Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise the time-critical electrical, pump and mechanical complications of myocardial infarction and choose the next diagnostic and escalation step.
Post-MI complications are best organised as recurrent ischaemia, electrical instability, pump failure, mechanical rupture, inflammation and thrombosis. The key exam and clinical move is to link the deterioration pattern to urgent bedside echocardiography and definitive specialist treatment.
Mechanical complications often present after an apparent period of stability and can deteriorate within minutes. Revascularisation reduces but does not abolish this risk, particularly after a large or late-presenting infarct.
Management is simultaneous: resuscitate, search for a reversible cause, restore coronary flow when indicated and involve interventional cardiology, cardiac surgery and critical care early.
Extensive transmural necrosis leaves less functioning myocardium and more structurally weakened tissue. Delayed or unsuccessful reperfusion therefore increases pump-failure, arrhythmic and mechanical-complication risk.
Acute stent thrombosis, persistent culprit occlusion or a new plaque event can extend injury or cause reinfarction. Recurrent pain with fresh ischaemic change is a warning pattern.
Anterior or apical injury favours severe left-ventricular dysfunction and mural thrombus; inferior infarction may involve the right ventricle, atrioventricular conduction or papillary muscle.
Inflammation, scar formation and altered loading can produce pericarditis, ventricular aneurysm, functional mitral regurgitation and chronic arrhythmic substrate after the acute necrotic phase.
Ischaemia disrupts membrane potentials, conduction and myocyte contraction. Ventricular arrhythmia, atrioventricular block, regional akinesis or immediate pump failure may therefore accompany the infarct.
During early healing, enzymatic breakdown temporarily reduces tissue strength. The free wall, interventricular septum or papillary muscle may rupture before a mature scar forms.
Surviving myocardium bears greater wall stress, promoting dilatation and fibrosis. Ventricular geometry may worsen functional mitral regurgitation and progress towards chronic systolic heart failure or aneurysm.
Akinetic or aneurysmal ventricular segments permit blood stasis over injured endocardium. Mural thrombus can form and later embolise into the systemic circulation.
Inflammation extending to the adjacent pericardium can cause early pleuritic pain. A later immune-mediated response may produce recurrent pericardial or pleural inflammation and effusion.
Palpitations, syncope, broad-complex tachycardia, VF or cardiac arrest; correct ischaemia, hypoxia and electrolyte disturbance while following the RCUK peri-arrest or ALS algorithm.
Abrupt pulmonary oedema, hypotension and a new apical systolic murmur after MI; the murmur may be soft when cardiac output is very low.
Acute heart failure or shock with a new harsh pansystolic murmur, often with a palpable thrill and biventricular failure.
Sudden collapse, hypotension, raised JVP, electromechanical dissociation or PEA; a contained rupture may present more subtly as a pseudoaneurysm.
Cold peripheries, confusion, oliguria, narrow pulse pressure and pulmonary or systemic congestion; consider LV, RV and mechanical causes.
Pleuritic positional pain and diffuse ST/PR change suggest pericarditis; embolic symptoms or a large anterior apical infarct should prompt assessment for LV thrombus.
Recurrent pressure-like pain with territorial ECG change favours coronary re-occlusion. Pleuritic, positional pain with diffuse changes and a rub suggests post-infarction pericardial inflammation.
Pleuritic pain, unexplained hypoxaemia, tachycardia and right-heart strain can reflect PE rather than recurrent infarction or left-sided failure. Definitive evaluation follows clinical probability.
New pulmonary oedema may reflect extensive ventricular injury, but abrupt shock or a new murmur raises acute mitral regurgitation or septal rupture. Urgent Doppler echocardiography discriminates.
Procedure-related bleeding can cause hypotension, tachycardia and oliguria after MI. Low filling pressures, falling haemoglobin or an identified bleeding source favour volume loss over cardiogenic congestion.
Abrupt severe chest or back pain, pulse disparity, neurological deficit or new aortic regurgitation suggests dissection. This can mimic coronary occlusion and changes antithrombotic decisions urgently.
Ventricular tachycardia or fibrillation can cause sudden arrest, while bradycardia and atrioventricular block may produce syncope or shock. Ongoing ischaemia and electrolyte disturbance can perpetuate either pattern.
Extensive left-ventricular injury causes pulmonary congestion and low output; right-ventricular infarction causes a different preload-sensitive phenotype. Both can progress to renal, hepatic and cerebral hypoperfusion.
Papillary-muscle rupture causes acute severe mitral regurgitation, septal rupture creates a left-to-right shunt, and free-wall rupture can cause haemopericardium and tamponade. Each can deteriorate rapidly and requires immediate specialist escalation.
Large anterior or apical akinesis can support mural thrombus. Systemic embolisation may cause stroke or limb and visceral infarction, while combined antithrombotic treatment increases management complexity.
Adverse remodelling can lead to chronic heart failure, ventricular aneurysm and scar-related arrhythmia. Early or immune-mediated pericarditis may cause recurrent pain and effusion.
A small pressure gradient in profound shock can make severe acute MR or a septal rupture surprisingly quiet.
Right-ventricular infarction and AV block are important causes of hypotension; bedside echo and right-sided ECG leads help distinguish them from LV congestion.
After MI, PEA should trigger immediate consideration of tamponade from free-wall rupture as well as the standard reversible causes.
Because it remains raised, reinfarction requires a new clinical/ECG pattern plus a convincing biomarker change or angiographic evidence.
Adding anticoagulation to antiplatelets raises bleeding risk; confirm the indication and agree the shortest safe combined plan with cardiology.
Attributing new pulmonary oedema to uncomplicated LV failure without listening for a murmur and obtaining urgent echo.
Waiting for a loud murmur before considering papillary-muscle or septal rupture.
Giving repeated fluid boluses to undifferentiated post-MI shock despite pulmonary congestion or a mechanical lesion.
Calling persistent troponin elevation reinfarction without new ischaemic evidence.
Delaying surgical or catheter-laboratory contact until vasoactive treatment has failed.
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Three days after an inferior myocardial infarction, a patient develops abrupt severe dyspnoea, hypotension and a new apical systolic murmur. Which complication is most likely?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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