BT_RA 1.4 Describe the anatomy of the vertebral column spinal cord and meninges relevant to the performance of central neuraxial block with appropriate surface markings.

Ellis and Lawson’s “Anatomy for anaesthetists” is worth a read through for some of the key areas of anatomy pertinent to anaesthetists. The answers to all of these are available there. In the exam you will be quizzed on a pretty narrow range of anatomy as it’s not easy to examine in a clinically relevant way without resorting to recollection of ‘factoids’. However, given the frequency with which you stick long sharp things into people’s spines, blindly aiming for a spot half the size of your little fingernail at seemingly ever-increasing distances from the surface, it behoves you to be au fait with the anatomy of the vertebral column and it’s contents.

T/F  the intercristal (Tuffier’s) line usually passes through the body of L3

T/F  the posterior rami of sacral nerves exit through the sacral hiatus

T/F  the dural sac terminates at L5/S1

T/F an epidural catheter advanced too far may exit the vertebral canal through an intervertebral foramen

T/F  the dural sac does not have posterior attachments

T/F  the subdural space is a potential space between the dura and arachnoid mater

Help to find some positive emotion

 

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Mermaid – Grand Prize Winner National Geographic Photographer of the Year

This morning I wrote a post on the benefits of cultivating and using positive emotion. Sometimes these emotions can be hard to find. I have just been looking at my emails and thought I must share this with you – the  National Geographic Travel Photographer of the Year  finalists and winning entries.

I would encourage you to scroll through the amazing photographs and feel the positive emotion flood through you….

Aim to pass the exam rather than avoid failing it

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UPDATE: I had linked to the wrong page in the first version of post this morning. All fixed now, although for those of you who were diverted to the recipe it will definitely help induce positive emotions (more on that below).

I have recently attended a resilience and wellbeing course where the concept of negativity bias was discussed.

I have mentioned the concept previously on this blog.

In the current course, the instructors discussed he research of Rozen and Roysman (2001) which showed we will generally be more motivated to avoid a negative outcome rather than to achieve a positive one. Hence our focus becomes on defeat (avoidance) rather than success. I often hear candidates say, “I really don’t want to fail the exam”. Less often do I hear, “I really want to pass the exam”

I propose that you actively counteract this tendency, when studying and talking about the exam, such that you talk about what you can do to pass the exam rather than what you can do to avoid failing.

Perhaps this seems like a very subtle change of reference and why does it matter because  the end result is the same – exam completed successfully.

The positive frame of reference enables you to capitalise on the benefits of using positive emotions to drive you. When we are driven by negative emotions we tend to become very singleminded and tunnel visioned. Our ability to problem solve and consider alternate approaches decreases. Perhaps single mindedness is a good thing for the exam. However the proposed benefits of reframing our experience to use positive emotion, is that we are able to “broaden and build” our thinking. When studying under a positive reference, you are likely to have greater mental flexibility, be able to consider more options and use more of your cognitive resources to achieve the task at hand.

Does this sound like something you would give a go?

Here is a TED talk given by one of the main investigators in the area, Barabara Fredrickson, talking about the benefits of operating under the effect of positive emotion.

I hope that all of you experience some positive emotion this weekend. It doesn’t have to be bliss (although that does sound good), but perhaps one of the others, serenity, interest, love, awe…

…and from now on when thinking or talking about the exam, talk about how you are going to pass!

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.

Onset of local anaesthetic block

A lower tissue pH will increase the speed of onset of local anaesthetic block. TRUE/FALSE

An increase in progesterone, increases the sensitivity to local anaesthesia. TRUE/FALSE

A large nerve axon has a faster onset of action with the same dose of local anaesthetic, compared to a small nerve. TRUE/FALSE

Fick’s law of diffusion covers all of the factors that affect onset of a local anaesthetic block. TRUE/FALSE

Ropivicaine has intrinsic vasodilatory actions which may reduce its length of action. TRUE/FALSE

 

Duration of Non-depolarising Neuromuscular Blocking Agents

NDMRs with a long duration of action have a clearance rate that is limited by the glomerular filtration rate. TRUE/FALSE

Intravenous calcium can be used to hasten the recovery from neuromuscular blockade. TRUE/FALSE

Magnesium and Lithium have opposing effects on the duration of action of NDMRs. TRUE/FALSE

Hypothermia increases the duration of vecuronium induced neuromuscular blockade. TRUE/FALSE

A patient with a 40% burn 2 weeks prior, is likely to be resistant to the effects of NDMRs. TRUE/FALSE

Onset time for Non-Depolarising Neuromuscular Blockade

Increasing the dose of Atracurium from 0.6mg/kg to 1.0mg/kg, increases the speed of onset of intubating conditions. TRUE/FALSE

Sevoflurane will slow the onset of non-depolarising neuromuscular blocking drugs. TRUE/FALSE

The gender difference in sensitivity to NDMRs is insignificant. TRUE/FALSE

The onset of action of NDMRs in peripheral muscles (versus central) is slower primarily due to differences in blood supply. TRUE/FALSE

The most potent NDMR has the slowest onset whereas the least potent NDMR has the fastest. TRUE/FALSE

Ephedrine increases the cardiac output, which causes the NDMR to reach the effect site more quickly. TRUE/FALSE

The onset of NDMRs may be delayed in someone with poor nutritional status. TRUE/FALSE

 

 

Anaesthesia – a novel prevention for jet lag? Bee prepared to be amazed!

Above is one of the fabulous tapestries hung in Christiansborg Palace, Copenhagen. Commissioned by the current Queen, this one depicts the Vikings (great travellers themselves).

Having recently undertaken long distance travel across many time zones, the prevention of jet lag has been on my mind. Some of my friends swear by melatonin, especially the controlled release form. I am a fan of the natural melatonin stimulant – sunlight. Exposure to intense natural light is supposed to increase nocturnal melatonin levels and it is a good excuse to get out an explore wherever you have just landed!

That’s all well and good, but what is the relevance to the title of this post? One of the fellow authors of this blog, slowlywaving, recently regaled me with the fascinating story regarding evidence that anaesthesia interrupts circadian rhythms. It all revolves around the study of bees.

Bees have a stong circadian timer which governs much of their behaviour and also helps with their navigation in conjunction with the sun compass. Amongst other things it enables them to judge how much time has passed whilst they have been in the hive so that when they leave the hive, they can maintain their heading back to a great source of nectar, even though the position of the sun may have changed dramatically.

A group of researchers decided to use bees to test the effect of anaesthesia on circadian rhythms. In our initial discussion, the thought was that the bees were anaesthetised with propofol and there was some discussion about how this could possibly be achieved (anyone trying cannulating a bee? do they even have veins? you can find the answer here if you are interested). As it turns out, isoflurane was used and the bees received a 6 hr daytime anaesthetic.

On awakening from the anaesthetic, the bees behaved in a manner consistent with them sensing a time 4-5 hours earlier than the actual time. They headed off to find their food at the bearing it would have been at, relative to the sun, several hours previously! They did a whole lot of fancy genetic testing and determined that the effect was related to dramatic slowing of the circadian rhythm. How cool! Interestingly night time perception was unchanged, which apparently fits with the hypothesis.

So how could we use this to prevent jet lag? Just imagine being anaesthetised (it would be much easier with propofol than isoflurane, assuming that it has the same effect) prior to being put on your long haul flight. You are then awoken at the same hour that you were anaesthetised, but in your new location and, voila, no jet lag!! Do you think it would take off? (sorry…)

The other fascinating part of the story revolves around tracking the bees. It involves tiny radar transponders and a disused airbase, but perhaps that can be a story for another day….

For those of you interested I have posted a copy of the article at aGasgal’s site

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

BT_GS 1.43 Outline the physiological basis of vomiting

Here’s a delightful topic. Given that it is one of the most frequent complications of anaesthesia (and one of the most frequent reasons for day surgery suddenly requiring an overnight stay) it pays to know a bit about the physiology and mechanics of the “big little problem”. If a patient has cricoid pressure applied prior to indiction and tries to have a coordinated vomit, you MUST release the cricoid pressure to mitigate the risk of oesophageal perforation (which still carries a 20-50% mortality rate, even with treatment). If you are interested, there is a case report from 1991 here.  The condition of oesophageal perforation due to vomiting was described over 250 years ago by Boerhaave, commenting on the death of the Grand Admiral of the Dutch Fleet.

The physiology necessary for the PEX is well covered in Power and Kam, Chapter 5.

In order of relevance for a change.

High:

T/F  the vomiting centre lies outside the blood brain barrier

T/F  afferents from the vestibular apparatus are relayed via the VIIIth nerve

Medium:

T/F  5HT3 receptors in the gut are implicated in PONV

T/F  afferents from pharyngeal touch receptors are mediated through the hypoglossal nerve

Low:

T/F   vomiting, like all PLOOTD posts, begins with deep inspiration

T/F  vomiting involves coordinated activation of both smooth and striated muscle