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Pharmacology. > 6. Inhalational > Flashcards

6. Inhalational Flashcards

1
Q

What three compartments do inhalational agents exist in?

A

Alveoli (PA)
Blood (Pa)
Brain (PB)

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2
Q

What happens to inhalational agents in the different compartments until equilibrium?

What is required of an inhalational agent to have an effect?

A

Initially PA > Pa > PB

After a period of time PA = Pa = PB

Dug must exert its partial pressure in the CNS to take effect. The driving pressure therefore depends on the PA and if this concentration drops then the brain concentration drops.

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3
Q

Is a MAC always accurate?

A

No not initially as the different departments haven’t equilibrated yet, and so lung concentration won’t represent the brain.

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4
Q

How do we quickly get brain concentration of volatiles up on induction?

A

Overpressure (give higher concentration than needed for anaesthesia to quickly increase concentration gradient).

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5
Q

What is a wash in curve?

What shape is it and why?

A

FA/Fi (y), plotted against time (x)

When FA/Fi = 1 this is equilibrium

Hyperbolic. Negative exponential curve - as the rate with which equilibrium is achieved decreases with time.

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6
Q

What is the most important factor effecting the wash in curve of volatiles?

What do wash in curves describe?

A

Blood:gas partition coefficient

Describe the speed of movement of the volatiles between different compartments.

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7
Q

What are two categories of ways equipment can reduce the actual concentration of volatile delivered to a patient vs. the dialled concentration?

A
  1. Dilution: with other gasses in the circuit
  2. Volatile absorption: by plastic, rubber and CO2 absorbers
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8
Q

What is the pumping effect?

A

(Diagram page 42 of pharma 6)

IPPV method that reduces dilution and increases volatile concentration delivered.

During respiratory cycle:
If pressure increases: gas in back bar moves back to vaporiser via bypass channel.
Pressure falls: gas in vaporiser moves to back bar to mix.
More effective at low flows, but increases gas in mix.

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9
Q

What can reduce the effect of the pumping effect?

A

Putting a non return valve downstream
Increasing resistance through the vaporiser and bypass channel
Reducing the vaporiser volume or lengthening the gas tube leaving the vaporiser

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10
Q

What patient physiological factors effect the speed that volatiles reach equilibrium with the brain?

Why?

A

High minute volume (faster wash in curve):

Low cardiac output: takes less away from the lungs allowing PA to build more quickly. Low CO also will preferentially deliver blood to the brain, allowing for faster CNS rise.

High FRC: increases the dilution of the volatile so decreases PA

Cerebral blood flow: higher = more volatile delivery. Hypercapnoea and volatile agent use increases cerebral vasodilation.

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11
Q

What factors increase and decrease FRC?

A

Increase: age, asthma, COPD, PEEP

Decrease: supine, GA, obesity, pregnancy, increased abdominal pressure e.g. ascites and fibrosis/oedema.

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12
Q

What Mac is usually safe in raised ICP? Why?

What should we not use in raised ICP?

A

Volatile agents increase cerebral blood flow and ICP, but usually a MAC of one is safe. Avoid nitrous.

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13
Q

How is potency related to the lipid solubility and O:G coefficient?

What about MAC and speed of onset?

A

Higher potency = higher lipid solubility = higher O:G = decreased MAC and slower onset speed as drug rapidly enter CNS reducing gradients.

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14
Q

What is a partition coefficient?

A

Reflects the relative solubility of a substance in two different compartments, of the same temp and volume at equilibrium

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15
Q

What is the blood:gas partition coefficient?

How is this related to speed of onset?

A

Solubility in blood relative to the partial pressure it exerts in the gas phase.

Higher B:G = more soluble = more quickly moved out of lungs = reduced gradient = slower onset.

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16
Q

What is the definition of MAC?

A

The minimum alveolar content of an anaesthetic agent at steady state that prevents reactive movement to a standard surgical stimulus in 50% of non pre medicated subjects at one atmosphere of pressure.

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17
Q

What is the Meyer Overton hypothesis?

A

The theory of anaesthetic action which proposes that the potency of an anaesthetic agent is related to its lipid solubility. Potency is described by the minimum alveolar concentration (MAC) of an agent and lipid solubility by the oil:gas solubility coefficient.

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18
Q

What are the different chemical structures of the volatiles?

A

Look at diagram on page 44 pharma 6.

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19
Q

What type of agents are all volatiles?

What does this mean for their lipid solubility?

A

All ethers except halothane

Ethers are larger and less lipid soluble and so halothane has the largest oil:gas coefficient

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20
Q

Are ethers more or less water soluble than halothane?

A

Less water soluble as they do not polarise.

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21
Q

What volatile ether is the most resistant to metabolism and why?

A

Desfluorane as the C-F bond has a higher difference in electronegativity that C-Cl etc.

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22
Q

What is the relationship between enflurane and isoflurane?

What are the differences in behaviour and why?

A

They are structural isomers.

Position of the C-F bond in isoflurane makes it less water soluble and more resistant to metabolism than enflurane

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23
Q

What is the concentration effect?

Compare des and nitrous?

A

Disproportionate rise of FA/FI when using high concentrations of nitrous compared to low concentrations.

Only used for nitrous, as it’s the only anaesthetic gas used in sufficiently high concentrations.

Usually speed is related to B:G coefficient. Lower = faster. Des = 0.42 and nitrous 0.47, so Des should be faster.

Low concentrations of nitrous are slower than des, but higher = faster. Due to the concentration effect.

It is the only agent used in high enough concentrations to greatly speed up the time to equilibrium. This is because nitrous is 20x more soluble in the blood than nitrogen and so leaves the alveoli to the blood 20x more rapidly. This means that fresh gas flow comes from upper airways to replace what was lost to avoid alveolar collapse. Results in augmented ventilation.

24
Q

What is the second gas effect?

A

This is when other gasses are brought to the alveoli alongs side nitrous during augmented ventilation to fill the alveoli and stop collapse. This allows for faster equilibrium (FA/FI ratio) and faster induction.

25
Q

What is diffusion hypoxia?

What does this mean for anaesthetics using nitrous.

A

Opposite of the second gas effect. N2O leaves the blood to alveoli more quickly than nitrous can enter the blood. Gas in alveoli gets diluted with nitrous.

All nitrous anaesthetics need supplemental oxygen after. Also need to be careful with patients at risk of obstruction once definitive airway removed e.g. OSA. As lower O2 stores in lungs.

26
Q

Should nitrous be used in upper airway surgery?

Why?

A

It supports combustion and so should be used if using laser or diathermy in the airways

27
Q

What effects offset of anaesthesia?

A

Low B:G coefficient will have a faster offset.

Higher minute volume blows more off, but if results in hypocapnoea it will cause cerebral vasoconstriction, prolonging the drug time in the CNS.

Higher fresh gas flow to washout gas from closed system e.g. circle.

Higher lipid solubility will mean there is a longer offset due to tissue redistribution e.g. halothane.

28
Q

What are the axis labelled as on a washout curve and why?

What kind of curve is this?

A

X = time

Y = FA/FAE. Cannot be FA/FI anymore as the curve would go to infinity, so needs to start at the concentration when the vaporiser is switched off.

Negative exponential curve

29
Q

What is context sensitive half time?

What determines this?

How does the 50% and 90% times change with different surgery lengths?

A

Is the decrement time in the context of the length of time tuned for administration. E.g. the time required for blood or plasma concentrations of a drug to decrease by 50% after discontinuation of drug administration.

Determined by the lipid solubility

Not much change in 50% drop, but 90% decrement times are increased after prolonged anaesthetics (esp. over 6h)

30
Q

How much of each of the volatiles metabolised?

Products?

How is sevo different?

What is the issue with halothane and what induces this?

A

Table on page 47, pharma 6.

Sevo is the only ether that isn’t metabolised to trifluoracetic acid.

Halothane is the most metabolised and occurs in the liver with CYP2E1, that attacks C halogen bonds. The trifluroacetic acid is implicated in halothane hepatitis, which is induced by chronic alcoholism, which increases the MAC of volatiles.

31
Q

Can the second gas effect occur independently to the concentration effect?

A

No, it is a direct consequence of the concentration effect

32
Q

What factors increase and decrease MAC?

A

Increase MAC: infants and kids, hyperthyroid, hyperthermia, hypernatraemia, chronic drug and alcohol use

Decrease: neonates and old, pregnancy, hypothyroid, hypothermia, hypotension, acute drugs/alcohol.

33
Q

What is critical temperature and pressure and what phases to gasses exist in, in relation to these values?

A

Critical temperature is the temp above which vapour cannot be liquified regardless of the pressure applied.

CP = pressure required to liquefy gas at its critical temperature.

Above critical temperature = all gas, no vapour
At/below critical temperature = liquid above the CP and gas below

34
Q

What is SVP?

How does this relate to temperature?

How is BP related to SVP and what happens when we add heat to this?

A

Pressure exerted by a vapour when in equilibrium with gas phase.

SVP rises with temperature

At BP, SVP = atmospheric pressure. Adding heat provides latent heat, but doesn’t change the temperature.

35
Q

What happens to the temperature of a liquid when molecules leave it using latent heat?

A

The liquid cools, unless more heat is being added.

36
Q

How is MAC related to potency?

A

Inversely proportional

37
Q

Why is Des in a heated vaporiser and what happens?

A

Des has lowest BP (23deg), meaning lots is vaporised at room temperature.
A standard vaporiser would need very high fresh gas flows to dilute high vapour concentration to a safe level.
Additional latent heat would leave rapidly as the des vaporises, giving a variable level of vapour released.

The TEC 6 beasts the des to provide a stable concentration and manually injects a controlled amount into the fresh gas flow.

38
Q

How does the chemical structure of volatiles affect the solubility?

A

Fluoride ions are lighter than CL or bromide.

Lower MW = less soluble

So more fluoride = less soluble.

39
Q

How are iso and enflurane related?

A

Structural isomers

40
Q

What does iso do to airways in awake people?

A

More pungent than sevo, causing coughing and breath holding.
Reduces airway resistance.

41
Q

What does sevo do to airway resistance?

A

Reduces it.

42
Q

What happens if we run more than one volatile at a time in terms of MAC?

A

MACs are additive so giving half a mac of two gasses would make a MAC of 1 e.g. sevo and nitrous

43
Q

What are the adverse effect of volatiles?

A

Resp: reduced Tv and non compensatory rise on RR. Causes rising CO2

CVS: dose dependent MAP reduction, halothane via CO, the rest by SVR. des and sevo increase HR and sevo can prolong QT.

CNS: cerebral metabolic depression (burst suppression at high concentrations). Uncouple cerebral metabolism with blood flow, so vasodilation and raised ICP with less response to CO2.

44
Q

Draw the different volatiles

A

Page 1 of formula sheet

45
Q

What can halothane do the liver?

A

Fulminant hepatitis due to trifluroacetic acid

46
Q

What is MH?

Genetics?

Triggers?

S/S?

Treatment?

A

AD condition (CH19) of mutation of ryanodone receptor (RYR1) on SR.
Gives uncontrolled free release of Ca from SR.

Triggered by volatiles and depolarising muscle relaxants.

S/S: initially see rising ETCO2, and tachy, then rising O2 requirement, muscle rigidity, and hyperpyrexia (late). See a mixed metabolic/resp acidosis, hyperkalaemia, myoglubinaemia and DIC.

Rx: stop trigger, clean circuit, hyperventilate, TIVA and non-depolarising. Danteolene (interacts with CCB’s) at 2.5mg/kg IV and repeats of 1mg/kg up to 10mg/kg.

47
Q

Why does N2O have a Mac of 103?

A

Equates to 103kpa. This is if given in a hyperbaric chamber where pressures count but not percentages. Given with O2 to avoid hypoxia.

48
Q

What does the critical temperature of N2O mean for its state?

A

36.5 deg

Breathed in as vapour and out as a gas.

49
Q

What does nitrous do?

A

Inhibits NMDA receptors.

50
Q

What are the good and bad effects of nitrous!

A

Good = analgesia and sedation

Bad = emetic, oxidises B12 so reduces methionine and DNA synthesis. Megaloblastic changes and anaemia after a few hours. Sub acute cord degeneration after repeats. Reduced Co in HF. Reduced Tv but compensatory RR.

51
Q

When should we avoid nitrous?

A

Large bowel obstruction, middle ear/eye surgeries, following craniotomy and pneumothorax.

52
Q

Where does the name xenon derive from?

A

The Greek xenon, meaning strange one.

53
Q

How is xenon made?

A

Fractional distillation of liquid air.

54
Q

What are the pluses and minuses of xenon?

A

Good: colourless, non+flammable, no greenhouse, no toxicity, neuroprotective, decreased RR but compensatory Tv.

Bad: expensive, apnoea at high doses. Slightly vagotonic.

55
Q

How does xenon work?

A

Inhibits glutamate and NMDA receptors.

Pharmacology. (22 decks)

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