Are your patients talking about this…..

Two posts in one day!! Thought I might as well post about this whilst it was back in my brain.

On June 7 Richard Fidler conducted an interview on ABC local radio, on the topic of consciousness and anaesthesia.

Two patients asked me about it within 24 hrs of it airing……

One, who had listened to it on the day of his procedure, was mildly terrified by the interview ( I hadn’t heard it at that stage, but did my best to reassure him).

I listened to the interview on my walk in to work the following morning.

The first patient of the day mentioned the interview to me. She was fascinated! She had me repeat a random word to her throughout the case to see if she could recall it after the event – she couldn’t! [although I didn’t hypnotise her]

It came to mind today as I was listening to one of my favourite podcasts, Chat10Looks3 , where the interview is discussed again.

It is worth listening to. Make up your own minds about it. It is always good to be cognisant of the information out patients are receiving about our specialty – the information doesn’t always come from us…..

BT_PO 1.93 Describe the physiology of sleep

I think this glass spinning wheel looks like something straight out of Sleeping Beauty. I haven’t really captured it’s brilliance, the gallery was shutting its doors as I happened upon it! It is worth taking a look the the artist Andy Paiko ‘s, website to view some more of his amazing creations. 

Clearly normal sleep and anaesthesia are not the same, but most of our patients, hopefully, sleep within 24 hrs of anaesthetic. Recent GA can have an impact on sleep and may exaggerate some of the normal physiological effects.  

BT_PO 1.93 Describe the physiology of sleep 

Arterial CO2 and O2 levels are unaffected by sleep TRUE/FALSE

Tidal volume reduces during sleep TRUE/FALSE

General anaesthesia often disrupts sleep architecture on the first post-operative night TRUE/FALSE

Responsiveness to increased arterial CO2 is reduced by sleep TRUE/FALSE

Loss of REM sleep on one night is often associated with increased REM sleep on subsequent nights TRUE/FALSE

BT_RA 1.12 Determinants of ICP and their regulation Pt 2

This sculpture by Barry Flanagan will hopefully put you in a thinking mood…..

Today a little exercise to work through.

It will enable you to answer the question, “How can you manipulate blood pressure to minimise cerebral blood volume ( within the limits of cerebral autoregulation)?”

Before we start, what is you first thought?

Over 90% of registrars, to whom I have posed this question, come up with the incorrect answer.

When I start to probe their reasoning, most draw a graph which relates cerebral blood flow to MAP. It is a reasonable place to start.  Have a go at drawing that graph.

Now write an equation that shows the relationship between flow and pressure.

What is the third variable?

If flow remains constant in the face of changing pressure, what else is changing? Which direction does this change occur in order to maintain constant flow at both a high and low MAP?

Returning to your original graph, what is the relative calibre of the blood vessels at each end of the flat portion of the curve?

Have you changed your answer to the original question?

I’ll be back on the weekend with some more on this ….

UPDATE 20/5: you can find some more on this topic here

BT_RA 1.12 Determinants of ICP and their regulation 

I am going to spend two days in this topic. 

Today to get you thinking about the topic and tomorrow, an exercise for you to help you clarify an issue that has tripped up many a registrar in vivas.

I have recently had a much more pleasant kind of trip, to Washington DC for the IARS meeting. For those of you who have been following this blog for a while, you may remember my post mentioning the work of Yayoi Kusama. Well, she currently has an exhibition in DC and I spotted one of her pumpkins!

BT_RA1.12  Outline the factors determining intracranial pressure and discuss its regulation
The Monroe- Kellie doctrine can be represented graphically as an elastance curve TRUE/FALSE

Reduction CSF production as ICP rises helps maintain a normal ICP TRUE/FALSE

An intact blood brain barrier is necessary for intravenous mannitol to decrease brain water TRUE/FALSE

Factors the reduce CMRO2 generally reduce cerebral blood volume TRUE/FALSE

Doses of volatile anaesthetic agents less than 1MAC cause an uncoupling of the relationship between CMRO2 and cerebral blood flow TRUE/FALSE

2017.1 : SAQ 12

Discuss the physiological consequences of total spinal anaesthesia caused by intrathecal administration of 20ml of  2% lignocaine at the L3/4 level. (Do not include management)

BT_RA 1.2

A great question to demonstrate understanding of the physiological consequences of neuraxial blockade. The effects can all be deduced from your knowledge of physiology and pharmacology. However there is a most excellent article in AIC(1974) in which TI Evans, a Victorian anaesthetist, administered 30-40ml of 1% lignocaine intrathecally at the lumbar level in 100 patients. He proceeded to tilt the table 10 to 15 degrees head down and administer oxygen until vocal cord paralysis and unconsciousness developed and he intubated them. There were excellent conditions for abdominal surgery. The curious can access this work online through the college library, as a bonus the same issue (2) has quite a nice article on electrical safety as well.

This will cause bradycardia TRUE/FALSE

The patient will have dilated gut TRUE/FALSE

The patient will become hyperthermic TRUE/FALSE

The patient will have dilated pupils TRUE/FALSE

The patient will be unconscious TRUE/FALSE

BT_GS 1.52 Explain the principles involved in the electronic monitoring of depth of sedation, including EEG analysis.

Although a unique EEG “neural correlate of consciousness” has not yet been identified, drugs that induce anaesthesia do have characteristic effects on the spontaneous EEG. However, it is important to note that these effects are not the same for different drugs, even though they may produce a similar clinical endpoint. Appreciating these differences is the key to understanding why commercial EEG monitoring devices may give misleading results when certain drugs are used.


T / F    The EEG during sevoflurane anaesthesia has less “randomness” than when awake.

T / F    Propofol causes burst-suppression of the EEG at levels which have little effect on spinal reflexes.

T / F    When burst-suppression is induced by propofol, total brain oxygen consumption is reduced by up to 90%.

T / F    Nitrous oxide causes similar changes to the EEG compared to sevoflurane.

T / F    Electrocortical silence cannot be produced with ketamine.



BT_PO 1.94 Outline the basis of the electroencephalogram

This is the first of three posts on the EEG – 1) the basic physiology, 2) how drugs affect the EEG, and 3) quantitative EEG monitors.

Inferring the state of consciousness by analysing electrical voltages on the surface of the forehead may seem a bit like trying to see who is winning the football by holding a voltmeter up to the TV screen. However, as reversible obliteration of consciousness is our core business, and the electroencephalogram (EEG) is one of the few ways to observe the effect of drugs on the brain, it is important to understand some basics of the EEG, in part so that the various claims made for quantitative EEG devices can be assessed critically.

Useful resources include the 8th Ed of Miller, especially Chapter 17, which is available online from the ANZCA website.

T / F    The frontal EEG is a mixture of electrical signals derived from the cerebral cortex as well as sub-thalamic structures and the limbic system.

T / F     An “activated” EEG means that the amplitude of the EEG waveform is reduced.

T / F    The amplitude of an awake EEG is about the same as the p-wave on a standard ECG.

T / F    The amplitude of the EEG decreases with age.

T / F   “Burst suppression” is defined as periods of electrical activity alternating with periods of isoelectric EEG.

BT_PO 1.97 Describe the dynamics and metabolism of cerebrospinal fluid

Ok. A break from pharmacodynamics today.

The single column of rock in this picture is the Totem Pole, a popular rock climbing destination off the Tasman Peninsula ( captured here from the Three Capes Track ).

It was the site of a terrible accident in 1998, but an even more amazing story last year.

If you read the article, you’ll find the link to today’s LO….

BT_PO 1.97 Describe the dynamics and metabolism of cerebrospinal fluid

Refer to the diagram below, which shows CSF formation and absorption to help answer the questions

Screen Shot 2017-03-08 at 7.43.10 pm


The blue line represents CSF production, which is independent of intraventricular pressure T/F

CSF reabsorption is zero when CSF pressure is low T/F

At normal CSF presssure, production of CSF is greater than reabsorption T/F

Increased absorption of CSF is a indefinite means of compensating for rising ICP T/F

CSF is a filtrate of plasma  T/F (no help from the graph there 😊 )

(You can find the unadulterated version of the graph in Ganong’s Review of Medical Physiology)



BT_PO 1.51 Autonomic nervous system

BT_PO 1.51

Describe the autonomic nervous system and its physiological roles including:

· Autonomic receptors and cellular effects of receptor activation

· Autonomic transmitters, their synthesis, release and fate

TRUE/FALSE  Sympathetic stimulation increases peristalsis

TRUE/FALSE  The nicotinic receptor sub-type found in autonomic ganglia is a G-protein coupled receptor

TRUE/FALSE  The acetylcholine muscarinic receptor is an example of a G-Protein coupled receptor

TRUE/FALSE  Noradrenaline is the neurotransmitter released from all post-ganglionic sympathetic neurons

TRUE/FALSE  The sino-atrial node is innervated by the right vagus