BT_PO 1.96 Discuss the significance of the blood brain barrier

Devilsadvocate has made a list of LOs we haven’t addressed yet and I’ll post on some of these orphans this week. I’ve used Ganong for this one but it should be in most of the basic texts.

Glucose passively diffuses into the brain     T/F

Circumventricular organs are within the blood brain barrier     T/F

Ions cross the blood brain barrier readily     T/F

Neurotransmitters cross the blood brain barrier readily     T/F

The blood brain barrier can be disrupted by acute severe hypertension     T/F

BT_RT 1.13 Discuss factors leading to a loss of cerebral autoregulation

Nyhavn, Copenhagen

Last week I put up a post on regulation of cerebral blood flow.

Today I thought we would focus on another component of the same LO – factors that result in loss of autoregulation.

BT_RT 1.13  Describe the cerebral circulation, the regulation of cerebral blood flow and factors leading to the loss of autoregulation

Some of the mechanisms behind the loss of autoregulation are complicated. I think that a basic understanding of general principles would be sufficient for this part of the LO.

All the statements which follow fall into that category.

Miller and Hemmings and Egan, both have reasonable chapters on this stuff (they are very similar in terms of content and style as they have the same three authors…)

In a brain with significant cerebrovascular disease, vessels in areas of brain distal to an atherosclerotic narrowing will tend to be vasodilated to maximise flow T/F

Cerebral autoregulation is well preserved in traumatic brain injury T/F

Severe hypercapnoea will obliterate cerebral autoregulation T/F

If cerebral autoregulation is lost, and PaCO2 is normal, avoiding hypotension will help minimise the risk of ischaemia T/F

Cerebral autoregulation is preserved with propofol based anaesthesia T/F

Over at aGasgal I have attached links to a couple more articles on cerebral blood flow for those of you who are interested.

BT_RT 1.13 Describe the regulation of cerebral blood flow 

Louisiana Museum, about 45 minutes by train from Copenhagen – would strongly recommend you visit if you are ever in the vicinity (that’s Sweden in the distance)

I have recently been in Copenhagen at the Euroanesthesia meeting. I went to an interesting talk on hypotension, where the speaker made a joke regarding people being tortured by the cerebral blood flow autoregulation curve in their primary exams. It seems a shame to limit the “torture” to the exam setting…..

I have posted on the effect of cerebral blood flow on ICP  previously. You may find it useful to look at that post in conjunction with this one.

BT_RT 1.13  Describe the cerebral circulation, the regulation of cerebral blood flow and factors leading to the loss of autoregulation

The basics of this topic are covered in most physiology textbooks. However I think that Hemmings and Egan Ch 8  covers it better than most.

The first four statements cover important core material

Cerebral blood flow is autroregulated to maintain a constant flow in face of changing cerebral perfusion pressure T/F

Cerebral blood vessels are maximally dilated at the lower end of the autoregulation plateau T/F

As a general rule, the higher the cerebral metabolic rate, the higher the cerebral blood flow T/F

The most important factor in cerebral autoregulation is autonomic nervous system activity T/F

The speaker for the talk mentioned above was Adrian Gelb, from UCSF. Part of his talk referenced this article, which he authored, on the effect of CO2 on cerebral autoregulation. The article covers a lot of non core material, but I thought that his conceptualisation was very interesting, for those of you looking to explore the topic in more depth.

The last few T/F statements come from the article

Increased PaCO2 narrows the autoregulation range of blood pressures, by lowering the upper limit and elevating the lower limit T/F

The combination of hyopcapnoea and low normal BP may put the brain at risk of ischaemia T/F

The lower limit of autoregulation may be affected by the cause of the hypotension T/F

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_PO 1.95 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_PO 1.95 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.