SS25 3-10 Inhaled Anesthetics Part 2 (Exam 3) Flashcards
What are the purposes of the anesthesia circuit?
- Delivers O₂ and inhaled anesthetics
- Maintenance of temperature & humidity
- Removal of CO₂ and exhaled drugs
Explain how the anesthesia circuit maintains temperature/ humidity.
Utilizes the nose/pharnyx to maintain natural moisture and warmth
What types of gas delivery systems are there?
- Rebreathing (Bain system)
- Non-rebreathing (self-inflating BVM system)
- Circle systems (Anesthesia machine)
- Why is the BVM system a great way to give volatile anesthetics?
- What is the key difference with the BVM reservoir bag?
- What can you add to BVM system?
**- Trick question! ** Non-rebreathing BVM system is not a good way for inhaled drugs. It’s very effective for O2 and air delivery.
- Must self-inflate
- Able to build on it: add peep; add another bag; add O2
Side note:The way the BVM is set up can control how much re-breathing we have
What type of system is depicted below?
Where is the aPL valve located on this system?
- Bain Circuit = Rebreathing
- Blue circle depicts aPL below.
List key characterictics of Bain circuit based on labeled points
- A: Patient end that connects to ETT
- B: Able to connect to supplemental O2 via side port
- C: Another O2 connector option
- D: Acts as typical reservior bag
- E: APL valve open/ shut to make bag inflate more or less (control positive pressure)
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
Bag inspiratory drive v. vent inspiratory drive
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
- ETT connection
When fresh gas flow (FGF) exceeds V̇m then you have _________________.
High Flow Anesthesia
When V̇m exceeds fresh gas flow (FGF) then you have _________________.
Low Flow Anesthesia
When would one see rapid changes in anesthetic, lack of rebreathing, wasteful volatile use, and cool dried air?
High Flow anesthesia
What are common indications for high flow delivery?
- Build up O2 reserve (Pre-oxygenate)
- Rid N2 (Denitrogenate)
- Esp. in elderly and comorbid populations
For high flow anesthesia, you want to ____ (increase/decrease) gas concentration and ____ (increase/decrease) flow rate.
- increase; increase
When would one see lower cost d/t less volatile use, less cooling/drying of air, and slow changes in anesthetic?
Low Flow anesthesia
What is Compound A?
- Metabolite produced during Low Flow Sevo anesthesia and CO2 absorbent
- Low flow anesthesia (LFA) is 2 L/min (lower than normal Vm)
- Nephrotoxin
- No longer a concern but was prevalent for decades so will still be in literature/ discussed
What is the CO2 absorbent made of?
- How is this rlt Compound A?
- What was the rat discovery?
- CO2 absorbent is made of Potassium (K+) and Sodium Hydroxide (NaOH)
- Increase CO2 absorbant eith low flow sevo created Compound A (nephrotoxin)
- Discovered it takes about 100 parts per million (ppm) to cause Acute tubular necrosis (ATN) in rats and 400 ppm to kill them
Scientific word for Compound A:
- Fluoromethyl-2,2-difluro-1-vinyl ether
What do we know about Compound A now in modern day?
- 75% or more is now made out of Ca(OH)₂
- No clinical date to support Compound A is a risk at LFA
- Breathing circuit trial: @ flows of 1, 3 , 6 L/min we had 19.7, 8.1, 2.1 ppm
- Showed no change in BUN/ creat, no proteinuria & no glucosuria
- D/t low ppm not clincally significant
What is the quickest way to get a patient to stop responding to surgical stimuli?
- Turn up gas concentration and flow rate
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
- inflammatory processes & epithelialdamage alters effectiveness
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?
- Coughing w/ ETT in place
- <10 years old
- URI
What anesthetic is generally the best at bronchodilating?
- Sevoflurane (1st)
- Isoflurane (2nd)
Inhaled anesthetic of choice for pediatric patients:
- Sevoflurane
Sevo! Sevo! Sevo!
Which anesthetic can function as a pulmonary irritant?
- This leads to?
- Which population is at an increased risk?
- Desflurane
- Worsening bronchospam
- Smokers
Which volatile anesthetic in the graph below caused the greatest increase in airway resistance?
Lowest?
- Desflurane = ↑ airway resistance
- Sevoflurane = ↓ airway resistance
T/F: Inhaled anesthetics have a dose-dependent skeletal muscle contraction mediated via spinal cord.
- False
- dose dependent skeletal muscle Relaxation
Which volatile gas has no effect on the relaxation of skeletal muscles?
- N₂O (Nitrous Oxide)
Will volatiles potentiate or inhibit depolarizind and non-depolarizing NMBD’s?
- If so, how?
- **Potentiates **
- via sensitization of nACh receptors at NMJ
- via enhancement of glycine at the spinal cord
Side note: Volatile anesthetics cause enhancement of glycine leading to skeletal muscle relaxation as a solo agent
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 what MAC level?
0.25
What molecule mediates ischemic preconditioning?
Adenosine
Why does ischemic preconditioning happen?
(IPRV)
- Increases PKC activity
- Phosphorylation of ATP sensitive K⁺ channels
- Production of ROS
- Better vascular tone regulation
PKC = Protein Kinase C
ROS = Reactive Oxygen Species
What does ischemic preconditioning prevent?
- Reperfusion injuries
- Cardiac dysrhythmias
- Contractile dysfunction
- Delays MIs for PTCA and CABG
At what dose does volatile depression of CMRO₂ and cerebral activity begin?
- 0.4 MAC as wakefulness changes to unconsciosness
At what MAC would we see EEG burst suppression?
What about total electrical silence?
- 1.5 MAC = burst suppression
- 2 MAC = EEG electrical silence
At what MAC does 50% of patients not move to supermaximal stimuli (ie: surgical cut)?
- 1.0 MAC
Which volatile causes the most EEG suppression?
- Trick question. They all affect EEG’s the same.
- ’‘SID’’
Isoflurane = sevoflurane = desflurane
Which volatiles have anticonvulsant activity?
- At high or low concetrations?
- With hypercarbia or hypocarbia?
- DIS: Des, Iso, &Sevo
- At high concentrations & with hypocarbia
Which volatile is a proconvulsant?
- Risk factors?
- Enflurane
- Especially above 2.0 MAC or PaCO2 < 30 mmHg
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 - 1.5 MAC):
- ↓ amplitude
- ↑ latency (delayed frequency)
What effects does volatiles have on cerebral blood flow (CBF)?
- Dose-dependent effects
- ↑ volatile adminstration = ↑ vasodilation = ↑ CBF
- Can lead to ↑ ICP
At what MAC onset do you start to see an ↑CBF due to volatile administration?
- Onset > 0.6 MAC
Occurs within minutes despite lack of BP change
Which volatile has less vasodilatory effects?
Sevoflurane
Which volatile has the greatest effect on increasing CBF/ICP?
Halothane
Which volatile is the best for neuro cases? Why?
- Sevoflurane
- Preserves autoregulation mechanism up to 1 MAC
Hesd injuries
Is Sevo isn’t available what is the next option for volatile use with CBF management?
- Iso and Des pretty much equal effects per Dr. Kane
What patient population is most at risk due to the ICP increasing effects of volatile agents?
Patients with space-occupying lesions
At what volatile dosage does ICP increase?
- How much of an increase do we typically see?
- Onset > 0.8 MAC
- Increase in ICP by 7 mmHg
What opposes increased ICP?
- Hyperventilation
T/F: Nitrous is a potent vasodilator
- True
- Avoid diffusion into airspaces (ie: pneumocephalus)
Explain autoregulation differences between Halo, Sevo, Iso, & Des.
- Sevo preserves to 1 MAC
- Halo lost by 0.5 MAC
- Iso & Des lost by 0.5 - 1.5 MAC
Autoregulation varies patient to patient
Based off image, explain autoregulation.
- ICP, MAP, PaCO2, & PaO2 autoregulated between 50 - 150 mmHg
- Our goal is tomaintain within autoregulation (MAP > 60 mmHg / within 20% of baseline)
- Volatiles can cause expected shifts outside of autoregulation; must be prepared to treat those
What do volatiles do to the respiratory system?
Dose-dependent:
- Respiratory depression
- ↑ rate (Tachypnea)
- ↓ VT
- The more volatile used, the faster & shallower the patient will breath
The more volatile used, the faster&shallower thr patient will breath
How do volatiles cause their respiratory depression?
- Direct depression of medullary ventilatory center
- Interference with intercostal muscles
- Rate change insufficent to miantin Vm or PaCO2
Describe physical change in breathing muscles during respirstory depression.
- Diaphragm descends and chest wall collapses inward
At what volatile dosage would apnea be seen?
1.5 - 2.0 MAC
T/F: All volatiles will blunt both the hypoxic and hypercarbic response
- False. N₂O does not blunt the hypercarbic response
- N₂O does not increase PaCO2
All volatiles blunt hypoxic response (including N2O)
How can the hypercarbic response be preserved while using volatile anesthetic gasses?
- Use N₂O and volatile together (less depression)
What usually mediates blunting of hypoxic response with volatile administration?
- At what MAC(s)?
- Mediated by Carotid bodies
- 0.1 MAC= 50 - 70% depression - 1.1 MAC = 100% depression
Based on image, explain CO2 response to volatile use.
- All volatiles have a significant increase in PaCO2 (except N2O)
- Use of N₂O-desflurane decreases CO2-induced hypercarbia compared to desflurane alone.
What is hypoxic pulmonary vasoconstriction (HPV)?
- Compesatory contraction of pulmonary artery smooth muscle to shunt blood away from poorly ventilated portions of the lung.
- Optimizes VQ
When is HPV most concerning?
- In One-lung ventilation
How fast is the HPV response?
- Fast: within 5 minutes regional blood flow is ½ of normal
- Max response lasts up to 2 - 4 hours
50% depression of HPV occurs at ___ MAC.
- 2 MAC
- Volatiles cause a dose-dependent decrease HPV response but we never give 2 MAC for an entire case so we shouldn’t see this ever
Which volatile(s) does not cause cardiac depression?
- N₂O (Nitrous)
How do volatiles effect MAP?
- What dose-dependent changes occur?
- Direct myocardial depression by altering Ca⁺⁺ entry and SR function
- Dose-dependent ↓ in contractility, SVR, CO, & MAP
Most decrease seen with Halothane use “ H for heart probs”
When is volatile depression of cardiac function most concerning?
- In diseased hearts with altered contractility
What effect does volatiles have on heart rate?
- Dose-dependent increases in HR
What volatile can cause significant tachycardia with overpressurization?
- Desflurane
- Iso and Des can cause increased tachycardia at lower MAC concentrations than Sevo
When will sevoflurane begin to cause increases in heart rate?
- Only when > 1.5 MAC
What variables cofound/ obscure the tachycardic effect of volatiles?
- Anxiety
- Concurrent opioids
- β blockade
- Vagolytics
Compare CI/CO effects of volatile usage.
- Dose- dependent decrease in CI/CO
- Halothane has most decrease in CO
- Isoflurane seems to maintain CO up to about 1 MAC
What volatile is sympathomimetic, causing a slight increase in CO?
N₂O
What’s coronary steal syndrome?
- Is it clinically significant?
- Volatiles induce coronary vasodilation on 20-50 mm vessels preferentially
- Redistribution of blood from ischemic to non-ischemic regions
- Not significant
What electrocardiac effect do volatiles have?
- This causes an increase risk of what arrythmia?
- QT prolongation via inhibition of K⁺ currents in healthy patients
- Torsades
Be aware of other meds being used that proolong QT as well (ie: Zofran)
Which volatile has minimal pro-arrhythmic activity?
N₂O
Which volatile is the choice for EP ablations and why?
- Which volatile is poor choice for EP studies and why?
- Sevoflurane; no negative effects with ablations
- Isoflurane increases refractoriness of accessory pathways making identification of arryhthmia location difficult.
Volatile neuroendocrine stress response: will cause a perioperative surge in
- ANS and HPA (Hypothalamus Pituitary Axis) activated
- Perioperative surge in catecholamines, ACTH, & cortisol
“We know a lot about volatiles thanks to Edmond Eger” - Dr. Kane
Volatiles suppress what important immune system components?
- Volatiles suppress Monocytes, Macrophages, and T-cells (MMT)
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
- Evidence shows GA increases metastasis and mortality
- TIVA may be better choice for Ca patients
What hepatic blood flow changes are seen with volatile administration?
- Total hepatic BF maintained
- Hepatic artery flow maintained
- Portal vein flow increased d/t vasodilation
What MAC dose does portal vein flow increase?
- 1 - 1.5 MAC
Which volatile(s) decrease portal vein flow?
- Halothane
- Halothane Hepatitis common
- Decreases O2 delivery
What is volatile hepatotoxicity?
-When is it a concern?
- Inadequate oxygenation of hepatocytes via ↓ blood flow, enzyme induction and ↑ O₂ demand
- Concern for patients with preexisting liver disease
What is Type 1 Volatile hepatotoxicity?
- Direct toxic or free radical effect 1-2 weeks post surgically
- Flu-like symptoms (N/V, lethargy, & fever)
-20% of patients; more common than Type 2
What is Type 2 Volatile Toxicity?
- Immune-mediated (IgA) response against hepatocytes caused by previous exposure to volatile
- Charecterized by eosinophilia & fever
- Occurs 1 month after exposure
- Higher mortality with Acute hepatitis and necrosis
Why we don’t use Halothane in US
Volatile of choice for severe liver disease?
- Why?
-Sevoflurane: Metabolized to vinyl halide
- Unable to stimulate antibody production causing a Type II reaction
What volatiles are metabolized into acetyl halides?
- What is the significance of this?
- Enflurane > Iso > Des
- Oxidixed by P450 to acetyl halides
- 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
- Foleys for surgeries > 2 hrs
- Expect lower UOP d/t volatiles and may be positioning (gravity) (not rlt to Vasopressin release)
How can the renal effects of volatile anesthetics be counteracted?
- Pre-Op Hydration
What other organ (besides the heart) undergoes protective ischemic preconditioning from volatile anesthetics?
- Kidneys
What toxic metabolites of volatiles can cause nephrotoxicity?
- Nephrotoxic presentation?
- Why is this not an issue typically?
- Fluoride metabolites
- Hyperosmolarity, HyperNa, Increased creatinine (HIH)
- Newer volatiles have lower solubility so they’re **exhaled prior to being metabolized **
What volatile is 70% metabolized and can cause fluoride metabolite nephrotoxicity more than any of the other volatiles?
Methoxyflurane
Removed from market
What measure is utilized in CO₂ absorbents today to help prevent the formation of compound A?
- 75% or greater concentrations of calcium hydroxide [Ca(OH)₂]
What volatile is predisposed to starting fires? Why?
- Sevoflurane
- Sevo + desiccated absorbent produces methanol and formaldehyde causing a heat and speeding up reactiom which can lead to spontaneous combustion
How is sevoflurane fire avoided?
- Add water to Sevo
- Check temp of absorbent cannister (should feel like room temp; shouldn’t be hot)
Malignant Hyperthermia:
- Causes
- MOA
- S&S
- Diagnostic test
- Treatment
- Caused by all inhaled Volatiles and Succs
- MOA: Hypermetabolic state of skeletal muscle: Excessive Ca release; muscle rigidity; Rhabdo
- S&S: Fever, hypercarbia, hypoxia
- Test: Caffeine contracture test
- Tx: Dantrolene
80% mortality (high)
MOA of Dantrolene:
- Ca-channel blocker
- Blocks intracellular Ca release
- Supportive care for Rhabdo
Which volatile anesthetics are emetogenic?
- All
Maybe just TIVA; no volatiles
What rate of PONV is seen with two triggering agents?
- Example of triggering agents?
- 25 - 30% PONV
- Volatile + Opioid
- Other risk factors: - Females, abd sx, pregos, red heads
Pre-op combo drugs
When is N₂O pro-emetic?
- Greater than 0.5 MAC
- Just don’t give it
Metabolic effects of volatiles:
(BMH)
- B12 deficiency
- Megaloblastic BM supression
- High plasma homocysteine levels
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 fetus
- High risk: 1st tri pregos
Which volatile anesthetic can cause megaloblastic bone marrow suppression?
- N₂O
- After 24 hrs after exposure; repeated exposured < 3 days cumulative intervals
- high risk: Immunocompromised patients
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
OB effects of volatile use:
- 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
- Increase volatile to dilate
When would an increase in uterine muscle tone be useful?
- Uterine atony (↑ blood loss)
- Decrease volatile
Why is N₂O useful in mom’s post delivery?
- Swiftly increases analgesia without opioid/benzos (use as the spinal starts to wear off)
- No effect on contractility
Which volatiles have a sweeter smell (non-pungent)?
- Halothane
- Sevoflurane
Halothane profile:
- molecular makeup?
- high or low potency?
- sweet or smelly odor?
- high, intermediate, or low solubility?
- Halogenated alkane
- Compatible with inhalation induction: high potency; sweet/ non-pungent odor
- Intermediate solubilty = wants to stay in blood (so slower induction and a slower wake up)
Benefit(s) of Halothane:
- Lower risk of N/V
- Non-flammable
What are the four major concerns of Halothane?
(CHPD)
- Catecholamine-induced arrhythmias
- Hepatic necrosis
- Pediatric brady-arrhythmias
- Decomposing into HCL acid (Thymol preservative added)
Which two volatiles can’t be used for induction due to their awful smell/pungent?
- Isoflurane
- Desflurane
Which volatile does not degrade, even after 5 years of storage?
Isoflurane
Isomer of Enflurane:
- Isoflurane (Forane)
Creation order: Halothane → Enflurane → Isoflurane
Which volatile is considered most famous/popular per lecture?
- Desflurane (Suprane)
Sevo also very popular
Isoflurane profile:
- high or low potency?
- sweet or smelly odor?
- high, intermediate, or low solubility?
- name of purification process?
- Is it nephro/hepatotoxic?
- Shelf life?
- Highly potent
- Highly pungent
- Intermediate solubiity
- $$$ to purify (Distillation)
- No, Resistant to metabolism (avoids toxicity)
- Stable; no deterioration after 5 years
Which inhaled volatile requires a vaporizer with a heating element?
- Desflurane
- Requires special vaporizer
Desflurane profile:
- molecular make up?
- what volatile is it very similar to?
- what is the difference b/w them?
- Fluorinated methyl ethyl ether
- Identical to Isoflurane except Fluoride substituted for Chloride
Desflurane profile:
- high, intermediate, or low potency?
- sweet or smelly odor?
- high or low vapor pressure?
- low potency
- low solubility (wants to leave blood and go to receptors)
- Most pungent (coughing, salivation, breath holding, laryngospasm occurs in greater than 6%)
What happens if you over-pressurize Desflurane?
- Mediated by what?
- Tachycardia d/t SNS stimulation
What does Des degrade into?
- Cause?
- How could this happen?
- Will degrade into Carbon monoxide (CO) if absorbent dehydrates
- Could happen if you forget to turn O2 flow meter off
List the order in which volatiles will degrade into carbon monoxide if the absorbent becomes exhausted.
-
Desflurane (worst) > Enflurane
> Isoflurane > Sevoflurane (trivial)
DEIS
Which volatile anesthetic would be the choice for inhalation induction? Why?
- Sevoflurane
- Smells sweet = Least airway irritation of modern volatiles
Sevo profile:
- molecular make up?
- high, intermediate, or low potency?
- Fluorinated methyl isopropyl ether
- low solubility
Neuro effects of Sevo:
- How does it effect ICP?
- How does it effect lidocaine-induced seizures?
- Least cerebral vasodilation
- Drug of choice (DOC) for increased ICP
- Supresses lidocaine-induced sz activity
Pop Quiz: What’s the blood:gas coefficient for Sevo and Des?
- Which one has the lower/poorer solubility? Clinical significance?
- Sevo = 0.69
- Des = 0.42 (lower solubility)
- The lower the solubilty the more it wants to leave blood and go to receptors in brain (VRG), fat, etc.
Sevo metabolism:
- Metabolite?
- Does is for CO and Compound A?
- Inorganic Fluoride
- All volatiles can form CO but Sevo is least likely
- We now know it won’t form toxic levels of Compound A from Low Flow
Sevo = super safe and predominant volatile
Nitrous Oxide (N₂O) profile:
- high or low potency?
- sweet or smelly odor?
- high, intermediate, or low solubility?
- Low potency
- Sweet/odorless
- Lowest solubility
How does N₂O produce skeletal muscle relaxation?
- Trick question! It does not.
- Unable to be sole anesthetic b/c can’t deliver1 MAC
What are the benefits of N₂O ?
- Good analgesic properties (ie: spinal wearing off, dentist fillings)
- 2nd gas effect
What’s 2nd gas effect?
- Quicker inhalation b/c N₂O diffuses in then out of pulmonary capillaries and they collapse causing the concentration
What are negatives of N₂O ?
- N/V > 50% @ 0.5 MAC
- ↑ PVR
- No surgeries with air filled spaces
- N₂O is contraindicated in what patient population? Why?
- Neonates
- May increase right-to-left shunt
- Jeopardizes arterial oxygenation
