Undifferentiated Chest Pain — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Margaret O'Sullivan is a 68-year-old retired schoolteacher presenting with two hours of central crushing chest pain radiating to the left arm and the jaw, with diaphoresis and nausea, on a background of type 2 diabetes, hypertension, hyperlipidaemia and hypothyroidism. She is a 30-pack-year ex-smoker with a strong family history of premature coronary disease — her father had an MI at 55 and her brother had a CABG at 60. ^[1]

Her main problem is an acute ST-elevation myocardial infarction — the ECG shows ST elevation of 2 mm in the inferior leads with reciprocal changes, and the troponin is elevated. The blood-pressure differential between the arms is 14 mmHg, which is within the normal range and does not raise the concern for aortic dissection. ^[1]

My immediate priorities are to activate the catheter lab for primary percutaneous coronary intervention, initiate the antiplatelet and anticoagulant therapy, control her pain and her sympathetic drive, and assess for the complications of the infarction — in particular, right ventricular involvement, which is common in inferior MI and which changes the fluid management. I will also manage her diabetes during the ACS — holding the metformin for the contrast of the angiogram, and using an insulin sliding scale if the glucose is high — and I will plan the secondary prevention, which is as important as the acute reperfusion." ^[1]

Examiner probing questions and model answers

Q1: "How do you use the Sgarbossa criteria, and when would you apply them?" ^[1]

"The Sgarbossa criteria (Sgarbossa and colleagues, 1996) are used to identify acute myocardial infarction in the setting of left bundle branch block, where the standard ST-elevation criteria do not apply ^[4]. The three criteria are: concordant ST elevation of 1 mm or more in a lead with a positive QRS complex — 5 points; concordant ST depression of 1 mm or more in V1 to V3 — 3 points; and excessively discordant ST elevation of 5 mm or more in a lead with a negative QRS complex — 2 points. A total score of 3 or more is highly specific for acute infarction. I apply them in the patient with a known or presumed new LBBB who presents with chest pain consistent with ACS. The key teaching point is that a new or presumed new LBBB in the right clinical context is a STEMI-equivalent that triggers the catheter-lab activation — the Sgarbossa criteria help me confirm the infarction, but their absence does not exclude it in the right clinical context. The modified Smith-Modified Sgarbossa criteria, which use a proportional ST to S-wave ratio of -0.25 or less instead of the absolute 5 mm cutoff, improve the sensitivity and are increasingly used in practice."

Q2: "How does the high-sensitivity troponin 0/1h algorithm work?" ^[1]

"The 0/1h algorithm (Mueller and colleagues, 2016, a multicentre evaluation in 1282 patients) uses the high-sensitivity troponin at presentation and at one hour to stratify the patient into rule-out, observe, or rule-in ^[3]. The cutpoints are assay-specific. A very low presentation troponin (below the limit of detection) with a small one-hour delta rules out myocardial infarction and allows safe early discharge or further assessment in the outpatient setting. A high presentation troponin or a large one-hour delta rules in myocardial infarction and triggers the invasive pathway. The intermediate group — the observe group — requires further serial troponins and observation. The algorithm is a Class I recommendation in the 2023 ESC ACS Guidelines, and it reduces the ED length of stay and the proportion of patients requiring prolonged observation ^[2]. The teaching point is that the troponin must be interpreted in the clinical context — an elevated troponin in a septic, tachycardic or uraemic patient may be type 2 injury (supply-demand mismatch) rather than type 1 infarction (plaque event), and the Fourth Universal Definition requires the dynamic rise or fall to distinguish the two ^[6]."

Q3: "How do you use the HEART score in practice?" ^[1]

"The HEART score (Backus and colleagues, 2013, validated in 2440 patients) is the risk-stratification tool designed specifically for the emergency department chest pain patient ^[1]. The five components — History, ECG, Age, Risk factors, Troponin — each scored 0 to 2, stratify the patient into low risk (score 0 to 3, MACE rate 1.7 per cent at six weeks), intermediate risk (score 4 to 6, MACE rate around 20 per cent) and high risk (score 7 to 10, MACE rate exceeding 50 per cent). In practice, I use it in the patient with chest pain of suspected cardiac origin who does not have a clear STEMI on the ECG — the patient in whom the question is 'how hard should I work this up?' The low-risk patient can be considered for early discharge with outpatient follow-up and a safety-net. The intermediate-risk patient requires admission for serial troponins and observation. The high-risk patient is admitted for urgent investigation and management. The HEART score outperformed the TIMI and GRACE scores because they were designed for the inpatient ACS population, not the undifferentiated ED patient. The teaching point is that the HEART score is a decision-support tool, not a substitute for clinical judgement — the registrar who discharges a patient on the basis of a low score without considering the clinical context and the patient's own risk tolerance has misused the tool."

Q4: "What if this patient had presented with breathlessness and fatigue instead of chest pain?" ^[1]

"Then she would have had an atypical presentation of ACS, which is the single largest source of missed diagnosis and delayed treatment. Women, the elderly and the diabetic patient frequently present without classic central crushing chest pain — they present with dyspnoea, fatigue, nausea, vomiting, epigastric discomfort, syncope, or just feeling unwell. The registrar who requires classic chest pain to investigate for ACS in these populations has excluded the majority of infarctions. The corollary is that I maintain a low threshold for the ECG and the troponin in the woman, the elderly and the diabetic patient who presents with any of these atypical symptoms, even without classic chest pain. The ECG and the troponin would still have identified her STEMI, and the management pathway would have been the same. The teaching point is that the registrar's index of suspicion — not the patient's pain description — determines whether the investigation is performed." ^[1]

Q5: "Her blood pressure is 152 over 94 in the right arm and 138 over 90 in the left. Is this dissection?" ^[1]

"The differential of 14 mmHg is below the 20 mmHg threshold that raises the concern for aortic dissection, and her clinical picture — the inferior STEMI, the classic cardiac pain, the cardiac risk factors — is overwhelmingly consistent with ACS ^[5]. The IRAD registry established that the clinical presentation of dissection is diverse, but the classic features — tearing interscapular pain maximal at onset, a pulse deficit, a new aortic regurgitation murmur, a widened mediastinum — are absent in this patient. I proceed to primary PCI, and the coronary angiogram will definitively exclude dissection as the cause. If the angiogram shows normal coronaries in the setting of an inferior STEMI pattern, I immediately reconsider dissection and proceed to an aortogram. The teaching point is that the blood pressure in both arms is a mandatory part of the chest pain examination — it is the single bedside sign that raises the dissection question, and it is omitted in the majority of assessments."

Q6: "What is your secondary prevention plan?" ^[1]

"The secondary prevention is the four pillars: antiplatelet therapy (dual for 12 months, then lifelong single), lipid-lowering (atorvastatin 80 mg, target LDL below 1.4 mmol per L), neurohormonal modulation (ACE inhibitor and beta-blocker, titrated to the maximum tolerated dose), and lifestyle (smoking cessation reinforcement, cardiac rehabilitation, Mediterranean diet, regular exercise). I add an SGLT2 inhibitor for the cardiorenal benefit. I arrange the echocardiogram to assess the ejection fraction and the wall-motion abnormality, and the cardiology follow-up at six weeks. The teaching point is that the secondary prevention is as important as the acute reperfusion — the patient who has the PCI and then stops the medications at three months has squandered the benefit of the intervention. I also address the psychosocial support — the anxiety and the depression after an ACS are commoner in women and are independent risk factors for a poor outcome." ^[1]