Undifferentiated Chest Pain — Written Clinical Reasoning

SAQ 1 — Integrated Diagnostic and Management Approach to the Acute STEMI Patient (20 marks, 30 minutes)

Prompt: Outline your integrated diagnostic and management approach to Mrs O'Sullivan's presentation, addressing: (a) the diagnostic interpretation of the ECG and the troponin, and the immediate catheter-lab activation; (b) the assessment for right ventricular involvement and the blood-pressure differential; (c) the antiplatelet and anticoagulant therapy; (d) the pain and sympathetic-drive control and the assessment for complications; (e) the diabetes management during the ACS; and (f) the secondary prevention plan and the common exam trap. [1]

Model Answer

(a) Diagnostic interpretation and catheter-lab activation (4 marks): [1]

Mrs O'Sullivan has an acute inferior ST-elevation myocardial infarction. The ECG shows ST elevation of 2 mm in the inferior leads (II, III, aVF) with reciprocal ST depression in I and aVL — the diagnostic pattern of an inferior STEMI from right coronary artery occlusion. The troponin of 45 ng per L is elevated above the 99th percentile, confirming myocardial injury. The pain is classic central crushing cardiac pain radiating to the arm and jaw with autonomic features. The diagnosis is an acute STEMI, and the immediate priority is to activate the catheter lab for primary percutaneous coronary intervention — the gold standard for STEMI if it can be delivered within the recommended door-to-balloon timeframe of 90 minutes [2]. If PCI is not available within the required timeframe, fibrinolysis (tenecteplase as a single weight-adjusted intravenous bolus) is the alternative, followed by transfer to a PCI-capable centre.

(b) Right ventricular involvement and the blood-pressure differential (3 marks): [1]

The inferior STEMI may involve the right ventricle in up to 40 per cent of cases. I will perform a right-sided ECG (V4R) — if ST elevation is present in V4R, the right ventricle is involved and the patient is preload-sensitive. This changes the fluid management: nitrates and diuretics may cause hypotension in the right-ventricular-infarct patient, and a careful fluid challenge (250 mL of normal saline) may be needed for hypotension. The blood-pressure differential of 14 mmHg between the arms (152/94 right, 138/90 left) is below the 20 mmHg threshold that raises the concern for aortic dissection, and the clinical picture (crushing cardiac pain, inferior STEMI, cardiac risk factors) is overwhelmingly consistent with ACS. I document the differential, and I am aware that dissection can compromise the right coronary artery giving an inferior MI pattern — but the coronary angiogram will definitively exclude this [6].

(c) Antiplatelet and anticoagulant therapy (4 marks): [1]

The 2023 ESC ACS Guidelines frame the antithrombotic therapy [2]:

• Aspirin 300 mg loading dose then 100 mg daily, lifelong.
• P2Y12 inhibitor — ticagrelor 180 mg loading then 90 mg twice daily, or prasugrel 60 mg loading then 10 mg daily (preferred over clopidogrel in the primary PCI setting unless contraindicated), or clopidogrel 300 to 600 mg loading then 75 mg daily if ticagrelor and prasugrel are contraindicated.
• Anticoagulation during the PCI — unfractionated heparin (100 units per kg) or bivalirudin, per the local protocol. [1]

Dual antiplatelet therapy is continued for 12 months after the primary PCI, then the patient transitions to lifelong single antiplatelet therapy (aspirin or a P2Y12 inhibitor, guided by the bleeding risk and the ischaemic risk). [1]

(d) Pain and sympathetic-drive control and the assessment for complications (3 marks): [1]

The pain and the sympathetic drive are controlled with morphine 2.5 to 5 mg intravenously (with an antiemetic such as metoclopramide 10 mg) and sublingual glyceryl trinitrate (unless hypotensive or the right ventricle is involved). The oxygen is given only if the SpO2 is below 90 per cent — routine high-flow oxygen in the non-hypoxaemic ACS patient is no longer recommended because it may increase infarct size. The complications I assess for are: heart failure (the Killip classification), arrhythmia (the inferior MI may cause bradycardia and heart block from vagal stimulation or AV nodal ischaemia), pericarditis, ventricular septal rupture, papillary muscle dysfunction (mitral regurgitation), and right ventricular infarction. [1]

(e) Diabetes management during the ACS (3 marks): [1]

I hold the metformin for the angiogram because of the risk of contrast-induced nephropathy and lactic acidosis, and I manage the hyperglycaemia with an insulin sliding scale if the glucose is above 10 mmol per L. The target during the acute ACS is a glucose of 6 to 10 mmol per L — the tight control showed a mortality benefit in the DIGAMI trial, but the hypoglycaemia risk must be managed. Once the acute phase resolves and the renal function is confirmed, I restart the metformin and optimise the oral therapy. I also ensure that an SGLT2 inhibitor is considered for the cardiorenal protection, in line with the current guidelines. [1]

(f) Secondary prevention plan and the common exam trap (3 marks): [1]

The secondary prevention is the four pillars: [1]

1. Antiplatelet therapy — dual for 12 months, then lifelong single.
2. Lipid-lowering — atorvastatin 80 mg daily, target LDL below 1.4 mmol per L.
3. Neurohormonal modulation — ACE inhibitor (or ARB) and a beta-blocker, titrated to the maximum tolerated dose.
4. Lifestyle — smoking cessation reinforcement, cardiac rehabilitation, Mediterranean diet, regular exercise. [1]

I arrange the echocardiogram to assess the ejection fraction and the wall-motion abnormality, and the cardiology follow-up at six weeks. [1]

The common exam trap in this patient is the anchoring error — stopping at the STEMI and missing the coexisting conditions or the complications. The registrar who activates the catheter lab and treats the STEMI but does not assess for right ventricular involvement, does not manage the diabetes, and does not plan the secondary prevention has provided incomplete care. The second trap is the blood-pressure differential — the registrar who ignores the 14 mmHg differential has omitted a mandatory part of the examination, and the registrar who over-interprets it as dissection has misclassified the patient. The integrated approach — the catheter-lab activation, the antithrombotic therapy, the right-ventricular assessment, the complication surveillance, the diabetes management, and the secondary prevention — is what keeps the STEMI patient safe. [1]

SAQ 2 — The Diagnostic Pathway for Pulmonary Embolism and the Role of Clinical Prediction Rules in Chest Pain (10 marks)

Prompt: A junior doctor asks you to explain: (a) the two-level Wells score and how it stratifies the pre-test probability of pulmonary embolism in a chest pain patient; (b) how the Wells score integrates with the D-dimer and CT pulmonary angiography in the validated diagnostic algorithm, with reference to the Christopher study; and (c) the synthesis of the evidence that you would give a colleague considering the overuse of CTPA in low-risk patients. [1]

Model Answer

(a) The two-level Wells score (3 marks): [1]

The two-level Wells score is a clinical prediction rule that stratifies the pre-test probability of pulmonary embolism into PE unlikely (score 4 or less) and PE likely (score more than 4) [7]. The components and weights are: clinical signs of DVT (leg swelling and pain with palpation of the deep veins) 3; PE is the most likely diagnosis or equally likely 3; heart rate greater than 100 1.5; immobilisation for at least 3 days or surgery in the previous 4 weeks 1.5; previous objectively diagnosed DVT or PE 1.5; haemoptysis 1; and malignancy (on treatment, treated in the last 6 months, or palliative) 1. The single highest-weighted subjective item — PE is the most likely diagnosis — is the one that most often determines which limb the patient enters, and the registrar who miscalculates this item has misclassified the patient.

(b) Integration with the D-dimer and CTPA (4 marks): [1]

The validated algorithm, established by the Christopher study (van Belle and colleagues, 2006, a prospective cohort of 3306 patients), combines the Wells score with the D-dimer and CTPA [8]. The patient classified as PE unlikely (score 4 or less) undergoes a D-dimer; if the D-dimer is negative, PE is safely excluded without imaging (the 3-month incidence of symptomatic VTE in this group was 0.5 per cent). The patient classified as PE likely (score more than 4), or the patient classified as PE unlikely with a positive D-dimer, proceeds to CTPA. The age-adjusted D-dimer (cutoff equals age multiplied by 10 in micrograms per litre for patients over 50) increases the proportion of patients in whom PE can be excluded without imaging, particularly in the older patient in whom a fixed cutoff of 500 micrograms per litre is rarely normal.

(c) Synthesis of the evidence for the colleague (3 marks): [1]

The synthesis I would give the colleague is that the validated algorithm — Wells score, then D-dimer if PE unlikely, then CTPA if PE likely or if the D-dimer is positive — safely excludes PE in a defined subset of patients and reduces the overuse of CTPA. The Christopher study demonstrated that the PE-unlikely plus negative-D-dimer strategy carries a 3-month VTE risk of 0.5 per cent, which is below the accepted threshold for clinical safety [8]. The overuse of CTPA — ordering it in every chest pain patient without applying the Wells score — exposes patients to unnecessary radiation, contrast nephropathy and the overdiagnosis of clinically insignificant subsegmental PE. The corollary is that the disciplined application of the Wells score and the D-dimer is not a compromise on safety; it is the evidence-based standard of care. The D-dimer is a rule-out test, not a rule-in test, and it is interpreted only in the PE-unlikely limb — ordering it in a patient with a high pre-test probability is an error because it will be positive and the test adds nothing.