Anaesthetic Gasses And Vapours Flashcards
Characteristics of voletile anaesthetic agents
Liquids with low boiling points (lower than water) and high saturated vapour pressure (higher than water) that evaporate easily
How are voletile anaesthetic distributed through the body at equilibrium
Same partial pressure all over (if not would be out of equilibrium and move down gradient) but varied concentrations dependant on partition coefficients
Phases of volatile anaesthetic distribution to brain
Delivery phase
Pulmonary phase
Circulatory phase
What is the delivery phase of volatile anaesthetic distribution
Introduction of agent into the inspired gas mixture
Why does the actual concentration of volatile inspired differ from the dialled concentration on the vapourisor
Dilution with existing gas
Uptake by co2 absorbers
Uptake by rubber or plastic components in the circuit
Where should concentration of volatile agents be measured in a circuit
As close to the patient as possible
What factors influence uptake of anaesthetic form inhaled gas to the blood
Inhaled concentration
Alveolar ventilation
Diffusion
Blood gas partition coefficient
Pp in the pulmonary artery
Pulmonary blood flow
Ventilation perfusion distribution
Concentration effect
Second gas effect
How can alveolar volatile levels be made to reach inspired levels faster
What acts to decrease the alveolar level
Increasing alveolar minute volume
Diffusion of the gas into the blood
What limits diffusion of voletile from alveoli to blood
Disease eg pulmonary fibrosis increasing thickness or emphysema reducing available area
What is the blood gas partition coefficient
What assumptions are made
The amount of agent that must be transferred to the blood to achieve equilibrium for a given tension
Assumes blood volume is known and there is no transfer on to other tissues.
What is the implication and effect of a low blood gas partition coefficient
Low blood solubility
Equilibrium reached after a small transfer of gas
Thus equilibrium reached rapidly
Which 4 anaesthetic agents have the lowest blood gas partition coefficient
What values
Xenon 0.12
Desflurane 0.42
N2O 0.44
Sevo 0.69
Which 3 anaesthetic agents have the highest blood gas partition coefficient
What values
Halothane 2.3
Enflurane 1.9
Isoflurane 1.43
Why does pp of volatile in pul artery effect uptake of volatile from alveoli
Increasing pp in artery decreases gradient so decreases uptake
What is the effect of pul blood flow on uptake of volatile agent
Increase flow clears concentrated blood thus increases rate of transfer
What is the concentration effect with respect to transfer of volatile agent from alveoli to blood
Uptake of volatile will leave a lower concentration for rest of the ventilatory cycle, thus lower tension, thus lower transfer for rest of that cycle (assuming lower proportion of other alveolar gases absorbed). Bigger effect proportionally when starting concentration is lower.
What is the second gas effect
If another alveolar gas is absorbed quicker than the volatile then the conc. increases thus faster uptake
What factors influence the circulatory phase of volatile delivery
Cardiac output
Cerebral blood flow
Distribution to other tissues
What is the formulae for uptake of volatile agent by tissues
Uptake = tissue blood flow x tissue:blood solubility x av tension difference
What is the effect of the differing distribution of blood flow to different organs on volatile distribution
Volatile follows blood thus large proportion of absorbed anaesthetic directed to the brain
What is the significance of cerebral auto regulation on distribution of volatile anaesthetic
In shock cerebral blood flow maintained thus even greater proportion of blood flow goes to brain thus equilibrium reached more rapidly
Hypoventilation during anaesthetic will increase co2 and further speed equilibrium
Hyperventilation (eg at induction) decreases co2 and thus would slow equilibrium
What is the effect of distribution of volatiles to other tissues on uptake to the brain
Initially decreases it as the agent is absorbed elsewhere
Then acts as a resevoir releasing it back into the blood and thus back to the brain after agent turned off - both acts as a damper to change and slows recovery
What is MAC
Minimum alveolar concentration
The concentration of anaesthetic agent that at equilibrium will prevent a reflex response to skin incision in 50% of subjects
What is the effect of altitude on MAC
Reduced pressure thus reduced concentration of anaesthetic for a given percentage
What is an AD95 for an anaesthetic
Anaesthetic dose to prevent response to surgical stimuli in 95%
MAC percentages for common anaesthetic agents (% v/v)
Halothane 0.75
Isoflurane 1.15
Sevoflurane 2.0
Enflurane 1.68
Desflurane 6.35
Xenon 71
Nitrous oxide 105
Characteristics of ideal volatile agent
Liquid at room temp
Low latent heat of vapourisation, low specific heat capacity
Saturated vapour pressure high
Stable
Non flammable
Inexpensive
Environmentally safe
Pleasant smell
Low blood gas solubility
High oil water solubility
Low mac
Analgesics effect
No side effects
Cardiovascularly stable
Non irritant
No increase in ICP
Minimal metabolism
Not effected by organ dysfunction
What are common halogens
Fluorine
Bromine
Chlorine
Iodine
Which volatile contains bromine
Halothane
Which three volatiles have the same carbon skeleton
What is it
Isoflurane
Enflurane
Desflurane
C - O - C - C
Effects of volatile agents on CNS
Dose dependant suppression of cerebral activity
Lowering oxygen consumption
Increased cerebral blood flow and thus ICP
Which volatile increases epileptiform activity on eeg
Enflurane
Which volatile agents effect cerebral blood flow and ICP the most
Halothane more than all others
Desflurane has slightly higher ICP effects compared to sevo and iso
Which volatile has analgesic properties
Nitrous only
Effect of volatiles on respiratory system
Dose dependant resorption depression
Reduced tidal volumes and increased rate (except sevo which lowers rate)
PaCO2 raises
Response to hypercapnia and hypoxia blunted
Bronchodialation (halothane and sevo)
Irritation (Desflurane and iso)
Effect of main volatiles on resp depression
D > I > H,S
What are the mechanisms of action of volatiles on cardiovascular depression
Contractility decrease Occurs by interference with calcium movement.
Usually increased heart rate (except halothane that decreases)
Decreased SVR - especially iso and sevo
Which voletile causes most cardiovascular depression
Halothane
What is the effect of volatiles on muscle relaxation
Dose dependant depression if nm function potentiating muscle relaxants
Effect of volatiles on metabolic rate
Decreases causing decrease in o2 consumption and co2 production
2 MAC decreases BMR by 30%
Which halogen is associated with lowest toxicity
Why
Fluorine
Decreased metabolism
What is produced when dry soda lime contacts desflurane or isoflurane
How to avoid
Carbon monoxide
Low flows - keeps air moist so no reaction
Impact of volatiles on immune system
Reduce neutrophil killing function by interfering with calcium flux and superoxide genratjon
Colours of volatile agent bottles
Hal - red
Iso - purple
Sevo - yellow
Effect of sevoflurane and soda lime mixing
Effect on body
> 65oC degrades to form compounds A-E,
Lower temps forms only compound A and small amounts compound B
Toxic renal, hepatic and brain effects
Effect of volatiles on salivary secretions
Increases
Elimination of volatiles
Des and iso - Most by lungs with 0.02 to 0.2 respectively hepatically metabolised
halothane - 20% metabolised in liver and metabolites excreted in urine for weeks
Sevo - 5% metabolised by cyp450
Boiling points of volatiles and SVP
Des - 22.8, 88.5
Iso - 48.5, 31.9
Halo - 50.2, 32.5
Sevo 58.6, 21.3
Which volatile vapourisor is different? Why?
Des
Due to high svp needs heated pressurised vapourisor with microprocessor control unit that injects gas into the incoming mixture.
What is the implication of the low blood/gas coefficient of des?
Rapid onset and also rapid offset - very controllable.
Why is des bad for a gas induction
Very irritant
Increases bronch and salivary secretions
Conc above 6% can stimulate coughing and laryngospasm esp in children
What needs to be done to halothane vapourisors
Why
Clean them
Thymol preservative doesn’t vapourise so builds up
Which volatile maintains cardiac contractility more than others
Des
Cardiovascular effects of halothane
Decreased contractility and rate due to vagal stimulation
Irritability resulting in pvcs
Sensitisation to catecholamines thus risk of arrhythmia with adrenaline administration
Which agent is good for inhalational induction where airway obstruction may be a significant issue? Why
Halothane
Non-irritant, Reduces secretions, causes bronchodilation,
Metabolites of halothane
Trifluroacetic acid
Chloride
Bromide
What is ‘steal’ in relation to volatiles
Dilation of healthy vessels diverts blood away from critically perfused non compliant vessels producing compromised areas
Effect of Sevo on resp function
Decreases tidal volumes and resp rate
Decreases hypoxic drive and co2 sensitivity
Reduces bronchial smooth muscle tone
Metabolite of sevoflurane
5% metabolised by cyp450
Produces fluoroisopropanol and inorganic fluoride ions
These can be toxic (renal)
What are wet and dry Sevo presentations? Why
Can either come with higher or lower water content
No convincing evidence either way but risk of breakdown of Sevo in contact with metal to an acid and water inhibits this.
Boiling point of nitrous oxide
Saturated vapour pressure of nitrous oxide
-88oC
5300
How is nitrous oxide presented
French blue cylinders
Pure liquid under pressure (44bar)
Filling ratio 0.75
Why is nitrous an issue around fire
Not flammable itself be decomposes to oxygen and nitrogen above 450oC
Effect of nitrous on cvs
Increases vascular tone and increases blood pressure
Issues with nitrous oxide
Diffuses into air filled spaces Causing expansion
Prolonged use interferes with Vit B12
How is nitrous oxide synthesised
Heating ammonium nitrate to 240
What happens to nitrous oxide cylinder pressure as it is used
Why
Stays the same until all liquid nitrous oxide used up then falls rapidly
The pressure is specific for the temperature (SVP) and is replenished from the liquid as gas is removed.
NB slight fall is seen due to temperature drop
Effect of nitrous oxide on spinal impulses
Suppresses them
How does nitrous oxide effect cvs
Suppressed myocardial contractility by direct effect but this is neutralised by increased sympathetic tone
Generally increased vascular tone giving rise in pvr and SVR
Effect of nitrous oxide on skeletal muscles
Increased activity
Does not potentiate nmb
How does nitrous oxide effect vitamins
Interacts with b12 converting movovalent cobalt to bivalent. This prevents it functioning as a coenzyme for methionine synthase, thus increase in homocysteine and decrease in methionine. This impairs dna synthesis and thus can cause megaloblastic anaemia
Time frame for nitrous to cause vitamin effects
6-24 Hrs but can be faster in seriously ill patients.
What is the coshh regulation limit on nitrous oxide exposure
Less than 100ppm over 8hrs
Why does nitrous oxide causes air space expansion
More soluble in blood than nitrogen (34 fold)
Diffuses into air filed spaces quicker than nitrogen diffuses out increasing the volume
How is nitrous oxide metabolised
Most excreted by lungs
How is entonox presented
French blue cylinder
Blue and white quarter shoulders
137 bar pressure, filling ratio 0.75,
Advantages of xenon as a voletile
Very cardiovascularly stable
Non irritant
Low blood gas coefficient so rapid onset and emergence
Excreted unchanged
Does not cause malignant hypothermia
Not irritant
Disadvantages of xenon as a volatile
Very expensive
Cannot be compressed to form liquid as critical temp 16o
Hard to monitor
Low potency (needs high concentrations to achieve Mac)
High viscosity so needs high driving pressure
