Before you get your hopes up I will not be revealing the intimate details of a viva but I will attempt to convey some of the thought processes that are employed in the creation of a viva. I can only speak for myself here but I suspect my colleague examiners do similar things.
It begins with an idea (as do most things) which is often formed during the actual viva exams. I think to myself, “Gee the candidates don’t know much about basic propofol pharmacokinetics.” Often this thought is engendered as I watch a colleague examine on a particular topic. I like to examine on topics that satisfy a few criteria:
- I think anaesthetists should know this stuff
- The topic is clinically relevant (hopefully these two aren’t mutually exclusive)
- I have seen a knowledge deficit about the topic in my trainees (if they already know it then someone else can ask them that!)
- The ‘answers’ or responses I want need to be in the set texts (this can be quite difficult and has scuppered a few viva ideas along the way)
- Another person with a FANZCA would at least understand most of what the viva was getting at
- The nature of the topic lends itself to being asked in a viva format
Once I have the idea I write down what the main points I want candidates to demonstrate an understanding of are. (I also need to make sure there is a learning objective pertaining to the viva!!) Each viva topic is only five minutes long so the path to pass responses needs to be direct and hopefully short. Next I hit the books and confirm that the topic is adequately covered. Occasionally I discover that my understanding of the topic is at odds with what the books say! Not uncommonly I may have to look at six different books and it is frustrating for all of us if they say six slightly different things. Next I need to formulate the questions to get the information I want. Each viva should ideally start with a simple and brief question to allow the candidate to answer the opening question correctly and begin in a good frame of mind. So, for a propofol PK viva I might ask “What is the induction dose of propofol for a healthy unpremedicated 20 year old?” Subsequent questions need to flow on naturally from the opening question. I like a diagram or two in a viva but it needs to be simple and easily drawn. Sometimes it may be better to provide a diagram. It may be deliberately incomplete. Lastly I run through the viva myself a few times to check the timing and make sure the flow of the viva is alright. Then the real hard work starts. Part 2 will elaborate.
It is a more potent agent than vecuronium T/F
If you drank it, it would paralyse you eventually T/F
Its duration of action is dependent on what time of the day you administer it T/F
It commonly causes stinging when injected* T/F
It is presented as a racemic mixture T/F
*Read this paper for a description of what it feels like to have rocuronium and suxamethonium injected when you are wide awake. Response of the bispectral index to neuromuscular block in awake volunteers. P Schuller et al. British Journal of Anaesthesia 2015; 115(Supp 1): i95-103.
Reading any clinical paper about rocuronium should allow you to answer the third question. Unfortunately, reading any of the recommended texts for the exam won’t be enlightening about this particular property of rocuronium.
It can sting on administration because it has a high pKa T/F
It has very poor bioavailability T/F
It can induce anaesthesia when used as a sole agent T/F
It tastes nice hence its popularity as a paediatric premed T/F
It has an active metabolite T/F
Despite what the practice of many trainees may suggest, the t1/2 keo of midazolam is significantly more than about thirty seconds.
Regarding a propofol ampoule:
It contains egg products so shouldn’t be given to patients with an egg allergy T/F
The contents are white because it contains soya bean oil$ T/F
It costs more than an ampoule of thiopentone T/F
It contains antimicrobial preservative T/F
If you drank a 100ml ampoule it would make you quite sleepy* T/F
$ Ask yourself what colour most oils are and what colour mayonnaise is and why they aren’t the same…
*In the trial of Michael Jackson’s cardiologist come ‘anesthesiologist’, Conrad Murray, an expert witness for the defence suggested that Jackson swigged a whole lot of propofol. This hypothesis was strongly refuted by the expert witness for the prosecution who happened to be none other than Steve Shafer. Who was correct?
Some answers for you. Again these mostly come from Dr Wilson’s “One Grand Chain”.
The first anaesthetic for a surgical procedure was given by William Ross Pugh in June, 1847 at Launceston. This is probably true and the actual date was the 7th of June. The patient was a woman with a mandibular tumour. Seems this is a popular condition to have treated under historically significant anaesthetics- Morton anaesthetized Gilbert Abbott who also had a lump in his neck. There is a statue of Pugh in Launceston that commemorates the event. There is reasonable evidence to suggest that Pugh wasn’t a properly qualified medical practitioner.
The first anaesthetic given in Australia was also by William Ross Pugh. This is probably true. Pugh’s anaesthetics are the best documented but there are a couple of other contenders for the title. Of these a Sydney dentist named John Belisario has the best case to challenge Pugh. Interestingly both men gave anaesthetics on the 7th June, 1847!
The pioneering anaesthetists would have had to make their own ether. This is true and it is not hard to do.
The first case of awareness under anaesthesia is also attributed to Pugh. This is true regarding anaesthetics administered in Australia. Pugh anaesthetized three patients on 7th June (attempted to actually, the third case was a failure due to equipment issues). The second patient had a cataract removed and was aware but didn’t report it to be painful. The first case of anaesthetic awareness occurred with the iconic first ‘successful’ demonstration of ether by Morton on 16 October, 1846. The patient, Gilbert Abbott, later reported being aware of the procedure and that it was indeed painful. Presumably it would have been a lot worse if he’d had no ether at all!
The first reported anaesthetic death in Australia is also attributed to Pugh. This is false. The first reported anaesthetic death was in April 1848. Like most ‘anaesthetic’ deaths there were several other contributing factors. The unfortunate patient was a middle aged woman named Ann Ryder who suffered two indignities on that fateful day: she was tossed from a carriage and sustained a compound fracture of the leg and she was also robbed. She was given ether and had her leg amputated. She briefly regained consciousness after the procedure but then became obtunded and was unable to be resuscitated. Pouring brandy down an obtunded person’s throat was a popular resuscitative measure at the time. It didn’t work in this instance.
No LO for this stuff but pretty interesting nonetheless. If you can’t be bothered to google the answers I will give them to you in a subsequent post. I am pretty biased but I think Morton’s successful public demonstration of general anaesthesia using ether on 16th October 1846 is the single most important medical discovery of the modern era. It is astonishing given the lack of social media and communication satellites in the 1840s that within months doctors were trying their hand at giving ether anaesthetics on the other side of the world including Australia. Indeed the first anaesthetics in Australia were given in June 1847. The apparatus used was based on a picture in a London newspaper published in January 1847. It took four months to sail from London to Australia so it was only a matter of weeks from reading about Morton’s discovery that Australians were giving it a crack. I don’t think many of us would try a novel technique on a patient that we’d only read about in a journal, especially when we needed to fashion our own apparatus!
The statements relate to historically significant events regarding anaesthetic practice in Australia. The definitive resource on Australian anaesthetic history is Gwen Wilson’s “One Grand Chain: The History of Anaesthesia in Australia”. Not a bad read. I got my copy gratis from the nice folk at the College library.
The first anaesthetic for a surgical procedure was given by William Ross Pugh in June, 1847 at Launceston. TRUE/ FALSE
The first anaesthetic given in Australia was also by William Ross Pugh. TRUE/ FALSE
The pioneering anaesthetists would have had to make their own ether. TRUE/ FALSE
The first case of awareness under anaesthesia is also attributed to Pugh. TRUE/ FALSE
The first reported anaesthetic death in Australia is also attributed to Pugh. TRUE/ FALSE
BT_GS 1.52 Explain the principles involved in the electronic monitoring of depth of sedation and anaesthesia, including the use of EEG analysis
Again, the comments relate to the beloved BIS again.
BIS has been validated as a depth of anaesthesia monitor in large clinical trials T/F
Burst suppression is seen in physiological sleep T/F
Propofol can cause an isoelectric EEG T/F
Volatile anaesthetics can suppress the EEG but not cause an isoelectric EEG T/F
Spindle formation on the EEG is only seen in slow wave sleep T/F
BT GS 1.52 Explain the principles involved in the electronic monitoring of depth of anaesthesia, including the use of EEG analysis.
The statements relate to BIS as this is the most commonly used ‘depth of anaesthesia’ monitor in Australasia. Entropy is pretty similar. A plea from a pragmatic anaesthetist- if you are going to use BIS then please make sure you are displaying the EEG trace on your monitor (and make sure you’ve turned the filter off). The dimensionless number by itself is close to useless. You should be able to interpret a raw EEG trace as well as you can an arterial waveform or ECG trace. I highly commend the ICETAP.org website as an educational resource. It is an excellent place to learn how to interpret the EEG and get the most clinically useful information from your processed EEG monitor. If you don’t know the answer to the third statement below then can I suggest you look at the paper by Whitlock et al in Anesthesiology 2011; 115: 1209-18. Figure 4 should astonish you if you haven’t already seen it.
The algorithm by which the BIS value is calculated has been made known to clinicians T/F
Ketamine can elevate the BIS reading because of its effect on the beta ratio T/F
There is a clear dose-response relationship between BIS values and end-tidal volatile concentrations T/F
There is a clear dose-response relationship between BIS values and plasma propofol concentrations T/F
SR denotes the Suppression ratio which is the percentage of time in the preceding 63s that the EEG has been suppressed. T/F
BT_PO 1.63 Describe glomerular filtration and tubular function
Regarding the proximal convoluted tubule:
Q. It reabsorbs 65% of filtered sodium and water. TRUE/ FALSE
Q. It reabsorbs 65% filtered chloride. TRUE/ FALSE
Q. Aquaporin channels are found on the luminal surface of the tubule cells. TRUE/ FALSE
Q. Most of the glucose is reabsorbed via the paracellular route. TRUE/ FALSE
Q. This is the principal site of urea secretion. TRUE/ FALSE
Most people don’t find pharmacokinetics particularly palatable. This book is arguably one of the most enjoyable ways you can learn about pharmacokinetics. This book doesn’t just entertain but it also gives you a sound understanding of PK concepts as they relate to the practising anaesthetist. It is under 200 pages and can be read in a day. It is fairly non PC which accounts for half its charm. Nothing in there about TCI sadly.
Addendum by woundedwildebeest… I got to see this post when it was a draft and bought the book. I definitely second this recommendation. Funny, educational, with even a dramatic twist on the last page. I’d suggest reading a chapter at a time and applying it in theatre before moving on to the next.