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IM2.1-24 | Acute Myocardial Infarction and Ischemic Heart Disease — PBL Case
CLINICAL SETTING
Dr Kavitha is the medical registrar on call at a district hospital in rural Tamil Nadu on a Sunday evening. Mr Rajan, a 56-year-old lorry driver, is brought in by his wife, who found him sitting on the kitchen floor, pale and sweating, complaining of severe burning in the upper abdomen and an 'unbearable weight on the chest' that started suddenly two hours ago after dinner. He initially thought it was acidity — he has a history of dyspepsia and took two antacid tablets without relief. He has smoked 20 cigarettes a day for 30 years and takes telmisartan 40 mg for hypertension. He says he has had occasional chest heaviness on climbing stairs for the past 4 months, always settling after rest, which he had dismissed as 'tiredness from driving long hours'. His wife adds: 'He is always tired. He never complains.' On arrival: BP 90/60 mmHg (right arm), HR 104/min, RR 22/min, SpO2 92% on room air. He is pale, diaphoretic, with cool peripheries. The junior doctor at triage writes 'acute gastritis, ?GERD' in the notes and starts an IV drip. Dr Kavitha arrives, picks up the case, and reads the triage note. She immediately orders an ECG. She turns to the final-year students in the emergency bay: 'Before we see the ECG — walk me through your differential and what you are most worried about.'
Trigger 1: The ECG and the First Decision
The ECG is brought in (12 minutes after arrival). Dr Kavitha holds it up for the students. It shows: sinus tachycardia at 104/min; normal axis; normal PR and QRS intervals; ST elevation 3–4 mm in leads II, III, and aVF; ST depression 2–3 mm in I, aVL, and V1–V4; and a dominant R wave in V1 with upright T wave. SpO2 has dropped to 89%. Mr Rajan is now more distressed, saying the pain is radiating to his jaw. The junior doctor suggests: 'We should give him sublingual nitrate for the pain and call the cardiologist.' Dr Kavitha pauses and says quietly: 'Before you give that nitrate — look at the ECG again. What does this pattern tell you about which parts of the heart are involved?'
DISCUSSION POINTS
- What does ST elevation in leads II, III, and aVF with ST depression in I, aVL, and V1–V4 indicate in terms of infarct territory and most likely culprit vessel?
- What is the significance of a dominant R wave with upright T wave in V1 in the context of inferior STEMI? What additional leads should be recorded and why?
- Why is sublingual nitrate potentially dangerous in this patient before additional ECG leads are obtained? What clinical and ECG features should be confirmed before any vasoactive drug is given?
Click to reveal Trigger 2: Right-Sided Leads and a Changed Management Plan (discuss previous trigger first!)
Trigger 2: Right-Sided Leads and a Changed Management Plan
Dr Kavitha orders right-sided (V3R–V6R) and posterior (V7–V9) leads. Right-sided leads show 2 mm ST elevation in V3R and V4R. Posterior leads (V7–V9) show 1.5 mm ST elevation. The cardiologist is available by telephone 3 hours away by road; the nearest primary PCI centre is 4.5 hours away by the district ambulance. Mr Rajan's BP is now 80/55 mmHg and his JVP is visibly elevated. Lung fields are clear on auscultation. The cardiologist advises: 'This is inferior + posterior + RV STEMI. Fibrinolysis is indicated — PCI is not achievable within the time window. Follow the pharmacoinvasive protocol.' The emergency nurse looks at Dr Kavitha: 'We have streptokinase and tenecteplase in the emergency kit. Which one do we use?'
DISCUSSION POINTS
- Compare streptokinase and tenecteplase as fibrinolytic agents: what are the key differences in mechanism, administration, antigenicity, and clinical preference in a patient who has not received streptokinase before?
- What antiplatelet regimen should accompany fibrinolysis in this patient, and why is ticagrelor NOT the correct choice here?
- The patient has hypotension (BP 80/55), elevated JVP, and clear lung fields. What is the specific pathophysiological explanation for this triad in RV infarction, and what is the immediate haemodynamic treatment?
Click to reveal Trigger 3: Two Hours After Fibrinolysis: Assessing Response (discuss previous trigger first!)
Trigger 3: Two Hours After Fibrinolysis: Assessing Response
Tenecteplase was given with aspirin 300 mg and clopidogrel 300 mg plus enoxaparin. Ninety minutes later, the repeat ECG shows only 25% reduction in ST elevation in the inferior leads. Mr Rajan's chest pain persists at 7/10. His BP has improved to 92/60 after IV fluid loading (500 mL normal saline). The on-call nurse asks: 'Should we give another dose of tenecteplase since the first didn't work?' Dr Kavitha shakes her head. A student asks: 'How do we know if thrombolysis has failed, and what do we do now?' The cardiology registrar at the PCI centre calls back: 'If fibrinolysis has failed, transfer urgently for rescue PCI — we can get him in within 2.5 hours of your call. What is the patient's current status?'
DISCUSSION POINTS
- What are the ECG and clinical criteria for successful versus failed fibrinolysis, and at what time point after administration should these be assessed?
- Why is re-administration of a fibrinolytic agent (repeat tenecteplase) contraindicated after failed thrombolysis?
- What is rescue PCI, how does it differ from primary PCI and pharmacoinvasive PCI, and what preparations should be made during transfer to the PCI centre?
Click to reveal Trigger 4: Post-PCI: The Ward Round, Complications, and Counselling (discuss previous trigger first!)
Trigger 4: Post-PCI: The Ward Round, Complications, and Counselling
Mr Rajan is transferred and undergoes successful rescue PCI with drug-eluting stent placement in the proximal RCA. He returns to the district hospital on day 3 for continuing care. His echocardiogram shows LVEF 40%, inferior hypokinesia, preserved RV function. On day 5, during morning rounds, a student notices a new finding: Mr Rajan develops sudden pleuritic chest pain, low-grade fever (38.1°C), and a pericardial friction rub. His repeat ECG shows diffuse saddle-shaped ST elevation in all leads except aVR. Troponin is minimally elevated. Dr Kavitha asks: 'What complication has developed, and how is this different from his original STEMI? Should we anticoagulate him?' Later that day, Mr Rajan asks the student assigned to him: 'Doctor, can I go back to driving? I need this job. And do I really need to take 5 tablets a day for the rest of my life?'
DISCUSSION POINTS
- What is Dressler syndrome (post-cardiac injury syndrome)? How does its ECG pattern differ from the original STEMI pattern, and what is the appropriate management — including whether anticoagulation should be continued?
- Construct the complete evidence-based discharge medication regimen for Mr Rajan (post-RCA STEMI, LVEF 40%, DES in situ). Name each drug, dose, duration, and the specific evidence-based indication.
- How would you counsel Mr Rajan about returning to work as a long-distance lorry driver after a STEMI? Address both the medical recovery timeline and the specific occupational and regulatory considerations for a Group 2 (commercial vehicle) driving licence.
Group Task Assignments
- Construct a triage decision tool (one page, point-of-care format) that a junior doctor or nurse in a district hospital can use to distinguish ACS from acute gastritis/GERD in a patient presenting with epigastric pain — specifying which clinical features, ECG findings, and biomarker thresholds require immediate escalation to a senior physician.
- Prepare a 5-minute patient education handout (in plain language, as if for a patient with secondary school education) that explains: what caused Mr Rajan's heart attack, why he must take all 5 medications without stopping, the single most important lifestyle change (smoking cessation), and when to return to the emergency department.
- Debate the proposition: 'In the Indian district hospital setting, a pharmacoinvasive strategy (fibrinolysis followed by routine PCI within 24 hours) provides equivalent outcomes to primary PCI for STEMI patients with a long transfer time.' What are the arguments for and against this strategy based on clinical trial evidence (STREAM, TRANSFER-AMI, CAPITAL AMI)?
- Design a 12-week cardiac rehabilitation programme for Mr Rajan that could be implemented at district hospital level — specifying the exercise prescription (type, frequency, intensity, duration), risk factor targets, psychological support components, and occupational rehabilitation plan.
Learning Issues
Research these questions and bring your findings to the discussion.
- [IM2.9] What are the clinical criteria that distinguish stable angina, unstable angina, NSTEMI, and STEMI — and how do the ECG and troponin findings for each entity differ?
- [IM2.10] What are the ECG diagnostic criteria for STEMI, and how do you localise the infarct territory and culprit vessel from the pattern of ST elevation and reciprocal changes? What is the ECG pattern of RV infarction and posterior STEMI?
- [IM2.19] What are the mechanical and arrhythmic complications of acute MI, what are their characteristic clinical presentations, and at what time point post-MI does each typically occur?
- [IM2.16] What are the indications for, and time targets of, primary PCI versus fibrinolysis in STEMI? What is the pharmacoinvasive strategy and rescue PCI, and when is each indicated?
- [IM2.23] What antiplatelet and anticoagulant regimens are recommended for STEMI managed with primary PCI versus fibrinolysis, and why does the choice of P2Y12 inhibitor differ between these two reperfusion strategies?
- [IM2.15] What is the complete post-MI discharge medication bundle, what is the evidence base for each drug class, and what are the LDL-C targets and escalation strategy for patients not reaching target on maximum statin therapy?
- [IM2.24] What are the key components of patient counselling after ACS, and how do occupational and driving restrictions apply to a commercial vehicle driver post-STEMI?