BT_PO 1.44 Describe the physiology of cardiac muscle and the mechanism of excitation contraction coupling

T/F  cardiac muscle is not striated

T/F  acetylcholine is released from the terminal ends of the cardiac conduction system, where it binds to muscarinic acetylcholine receptors on the myocytes

T/F  cardiac myocytes are connected to each other via gap junctions, to increase the speed of electrical conduction and enable the heart to contract “as one”

T/F  an increase in the force of myocardial contraction is brought about by recruitment of additional myocardial motor units

T/F  contractility is proportional to intracellular calcium concentration

T/F  entry of extracellular calcium via T tubules triggers further calcium release from sarcoplasmic reticulum


  • Ganong
  • Pappano & Weir

BT_PO 1.59 Describe the pharmacology of drugs used to manage myocardial ischaemia/infarction, including: nitrates, beta blockers, calcium antagonists, anti-platelet agents, anti- coagulants and fibrinolytic agents

T/F  the main mechanism by which glyceryl trinitrate can treat myocardial ischaemia, is by direct coronary artery vasodilation

T/F  tachyphylaxis can develop if glyceryl trinitrate is given continuously (e.g. transdermal patch), without a ‘rest’ period

T/F  beta blockers help reduce myocardial ischaemia mainly by reducing contractility – the decreased wall tension corresponds to decreased oxygen demand

T/F  the calcium channel blockers most appropriate for angina, are from the dihydropyridine group

T/F  aspirin is useful with myocardial ischaemia because it decreases vascular endothelial prostaglandin synthesis – this reduces platelet adhesion

T/F  tirofiban can be used IV for unstable angina – this must be ceased at least 24 hours pre-operatively to reduce bleeding risk


  • various bits of Hemmings & Egan, Evers & Maze, Stoelting

BT_GS 1.69a Describe how a patients temperature is monitored and discuss the indications for temperature monitoring with the advantages and disadvantages of particular sites and methods (also refer to monitors and monitoring standards, which is covered in the Safety and quality in anaesthetic practice clinical fundamental)

T/F  a 1 degree increment on the Celsius scale equals a change of 0.1 Kelvin

T/F all anaesthetised patients being actively warmed, must have their core temperature continually monitored

T/F temperature probes commonly used in anaesthesia incorporate a thermocouple which consists of two wires joined together, each being a different metal

T/F  a temperature probe placed in the oropharynx can underestimate core temperature – it should be placed in the oesophagus

T/F  urinary catheters with a built-in temperature probe can be useful with head and neck surgery, or in patients destined for ICU

T/F  a tympanic thermometer emits a beam of infrared light onto the tympanic membrane – this is then reflected back to a sensor at a given wavelength which corresponds to temperature

T/F  digital thermometers (e.g. for use per axilla) incorporate a thermistor, which consists of a small bead of a metal oxide – its electrical resistance increases as temperature increases


  • ANZCA PS 15
  • Davis & Kenny
  • look at the equipment in your hospital

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

A bit of a glitch

Hi everyone.

There seems to be a bit of a problem in the land of “WordPress meets my computer” and I can’t access any of the site material, other than the already published posts. I also can’t write a new post ( I am currently on my phone which has limited functionality).

I’ll try again a bit later today….

This fabulous table top is constructed from materials found in the Great Pacific garbage patch (I can remember the creators name)

BT_PO 1.19 Describe altered lung mechanics in common disease states

Notre Dame Cathedral

Ok, well that is Murphy’s Law in action. After trying repeatedly to get the site working, as soon a I posted that last message, it was back in action!

Sorry for the absence of a post yesterday – lucky we had two on Monday.

I think this may be the last respiratory LO yet to receive a post!


BT_PO 1.19 Describe altered lung mechanics in common disease states

In patient’s with CPOD, the diaphragm becomes less efficient, worsening ventilatory capacity T/F

Loss of compliance of the chest wall is a significant contributory to respiratory failure in patients with circumferential chest wall burns T/F

Hyperinflation of the lungs, due to gas trapping associated with COPD, results in improved intercostal muscle efficiency T/F

There is a restriction to inspiratory flow more than expiratory flow with obstructive airways disease T/F

With Easter around the corner here is something to think about. It has been postulated that many people who were crucified died from asphyxia or ventilatory failure. Can you postulate how this might occur thinking about the mechanics of breathing?


IV Fluids

T/F the lactate in Hartmann’s can worsen a lactic acidosis

T/F Hartmann’s is contraindicated in patients with diabetes

T/F 5% glucose is used to provide IV water without causing haemolysis

T/F the rationale of 4% and a fifth is to meet the normal daily requirement of sodium

T/F 4% and a fifth can cause hyponatrarmia in unwell patients

Discussion point – it is common practise in neuroanaesthesia to use 0.9% saline instead of Hartmann’s – can you think of a rationale for this? Is it routinely necessary?

Exams with children

When I sat my primary examinations, someone said to me that people with children were more likely to pass this exam. Is this true? Who knows? But it was an interesting point and one that has stayed with me over the years.

This is a difficult exam and one that requires a huge amount of time if you want to pass. Having children, regardless of their age, in your life around the time of the preparation for the examination and the examination itself makes a tough time even harder. We now have trainees who are post graduate when they start medicine, meaning that we seem to be seeing more and more trainees that have children during their training.


This post is aimed to give some useful tips to those trainees sitting this exam with children, or with other life events. It is based on opinion, experience and a smidgen of research.

  1. This is a family decision. You will need to lean heavily on partners, extended family, friends, other school parents and neighbours. Be proactive and get people ready to help once you start studying.
  2. Get outside help. A nanny, cleaner or daycare can be a big financial hit, but it’s a short-term hit. If you need to pay to have your life made easier, then take it and pass the exam.
  3. Make yourself a priority. You only want to sit once so look after yourself. Sleep well, eat healthily, exercise and keep your mental health steady.
  4. Make yourself a priority, until you need to help. There are times when you will have to miss times with your children, and then there are times you will need to miss study time.
  5. Be realistic. Add an extra 10% of study time into your plan as life will inevitably get in the way at times.
  6. Be organised. Plan your hours of study around times when the children are asleep or at school or you have help. This might mean studying into the night once the kids are asleep, or getting up early to get the hours in. It does no one any favours if you are studying inefficiently and if you have a routine, the children learn your routine.
  7. Don’t be a perfectionist. If your kids need screen time or scrambled eggs for dinner sometimes to get you through, remember you are still setting a wonderful example for them.
  8. Sacrifice free time for family time. Have breaks. See the kids. Thank your partner.
  9. In the era of social media, tap into online support groups for practical tips and support from other studying parents.

Do people with children have a higher rate of passing this exam? Again, I don’t know but I can see that this might be true. It is an added pressure that requires organisation, efficiency and dedication. Having children can also put times like this in perspective.

If anyone has any extra tips for other trainees sitting the exam with children then please share them here. And good luck to everyone sitting the viva examinations in a few weeks!


BT_PM 1.12 Describe opioid receptors

I don’t have any nice new poppy photos, so we will go with a water lilly instead

I think this is another LO where you what you learn should be directed towards how it affects function rather than just memorising in detail the intricacies of the receptor itself.

The top 4 statements are core. The last one is the most interesting (I’ll try to find a good concise article on it for those who are interested and will update the post when I have). You will find the answers to the rest in, you guessed it, Hemmings and Egan 2e. There is also a nice summary article in BJA Education here.

BT_PM 1.12 Describe opioid receptors

Opioid receptors are G-protein coupled receptors  T/F

Opioid receptors are found only on post synaptic cell membranes T/F

Activation of opioid receptors increases potassium conductance and  causing membrane hyperpolarisaton T/F

All opioid receptor subgroups have their own endogenous ligand, with B endorphin the ligand for the mu opioid receptor T/F

Opioid receptors are subject to significant genetic polymorphism which effects nociception and analgesia T/F


BT_GS 1.22 Describe the mechanisms of action and potential adverse effects of buffers, anti-oxidants, anti-microbial and solubilising agents added to drugs

T / F glycerol is part of the formulation of propofol – it is added as an emulsifying agent

T / F the intravenous formulation of paracetamol contains mannitol and povidone – both are to improve solubility

T / F amiodarone is formulated in alcohol and polysorbate 80 – these can cause hypotension with a rapid bolus

T / F phenytoin is soluble in water if the pH is < 3 – therefore hydrochloric acid is added to the ampoule

T / F sodium metabisulphite is added to some drugs ampoules as an anti-oxidant and anti-microbial – it is required to make morphine suitable for intrathecal use


  1. MacPherson R. Pharmaceutics and the anaesthetist. Anaesthesia, 2001; 56: 965-79
  2. MIMS and/or product info leaflets for each drug