How to use physiology viva questions
A physiology viva tests whether you can explain a process aloud, not just recognise the correct sentence in a textbook. A strong answer normally does four things:
- defines the process or variable;
- gives the mechanism in a logical sequence;
- applies it to the finding, graph or patient described;
- states a limitation, control mechanism or clinical implication where relevant.
The common failure is not always a lack of knowledge. Candidates often begin with an isolated fact, omit the causal link, or continue speaking after they have answered the question. Oral practice should therefore train both recall and answer structure.
For each question, take a short pause, state your framework, then work from cause to effect. If you do not know a detail, identify what you do know and explain how you would reason towards it. Do not invent a value or claim that a variable is regulated when it is merely correlated with another variable.
This article uses three complete stations: resting membrane potential, acid–base interpretation and cardiovascular responses to exercise. They cover the kinds of explanation that recur across physiology viva questions without assuming a particular university or professional examination format.
Set a usable answer frame
Before practising, use the following frame:
- Define: What is being measured or explained?
- State the baseline: What is the normal direction, range or relationship, if you know it?
- Explain the mechanism: Name the channels, receptors, pressures, hormones or equations involved.
- Apply it: Link the mechanism to the result in the station.
- Qualify it: Give one important exception, limitation or compensatory response.
A viva answer should sound like reasoning rather than a memorised paragraph. Say the main conclusion first, then justify it. For example: the resting membrane potential is mainly determined by potassium permeability; the reason is that resting potassium conductance is much greater than sodium conductance, so the membrane potential lies closer to the potassium equilibrium potential than to the sodium equilibrium potential.
Build stations from your own material
Start with lecture outcomes, practical data, diagrams and tutorial questions. Convert each topic into an opening question, two probing questions and one interpretation task. A station should make you explain a relationship, not recite a heading.
A useful station set covers several levels:
- a definition, such as clearance or compliance;
- a mechanism, such as excitation–contraction coupling;
- a calculation or graph, such as interpreting a pressure–volume loop;
- an application, such as the response to haemorrhage or exercise;
- a limitation, such as why a measured value may not represent a steady state.
A station table helps you rehearse the opening move before you record yourself. The examples below are written as practice stations, not as claims about the format or marking scheme of a particular examination.
A physiology viva station table can be organised like this:
The aim is not to memorise a single polished script. Use the station to practise changing direction when a follow-up question exposes a missing link. Record one attempt, listen once for scientific accuracy and once for communication, then repeat the same station after correcting only the weakest part.
Here is a set of five stations that can be used across several study sessions.
Station 1: Resting membrane potential
Opening answer
Start with the conclusion: the resting membrane potential is closer to the potassium equilibrium potential because the resting membrane is much more permeable to potassium than to sodium. Potassium tends to diffuse out of the cell down its concentration gradient, leaving the inside relatively negative. The sodium–potassium pump maintains the sodium and potassium gradients by moving three sodium ions out and two potassium ions in per ATP hydrolysed, but the pump is not the main immediate source of the voltage.
A strong answer distinguishes permeability from concentration gradient. The Nernst equation gives the equilibrium potential for one ion at a specified concentration ratio. The Goldman–Hodgkin–Katz equation considers several ions and their relative permeabilities. Because potassium permeability dominates at rest, the actual membrane potential is near, but not identical to, the potassium equilibrium potential. A small resting sodium permeability makes it less negative than the potassium equilibrium potential.
If asked what happens when potassium concentration outside the cell rises, explain the direction carefully. The potassium concentration gradient becomes smaller, so the potassium equilibrium potential becomes less negative. The resting membrane potential therefore tends to depolarise. Severe changes can alter excitability and conduction because voltage-gated sodium channels depend on membrane voltage and may become inactivated during sustained depolarisation.
What the examiner is listening for
Keep the causal chain visible: relative permeability, potassium movement, charge separation and the role of the pump. Do not say that the pump directly creates the entire resting potential. It contributes a small electrogenic effect and, more importantly, preserves the gradients that make the membrane potential possible.
A complete response to the station could sound like this:
Examiner
Why is the resting membrane potential of a typical neurone closer to the potassium equilibrium potential than to the sodium equilibrium potential?
The answer linked high resting potassium permeability to potassium efflux and a negative intracellular voltage.
ImproveState explicitly that the Goldman–Hodgkin–Katz relationship includes relative permeability, not concentration alone.
The distinction between Nernst and Goldman–Hodgkin–Katz was present, but the effect of increased extracellular potassium was not fully developed.
ImproveExplain that reducing the potassium gradient shifts the potassium equilibrium potential in a less negative direction.
The main conclusion came first and the sodium–potassium pump was correctly described as maintaining gradients.
ImproveAdd that the pump has a small direct electrogenic contribution but is not the main immediate voltage source.
A strong answerThe resting membrane potential is closer to the potassium equilibrium potential because resting potassium permeability is much greater than resting sodium permeability. Potassium diffuses out of the cell down its concentration gradient, leaving the cell interior negative, while the small sodium leak shifts the voltage away from the potassium equilibrium potential. The Goldman–Hodgkin–Katz equation accounts for both concentration gradients and relative permeabilities. The sodium–potassium pump maintains the gradients by moving three sodium ions out and two potassium ions in, with only a small direct electrogenic effect.
That is a MySummaries station, filled with physiology material. Yours is written from your own notes. Start free
The key repair is precise wording. If you say the pump creates the resting potential, the listener cannot tell whether you understand the difference between maintaining gradients and producing the immediate voltage. Practise saying that distinction in one sentence.
Station 2: Metabolic acidosis
Opening answer
For an acid–base station, identify the pH direction first, then decide whether the primary change is respiratory or metabolic. In the example station, the pH is 7.25, so the blood is acidemic. The bicarbonate is low at 15 mmol/L, indicating a primary metabolic acidosis. The carbon dioxide tension is also low, which is consistent with respiratory compensation through increased alveolar ventilation.
Do not call the low carbon dioxide the cause simply because it is abnormal. The low bicarbonate is the primary abnormality in this pattern. The lungs respond relatively quickly by reducing carbon dioxide, while renal compensation for a respiratory disturbance would take longer. You should still check whether the compensation is appropriate rather than assuming that any second abnormality is compensation.
An examiner may ask how you would investigate the cause. Keep the answer physiological before becoming clinical: assess lactate and perfusion if lactic acidosis is possible, review renal function, consider gastrointestinal bicarbonate loss, check ketones where clinically relevant, and calculate the anion gap if sodium and chloride are available. The formula commonly used is sodium minus chloride minus bicarbonate. Interpret it with the laboratory’s reference range and the clinical context.
A good oral answer distinguishes compensation from correction. Compensation reduces the change in pH but does not remove the original metabolic problem. If ventilation cannot increase, the carbon dioxide may remain high and the acidemia may become more severe.
The station can be marked for whether the candidate explains the numbers, rather than merely labelling the disorder:
Examiner
A patient has a pH of 7.25, bicarbonate of 15 mmol/L and a low carbon dioxide tension. Explain the disturbance and the compensation.
The response correctly identified a primary fall in bicarbonate and linked the low carbon dioxide to increased ventilation.
ImproveExplain that increased alveolar ventilation removes carbon dioxide and reduces carbonic acid, partially limiting the fall in pH.
The pH and bicarbonate were interpreted correctly, but compensation was accepted without checking its appropriateness.
ImproveSay that expected compensation should be assessed using the relevant clinical rule and that an additional respiratory disorder may coexist.
The diagnosis was clear but the answer moved quickly into causes without explaining the physiological sequence first.
ImproveUse the order pH, primary variable, compensatory variable, then likely causes and further tests.
A strong answerThis is an acidemia because the pH is 7.25. The low bicarbonate identifies a primary metabolic acidosis. The low carbon dioxide is a compensatory respiratory response: increased alveolar ventilation removes carbon dioxide, reducing carbonic acid and limiting the fall in pH. I would check whether the degree of carbon dioxide reduction is appropriate, because an additional respiratory disorder may be present. I would then investigate the cause, including lactate, renal function, ketones and gastrointestinal bicarbonate loss, and calculate the anion gap if the required electrolytes are available.
When practising acid–base physiology, always say which abnormality is primary. That single habit prevents many answers from becoming a list of laboratory values without interpretation.
Station 3: Cardiovascular responses to exercise
Opening answer
Dynamic exercise increases the metabolic demand of active skeletal muscle. The central response is an increase in cardiac output, which equals heart rate multiplied by stroke volume. Heart rate rises through withdrawal of parasympathetic activity followed by increased sympathetic activity. Stroke volume rises through increased venous return, increased contractility and reduced end-systolic volume.
Venous return is supported by the skeletal muscle pump, the respiratory pump and sympathetic venoconstriction. Increased venous return raises end-diastolic volume, so the Frank–Starling mechanism contributes to the increase in stroke volume. Sympathetic stimulation also increases myocardial contractility through beta-1 adrenergic receptors and increases conduction through the atrioventricular node.
Blood flow is redistributed. Arterioles in active skeletal muscle dilate in response to local metabolic factors, while sympathetic vasoconstriction limits flow to some less immediately active vascular beds. The total systemic vascular resistance may fall even though cardiac output rises, because the resistance change in the exercising muscle beds is substantial. Mean arterial pressure is maintained or rises modestly because cardiac output increases and the fall in systemic vascular resistance is not complete.
Avoid saying that sympathetic stimulation constricts every vessel during exercise. Local metabolic vasodilation in active muscle modifies the sympathetic response. Also distinguish dynamic exercise from sustained isometric contraction, where the haemodynamic response can differ because muscle compression affects vascular resistance and venous return.
The full practice attempt below shows how a candidate can earn most of the available platform marks while still needing to qualify the blood-pressure response.
Examiner
Explain how cardiac output changes during dynamic exercise and how the body achieves that change.
The answer correctly connected autonomic changes, venous return, contractility and cardiac output.
ImproveMake the equation cardiac output equals heart rate multiplied by stroke volume the organising statement rather than adding it halfway through.
The candidate explained local muscle vasodilation and the fall in systemic vascular resistance accurately.
ImproveState that mean arterial pressure is usually maintained or rises modestly, rather than implying a fixed response at every workload.
The main response was well ordered and included the skeletal muscle pump and Frank–Starling mechanism.
ImproveBriefly distinguish dynamic exercise from isometric exercise if asked about generalisation.
A strong answerDuring dynamic exercise, cardiac output increases because it equals heart rate multiplied by stroke volume. Heart rate rises first through vagal withdrawal and then sympathetic beta-1 stimulation. Stroke volume increases because venous return raises end-diastolic volume through the skeletal muscle and respiratory pumps, while sympathetic stimulation increases contractility and reduces end-systolic volume. Active skeletal muscle arterioles dilate because of local metabolites, so systemic vascular resistance can fall even as cardiac output rises. Mean arterial pressure is therefore maintained or may rise modestly, depending on exercise intensity and the balance between cardiac output and resistance.
Review the spoken answer, not only the score
After each recording, listen for five specific problems:
- Did you answer the exact opening question before giving background?
- Did every named mechanism lead to a physiological consequence?
- Did you distinguish cause, response and association?
- Did you define an equation’s variables before using it?
- Did you stop after the conclusion, or continue into unrelated facts?
A transcript makes vague self-criticism more useful. Mark the phrase that was too brief and the phrase where the mechanism disappeared. For example, saying refer for further assessment is not an explanation when the station asks how ventilation changes carbon dioxide. Replace it with the physiological action and its consequence.
The patient compensates by breathing more, so the carbon dioxide falls. This corrects the acidosis. The kidneys may also help later by retaining bicarbonate and excreting acid. I would then investigate the underlying cause.
This corrects the acidosis.
The statement does not explain that respiratory compensation reduces carbonic acid and only partially limits the pH change; it also treats later renal handling as an immediate response without specifying the time course.
Say: Say: Increased alveolar ventilation removes carbon dioxide, reducing carbonic acid and partially limiting the fall in pH. Renal generation and retention of bicarbonate is a slower response and does not identify the original cause.Use the replacement sentence in your next attempt, then remove it from your notes. The goal is retrieval under pressure, not dependence on a script.
A short debrief routine
Immediately after a station, record three lines:
- The mechanism I explained accurately.
- The mark I probably lost.
- The one sentence I will add next time.
Do not rewrite the entire answer. If the problem was that you named the Frank–Starling mechanism without explaining preload, repair that link. If the problem was poor prioritisation, rehearse the first two sentences only. Return to the station after a delay and test whether the correction has become available without prompting.
For difficult topics, create a short audio explanation after you have corrected the answer. Listen while walking or travelling, but do not treat passive listening as a substitute for speaking. The useful test is whether you can pause the recording and continue the explanation yourself.
How MySummaries helps
MySummaries can turn your physiology notes, practical data and lecture slides into a revision board, then use that board to create oral stations. You can record an answer, receive feedback against the platform’s physiology practice criteria, review the marked wording, and return to the weak mechanism rather than repeating the whole topic. Its spaced-repetition cards can preserve equations, definitions and thresholds while the oral practice tests whether you can use them in sequence.
You can start with your own material at portal.mysummaries.app.