Stan's gold medal viva exam

By popular demand, here is the actual physiology and pharmacology viva that Stan was examined on for the part 1 ANZCA exam!

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Some links and formulas!

How does it measure cardiac output?

Using thermodilution and utilisation of Stewart Hamilton’s equation of:

(Tb-Ti)*Volume*k/intergration of change in T

What is venous admixture?

Venous admixture is the amount of mixed venous blood that needs to be added to end-capillary blood to account for the difference seen in pO2 between arterial blood and end-capillary blood.

It is calculated using the equation:

Qs/Qt = Cc’O2 – CaO2 / Cc’O2 – CvO2

Alveolar gas equation.

PAO2 = FiO2 (Patm – PH2O) – pCO2/R

 Is there anything else at the end?

Yes there is a correction factor (+F) which is FiO2 * pCO2 * (1-R)/R and this is normally less than 2mmHg.

O2 content = SaO2 * Hb * 1.34 (Huffner’s constant which ideally is 1.39) + pO2 * 0.003

the isoshunt diagram is figure 8 here:
https://erj.ersjournals.com/content/44/4/1023.figures-only

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Check out https://anaesthesiacollective.com/education/first-part-exam/ for general information and a collection of model answers

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Transcript

 What is the balloon used for in a pulmonary artery catheter?

To wedge the pulmonary artery and produce a static column of fluid.

What else?

(Pause) I can’t think of anything else at this moment in time.

Well why do we blow up the balloon at the start?

I don’t know. (Can feel the examiner getting slightly frustrated)

What’s the path the balloon travels?

SVC, right atrium, right ventricle, pulmonary artery.

So how do you get the catheter to get into the right place?

(Dawns on me at this moment that he wants me to say) Aids in the direction of the catheter.

Correct. It’s for flow direction. Now can you draw me a trace.

Trace drawn:

y axis: pressure, x axis: time

Right atrium, a, c, v wave. Pressure about 5mmHg.

Right ventricle: Systolic 25mmHg, Diastolic 0mmHg.

Pulmonary artery: Systolic 25mmHg, Diastolic 8mmHg

Wedge pressure: a, c, v wave. Pressure about 10mmHg.

Hold on, is the wedge pressure higher or lower than the pulmonary diastolic pressure.

(I always though the most important pressure was the pulmonary artery mean which is 15mmHg which still provided a pressure gradient to the left atrium, but given the examiner interrupted me I knew he thought differently so I said) No sorry, it’s lower.

How does it measure cardiac output?

Using thermodilution and utilisation of Stewart Hamilton’s equation of:

(Tb-Ti)*Volume*k/òDT

Can you draw me a diagram and explain?

Diagram drawn:

y axis: Change in temp

x axis: time

So a larger AUC represent a smaller cardiac output. A smaller AUC represents a larger cardiac output as more blood is able to minimise the change in temp.

What is this – points to (Tb-Ti)*Volume*k?

Amount of injectate.

What is continuous cardiac output monitoring?

Uses a proximal heating element and a thermistor distally to measure the change in temp over time.

What else can you measure using a pulmonary artery catheter?

CVP, right ventricle pressure, core temperature, left atrial pressure which equals left ventricular end-diastolic pressure which is an index of preload. (I missed out mixed venous O2)

How do you standardize cardiac output measurement?

CO divided by BSA

Okay, let’s completely change topic. What is an acid?

An acid is a substance which donates a hydrogen ion according to the Bronsted Lowry theory.

How does the body handle an acid?

By buffering, compensation and correction. How it works depends on whether it is a respiratory or metabolic acidosis.

Okay, how do kidneys excrete an acid load?

Via titrateable acids and glutamine. (Should have said ammonium!)

What do you mean by glutamine?

Glutamine is broken down to H+ which is excreted and OH- which is absorbed. (Should have said glutamine!)

What are the important substances which allow the kidneys to excrete an acid load?

Phosphate is the most important.

Anything else?

Bicarbonate.

And acetoacetate and beta hydroxybutyrate in pathological conditions such as DKA.

What about the substance that glutamine becomes?

Ammonium.

You are doing a case and the consultant hands you a blood gas result and tells you there is an acidaemia. How do you read it?

It depends on whether the result is pH stat or alpha stat. (Should have probably said I would determine the clinical scenario first).

Which one do you use?

Alpha stat because of intracellular imidazole groups.

Okay, what would you look at next?

I would look at the pCO2 to see if this is the cause of the acidaemia.

It CO2 an acid according the Bronsted?

No it’s not but it forms carbonic acid which is an acid.

Agree. What would you look at the next?

Next I would look at the bicarbonate.

(Interrupts me) Even before that, what else could you look at?

The base excess.

What is base excess?

Bases excess is the amount of acid or base that needs to be added to the blood to return it to a pH of 7.4 at a pCO2 of 40mmHg and temp of 37. 

Did you tell me what pH was an acidaemia?

No I didn’t. But a normal pH range depending on the calibration of the machine is 7.35-7.45, so anything less than 7.35.

What is the normal base excess?

-2 to +2

What is significant?

(Had no idea) It depends on the severity of the acidaemia. For example if the pH is 7.1 and the BE is -5, I would consider that significant.

What are its units?

I don’t know but going from 1st principles, it should be mmol/L.

Correct. Finally is albumin an acid?

Well according to Stewart’s hypothesis it is.

How about Bronsted’s theory?

(Given he asked this I deducted it must be so I said) Well it does donate a H+ so it is.

Correct.

What is shunt?

Shunt is blood that goes from the right side of the heart to the left side in a circuit and does not participate in gas exchange.

There is physiological and pathological shunt.

Physiological shunt includes:

1.      Bronchial veins

2.      Thebesian circulation

(Interrupts me) How much do the bronchial veins contribute to shunt?

Very small. Less than 1%.

What is the thebesian circulation?

These are venous tributaries from the heart which drain into the left atrium.

What is the colour of its blood?

It would be dark blue.

Okay go on.

So the pathological causes would be V/Q mismatch.

(Interrupts me) Is V/Q mismatch a shunt?

No you’re right, it’s not. It contributes to venous admixture but is not a shunt. 

Okay, anything else?

So other causes would be atelectasis, pneumonia and congenital right to left shunts.

What is venous admixture?

Venous admixture is the amount of mixed venous blood that needs to be added to end-capillary blood to account for the difference seen in pO2 between arterial blood and end-capillary blood.

It is calculated using the equation:

Qs/Qt = Cc’O2 – CaO2 / Cc’O2 – CvO2

What do you need to measure CaO2?

An arterial line.

CvO2?

Pulmonary artery catheter.

Yes like we talked about previously. (and reminding me of what I missed out!)

Cc’O2?

You need to know the ideal alveolar pO2 which is calculated using the Alveolar gas equation.

PAO2 = FiO2 (Patm – PH2O) – pCO2/R

Is there anything else at the end?

Yes there is a correction factor (+F) which is FiO2 * pCO2 * (1-R)/R and this is normally less than 2mmHg.

In what instances does it become significant?

Reading off my formula – Elevated pCO2, very low R. (forget to say high FiO2 which is probably the most important factor).

What is the respiratory quotient?

Respiratory quotient is the amount of CO2 produced divided by the amount of O2 consumed at steady state. It is dependent on the substrates used for energy. For example, carbohydrates have a RQ of 1, and fats have a RQ of 0.7. 

What is the RQ of alcohol?

I don’t know. (It’s about 0.67)

What is the content equation? 

O2 content = SaO2 * Hb * 1.34 (Huffner’s constant which ideally is 1.39) + pO2 * 0.003

Why is it 1.34 and not 1.39?

1.39 is with deoxy and oxyHb. However, because of the presense of other Hb such a sulfaHb, metHb, carboxyHb, this value becomes 1.34.

What is this? (pointing to 0.003)

This is Henry’s solubility coefficient based on his law which is the amount of O2 dissolved for a given pO2.

How do you measure SaO2?

Indirect and direct ways of measuring it.

Indirect includes pulse oximetry.

Direct includes using infra red absorption on a blood sample (I forgot the name!)

(I should also have said by measurement of pO2, many machines indirectly solve for SaO2 using a HbO2 dissociation curve/algorithm.)

Do you know what it’s called?

I can’t remember.

Co-oximetry. How else can you measure content?

By using the Lloyd-Haldane and Van Slyke technique, using saponin to lyse the blood cell to release O2 (I forget to say the addition of potassium cyanide), and then there is a manometer which measure the pressure change.

Can 100% O2 fix a true shunt?

It depends on the degree of shunt.

No, just the shunt itself?

No.

What happens when you cut your hand with a knife?

A number of things happen:

1.      Polysynaptic/withdrawal reflex.

2.      Pain pathway

3.      Sympathetic response

4.      Immunogical response

5.      Coagulation response

Describe the withdrawal reflex?

The afferents synapse in the dorsal horn where locally they cause activation of the alpha motor neurons on the flexor muscle and inhibition on the extensor muscle.

What is this reflex called?

It’s a monosynaptic if you’re talking about one reflex arc. However there are many other levels involved including movement of the other arms and legs to make it a polysynaptic reflex.

What happens to the other hand?

(Mouth talked before brain could think) It flexes too.

No. It actually extends. Tell me about the pain pathway?

The transmission of pain can be divided into:

1.      Physiological

2.      Pathological

3.      Modulation

Physiological can be divided into 1st order, 2nd order and 3rd order neurons.

1st order neurons are Ad fibres which are myelinated and are mechanothermal, and unmylenated C fibres which are unmyelinated and polymodal.

How fast to they travel?

Ad fibres 10-15m/s (actually 10-30m/s)

Unmyelinated C fibres 0.5-1m/s

Can you draw me a diagram with the spinal cord?

Diagram drawn showing Ad fibres synapsing on substantia gelatinosa I and V, and C fibres synapsing on substantia gelatinosa I and II. They then cross via Lissauer’s tract and go up via the spinothalamic tracts. There are 2 types – paloespinothalamic which is the primitive form and ends in the medulla and subjected to modulation. It transmits diffuse pain. The other is the neospinothalamic which ends directly in the thalamus and transmits sharp pain.

Why do people rub their hands when they cut their hand?

It produces a wider area of signals through the spinal cord and so decrease the primary afferent pain stimulus.

Describe the sympathetic pathway?

Sympathetic output is primarily a thoracolumbar output.

At what levels does it come out?

T1 to about L2

Continue.

So it starts from the vasomotor centre in the medulla, exits at the spinal cord and is important in a number of actions including increasing the heart rate and getting the body ready for flight or fight response. (I missed out describing its preganglionic and postganglionic innervation)

What are the stress hormones released?

Cortisol is primarily the main stress hormones.

Are there any other hormones?

*BELL*

Answer would have been adrenaline, noradrenaline, renin-angiotensin-aldosterone


What is MAC?

MAC is the minimum alveolar concentration of a volatile which prevents movement to a supramaximal stimulus. It is measured at standard pressure, with 100% O2, and after 15 minutes once end tidal equilibrium has been achieved with no other drugs such as induction agents (this could be wrong and probably benzodiazepines is more correct), opioids or muscle relaxants.

If you don’t use induction agents, how do you get them off to sleep?

With the volatile. (This could be possible with halothane and sevoflurane, but may not be desirable using isoflurane and desflurane).

Why do we use it?

We use it as:

1.      A measure of potency between other volatiles where it is a constant when multiplying it’s oil/gas coefficient with its MAC.

2.      An objective measure of awareness

3.      And there are also other MAC numbers avaialble.

How else is it relevant?

(Not too sure what he was getting at here). Well MAC represent the mean, mode and median of the response.

What happens to MAC when you give 70% N2O with sevoflurane?

MAC in this case is additive. So with 70% N2O, this is about 0.7 MAC and you need another 0.3 MAC of sevoflurane to get 1 MAC.

What are the different types of MACs?

There is MAC awake which is about 0.3. There is MAC BAR which depending on the volatile is about 1.5.

What is BAR in MAC BAR?

Blocking of Autonomic Response.

Does N2O have the same MACawake values as volatiles? 

No it actually has higher MAC awake value.

Why?

Because N2O is much less potent than the other volatiles having a MAC value of 104%.

Can you draw me a MAC-response curve with MAC?

Graph drawn with y-axis response, x-axis MAC, and steep sigmoid curve with ED50 at MAC 1.

MACawake?

Graph drawn with ED50 at MAC 0.3

MACBAR?

Graph drawn with ED50 at MAC 1.5

Is there another type of stimulus that can be used other than a surgical incision?

Yes you can use a nerve stimulator.

And what kind of stimulus would you give?

You would give a supramaximal stimulus which is 2-3 x more than the threshold potential to depolarise all composite nerve fibres.

And what does the response have to be to be considered positive?

It has to be purposeful movement.

What are the side effects of atropine?

Side effects are dose dependent and for the cardiovascular system, this would include tachycardia increasing myocardial O2 demand and decreasing O2 supply, and because it is a tertiary amine it cross the BBB and can cause sedation and confusion. There are also idiosyncratic reactions like anaphylaxis and other adverse reactions. (The mnemonic completely escaped me with this question – red as a beet, mad as a hatter, dry as a bone, blind as a bat, hot as a hare).

What do patients also complain about when you give this a pre-med?

Dry mouth

What would someone look like with an atropine overdose? 

Confused and tachycardic.

What would be the colour of their skin? 

(Wasn’t sure and guessed wrongly) Pale.

What happens to their temperature?

It goes up especially in children because atropine inhibits their ability to sweat.

So what happens to the colour of their skin?

So they vasodilate and become red.

Have you heard of anticholinergic sydrome?

Yes

What other drug can cause this?

Hyoscine or scopolamine.

How do you treat central anticholinergic syndrome?

You would use an anticholinesterase agent which has a tertiary amine that crosses the BBB like physostigmine.

Why don’t we use physostigmine anymore in our practise?

(I had no idea we didn’t use it anymore in our practise but deduced it was from its side effects). Because of its ability to cross the BBB, not only were there muscarinic effects, but also central nicotinic effects which may cause seizures, muscle fasciculations and paralysis.

What else can physostigmine be used to treat?

I don’t know but possible benzodiazepine overdose. (Partly guessed correct. Can also be used for TCAs and antihistamine ODs).

Can atropine cause a bradycardia? 

Yes it can in small doses. 

Why?

I think it’s a partial agonist effect. (This is wrong. It’s been described as either a central effect or a Bezold-Jarisch reflex).

What are the differences between atropine and glycopyrrolate?

Glycopyrrolate has a quaternary ammounium and so does not cross the BBB and cause sedation or confusion.

What about the time to onset?

Yes, atropine has a faster onset of action than glycopyrrolate. 1 vs 3 mins.

What is anaphylaxis?

Anaphylaxis is a Type I hypersensitivity reaction mediated by IgE and requires prior sensitisation. On exposure to the antigen again, this releases mediators such as histamine which causes hypotension, bronchoconstriction and urticaria. 

Can you tell me more about how and what mediators released?

With the sensitisation event, IgE is exposed on mast cells and basophils and when exposed to the antigen, they cross link and release large amount of histamine, serotonin, bradykinin, prostaglandings, slow releasing factors of anaphylaxis (leukotrienes).

Yes, quite an inflammatory soup. How would you treat it?

Treatment would be:

(Forgot to say remove the offending agent), O2, adrenaline, H1 antagonist such as promethazine and finally a steroid like dexamethasone.

Why adrenaline?

Adrenaline is a potent a and b adrenoceptor agonist which reverses the hypotension, bronchodilates and stabilises mast cells to prevent further degranulation.

Why steroids?

Steroids would not be the first line but is used because it decreases the production of prostaglandins and slow releasing factors of anaphylaxis.

Can you tell me more about the pathway?

So these mediators are produced from membrane phospholids and converted into arachodonic acid via phospholipase A2 which are then made into prostaglandins and leukotrienes via COX I and II. So steroids inhibit phospholipase A2 (via increase production of phospholipase A2 inhibitor) and decrease the conversion of phospholipids to arachodonic acids.

What are the different types of histamine receptors?

So there are H1, H2 and H3 receptors.

H1 are Gq proteins and cause vasodilation and bronchoconstriction. (Forgot to mention important in the transmission of nausea and vomiting in the nucleus solitaruis and vestibular nucleus).

H2 are Gs protiens and cause an increase in gastric acid secretion.

H3 and Gi proteins which are presynaptic and cause negative feedback inhibition.

What would you use to block H1 receptors?

Promethazine.

What would you use to block H2 receptors?

Ranitidine.

We used to use cimetidine in the past. Why don’t we use it anymore?

Because it inhibits cytochrome P450, and so can potentiate the effects of other drugs which are dependent on this system for metabolism.

How else do you treat bronchoconstriction?

So apart from adrenaline you can use a b2 agonist such as salbutamol. You can also use aminophylline. 

(Examiner interrupts) So how does aminophylline work?

Aminophylline is a phosphodiesterase inhibitor which decreases the breakdown of cAMP and cGMP which decreases Ca2+ influx and causes bronchodilation.

How is oxygen made?

Oxygen is made either by fractional distillation or filtered through an artificial zeolite made of silica.

With fractional distilllation, air is cooled to -180°C and compressed to 5 bar and when the temperature is increased, N2 boils off first as it has a lower boiling point leaving O2.

With filtration, gases such as N2 and H2O are trapped leaving O2.

What are its physicochemical properties?

Oxygen is a clear, colourless gas that has a MW of 32. It has a boiling point of -180°C and a critical point of -120°C. (Missed out saying it is odourless as well as supporting combustion).

In the hospital setting, O2 is cooled and compressed as a liquid and comes out of the mains at a pressure of 4 BAR, and is also stored in cylinders at 137 BAR.

How is oxygen stored in the body?

It’s primarily stored in haemoglobin.

Anywhere else?

It’s also stored in your functional residual capacity, dissolved in blood and tissue and in myoglobin.

What are the pharmacokinetics once it enters the cell?

It enters the mitochondria and allows oxidative phosphorylation to occur, and is converted by cytochrome aa3/oxidase to H2O.

Okay we are probably going into physiology here. What are the potential toxicities with oxygen?

First it causes pulmonary toxicity thought to be due to production of oyxgen radicals and lipid perodixation. It is associated with high concentrations of O2, for example using 60% of O2 for more than 24 hours.

Secondly it can cause convulsion but only at atmospheres more than 2, which is only relevant for hyperbaric conditions.

What other gaseous mixture is made with oxygen?

This would be Entonox which is a 50:50 mix of oxygen and N2O and utilises the Poynting effect.

Can you tell me a bit more about this effect?

So by mixing the two gases, it changes both their physiochemical properties where the boiling point is now -6°C. This is relevant because if it is exposed to temperature lower than this, it becomes a liquid and then when used again, the O2 comes out first and so doesn’t provide any analgesia to the patient, and then afterwards it gives out a hypoxic mixture predominantly of nitrous oxide and causes death.

What is diffusion hypoxia?

This is implicated with the use of N2O because of it’s high concentrations and low solubility, when it is turned off and washes out into the alveoli, it dilutes the oxygen in the alveoli causing hypoxia. That is why it is important to make sure there is 100% O2 when washing out N2O.

Apart from N2O, what other gases have analgesic effects?

*BELL*

Would have said xenon. Other volatiles also have some analgesic effects, (the concept of MAC) especially methoxyflurane.