2019.1 SAQ 5 – steep head down

Discuss the cerebral effects of prolonged anaesthesia in the steep head-down position.

BT_PO 1.95 Discuss the determinants and control of:
 intracranial and intraspinal pressure
 cerebral blood flow and autoregulation
 cerebral perfusion pressure

IT_GS 1.9 Outline the physiological changes that occur with and the implications for anaesthetic management of the following patient positions:
 supine
 Trendelenberg and reverse Trendelenberg
 lateral
 lithotomy
 prone

T/F reverse Trendelenberg means “head down”

T/F the head-down position increases both cerebral arterial, and cerebral venous pressures, by the same amount

T/F following from the above statement, cerebral perfusion pressure would remain unchanged

T/F despite an increase in cerebral capillary hydrostatic pressure, cerebral oedema does not develop if the blood brain barrier is intact

T/F intracranial pressure may increase due to (i) increased cerebral venous blood volume, (ii) increased arterial blood volume, and (iii) cerebral oedema

T/F applying PEEP would have no impact on cerebral venous pressure

BT_PO 1.92 Outline the basic electrophysiology of nerve conduction

T/F  the resting membrane potential of a nerve is about minus 90 mV

T/F  in a nerve, voltage gated sodium channels are opened at a threshold of minus 40 mV

T/F  voltage gated potassium channels are also triggered to open at threshold

T/F  there is no refractory period with a nerve action potential (this is only seen in cardiac action potentials)

T/F  saltatory conduction (i) increases the speed of conduction, and (ii) decreases the energy expended by the nerve cells

T/F  repolarisation of a nerve cell occurs when the sodium-potassium pumps actively pump out the sodium which entered the cell during depolarisation


any standard physiology book, including Kam & Power, Ganong, Guyton

BT_PO 1.86 Describe the role of the hypothalamus in the integration of neuro-humoral responses

T/F   osmoreceptors are located in the hypothalamus – when osmolality increass, ADH is released from the posterior pituitary

T/F   the hypothalamus can suppress appetite via the satiety centre, by sensing blood glucose levels

T/F    the posterior hypothalamus contributes to the control of the sympathetic nervous system

T/F   the hypothalamus integrates body temperature regulation – responses to a fall in body temperature are triggered by the anterior hypothalamus

T/F  fever occurs when pyrogenic cytokines alter the “set point” of the hypothalamus to higher than 37 degrees

T/F  the hypothalamus secretes thyroid stimulating hormone (TSH) which stimulates T3 and T4 release from the thyroid gland


  1. Kam & Power 3rd edition, page 66-67
  2. Ganong 24th edition, chapter 17

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


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

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