Reperfusion and infarction complications

Clinical comparison: ECG Localization, Culprit Arteries, and Clinical Correlates

• Anteroseptal: Diagnostic Leads: V1, V2, V3, V4; Reciprocal Leads: None or minimal; Culprit Vessel: LAD; High-Yield Clinical Hazards: High risk of bundle branch block, ventricular septal rupture, heart failure
• Extensive Anterior: Diagnostic Leads: V1–V6, I, aVL; Reciprocal Leads: II, III, aVF; Culprit Vessel: Proximal LAD / LMCA; High-Yield Clinical Hazards: Cardiogenic shock, acute pulmonary oedema, primary ventricular fibrillation
• Lateral: Diagnostic Leads: I, aVL, V5, V6; Reciprocal Leads: II, III, aVF; Culprit Vessel: LCx or Diagonal branch; High-Yield Clinical Hazards: Frequently subtle on initial 12-lead ECG; may cause refractory angina
• Inferior: Diagnostic Leads: II, III, aVF; Reciprocal Leads: I, aVL; Culprit Vessel: RCA (85%) or LCx (15%); High-Yield Clinical Hazards: Sinus bradycardia, transient Wenckebach or complete AV block, RVMI
• Right Ventricle: Diagnostic Leads: V4R (V1R–V6R); Reciprocal Leads: None; Culprit Vessel: Proximal RCA; High-Yield Clinical Hazards: Profound preload dependence; severe hypotension with nitrates/diuretics
• Posterior: Diagnostic Leads: V7, V8, V9; Reciprocal Leads: V1, V2, V3 (mirror image); Culprit Vessel: LCx or PDA; High-Yield Clinical Hazards: Overlooked as anterior ischaemia; mandates posterior lead placement

Acute Medical Management & Reperfusion Pathways

Time to myocardial reperfusion is the single greatest determinant of survival in acute STEMI. The Australian standard of care dictates immediate dual antiplatelet therapy, anticoagulation, and rapid triage to reperfusion.

Initial Medical Stabilization

• Aspirin: $300\text{ mg}$ oral soluble/chewed loading dose administered immediately to all patients without confirmed anaphylaxis.
• P2Y12 selection: Check bleeding risk and the reperfusion plan. Prasugrel is contraindicated after prior stroke/TIA; age at least 75 years or weight below 60 kg requires particular caution and regimen selection. Fibrinolysis uses a different antiplatelet pathway from primary PCI.
• Anticoagulation: Intravenous unfractionated heparin (UFH, bolus $70\text{ to }100\text{ units/kg}$) or enoxaparin ($1\text{ mg/kg}$ subcutaneously twice daily, dose-adjusted for age and renal function).
• Oxygen: In ACS, give supplemental oxygen for hypoxaemia; routine oxygen is not recommended when SpO2 is at least 90%. Respiratory failure or another illness may require a different target. Monitor saturation and ventilation rather than prescribing oxygen solely because chest pain is present.
• Nitrates & Analgesia: Sublingual glyceryl trinitrate ($400\text{ mcg}$ spray or tablet every 5 minutes, up to 3 doses) provided systolic BP $> 90\text{ mmHg}$, heart rate is $50\text{ to }100\text{ bpm}$, and no phosphodiesterase-5 inhibitors (e.g., sildenafil within 24 hours, tadalafil within 48 hours) or RVMI are present. Intravenous titrated opioids (fentanyl $25\text{ to }50\text{ mcg}$ or morphine $2.5\text{ to }5\text{ mg}$) provide analgesia and reduce sympathetic drive.

Reperfusion Strategy Selection

• Primary Percutaneous Coronary Intervention (PCI): The gold standard reperfusion modality. Indicated when the anticipated delay from first medical contact (FMC) to balloon inflation is $\le 120\text{ minutes}$ (or $\le 90\text{ minutes}$ if presenting to a PCI-capable hospital).
• Fibrinolysis: If primary PCI cannot be provided within the guideline delay and presentation is appropriate, give fibrinolysis as soon as possible, ideally within thirty minutes of first medical contact, after checking contraindications. Use the age/weight-adjusted antithrombotic pathway, arrange immediate transfer and assess reperfusion. Successful lysis requires subsequent angiography, generally within 2–24 hours; failed reperfusion requires rescue PCI.
• Pharmacoinvasive Strategy: Following fibrinolysis, immediate transfer to a PCI-capable facility is mandatory. Assess ECG at 60 to 90 minutes post-lysis: if ST resolution is $< 50\%$, lysis has failed and rescue PCI is performed immediately. If ST resolution is $\ge 50\%$, routine diagnostic angiography and PCI are performed within 2 to 24 hours.

Mechanical and Electrical Complications

Mechanical complications typically present between day 2 and day 7 post-infarction as necrotic myocardium softens, presenting with sudden haemodynamic collapse and acute pulmonary oedema:

1. Acute Mitral Regurgitation (Papillary Muscle Rupture): Most commonly affects the posteromedial papillary muscle because it receives a single blood supply from the posterior descending artery (RCA or LCx). Conversely, the anterolateral papillary muscle has dual supply from the LAD and LCx. Clinical findings include sudden pulmonary oedema, hypotension, and a new harsh holosystolic murmur maximal at the apex radiating to the axilla. Echocardiography is diagnostic, and emergent surgical valve repair or replacement is lifesaving.
2. Ventricular Septal Rupture (VSR): Transmural necrosis of the interventricular septum creates a left-to-right shunt. Manifests as sudden biventricular failure, cardiogenic shock, and a harsh pansystolic murmur accompanied by a palpable thrill along the left lower sternal border. Pulmonary artery catheterization shows a step-up in oxygen saturation between the right atrium and right ventricle.
3. Left Ventricular Free Wall Rupture: Catastrophic transmural tear resulting in acute haemopericardium, cardiac tamponade, and pulseless electrical activity (PEA) arrest. Mortality approaches 90% without emergent surgical salvage.
4. Conduction disturbances: Inferior infarction can cause AV nodal block; anterior infarction may damage the His–Purkinje system. An unstable bradyarrhythmia requires urgent resuscitation and pacing assessment. Permanent pacing depends on persistence after reversible causes and acute ischaemia have been addressed.

Primary references (checked 7 October 2026): Heart Foundation ACS guideline.