BT_RA 1.8 Describe the principles of ultrasound imaging and the safe use of ultrasound equipment for regional anaesthesia

T/F  the frequency and amplitude of a wave are synonymous terms

T/F  one Hertz = 100 cycles per second

T/F  ultrasound consists of high frequency sound waves above the human hearing range (medical ultrasound is 2.5 – 15 MHz)

T/F  Ultrasound waves are produced by a piezo-electric crystal *. The crystal vibrates in response to an electric current.

T/F  choosing an ultrasound transducer with a higher frequency will produce a higher resolution image, at a greater depth **

T/F ultrasound waves are propagated through all tissues at the same velocity

T/F  when using ultrasound for an invasive procedure, the probe must be covered by a sterile cover, and sterile gel must be used (see ANZCA PS 28)

References

  1. Cross & Plunkett 2nd ed, page 87-88
  2. Magee & Tooley 2nd ed, page 148-150
  3. ANZCA PS 28 – Infection Control in Anaesthesia, 2015

* What does “piezo” mean?

** Have a look at your ultrasound machine(s) at work. What is the frequency of the probes you usually use for nerve blocks or line insertions, compared with probes for obstetric scans, or FAST trauma scans?

BT_RT 1.14 Discuss cerebral perfusion pressure

T/F  cerebral perfusion pressure = mean arterial pressure – intracranial pressure

T/F  cerebral perfusion pressure is the only determinant of cerebral blood flow

T/F  PEEP can decrease cerebral perfusion pressure

T/F  after traumatic brain injury, the recommended range for cerebral perfusion pressure is 60-70 mmHg (see reference 2)

T/F  sevoflurane may decrease CPP, but increase CBF

T/F  the cerebral circulation has minimal sympathetic innervation

References:

  1. Miller 8th edition, Chapter 17
  2. Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury, 4th edition. 2016, page 181

Do you know any great primary teachers?

Because they could become great primary examiners.

Do you have any tutors who have been fellows of the college for at least 3 years? Who have a contagious passion for the sciences underpinning anaesthesia? Who seem to know a bit about the topic? Who might be reluctant to apply without a bit of a nudge? Or are you a tutor reading this?

We have vacancies for primary examiners. First step is to email primaryexam@anzca.edu.au to get the application documents and ask any questions. The applications are considered twice a year and and successful fellows are invited to a weekend training workshop before the following vivas. At the workshop they are allocated a mentor who helps them prepare for and at their first viva examination. If someone applied now they’d be considered in May. It’s hard work but satisfying.

We’d love you to encourage any tutors you admire.

French Gauge

Despite the obvious benefits of using the metric system and SI units, the medical community persists with various types of bizarre systems of measurement.

One such system is the French catheter scale. To make matters even more confusing, it can be abbreviated in 5 ways:

  • FR or Fr
  • FG (meaning French Gauge)
  • CH or Ch (meaning Charriére)

Joseph Charriére (1803-1876) was the inventor of the French catheter scale. He was a manufacturer of surgical instruments. He worked at a time when there was no standardised system of measurement – different industries and different countries could all do their own thing!

The basic principle of the French catheter scale is that the diameter of the catheter (in mm) is one-third the French size.

So a 10 FR catheter has a diameter of 3.33 mm. Note that this is the outer diameter – so catheters of the same FR size could have different lumen diameters depending on their wall thickness.

Here are 3 common anaesthetic examples:

(1) Y suction catheter

Y suction catheter

The manufacturers of this particular Y suction catheter have just labelled it as “14” without telling you that this is the FR size. The outer diameter is not stated on the packet, but we can work it out to be (14 / 3) = 4.6 mm.

(2) Intubating Bougie

bougie

For this particular bougie, the manufacturer helpfully tells you it’s 14 Fr, and the OD is 4.6 mm (we already worked this out in Example 1). The smallest ETT this bougie will go down is a 5.0 mm. (NB the sizes of ETT’s refer to their internal diameters).

(3) Double Lumen ETT

DLT

This manufacturer states the size as 37 Fr/Ch …. I wonder how many clinicians know that Fr and Ch are actually the same thing? They also state it is a 12.3 mm tube – but unfortunately, they don’t specify that this is the outer diameter (OD)*. Double lumen tubes change shape along their length, so 12.3 mm only applies to the OD at the widest point. The internal diameter of the tracheal and bronchial lumens are each different, and also change shape along the length of the tube!!

* the size in mm stated on a DLT refers to its outer diameter, but for all other ETT’s the size in mm refers to its inner diameter.

I’m sure you can think of other examples… how about urinary catheters, nasogastric tubes, intercostal catheters, and surgical drains!!

It would probably be impossible to change from this system, because it has become so ingrained. Even though few people know the true size of many of these tubes, they seem to know which one to use!

BT_GS 1.15 Define tachyphylaxis, tolerance, addiction, dependence and idiosyncrasy and describe mechanisms of tolerance

T/F  tolerance is the diminished response to a drug, which occurs due to repeated exposure

T/F  tachyphylaxis is a form of tolerance that occurs rapidly (often within a few doses), usually due to depletion of neurotransmitter

T/F  ephedrine and metaraminol are equally likely to produce tachyphylaxis

T/F  mechanisms of opioid tolerance can include: receptor downregulation; metabolic enzyme induction; and alterations to second messenger systems

T/F  patients who develop tolerance to the analgesic and sedative effects of opioids, will still exhibit miosis even to small doses

T/F  physical drug dependence occurs when continued administration of a drug is required for normal function and/or to prevent a withdrawal syndrome

T/F  drug dependence and drug addiction are the same thing

Reference
1. Goodman & Gillman 13th edition, Chapter 24 and 20

BT_GS 1.56 Describe the clinical features and management of inadequate reversal of neuromuscular blockade

T/F  adequate reversal of neuromuscular blockade exists when the TOF ratio is > 0.9

T/F  It is difficult to clinically detect fade when the TOF ratio is > 0.7. In this scenario, double burst stimulation (DBS) can improve the detection of fade.

T/F  after giving 0.6 mg/kg rocuronium, complete spontaneous recovery would occur in 30 minutes

T/F  vital capacity and head lift can be used to clinically determine adequate reversal of neuromuscular block

T/F  the maximum antagonistic effect of neostigmine occurs in 10 minutes – if full reversal has not occurred within this time, a second dose should be given

T/F  inadequate reversal usually results in an inability to breathe effectively – this frightening scenario is remembered by many of these patients

T/F  even a very “slight” degree of residual neuromuscular block can significantly increase the incidence of postoperative respiratory complications

T/F  residual paralysis decreases the hypoxic ventilatory drive – due to inhibition of neuronal nicotinic receptors on the carotid body

Reference
1. Miller 8th edition Chapters 34, 35, 53

BT_PO 1.103 Describe the storage, synthetic, metabolic, immunological and excretory functions of the liver and identify the physiological consequences of hepatic disease

T/F  liver failure can result in hypoglycaemia due to limited / absent –  (i) glycogen storage and (ii) gluconeogenesis

T/F  liver disease can result in coagulopathy, because the liver produces all of the clotting factors

T/F  Kupffer cells are macrophages which line the hepatic sinusoids – with severe liver disease these may be absent, placing the patient at risk of sepsis from GIT flora

T/F  biliverdin (from haem breakdown) undergoes active transport into hepatocytes where it is metabolised to bilirubin – this is why liver disease can produce jaundice

T/F  one cause of hepatic encephalopathy is high ammonia levels – this results from impaired conversion of nitrogenous compounds (derived from protein), to urea. Lactulose is used in patients with encephalopathy because it decreases intestinal ammonia production.

T/F  portal hypertension leads to intestinal wall oedema, which reduces the absorptive capacity of the GIT

T/F  (not in the primary exam) gynaecomastia occurs in men with chronic liver disease because the free oestrogen : testosterone ratio is altered by a reduction in sex-hormone binding globulin

References
1. Miller 8th edition, Chapter 22
2. Kam and Power 3rd edition, Chapter 6

BT_SQ 1.17 Discuss the safety of methods for maintaining body temperature during anaesthesia and sedation, including active warming of patients

T/F  patients being actively warmed during anaesthesia must have their core temperature continually monitored (see ANZCA PS 18)

T/F  a simple layer of insulation can reduce heat loss by approximately 30% – there is no clinically important difference between insulation types (cotton blanket, surgical drapes, plastic sheet, ‘space’ blanket)

T/F  mattresses containing circulating warm water are nearly ineffective, because there is very little capillary blood flow through the posterior skin surface

T/F  compared with an obese adult, in a frail thin adult, there is a greater risk of intraoperative hypothermia, and a greater risk of over-heating with forced air warming devices

T/F  forced air warmers cannot cause skin burns because the maximum air temperature is 43 degrees C

T/F  forced air warmers should not be turned on until after surgical draping is complete, because they blow germs around the theatre **

T/F  ‘space’ blankets are highly flammable (click here)

References
1. ANZCA PS 18
2. Miller 8th edition, Chapter 54

** is there any actual evidence for or against this statement?

Australian Anaesthetic History part 3

frontcover_jpg

I have just finished reading this book. It is a biography about William Russ Pugh who, as I’m sure you’ll all remember, was the first person to administer an anaesthetic for a surgical procedure in Australia*. The biography was written by John Paull, a retired anaesthetist, and if you want a copy visit his website jdpaull.com.au

I did a post about the topic a while ago which was written before I had read this book. https://primarydailylo.wordpress.com/2017/07/07/australian-anaesthetic-history-part-1/

When I say ‘read’ I must admit I ended up flicking through this rather dry tome- there are 570 pages and many of them are filled with excerpts from the papers of the times. Only one chapter is devoted to telling the tale about the anaesthetics. It seems Pugh was not a huge fan and he devoted the majority of his time to surgical pursuits rather than anaesthetic ones. Nonetheless he was certainly the innovator and all credit is due to him for reading an article about Morton’s exploits and then going on to make his own ether, make his own apparatus, rustle up some patients and then proceed to anaesthetize them. Really remarkable that it worked at all. He also did the important task of writing to his peers to inform them about it. He recognised the limitations of ‘etherisation’ and acknowledged his failures with the technique. As the title of Paull’s book suggests, Pugh really was more than an anaesthetist and was an accomplished surgeon, scientist, philanthropist and champion for civil rights and child protection amongst other things. He also had a gift for rubbing people the wrong way (possibly reflecting his more abrasive surgeon’s character). An astonishing number of court appearances are documented in the biography.

Looking at my previous post I realise there is an error which I would like to correct now. I said there were grounds to suspect Pugh wasn’t properly qualified- this is incorrect. Pugh was qualified and indeed was involved with accrediting doctors in Launceston.

Below is a picture of the statue that was made in recognition of his notable achievement. It is near his former home in Launceston. Pugh lived to the venerable age of 91.

r0_0_3008_1999_w1200_h678_fmax

*Yes, it was in Launceston and yes that still counts!

IT GS 1.5 Describe the chemical composition of crystalloids and colloids used in clinical practice and their effects when used in volume replacement.

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Twenty years late I happened across this article:

https://onlinelibrary-wiley-com.ezproxy.anzca.edu.au/doi/10.1111/j.1365-2044.1997.090-az0082.x

If the shortcut doesn’t work it is from Anaesthesia 1997 52:422-27 and the punny title is ‘Is Hartmann’s the solution?’. Like most articles in Anaesthesia it is brief and to the point. The authors legitimately bemoan the deficit of knowledge about a fluid that we give to every other patient and conducted a survey  of FRCA candidates to test their knowledge which was poor. They also looked in their Hospital library for information about Hartmann’s which was also lacking.

Being newly informed about the physiology of Hartmann’s, I too looked in the set texts (current ones obviously) to see if the answers to my questions below are contained within. I am disappointed to inform you that the situation has not improved. Goodman and Gilman has nothing, nor does Power and Kam. Stoelting has hardly anything and Hemmings and Egan mainly bangs on about starch. Miller has a bit but gets bogged down about acetate and lactate toxicity which is utterly irrelevant for ninety nine percent of our patients. The best resources apart from the article of course are Yentis’s A-Z and Brandis’s notes on his anaesthesiamcq.com website- but you have to look in both the fluid physiology and acid-base physiology sections to get all the lowdown on Hartmann’s. Interestingly every text quotes slightly different values for the constituents of a bag of Hartmann’s- the definitive answer being what’s actually written on the bag of course! (They aren’t all the same.)

Seems unfair to expect you to know this* but I do think you should know about a drug that you give to just about every patient that is under your care. All the answers are in the article (or a composite of seven textbooks…).

T/F Administration of Hartmann’s can elevate a patient’s BSL.**

T/F Hartmann’s contains magnesium

T/F Hartmann’s contains calcium and potassium in similar concentrations

T/F Lactate metabolism by the liver generates bicarbonate

T/F Hartmann’s has a modest caloric content

T/F Administration of large amounts of Hartmann’s can cause lactic acidosis. (see what Miller says about this)

Not examinable but worthy of knowing:

T/F Hartmann’s fluid and Hartmann’s procedure are named after the same person.

*Examiners have and will continue to ask you about the contents of a bag of Hartmann’s and their implications. Note the LO is for the IT training period.

**Do your anaesthetic assistants ever query you when you hang a bag of CSL for a diabetic patient?