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IM2.{14-16,19-20,23} | ACS Acute Management — SDL Guide

Learning Objectives

• Describe the indications for CCU admission and the components of supportive care in ACS
• Discuss the medications used in ACS — antiplatelet agents, anticoagulants, nitrates, beta-blockers, ACE inhibitors, and GPIIb/IIIa inhibitors — with their indications, contraindications, and mechanisms
• Describe the indications for thrombolysis, primary PCI, and CABG in ACS
• Describe the pathogenesis, recognition, and management of ACS complications — arrhythmias, cardiogenic shock, LV dysfunction, papillary muscle rupture, and pericarditis
• Discuss the assessment and relief of pain in ACS

INSTRUCTIONS

This module covers the full arc of ACS acute management: from the moment of admission through CCU supportive care, pharmacotherapy, reperfusion decision-making, complication management, and pain control. Every drug and procedural decision has a specific indication, contraindication, and timing window that must be understood mechanistically, not merely memorised.

References

• Harrison's Principles of Internal Medicine, 21st ed., Ch. 295 — Ischaemic Heart Disease (textbook)
• API Textbook of Medicine, 10th ed., Ch. on ACS Management (textbook)
• ESC 2023 Guideline for Acute Coronary Syndromes (guideline)
• ACC/AHA 2022 Guideline for Chest Pain and ACS Management (guideline)

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Version 2.0 | NMC CBUC 2024

Clinical Presentation of ACS Complications

Understanding the clinical presentations of ACS complications is the foundation for recognising them at the bedside — before haemodynamic collapse makes intervention more difficult. The complications of ACS can be classified into electrical (arrhythmias and conduction disturbances), mechanical (structural failures of the heart), and inflammatory/pericardial (pericarditis). Each has a characteristic timing after MI onset, a pathological mechanism directly tied to the infarct territory, and a clinical presentation that is recognisable if you know what to look for. The electrical complications tend to dominate the first 24 hours, the mechanical complications emerge on days 2–5 as the necrotic myocardium undergoes enzymatic softening, and the pericardial complications span from day 1 (early epistenocardial pericarditis) to weeks 2–8 (Dressler syndrome). Knowing this temporal pattern converts complication recognition from memorisation into pattern-based clinical reasoning — if it is day 3 and a new murmur appears, you are immediately thinking papillary muscle rupture or VSD; if it is day 1 and the patient has pleuritic pain, you are thinking early pericarditis.

Electrical complications — arrhythmias:
- Ventricular fibrillation (VF): the most common cause of sudden death in the first 24 hours of STEMI, due to re-entry circuits in the border zone of ischaemic and non-ischaemic myocardium. Presents as sudden haemodynamic collapse without a palpable pulse; ECG shows chaotic high-amplitude waveforms with no discernible P or QRS complexes. Immediate defibrillation is the only effective treatment — precordial thump is no longer recommended (Class III in current guidelines). CPR while charging the defibrillator.
- Ventricular tachycardia (VT): monomorphic VT (regular wide-complex tachycardia at >100/min) in the context of acute MI indicates significant myocardial ischaemia. Sustained VT >30 seconds or causing haemodynamic compromise requires synchronised DC cardioversion. Lidocaine (1–1.5 mg/kg IV bolus) or amiodarone (150 mg IV over 10 minutes) are pharmacological options for termination or suppression.
- Accelerated idioventricular rhythm (AIVR): a regular wide-complex rhythm at 60–100/min occurring in the first 12–24 hours post-MI or after successful reperfusion — the 'reperfusion arrhythmia'; usually benign and self-terminating; does NOT require treatment and should not be confused with VT (rate distinguishes them)
- Sinus bradycardia with inferior STEMI: Bezold-Jarisch reflex (vagal activation) causes sinus bradycardia or Mobitz type I (Wenckebach) AV block — usually resolves with reperfusion; atropine (0.5 mg IV, repeated to 3 mg total) if symptomatic bradycardia (HR <40, haemodynamic compromise). Complete heart block (CHB) with inferior STEMI: indicates involvement of the AV nodal artery (branch of RCA); usually transient with reperfusion but may require temporary pacing (transcutaneous pacing as bridge, then transvenous if persistent).
- New LBBB or complete heart block with anterior STEMI (LAD occlusion with septal involvement): indicates bilateral bundle branch block territory infarction; high risk of progression to complete heart block or asystole; prophylactic temporary pacemaker required.
- Atrial fibrillation (new onset): occurs in ~10% of STEMI patients, usually in the context of LV dysfunction or haemodynamic compromise; associated with increased thromboembolic risk (anticoagulation) and rate or rhythm control as indicated

Mechanical complications — these are life-threatening structural failures occurring 2–5 days post-MI (peak at day 3–5 as necrotic myocardium undergoes autolytic softening):
- Free wall rupture: catastrophic — sudden haemodynamic collapse, electromechanical dissociation (EMD/PEA on monitor, organised QRS without pulse), cardiac tamponade (elevated JVP, hypotension, muffled heart sounds — Beck's triad). Rare (1–3% of untreated STEMI), more common in older women, first MI, anterior location, and hypertension. Emergency pericardiocentesis for temporising, followed by immediate surgical repair.
- Ventricular septal defect (VSD): septal rupture due to necrosis of the interventricular septum (proximal LAD territory). Presents as sudden haemodynamic deterioration with a new harsh pansystolic murmur at the left sternal border, confirmed by echo (colour Doppler shows L→R shunt across the septum). Surgical repair or transcatheter closure urgently after initial stabilisation with vasodilators (if not in shock) and intra-aortic balloon pump.
- Papillary muscle rupture: ischaemia of the posteromedial papillary muscle (single RCA supply, unlike anterolateral which has dual supply) causes partial or complete rupture, producing acute mitral regurgitation. Presents as a new pansystolic murmur at the apex radiating to the axilla, with acute pulmonary oedema (the regurgitation is acute, the LA has no time to dilate, LV pressure transmitted backwards). Surgical mitral valve repair/replacement urgently. Echo differentiates from VSD by murmur quality and colour Doppler findings.

Pericardial complications:
- Early pericarditis (epistenocardial pericarditis): inflammatory reaction of the pericardium overlying the infarcted zone, occurring on day 1–2. Presents as sharp, pleuritic chest pain (worse supine, better sitting forward), pericardial friction rub on auscultation. ECG: widespread saddle-shaped ST elevation (but this may be difficult to distinguish from residual STEMI changes in the acute phase). Treated with high-dose aspirin (1000 mg TDS × 2 weeks) or colchicine (0.5 mg BD × 3 months) — NSAIDs other than aspirin are avoided in the acute MI phase as they impair myocardial healing.
- Dressler syndrome: autoimmune pericarditis occurring 2–8 weeks post-MI (immune complex deposition in the pericardium). Presents with fever, pericarditic chest pain, pleural effusion, pericardial rub. Treat with NSAIDs or colchicine; corticosteroids if refractory. Anticoagulation risk increases with large effusion.

Timeline of ACS Complications After MI

Pathophysiology: Why Each ACS Complication Occurs

Each ACS complication has a specific pathophysiological mechanism tied to the territory and depth of infarction, the time course of myocardial necrosis, and the structure-specific vulnerability of different cardiac components. Understanding these mechanisms is not merely academic — it predicts which complication is most likely in a given clinical scenario and explains why the management of each complication differs fundamentally.

Arrhythmic mechanism: In the first minutes to hours of coronary occlusion, the ischaemic zone generates electrical heterogeneity — adjacent cells have different resting potentials, action potential durations, and refractory periods. This heterogeneity creates re-entry circuits in the peri-infarct border zone, which are the substrate for VF and VT. The longer the ischaemia, the more extensive the zone of heterogeneity and the greater the arrhythmic risk. Reperfusion (by PCI or thrombolysis) reduces arrhythmic risk by restoring homogeneous conduction, though it can itself cause brief arrhythmia (reperfusion arrhythmia = AIVR). Hypokalaemia, hypomagnesaemia, and acidosis amplify arrhythmic risk — electrolyte correction is a critical supportive measure.

Conduction disturbance mechanism: The AV node is supplied by the AV nodal artery, a branch of the RCA in 90% of individuals. Inferior STEMI (RCA occlusion) can therefore interrupt AV nodal blood supply, causing Wenckebach (Mobitz I) or complete heart block. This is typically infra-nodal (His bundle level), generally resolves with reperfusion, and responds to atropine. In contrast, anterior STEMI involving the septum (proximal LAD) causes bilateral bundle branch block (RBBB + LAFB or LPFB) or complete heart block — this is a His-Purkinje level block, does NOT respond to atropine, and requires pacemaker insertion.

Mechanical complication mechanism: The necrotic myocardium undergoes two phases of structural change: early oedema and softening (hours 1–72), and then enzymatic autolysis by macrophage-mediated matrix metalloproteinases (days 3–5). The softened myocardium is mechanically vulnerable — it can rupture (free wall, septum) or fail to support the attached papillary muscle. The posteromedial papillary muscle is uniquely vulnerable because it receives its entire blood supply from a single vessel (the right posterior descending artery from the RCA), whereas the anterolateral papillary muscle has dual supply (LAD + LCx). This explains why papillary muscle rupture occurs predominantly in inferior STEMI (RCA territory) rather than anterior MI. The pressure gradient between the LV and the RV (or LA) determines the haemodynamic impact of VSD (L→R shunt, volume overload of the RV) and papillary muscle rupture (acute MR, massive LA pressure elevation and pulmonary oedema).

Dressler syndrome mechanism: Autoimmune pericarditis and pleuritis developing weeks after MI is caused by immune sensitisation to cardiac antigens (myosin, actin) released from the necrotic myocardium. T-lymphocyte activation and immune complex deposition in the pericardium produce the inflammatory response. The time course (2–8 weeks) is consistent with the adaptive immune response cycle. The same mechanism may occur weeks to months after cardiac surgery ('post-cardiac injury syndrome' or 'post-pericardiotomy syndrome').

Diagnosis and Investigation in Acute ACS Management

The diagnostic investigation in ACS acute management overlaps with the diagnostic module but focuses here on specific investigations that directly drive management decisions — distinguishing STEMI from NSTEMI (reperfusion vs risk-stratified invasive), identifying complications (echo, haemodynamic monitoring), and risk-stratifying severity (Killip class, GRACE score, TIMI score).

The CCU (Coronary Care Unit) admission criteria derive directly from these diagnostic assessments. A patient with suspected ACS requires CCU admission when any of the following are present: confirmed STEMI or high-risk NSTE-ACS (GRACE score >140), haemodynamic instability (Killip class II–IV, hypotension, tachycardia indicating low cardiac output), high-grade arrhythmia (VT, VF, CHB, new LBBB), or clinical need for continuous monitoring during the diagnostic phase. The CCU provides continuous cardiac monitoring, defibrillator availability, and immediate access to reperfusion therapy. Lower-risk patients (GRACE score <109, NSTE-ACS with negative troponin on serial testing) may be managed in a monitored step-down unit or observation ward.

The GRACE score is the validated risk stratification tool for NSTE-ACS and guides the timing of coronary angiography: GRACE >140 (high risk) → immediate invasive (angiography within 24 hours); GRACE 109–140 (intermediate) → early invasive (within 72 hours); GRACE <109 (low risk) → selective invasive (guided by stress imaging or non-invasive assessment). The TIMI risk score (7 variables: age ≥65, ≥3 CAD risk factors, prior stenosis ≥50%, ST deviation, ≥2 anginal events in 24h, aspirin use in past 7 days, elevated cardiac markers) is used at NSTE-ACS presentation: score 0–2 = low risk; 3–4 = intermediate; 5–7 = high risk.

Haemodynamic monitoring in cardiogenic shock (Killip IV): Continuous intra-arterial blood pressure monitoring (radial arterial line) provides real-time BP measurement more accurately than non-invasive cuffs in shock. Central venous pressure monitoring guides fluid management in RV infarction. Pulmonary artery catheterisation (Swan-Ganz catheter) may be used to measure pulmonary capillary wedge pressure (PCWP) — elevated PCWP (>18 mmHg) confirms LV failure (vs. volume depletion); very high PCWP (>25 mmHg) correlates with pulmonary oedema. However, routine Swan-Ganz use in ACS cardiogenic shock is not supported by randomised trials (ESCAPE trial) — clinical and echocardiographic assessment usually suffices.

Bedside echocardiography (point-of-care ultrasound, POCUS) provides rapid assessment of LVEF, regional wall motion, pericardial effusion, and mechanical complications in haemodynamically unstable ACS patients. A LVEF <30–35% in anterior STEMI indicates extremely high risk of cardiogenic shock and should prompt early escalation of support (inotropes, intra-aortic balloon pump or mechanical circulatory support).

ACS Management Pathway: STEMI vs NSTE-ACS