The ACEM Primary assesses foundational sciences and their application to emergency medicine. Its assessment typically includes written components and structured oral or viva-style assessment; check the official ACEM website for current examination details. The questions below practise core concepts, not an official paper. For each one, choose the best answer in the question panel, then use the explanation and discussion that follow to check your reasoning.
In MySummaries, a question set can be built from the candidate’s own revision board. Here is a practice set spanning mechanisms, data interpretation and clinical application.
1. Acute respiratory compensation
This tests whether you can distinguish the expected immediate renal response from compensation after a longer period of raised carbon dioxide.
A patient has an acute rise in PaCO₂ from 40 to 60 mmHg. If the primary disturbance is acute respiratory acidosis, what approximate change in plasma HCO₃⁻ is expected from compensation?
In acute respiratory acidosis, buffering raises HCO₃⁻ by approximately 1 mmol/L per 10 mmHg increase in PaCO₂. Renal compensation takes longer; in chronic respiratory acidosis the rise is approximately 3–4 mmol/L per 10 mmHg.
The strongest distractor is the 3–4 mmol/L figure: it describes the approximate chronic renal response, not the immediate response. State whether a disturbance is acute or chronic before applying a compensation rule.
2. The oxyhaemoglobin dissociation curve
This tests how changes in tissue conditions affect haemoglobin’s oxygen affinity and unloading.
Which change shifts the oxyhaemoglobin dissociation curve to the right and promotes oxygen unloading in tissues?
An increased hydrogen ion concentration (lower pH) shifts the curve to the right through the Bohr effect, reducing haemoglobin’s oxygen affinity and promoting unloading. Increased PaCO₂, temperature and 2,3-BPG also shift it right.
Reduced PaCO₂ is a tempting alternative, but it tends to shift the curve left. In an answer, connect the shift to its consequence: rightward shift means lower affinity and easier oxygen release at a given tissue PO₂.
3. Local anaesthetic action
This tests the ion channel mechanism behind local anaesthesia and why nerve conduction fails.
What is the primary mechanism by which local anaesthetics prevent action potential propagation in peripheral nerves?
Local anaesthetics block voltage-gated sodium channels, reducing the inward sodium current required for the action potential upstroke and propagation. Presynaptic calcium-channel blockade is not their primary mechanism in peripheral nerve conduction.
The key distinction is between preventing the nerve action potential and blocking neurotransmitter release at a synapse. A concise answer should name the channel, the affected ion current and the effect on propagation.
4. Ventricular action potential
This tests identification of the current responsible for rapid depolarisation in working ventricular myocytes.
Which ion current is chiefly responsible for phase 0, the rapid upstroke of the action potential in a working ventricular myocyte?
Phase 0 in a working ventricular myocyte is the rapid opening of fast voltage-gated sodium channels and inward sodium current. L-type calcium current contributes to the plateau phase; nodal tissue has a different phase 0 mechanism.
The L-type calcium option is the strongest distractor because calcium is central to the ventricular plateau. Keep the cell type in view: the rapid upstroke in nodal cells is calcium-mediated, unlike that in working ventricular muscle.
5. Aldosterone and potassium
This tests the renal mechanism linking a hormone to potassium handling.
In the cortical collecting duct, what is the main effect of aldosterone on potassium handling by principal cells?
Aldosterone increases ENaC activity and basolateral Na⁺/K⁺-ATPase activity in principal cells. The resulting sodium reabsorption and electrochemical conditions favour potassium secretion into the tubular lumen.
The thick ascending limb is involved in potassium transport, but it is not the principal-cell site being tested here. Explain the sequence: aldosterone increases sodium reabsorption, making the lumen relatively negative and favouring potassium secretion.
6. Competitive antagonism
This tests the effect of a reversible competitive antagonist on an agonist concentration–response curve.
What is the usual effect of a reversible competitive antagonist on an agonist concentration–response curve, assuming sufficient agonist concentrations can be tested?
A reversible competitive antagonist competes at the same receptor site and can be overcome by increasing agonist concentration. The curve shifts right, indicating reduced potency, while the maximal response is preserved.
A reduced maximum is more characteristic of insurmountable antagonism or non-competitive effects. In a viva, define the interaction, then state what happens to potency and maximal efficacy.
7. Anion gap interpretation
This tests calculation with stated units and recognition of a raised anion gap metabolic acidosis.
A blood test shows Na⁺ 140 mmol/L, Cl⁻ 104 mmol/L and HCO₃⁻ 16 mmol/L. Using anion gap = Na⁺ − (Cl⁻ + HCO₃⁻), what is the anion gap, and what does it indicate?
The calculation is 140 − (104 + 16) = 20 mmol/L. This is a raised anion gap by commonly used reference ranges and, with low bicarbonate, supports a high-anion-gap metabolic acidosis. Interpret against the local laboratory range and clinical context.
The 36 option omits bicarbonate from the subtraction; 260 adds rather than subtracts. Show the arithmetic and units, then relate the result to the acid–base pattern rather than treating the number in isolation.
8. Arterial oxygen content
This tests calculation of oxygen content and the importance of haemoglobin concentration.
Estimate arterial oxygen content using CaO₂ = (1.34 × Hb × SaO₂) + (0.003 × PaO₂). Hb is 100 g/L, SaO₂ is 0.98 and PaO₂ is 100 mmHg. Use Hb in g/dL.
Convert Hb to 10 g/dL. Bound oxygen is 1.34 × 10 × 0.98 = 13.13 mL/dL; dissolved oxygen is 0.003 × 100 = 0.3 mL/dL. Total is approximately 13.4 mL O₂/dL.
The 20 mL/dL distractor assumes a higher haemoglobin concentration. The calculation also shows why a normal PaO₂ does not guarantee normal oxygen content: most oxygen is carried bound to haemoglobin.
9. Mean arterial pressure and systemic vascular resistance
This tests the relationship between cardiac output, vascular resistance and pressure.
If cardiac output remains constant and systemic vascular resistance falls substantially, what is the expected direction of change in mean arterial pressure?
Mean arterial pressure is approximately cardiac output multiplied by systemic vascular resistance, with central venous pressure usually small enough to be omitted in a simplified relationship. If cardiac output is constant and resistance falls, mean arterial pressure falls.
The relationship is approximate, but useful for explaining haemodynamic changes. Avoid saying that pressure depends on heart rate alone: cardiac output also depends on stroke volume, and vascular resistance matters.
10. Cerebral perfusion pressure
This tests a straightforward calculation and its physiological meaning.
A patient has a mean arterial pressure of 80 mmHg and an intracranial pressure of 25 mmHg. Using CPP = MAP − ICP, what is the cerebral perfusion pressure?
CPP = MAP − ICP = 80 − 25 = 55 mmHg. The calculation illustrates that raised intracranial pressure reduces the pressure gradient available to perfuse the brain.
The 105 option adds the pressures rather than calculating the gradient. In an acute-care answer, give the equation, substitute the values and then state the clinical implication: either reduced MAP or increased ICP lowers CPP.
A short-answer mark-up
The written components typically assess explanation and application as well as recall. Practise presenting the mechanism in a logical order: identify the primary disturbance, give the expected response, and interpret the numbers. This marked example shows how one incomplete detail can cost a mark.
A patient’s PaCO₂ rises acutely from 40 to 60 mmHg. Explain the expected change in HCO₃⁻ and contrast it with chronic respiratory acidosis.
3/4In acute respiratory acidosis, HCO₃⁻ rises by about 1 mmol/L for each 10 mmHg increase in PaCO₂ due to buffering. In chronic respiratory acidosis it rises more because the kidneys retain bicarbonate.
The acute rule and the renal mechanism are correct. The chronic comparison is directionally right but needs the approximate expected magnitude to make the contrast precise.
Missed
−State the chronic compensation rule: HCO₃⁻ rises approximately 3–4 mmol/L per 10 mmHg increase in PaCO₂.
Model answerThe primary disturbance is respiratory acidosis because PaCO₂ has risen. In an acute rise, HCO₃⁻ increases by approximately 1 mmol/L per 10 mmHg PaCO₂ rise, mainly through buffering. With chronic respiratory acidosis, renal compensation increases HCO₃⁻ by approximately 3–4 mmol/L per 10 mmHg. These are approximate rules; interpret the measured values in clinical context.
That is a MySummaries paper, filled with ACEM Primary material. Yours is written from your own notes. Start free
This is a platform-style feedback example, not an official ACEM marking scheme. The missed point is specific: the candidate named renal compensation but did not quantify the chronic response.
Choose the next revision target
After a practice set, group errors by the underlying skill: mechanism, calculation, units or clinical interpretation. Revisit errors caused by a missing concept differently from those caused by rushed arithmetic. A board could rank repeated weak areas like this:
Turn a repeated error into a precise retrieval prompt, rather than rereading an entire topic. For example, a question about acute versus chronic compensation should require the candidate to recall both approximate rules and explain why they differ.
You lost this mark twice: in chronic respiratory acidosis, approximately how much does HCO₃⁻ rise for each 10 mmHg increase in PaCO₂, and why is the acute rise smaller?
How MySummaries helps
MySummaries turns your own notes into a revision board, then uses that material to generate practice questions, marked written answers and flashcards for repeated weak points. Build a board from your ACEM Primary resources at portal.mysummaries.app.