Contents
Overview
Acute coronary syndromes (ACS) may present de novo in the ICU or complicate pre-existing critical illness. The critically ill patient poses particular diagnostic and therapeutic challenges: altered physiology, polypharmacy, haemodynamic instability, and frequent troponin elevation from non-ischaemic causes.
ACS in the ICU carries a high mortality, particularly when complicated by cardiogenic shock, ventricular arrhythmia, or mechanical complications.
Pathophysiology
The majority of ACS results from disruption of an atheromatous plaque, with subsequent platelet aggregation, thrombus formation, and coronary artery occlusion. The extent of myocardial injury depends on the duration and completeness of occlusion, coronary collateral supply, and myocardial oxygen demand.
A clinically important distinction in ICU patients is between:
Type 1 MI — atherothrombotic plaque rupture or erosion causing coronary thrombosis.
Type 2 MI — supply-demand mismatch without primary plaque rupture. Occurs in the context of tachycardia, hypotension, hypoxia, anaemia, or vasospasm. Common in critical illness. Troponin elevation in this setting does not indicate coronary artery disease and does not warrant the same interventional approach.
Differentiating type 1 from type 2 is essential, as management strategies differ fundamentally.
Classification
STEMI — ST elevation ≥1 mm in two or more contiguous limb leads, or ≥2 mm in V1–V3, or new left bundle branch block. Indicates complete occlusion requiring immediate reperfusion.
NSTEMI — Troponin rise with ischaemic symptoms, ECG changes (ST depression, T-wave inversion), or both, but without ST elevation criteria. Indicates partial or intermittent occlusion.
Unstable angina — Ischaemic symptoms without troponin elevation. Increasingly rare with high-sensitivity troponin assays.
Mechanical complications of MI:
- Ventricular free wall rupture
- Ventricular septal defect (VSD)
- Papillary muscle rupture → acute mitral regurgitation
- Right ventricular infarction
These typically present 2–7 days post-MI with sudden haemodynamic deterioration and require urgent surgical or percutaneous intervention.
Management
STEMI
Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion strategy. Target door-to-balloon time is under 90 minutes.
Thrombolysis is used only when PPCI is unavailable within 120 minutes of first medical contact and there are no contraindications.
Antiplatelet therapy: aspirin 300 mg loading dose, then 75 mg daily. Add a P2Y12 inhibitor (ticagrelor 180 mg loading, or prasugrel in suitable patients). Clopidogrel is an alternative if others are contraindicated.
Anticoagulation: unfractionated heparin during PCI; alternatives include bivalirudin or enoxaparin depending on bleeding risk and institutional preference.
Beta-blockade: initiate once haemodynamically stable. Avoid if bradycardia, heart block, or acute decompensated heart failure.
NSTEMI
Risk stratification guides the urgency of invasive strategy:
- GRACE score >140, troponin rise, dynamic ECG changes, haemodynamic instability, or ventricular arrhythmia → early invasive strategy within 24 hours
- Lower-risk patients → invasive strategy within 72 hours
Antiplatelet and anticoagulation therapy as for STEMI, without the urgency of immediate catheterisation.
Cardiogenic Shock
Cardiogenic shock complicates 5–10% of STEMI. Managed with immediate PPCI of the culprit vessel. Inotropic support with dobutamine or adrenaline. Mechanical circulatory support (intra-aortic balloon pump, Impella, or venoarterial ECMO) is considered in refractory shock.
The CULPRIT-SHOCK trial demonstrated that immediate multivessel PCI worsens 30-day mortality compared with culprit-only revascularisation — staged procedures are performed once stabilised.
Nitrates
Glyceryl trinitrate reduces ischaemic pain and preload. Avoid in right ventricular infarction (inferior STEMI with right-sided ST changes) and in the presence of hypotension or recent phosphodiesterase-5 inhibitor use.
Key Trials
DANAMI-2 — Randomised 1572 patients with STEMI to primary PCI vs thrombolysis. PCI reduced the composite of death, reinfarction, and stroke at 30 days (8.0% vs 13.7%), establishing PPCI as the preferred reperfusion strategy.
PLATO — Compared ticagrelor with clopidogrel in 18,624 ACS patients. Ticagrelor reduced death from vascular causes, MI, or stroke (9.8% vs 11.7%) without a significant increase in overall major bleeding. Ticagrelor is now preferred over clopidogrel in ACS.
CULPRIT-SHOCK — In 706 patients with STEMI and cardiogenic shock, culprit-only PCI reduced 30-day mortality compared with immediate multivessel PCI (43.3% vs 51.6%). Staged revascularisation of non-culprit vessels is performed after recovery.
Viva Questions
How do you distinguish type 1 from type 2 MI in a critically ill patient?
Type 1 MI results from plaque rupture with coronary thrombosis and tends to present with a typical ischaemic pattern — new ST changes, regional wall motion abnormality on echocardiography, and a troponin rise with the characteristic rise-and-fall kinetics. Type 2 MI occurs when myocardial oxygen demand exceeds supply in the absence of primary plaque rupture, commonly seen in the context of hypotension, sepsis, tachyarrhythmia, anaemia, or hypoxia. The troponin rise may be more modest and the ECG changes less specific. Echocardiography can help identify regional wall motion abnormalities suggesting a coronary territory, but non-ischaemic myocardial injury (myocarditis, takotsubo) may also produce regional changes. Coronary angiography is the definitive investigation when type 1 MI is suspected and the patient is stable enough to proceed. In type 2 MI, the priority is to identify and correct the underlying precipitant rather than pursuing coronary intervention.
How would you manage STEMI in a ventilated ICU patient?
The principles remain the same: achieve reperfusion as rapidly as possible. The patient should be transferred to a cardiac catheterisation laboratory for PPCI if this can be done within 90 minutes. Aspirin 300 mg and a P2Y12 inhibitor should be administered via nasogastric tube if the patient cannot swallow. Anticoagulation with unfractionated heparin is given procedurally. Haemodynamic support must be established before and during transfer — ensure adequate vasopressor and inotropic infusions, and consider mechanical circulatory support if cardiogenic shock is present. The anaesthetic and ICU team should accompany the patient to the catheterisation laboratory. Post-procedure, the patient returns to the ICU for ongoing monitoring, management of arrhythmias, and assessment for mechanical complications.
What are the mechanical complications of MI and how do you recognise them?
The three principal mechanical complications are ventricular free wall rupture, ventricular septal defect, and acute mitral regurgitation due to papillary muscle rupture. All typically present 2–7 days after MI with sudden haemodynamic deterioration. Free wall rupture causes cardiac tamponade and electromechanical dissociation — it is usually rapidly fatal. VSD presents as a new pansystolic murmur with a step-up in oxygen saturation from right atrium to right ventricle on Swan-Ganz catheterisation, and haemodynamic deterioration; echocardiography confirms the defect. Acute mitral regurgitation from papillary muscle rupture (more commonly the posteromedial papillary, supplied by a single artery) causes flash pulmonary oedema; echocardiography shows the flail leaflet and severe regurgitation. All three require urgent surgical or percutaneous intervention. Intra-aortic balloon pump and/or mechanical circulatory support stabilise patients as a bridge to definitive treatment.
What is the evidence for intra-aortic balloon pump in cardiogenic shock?
The IABP-SHOCK II trial randomised 600 patients with cardiogenic shock complicating MI to IABP or no IABP, all undergoing early revascularisation. There was no difference in 30-day mortality (39.7% vs 41.3%), and no benefit was seen at 12 months. Despite this, IABP is still used in some centres as a bridge to definitive mechanical support or surgery, particularly in the context of mechanical complications. Percutaneous ventricular assist devices (Impella) and venoarterial ECMO are increasingly used in refractory cardiogenic shock, though high-quality evidence demonstrating mortality benefit remains limited.