Medicine — Cardiology, NMC MBBS licence examination syllabus (Nepal Medical Council).
Acute coronary syndromes: the ECG decides, not the troponin
You commit to the biggest decision in cardiology before the blood test comes back.
A patient with chest pain arrives. Within ten minutes you must decide whether to activate a catheter laboratory, call for thrombolysis, or admit and observe. The troponin that would settle the diagnosis takes hours to become reliable — and by then, if this is a complete occlusion, a substantial amount of myocardium is already dead.
So acute coronary syndrome is taught in an unusual order: not diagnosis-then-treatment, but one ECG finding that triggers immediate action, with the rest of the diagnosis filled in afterwards. Understanding why that is — why ST elevation alone justifies committing to reperfusion — is most of what this chapter is for.
🩺 Where this lives: The phrase "time is myocardium" is not rhetoric. In a complete coronary occlusion, myocardium begins to die within roughly twenty to thirty minutes and the infarct extends progressively over the following hours. Every minute between the door and the balloon is muscle that will not come back, which is why STEMI pathways are built around minutes rather than hours — and why a doctor who waits for a troponin before acting on ST elevation has already made the most expensive mistake available.
One event, three outcomes
All three acute coronary syndromes begin the same way: an atherosclerotic plaque ruptures, platelets aggregate on the exposed core, and a thrombus forms. What separates them is how completely that thrombus blocks the artery, and therefore how much muscle dies.
Read that figure as a single spectrum rather than three diseases. Unstable angina and NSTEMI differ only by troponin — the same ECG, the same initial treatment, and the distinction is made retrospectively by whether cells died. STEMI is separated by the ECG, and that separation is what changes management immediately.
WHY ST ELEVATION MEANS SOMETHING DIFFERENT
PARTIAL occlusion
Blood still reaches the outer myocardium. The
SUBENDOCARDIUM — the innermost layer, furthest from
the epicardial vessels and under the highest wall
stress — is starved first.
→ ST DEPRESSION or T wave inversion
→ unstable angina or NSTEMI
COMPLETE occlusion
The full thickness of the wall is ischaemic.
→ ST ELEVATION
→ STEMI, and an artery that must be opened NOW
This is why the ECG can commit you to treatment: ST
elevation is a statement about a vessel being shut, and
a shut vessel is a mechanical problem with a mechanical
answer.
The presentation, and how it misleads
🔍 Typical, and then the ones that are missed
TypicalCentral, crushing or heavy chest pain lasting more than 20 minutes, radiating to the jaw or left arm, with sweating, nausea and breathlessness. Not relieved by rest or nitrates — the feature that distinguishes it from stable angina.
Atypical, and dangerousDiabetic patients (autonomic neuropathy blunts the pain), elderly patients, and women present more often without classic pain — instead with breathlessness, fatigue, collapse, confusion or epigastric discomfort. These are the infarcts that get sent home.
SignsOften unremarkable, which is itself worth knowing. Look for signs of complications: hypotension, a new murmur, raised JVP, pulmonary crackles, or an arrhythmia.
💡 Exam angle: the silent infarct in a diabetic patient is asked repeatedly, and the mechanism is the answer — autonomic neuropathy reduces the perception of cardiac pain. A question describing an elderly diabetic with sudden breathlessness, sweating and no chest pain is asking whether you will still order an ECG. The reasoning connects directly to the diabetes chapter's neuropathy section.
Reading the ECG
WHAT COUNTS AS ST ELEVATION
≥ 1 mm (0.1 mV) in two CONTIGUOUS limb leads
≥ 2 mm in two contiguous chest leads
(thresholds differ slightly by sex and by lead V2–V3)
"Contiguous" matters — it means the leads look at
neighbouring parts of the heart. Elevation scattered
across unrelated leads suggests pericarditis rather
than infarction.
TREATED AS A STEMI EQUIVALENT
NEW left bundle branch block with a compatible history
Posterior MI — tall R waves and ST DEPRESSION in V1–V2,
which is the mirror image of elevation at the back.
Confirm with posterior leads. This is the infarct most
often missed, because the pattern looks like the
opposite of what you are hunting.
Troponin, and why one value is not an answer
💡 Exam angle: two points recur. First, a normal troponin drawn early does not exclude infarction — it rises over 3–6 hours, so a single sample taken on arrival proves nothing and must be repeated. Second, troponin means myocardial injury, not infarction. It rises in sepsis, pulmonary embolism, heart failure, myocarditis and renal impairment. A raised troponin in a patient with no ischaemic story is a question about the cause, not a diagnosis of MI.
Immediate management
THE INITIAL DRUGS, AND WHY EACH
ASPIRIN irreversible COX-1 inhibition
Loading dose, chewed for faster absorption. The single
most evidenced drug in this presentation.
SECOND ANTIPLATELET P2Y12 inhibitor
Ticagrelor, prasugrel or clopidogrel — dual antiplatelet
therapy is the standard, with the choice guided by local
protocol, bleeding risk and planned intervention.
ANTICOAGULATION heparin or an alternative
Prevents further thrombus propagation.
ANALGESIA opioid if needed
Pain drives sympathetic activation, which raises
myocardial oxygen demand. Treating it is not just comfort.
OXYGEN — ONLY IF HYPOXIC
Routine oxygen in a normoxic patient is NOT beneficial
and may cause harm through coronary vasoconstriction.
Give it for saturations below target, not reflexively.
NITRATES — with two exceptions below
The nitrate exceptions matter clinically and are heavily examined. In inferior STEMI with right ventricular involvement, cardiac output depends on right ventricular preload; a nitrate drops preload and can cause profound hypotension. The same applies after a phosphodiesterase-5 inhibitor such as sildenafil, where the combination produces severe, refractory hypotension. In both cases the "routine" drug is the harmful one — which is exactly the shape of question examiners like.
Reperfusion in STEMI
🔍 The two strategies
Primary PCIMechanically opening the artery with a catheter and stent. The preferred strategy where it can be delivered promptly, because it opens more arteries more reliably than drugs do.
ThrombolysisA drug that dissolves the clot. Used where PCI is not available within the target time — a common situation outside major centres. Effectiveness falls sharply with delay, so it is most valuable early.
ChoosingThe decision is time-based: if PCI can be delivered within the locally agreed window, transfer for it; if not, thrombolyse without delay and transfer afterwards. A patient thrombolysed promptly does better than one who waits hours for a catheter laboratory.
Thrombolysis contraindicationsAnything that makes bleeding catastrophic: previous intracranial haemorrhage, recent ischaemic stroke, known intracranial neoplasm or vascular malformation, active bleeding, suspected aortic dissection, recent major trauma or surgery.
Complications
EARLY — hours to days
ARRHYTHMIA ventricular fibrillation is the
commonest cause of early death, which
is why these patients are monitored
HEART FAILURE and cardiogenic shock
BRADYCARDIA / BLOCK particularly in INFERIOR MI, since the
RCA usually supplies the AV node
PERICARDITIS early, over the infarcted segment
LATER — days to weeks
MECHANICAL RUPTURE free wall (tamponade), septum (new
murmur, shunt), papillary muscle
(acute mitral regurgitation) —
typically several days after infarction
and often catastrophic
MURAL THROMBUS and systemic embolism
VENTRICULAR ANEURYSM with persistent ST elevation
DRESSLER SYNDROME immune-mediated pericarditis weeks
later
A new murmur with sudden deterioration after an MI is a
mechanical complication until proven otherwise.
Secondary prevention
The admission is the acute problem; the discharge prescription is what determines the next ten years. Every patient leaves on the same core regimen unless there is a specific reason not to.
THE FIVE THAT CHANGE OUTCOME
1. ASPIRIN lifelong
2. SECOND ANTIPLATELET for a defined period
3. STATIN high intensity
4. ACE INHIBITOR especially with LV dysfunction
5. BETA-BLOCKER reduces mortality post-MI
Plus: cardiac rehabilitation, smoking cessation, blood
pressure and glycaemic control.
Note how many of these are the SAME interventions the
diabetes chapter argued for. Cardiovascular risk
management is one subject wearing several names.
Clinical reasoning: four presentations
🔍 Case 1 — the ten-minute decision
PresentationA 58-year-old with 40 minutes of crushing central chest pain, sweating and vomiting. ECG shows 3 mm ST elevation in II, III and aVF. Troponin not yet back.
ReasoningInferior STEMI. The ECG is diagnostic and the troponin is irrelevant to the decision — waiting for it wastes myocardium.
AnswerActivate reperfusion immediately: primary PCI if achievable in the local window, otherwise thrombolysis. Give aspirin, a second antiplatelet and anticoagulation. And because it is inferior — do right-sided leads before reaching for a nitrate.
🔍 Case 2 — the harmful reflex
PresentationThe same patient. V4R shows ST elevation, confirming right ventricular involvement. BP 96/58. A colleague draws up GTN for ongoing pain.
TrapNitrates are standard for ischaemic chest pain, so giving one feels automatic.
ReasoningA failing right ventricle depends on preload to fill the left side. Nitrates reduce preload, and in RV infarction that can cause abrupt, severe hypotension.
AnswerWithhold the nitrate. These patients are preload-dependent and are managed with cautious fluid loading and reperfusion. This is the RV-infarct question in its usual disguise.
🔍 Case 3 — the atypical presentation
PresentationA 74-year-old woman with type 2 diabetes: two hours of breathlessness, nausea and clamminess. No chest pain at all. Looks unwell.
Key cluesDiabetic, elderly, female — three groups in which infarction presents without pain.
ReasoningAutonomic neuropathy blunts cardiac pain perception. The absence of chest pain is not evidence against an acute coronary syndrome in this patient; it is expected.
AnswerECG immediately, and serial troponins. A low threshold for suspecting ACS in these groups is the entire teaching point — these are the infarcts that get discharged as indigestion.
🔍 Case 4 — the negative troponin
PresentationA 49-year-old arrives 90 minutes after the onset of severe chest pain, now settled. ECG normal. Troponin on arrival is normal. He asks to go home.
TrapA normal ECG plus a normal troponin looks like a clean discharge.
ReasoningTroponin does not rise measurably until roughly 3–6 hours after myocardial injury. At 90 minutes a normal value tells you almost nothing.
AnswerRepeat the troponin after the appropriate interval and repeat the ECG, looking at the change rather than the single value. Discharging on one early negative sample is how NSTEMIs are missed.
Commonly confused
Confusion
The distinction
Why it matters
Unstable angina vs NSTEMI
Troponin — raised means cells died
Initial management is the same; the distinction is retrospective.
NSTEMI vs STEMI
ST elevation on the ECG
Only STEMI needs immediate reperfusion.
Stable angina vs ACS
Stable angina is predictable and relieved by rest
Pain at rest lasting over 20 minutes is an emergency.
Troponin rise vs infarction
Troponin means injury from any cause
Sepsis, PE and renal failure raise it without an MI.
Posterior MI vs anterior ischaemia
Posterior gives ST DEPRESSION in V1–V2 with tall R waves
It is a STEMI equivalent, and it looks like its opposite.
Nitrates always vs nitrates usually
Contraindicated in RV infarction and after PDE5 inhibitors
The routine drug becomes the harmful one.
Rapid revision
MUST-KNOW FACTS
1. All ACS begins with plaque rupture and thrombus formation.
2. Partial occlusion → subendocardial ischaemia → ST depression / T inversion.
3. Complete occlusion → full-thickness → ST ELEVATION.
4. Unstable angina and NSTEMI differ ONLY by troponin.
5. The ECG, not the troponin, drives the STEMI decision.
6. ECG within 10 minutes of arrival.
7. STEMI criteria: ≥1 mm in two contiguous limb leads, ≥2 mm in two chest leads.
8. New LBBB with a compatible history is a STEMI equivalent.
9. Posterior MI: ST depression + tall R in V1–V2 — easily missed.
10. V1–V4 anterior (LAD) · II, III, aVF inferior (RCA) · I, aVL, V5–V6 lateral (circumflex).
11. Inferior STEMI → do right-sided leads (V4R).
12. RV infarction is PRELOAD-DEPENDENT — no nitrates; give fluid.
13. Nitrates also contraindicated after a PDE5 inhibitor.
14. Oxygen only if hypoxic — routine oxygen may harm.
15. Aspirin, a second antiplatelet, anticoagulation and analgesia for all.
16. Reperfusion: primary PCI preferred; thrombolysis if PCI is not timely.
17. Troponin rises at 3–6h, peaks 12–24h, stays raised up to 10 days.
18. One early normal troponin does NOT exclude infarction — repeat it.
19. Troponin means myocardial injury, not necessarily MI.
20. Silent infarcts: diabetic, elderly and female patients.
21. VF is the commonest cause of early death — monitor these patients.
22. New murmur plus deterioration post-MI = mechanical complication.
23. Secondary prevention: aspirin, P2Y12, statin, ACE inhibitor, beta-blocker.
💡 Exam angle: the reliable threads are (a) acting on ST elevation without waiting for troponin, (b) the RV-infarct nitrate contraindication, (c) an early negative troponin proving nothing, (d) silent infarction in diabetic and elderly patients, and (e) recognising posterior MI from ST depression in V1–V2. Four of those five are situations where the obvious reading is the wrong one — which is the pattern this whole topic is built around.
Syllabus points
Plaque rupture and the ACS spectrum
Why partial occlusion depresses ST and complete elevates it
Typical presentation and the atypical ones that get missed
ECG criteria and STEMI equivalents
Lead territories and their coronary arteries
Posterior MI and why it is missed
Troponin kinetics and what a raised value means
Immediate management and the nitrate contraindications
Reperfusion: PCI versus thrombolysis
Early and late complications
Secondary prevention
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