Inhaled Anesthetics Part 2 (Exam III)

Question 1

What are the purposes of the anesthesia circuit?

Answer 1

• Delivery of O₂ and inhaled anesthetics
• Maintenance of temperature & humidity
• Removal of CO₂ and exhaled drugs

S2

Question 2

What types of gas delivery systems are there?

Answer 2

• Rebreathing (Bain system)
• Non-rebreathing (BVM system)
• Circle systems (Anesthesia machine)

S2

Question 3

What type of system is depicted below?
Where is the aPL valve located on this system?

Answer 3

• Bain Circuit
• Blue circle depicts aPL below.

S3

Question 4

In the figure below, what portion of the anesthesia circle system is indicated by 1?

Answer 4

Inspiratory Unidirectional Valve

S5

Question 5

In the figure below, what portion of the anesthesia circle system is indicated by pink arrow?

Answer 5

Fresh Gas Inlet (O₂ & medical air)

S5

Question 6

In the figure below, what portion of the anesthesia circle system is indicated by 2?

Answer 6

CO₂ Absorber

S5

Question 7

In the figure below, what portion of the anesthesia circle system is indicated by 3?

Answer 7

Bag/Ventilator Selector Switch

S5

Question 8

In the figure below, what portion of the anesthesia circle system is indicated by 4?

Answer 8

APL Valve

S5

Question 9

In the figure below, what portion of the anesthesia circle system is indicated by 5?

Answer 9

Expiratory Unidirectional Valve

S5

Question 10

In the figure below, what portion of the anesthesia circle system is indicated by 6?

Answer 10

Expiratory Limb

S5

Question 11

In the figure below, what portion of the anesthesia circle system is indicated by 7?

Answer 11

Y-Piece

S5

Question 12

When fresh gas flow (FGF) exceeds V̇_T then you have _________________.

Answer 12

High Flow Anesthesia

S6

Question 13

When V̇_T exceeds fresh gas flow (FGF) then you have _________________.

Answer 13

Low Flow Anesthesia

S6

Question 14

When would one see lack of rebreathing, wasteful volatile use, and cool dried air?

Answer 14

High flow anesthesia

S6

Question 15

When would one see lower volatile use, less cooling/drying of air, and slow changes in anesthetics?

Answer 15

Low flow anesthesia

S7

Question 16

Do volatiles cause bronchostriction or bronchodilation?

Answer 16

Bronchodilaton

S10

Question 17

How do volatiles cause bronchodilation?

Answer 17

• Blockage of VG Ca⁺⁺ channels
• Depletion of SR Ca⁺⁺

S10

Question 18

Is the bronchodilatory effect of volatiles still present in someone with reactive airway disease?

Answer 18

• No (or very little effect). Bronchodilatory effects of volatiles require an intact epithelium, normal inflammatory processes, etc.

S10

Question 19

Will volatiles cause bronchospasm on their own (in a patient with no history of bronchospasm)?

Answer 19

No

Histamine release or vagal afferent stimulation needed to cause spasm.

S10

Question 20

In a patient without history of bronchospasm, how much would you anticipate PVR to change with 1-2 MAC?

Answer 20

PVR would be unchanged in patient with no history of bronchospasm.

S10??

Question 21

What risk factors increase risk of bronchospasm?

Answer 21

• COPD
• Coughing w/ ETT in place
• <10 years old
• URI

S10

Question 22

What anesthetic is generally the best at bronchodilating?

Answer 22

• Halothane (1st)
• Sevoflurane (2nd)

S11

Question 23

Which anesthetic can function as a pulmonary irritant (especially in smokers)?

Answer 23

Desflurane

S11

Question 24

Which volatile anesthetic in the graph below caused the greatest increase in airway resistance?
Lowest?

Answer 24

• Desflurane = ↑ airway resistance
• Sevoflurane = ↓ airway resistance

S11

Question 25

Inhaled anesthetics engender a dose-dependent skeletal muscle relaxation. T/F?

Answer 25

True ## Footnote S12

Question 26

Which volatile gas has **no effect** on the relaxation of skeletal muscles?

Answer 26

N₂O ## Footnote S12

Question 27

Will volatiles potentiate or inhibit NMBD's? How?

Answer 27

Potentiate via sensitization of nACh receptors at NMJ. ## Footnote S12

Question 28

How do volatile anesthetics cause skeletal muscle relaxation as a solo agent?

Answer 28

Volatiles cause skeletal muscle relaxation via enhancement of glycine at the spinal cord. ## Footnote S12

Question 29

What is ischemic preconditioning?

Answer 29

With people who are susceptible of having M.I., there’s a thought that if you expose them to a little of anesthetic gas, it preconditions them and decreases their likelihood from getting M.I. ## Footnote S13

Question 30

Ischemic preconditioning with volatile anesthetics can occur as low as ______ MAC.

Answer 30

0.25 ## Footnote S13

Question 31

Why does ischemic preconditioning happen?

Answer 31

- ↑ PKC activity - Phosphorylation of ATP sensitive K⁺ channels - Production of ROS (Reactive Oxygen Species) - Better regulation of vascular tone. ## Footnote S13

Question 32

What molecule mediates ischemic preconditioning?

Answer 32

Adenosine ## Footnote S13

Question 33

What does ischemic preconditioning prevent?

Answer 33

- Reperfusion injuries - Cardiac dysrhythmias - Contractile dysfunction - Delays MI's in CAD patients. ## Footnote S13

Question 34

At what dose does volatile depression of CMRO₂ begin?

Answer 34

0.4 MAC ## Footnote S15

Question 35

At what MAC would we see EEG burst suppression? What about total electrical silence?

Answer 35

- 1.5 MAC = burst suppression - 2 MAC = EEG silence ## Footnote S15

Question 36

Which volatile causes the most EEG suppression?

Answer 36

Trick question. They all affect EEG's the same. ## Footnote S15

Question 37

Which volatiles have anticonvulsant activity?

Answer 37

Des, Sevo, & Iso at high concentrations & with hypocarbia. ## Footnote S16

Question 38

Which volatile is a proconvulsant?

Answer 38

Enflurane ## Footnote S16

Question 39

Give an example of a somato-sensory evoked potential (SSEP).

Answer 39

Stimulation of the foot evoking an electrical response in the CNS. ## Footnote S16

Question 40

Give an example of a motor-evoke potential (MEP).

Answer 40

Direct stimulation of the brain eliciting a twitch response in the hand. ## Footnote S16

Question 41

You have a case where SSEPs and MEPs need to be monitored, what general anesthetics options do you have?

Answer 41

- TIVA - N₂O 60% and 0.5 MAC volatile. ## Footnote S16

Question 42

What specific effects will volatile agents have on SSEPs and MEPs?

Answer 42

Dose-dependent (0.5 - 1.5MAC): - ↓ amplitude - ↑ latency (delayed frequency) ## Footnote S16

Question 43

What occurs with cerebral blood flow with volatile administration?

Answer 43

Dose dependent: - ↑ CBF due to dilated vessels - ↑ ICP ## Footnote S17

Question 44

At what MAC would you expect to start to see an increase in CBF due to volatile administration?

Answer 44

At > 0.6 MAC ## Footnote S16

Question 45

Which volatile has less vasodilatory effects?

Answer 45

Sevoflurane | good for neuro patients ## Footnote S16

Question 46

Which volatile has the greatest effect on increasing CBF? (and thus ICP)

Answer 46

Halothane ## Footnote S17

Question 47

How much Nitrous to give due to potent vasodilating effect?

Answer 47

< 1 MAC ## Footnote S17

Question 48

Which volatile is the best for neuro cases? Why?

Answer 48

Sevoflurane (preserves autoregulation mechanism up to 1 MAC). ## Footnote S17

Question 49

Slide 18

Question 50

What patient population is most at risk due to the ICP increasing effects of volatile agents?

Answer 50

Patients with CNS occupying tumor/lesion. ## Footnote S19

Question 51

What average ICP increase is seen with volatile use?

Answer 51

7mmHg ## Footnote S19

Question 52

At what volatile dosage does ICP increase?

Answer 52

> 0.8 MAC ## Footnote S19

Question 53

What do volatiles do to the respiratory system?

Answer 53

Dose dependent: - Tachypnea - ↓ V_T ## Footnote S20

Question 54

How do volatiles cause their respiratory effects?

Answer 54

- Direct depression of medullary ventilatory center. - Interference with intercostal muscles. ## Footnote S20

Question 55

Rate change insufficient to maintain Vm or PaCO2 SLIDE @ 20

Question 56

At what volatile dosage would apnea be seen?

Answer 56

1.5 - 2 MAC ## Footnote S20

Question 57

All volatiles with blunt both the hypoxic and hypercarbic response. T/F?

Answer 57

False. N₂O does not blunt the hypercarbic response. ## Footnote S21

Question 58

How can the hypercarbic response be preserved whilst using volatile anesthetic gasses?

Answer 58

- Use N₂O and volatile together. ## Footnote S21

Question 59

What effect is seen in the graph below?

Answer 59

Use of N₂O-desflurane decreasing CO₂ induced hypercarbia compared to desflurane alone. ## Footnote S22

Question 60

What is hypoxic pulmonary vasoconstriction?

Answer 60

Contraction of pulmonary arteries to shunt blood away from poorly ventilated portions of the lung. ## Footnote S23

Question 61

When is the blunting of HPV most concerning?

Answer 61

When one lung ventilation is being utilized. ## Footnote S23

Question 62

How fast is the HPV response?

Answer 62

Fast: within 5 minutes regional blood flow is ½ of normal. ## Footnote S23

Question 63

50% depression of HPV occurs at ___ MAC.

Answer 63

2 ## Footnote S23

Question 64

Which volatile(s) **does not** cause cardiac depression?

Answer 64

N₂O ## Footnote S24

Question 65

How do volatiles cause hypotension?

Answer 65

- Direct myocardial depression by altering Ca⁺⁺ entry and SR function. ## Footnote S24

Question 66

Slide 25

Question 67

Volatiles will cause a dose-dependent decrease in __ , __ , and CO.

Answer 67

contractility ; SV ## Footnote S26

Question 68

When is volatile depression of cardiac function most concerning?

Answer 68

With pathologic hearts (particularly pathologies of ↓ contractility) ## Footnote S24

Question 69

What volatile can cause significant tachycardia with overpressurization?

Answer 69

Desflurane ## Footnote S25

Question 70

When will sevoflurane begin to cause increases in heart rate?

Answer 70

Only at > 1.5 MAC ## Footnote S25

Question 71

What variables confound the tachycardic effect of volatiles?

Answer 71

- Anxiety - Concurrent opioids - β blockade - Vagolytics ## Footnote S25

Question 72

What volatile is slightly sympathomimetic, causing a slight increase in CO?

Answer 72

N₂O ## Footnote S26

Question 73

Is the coronary steal effect of volatiles clinically significant?

Answer 73

Nope ## Footnote S26

Question 74

What electrocardiac effect do volatiles have?

Answer 74

QT prolongation via inhibition of K⁺ currents. | increse risk of Torsades ## Footnote S27

Question 75

Which volatile has minimal pro-arrhythmic activity?

Answer 75

N₂O ## Footnote S27

Question 76

What volatile is the gas of choice and which one is not the gas of choice for EP ablations and? Why?

Answer 76

- Sevoflurane - Other volatiles increase refractoriness of accessory pathways making identification of arryhthmia location difficult such as ISOFLURANE *Sevo gang*. ## Footnote S27

Question 77

Volatile neuroendocrine modulation will cause a perioperative surge in __, ___, and ___.

Answer 77

catecholamines; ACTH; & cortisol ## Footnote S28

Question 78

Volatiles will suppress what important immune system components?

Answer 78

Volatiles suppress **monocytes, macrophages, and T-cells.** ## Footnote S28

Question 79

What does the total neuroendocrine profile of volatile anesthetics suggest for cancer patients undergoing surgery?

Answer 79

Neuraxial anesthesia is likely better than GA for cancer patients. ## Footnote S28

Question 80

What hepatic blood flow changes are seen with volatile administration?

Answer 80

Portal vein dilation = ↑ portal vein flow. ## Footnote S29

Question 81

Which volatile is the only one that decreases portal vein flow?

Answer 81

Halothane (likely contributes to halothane hepatitis) ## Footnote s29

Question 82

What is volatile hepatotoxicity? When is it a concern?

Answer 82

- Inadequate oxygenation of liver cells via ↓ blood flow and ↑ O₂ demand. - Concern for patients with preexisting liver disease. ## Footnote S30

Question 83

What is Type 1 Volatile hepatotoxicity?

Answer 83

- Direct toxicity or free radical effect 1-2 weeks post surgically with N/V & fever in 20% of patients. ## Footnote S30

Question 84

What is Type 2 Volatile Toxicity?

Answer 84

- Reaction caused only with previous exposure to volatile with eosinophilia, fever, and higher mortality rate from hepatitis and necrosis. - 1 month after exposure ## Footnote S30

Question 85

Which volatile is the choice anesthetic for severe liver disease? Why?

Answer 85

Sevoflurane: broken down to vinyl halide and won't stimulate antibody production causing a Type II reaction. *Sevo the GOAT gas fr* ## Footnote S31

Question 86

What volatiles are metabolized into acetyl halides? What is the significance of this?

Answer 86

Enflurane > Iso > Des - **Acetyl halides can cause antibody reactions** especially with previous exposure to halothane or enflurane. ## Footnote S31

Question 87

What are the renal effects of volatile anesthetics?

Answer 87

Dose dependent decrease in RBF, GFR, and UO from CO depression. ## Footnote S32

Question 88

How can the renal effects of volatile anesthetics be counteracted?

Answer 88

Hydration (both pre-operative and intra-operative). ## Footnote S32

Question 89

What other organ (besides the heart) undergoes protective ischemic preconditioning from volatile anesthetics?

Answer 89

Kidneys ## Footnote S32

Question 90

What toxic metabolites of volatiles can cause nephrotoxicity? Why is this not an issue typically?

Answer 90

- Fluoride metabolites - Newer volatiles are exhaled prior to being metabolized. ## Footnote S33

Question 91

What volatile is 70% metabolized and can cause fluoride metabolite nephrotoxicity more than any of the other volatiles?

Answer 91

Methoxyflurane ## Footnote S33

Question 92

What measure is utilized in CO₂ absorbents today to help prevent the formation of compound A?

Answer 92

75% or greater concentrations of calcium hydroxide. ## Footnote S34

Question 93

What does Sevoflurane mixed with CO2 create? And what kind of toxin is it?

Answer 93

creates Compound A which is a nephrotoxin | Compound A not seein in U.S. anymore d/t change from K & NaOH to CaOH ## Footnote S34

Question 94

What volatile is predisposed to starting fires? Why?

Answer 94

- Sevoflurane - Sevo + baralyme (absorbent) produce methanol and formaldehyde causing a heat and and eventual explosion. ## Footnote S35

Question 95

How is sevoflurane fire avoided?

Answer 95

- Addition of H₂O to Sevo - Check temp of absorbent cannister - Exchange exhausted absorbents ## Footnote S35

Question 96

What triggers Malignant Hyperthermia? The s/s? The treament?

Answer 96

Triggers: all volatile agents and succinylcholine Symptoms: ↑ body temp, CO2 production, O2 consumption Treatment: Dantrolene Blocks intracellular Ca++ release Supportive care of rhabdomyolysis ## Footnote S36

Question 97

Which volatile anesthetics are emetogenic?

Answer 97

All ## Footnote S37

Question 98

What rate of PONV is seen with two triggering agents? (ex. desflurane and fentanyl)

Answer 98

25 - 30% PONV ## Footnote S37

Question 99

When is N₂O emetogenic?

Answer 99

At greater than 50% or 0.5 MAC ## Footnote S37

Question 100

Why is N₂O administration in a pregnant patient with B₁₂ deficiency dangerous?

Answer 100

N₂O will oxidize the cobalt ion in B₁₂ thus inhibiting methionine synthase = inhibition of DNA synthesis in fetu. ## Footnote S38

Question 101

Which volatile anesthetic can cause bone marrow suppression?

Answer 101

N₂O ## Footnote S38

Question 102

What is the result from increases in plasma homocysteine levels from N₂O administration?

Answer 102

If the patient also has low B vitamins and atherosclerosis, then N₂O increases risk of myocardial events. ## Footnote S38

Question 103

What is/are the obstetric effects of volatile anesthetics?

Answer 103

Dose-dependent (0.5 - 1.0 MAC) decrease in uterine smooth muscle contractility. ## Footnote S39

Question 104

When would a decrease in uterine muscle tone be useful?

Answer 104

With retained placenta ## Footnote S39

Question 105

When would an increase in uterine muscle tone be useful?

Answer 105

Uterine atony (↑ blood loss) ## Footnote S39

Question 106

Why is N₂O useful in mom's post delivery?

Answer 106

Swiftly increases analgesia without opioid/benzo's (use as the spinal starts to wear off). ## Footnote S39

Question 107

Which volatiles have a sweeter smell?

Answer 107

- Halothane - Sevoflurane ## Footnote S40

Question 108

What is the only real benefit of halothane?

Answer 108

↓ N/V ## Footnote S40

Question 109

What are the four major concerns of halothane?

Answer 109

- Catecholamine-induced arrhythmias - Pediatric bradycardia - Hepatic necrosis - Decomposing into HCl acid. ## Footnote S40

Question 110

Which two volatiles can't be used for induction due to their awful smell?

Answer 110

- Isoflurane - Desflurane ## Footnote S41

Question 111

Which volatile does not degrade, even after 5 years of storage?

Answer 111

Isoflurane ## Footnote S41

Question 112

If a vaporizer has a heating element, then the gas for that vaporizer can be assumed to be ____________.

Answer 112

Desflurane ## Footnote S42

Question 113

List the order in which volatiles will degrade into carbon monoxide if the absorbent becomes exhausted/dehydrated.

Answer 113

**Desflurane** (worst) > Enflurane > Isoflurane > Sevoflurane (trivial) *Sevo on top per usual*. ## Footnote S42

Question 114

Which volatile anesthetic would be the choice for inhalation induction? Why?

Answer 114

- Sevoflurane - Least airway irritation & smells sweet. *Yet another example of sevo superiority*. ## Footnote S43

Question 115

Which volatile causes the least increase in ICP?

Answer 115

Sevoflurane *In Sevo, we trust*. ## Footnote S42

Question 116

How does N₂O produce skeletal muscle relaxation?

Answer 116

Trick question. It does not. ## Footnote S44

Question 117

What are the benefits of N₂O ?

Answer 117

- Good analgesia - 2nd gas effect ## Footnote S45

Question 118

What are the major cons of N₂O ?

Answer 118

- N/V @ 0.5 MAC - ↑ PVR - No surgeries with air filled spaces ## Footnote S45