Inhaled Anesthetics Part 2 (Exam III) Flashcards
What are the purposes of the anesthesia circuit? (3)
- 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 (BVM system)
- 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.
In the figure below, what portion of the anesthesia circle system is indicated by 1?
Inspiratory Unidirectional 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?
8?
6 = Expiratory Limb
8 = Inspiratory 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 bronchoconstriction 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 bronchospasm on their own (in a patient with no history of bronchospasm)?
No
Histamine release or vagal afferent stimulation needed to cause spasm.
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.
What risk factors increase risk of bronchospasm? (4)
- COPD
- Coughing w/ ETT in place
- <10 years old
- URI
What anesthetic is generally the best at bronchodilating?
- Sevoflurane
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 provide 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 sensitization of nACh receptors at NMJ.
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.
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?
- ↑ 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? (4)
- Reperfusion injuries
- Cardiac dysrhythmias
- Contractile dysfunction
- Delays MI’s in CAD patients.
At what MAC 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 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? At what MAC?
Dose-dependent (0.5 - 1.5MAC):
- ↓ amplitude
- ↑ latency (delayed frequency)
What occurs with cerebral blood flow with volatile administration?
Dose dependent:
- ↑ CBF due to vasodilation ⇒ ↑ 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 volatiles have the greatest effect on increasing CBF? (and thus ICP)
Halothane and N₂O
Which volatile is the best for neuro cases? Why?
Sevoflurane
(preserves autoregulation mechanism up to 1 MAC & minimal cerebral vasodilation).