Inhaled Anesthetics Part 2 (Exam III) Flashcards
need to separate concept with inhaled gas info
What are the purposes of the anesthesia circuit?
- Delivery of O₂ and inhaled anesthetics
- Maintenance of temperature & humidity
- Removal of CO₂ and exhaled drugs
S2
What types of gas delivery systems are there?
- Rebreathing (Bain system)
- Non-rebreathing (BVM system)
- Circle systems (Anesthesia machine)
S2
What type of system is depicted below?
Where is the aPL valve located on this system?
- Bain Circuit
- Blue circle depicts aPL below.
S3
In the figure below, what portion of the anesthesia circle system is indicated by 1?
Inspiratory Unidirectional Valve
S5
In the figure below, what portion of the anesthesia circle system is indicated by pink arrow?
Fresh Gas Inlet (O₂ & medical air)
S5
In the figure below, what portion of the anesthesia circle system is indicated by 2?
CO₂ Absorber
S5
In the figure below, what portion of the anesthesia circle system is indicated by 3?
Bag/Ventilator Selector Switch
S5
In the figure below, what portion of the anesthesia circle system is indicated by 4?
APL Valve
S5
In the figure below, what portion of the anesthesia circle system is indicated by 5?
Expiratory Unidirectional Valve
S5
In the figure below, what portion of the anesthesia circle system is indicated by 6?
Expiratory Limb
S5
In the figure below, what portion of the anesthesia circle system is indicated by 7?
Y-Piece
S5
When fresh gas flow (FGF) exceeds V̇T then you have _________________.
High Flow Anesthesia
S6
When V̇T exceeds fresh gas flow (FGF) then you have _________________.
Low Flow Anesthesia
S6
When would one see lack of rebreathing, wasteful volatile use, and cool dried air?
High flow anesthesia
S6
When would one see lower volatile use, less cooling/drying of air, and slow changes in anesthetics?
Low flow anesthesia
S7
Do volatiles cause bronchostriction or bronchodilation?
Bronchodilaton
S10
How do volatiles cause bronchodilation?
- Blockage of VG Ca⁺⁺ channels
- Depletion of SR Ca⁺⁺
S10
Is the bronchodilatory effect of volatiles still present in someone with reactive airway disease?
- No (or very little effect). Bronchodilatory effects of volatiles require an intact epithelium, normal inflammatory processes, etc.
S10
Will volatiles cause bronchospasm on their own (in a patient with no history of bronchospasm)?
No
Histamine release or vagal afferent stimulation needed to cause spasm.
S10
In a patient without history of bronchospasm, how much would you anticipate PVR to change with 1-2 MAC?
PVR would be unchanged in patient with no history of bronchospasm.
S10??
What risk factors increase risk of bronchospasm?
- COPD
- Coughing w/ ETT in place
- <10 years old
- URI
S10
What anesthetic is generally the best at bronchodilating?
- Halothane (1st)
- Sevoflurane (2nd)
S11
Which anesthetic can function as a pulmonary irritant (especially in smokers)?
Desflurane
S11
Which volatile anesthetic in the graph below caused the greatest increase in airway resistance?
Lowest?
- Desflurane = ↑ airway resistance
- Sevoflurane = ↓ airway resistance
S11
Inhaled anesthetics engender a dose-dependent skeletal muscle relaxation. T/F?
True
S12
Which volatile gas has no effect on the relaxation of skeletal muscles?
N₂O
S12
Will volatiles potentiate or inhibit NMBD’s? How?
Potentiate via sensitization of nACh receptors at NMJ.
S12
How do volatile anesthetics cause skeletal muscle relaxation as a solo agent?
Volatiles cause skeletal muscle relaxation via enhancement of glycine at the spinal cord.
S12
What is ischemic preconditioning?
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.
S13
Ischemic preconditioning with volatile anesthetics can occur as low as ______ MAC.
0.25
S13
Why does ischemic preconditioning happen?
- ↑ PKC activity
- Phosphorylation of ATP sensitive K⁺ channels
- Production of ROS (Reactive Oxygen Species)
- Better regulation of vascular tone.
S13
What molecule mediates ischemic preconditioning?
Adenosine
S13
What does ischemic preconditioning prevent?
- Reperfusion injuries
- Cardiac dysrhythmias
- Contractile dysfunction
- Delays MI’s in CAD patients.
S13
At what dose does volatile depression of CMRO₂ begin?
0.4 MAC
S15
At what MAC would we see EEG burst suppression?
What about total electrical silence?
- 1.5 MAC = burst suppression
- 2 MAC = EEG silence
S15
Which volatile causes the most EEG suppression?
Trick question. They all affect EEG’s the same.
S15
Which volatiles have anticonvulsant activity?
Des, Sevo, & Iso at high concentrations & with hypocarbia.
S16
Which volatile is a proconvulsant?
Enflurane
S16
Give an example of a somato-sensory evoked potential (SSEP).
Stimulation of the foot evoking an electrical response in the CNS.
S16
Give an example of a motor-evoke potential (MEP).
Direct stimulation of the brain eliciting a twitch response in the hand.
S16
You have a case where SSEPs and MEPs need to be monitored, what general anesthetics options do you have?
- TIVA
- N₂O 60% and 0.5 MAC volatile.
S16
What specific effects will volatile agents have on SSEPs and MEPs?
Dose-dependent (0.5 - 1.5MAC):
- ↓ amplitude
- ↑ latency (delayed frequency)
S16
What occurs with cerebral blood flow with volatile administration?
Dose dependent:
- ↑ CBF due to dilated vessels
- ↑ ICP
S17
At what MAC would you expect to start to see an increase in CBF due to volatile administration?
At > 0.6 MAC
S16
Which volatile has less vasodilatory effects?
Sevoflurane
good for neuro patients
S16
Which volatile has the greatest effect on increasing CBF? (and thus ICP)
Halothane
S17
How much Nitrous to give due to potent vasodilating effect?
< 1 MAC
S17
Which volatile is the best for neuro cases? Why?
Sevoflurane
(preserves autoregulation mechanism up to 1 MAC).
S17
Slide 18
What patient population is most at risk due to the ICP increasing effects of volatile agents?
Patients with CNS occupying tumor/lesion.
S19
What average ICP increase is seen with volatile use?
7mmHg
S19
At what volatile dosage does ICP increase?
> 0.8 MAC
S19
What do volatiles do to the respiratory system?
Dose dependent:
- Tachypnea
- ↓ VT
S20
How do volatiles cause their respiratory effects?
- Direct depression of medullary ventilatory center.
- Interference with intercostal muscles.
S20
Rate change insufficient to maintain Vm or PaCO2
SLIDE @ 20
At what volatile dosage would apnea be seen?
1.5 - 2 MAC
S20
All volatiles with blunt both the hypoxic and hypercarbic response. T/F?
False.
N₂O does not blunt the hypercarbic response.
S21
How can the hypercarbic response be preserved whilst using volatile anesthetic gasses?
- Use N₂O and volatile together.
S21
What effect is seen in the graph below?
Use of N₂O-desflurane decreasing CO₂ induced hypercarbia compared to desflurane alone.
S22
What is hypoxic pulmonary vasoconstriction?
Contraction of pulmonary arteries to shunt blood away from poorly ventilated portions of the lung.
S23
When is the blunting of HPV most concerning?
When one lung ventilation is being utilized.
S23
How fast is the HPV response?
Fast: within 5 minutes regional blood flow is ½ of normal.
S23
50% depression of HPV occurs at ___ MAC.
2
S23
Which volatile(s) does not cause cardiac depression?
N₂O
S24
How do volatiles cause hypotension?
- Direct myocardial depression by altering Ca⁺⁺ entry and SR function.
S24
Slide 25
Volatiles will cause a dose-dependent decrease in __ , __ , and CO.
contractility ; SV
S26
When is volatile depression of cardiac function most concerning?
With pathologic hearts (particularly pathologies of ↓ contractility)
S24
What volatile can cause significant tachycardia with overpressurization?
Desflurane
S25
When will sevoflurane begin to cause increases in heart rate?
Only at > 1.5 MAC
S25
What variables confound the tachycardic effect of volatiles?
- Anxiety
- Concurrent opioids
- β blockade
- Vagolytics
S25
What volatile is slightly sympathomimetic, causing a slight increase in CO?
N₂O
S26
Is the coronary steal effect of volatiles clinically significant?
Nope
S26
What electrocardiac effect do volatiles have?
QT prolongation via inhibition of K⁺ currents.
increse risk of Torsades
S27
Which volatile has minimal pro-arrhythmic activity?
N₂O
S27
What volatile is the gas of choice and which one is not the gas of choice for EP ablations and? Why?
- Sevoflurane
- Other volatiles increase refractoriness of accessory pathways making identification of arryhthmia location difficult such as ISOFLURANE
Sevo gang.
S27
Volatile neuroendocrine modulation will cause a perioperative surge in __, ___, and ___.
catecholamines; ACTH; & cortisol
S28
Volatiles will suppress what important immune system components?
Volatiles suppress monocytes, macrophages, and T-cells.
S28
What does the total neuroendocrine profile of volatile anesthetics suggest for cancer patients undergoing surgery?
Neuraxial anesthesia is likely better than GA for cancer patients.
S28
What hepatic blood flow changes are seen with volatile administration?
Portal vein dilation = ↑ portal vein flow.
S29
Which volatile is the only one that decreases portal vein flow?
Halothane (likely contributes to halothane hepatitis)
s29
What is volatile hepatotoxicity?
When is it a concern?
- Inadequate oxygenation of liver cells via ↓ blood flow and ↑ O₂ demand.
- Concern for patients with preexisting liver disease.
S30
What is Type 1 Volatile hepatotoxicity?
- Direct toxicity or free radical effect 1-2 weeks post surgically with N/V & fever in 20% of patients.
S30
What is Type 2 Volatile Toxicity?
- Reaction caused only with previous exposure to volatile with eosinophilia, fever, and higher mortality rate from hepatitis and necrosis.
- 1 month after exposure
S30
Which volatile is the choice anesthetic for severe liver disease? Why?
Sevoflurane: broken down to vinyl halide and won’t stimulate antibody production causing a Type II reaction.
Sevo the GOAT gas fr
S31
What volatiles are metabolized into acetyl halides? What is the significance of this?
Enflurane > Iso > Des
- Acetyl halides can cause antibody reactions especially with previous exposure to halothane or enflurane.
S31
What are the renal effects of volatile anesthetics?
Dose dependent decrease in RBF, GFR, and UO from CO depression.
S32
How can the renal effects of volatile anesthetics be counteracted?
Hydration (both pre-operative and intra-operative).
S32
What other organ (besides the heart) undergoes protective ischemic preconditioning from volatile anesthetics?
Kidneys
S32
What toxic metabolites of volatiles can cause nephrotoxicity?
Why is this not an issue typically?
- Fluoride metabolites
- Newer volatiles are exhaled prior to being metabolized.
S33
What volatile is 70% metabolized and can cause fluoride metabolite nephrotoxicity more than any of the other volatiles?
Methoxyflurane
S33
What measure is utilized in CO₂ absorbents today to help prevent the formation of compound A?
75% or greater concentrations of calcium hydroxide.
S34
What does Sevoflurane mixed with CO2 create? And what kind of toxin is it?
creates Compound A which is a nephrotoxin
Compound A not seein in U.S. anymore d/t change from K & NaOH to CaOH
S34
What volatile is predisposed to starting fires? Why?
- Sevoflurane
- Sevo + baralyme (absorbent) produce methanol and formaldehyde causing a heat and and eventual explosion.
S35
How is sevoflurane fire avoided?
- Addition of H₂O to Sevo
- Check temp of absorbent cannister
- Exchange exhausted absorbents
S35
What triggers Malignant Hyperthermia?
The s/s?
The treament?
Triggers: all volatile agents and succinylcholine
Symptoms: ↑ body temp, CO2 production, O2 consumption
Treatment:
Dantrolene
Blocks intracellular Ca++ release
Supportive care of rhabdomyolysis
S36
Which volatile anesthetics are emetogenic?
All
S37
What rate of PONV is seen with two triggering agents? (ex. desflurane and fentanyl)
25 - 30% PONV
S37
When is N₂O emetogenic?
At greater than 50% or 0.5 MAC
S37
Why is N₂O administration in a pregnant patient with B12 deficiency dangerous?
N₂O will oxidize the cobalt ion in B12 thus inhibiting methionine synthase = inhibition of DNA synthesis in fetu.
S38
Which volatile anesthetic can cause bone marrow suppression?
N₂O
S38
What is the result from increases in plasma homocysteine levels from N₂O administration?
If the patient also has low B vitamins and atherosclerosis, then N₂O increases risk of myocardial events.
S38
What is/are the obstetric effects of volatile anesthetics?
Dose-dependent (0.5 - 1.0 MAC) decrease in uterine smooth muscle contractility.
S39
When would a decrease in uterine muscle tone be useful?
With retained placenta
S39
When would an increase in uterine muscle tone be useful?
Uterine atony (↑ blood loss)
S39
Why is N₂O useful in mom’s post delivery?
Swiftly increases analgesia without opioid/benzo’s (use as the spinal starts to wear off).
S39
Which volatiles have a sweeter smell?
- Halothane
- Sevoflurane
S40
What is the only real benefit of halothane?
↓ N/V
S40
What are the four major concerns of halothane?
- Catecholamine-induced arrhythmias
- Pediatric bradycardia
- Hepatic necrosis
- Decomposing into HCl acid.
S40
Which two volatiles can’t be used for induction due to their awful smell?
- Isoflurane
- Desflurane
S41
Which volatile does not degrade, even after 5 years of storage?
Isoflurane
S41
If a vaporizer has a heating element, then the gas for that vaporizer can be assumed to be ____________.
Desflurane
S42
List the order in which volatiles will degrade into carbon monoxide if the absorbent becomes exhausted/dehydrated.
Desflurane (worst) > Enflurane
> Isoflurane > Sevoflurane (trivial)
Sevo on top per usual.
S42
Which volatile anesthetic would be the choice for inhalation induction? Why?
- Sevoflurane
- Least airway irritation & smells sweet.
Yet another example of sevo superiority.
S43
Which volatile causes the least increase in ICP?
Sevoflurane
In Sevo, we trust.
S42
How does N₂O produce skeletal muscle relaxation?
Trick question. It does not.
S44
What are the benefits of N₂O ?
- Good analgesia
- 2nd gas effect
S45
What are the major cons of N₂O ?
- N/V @ 0.5 MAC
- ↑ PVR
- No surgeries with air filled spaces
S45
