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.
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.
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.
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
• 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.
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…
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.
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)
• 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.
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.
A trainee who purchased my exam primer astutely noted that I have made contradictory statements regarding the effect of the Trendelenburg position on cerebral perfusion pressure. In the ‘physiology of the pneumoperitoneum’ bit I say that the map rises more than cvp in the head down position and in the ‘cerebral blood flow and intracranial pressure’ bit I say cvp rises more than map! To complicate matters there are references to support both these statements. I find the contradicting statements irksome at the least.
None of us would be too fazed by this state of affairs if it weren’t for the fact that there have been SAQs asked about this in the primary and it is also a subject worthy of the final exam. Why do examiners ask about it? Well, because of the increasing prevalence of robotic surgery which is predominantly conducted in the steep head down position for urological and gynaecological surgery. (Most gynaecological surgery seems to be done in this position in my hospital incidentally.) Most of the implications relate to positioning related injuries.
Discuss the cerebral effects of prolonged anaesthesia in the steep head-down position.
The above SAQ was asked in the 2019.1 exam. The exam report isn’t enlightening. A protracted search through all the recommended texts finds approximately nil written about the topic. The best I could find was in Miller’s chapter ‘Anesthesia for Robotic Surgery’ which says ICP goes up a bit as does IOP and regarding the cardiovascular effects: “Studies demonstrate a variety of conclusions with respect to the effect of Trendelenburg position on cardiac index and output”. Useless. The invaluable Dr Yartsev (Deranged Physiology) has managed to find an old paper reporting minimal changes in BP/CO/SVR in ICU patients tipped 20 degrees head down. PAOP went up a little bit presumably due to the increased preload.
Invariably patients in the head down position undergoing surgery have haemodynamics further complicated by the existence of concomitant pneumoperitoneum and anaesthesia. All the books bang on about how hypercapnia increases CBF blah de blah but the attending anaesthetist is controlling this appropriately with an increase in ventilation, aren’t they?
More contemporary studies report conflicting results as alluded to above. The best study I could find is this one https://doi.org/10.1093/bja/aer448 This is a small study published in the 2012 BJA involving 14 patients undergoing robotic prostatectomy in the steep head down position with a pneumoperitoneum. Intravascular pressures were measured at the tragus. Anaesthesia was maintained with 1MAC sevoflurane and 5 of PEEP was applied. The graph below is taken from Fig 3 of the paper.
CVP and MAP both rose by the same amount when initially tipped head down as you would expect purely from the hydrostatic pressure effect. CVP remains more elevated than MAP as Trendelenburg is maintained- I assume this is due to the baroceptor response to the increased BP. Consequently, CPP is reduced but not by much (average of 9mmHg). When they were moved back supine, pressures fell a bit presumably due to the fall in preload. As long as CO2 is controlled and MAP is kept in the autoregulatory range (whatever that is) then cerebral perfusion should be fine when you’re having your robotic surgery.
However, there are some other concerns of importance to the anaesthetist. CVP is increased and the hydrostatic pressure on the cerebral venous side is undoubtedly increased. Valves in the central veins may ameliorate the degree of this rise in hydrostatic pressure as the column of venous blood is not continuous if they are competent. Veins will be distended with the increase in pressure and this equates with an increase in cerebral blood volume. These factors are thought to be implicated in the modest increase in ICP/IOP seen (a few mmHg) and more importantly in the development of oedema in dependent tissues notably the periorbital tissues. There is no study directly measuring ICP, they all use surrogate measures, most commonly the optic nerve sheath diameter. If you’ve never seen chemosis before then look at these people when they wake up. Presumed cerebral oedema has been implicated in the increased incidence of emergency delirium in these patients. If you crank up the PEEP this presumably further increases CVP.
All of the above sounds sort of reasonable. But what if your patient has a crappy heart or crappy lungs or benign intracranial hypertension or they’re hypovolaemic or you’re running a ketamine infusion along with propofol and remi and dexmedetomidine?
If we pretend things are simple and that cvp goes up a bit more than map and cpp is slightly reduced but remains in the autoregulatory range then we can probably satisfy the examiners. I was feeling a bit relieved until I came across this study which was published in the 2010 BJA by the same authors!
https://doi.org/10.1093/bja/aeq018 30 patients undergoing robotic prostatectomy with pneumoperitoneum in steep head down position. Diagram below is taken from their Fig 1. Same anaesthetic.
If you focus on the bottom right panel you see CPP increases a bit initially then falls back to pre-Trendelenburg values. This is because MAP increases more than CVP- this is different to their 2012 study I quoted earlier. So, like most things in this world, things are complex, and the answer is not clear cut.
Firstly, I want to thank all the people to date who have purchased my book. It has been well received and I earnestly hope it aids you in your quest to pass the exam.
The actual cover is reprised below- the back cover is a bit different from my earlier post.
Buy it from the Australian amazon site: amazon.com.au I have had several queries from people saying it has been out of stock- this is only on the American site. It has always been in stock on Amazon Australia. Interestingly I have sold quite a few copies in the US, Canada as well as the UK.
I have become aware of a couple of errors and have rectified these on the current version of the book that you would buy now. I would like to highlight these corrections for owners of earlier versions of the book.
p27 100% oxygen- “The 47 refers to the the saturated vapour pressure of water at seal level at standard temperature…” This should be body temperature, not standard temperature.
p166 pulse oximetry- my explanation of how carboxyhaemoglobin causes an elevated oximetry reading was a bit clunky. My revised explanation is reprised here: Carboxyhaemoglobin (COHb) has a similar absorbance pattern to oxyhaemoglobin so will tend to artefactually elevate the reading towards 100%. This is the simple explanation provided in the books, but it is more complex than that: COHb has a little absorbance of red light but none of infrared, so its presence alone should cause an elevated R ratio (AC660/AC940) which correlates with a reduced saturation! So why do the sats read high? The explanation is that CO binds very tightly to haemoglobin and there is reduced deoxyhaemoglobin present. A reduction in deoxyhaemoglobin causes a greater fall in AC660 absorbance than AC940 since it is a log scale and so the R ratio is smaller which correlates with an increased saturation value.
Admittedly the above is pretty niche material but the perfectionist trainee should be satisfied. I also share with you what MAK95 (not MAC95) means.
The Cynical Anaesthetist has finally finished his long awaited exam primer book. It has been published on Amazon in both hardcopy paperback form and as a Kindle eBook. The paperback is $88 and the eBook is $70. The content is identical but there is a bit of colour in the Kindle version. The paperback is 263 pages long and A4 size. Obviously, the main incentive for writing the book is to help people pass the exam. I am totally biased of course, but I think this book will be a very valuable tool for you to use in your exam preparation. I asked a group of my colleague examiners to peruse and comment on the book prior to publication and have incorporated their insightful and much appreciated contributions. The cover and table of contents are reproduced below.
I have learnt a lot in the course of writing this book. The phrase “All killer, no filler” is apt. I have gone to lengths to include material that is very commonly asked in the exam and is poorly explained by the recommended texts. It is probably the book with the most comprehensive and up to date treatment of the encephalogram and BIS monitor. It also has quite detailed and comprehensive entries on the propofol plasma time curve and offset of a propofol infusion. The morbidly obese patient has been catered for. I can’t claim to have written a book without any errors in it, but have gone to lengths to do my very best to find and correct them. The SHORT AND SWEET section incorporates 500 short format questions and answers that traverse the entire breadth of the curriculum. They are similar in style to the QUICK QUIZ questions in Kerry Brandis’ The Physiology Viva.
As the title says, this is a companion book. It doesn’t claim to incorporate everything you need to pass the exam in a mere 263 pages. But it does plug quite a few gaps and represents the only book of its kind- a book written by an examiner for the ANZCA primary exam. I hope you find it helpful.
I hadn’t noticed that the patient was sunburned until we started positioning. The oximeter had fallen off the finger and the assistant was leaning on the BP cuff whilst tucking in the warming blanket. All you would need is the nurse to ring from recovery to ask for a mod for the parturient with a BP of 100 and everything would be completely normal.
The title of the post rather gives it away, but at the start of a crisis it can often be difficult to realise that it is even happening. The thing that made me reach for the adrenaline was that I noticed that the ETCO2 was low.
Here is a portion of the anaesthetic record, reproduced with permission. The jagged parts are artefact.
The ETCO2 is the gray filled area at the bottom, with units in mmHg. Initially the patient was mask ventilated, which is why the trace has gaps in it. The green line is the plethysmograph amplitude. You can see that by 8 minutes after induction both the CO2 and the plethysmograph amplitude are dropping. The purple syringes are doses of adrenaline. The CO2 immediately rose with the first dose. Just as I was giving the adrenaline the trace was starting to show bronchospasm—which went away immediately.
The agent responsible was found to be rocuronium. Apparently the rate of rocuronium anaphylaxis has increased since COVID, which the allergy specialist thinks might be a result of greater use of cough suppressants.
The important take away messages are:
Anaphylaxis rash may look like a sunburn
If you see a low CO2, think low cardiac output
BT_PO 1.27 Discuss West’s zones of the lung
I am not brave enough to suggest that this is the only possible reason, but…
Low cardiac output states can cause hypocapnoea in a ventilated patient because:
Pulmonary hypotension increases anatomical shunt
Pulmonary hypotension increases West zone 1
Pulmonary hypotension increases West zone 3
Systemic hypotension increases the relative proportion of bronchial artery blood flow
Systemic hypotension decreases CO2 carriage in the blood
Primary LO of the Day 
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