Undifferentiated Chest Pain — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret O'Sullivan, 68 years old, retired schoolteacher. [1]

Presenting complaint: Two hours of central crushing chest pain that started at rest, radiating to the left arm and the jaw, associated with diaphoresis and nausea. She is now breathless on minimal exertion. [1]

Past history: Type 2 diabetes (HbA1c 64 mmol/mol, on metformin 1 g twice daily and gliclazide 80 mg daily), hypertension (on perindopril 5 mg daily and amlodipine 10 mg daily), hyperlipidaemia (on atorvastatin 40 mg daily, LDL 2.1 mmol per L), hypothyroidism (on thyroxine 100 micrograms daily). She smoked 30 pack-years and stopped ten years ago. Her father had an MI at 55 and her brother had a CABG at 60. She is normally independent, walking 30 minutes daily. [1]

Examination findings (trainee elicits):

• Alert and diaphoretic, in pain.
• Blood pressure 152/94 in the right arm, 138/90 in the left arm.
• Heart rate 96 in sinus rhythm.
• Respiratory rate 20, SpO2 97 per cent on room air.
• Temperature 36.8.
• Heart sounds normal with no added sounds and no murmurs.
• Chest clear.
• No peripheral oedema. All peripheral pulses present and symmetrical. [1]

Investigations (available results):

• ECG: ST elevation of 2 mm in the inferior leads (II, III, aVF) with reciprocal ST depression in I and aVL.
• Troponin at presentation: 45 ng per L (99th percentile 14).
• Chest X-ray: clear lung fields, normal cardiac silhouette, no widened mediastinum. [1]

Drug chart (current): metformin 1 g twice daily, gliclazide 80 mg daily, perindopril 5 mg daily, amlodipine 10 mg daily, atorvastatin 40 mg daily, thyroxine 100 micrograms daily. [1]

Candidate's structured presentation (model)

Opening statement (SASPOP): [1]

"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 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 ECG shows an inferior STEMI with reciprocal changes, and her troponin is elevated. This is an acute ST-elevation myocardial infarction. My immediate priority is to activate the catheter lab for primary percutaneous coronary intervention, while I 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. I will also manage her diabetes during the ACS and plan the secondary prevention." [1]

Management plan: [1]

1. Activate the catheter lab. Primary PCI is the gold standard for STEMI if it can be delivered within the recommended door-to-balloon timeframe. If PCI is not available in time, fibrinolysis (tenecteplase) is the alternative, followed by transfer to a PCI-capable centre.
2. Antiplatelet and anticoagulant therapy. Aspirin 300 mg loading then 100 mg daily; a P2Y12 inhibitor (ticagrelor 180 mg loading then 90 mg twice daily, or prasugrel 60 mg loading then 10 mg daily); unfractionated heparin during the PCI.
3. Pain and sympathetic-drive control. Morphine 2.5 to 5 mg intravenously with metoclopramide; sublingual glyceryl trinitrate (unless hypotensive or right ventricle involved). Oxygen only if SpO2 below 90 per cent.
4. Assess for right ventricular involvement. Right-sided ECG (V4R). If ST elevation is present, the right ventricle is involved and the patient is preload-sensitive — avoid nitrates and diuretics, give fluid if hypotensive.
5. Assess for complications. Heart failure (Killip classification), arrhythmia (inferior MI may cause bradycardia and heart block), pericarditis, ventricular septal rupture, papillary muscle dysfunction.
6. Diabetes management. Hold metformin for the contrast of the angiogram. Insulin sliding scale if glucose above 10 mmol per L. Target 6 to 10 mmol per L. Restart metformin once the renal function is confirmed post-angiogram.
7. Secondary prevention. Dual antiplatelet therapy for 12 months; atorvastatin 80 mg (target LDL below 1.4 mmol per L); ACE inhibitor and beta-blocker titrated to maximum tolerated dose; cardiac rehabilitation; smoking cessation reinforcement; echocardiogram to assess the ejection fraction and the wall-motion abnormality. [1]

Communication and shared decision-making: Explain to Mrs O'Sullivan and her family that she is having a heart attack, that the priority is to open the blocked artery as quickly as possible, and that the next 24 hours are critical. Surface the secondary prevention plan — the medications, the rehabilitation, the lifestyle changes — and explain that the long-term outcome depends as much on the adherence to the secondary prevention as on the acute intervention. Address the anxiety and the depression, which are commoner after an ACS in women and are independent risk factors for a poor outcome. [1]

Examiner discussion questions

Q1: "Walk me through the ECG interpretation and how it determines the management." [1]

"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 acute inferior STEMI from right coronary artery occlusion. This is a STEMI that triggers immediate catheter-lab activation for primary PCI, guided by the 2023 ESC ACS Guidelines [1]. The reciprocal changes confirm the territorial nature of the infarction and they distinguish it from the diffuse concave ST elevation of pericarditis. The inferior STEMI raises the question of right ventricular involvement — I will perform a right-sided ECG (V4R), and if ST elevation is present, the right ventricle is involved, making the patient preload-sensitive. The teaching point is that the ECG within 10 minutes is the single highest-yield investigation in chest pain, and the STEMI-equivalent patterns — the new LBBB, the Wellens syndrome, the De Winter T waves, the posterior MI — are the patterns the registrar must recognise to trigger the catheter-lab activation [3]."

Q2: "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 [4]. 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 document the differential, and I proceed to primary PCI. 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."

Q3: "How do you interpret the troponin, and when would you repeat it?" [1]

"The troponin of 45 ng per L is elevated above the 99th percentile of 14, which confirms myocardial injury [5]. In the setting of the STEMI on the ECG and the classic chest pain, this is diagnostic of an acute type 1 myocardial infarction (a plaque event). I do not need to wait for a serial troponin to make the diagnosis or to activate the catheter lab — the STEMI on the ECG is sufficient. The serial troponin is useful for confirming the dynamic rise and for prognostication (the peak troponin correlates with the infarct size). The teaching point is that the troponin is interpreted in the clinical context — the elevated troponin with the STEMI is type 1 infarction; the elevated troponin in a septic, tachycardic or uraemic patient without chest pain or ECG changes may be type 2 injury (supply-demand mismatch), and the job of the registrar is to distinguish the two [2]."

Q4: "What if she develops complete heart block during the infarction?" [1]

"Complete heart block occurs in up to 10 per cent of inferior STEMIs, typically from ischaemia of the AV node (supplied by the right coronary artery in 90 per cent of patients). The management is transcutaneous pacing as a bridge, with the recognition that the inferior-MI heart block is often transient and resolves with reperfusion. If the heart block persists or is symptomatic with hypotension, a temporary transvenous pacemaker is inserted. The teaching point is the difference between the inferior-MI heart block (usually transient, often has a stable escape rhythm, resolves with reperfusion) and the anterior-MI heart block (from extensive septal and bundle-branch infarction, a sign of a large infarct with a poor prognosis, more likely to need a permanent pacemaker)." [1]

Q5: "How do you manage her diabetes during the admission?" [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. 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. The long-term glycaemic target is an HbA1c of 53 mmol per L or less." [1]

Q6: "What is the single most important lesson from this case for a registrar managing undifferentiated chest pain?" [1]

"The single most important lesson is that the systematic approach — the ECG within 10 minutes, the pain-character history, the focused examination, the risk stratification — identified this STEMI within minutes and triggered the time-critical pathway. The registrar who added the pain-character history to the classic crushing central pain, the diaphoresis, the nausea and the cardiac risk factors, and who got the ECG within 10 minutes, has done everything right. The corollary is the atypical patient — the woman with dyspnoea and nausea, the elderly patient with confusion, the diabetic with fatigue — and the registrar who maintains the low threshold for the ECG and the troponin in these populations will catch the atypical ACS that the classic approach would miss [6]."

DCE Short Case — The Systematic Cardiovascular Examination in the Chest Pain Patient

Instruction

"You are the medical registrar assessing a 65-year-old man on the ward with a history of central chest pain on exertion over the past two months. Examine his cardiovascular system, present your findings, and offer a differential diagnosis. You have 5 minutes to outline your examination approach and 5 minutes for discussion." [1]

Provided data: The patient is a 65-year-old man, a current smoker of 40 pack-years, with central exertional chest pain that resolves with rest over two months. On examination: blood pressure 145/85, heart rate 78 in sinus rhythm, respiratory rate 16, SpO2 98 per cent on room air. An ejection systolic murmur is audible at the upper right sternal edge, radiating to the carotids, with a slow-rising pulse. [1]

Presentation template

"I have examined this man's cardiovascular system. At the end of the bed he is comfortable at rest. His pulse is 78 in sinus rhythm, regular, slow-rising in character. His blood pressure is 145 over 85. His JVP is not elevated. His hands show tendon xanthomata and corneal arcus, consistent with hyperlipidaemia. His apex is not displaced and is sustained in character. On auscultation, there is an ejection systolic murmur at the upper right sternal edge, radiating to the carotids, with a soft second heart sound. His chest is clear. He has no peripheral oedema and all his peripheral pulses are present. My findings are consistent with aortic stenosis — the slow-rising pulse, the sustained apex, the ejection systolic murmur radiating to the carotids, and the soft second heart sound. The exertional chest pain may represent angina from the aortic stenosis, or coexisting coronary disease given his smoking history. I would arrange an echocardiogram to quantify the valve gradient, an ECG, and I would assess for coexisting coronary disease with a coronary angiography or a CT coronary angiography." [1]

Discussion

Examiner: "What is your differential diagnosis for the murmur, and how would you discriminate?" [1]

"The leading diagnosis is aortic stenosis — the slow-rising pulse (pulsus parvus et tardus), the sustained apex, the ejection systolic murmur at the aortic area radiating to the carotids, and the soft second heart sound are the classic tetrad. The differential within the systolic murmurs includes hypertrophic obstructive cardiomyopathy (the murmur is at the lower left sternal edge, it increases with Valsalva, and there may be a bifid apex beat), mitral regurgitation (the murmur is at the apex, radiating to the axilla, with a soft first heart sound), and a ventricular septal defect (a pansystolic murmur at the lower left sternal edge). The echocardiogram discriminates these definitively — the aortic valve gradient, the valve area, the left ventricular function, and the wall-motion abnormalities. The teaching point is that the murmur of aortic stenosis is distinguished from the flow murmur of severe anaemia or hyperthyroidism by the peripheral signs — the slow-rising pulse and the sustained apex are the signatures of the fixed outflow obstruction." [1]

Examiner: "His chest pain is on exertion. Is this angina?" [1]

"Yes, most likely. The exertional chest pain in a patient with aortic stenosis may represent angina from the increased myocardial oxygen demand in the hypertrophied left ventricle against the fixed outflow obstruction, or it may represent coexisting coronary disease (the risk factors — smoking, hyperlipidaemia — are present in both). The discriminator is the coronary angiography, which I would arrange alongside the echocardiogram. The teaching point is that the angina of aortic stenosis can occur with normal coronaries — the hypertrophied myocardium outstrips its oxygen supply, and the management is the valve replacement, not the coronary intervention." [1]

Examiner: "What is the lesson about the missed diagnoses in the chest pain patient with a murmur?" [1]

"The lesson is that the chest pain patient with a murmur must not be assumed to have ACS alone — the aortic stenosis, the hypertrophic cardiomyopathy, and the mitral valve prolapse are the valvular causes of chest pain that the systematic cardiovascular examination identifies. The registrar who examines only the ECG and the troponin in a chest pain patient, without the full cardiovascular examination, has missed the valvular diagnosis that the stethoscope would have revealed. The corollary is the integration — the murmur, the pulse character, the apex character, and the heart sounds are not isolated observations but a single picture that, read together, identifies the valvular cause of chest pain that the troponin alone would miss." [1]