Acute Coronary Syndrome (ACS) STEMI ❤️ ✅

Related Subjects: | AP of the Coronary Arteries |Acute Coronary Syndrome: Overview |Atherosclerosis |Ischaemic heart disease |Assessing Chest Pain |Acute Coronary Syndrome (ACS): Complications |ACS - General |ACS - STEMI |ACS - NSTEMI |ACS - GRACE Score |ACS - ECG Changes |Cardiac Troponins |ACS - Post MI arrhythmias |ACS: Right Ventricular STEMI |ACS: Sgarbossa Criteria |Wellen's syndrome

📊 Initial Management of Acute STEMI

🫀 Site of Coronary Artery Occlusion in STEMI

1. Right coronary artery occlusion
   • ST depression in lead I.
   • ST elevation in lead III greater than in lead II.
   a. Proximal occlusion

   • ST elevation more than 1 mm with positive T wave in lead V₄R.
   b. Distal occlusion

   • ST isoelectric with a positive T wave in lead V₄R.
2. Left circumflex artery occlusion
   • ST elevation in lead II greater than lead III.
   • ST isoelectric or elevated in lead I.
   • ST isoelectric or depressed with negative T wave in V₄R.
   a. Extension to posterior wall

   • ST depression in precordial leads.
   b. Extension to lateral wall

   • ST elevation in leads I, aVL, V₅ and V₆.
3. Left anterior descending artery occlusion
   a. Proximal to first septal branch and first diagonal branch

   • ST elevation in leads aVR and aVL.
   • ST depression in leads II, III and aVF.
   • ST elevation in lead V₁ >2 mm and leads V₂ to V₄.
   • ST isoelectric or depressed in leads V₅ and V₆.
   • Acquired intra-Hisian block or RBBB may occur.
   b. Distal to first septal branch, proximal to first diagonal branch

   • ST elevation in leads I and aVL.
   • ST depression in lead III, with lead II isoelectric.
   • ST elevation in leads V₂ to V₆ but not in lead V₁.
   c. Distal to first diagonal branch, proximal to first septal branch

   • ST depression in aVL, highest in lead III.
   • ST elevation in inferior leads, highest in lead III.
   • ST elevation in leads V₁ to V₄.
   d. Distal LAD

   • ST depression in aVR.
   • ST elevation in inferior leads, highest in lead II.
   • ST elevation in leads V₃ to V₆.
4. Left main coronary artery occlusion
   • ST elevation in lead aVR.
   • ST elevation in lead V₁, usually lower than in aVR.
   • ST depression in leads II and aVF.
   • ST depression in precordial leads to the left of V₂.

🖼️ STEMI ECG Examples

🫀 Management of Acute STEMI - NICE NG185 + ESC 2023 aligned

🚨 Key principle: STEMI is a time-critical reperfusion emergency. Do not delay reperfusion for CXR, routine bloods or waiting for troponin.
NICE timing logic: offer primary PCI if it can be delivered within 120 minutes of the time fibrinolysis could have been given; otherwise offer fibrinolysis if within 12 hours, appropriate and not contraindicated.
Time = myocardium ⏱️

⚡ Pathophysiology - why speed matters

• Cause: usually plaque rupture or erosion → platelet activation + thrombin generation → acute coronary thrombotic occlusion.
• Wavefront necrosis: infarction spreads from endocardium to epicardium over hours; early reperfusion salvages myocardium and preserves LV function.
• Electrical instability: acute ischaemia increases VT/VF risk early; hence monitoring and defibrillator readiness.

🩺 Clinical features - typical and atypical

• Typical pain: central crushing/tight chest pain lasting >20 minutes, with or without radiation to jaw, left arm, neck or back.
• Associated symptoms: dyspnoea, sweating 😰, nausea/vomiting, palpitations, syncope or sense of doom.
• Atypical presentations: older adults, women, diabetes and CKD may present with dyspnoea, collapse, epigastric discomfort, confusion or minimal pain.
• Examination clues: hypotension/shock, pulmonary oedema, new pansystolic murmur, bradycardia in inferior/RV MI, or arrhythmia.

📉 ECG diagnosis - STEMI and STEMI equivalents

• ST elevation in ≥2 contiguous leads supports STEMI when consistent with symptoms and clinical context.
• V2–V3: use sex/age-specific thresholds; commonly ≥2 mm in men and ≥1.5 mm in women, with higher thresholds often used in younger men.
• Other leads: ≥1 mm ST elevation in at least 2 contiguous leads.
• Posterior MI: ST depression V1–V3 with tall R waves → record V7–V9; posterior ST elevation supports STEMI pathway.
• Right ventricular MI: consider with inferior STEMI + hypotension → record V3R/V4R; avoid nitrates if RV infarct suspected.
• LBBB or paced rhythm: new LBBB alone is not diagnostic, but ischaemic symptoms with concordant ST changes or strong clinical suspicion should trigger urgent senior/cardiology review and possible STEMI pathway activation.
• Repeat ECGs: repeat if symptoms persist or evolve because dynamic STEMI can be missed on the first trace.

🧪 Troponin - do not wait for it

• Troponin supports diagnosis and risk assessment, but STEMI is a clinical + ECG diagnosis requiring immediate reperfusion when clear.
• High-sensitivity troponin may be normal early, so a normal initial troponin does not exclude acute coronary occlusion.
• Bedside echo can help if the diagnosis is unclear, for example regional wall motion abnormality, but should not delay reperfusion when STEMI is clear.

🚑 Immediate actions - first 5–10 minutes

• ABCDE, activate cath lab / STEMI pathway early, and involve a senior decision-maker.
• Cardiac monitor + defibrillator ready ⚡; treat VT/VF according to ALS.
• 12-lead ECG and repeat if evolving; consider posterior and right-sided leads when indicated.
• IV access x2, point-of-care glucose and bloods, but do not delay reperfusion.
• Oxygen only if hypoxaemic: target 94–98%, or 88–92% if at risk of hypercapnic respiratory failure.
• Do not delay reperfusion for CXR unless there is strong suspicion of aortic dissection or another diagnosis requiring immediate imaging.

💊 Symptom relief - analgesia and anti-ischaemic treatment

• Opioid analgesia: IV morphine or diamorphine titrated to pain, plus antiemetic such as metoclopramide or ondansetron if needed.
• GTN: sublingual or IV for ongoing pain and hypertension if no contraindications.
• Avoid GTN in hypotension, suspected RV infarct, severe aortic stenosis or recent PDE5 inhibitor use.
• Positioning: upright if pulmonary oedema; supine/legs elevated if hypotensive while treating shock.

🩸 Antiplatelet therapy - NICE NG185

✅ Core: aspirin + a P2Y12 inhibitor. NICE specifies prasugrel + aspirin for STEMI undergoing primary PCI in people not already taking an oral anticoagulant, with age, weight and bleeding cautions.

• Aspirin: 300 mg loading dose as soon as possible, chewed/crushed if needed, then 75 mg daily long-term unless contraindicated.
• If primary PCI is planned and not on oral anticoagulant: offer prasugrel + aspirin.
• Prasugrel cautions: avoid if previous stroke/TIA; consider alternatives if age ≥75 years, body weight <60 kg, frailty or high bleeding risk.
• If prasugrel is unsuitable, consider ticagrelor or clopidogrel with aspirin according to cardiology/local pathway.
• If already taking an oral anticoagulant: offer clopidogrel + aspirin.
• If STEMI is not treated with PCI: offer ticagrelor + aspirin unless bleeding risk is high; if high bleeding risk, consider clopidogrel + aspirin or aspirin alone. If fibrinolysis is used, follow the local fibrinolysis protocol for the immediate P2Y12 choice and timing.

🧬 Antithrombin / anticoagulation - match to strategy

• Primary PCI with radial access: offer UFH with bailout glycoprotein IIb/IIIa inhibitor.
• If femoral access is needed: consider bivalirudin with bailout glycoprotein IIb/IIIa inhibitor.
• If fibrinolysis is given: give an antithrombin at the same time, according to local protocol.
• Avoid routine pre-hospital fibrinolysis or routine GP IIb/IIIa inhibitor use when primary PCI is planned.
• Renal function: adjust dosing where relevant and monitor bleeding risk closely.

⚡ Reperfusion strategy - NICE NG185 + ESC 2023 framing

• Primary PCI preferred: offer coronary angiography with follow-on primary PCI if indicated when presentation is within 12 hours of symptom onset and primary PCI can be delivered within 120 minutes of the time fibrinolysis could have been given.
• Fibrinolysis: offer if within 12 hours, timely primary PCI is not achievable, and there are no contraindications to fibrinolysis.
• Cardiogenic shock: offer urgent coronary angiography with follow-on PCI if indicated; consider even after 12 hours if ongoing ischaemia or shock persists.
• Late presenters >12 hours: consider angiography/PCI if ongoing ischaemia, haemodynamic instability, malignant arrhythmias or shock.
• System delay: where possible, bypass non-PCI centres and move directly to cath lab in confirmed STEMI.

💉 If fibrinolysis is used - what next?

• Give antithrombin at the same time as fibrinolysis.
• Repeat ECG at 60–90 minutes after fibrinolysis.
• Failed reperfusion: persistent ST elevation or ongoing pain → offer immediate coronary angiography with follow-on PCI if indicated; do not repeat fibrinolysis.
• Recurrent ischaemia: seek urgent cardiology advice and consider angiography/PCI.
• Successful fibrinolysis and stable: consider angiography during the same admission.

🩻 Cath lab / in-hospital strategy - NICE NG185

• Access: radial preferred when feasible.
• Stent choice: offer drug-eluting stent if stenting is indicated.
• Thrombus management: thrombus aspiration may be considered during primary PCI, but mechanical thrombus extraction should not be used routinely.
• Multivessel disease:
  • If no shock: offer complete revascularisation, often during index admission or staged.
  • If cardiogenic shock: consider culprit-only revascularisation during the index procedure.
• LV function: assess LV function in all STEMI patients, ideally before discharge or in early follow-up.

🧠 Special situations - high yield

• Inferior STEMI + hypotension: think RV infarct; record right-sided leads; avoid nitrates; treat with cautious fluids and urgent reperfusion.
• Posterior MI: record V7–V9; treat as STEMI equivalent if posterior ST elevation is present.
• Cardiac arrest with ROSC: if ECG/clinical picture suggests acute coronary occlusion, urgent cath lab discussion is warranted according to local network protocol.
• Suspected aortic dissection: tearing pain radiating to back, pulse/BP differential, new aortic regurgitation murmur or mediastinal widening → avoid anticoagulants/thrombolysis and image urgently.

💓 Beta-blockers, ACEi/ARB, MRA - inpatient and discharge

• ACE inhibitor / ARB: start when haemodynamically stable, especially with LV dysfunction, anterior MI, diabetes, hypertension or CKD; titrate to target doses.
• Beta-blocker: offer after MI unless contraindicated; particularly important with LV dysfunction, heart failure, arrhythmia or ongoing angina. Avoid or withhold in shock, acute pulmonary oedema, severe bradycardia, heart block or severe asthma.
• Aldosterone antagonist, e.g. eplerenone: consider if LVEF ≤40% with heart failure or diabetes after MI; monitor potassium and renal function closely.
• High-intensity statin: start early unless contraindicated and continue long-term.

🩹 Secondary prevention - what saves lives long-term

• DAPT: aspirin + P2Y12 inhibitor as directed, often up to 12 months; shorter if bleeding risk high, longer only in selected high-ischaemic-risk cases under specialist advice.
• Statin: high-intensity statin long-term; consider add-on lipid therapy in very high-risk patients if targets are not met.
• BP, diabetes, smoking: aggressive risk factor control; smoking cessation has one of the largest absolute benefits.
• Cardiac rehab: structured rehab improves outcomes and adherence; include exercise prescription, education and psychosocial support.
• Vaccination: influenza and other vaccinations according to risk group/local policy to reduce infection-triggered events.

📅 Inpatient monitoring and complications to watch for

• Arrhythmias: VT/VF early; AF; bradyarrhythmias in inferior MI; monitor and treat according to ALS/cardiology guidance.
• Heart failure / pulmonary oedema: diuretics, nitrates if BP allows, ventilatory support if needed, and assess LVEF.
• Mechanical complications, often 2–7 days: papillary muscle rupture causing acute MR, VSD, free wall rupture causing tamponade; suspect if sudden shock or new murmur.
• Pericarditis: pleuritic pain and pericardial rub early; Dressler syndrome later.

📊 Risk stratification - use the right tools

• Reperfusion decisions in STEMI are ECG + time + clinical status driven, not primarily GRACE/TIMI driven.
• After reperfusion, prognosis is guided by:
  • Killip class / heart failure severity.
  • LVEF on echo.
  • Extent of coronary disease and success of revascularisation.
  • Bleeding risk, renal function, frailty and complications during admission.
• GRACE is primarily a NSTEMI/unstable angina risk tool and is not the main determinant for acute STEMI reperfusion.

💡 Teaching pearl: A normal early troponin does not exclude STEMI. The life-saving decision is whether the ECG and clinical picture require immediate reperfusion. STEMI is a coronary occlusion problem first; troponin is confirmatory, but reperfusion is therapeutic.

🧠 Pathophysiology pearl: STEMI usually occurs when plaque rupture or erosion triggers platelet-rich thrombus and complete coronary occlusion. Myocardial necrosis spreads as a wavefront from subendocardium to epicardium, so every delay reduces salvageable myocardium. This is why the pathway prioritises rapid ECG recognition, antithrombotic therapy and immediate reperfusion.

📚 References - guidelines

• NICE NG185: Acute coronary syndromes - overview
• NICE NG185: Recommendations - STEMI pathway, antiplatelets, anticoagulation and reperfusion timings
• NICE NG185: STEMI visual summary
• ESC 2023 Guidelines: Acute Coronary Syndromes
• ESC 2023 ACS Guidelines - PubMed record