Inhaled Anesthetics Part 2 (Exam III) Flashcards
What are the purposes of the anesthesia circuit?
- Delivery of O₂ and inhaled anesthetics
- Maintenance of temperature & humidity
- Removal of CO₂ and exhaled drugs
What types of gas delivery systems are there?
- Rebreathing (Bain system)
- Non-rebreathing (self-inflating BVM )
- Circle systems (Anesthesia machine)
What type of system is depicted below?
Where is the aPL valve located on this system?
- Bain Circuit
- Blue circle depicts aPL below. (Escape/overflow valve)
In the figure below, what portion of the anesthesia circle system is indicated by 1?
Inspiratory Unidirectional Valve (one way valve)
In the figure below, what portion of the anesthesia circle system is indicated by pink arrow?
Fresh Gas Inlet (O₂ & medical air)
In the figure below, what portion of the anesthesia circle system is indicated by 2?
CO₂ Absorber
In the figure below, what portion of the anesthesia circle system is indicated by 3?
Bag/Ventilator Selector Switch
In the figure below, what portion of the anesthesia circle system is indicated by 4?
APL Valve
In the figure below, what portion of the anesthesia circle system is indicated by 5?
Expiratory Unidirectional Valve
In the figure below, what portion of the anesthesia circle system is indicated by 6?
Expiratory Limb
In the figure below, what portion of the anesthesia circle system is indicated by 7?
Y-Piece
When fresh gas flow (FGF) exceeds V̇T then you have _________________.
High Flow Anesthesia
When V̇T exceeds fresh gas flow (FGF) then you have _________________.
Low Flow Anesthesia
When would one see lack of rebreathing, wasteful volatile use, and cool dried air?
High flow anesthesia
When would one see lower volatile use, less cooling/drying of air, and slow changes in anesthetics?
Low flow anesthesia
Do volatiles cause bronchostriction or bronchodilation?
Bronchodilaton
How do volatiles cause bronchodilation?
- Blockage of VG Ca⁺⁺ channels
- Depletion of SR Ca⁺⁺
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.
Will volatiles cause bronchodilation on their own (in a patient with no history of bronchospasm)?
No
baseline pulmonary resistance unchanged by 1-2 MAC
Histamine release or vagal afferent stimulation needed to cause spasm.
In a patient without history of bronchospasm, how much would you anticipate Pulmonary resistance to change with 1-2 MAC?
Baseline pulmonary resistance would be unchanged in patient with no history of bronchospasm.
What risk factors increase risk of bronchospasm?
- COPD
- Coughing w/ ETT in place
- <10 years old
- URI
What anesthetic is generally the best at bronchodilating?
- (#1) Sevoflurane (best in decreasing respiratory system resistance & not pungent)
- Halothane
Which anesthetic can function as a pulmonary irritant (especially in smokers)?
Desflurane
Which volatile anesthetic in the graph below caused the greatest increase in airway resistance?
Lowest?
- Desflurane = ↑ airway resistance
- Sevoflurane = ↓ airway resistance
Inhaled anesthetics engender a dose-dependent skeletal muscle relaxation. T/F?
True
Which volatile gas has no effect on the relaxation of skeletal muscles?
N₂O
Will volatiles potentiate or inhibit NMBD’s? How?
-Potentiate via inhibition of nACh receptors at NMJ.
-enhance glycine at spinal cord
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.
- Depress excitatory AMPA & NMDA (glutamate receptors)
- Enhance inhibitory glycine receptors
- Act on sodium channels (block presynaptic release of glutamate)
What is ischemic preconditioning?
Brief periods of ischemia preparing the heart for longer periods of ischemia.
Ischemic preconditioning with volatile anesthetics can occur as low as ______ MAC.
0.25
Why does ischemic preconditioning happen?
Mediated via Adenosine
- ↑ PKC activity
- Phosphorylation of ATP sensitive K⁺ channels
- Production of ROS (Reactive Oxygen Species)
- Better regulation of vascular tone.
What molecule mediates ischemic preconditioning?
Adenosine
What does ischemic preconditioning prevent?
“Reperfusion injuries”
- Cardiac dysrhythmias
- Contractile dysfunction
- Delays MI’s in CAD patients. (PTCA, CABG)
At what dose does volatile depression of CMRO₂ begin?
0.4 MAC
At what MAC would we see EEG burst suppression?
What about total electrical silence?
- 1.5 MAC = burst suppression
- 2 MAC = EEG silence
Which volatile causes the most EEG suppression?
Trick question. They all affect EEG’s the same.
Which volatiles have anticonvulsant activity?
Des, Sevo, & Iso
Sevo might cause seizures in pediatrics and healthy adults “at high concentrations & with hypocarbia.”
Which volatile is a proconvulsant?
Enflurane
Give an example of a somato-sensory evoked potential (SSEP).
Stimulation of the foot evoking an electrical response in the CNS.
Give an example of a motor-evoke potential (MEP).
Direct stimulation of the brain eliciting a twitch response in the hand.
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.
What specific effects will volatile agents have on SSEPs and MEPs?
Dose-dependent (0.5 - 1.5MAC):
- ↓ amplitude
- ↑ latency (delayed frequency)
What occurs with cerebral blood flow with volatile administration?
Dose dependent:
- ↑ CBF due to dilated vessels
- ↑ ICP
At what MAC would you expect to start to see an increase in CBF due to volatile administration?
At > 0.6 MAC
Which volatile has less cerebral vasodilatory effects?
Sevoflurane
Which volatile has the greatest effect on increasing CBF? (and thus ICP)
Halothane! Fallow by enflurane
ISO and DES are the same
N2O is a potent vasodilator (but we give < 1 MAC)
Which volatile is the best for neuro cases? Why?
Sevoflurane
(preserves CBF autoregulation mechanism up to 1 MAC).
What patient population is most at risk due to the ICP increasing effects of volatile agents?
Patients with CNS occupying tumor/lesion.
What average ICP increase is seen with volatile use?
7mmHg
At what volatile dosage does ICP increase?
> 0.8 MAC
What do volatiles do to the respiratory system?
Dose dependent:
- Tachypnea
- ↓ VT
How do volatiles cause their respiratory effects?
- Direct depression of medullary ventilatory center.
- Interference with intercostal muscles (diaphragm descends, chest wall collapses inward)
At what volatile dosage would apnea be seen?
1.5 - 2 MAC
All volatiles with blunt both the hypoxic and hypercarbic response. T/F?
False. N₂O does not blunt the hypercarbic response.
How can the hypercarbic response be preserved whilst using volatile anesthetic gasses?
- Use N₂O and volatile together.
What effect is seen in the graph below?
Use of N₂O-desflurane less depression hypercarbia response compared to desflurane alone.
What is hypoxic pulmonary vasoconstriction?
Contraction of pulmonary arteries to shunt blood away from poorly ventilated portions of the lung.
When is the blunting of HPV most concerning?
When one lung ventilation is being utilized.
How fast is the HPV response?
Fast: within 5 minutes regional blood flow is ½ of normal.
Maximal response lasting for 2-4 hours
50% depression of HPV occurs at ___ MAC.
2
Which volatile(s) does not cause cardiac depression?
N₂O
How do volatiles cause hypotension?
- Direct myocardial depression by altering Ca⁺⁺ entry and SR function
Dose dependent
- decreased contractility, SV & CO (more w/ Halothane)
- decreased in MAP primarily due to decreased in SVR (Des, Sevo, Iso)
Volatiles will cause a dose-dependent decrease in ______ , ______ , and CO.
contractility ; SV
When is volatile depression of cardiac function most concerning?
With pathologic hearts (particularly pathologies of ↓ contractility)
What volatile can cause significant tachycardia with overpressurization?
Desflurane
When will sevoflurane begin to cause increases in heart rate?
Only at > 1.5 MAC
What variables confound the tachycardic effect of volatiles?
- Anxiety
- Concurrent opioids
- β blockade
- Vagolytics
What volatile is slightly sympathomimetic, causing a slight increase in CO?
N₂O
Is the coronary steal effect of volatiles clinically significant?
Nope
What electrocardiac effect do volatiles have?
-QT prolongation via inhibition of K⁺ currents.
- increase risk of Torsade’s
Which volatile has minimal pro-arrhythmic activity?
N₂O
What volatile is the gas of choice for EP ablations? Why?
- Sevoflurane
- Other volatiles (iso) increase refractoriness of accessory pathways making identification of arryhthmia location difficult.
Sevo gang.
Volatile neuroendocrine modulation will cause a perioperative surge in _______, _______, and _______.
catecholamines; ACTH (Adrenocorticotropic hormone); & cortisol
Volatiles will suppress what important immune system components?
Volatiles suppress monocytes, macrophages, and T-cells.
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.
What hepatic blood flow changes are seen with volatile administration?
Portal vein dilation = ↑ portal vein flow at 1-1.5 MAC.
Which volatile is the only one that decreases portal vein flow?
Halothane (likely contributes to halothane hepatitis)
What is volatile hepatotoxicity?
When is it a concern?
- Inadequate oxygenation of hepatocytes via ↓ blood flow, enzymes induction and ↑ O₂ demand.
- Concern for patients with preexisting liver disease.
What is Type 1 Volatile hepatotoxicity?
- Direct toxicity or free radical effect
- 1-2 weeks post exposure
- Nausea, lethargy, fever “flue like s/s”
- 20% of patients.
What is Type 2 Volatile Toxicity?
- immune-mediated response against hepatocytes: eosinophilia, fever
- high mortality: acute hepatitis, hepatic necrosis
- needs prior exposure
- 1 month after exposure onset?
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
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.
What are the renal effects of volatile anesthetics?
Dose dependent decrease in RBF, GFR, and UO from CO depression.
How can the renal effects of volatile anesthetics be counteracted?
Hydration (both pre-operative and intra-operative).
What other organ (besides the heart) undergoes protective ischemic preconditioning from volatile anesthetics?
Kidneys
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.
What volatile is 70% metabolized and can cause fluoride metabolite nephrotoxicity more than any of the other volatiles?
Methoxyflurane
What measure is utilized in CO₂ absorbents today to help prevent the formation of compound A?
75% or greater concentrations of calcium hydroxide.
What volatile is predisposed to starting fires? Why?
- Sevoflurane
- Sevo + desiccated absorbent produce methanol and formaldehyde causing a heat and and eventual spontaneous combustion.
How is sevoflurane fire avoided?
- Addition of H₂O to Sevo
- Check temp of absorbent cannister
- Exchange exhausted absorbents
Which volatile anesthetics are emetogenic?
All
What rate of PONV is seen with two triggering agents? (ex. desflurane and fentanyl)
25 - 30% PONV
When is N₂O emetogenic?
At greater than 50% or 0.5 MAC
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.
Which volatile anesthetic can cause bone marrow suppression?
N₂O
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.
What is/are the obstetric effects of volatile anesthetics & at what MAC dose?
Dose-dependent (0.5 - 1.0 MAC) decrease in uterine smooth muscle contractility.
When would a decrease in uterine muscle tone be useful?
With retained placenta
When would an increase in uterine muscle tone be useful?
Uterine atony (↑ blood loss)
Why is N₂O useful in mom’s post delivery?
Swiftly increases analgesia without opioid/benzo’s (use as the spinal starts to wear off).
Which volatiles have a sweeter smell?
- Halothane
- Sevoflurane
- N2O (can also be odorless)
What is the only real benefit of halothane?
↓ N/V
What are the four major concerns of halothane?
- Catecholamine-induced arrhythmias
- Hepatic necrosis
- Pediatric bradycardia
- Decomposing into HCL acid. (Thymol preservative add to prevent)
Which two volatiles can’t be used for induction due to their awful smell?
- Isoflurane
- Desflurane
Which volatile does not degrade, even after 5 years of storage?
Isoflurane
If a vaporizer has a heating element, then the gas for that vaporizer can be assumed to be ____________.
- Desflurane
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.
Which volatile anesthetic would be the choice for inhalation induction? Why?
- Sevoflurane
- Least airway irritation & smells sweet.
Yet another example of sevo superiority.
Which volatile causes the least increase in ICP?
Sevoflurane
In Sevo, we trust.
How does N₂O produce skeletal muscle relaxation?
Trick question. It does not.
What are the benefits of N₂O ?
- Good analgesia “use in thin spinals”
- 2nd gas effect
What are the major cons of N₂O ?
- N/V > 0.5 MAC (50%)
- ↑ PVR (neonates increase right-to-left shunt. Jeopardize arterial oxygenation)
- No surgeries with air filled spaces
