agent increase the rate of rise of FA/FI?

A
  • The agent will cause more myocardial depression -> depressed CO, leading to less uptake by the blood , less by the tissues, and more in the alveoli so FI rises faster
173
Q

Greater minute ventilation increases FA/FI more rapidly, why?

A
  • More agent to the lungs and tissues
  • Increased ventilation affects soluble agents more than insoluble agents - insoluble agents rise so fast that there is no difference
174
Q

Infants have a higher _____ than adults?

A
  • Minute ventilation
175
Q

Faster induction occurs in kids or adults?

A
  • Kids because of increased proportion of CO to VRG

Pharmacology of Anesthesia (6 decks)

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