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

IT_AM 1.6 Outline the equipment required to be immediately available for basic airway management and the cant intubate, cant oxygenate (CICO) situation

I had to do one of these sessions recently, so it seemed like the perfect time to do this . The college has a document of course: http://www.anzca.edu.au/documents/ps61-2017.pdf  but it doesn’t list any of the equipment you need.

The “vortex” crowd have a magnificent website: http://vortexapproach.org/ and has a plethora of resources on it, including CICO kits.

I won’t sport with your intelligence by asking about equipment you must have for basic airway management* (it’s all in PS55 and it does include scissors, but no warning not to run with them). So, which of the following must you have during a CICO?

T/F  a declared team leader

T/F  a second generation LMA

T/F  a bougie

T/F  a scalpel

T/F  nerves of steel

T/F  gloves

T/F  a size 8.0 cuffed ET tube

T/F  a videolaryngoscope

T/F  an oxygen insufflation device that allows expiration via the cannula

T/F  a large (14G) cannula

T/F  a big voice and a small ego

 

 

SS_PA 1.79 Describe the difference in pharmacokinetics of local anaesthetic agents in neonates and children from adults and the implications for regional blockade

Just when you thought it was safe to go back in the water… another difficult paediatric topic! Good news is that we have now covered all the paediatric LOs examinable in PEX on PLOOTD at least once.

The really important points apply to neonates rather than older children and so this is unlikely to be very relevant until you do a specialised paediatric term. There are a host of competing factors that might make local anaesthetics potentially more or less toxic in neonates. These are well-covered in Miller 8e Ch 92, but I wouldn’t spend too much of your precious study time teasing out the detail. The main points are: Lower α1-acid glycoprotein level in neonates tend to increase the free fraction of LAs, however, red cells sequester LA and the higher haematocrit and greater ECF make the distribution volume higher thus reducing the effective plasma concentration. Metabolism by some of the CYPs is slower but hepatic blood flow is relatively greater. Elimination half lives are generally longer. The upshot is that caution is required and whilst single shot doses are pretty much the weight-based ones you that should know well, you should use reduced infusion rates and reduced repeat boluses in neonates, infants and children.

These are all very hard, so don’t be dispirited if you don’t know the answers. They are for the very interested!

T/F  the time to peak plasma concentration is increased for ropivacaine given epidurally in infants relative to adults

T/F  the maximum plasma concentration is decreased for ropivacaine given epidurally in infants relative to adults

T/F children with right-to-left-cardiac shunts exhibit higher plasma concentrations of local anaesthetic

 

See one, teach one, do one

The title of this post is not a misprint.
Many of us have grown up with the mantra “See One, Do One, Teach One” or even this one:  “Those that can’t do, teach” which is often used in a derogatory fashion to disparage teachers.  The quote comes from George Bernard Shaw but is usually taken out of context.
There is another interpretation for the Shaw quote, which says that before you can do something you need to be able to teach it.
What has this all got to studying?
You have spent hours getting the information into your brain, but how long have you spent getting it out? Probably far less.
What is the best way to get information out of you brain? Teach someone.
I recently came across a useful hierarchy:
Talking is more effective than writing which in turn more effective than typing and explaining is better than just talking.
So who to explain things to?
  1. Another person in person
  2. Another person over the phone
  3. Your dog or cat
  4. Your drink bottle
You might notice that the list doesn’t include “Explain it to yourself” – this is because it is important to talk out loud.
What has all this got to do with the Primary Exam?
Well, have a think about the various components of the Primary Exam and how much value is placed on each method of getting information out.

SS_PA 1.53 Describe the changes in the pharmacodynamics of volatile agents, analgesics, opioids and neuromuscular blocking agents in the neonate and the changes that occur with growth and development and the implications for anaesthesia

This is the last paediatric one for a while. However, it’s probably the most relevant one so plenty of questions. Miller has a nice chapter on this (8e Ch93). Given that yesterday’s post was so short, you get some bonus statements today!

When sevoflurane first came out it was heinously expensive compared to halothane and so we weren’t allowed to use it very often at the parsimonious unnamed children’s hospital in Victoria. Halothane inductions took a while (why? and why particularly with spontaneous ventilation?) and the advice was “when you think they are anaesthetised, wait another couple of minutes” before instrumenting the airway. We could use sevoflurane for quick inductions (to save money) but not for the case. Halothane also took a lot longer to wear off than sevoflurane (why?), so the Recovery Room was a quiet, full place. When sevoflurane came into routine use it was often called “screamothane” by the Recovery staff. Why was that?

T/F  MAC of sevoflurane for neonates is about 3.3%

T/F  the incidence of emergence excitement and agitation is higher with sevoflurance than halothane

T/F  the induction dose of propofol should be reduced in infants compared to older children

T/F  TCI propofol should not be used in children because of the risk of propofol infusion syndrome

T/F the required dose of suxamethonium in infants is twice that of older children

Enough of the easy ones, how about these:

T/F  ketamine as a sole anaesthetic agent preserves the gag reflex

T/F  rocuronium can be administered intramuscularly in children

T/F  sugammadex may not be administered to children under 12

And finally, for the real experts:

T/F  clearance of alfentanil is reduced in children compared to adults

T/F  newborns have a slower clearance of morphine than older neonates

SS_PA 1.26 Describe glucose homeostasis in the neonate and explain the changes that occur with growth and development

An MCQ possibly, but if you had a SAQ or viva on this topic, I think you could rightly feel robbed! There’s a little bit in Power and Kam, and, frankly, it’s plenty. So it’s the shortest post ever on PLOOTD.

 

T/F  premature babies have inadequate stores of glycogen

T/F  glycogen stores in the normal neonate are exhausted within 1 hour of birth

 

SS_PA 1.54 Describe the pharmacology of agents used for premedication in children, including midazolam, clonidine and ketamine

More paediatrics. The clinical pharmacology of these drugs is not much different in children than adults, however it is more likely that you will give children premedication, and more likely that it will be oral. Many of us put the drugs in undiluted cordial to mask the bitter taste of drugs like midazolam.

Most of the drugs can be given intranasally with Mucosal Atomiser Device, but most of them burn a bit too, so children are not usually delighted with this approach. I’ve enjoyed some success with intranasal fentanyl in children who have refused oral premeds. It’s very fast acting and well-tolerated. It’s popular in Emergency Departments. Here is a practice guideline from the Royal Children’s Hospital, Melbourne.

 

T/F  an oral dose of midazolam 0.1mg/kg will usually result in a compliant child who will separate easily

T/F  oral premedication with “MiKe” (midazolam 0.3mg/kg + ketamine 3mg/kg) will usually result in a deeply sedated child

T/F  clonidine has a low oral bioavailability in children

T/F  clonidine has a t1/2 of 12-24 hours

T/F  ketamine may be administered intranasally (3-6mg/kg) to achieve sedation

 

SS_PA 1.27 Describe vital signs for children of different ages

What you need to know for this exam is pretty much what you need to know in clinical practice, unlike some of the other areas! These are all taken from Power and Kam; incidentally, the sections on maternal, neonatal and perinatal physiology are all as comprehensive as you will need to get through the Exam comfortably.

T/F  respiratory rate of a newborn is 30-40 breaths per minute

T/F  a heart rate of 100 bpm is normal for for a 5 yo

T/F  normal systolic blood pressure for a neonate is 70-90 mmHg

T/F  a systolic blood pressure of 100 mmHg in a 5 year old is probably abnormal