Myocardial Infarction — Clinical Deep Dive
Myocardial Infarction is defined as myocardial cell death due to prolonged ischaemia. Clinically, it is diagnosed when there is a rise and/or fall of cardiac troponin (cTn) with at least one value above the 99th percentile upper reference limit (URL) AND at least one of:
- ① Symptoms of acute myocardial ischaemia
- ② New ischaemic ECG changes
- ③ Development of pathological Q waves
- ④ Imaging evidence of new loss of viable myocardium or new RWMA
- ⑤ Identification of coronary thrombus by angiography or autopsy
MI Classification Types:
Spontaneous MI due to atherosclerotic plaque rupture, erosion, fissuring, or dissection causing intraluminal thrombus → myocardial ischaemia → necrosis. This is the "classic heart attack."
MI secondary to oxygen supply-demand mismatch — NOT due to acute coronary plaque disruption. Causes: tachyarrhythmia, hypotension, severe anaemia, coronary spasm, coronary embolism, respiratory failure.
MI resulting in death when biomarker values are unavailable. Sudden cardiac death with symptoms suggestive of ischaemia + presumed new ECG changes or VF, but death occurs before blood samples or troponin rise.
MI related to PCI (≤48 hrs). Troponin >5× URL with normal baseline OR >20% rise if elevated baseline + ischaemic symptoms/ECG/angiographic findings/imaging.
MI related to stent thrombosis — documented by angiography or autopsy using Academic Research Consortium criteria.
MI related to CABG. Troponin >10× URL within 48 hours + new pathological Q waves OR angiographic graft/native artery occlusion OR new RWMA.
The ischaemic cascade is the sequential pathophysiological response to myocardial oxygen deprivation. From my ICU experience, understanding this cascade is critical for timing interventions:
Aerobic metabolism ceases. Shift to anaerobic glycolysis → lactate accumulation → intracellular acidosis. ATP production drops from 36 to 2 molecules per glucose. Creatine phosphate reserves depleted within seconds.
ATP depletion impairs calcium reuptake into sarcoplasmic reticulum → diastolic relaxation failure → ↑ LVEDP. This is detectable by Doppler echo (E/A reversal) BEFORE any systolic impairment. Clinically: dyspnoea, pulmonary congestion onset.
Regional wall motion abnormalities appear. Hypokinesis → akinesis → dyskinesis. If >40% of LV wall involved → cardiogenic shock. The LVEF begins to decline. This is the "stunned" myocardium phase — potentially reversible with reperfusion.
ECG changes follow functional impairment. Sequence: Tall hyperacute T waves → ST elevation → Q wave development. In the ER, I've seen hyperacute T waves precede ST elevation by 15–30 minutes — this is the window where early recognition saves lives.
Adenosine, bradykinin, & lactate stimulate cardiac nociceptors (C-fibres via sympathetic afferents → T1–T5 dorsal root ganglia). Referred pain: left arm, jaw, epigastrium. Inferior MI → vagal activation (Bezold-Jarisch reflex) → bradycardia + hypotension. Anterior MI → sympathetic surge → tachycardia + hypertension.
Necrosis begins subendocardially and progresses transmurally over hours (Reimer & Jennings "wavefront of necrosis"). Subendocardium is most vulnerable due to: highest metabolic demand, highest wall tension (Laplace's law), compression during systole, furthest from epicardial coronary supply. This is WHY "time is muscle" — every minute of delay = more transmural extension.
Correlating ECG leads with coronary territory is the single most important skill in acute MI management. From my experience, getting this right in the first 5 minutes dictates the entire treatment pathway:
| ECG Leads | Territory | Artery | Clinical Pearl |
|---|---|---|---|
| V1–V4 | Anterior | LAD | Highest mortality. Pump failure, cardiogenic shock. "Widow maker" if proximal LAD. |
| II, III, aVF | Inferior | RCA (85%) / LCx (15%) | Always check V4R for RV infarct. Avoid nitrates + diuretics if RV involved → volume dependent. |
| I, aVL, V5–V6 | Lateral | LCx / Diagonal | Often "electrically silent" — LCx occlusion may show only subtle changes. High index of suspicion needed. |
| V1–V3 (reciprocal ST↓) | Posterior | LCx / PDA | Check V7–V9 (posterior leads). Tall R in V1 + ST depression V1-V3 = posterior MI until proven otherwise. |
| V3R, V4R | Right Ventricle | Proximal RCA | Hypotension + clear lungs + elevated JVP = RV MI triad. Fluid challenge, NOT diuretics. Avoid morphine & nitrates. |
STEMI
- Pathology: Complete thrombotic coronary occlusion → transmural ischaemia
- ECG: ST elevation ≥1mm in ≥2 contiguous leads (≥2mm in V1-V3 for men ≥40, ≥2.5mm in V1-V3 for men <40, ≥1.5mm in V1-V3 for women)
- Troponin: Markedly elevated — but DO NOT wait for troponin to initiate reperfusion
- Management: Emergent reperfusion — Primary PCI (preferred) within 90 min OR Thrombolysis within 30 min if PCI not available within 120 min
- STEMI Equivalents: New LBBB (Sgarbossa criteria), de Winter T waves, Wellens syndrome (LAD), posterior MI pattern, isolated ST elevation in aVR (left main / 3-vessel)
NSTEMI / Unstable Angina
- Pathology: Partial/subtotal occlusion OR complete occlusion with collateral supply → subendocardial ischaemia
- ECG: ST depression ≥0.5mm, T-wave inversion, or transient ST elevation, or even normal ECG
- Troponin: Elevated in NSTEMI; normal in Unstable Angina (UA). High-sensitivity troponin (hs-cTn) with serial measurements at 0h/1h or 0h/3h protocol
- Risk Stratification: GRACE score determines timing of angiography: Very high risk → <2h, High risk → <24h, Intermediate → <72h, Low risk → non-invasive testing first
- Very High Risk Criteria: Haemodynamic instability, recurrent/ongoing chest pain refractory to medical Rx, life-threatening arrhythmias, mechanical complications, acute HF, recurrent dynamic ST/T changes
⚡ CLINICAL PEARL FROM ICU EXPERIENCE
"In my years in the CCU, I've learned that the first 10 minutes are about RECOGNITION, the next 20 are about STABILIZATION, and everything after is about REPERFUSION. The biggest killer isn't the MI itself — it's delay."
2-4mg IV q5-15min PRN. Reserve for pain refractory to nitrates. ⚠️ AVOID in RV infarct, hypotension, respiratory depression. Modern guidelines de-emphasize morphine — may mask ongoing ischaemia and delay recognition of complications. Fentanyl 25-50mcg IV is an alternative.
Only if SpO₂ <90% or respiratory distress. AVOID routine O₂ in normoxic patients — DETO₂X trial showed potential harm with hyperoxia (coronary vasoconstriction, increased ROS). Target SpO₂ 94-98%.
GTN 0.4mg SL q5min ×3, then IV infusion (5-200 mcg/min) titrate to pain relief and BP. CONTRAINDICATIONS: SBP <90, HR <50 or >100, RV infarct, PDE5 inhibitor use within 24-48 hrs, severe aortic stenosis. Mechanism: venodilation → ↓ preload → ↓ MVO₂, plus coronary vasodilation.
Aspirin: 325mg chewable (NOT enteric-coated) stat → 81mg daily thereafter. Irreversible COX-1 inhibition → blocks TXA₂ synthesis → ↓ platelet aggregation.
P2Y12 Inhibitor (load ASAP):
• Ticagrelor 180mg load → 90mg BID (preferred per ESC/AHA — faster onset, reversible, superior to Clopidogrel per PLATO trial)
• Prasugrel 60mg load → 10mg daily (contraindicated if prior stroke/TIA, age ≥75, weight <60kg)
• Clopidogrel 600mg load → 75mg daily (if ticagrelor/prasugrel contraindicated or unavailable, or with thrombolysis)
Beta-Blockers: Metoprolol 5mg IV q5min ×3 (if haemodynamically stable, no HF, no AV block) → then oral 25-50mg q6-12h. ↓ HR, ↓ contractility, ↓ MVO₂, ↓ arrhythmia risk. AVOID if: Killip III-IV, SBP <120, HR <60, PR >0.24s, 2nd/3rd degree AV block, active wheeze.
Anticoagulation: UFH 60 U/kg bolus (max 4000U) → 12 U/kg/hr (max 1000U/hr) for PCI pathway. Enoxaparin 0.5mg/kg IV for thrombolysis pathway.
SBP <90 for >30min, CI <2.2, PCWP >18. Usually >40% LV mass infarcted. Mortality 50-80%. Management: Emergent PCI, IABP/Impella, vasopressors (norepinephrine first-line), dobutamine for inotropy.
Day 3-5 post-MI (or Day 1 with thrombolysis). Sudden haemodynamic collapse + PEA. Pericardial tamponade → beck's triad. Almost universally fatal without emergent surgery. Risk factors: first MI, anterior, female, age >70.
Day 3-5. New harsh pansystolic murmur + thrill at left sternal border. Acute L→R shunt → biventricular failure. Confirm by echo with colour Doppler + step-up in O₂ sat from RA→RV. Surgical repair; Impella or IABP as bridge.
Papillary muscle rupture (posteromedial > anterolateral, because posteromedial has single blood supply from PDA). Acute severe MR → flash pulmonary oedema. New systolic murmur (may be soft due to equalization of pressures). Emergent surgery.
Weeks to months post-MI. Persistent ST elevation on ECG (>6 weeks). Thin dyskinetic wall → thrombus formation risk → systemic embolism. Anticoagulation needed. May cause refractory HF or VT.
2-10 weeks post-MI. Autoimmune pericarditis: fever, pleuritic chest pain, pericardial friction rub, pericardial effusion. ESR/CRP elevated. Treatment: Aspirin high-dose + Colchicine. Avoid anticoagulation (haemorrhagic pericarditis risk).