A 1-liter hemorrhage leads to decreased blood volume, resulting in reduced venous return, cardiac output, and tissue perfusion. The body compensates through vasoconstriction and increased heart rate and hormonal responses.

Viva Questions & Answers

Station 1: Physiological Effects of Acute 1 Litre Blood Loss

Immediate Effects:
- Activation of baroreceptors → Sympathetic nervous system stimulation.
- Inhibition of para-sympathetic nervous system
- Increased heart rate, stroke volume, vasoconstriction, venoconstriction.
- Peripheral vasoconstriction to maintain blood pressure.
- Note – Hb and Electroylte composiiton unaltered.
Intermediate Effects:
- Renin-angiotensin-aldosterone system (RAAS) activation.
- Reduced renal perfusion → Renin release → Angiotensin II (vasoconstrictor) → Aldosterone release → Sodium and water retention.
- ADH release → Fluid reabsorption in kidneys.
Delayed Effects:
- Capillary fluid shifts: Reduced hydrostatic pressure → Fluid movement from interstitial to intravascular space.
- Starling’s forces: Balance between hydrostatic and oncotic pressures drives this shift.
- Restoration of circulating volume. With a comparative anaemia as volume restored but circulating RBC count less.
Key Formula Mentioned:
- Starling Equation: Describes fluid movement across capillaries, governed by hydrostatic and oncotic pressures.

⠀

Station 2: Nerve Conduction & Resting Membrane Potential

Resting Membrane Potential:
- Typically -70 mV in neurons.
- Maintained by Na⁺/K⁺ ATPase pump: 3 Na⁺ out, 2 K⁺ in → Creates electrochemical gradient.
- High extracellular Na⁺, high intracellular K⁺.
Depolarisation:
- Triggered by neurotransmitter binding at postsynaptic membrane → Na⁺ influx, K⁺ efflux.
- Action potential propagates via voltage-gated sodium channels.
- Saltatory conduction in myelinated nerves via (Nodes of Ranvier) betwixt myeline sheaths
Refractory Periods:
- Absolute refractory period: No depolarisation possible.
- Relative refractory period: Requires supranormal stimulus.
Peripheral Nerve Fibre Classification:
- A fibres: Myelinated, fast conduction (alpha motor, sensory fibres).
- B fibres: Lightly myelinated (preganglionic autonomic).
- C fibres: Unmyelinated, slow conduction (pain, temperature, postganglionic autonomic).

⠀

Station 3: Acid-Base Balance & Anion Gap

Definition of pH:
- pH = –log₁₀[H⁺].
Buffer Systems:
- Immediate response: Intracellular and extracellular buffers (bicarbonate, haemoglobin, phosphate, proteins).
- Intermediate response: Respiratory compensation (↑respiratory rate to ↓CO₂).
- Delayed response: Renal compensation (H⁺ excretion, HCO₃⁻ reabsorption).
Henderson-Hasselbalch Equation:
- Used to describe pH regulation based on bicarbonate and CO₂ levels.
Anion Gap:
- Formula: [Na⁺] + [K⁺] – ([Cl⁻] + [HCO₃⁻]).
- Helps differentiate causes of metabolic acidosis:
  - Raised anion gap metabolic acidosis (HAGMA): CATMUDPILES mnemonic.
  - Normal anion gap metabolic acidosis: Bicarbonate loss (e.g., renal tubular acidosis, diarrhoea).

CAT MUDPILES ?

Mnemonic for Causes of Raised Anion Gap Metabolic Acidosis (HAGMA)

Letter	Cause	Notes
C	Carbon monoxide poisoning, Cyanide poisoning, Congenital heart failure	Impaired oxygen utilisation, leading to lactic acidosis
A	Aminoglycosides (e.g., gentamicin)	Renal tubular toxicity contributing to acidosis
T	Theophylline toxicity, Toluene (solvent abuse)	Organic acid accumulation
M	Methanol poisoning	Formic acid production (toxic metabolite)
U	Uraemia (advanced renal failure)	Accumulation of sulphates, phosphates, organic acids
D	Diabetic ketoacidosis (DKA), starvation, alcoholic ketoacidosis	Ketone body accumulation
P	Paracetamol overdose, Paraldehyde ingestion	Pyroglutamic acidosis, metabolic toxins
I	Iron overdose, Isoniazid toxicity, Inborn errors of metabolism	Metabolic derangements, lactic acidosis
L	Lactic acidosis	Tissue hypoperfusion, sepsis, shock, malignancy
E	Ethanol, Ethylene glycol poisoning	Toxic alcohols, oxalic acid formation
S	Salicylate overdose (aspirin)	Mixed respiratory alkalosis + metabolic acidosis

Key Takeaways

Acute blood loss triggers a tiered response: rapid sympathetic activation, RAAS-mediated volume retention, and delayed capillary shifts.
Clear knowledge of the resting membrane potential and action potential propagation is crucial. Remember ion gradients and refractory periods.
- Cross your fingers you run out of time before Nernst rocks up
Acid-base homeostasis is maintained by buffers, respiratory, and renal mechanisms—understand timing and underlying principles.
Anion gap calculation is essential in metabolic acidosis evaluation. Familiarity with CATMUDPILES ensures comprehensive differential diagnosis.

Debrief

This viva covered essential physiology areas often tested in the FRCA Primary. A key exam strategy is to structure responses clearly—using frameworks like immediate, intermediate, delayed.

Additionally, confidently stating formulae (Starling equation, Henderson-Hasselbalch) and their clinical relevance can progress a station smoothly. For acid-base discussions, fluency with the anion gap formula and mnemonics like CATMUDPILES is invaluable. Always verbalise your structure early (e.g., “I’ll break this down into three parts…”), keep answers concise but accurate, and avoid hesitations on key numbers like resting membrane potential or normal pH values.

If you aren’t sure move on – and if the examiner really wants to know if you know – they will ask.

Practice Practice Practice!

References & Further Reading

Guyton & Hall Textbook of Medical Physiology – Blood Loss Response & RAAS. (my favorite textbook)
West’s Respiratory Physiology – Acid-Base Regulation.
https://www.ncbi.nlm.nih.gov/books/NBK538143/ – Conduction – Stat Pearl
Resuscitation Council UK – Acid-Base Disorders Quick Reference Guide.
Ganong’s Review of Medical Physiology – Peripheral Nerve Classification.

“Thanks for listening guys… Every day you are getting better at this. Take it day by day, don’t overcook yourself, don’t freak out, and keep studying!”

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Transcript

Gas, Gas, Gas Episode: 1 Litre Blood Loss, Membrane Potential, and Acid-Base Balance

Introduction and Casual Pre-Viva Banter

00:00-03:30

Please listen carefully. Hello, and welcome to Gas, Gas, Gas, the podcast that covers the FRCA primary exam. We’re going to fit into your day and give you as much of your life back as you could possibly imagine. I’m here to make your studying easier – listen to us on your commute, in the gym, in the shower, or when you’re ironing your scrubs. Expect facts, concepts, model answers and the odd tangent. Check out the show notes for all the detail, and remember to follow the show so that you never miss an episode. Let’s get on with it.

Hello Tom and welcome to your Physiology Viva. Obviously we are smashing through these at a tremendous rate. But most importantly, what’s your opinion about this cardigan I’ve got on, eh? Although it’s a bit hot.

Hey, why would you buy a cardigan and then pull it over your head? Hey? You’re an animal. Yeah, that’s the whole joy of a cardigan. And why not go through the intermediate process of unbuttoning and see if that’s a nice balance? You really don’t deserve a cardigan.

Oh, I didn’t realise you felt so strongly about cardigan donning and doffing techniques, Tom. Sorry, I’ll buck up my ideas.

Anyway, focusing back on the task at hand there, Tom. How do you think your Physiology Viva question answering techniques have been going?

I don’t even know how to answer that question. It’s – I think I vaguely feel as though I know lots of physiology and then I keep getting asked questions where I go, “mmm.”

Yeah, how do you feel about the Nernst equation?

Oh, I do not know the Nernst equation and I can only vaguely recollect what it’s useful for. I did listen to some neuroscience lectures before medical school from MIT by a really monotone neuroscientist over there, and he I think was involved in all of the squid neuron experiments they like to reference, and he was very much a fan of the Nernst equation and used to love talking about acceleron stuff, which I think is the original German name for adrenaline.

That’s some niche knowledge, Tom. Unfortunately, I’ve not done Nernst equation questions for you today, but maybe next time. I suppose they have actually – they wrote a syllabus didn’t they? They did. It’s just rather broad.

Right. So are you ready for your timed three five-minute stations physiology viva? Yeah, I’m always ready.

Physiological Effects of 1 Litre Blood Loss

03:30-08:30

Summary: Tom explains the immediate, intermediate, and delayed physiological responses to significant volume loss.

So, Tom, welcome. This is your Physiology Viva. What are the physiological effects of the sudden loss of one litre of circulating volume?

When a large volume of your circulatory volume is lost, it has some immediate effects, intermediate effects and delayed effects.

Immediate Effects

The immediate effects are for baroreceptors within the carotid body and the aortic arch to sense that pressure within the vascular system has dropped. This leads to activation of the sympathetic nervous system via central pathways. It leads to secretion of antidiuretic hormone from the posterior pituitary, which promotes reabsorption of fluid from the distal convoluted tubule.

And sort of backtracking a little bit to more immediate effects: you have an increase in heart rate via that sympathetic activation, which helps maintain blood pressure. You have increase in stroke volume. You have venoconstriction, which moves blood from capacitance vessels such as within the liver to try and replace the circulating volume that’s lost, and you have peripheral vasoconstriction from that sympathetic activation as well, by action at adrenergic receptors in smooth muscle. All of these things help to maintain blood pressure.

Intermediate Effects

The intermediate effects involve retaining fluid. So I already mentioned secretion of antidiuretic hormone because I was thinking of the neuronal pathways that link to the central nervous system. But on top of this, there will be a drop in blood pressure detected by the perfusion to the kidney.

So, by having reduced venous pressure within the venules of the kidney, you get reduced sodium flux at the macula densa, which leads to the release of renin from the juxtaglomerular apparatus, the secretion of aldosterone and that promotes fluid retention in order to try and maintain blood pressure.

This – the same system, so the secretion of renin from the juxtaglomerular apparatus as well as promoting the release of aldosterone will lead to the activation of angiotensin, to conversion of angiotensin I to angiotensin II, in fact, which is a potent vasoconstrictor and will itself lead to further activation of the sympathetic nervous system and secretion of catecholamines.

They’re the mechanisms that spring to mind immediately.

Fluid Shifts and Starling Forces

And any other fluid shifts? You mentioned capacitance vessels, but is there any other store of fluid that can be mobilised?

Yes. So yeah, I suppose we talked there about immediate and intermediate actions rather than the delayed ones. So fluid will move from the interstitial space into the vascular space to replace that fluid which is lost, and it will do that in response to reduced hydrostatic pressure in the vessels within blood vessels essentially, and the reduction in Starling forces.

So as that fluid shifts across, it will also draw fluid from the intracellular compartment as well to some extent and lead to replacement of the lost volume to a point.

Have you got any formulaic way of framing that shift of fluid?

So I can talk about the percentage blood loss compared to the physiological effects, and I can give an idea of what percentage of total body fluid is in each compartment. But I haven’t – I was trying to get towards the Starling equation.

Oh yes, I mentioned Starling’s forces there, so it would be useful to draw a diagram here, but what factors are there?

Yeah, so the diagram I’m thinking of really just summarises the fact that there is hydrostatic pressure within blood vessels and there is oncotic pressure within blood vessels, and the same exists in the interstitial space around them. And the balance of those forces decides whether at capillary level, fluid shifts into or out of that space. When we lose volume from the vascular space, we get a reduction in hydrostatic pressure, as I mentioned earlier, causing fluid shift inside, but also as fluid shifts into the vascular space.

And that’s your five minutes, Tom. We’re going to move on.

Resting Membrane Potential and Nerve Conduction

08:30-13:30

Summary: Tom discusses resting membrane potential, depolarisation, and nerve fibre classification.

How would you define the resting membrane potential? What is it?

The resting membrane potential is the potential difference across a cell membrane in normal physiological conditions when electrolytes are sitting in equilibrium either side of a cell membrane. So a neuron resting membrane potential is normally around minus seventy millivolts and it’s dictated by the concentration of cations and anions either side of the cell membrane.

Through the action of sodium-potassium ATPase pumps, the primary driver behind resting membrane potential will be the raised concentration of potassium within the cell and the raised sodium concentration outside of a cell.

Could you just elaborate a little bit further on how those ionic differences are maintained?

Yes, so the sodium-potassium ATPase pump is a transmembrane protein that utilises adenosine triphosphate in order to consume energy and to move sodium and potassium in opposite directions against their concentration gradients. So potassium moves within the cell and sodium moves out of the cell. This sets up an electrochemical gradient and results in a resting membrane potential.

Depolarisation and Action Potentials

And what triggers depolarisation of this cell, this nerve cell, for example?

So, depolarisation of nerve cells is often thought of as an all or nothing response. It begins by reactions typically on the postsynaptic membrane of a neuron. So a preceding neuronal cell under the influence of various factors can release neurotransmitters into the synaptic cleft between neurons, and when they do this, they cause downstream effects at the postsynaptic membrane in the subsequent cell within the chain.

Typically these reactions lead to the rapid influx of sodium in response to binding of neurotransmitter to a receptor on the postsynaptic membrane and efflux of potassium. There’s also important calcium release intracellularly, normally stored mainly in sarcoplasmic reticulum, but this mechanism varies a little bit from cell type to cell type.

How is it conducted down the nerve?

So action potentials are conducted down a nerve via saltatory conduction and do so with rapid propagation of voltage-dependent opening of sodium channels and a rapid change in the resting membrane potential, which jumps between so-called nodes of Ranvier in myelinated cells. And in demyelinated cells, there is slightly slower conduction down the length of the neuron, but still via voltage-dependent sodium channels.

And can a nerve that’s been depolarised immediately depolarise again?

No, so after depolarisation of all cells that depolarise, there is an absolute refractory period and a relative refractory period. During the absolute refractory period it’s impossible for a cell to depolarise again, no matter how strong the stimulus from the postsynaptic membrane that normally starts conduction and depolarisation. In the relative refractory period, you can produce further conduction, but you need a supranormal stimulus in order to do so.

Peripheral Nerve Fibre Classification

You mentioned there that some nerve fibres are myelinated and some are not. Could you just classify those peripheral nerve fibres for me?

So we could name some of them via the parts of the nervous system they affect. So autonomic nerves are unmyelinated, which means they have slower conduction but are particularly susceptible to uptake of local anaesthetics, for instance, hence early effects on the sympathetic nervous system during spinal and epidural anaesthesia.

We have motor nerve fibres which are myelinated in order to facilitate rapid conduction and coordinated contraction of muscles. The same applies to primary and secondary neurons within spinal reflex pathways. They are also myelinated.

Then we have sensory fibres travelling through the spinothalamic tracts to the brain. So there are different types of nerve fibre such as C fibres and A-delta fibres. C fibres typically are unmyelinated. That’s as much as I can remember now.

And actually, as we have it, that’s your five minutes on that topic area.

pH and Acid-Base Balance

13:30-20:00

Summary: Tom explains pH, buffering systems, and the maintenance of acid-base homeostasis.

And this is your last five minutes because I’ve now organised it, Tom. And it’s one of your favourite topics as I understand it. Can you define pH?

pH is the negative log to the base ten of the hydrogen ion concentration in an aqueous solution.

And what is the relationship between hydrogen ions and pH?

So the relationship is defined by the equation I’ve just described. But the pH scale itself really is just a way of expressing hydrogen ion concentration. The relationship between specific chemicals and the resultant hydrogen ion concentration can be described by the acid dissociation constant.

So acid dissociation constant is the concentration of hydrogen ions times the conjugate base concentration divided by the conjugate acid concentration, and the negative logarithm of this is known as the pKa.

Well, talk me through the Henderson-Hasselbalch equation.

The Henderson-Hasselbalch equation relates the acid dissociation constant with the concentration of conjugate acid and conjugate base. So the pH is equal to the pKa plus the log to the base ten of the concentration of conjugate base over the concentration of conjugate acid.

Acid-Base Balance Homeostasis

How is normal acid-base balance maintained in a human?

So, acid-base balance can be divided into rapid, intermediate and delayed homeostatic responses.

Rapid responses are buffer action and respiratory action. So when hydrogen ion concentration increases in the plasma, buffer systems immediately act to stabilise the pH of solution. So a buffer is a weak acid that moves towards – well, it’s in equilibrium between its conjugate acid and conjugate base, and by Le Chatelier’s principle, it acts to oppose any change made within the system that it’s sitting in. Good examples would be histidine residues in haemoglobin, which absorb hydrogen ions when they’re produced during CO₂ transport.

But you also mentioned respiratory compensation. What’s that?

Respiratory compensation really involves the body’s response to PCO₂. So as PCO₂ increases, pH decreases, and in order to achieve homeostasis, the respiratory centres in the brain respond to increased PCO₂ by increasing respiratory rate and tidal volume, thus reducing the PCO₂ and increasing the pH.

The delayed responses that I’m talking about involve primarily renal handling of acid and bases. So in the proximal convoluted tubule in response to reduction in pH, bicarbonate is reabsorbed and in the distal collecting ducts H⁺ ions are secreted in response to a decrease in pH.

All of this together aims to keep tight control on physiological pH, which is important for the action of lots of enzymes which are biologically essential.

Anion Gap and MUDPILES

So what is the anion gap?

Anion gap is defined as sodium concentration in plasma plus the potassium concentration in plasma minus the chloride concentration plus the bicarbonate concentration. It’s a theoretical construct designed to help us understand acidosis and its causes. The theory itself doesn’t give an explanation of mechanism, but it does help us divide up aetiologies. So MUDPILES is the typical…

And that is your five minutes there, Tom. But you’ve got thirty seconds to tell me what MUDPILES is, just for the listeners.

So MUDPILES tells you causes of raised anion gap metabolic acidosis, so that includes methanol, uremia, DKA, paracetamol, isoniazid, lactic acidosis, ethylene glycol, salicylates. Yeah, I didn’t do that in order ’cause I’m in a hurry, but multiple causes of raised anion gap acidosis.

Host’s Comprehensive Review and Clinical Teaching

20:00-25:00

Summary: James provides detailed corrections and additional clinical information.

So we’re just all on the same page here, listeners. The acronym we really should be learning is CAT MUDPILES. And the full differential for high anion gap metabolic acidosis is:

C – Carbon monoxide plus cyanide plus congestive heart failure
A – Aminoglycosides like gentamicin
T – Theophylline or toluene if you’ve been sniffing plenty of glue
M – Methanol
U – Uraemia
D – DKA or ketoacidoses, because starvation and boozing also causes ketoacidosis
P – Paracetamol, paraldehyde
I – Iron overdose, isoniazid and inborn errors of metabolism
L – Lactic acidosis
E – Ethanol and ethylene glycol
S – Salicylates, i.e. aspirin overdose

If you can reel all that out at the examiner, they’ll probably be blown to smithereens.

So non-anion gap acidosis means that there’s a problem with bicarbonate – inappropriate bicarbonate secretion, essentially. So renal tubular acidosis or a lack of hydrogen ion secretion. So renal tubular acidosis – more than one type, so it can be inappropriate secretion of bicarbonate or inappropriate secretion of hydrogen ions, but also inappropriate retention of hydrogen ions or inappropriate loss of bicarbonate would cause the acidosis.

What about if I just drank an inordinately large amount of vinegar?

Oh God, you’d have to drink a lot. Well, it’s a weak acid, isn’t it? So wouldn’t it just help with your buffering? I don’t know. I once drank a pint for a bet. It wasn’t very nice. I got a terrible heartburn.

No, it definitely can cause profound acidosis. I know that in Bristol someone was admitted after drinking pints and pints of cider vinegar as a home remedy, and they’d given themselves like a pH of about 7.0. They felt quite ropey.

Post-Viva Discussion and Exam Technique

25:00-30:00

Summary: Discussion of performance feedback and exam strategies.

That is your physiology viva over there, Tom. Nice and brisk. I quite like the “what’s it” – you say immediate, something, delayed effects. What’s the middle one?

Immediate, intermediate, and delayed effects. It was a tip given by a consultant at work and I like it as an approach sometimes, but sometimes whilst I’m saying it, I think, “oh god, I’m not sure if I can actually carve it up that way.” Anyway.

Yeah, it makes it sound slick, but that’s half the battle.

Any thoughts, any questions?

No, I think I’m just being a bit wordy, need to make it a bit snappier, but getting there.

Yeah, still a bit – you’ve just got to go for the jugular and like if you’re going to say the buzzword, get it in. Just say it. Just get it in there. I think with the buffering, I’d be tempted to, because you kind of fudged it – it felt like you were saying that there was extracellular and intracellular buffers and breathing were like both quite rapid. When I’d sort of framed that those intra- and extracellular buffers, you know, the phosphates and the proteins and the haemoglobin, as you say, are like instant, almost instantaneous. And then you’ve got the respiratory effects, then you’ve got your renal effect.

Yeah, I should have put respiratory in the middle. I think I planned on doing that and then I don’t know why I changed my mind.

I would have thought so. You could just say in order of the time it takes for them to activate: your extracellular buffers and your intracellular buffers work very quickly. And then your respiratory system tries to compensate. And then your kidneys eventually catch up – this can take days as a timeline.

Well, thank you very much, Tom. That was your physiology viva. I didn’t hear a single drop of sweat land on your glasses.

Yeah, well, I did a tour in Afghanistan, and ever since I’ve been entirely incapable of sweating.

Host’s Final Teaching Points and Episode Wrap-up

30:00-32:00

Summary: James provides final exam technique advice and episode conclusion.

Well, thank you everyone for listening to what is the 16th VivaCast episode that we put together. Everyone will be happy to know that Tom did in fact pass his viva, which gives you a reasonable reflection of what they’re expecting in the standards they’re after.

It’s always important to have some structure. I think the immediate, intermediate, and delayed effects, you can probably shoehorn into most things. Have a few things you can fall back on as structures like pre-intra-post-operative. Have a few buzz phrases to open up questions to give you a chance to think, and sometimes very briefly repeating the question back to the examiner gives you time to process in your brain, which lets you start talking.

You can then open up with a phrase and then say, “and I like to structure this in…” Bang, bang, bang. Get your three fingers up for your three points. Go through each point. Move on. Everyone has a different style. You need to find your own and practice, practice, practice.

Hopefully, Tom’s going to come back and do a little bit more viva action. But if you are preparing for the viva and you want to get on this show, be put through your paces, get some direct feedback, and obviously fame, then please email me, direct message me on Blue Sky, message me on Facebook, send a carrier pigeon – less likely to work – or leave a comment on the show.

And in the meantime, buckle up for the next episode of Gas, Gas, Gas. We’re going to return to some core science stuff. The final element of the pharmacokinetics of propofol sort of series, we’re going to talk TIVA and we’re going to have a dive into the various TIVA models, the differences, the pitfalls, and the things you should know.

Cheerio, and see you next time!

Closing

32:00-32:30

Thanks for listening to the episode guys. If you found it useful or awful, please like and subscribe and rate the show. Definitely, go check out the show notes on gasgasgas.uk. We all know that this is a bucket of content. I want you to take some time for yourself and don’t overcook it. Don’t freak out, keep studying.

PhysiologyVivacast Articles

VivaCast 16 – 1 Litre Blood Loss, Nerve conduction and pH

Article Spring Board

What are the physiological effects of a 1-liter hemorrhage?