Now for the vivas- what to do

The written is done- forget about it now, you can’t change it. If you’d worked through the SAQ sets in my book you would have covered 9/15 of the SAQs. If you’d gone through a few recent exams, you’d have practised a few more. The invites for the vivas aren’t all that far away. So, this is what I suggest you focus your efforts on doing in the lead up to the vivas.

SAQ topics will not be reprised in the vivas. Go through the paper and identify major chunks that weren’t asked about. Focus on the core stuff particularly. Here’s some areas that I reckon may crop up in the vivas:

• renal physiology- not anyone’s favourite topic
• volatiles
• liver/ endocrine physiology
• pain
• there was nothing on local anaesthetics
• plenty of equipment/monitoring topics still eg NMT, ventilator, BIS, oximetry
• both CVS/resp physiology fairly light
• plenty more stuff that can (& will) be asked about propofol

The best preparation is undoubtedly prac vivas- don’t be scared to ask all and sundry for them. Regs who’ve already done it are a valuable resource. Ask all your bosses- worst case they say no. There’s lots of past viva stuff on the Net- they are better than nothing but not as good as a prac viva. You can use them as fodder for practice with your study group. Prac viva workshops both paid and unpaid are of questionable value IMHO- actual examiners rarely feature- people commonly reprise a viva that they personally had in the exam. Never fails to surprise me how recollections can be so disparate to what was actually asked!

My book- work your way through the opening viva questions p214. You can forget about the most commonly asked question ever “What is MAC?”

Work your way through the diagrams p217.

Lastly, I think it’s beneficial to work through the Short & Sweet sets- keeps your brain nimble and helps lodge an assortment of facts into your head so they are second nature when you’re asked to produce them.

See you in October

Solutions to the Puzzle Pages

How did you go?

ANSWERS

1. A, sats99/HR60/CO240/BP100
2. The drugs are desflurane, sevoflurane, nitrous oxide, methoxyflurane and Xenon. The rest is self-explanatory.
3. They all start with ‘M’ and are all relaxing.
4. All Cat A in pregnancy.
5. All come as lipid formulations.
6. Anagrams of drugs all missing one letter: morphine, nitrous, oxytocin, paracetamol, ether.
7. YO₂ is CO₂ and its pin index is 1,6.
8. Buprenorphine 40, oral morphine equivalents provided by 1mg of each drug.
9. A adrenaline, B clonidine, C adenosine, D phentolamine, F propranolol
10. Desflurane is blood. (yellow belly, purple heart, red eye, blue blood)
11. Sevoflurane and nitrous oxide is one combination that satisfies those interactions.
12. Sevoflurane, propofol, sodium nitroprusside, lignocaine, morphine, oxytocin.
13. ANALGESIA; LASAGNE/LEASING/SEALING; EASING/GENIAL/LASING/LINAGE/SIGNAL/SILAGE/SINGLE; AGAIN/AGILE/ALGAE/ALIGN/ANGEL/ANGLE/GLANS/GLEAN/SINGE/SLANG/SLING; GAIN/GALA/GALE/GLEN/GLIA/SAGA/SAGE/SANG/SIGN/SING/SLAG/SNAG.
14. G,N,U. Beginning bottom left: ‘Quote Gentlemen this is no humbug’.
15. Why? ABC/ IVDU/ PEG/ VWF/ LMWH/ QRS/ JZ/ NOK/ XRT. Only letter not used is ‘Y’.
16. Anaesthesia is fun but the exams are tough! Substitution cypher beginning with ANESTHIC.
17. Ether Dome 16^th October 1846; Gower Lane London 19 December 1846; Launceston 7 June 1847; Wellington 27 September 1847. Place and time first anaesthetics given in USA, UK, Australia and New Zealand.
18. N for neostigmine. Fentanyl, propofol, rocuronium, cephazolin, dexamethasone, etc. Reversal at end.

Puzzle Pages in The ANZCA Primary Exam Companion

Thank you again to the many of you who have purchased my book and special thanks to those who have given feedback and identified errors/ typos. I have endeavoured to correct them all- the great thing about Amazon is that you can edit the manuscript since it is a print-on-demand product.

I have decided to add a couple of puzzle pages to the book. I have reproduced the pages below for the the many who have bought a version of the book without these pages. The questions and clues are provided. I will post the solutions to them all in a week or so. Happy puzzling.

PUZZLE PAGES

All study and no play makes Johnny/Jill a dull person. Here is a page where I have melded knowledge with fun (perhaps). They get progressively trickier. Clues and answers are on the next page.

1. Which is correct?

A)  Y99G60W40R100   B)  Y100G40W60R99   C)  Y60G100W99R40

2. Complete the table

DRUG	SVP	BP	MAC (%)
	667	23
			2
			104
	20	104
Xenon	–	-108

3. What links these? Massage, music, mivacurium, meditation, manicure

4. What links these drugs? Thiopentone, paracetamol, suxamethonium, lignocaine, metoclopramide

5. What links these drugs? Propofol, diazepam, etomidate, morphine, bupivacaine

6. What links these? Phonier, suitor, oxyntic, metacarpal, here

7. If X₂O is 3,5 and O₂ is 2,5 what is YO₂?

8. What is the next number in this sequence? T0.2,M1, O1.5, H5, B?

9. In the table below E is yohimbine and G is caffeine. What are the other letters? (more than one solution)

	α1	α2	β1	β2	A1
+	A	B	A	A	C
–	D	E	F	F	G

10. If sevoflurane is belly, isoflurane is heart and halothane is eye; then what is desflurane?

11. If X + X =2 for MAC and X + Y=2 for MAC and X + Y=1.5 for hypnosis, what are X and Y?

12. Identify the following drugs from their chemical formula:

C4H3F7O, C12H18O, Na2[Fe(CN)5(NO)], C14H22N2O, C17H19NO3, C43H66N12O12S2.

13. How many words can you make from this word cube? Words contain at least 4 letters, all must contain ‘G’, no plurals, proper nouns or verb forms ending in ‘s’. (>30 words- very good)

S	I	A
E	G	L
A	N	A

14. What are the top 3 letters of this word triangle?

15. A) All resuscitation algorithms begin with these three letters.

B) Most people with hepatitis C have done this.

C) Feeding tube that bypasses the mouth.

D) Only clotting factor not made by liver.

E) Clexane is one.

F) This complex is normally narrow.

G) A zone where radiologists and gynaecologists intersect.

H) For a child, this is normally their parents.

I) Radiotherapy.

J) What is the remaining question?

16. What message is encoded below?

AKATQRCTQBA BQ HUK NUR RCT TXAJQ APT RLUIC!

17. What links these? What dates are associated?

42.3635N 71.0679W, 51.5224N 0.1326W, 41.4391S 147.1358E, 41.2867S 174.7730E

18. What is the next letter in this sequence? F, P, R, C, D, M, O, G, ?

CLUES

1. Look at your anaesthetic monitor
2. 4^th one is used by ambos
3. They share a common effect
4. Think categories
5. Think pharmaceutics
6. Anagrams
7. Cylinders
8. OME
9. Receptor agonists and antagonists
10. Colours
11. Isobolograms
12. all used by anaesthetists
13. don’t need any clues for this one
14. famous quote
15. what letter isn’t used in these acronyms
16. substitution cypher
17. plug in the coordinates
18. standard anaesthetic

More Eleveld

I had a chance to use Eleveld TCI on the latest B Braun Space pump yesterday. The pump itself is a big improvement over the old one and well worth taking a look at.

The first patient had a BMI of 44. The pump was giving about 70ml/hr, while my computer predicted 100ml/hr. I scratched my head for a while, before I realised that the B Braun implementation uses adjusted body weight. When I changed my computer to ABW, it tracked the pump’s output perfectly.

Adjusted Body Weight(ABW) = IBW + 0.4 * (TBW – IBW).

As I mentioned before, the Alaris pump uses Total Body Weight.

Take a look at the concentrations predicted by the TBW algorithm if you use the ABW algorithm in a patient with a BMI of 23.4.

Now a look at the difference with a BMI of 44.

This is not currently examinable, but given its importance it will soon become something that everyone needs to know.

•T/F The output from an Eleveld model is brand independent.

So which is the right one? The paper doesn’t say which weight was actually used, and there is no comparison of TBW vs ABW. The inter-patient variability for any TCI model is greater, anyway, than the difference between the two implementations, so at the moment we have no reason to recommend one over the other. You will, however, need to know which implementation your pump uses.

In case you are thinking you should just stick with Schnider, you should realise that some pumps use the a fixed time to peak effect and calculate the ke0 for the individual patient, and others use a fixed ke0, which means the TTPE will vary. There is also debate over which ke0 should be used with Marsh. The Alaris pump uses the original value.

TCI is a useful tool, but don’t be tempted to confuse it with reality!

Which body mass?

Congratulations to those who sat the written this week. I am no longer on the exam panel so the post on the Lean Body Mass formula was completely fortuitous 😀 Interestingly if you read Eleveld’s paper they discuss using Adjusted Body Weight. This site currently uses adjusted body weight with the Eleveld models, although as far as I can see the BD pumps use Total Body Weight (TBW), so this may change.

Adjusted Body Weight(ABW) = IBW + 0.4 * (TBW – IBW).

The easiest approximation for Ideal Body Weight is IBW = 22 * height².

If we look at a 1.73m tall patient who weights 151kg:

TBW = 151kg

IBW = 65.8kg

ABW = 100kg

In contrast James’ formula gives a LBM of 48.8.

T/F • 100mg (2*LBM) of propofol is a suitable induction dose for this patient.

Hemmings and Egan 2018 discuss this at greater length in chapter 5. You can also find some information in this paper, as well as in The First Year pp 200-1, 204.

As an aside on a different topic:

I have been asked how sensitive these models are to changes in the micro-rate constants. Go back to the graph of effect site concentration for Schnider. I have put sliders in so you can change the volumes of the compartments and the clearances from the compartments. (The constants for a compartment can be specified as micro-rates or volume & clearance, but volume & clearance are easier to conceptualise.)

The sliders are set to vary over an order of magnitude in each direction—any less and it is hard to see any difference. That should answer the above question.

What is the effect site?

With TCI we usually target effect site concentrations rather than plasma concentrations.

T/F • The effect site is the brain

The effect site is customarily described as a department of negligible volume. In practice it is implemented as 1/10,000 of the size of the central compartment—which equates to something like half a ml. This is significantly smaller than the brain of any vertebrate more advanced than a hospital manager.

Clearly, therefore, the effect site cannot be the brain, but does it represent brain concentrations? We don’t normally instrument the brain to measure concentrations of propofol. We do, however, have data for other drugs. Using microdialysis catheters, Roberts et al found the concentration of cefazolin in tissues was about 1/10th the concentration in the plasma. This was similar to the unbound plasma concentration.

Propofol is more than 98% protein bound, so as a first guess we might expect the brain concentration to be 1-2% of plasma concentration.

Look at graph of effect site concentration for Schnider. Click on plasma concentration to show the plasma concentration. You might find the following easier to see if you change the graph to logarithmic.

Try altering the ke0. Are there any values of ke0 where the effect site concentration remains at 2% of the plasma concentration?

The bottom line is that ke0 can introduce a delay, but it cannot maintain a concentration gradient between the central and effect compartments.

This is important and highly examinable

What function does the ke0 serve?

If you are unsure you can find the answer in this review article.

The function of the effect compartment is to adjust the plasma concentration to make observed effect proportional to concentration. A better term would be normalised plasma concentration. Until such time as we can measure brain concentrations there is no practical difference—so long as you realise that it is a mathematical construct rather than reality.

Paediatric TCI

In the past you had to use a different TCI model for paediatrics, such as Kataria or Paedfusor. Compare how Schnider compares with Kataria in a 5 year old. How does Schnider compare to the Paedfusor? Answer the following:

• T/F The Schnider model is appropriate for use in paediatrics

Now look how Marsh compares with Kataria in the same patient.

• T/F The Marsh model is appropriate for use in paediatrics

You can see that central volume of Kataria and Paedfusor are considerably higher than either Schnider or Marsh.

• T/F The blood volume of a 5 year old is 450ml/kg

This is examinable as a viva question

How can a paediatric TCI models have a central compartment of nearly half the body weight?

If you look at how Eleveld compares with Kataria in this patient, you can see that at least in the short term Eleveld correlates better than Schnider. Likewise for the Paedfusor.

The following graphs come from Hara et al 2017.

This graph shows the percentage of the expected plasma concentration delivered by the Paedfusor model in children. The white band indicates good performance. In most cases the actual values are between about -50% and 10% of the set value.

Look at the graph for Kataria.

• T/F Paediatric TCI models are more accurate than adult models

Compare these graphs with Eleveld.

• T/F Specialised paediatric TCI models are more accurate than Eleveld in children.

In summary Eleveld will allow you to inaccurately target plasma concentrations over a wider range of age and weight than previous models. What about the brain? More to follow…

Extensively revised version of The First Year now available

It has been five years since I revised this book and there’s an awful lot of changes. It is in a different font and fifty pages longer and of course much better! A summary of the new bits is below. The pdf file will be freely available via the College library. If you want to buy a hard copy it is available for sale on Amazon for $88- same price as my exam primer.

What’s new in the revised version of The First Year?

• Well- quite a lot. Every chapter has been altered in some way.
• The font has been changed to the more readable calibri.
• There is a new chapter on how the pulse oximeter works as well as a set of fifty questions you should know the answer to by the end of the year with answers.
• The new DRGA curriculum and structure has been addressed.
• The chapters on interpretation of the EEG waveform and Propofol TCI have been completely rewritten and expanded and greatly improved in terms of graphics and explanation.
• The ‘Preparing for the Primary Exam’ section is completely revamped and has mostly been supplanted by the equivalent chapter from my exam primer.
• There is a new bit on cases you probably shouldn’t do.
• The cost of things has been updated.
• References have all been updated.
• The perioperative medicine sections have been updated including recent major ANZCA trials.
• MTP and ROTEM algorithms have been updated.
• The book is over fifty pages longer.

It is still the only one-stop-for-the-lot book available on the market.

Eleveld TCI

BT_GS 1.59
Describe the pharmacological principles of and sources of error with target controlled infusion.

The Eleveld model has an extra parameter—Opioids (used or not used). The idea is that opioids may slow the metabolism of propofol.

I find the Opioid mode gives scarily low doses. The last patient I used it on opened her eyes at the end of the case at an effect site concentration of 3.5—before I had turned the infusion off.

The solid yellow line in this graph shows the effect site concentration with a TCI propofol infusion using the No Opioid model. The dotted yellow line is the effect site concentration predicted by the Schnider model for the same infusion rate.

• T/F At 30 minutes there is not much difference between the Schnider and Eleveld No Opiate model.

This graph shows the same thing using the Eleveld Opioid model. You can see that it is giving a lower dose than the previous model, and that this difference increases with time.

Eleveld can be used over a much greater range of weights than Schnider. Schnider uses James’ formula for lean body mass, which is an inverted parabola. This means that at high weights the lean body mass decreases. The peak is not a fixed value but varies with height and sex. (For those who are interested the peak is at 1.1 x height² / 256 for men and 1.07 x height² / 296)

Change the weight up and down in the compartment model for Schnider. Observe how weight affects clearance.

• T/F The clearance in the Schnider model decreases above a body weight of 120.

The reason for this is that body mass is only part of the calculation of clearance. Go back to the comparison of the Eleveld no opioid model vs the Schnider model and try entering a high value for weight.

This is examinable

• T/F The Schnider model can be used in patients with high body weights.

Is Eleveld more accurate than Schnider?

These graphs from a paper by Tobias Hüppe show the ratio of measured concentration to expected plasma concentration over time. You can see that in both cases the actual concentration is between about half and twice what you thought. This is consistent with other studies. Using your knowledge of the volatile kinetics answer this question:

This concept is also examinable, although more a viva question than a MCQ

• T/F TCI infusions have less inter-patient variability than volatile agents.

More to come…

Eleveld TCI Propofol

BT_GS 1.59
Describe the pharmacological principles of and sources of error with target controlled infusion.

DON’T PANIC—I can’t see this being asked in the near future. I am posting this to help you understand how to use this relatively new algorithm. It may also give you a better idea about compartmental modelling in general.

Those of you who use the Alaris pumps are probably starting to see their new Nexus pump with the Eleveld algorithm. They were very clever in their marketing to us, as they bound the doctors who saw their presentation with a non disclosure agreement. This effectively stopped up from assessing the alternatives (which have had Eleveld for years).

If you try to read the paper above, the implementation is very complicated. If you can understand the equations you are doing much better than I did. (If you want to know how to actually do it, there are spreadsheets at the bottom of this page which show how to implement the No Opiate model).

Look at the diagram here, and answer the following:

• T/F The Eleveld model is a three compartment model.

Look at the central compartment model for the Schnider and Eleveld (No Opiate) model for propofol. Try changing the values for age, height, weight and sex.

• T/F Central compartment volume is fixed in both Schnider and Eleveld models.

Look at the different time to peak effect values for the Schnider and Eleveld (No Opiate) model for propofol.

• T/F TTPE is model invariant.

This is actually quite different to our usual understanding. If you change the age parameter on the Compartment Models page you will notice that the time to peak effect (TTPE) also varies with age—which is sensible, but different to most other models.

As the TCI infusion will not restart until after the TTPE is reached, you will notice a big difference when using Eleveld rather than Schnider. The combination of a larger central compartment volume and a longer TTPE also means the initial bolus is much larger. Personally I think the Schnider bolus is too low and I much prefer the Eleveld. You will find though that you either need to decrease the dose of adjuvant drugs or put up with a longer apnoea.

Here are the context sensitive half time (CSHT) values predicted using the Eleveld (No Opiate) model. For those who are interested, I have discussed the origin of the CSHT values in your textbooks here.

• T/F The CSHT of propofol after an 8 hour infusion is 40 minutes.

More to follow…