Inhalational anaesthetic agents Flashcards

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1
Q

What is the difference between a vapour and a gas

A

A vapour is a substance that can exist as a liquid at room temperature (i.e. room temperature is below its critical temperature). A substance whose critical temperature is below room temperature cannot exist as a liquid at room temperature regardless of the amount of pressure exerted and is considered a gas.

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2
Q

What does the dial indicator of ‘1%’ mean

A

The vapour occupies 1% of the outflow from the vaporizer

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3
Q

Define MAC

A

This is the mean alveolar concentration of the volatile agent required to prevent 50% of patients moving when subjected to a standard midline incision

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4
Q

What determines potency: partial pressure of VA administered or concentration of VA delivered?

A

Partial pressure of volatile agent delivered

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5
Q

Why is partial pressure of VA delivered independent of atmospheric pressure

A

If 1% is dialled into the vaporizer then 1% of isoflurane is delivered at 20ºC and 100kPa (SVP of isoflurane is 32kPa)

Inside the vaporizer:
32kPa/100kPa x 100/1 = 32%

1/100 x 100kPa/1 = 1kPa

If 1% is dialled into the vaporizer then 0.5% of isoflurane is delivered at 20ºC and 200kPa (SVP of isoflurane is 32kPa)

Inside the vaporizer:
32kPa/200kPa x 100/1 = 16%

0.5/100 x 200kPa/1 = 1kPa

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6
Q

As vaporizers are calibrated in % and because one atmosphere is approximately 100kPa, there is a simple relationship between % and partial pressure of the agent: 1% = 1kPa. How is it possible for N2O to have a MAC of 103 (above 101.325 =atm pressure)

A

This means that the MAC of N2O cannot be achieved at atmospheric pressure.

The MAC values are quoted in terms of % concentration but their potency is actually determined by PARTIAL PRESSURE rather than % concentration.

Partial pressure is independent of atmospheric pressure. In a hyperbaric chamber a MAC of 103kPa can be obtained because the atmospheric pressure is increased e.g. 150 kPa

103kPa/150kPa = 69%

Is a concentration of 69% of N2O is delivered to a patient at Pb of 150 –> MAC of 103 kPa is obtained.

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7
Q

How do vaporizer adjust for changes in altitude?

A

They have mechanisms which ensure the delivery of a set partial pressure of anaesthetic agent (not concentration as displayed on the dials. The percentage of agent delivered will vary with altitude but the Partial pressure and the MAC remain unchanged

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8
Q

How are MAC values calculated

A

In volunteers just breathing anaesthetic agent n oxygen. (No other gases present)

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9
Q

How does the MAC change when N2O is added?

A

The MACs are additive e.g. half MAC N2O + half MAC Isoflurane = 1 MAC. (same calculation is releavant for sevo and iso together but this is NOT done in practice

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10
Q

What factors reduce MAC

A
IV anaesthetics used by infusion
N2O
Adjuvant medications (benzodiazepines, opioids, a2-adrenergic agonists)
Acute alcohol intoxication
Chronic amphetamine use (depleted CATS)

Reduced GCS
Hypothermia
Hypothyroidsim
Increasing age

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11
Q

What factors increase MAC

A

Chronic alcohol dependence
Exogenous catecholamine use and stimulus
Anxiety and stress

Hyperthyroidism
Hyperthermia
Young age

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12
Q

What effects the speed of onset of anaesthesia when using a volatile agent for induction?

A

How quickly FA/Fi approaches 1

How rapidly the alveolar concentration equals the inspired concentration of volatile anaesthetic

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13
Q

What is overpressure with regard to inhalation induction

A

Overpressure involves setting the initial concentration on the vaporizer above that needed for maintenance during induction and then, over 5 minutes or so, reducing it towards a maintenance value of approximately 1 MAC.

Incremental increases over a minute or so will minimize airway irritation (also airway irritation much less with sevoflurane)

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14
Q

Why do we use an intravenous induction in adults?

A

To avoid the unpleasantness of breathing a volatile –> do not delay initiating the volatile

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15
Q

What are the main reasons why N2O is used?

A

It is used as a carrier gas as it reduces the MAC required for a volatile agent and has useful analgaesic action

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16
Q

Explain the second gas effect

A

N2O has a very low B:G partition co-efficient (0.47)
Nitrogen has a relatively high B:G part. coeff. (0.015)

The B:G partition co-efficient for N2O is 30 x GREATER than that of Nitrogen.

Rate of diffusion = ∆P x SA x Solubility / √MW x L

∆P = partial pressure gradient
SA = Surface Area for gas exchange
Solubility = B:G partition co-efficient
MW = Molecular weight
L = Thickness of the diffusion barrier

In comparing N2 to N2O in lungs –> since N2O will replace N2 the ∆P is the same (constant), SA, L - constant (same lungs).

The variables are therefore MW and Solubility of each gas

For N2:
MW = 28 g/mol
B:G = 0.015

Relative Rate of diffusion = 0.015/√28 = 0.0028

For N2O
MW = 44 g/mol
B:G = 0.47

Relative Rate of diffusion = 0.0708 –>THIS IS 25 TIMES FASTER THAN N2.

17
Q

Define the concentration effect and draw the FA/Fi graph for all the volatile agents and N2O to illustrate this effect

A

The concentration effect is an observed phenomenon that describes the disproportionate
rate of rise of the alveolar fraction compared with the inspired fraction when high
concentrations of N2O are inspired.

18
Q

What implications does the difference in B:G coefficients for N2O and N2 have for anaesthetists

A
  1. Second gas effect
  2. Diffusion hypoxia

N2O diffuses 25 x faster than N2. When an anaesthetic agent is co-administered with N2O the effect of rapid diffusion of N2O out of the alveoli with relative slow diffusion of Nitrogen into the alveoli leads to a pressure gradient between the alveoli and the adjacent respiratory bronciles and other airways bringing more alveolar gas into the alveoli –> the effect is concentration of both the N2O and the volatile agent and increased FA of both and the increase concentration of the latter is the outcome of the second gas effect.

Diffusion hypoxia occurs because, during emergence in a patient in whom N2O was administered N2O leaving the blood and moving into the alveoli occurs at a faster rate than Nitrogen which is leaving the alveoli and entering the blood –> this has the effect of diluting the gases in the alveoli.

19
Q

What effects do all volatile agents have on RR and Vt

A

Increase RR and decrease VT
As tidal ventilation decreases dead space remains unchanged and hence alveolar ventilation decreases and may become inadequate with high concentrations of volatile.

20
Q

What effect does N2O have on minute ventilation

A

Minimal

21
Q

Briefly describe the technique for inhaled induction with sevoflurane

A

Minute 1: incremental dial up of sevo to 8 % starting with 0% but arriving at 8% by one minute

When patient is almost asleep (at about 2 mins) dial down to 3% to MAINTAIN TIDAL VENTILATION. If 8 % is continued –> Vt could drop to 40 ml and RR up to 22 but this means VA = 0

22
Q

Which volatile agents cause decreased SVR and reduced myocardial contractility

A

All volatile agents

Isoflurane

  • drops SVR slightly more than sevoflurane + accompanied by a reflex tachycardia
  • Also has been associated with coronary steal

Sevoflurane
- less pronounced drop in SVR, BP and HR better preserved

23
Q

What effect does N2O have on the CVS

A

Minimal reduction in cardiac contractility - usually offset by increased SNS activity

24
Q

What are the implications related to the vasodilation of coronary vessels caused by volatile anaesthetic agents

A

Volatile anaesthetic associated coronary vasodilation may reduce perfusion in coronary vessels distant to stenosed regions of these vessels precipitating ischaemia.

25
Q

In practice is coronary steal a factor in perioperative myocardial ischaemia?

A

As long as coronary perfusion pressure is maintained, no.

26
Q

What is the extent of metabolism of N2O, isoflurane and sevoflurane and what is the clinical relevance?

A

N2O - 0%

Isoflurane - 0.2%

Sevoflurane - 3 - 5% (High number of Fl- ions produced which are known to cause renal impairment –> despite this sevoflurane does not appear to impair renal impairment even after prolonged exposure

27
Q

What compounds are synthesized when sevoflurane interacts with CO2 absorbers (NaOh, KOH containing) and which of these are potentially toxic - describe the toxicity

A

Compounds A to E

Compound A - potential to produce renal toxicity but there have been no reports of actual renal toxicity despite potentially toxic levels being reached

28
Q

Is N2O a trigger for malignant hyperthermia

A

NO. All volatiles are

29
Q

What other important side effect is possible with N2O

A

Megaloblastic anaemia

30
Q

Which volatile agent causes some SNS stimulation at a MAC >1.5 or when the concentration is increased too rapidly

A

Desflurane

31
Q

Which volatile agent can sensitize the heart to catecholamines which may lead to arrhythmias

A

Halothane

32
Q

Which volatile agent causes coronary artery vasodilation and may lead to the ‘coronary steal syndrome’ and is therefore avoided in patients with marked coronary artery disease

A

Isoflurane

33
Q

Which volatile agent has the reduces myocardial contractility the most

A

Halothane

34
Q
What effect do the following agents have on heart rate
Isoflurane
Desflurane
N2O
Sevoflurane
Halothane
A
Isoflurane - Marked increase HR
Desflurane - Moderate increase HR
N2O - Mild increase HR
Sevoflurane - no effect
Halothane - Decrease HR
35
Q

Summarize the effects of the volatile effects on the CVS

A
HR
Isoflurane increases HR significantly
Halothane decreases HR
Desflurane increase HR moderately
Sevoflurane - no effect
N2O - mild increase HR

BP
All agents reduce BP

Contractility
All agents reduce contractility and Halothane has the greatest reduction. N2O the mildest.

SVR
All agents reduce SVR except N2O with a mild increase in SVR

36
Q

What are the CVS effects of muscle relaxants

A

SUX may cause bradycardia after 2nd dose from stimulation of cardiac M receptors. Prevented by giving atropine prior to second dose of SUX

Atracurium and mivacurim
- my cause histamine release causing BS and hypotension after RAPID IV injection –> reduced by slow injection

37
Q

How can the CVS response during extubation be minimized

A
  1. Ensure adequate reversal of muscle relaxation
  2. Optimize analgaesia
  3. Deep extubation as an option
  4. LMA less SNS than ETT
  5. Short acting BB
38
Q

Why does hypotension occur during central neuraxial blockade

A

Denervation of the sympathetic outflow, which causes a decrease in vascular resistance. The higher the block the more pronounced the hypotension, because of the greater SNS blockade leading to greater vasodilatation.

39
Q

When does bradycardia occur in neuraxial blocks

A

Bradycardia occurs when the cardiac sympathetic fibres are blocked (T1-T4).