Inhaled Anesthetics-Part 2 (3) Flashcards
What are different ways to deliver anesthetic gas?
- Rebreathing (Bain)
- Non-rebreathing (self-inflating BVM/AMBU)
- Circle systems
What are the functions of the anesthesia circuit?
- Deliver O2
- Deliver inhaled drugs
- Maintain temp and humidity
- Remove CO2 and exhaled drugs
What gas delivery system is this?
Bain Circuit
What gas delivery system is this?
Non-rebreathing (AMBU or BMV)
Not used alot for anesthesia gas (used for O2)
How are different Bain Circuits named?
Alphabetically (A,B,C etc)
What does the circle system have that the bain and BMV do not have?
CO2 absorbent
What type of circuit is this?
Circle system
What parts does the circle system have?
- Fresh gas inlet
- Inspiratory and expiratory limbs
- Reservoir bag
- CO2 absorbent
- One way valves
- Y piece
What is the downside of a circle system?
Stationary→ have to go on transport circuit when leaving room
How does high flow inhalation relate to minute ventilation (Vm)?
Fresh gas flow is greater than minute ventilation
What is the difference in low flow and high flow ventilation?
How it relates to minute ventilation:
High flow: FGF >Vm
Low flow: FGF< Vm
When is it common to use high flow anesthesia?
When first inducing the patient→ using high flow O2 to build up O2 reserves and get rid of N2
De-nitrogenate and build up O2 reserve
How does high flow anesthetic impact anesthetic gas?
Cause rapid changes in anesthetic
Turning gas MAC up and increasing flow rate= increases concentration and delivery rate
If a patient is moving during procedure and you dont have any IV drugs on hand, what is the fastest thing to get them deeper?
Turn gas concentration up and flow up at the same time
How does high flow prevent rebreathing?
There is always fresh gas and CO2 is always cleared by the fast flow of O2
High flow is _________ by using excess fresh gas and volatile than needed.
Wasteful
Why might humidification be added to high flow O2?
High flow cools and dries delivered volume
How does Low Flow anesthesia differ from High flow?
- FGF< Vm
- Low cost
- Less cooling/ drying
- VERY slow changes in anesthetic
What can be done if it looks like the case is almost finished and you have turned the vapor off and turned the O2 up to wash out the gas, but the surgeon messes up a sitch?
Can turn O2 back down to low flow→ gives more time for anesthetic to leave the circuit
What was a PRIOR concern with low flow anesthetics and Sevoflurane?
Compound A production
What factors influence price of anesthetics?
- Cost of liquid in mL
- Volume percent of anesthetics delivered (Potency)
- Fresh gas flow rate
What are benefits of volatile anesthetics?
Bronchodilation
What is the MOA of volatile anesthetics causing bronchodilation?
Relax airway smooth muscle:
* Block VG Ca++
* Deplete Ca++ in SR
What alters the bronchodilation effects of volatiles?
Inflammatory processes w/ epithelial damage
Need intact epithelium to get best bronchodilation
If a healthy patient doesnt have bronchospasm, does the volatile anesthetic still cause bronchodilation?
No, baseline pulmonary resistance is unchanged (does not have increased bronchodilation from volatiles)
Which patient population would have the best bronchodilation response to volatile anesthetics?
If a patient goes to the OR and is healthy with intact epithelium and has bronchospasm
What are risk factors for bronchospasm?
- Cough response with ETT
- Age <10
- URI
Which volatile is the least irritating and best at bronchodilating?
Sevo
Which volatile may worsen bronchospasm (esp. in smokers) d/t pungency and irritation?
Desflurane
Which volatile would you want to avoid in smokers?
Desflurane
Which agents are best at decreasing respiratory resistance? (bronchodilating)
Sevo
Halo
Iso
Thiopental/Des (worst)
Volatile anesthetics have a dose dependent __________ ___________ relaxation
skeletal muscle
Do all inhalation agents have relaxation effects on skeletal muscles?
Not Nitrous Oxide
How do volatiles potentiate depolarizing and non depolarizing NMBs?
- nACH receptors at neuromuscular junction
- Enhance glycine at the SC
What is ischemic preconditioning and how do the volatiles do this?
- Small exposure to ischemia prior to longer periods of ischemia with in a few days→ the ischemia isnt as bad
*If you expose pt to small amount of volatile then they are exposed to it again a few days later→ it isnt as damaging to the myocardium because their body has already seen it
What dose can Ischemic preconditioning occur at?
as low as 0.25 MAC
What is ischemic preconditioning process mediated by?
Adenosine:
* Increases protein kinase C activity
* Phosphorylates ATP sensitive K+ channels
* Production of reactive O2 species (ROS)
* Better regulate vascular tone
Ischemic preconditioning prevents ___________ injury.
Reperfusion
*cardiac dysrhythmias
* contractile dysfunction
* clinically apparent in delaying MI for PTCA, CABG
What are negative aspects of volatile anesthetics?
- Decrease CMRO2 and cerebral activity
- Increase CBF (may increase ICP)
- Potential loss of cerebral autoregulation
- Respiratory depression
- Blunts hypoxic and hypercarbic response
- Dose dependent decrease in HPV
- Direct Myocardiacldepressant
- Increase HR
- Decrease CO
- Prolonged QTc
- ANS and HPA activated
- Decrease RBF
- malignant hyperthermia
At what dose does CMRO2 and cerebral activity decrease with volatile anesthetics? What is the MAC for burst suppression and isoelectic?
Approx 0.4 MAC (as wakefulness changes to unconsciousness)
1.5 MAC burst suppression
2 MAC: electrical silence
Which volatile anesthetic has the least impact on CNS activity?
They are all equal: Iso=Sevo=Des
CNS activity doesnt affect choosing a volatile
Which volatiles have potential for anticonvulsant activity at high concentrations?
Des, Iso, Sevo (all work about the same)
High concentrations and with hypocarbia
Which volatile causes seizures? At what dose?
Enflurane→ especially above 2 MAC or PaCO2 <30 mmHg
How do volatile anesthetics affect SSEPs and MEPs?
Dose related decrease in amplitude and increase latency (0.5-1.5 MAC)
Increased latency= spread them further apart
What dose of volatile can be used that will not interfere when using SSEP and MEPs monitoring? (back cases)
up to 0.5 MAC volatile
would have to give something else to add with the 0.5 MAC (N2O or synergistic gtt)
What is SSEP?
somoatosensory evoked potentials→ ex: stimulate pts toe, signal goes from toe to brain to brain recognizes the signal
What is MEP?
Motor evoked potential→ ex: stimulate brain motor cortex and cause motor response to stimulation
Can you give 0.5 MAC of 2 different volatiles?
No, if giving 2 different anesthetic gases one would have to be nitrous
Machine will not let you open 2 vaporizers at the same time
What cases do we use SSEP and MEP?
Spinal cord/back cases (EEG tech in OR doing these)
If we are doing a back case with SSEP/MEP we cant use more than _____ MAC of volatile d/t decrease in amplitude and increase in latency.
0.5
What is the total MAC of 60% N2O and 0.5 MAC Sevo?
60% N2O= 104 MAC= about 0.5 MAC
0.5 MAC volatile
= 1MAC total
If you can only use 0.5 MAC of volatile to maintain SSEP and MEP, would it be better to give boluses of narcotic or start a gtt?
Narcotic gtt→ more consistent
Why does CBF increase with volatile anesthetics?
Volatiles cause vasodilation→ increase CBF d/t decreased cerebral vascular resistance
At what dose of volatile does CBF start to increase?
0.6 MAC and greater
* Onset occurs in minutes despite lack of BP change
What patients are we concerned about using volatile anesthetics with based on the CNS effects?
Neuro patients/ head injuries d/t risk for increased ICP
Which volatile has less vasodilatory effect causing less increase in CBF?
Sevo
Which volatile is best for neuro patients/ head traumas? What if you dont have sevo?
Sevo
Iso and Des are same in regards to CBF effect
Which volatile cause the biggest increase in CBF?
(big increase) Halothane → enflurane→ iso/des → sevo (less increase)
_______ is a potent vasodilator, so you wouldnt choose this for patients at risk for increase ICP or with pneumocephalus
Nitrous
At what dose is autoregulation lost with halothane, sevo, and iso/des?
Halothane: Lost by 0.5 MAC
Sevo: autoreg preserved to 1 MAC
Iso/Des: Lost 0.5-1.5 MAC
All volatiles lose autoregulation at around 1 MAC
If BP stays between ____ and _____ then we have enough O2 and blood flow to the brain
50 mmHg to 150 mmHg (autoregulation zone)
What MAC does increase ICP occur? How much does ICP increase with volatiles?
Onset >0.8 MAC
Increases about 7mmHg
_______ opposes increased intracranial pressure
Hyperventilation (decrease in CO2)= vasoconstriction
Which patients are most at risk for developing increased ICP from volatiles?
Patients with space-occupying lesions (wouldnt be able to tolerate any more pressure?)
Volatiles cause dose dependent respiratory depression. What does this do to rate and VT?
Increases rate: not sufficient to maintain minute ventilation or PaCO2
Decreases Vt
What is the MOA of volatiles causing respiratory depression?
*Direct depression of medullary ventilatory center
- Interferes with intercostal muscles→ diaphragm descends, chest wall collapses inward
At what dose dose apnea from volatile agents occur?
1.5-2.0 MAC
Volatiles blunt ________ and _______ responses
Hypoxic response
Hypercarbic response
decreases bodys need to take a breath in response to low O2 or high CO2
Hypoxic response in the body is normally mediated by _____ ______.
carotid bodies
At ____ MAC 50-70% hypoxic response is depressed and _____ MAC 100% depression of hypoxic response
0.1 MAC
1.1 MAC
Which volatiles blunt hypoxic response?
All volatiles AND nitrous
Lasts up to several hours post op
Which volatiles blunt hypercarbic response?
Nitrous does NOT increase PaCO2
Can substitute for part of MAC for less depression
At what dose do volatiles cause 50% decrease in hypoxic pulmonary vasoconstriction?
2 MAC= 50% depression of HPV
Wont be giving enough volatile to see HPV depressed
What is hypoxic pulmonary vasoconstriction?
Normal contraction of pulmonary artery smooth muscle to divert blood to better ventilated areas
*Optimized V/Q
*Maximal response lasts 2-4 hours
When is HPV response most concerning?
1 lung ventilation cases
What effects do volatiles have on cardiac contractility?
- Dose dependent decrease in contractility, SV, and CO
- Decrease in MAP d/t decrease in SVR
Which patient population has a greater significance in CV depression with volatile anesthetics?
Patients with heart disease that already have altered contractility
Does nitrous cause cardiac depression?
No
What do volatiles do to heart rate? What dose causes HR increase with sevo, iso, and des?
Increase HR→ more volatile= higher HR
Sevo: >1.5 MAC
Iso and Des: lower concentrations have increase HR
What happens from CV standpoint with high doses of desflurane? Who would this be an issue for?
VERY tachycardic
* Not good with ischemia or aortic stenosis
* Need to titrate des slowly
Cannot rapidly jack up the des with induction in these patients
What things may affect the tachycardia from increased desflurane with induction?
*Anxiety (increase)
*Opioids (decrease)
*Beta-blockade (decrease)
*Vagolytic/anticholinergic administration (increase)
Volatiles cause a _________ in cardiac output
Decreases: Mild increase in HR but decreases in SVR so CO is decreased
Which inhalation agent works as a sympathomimetic causing a mild increase in cardiac output?
Nitrous
How can volatiles lead to cardiac dysrhythmias?
*Prolonged QT interval in healthy patients→ inhibition of K+ current
* Potentially increase risk of torasades
What drugs should be avoided in patient that already have prolonged QT interval?
Other drugs that prolong QTc (creates additive effects)
EX: ondansetron, amiodarone
Does nitrous cause dysrhythmias?
Minimal proarrhythmic effect
What volatiles should be avoided with ablations studies?
*ablation studies= trying to cause dysrhythmias
*Iso increases refractoryiness of accessory pathways
*Sevo has no effect→ better to avoid volatiles when trying to cause dysrhythmias and use procedural sedation
How do volatiles affect neuroendocrine system?
Causes neuroendocrine stress response
*ANS and HPA activated
* Perioperative surge in catecholamines, ACTH, cortisol
There is evidence that GA with volatiles increases occurrence of ___________.
Cancer: Increases metastasis and mortality
Volatile anesthetics suppress _________, __________, and ________ cells
Monocytes, macrophages, and T cells
Some studies show this if you have known cancer, then using __________ or _______ anesthesia may be better than GA
TIVA or Neuraxial
How do volatile anesthetics impact hepatic blood flow?
Maintain total and hepatic artery flow
Increase portal vein flow (vasodilation) → at 1-1.5 MAC
Iso=Sevo=Des (all about the same liver wise)
What is the one volatile that decreases hepatic flow?
Halothane→ Decreases O2 delivery (caused hepatitis)
What causes hepatotoxicity?
Inadequate oxygenation of hepatocytes
* Decreased blood flow, enzyme induction, increased O2 demand
What is type 1 hepatotoxicity?
- 20% of patients (most patients)
- 1-2 weeks after exposure
- Direct toxic effect or free radical effect
- Nausea, lethargy, fever (flu like)
What is type 2 hepatotoxicity?
- Less common than type 1
- Immune-mediated response against hepatocytes
- Ig antibodies: eosinophilia, fever
- 1 month after exposure
- High mortality→ acute hepatitis, hepatic necrosis
What is one of the reasons we dont see hepatitis as a side effect in modern volatile anesthetics? What are Iso/Des metabolized into?
- The way they metabolize
- Iso/Des are oxidized by CYP450 to acetyl halides metabolites→ they are capable of causing antibody reactions but they dont
What is sevo metabolized to?
Vinyl Halide
Not able to stimulate antibody formation
How can reduced RBF, GFR, and urine output from volatiles be prevented?
- Preop hydration
__________ can also present as low urine output
Positioning→ If head down then the urine wont flow as well
When do we put foleys in?
In cases than are 2 hours or longer
What component do most volatile anesthetics have that can cause metabolites?
Fluoride
What was the 1st volatile that was discovered to cause fluoride toxicity?
Methoxyflurane
*70% metabolism in the kidney
* removed from market
How does fluoride toxicity present?
- Hyperosmolarity
- Hypernatremia
- Increased creatinine
Where are most of the current (newer) volatiles metabolised?
Most of them are exhaled and not metabolized in the kidneys because they are poorly soluble (dont like to stay in the blood)
What is Compound A?
Fluoromethyl-2,2-difluro-1-vinyl ether
*nephrotoxin metabolite
What was thought to cause formation of compound A?
Made between Sevo and low flow anesthetic (Less than 2L/min)
What did CO2 absorbent use to be made from that caused formation of compound A with low flow sevo? What is CO2 absorbent made with now?
Potassium and sodium hydroxide
Now CO2 absorbent is made with calcium hydroxide
How many parts per million of compound A does it take to cause ATN in rats? How many ppm to be fatal in rats?
100ppm
400 ppm fatal
What were the ppm tested in the anesthesia circuit at 1L, 3L, and 6L sevo?
1L: 19.7 ppm
3L: 8.1 ppm
6L: 2.1 ppm
WAY less than fatal amount of 400 ppm or ATN amount of 100ppm→ come to the conclusion that low flow anesthesia and sevo has nowhere near the amount of compound A to be dangerous
Why is it important to check temperature of absorbent cannister with sevo administration?
Sevo reacts chemically with desiccated absorbent
*Produces methanol and formaldehyde
* Reacting with heat leads to faster reaction and more heat then spontaneously combusts
* Additional water added to sevo absorbent
How is malignant hyperthermia diagnosed?
Caffeine contracture test
What are triggers for malignant hyperthermia?
Volatile agents
Succinylcholine
What causes malignant hyperthermia?
Hypermetabolic state of skeletal muscle
* Excessive release of Ca++
* Muscle rigidity
* Rhabdo
* Hypercarbia
What are symptoms of malignant hyperthermia?
*Co2 production
* O2 consumption
* Increase body temp
What is the mortality rate of malignant hyperthermia if untreated and what is the treatment?
80% mortality if untreated
Tx: Dantrolene (CCB)→ blocks intracellular Ca++ release and supportive care for rhabdo
Which volatiles cause PONV?
*All volatiles are emetogenic
* Nitrous >0.5 MAC (dont use with hx N/V)
How common is PONV with GA?
25-30%
2 risk factors: volatiles and opioids
Tx with multiple different meds
How does nitrous cause B12 deficiency?
Oxidizes cobalt ion in B12→ inhibits methionine synthase→ inhibits DNA synthesis
*be careful with Nitrous and 1st semester of pregnancy (fetus at risk)
Which volatile suppresses bone marrow?
- N2O
- 24 hours after exposure
- want to be cautious with immunosupressed patients and pediatric cancer patients?
Volatiles increase plasma homocysteine levels. What does this do?
Associated with low B vitamins and increase levels of atherosclerosis
more MI events post op
How do volatiles impact OB population?
Dose-dependent (0.5-1.0 MAC) decrease in uterine muscle contractility
*useful with retained placenta
*worsens blood loss in uterine atony
If a pt is post c section and you cant get the bleeding to stop, what should you do with the volatile?
TUrn it off
How does nitrous effect uterine contractility?
No effect; just increases analgesia
What is the solubility of halothane?
High potency and intermediate solubility
* wants to stay in the blood (slow induction and slow wake up)
Is Halothane still on the market?
No, causes hepatitis
Halothane is a halogenated ________
Alkane
Which volatile has lower risk for N/V d/t sweet non pungent odor and is non-flammable?
Halothane
What are concerns with halothane?
*Catecholamine-induced arrythmias
* Occasional Hepatic necrosis
* Pediatric Brady-arrythmias
* Decomposition to HCl Acid
What is another name for isoflurane? What is it an isomer of?
Forane
Isomer of enflurane (highly potent and highly pungent)
Why is it a good think that iso is resistant to metabolism?
Unlikely to cause organ toxicity
What is the solubility of iso? Is it stable?
Intermediate solubility
Very stable (no deterioration after 5 years)
*Expensive to purify
How does Desflurane composition differ from Isoflurane?
*Fluorinated methyl ethyl ether
* Identicle to iso (F Sub for Cl-)
* decreased solubility (wants to leave the blood and go to fat) and potency
* Increase vapor pressure
Why did Des use to require a special vaporizer?
Use to have heated vapor pressurizer bc vapor pressure is so close to atmospheric pressure
Which volatile in practice is the most pungent?
Desflurane
Last choice for inhalation induction
*coughing, salivation, breath holding, laryngospasm (with >6% FI)
What happens when Des is over-pressurized?
Increasing MAC with induction= SNS stimulation
*VERY rapid HR
*avoid with aortic stenosis and cardiac ischemia
What happens to Des if the CO2 absorbent is dehydrated?
Degrades to CO
What is another name for desflurane?
Suprane
What is another name for sevoflurane and what is the chemical structure?
Ultane
Fluorinated methyl isopropyl ether
How does Sevo solubility compare to Des?
Sevo has low solubility (not as low as Des)
Which volatile has the least airway irritation?
Sevo: Sweet smelling not pungent
How is sevo metabolised?
- Inorganic fluoride
- Least likely to form CO
- Compound A (low risk)
***VERY SAFE
Which volatile suppresses lidocaine induced seizure activity?
Sevo
Is Nitrous oxide ever the sole anesthetic?
Usually not, supplement
Low solubility and potency (sweet smelling/odorless)
No skeletal muscle relaxation
Cant deliver 1 MAC (1 MAC= 104)
What are pros and cons of routine nitrous?
Pro→ Good analgesia, 2nd gas effect (quicker inhalation
Cons→ N/V in 50% (around 0.5 MAC) , Increase PVR (increase R-L shunt in neonates and jeopardize arterial oxygenation)
