2018.1 SAQ 11


Describe the respiratory response to hypoxaemia in both the awake and anaesthetised patient.

You could give a very brief but pertinent answer to this question by stating that the responses are very different!  Being reliant on oxygen for sustaining life we have evolved powerful mechanisms to combat hypoxia/ hypoxaemia (not the same thing but usually co-exist) but these same mechanisms are mostly ablated when we anaesthetize our patients.

T/F  The peripheral chemoreceptors are located in the carotid sinus

T/F  Hypercarbia impairs the ventilatory response to hypoxaemia

T/F  Volatile agents will mostly ablate the ventilatory response to hypoxaemia at low MAC values

T/F  If you underwent bilateral carotid endarterectomy you would lose your ability to respond to hypoxaemia

T/F  Sustained hypoxaemia causes a triphasic response in the awake subject

T/F  Hypoxic pulmonary vasoconstriction is markedly impaired by 1 MAC volatile

All the answers are in Nunn of course. Possibly the only physiology text you should contemplate reading from cover to cover.

2018.1 SAQ 7 Propofol dosing

Justify the dose of propofol you would expect to use to induce anaesthesia in the following scenarios, using pharmacokinetic (PK) and pharmacodynamic (PD) principles.

  • 4 yo child weighing 15kg
  • 75 yo man weighing 70kg
  • 40 yo man weighing 70kg with severe hypovolaemic shock

The diagram below was conceived for entertainment value but is grounded in reasonably solid pharmacological principles. You really should have a pretty good idea about the answers to the T/F statements below. This is fundamental to our clinical practice after all.


Children have significantly reduced PD sensitivity to intravenous anaesthetic agents T/F

An increase in cardiac output will shorten the onset of effect of propofol but increase the dose required to cause loss of consciousness T/F

Shock reduces the induction dose of propofol for both PD and PK reasons T/F

There will be a relatively larger proportion of cardiac output going to the brain of a shocked patient T/F

The intravascular volume of an elderly man is not greatly different to that of a forty year old T/F


BT_GS 1.44 describe the clinical pharmacology of drugs used in management of PONV


I’m not a fan of Maxolon. This is a bit of an understatement actually. The main thing that bugs me about its still prevalent use in Australian hospitals is that it doesn’t actually work!! That is because it is not prescribed at a dose which is efficacious. The effective dose of metoclopramide for the treatment of PONV is 0.5mg/ kg. Consequently 10mg given to a 100kg patient is unlikely to help the cause. You may provoke an acute dystonic reaction if you’re unlucky. You may also provoke a raging tachycardia as the plastic ampoules look very similar to those of atropine (particularly when they were both in black print unlike the photo above). Since ondansetron is actually cheaper than Maxolon in my hospital I can think of no circumstances in which I would prescribe it.

Regarding metoclopramide:

It is not recommended by SAMBA* for the prevention or treatment of PONV T/F

The Australian TGA recommends a maximum dose in adults of 10mg three times a day. T/F

Despite avidly crossing the placenta, metoclopramide is the only antiemetic agent with a Category A rating for use in pregnancy T/F

Metoclopramide’s pro kinetic actions are negligible in the presence of anticholinergic therapy T/F

Metoclopramide may stimulate the secretion of prolactin and prolong the duration of sux T/F


Look in Stoelting if you’re not sure about the last one.

*You should know who SAMBA are- they’re not latin dance fans either.


BT PO 1.125 Outline the pharmacology of cancer chemotherapeutic agents

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Methotrexate is used in the medical treatment of ectopic pregnancy T/F

Vincristine may be administered both intravenously and intrathecally T/F

Vincristine is more likely to cause constipation than diarrhoea T/F

Anthracycline antibiotic agents like daunorubicin cause reversible cardiotoxicity T/F

Patients on chemotherapy who are febrile are almost always neutropaenic T/F

Answers about Archie and his airway

The Laryngeal Mask Airway (LMA) was just one of numerous patents that Brain applied for.  This is true. The LMA was the thirteenth patent he applied for. While not gifted in the sciences at school he had a flair for construction. He built his own guitar at the age of fourteen.

The first published study involving the LMA was a case series of women undergoing gynaecological laparoscopy.  This is also true. The paper was published in the BJA in 1983 and was titled “The laryngeal mask- a new concept in airway management”.

The LMA was first commercially available in 1983. False. The first commercial devices were available in the UK in 1988. Not all that long ago really! It took years for Brain to perfect his device and develop it as a medical device.

Australia was the first place to use the Proseal LMA.  This is true and was again relatively recently in 2000. I don’t know why. Perhaps he knew he had a willing advocate down under in the person of Joe Brimacombe!

There are over twenty different methods described to insert a LMA. This is true and they are all described in Brimacombe’s book. You only need one, however.

Dr Brain was born on July 2, 1942. His father was a diplomat and was knighted. Surely his son deserves a knighthood also?

5 things you probably didn’t know about Archie Brain

I hope I am not being presumptuous in assuming that all of you know who Archie Brain is. The next sentence will give you a rather substantial clue regardless. I reckon his invention of the laryngeal mask was worthy of the Nobel Prize for Medicine. His invention is certainly the most significant advance in the field of anaesthesia for my generation. It is very fortunate that propofol joined the arsenal at roughly the same time. White stuff + LMA is probably the commonest anaesthetic combo in the world today. Interestingly enough the first anaesthetics using the LMA were done with a combination of thiopentone and muscle relaxant. Trying to insert a LMA with just thiopentone is fraught with peril but the contemporary anaesthetic trainee has barely seen a vial of thiopentone these days let alone tried to insert a LMA under the influence of this venerable barbiturate. For a fascinating and comprehensive history about all things concerning Brain and his invention one should consult Joe Brimacombe’s definitive Laryngeal Mask Anesthesia: Principles and Practice. I would confidently assert that Brimacombe has inserted more LMAs than anyone else on the planet. Despite the American spelling of his textbook he is a pom who practices in Far North Queensland. To say he is an ardent fan of the Proseal LMA would be an understatement. LMAs are so popular in Cairns that they mandate intubating people each April so they don’t forget what to do with a laryngoscope.

The Laryngeal Mask Airway (LMA) was just one of numerous patents that Brain applied for.  TRUE/ FALSE

The first published study involving the LMA was a case series of women undergoing gynaecological laparoscopy.  TRUE/ FALSE

The LMA was first commercially available in 1983.  TRUE/ FALSE

Australia was the first place to use the Proseal LMA.  TRUE/ FALSE

There are over twenty different methods described to insert a LMA.  TRUE/ FALSE

BT_GS 1.44 Describe the clinical pharmacology of drugs used in the management of PONV


Regarding ondansetron:

It is significantly more expensive than metoclopramide*     T/F

It prolongs the QT period to a similar degree to that of droperidol     T/F

A common adverse effect is constipation                               T/F

It doesn’t impair the analgesic efficacy of tramadol             T/F

The wafer formulation has an intense bitter taste                 T/F


*At the time of writing, an amp of Maxolon costs about 40 cents in my hospital.

BT GS 1.12 Explain and describe the clinical application of concepts related to intravenous and infusion kinetics

Admittedly, this is a rather dry topic.  It is of unequivocal importance to anaesthetists however as our practice revolves around giving drugs that have potent pharmacodynamics effects with rapid onset and offset of action.

Regarding the time to peak effect (TTPE):

Is indicated on a plasma time curve for a bolus dose where the effect site curve crosses the plasma concentration curve TRUE/FALSE

Will be relatively short for any drug that rapidly redistributes TRUE/FALSE

Will be relatively short for drugs with a large keo TRUE/FALSE

Will always be longer than the t ½ keo TRUE/FALSE

Is considered to be a dose insensitive parameter TRUE/FALSE

BT PO 1.91 Outline the pharmacology of glucagon (& other things)


Coming in an aesthetically pleasing little orange container, glucagon is a drug anaesthetists administer infrequently. Funnily enough the most common indication that we give glucagon for has nothing to do with hypoglycaemia. Rather it is given to treat suspected spasm of the sphincter of Oddi demonstrated on an intraoperative cholangiogram when performed during a lap chole. The second most common indication in our sphere of influence is probably the management of impacted food boluses. Both of these indications relate to the smooth muscle relaxant action of glucagon.


Glucagon is an anabolic hormone TRUE/FALSE

Glucagon is synthesized by the alpha cells of the islets of Langerhans TRUE/FALSE

Glucagon is effective in the management of beta blocker overdose because it  firmly binds to adrenoceptors TRUE/FALSE

Glucagon is an inotrope and chronotrope TRUE/FALSE

Glucagon binds to a G protein coupled receptor and inhibits adenylate cyclase activity and thus reduces cAMP TRUE/FALSE