Add a suitable educational image showing coronary artery occlusion and myocardial injury here.
Why this topic matters: Myocardial infarction (MI) is time-critical myocardial injury caused by an acute imbalance between coronary oxygen supply and demand, most often from a ruptured atherosclerotic plaque and thrombus. Every minute of untreated coronary occlusion can increase myocardial damage. Nurses and emergency-care students must recognise atypical presentations, obtain and interpret the urgency of an ECG, activate the acute coronary syndrome (ACS) pathway, support reperfusion, monitor for complications and coordinate safe secondary prevention.
Learning objectives
- Define myocardial infarction and distinguish myocardial injury, ischaemia, infarction and acute coronary syndrome.
- Classify infarction into STEMI, NSTEMI, type 1, type 2, MINOCA and other clinically important categories.
- Explain coronary plaque rupture, thrombosis, oxygen mismatch, necrosis and ventricular remodelling.
- Recognise typical, atypical and silent presentations, including presentations in women, older adults and people with diabetes.
- Perform a structured first-contact assessment using ABCDE, OPQRST, vital observations and a 12-lead ECG pathway.
- Describe the roles and limitations of serial ECGs, high-sensitivity troponin, imaging and coronary angiography.
- Outline pre-hospital, emergency-department, catheter-laboratory, inpatient and discharge management for STEMI and NSTEMI.
- Explain the safe use and nursing monitoring of antiplatelets, anticoagulants, nitrates, analgesics, statins, beta-blockers, ACE inhibitors and other therapies.
- Anticipate early and late complications, including dysrhythmia, acute heart failure, cardiogenic shock and mechanical rupture.
- Provide patient-centred education, rehabilitation, risk-factor control and a written safety-net plan.
1. Definition and core concepts
Myocardial infarction is myocardial cell death caused by prolonged ischaemia. In clinical practice, MI requires evidence of acute myocardial injury—usually a rise and/or fall in cardiac troponin with at least one value above the assay’s 99th-percentile reference limit—together with evidence of acute ischaemia such as symptoms, new ECG changes, imaging evidence of new loss of viable myocardium or identification of a coronary thrombus. A raised troponin alone means myocardial injury; it does not automatically mean type 1 MI.
Acute coronary syndrome (ACS) is the emergency spectrum produced by acute coronary blood-flow reduction. It includes unstable angina, NSTEMI and STEMI. Unstable angina causes ischaemic symptoms without detectable myocardial necrosis, whereas NSTEMI and STEMI cause necrosis. STEMI usually has persistent ST-segment elevation or an equivalent occlusion pattern requiring immediate reperfusion. NSTEMI generally has no persistent ST elevation but can still be life-threatening and may need urgent angiography.
Safety principle: Treat suspected MI as an emergency before the diagnosis is fully confirmed. A patient can have a serious infarction with mild pain, a normal first ECG, no pain at all, or an initially non-diagnostic troponin.
2. Classification of myocardial infarction
| Classification | Meaning | Clinical implication |
|---|---|---|
| STEMI | Acute coronary occlusion with persistent ST-segment elevation or an accepted STEMI-equivalent pattern. | Activate the immediate reperfusion pathway. Primary PCI is preferred when it can be delivered within the local system target; fibrinolysis may be considered when timely PCI is unavailable and no contraindication exists. |
| NSTEMI | Acute myocardial necrosis with a rise/fall in troponin and clinical evidence of ischaemia, without persistent ST elevation. | Stabilise, risk-stratify, give guideline-directed ACS treatment and arrange invasive assessment according to risk and available services. |
| Type 1 MI | Spontaneous MI from a primary coronary event such as plaque rupture, erosion, fissure or dissection with thrombus. | Antithrombotic treatment and coronary reperfusion or revascularisation are considered according to STEMI/NSTEMI findings. |
| Type 2 MI | MI caused by oxygen supply–demand imbalance without an acute primary coronary thrombus, for example severe anaemia, sepsis, hypoxaemia, hypotension or tachyarrhythmia. | Correct the trigger urgently while assessing whether underlying coronary disease and additional ACS treatment are present. |
| MINOCA | MI with no obstructive coronary artery disease on angiography; possible causes include spasm, embolus, spontaneous coronary dissection, myocarditis or Takotsubo syndrome. | It is a working diagnosis, not the end of evaluation. Echo, cardiac MRI and specialist assessment may identify the actual cause. |
| Periprocedural or post-procedural MI | Myocardial injury meeting specific biomarker and clinical criteria after PCI or cardiac surgery. | Interpret troponin with the procedure, ECG, imaging and clinical course; notify the cardiology team. |
3. Causes and risk factors
3.1 Common coronary causes
- Atherosclerotic plaque rupture or erosion with platelet activation and thrombus formation.
- Progressive plaque narrowing that becomes unstable during exertion, hypotension or inflammation.
- Coronary vasospasm, sometimes associated with tobacco, stimulants or vasoactive drugs.
- Spontaneous coronary artery dissection, particularly in some younger patients and peripartum patients.
- Coronary embolism from atrial fibrillation, endocarditis, prosthetic valves or intracardiac thrombus.
- Acute stent thrombosis or graft failure.
3.2 Conditions that can precipitate supply–demand mismatch
- Severe anaemia or acute blood loss, reducing oxygen-carrying capacity.
- Hypoxaemia from respiratory disease, pulmonary oedema or airway compromise.
- Sepsis, fever and systemic inflammation, increasing metabolic demand.
- Prolonged tachycardia, atrial fibrillation with rapid ventricular response or sustained hypertension.
- Profound hypotension, dehydration or shock, reducing coronary perfusion.
- Thyrotoxicosis, stimulant toxicity or severe agitation.
- Severe aortic stenosis, hypertrophic cardiomyopathy or advanced heart failure.
3.3 Modifiable and non-modifiable risk factors
| Risk factor | How it increases risk | Nursing opportunity |
|---|---|---|
| Tobacco use | Damages endothelium, promotes vasoconstriction, thrombosis and atherosclerosis. | Ask without judgement, document use, offer cessation referral and involve family support with consent. |
| Hypertension | Increases arterial wall stress and left-ventricular workload. | Use accurate BP technique, support adherence and identify barriers to follow-up. |
| Diabetes | Accelerates vascular disease and may blunt pain perception through neuropathy. | Teach glucose control, medicine adherence, foot care and cardiovascular review. |
| Dyslipidaemia | Promotes lipid deposition and plaque formation. | Explain statin adherence, diet, laboratory monitoring and follow-up. |
| Obesity and inactivity | Increase blood pressure, insulin resistance and cardiac workload. | Agree realistic nutrition, activity and rehabilitation goals rather than unsafe sudden exercise. |
| Chronic kidney disease | Is associated with vascular inflammation, calcification and altered medicine clearance. | Monitor renal function, electrolytes, contrast risk and medicine adjustments. |
| Age, family history and genetic risk | Influence baseline atherosclerotic risk and plaque biology. | Take a complete family history and never dismiss symptoms because the patient is young or female. |
| Previous MI, stroke or peripheral arterial disease | Indicates established systemic atherosclerosis. | Verify secondary-prevention medicines and communicate the high-risk history during handover. |
4. Pathophysiology
- Endothelial injury allows LDL particles and inflammatory cells to enter the coronary arterial wall.
- Atherosclerotic plaque develops a lipid core and fibrous cap. A vulnerable cap can rupture or erode.
- Exposure of thrombogenic material activates platelets and the coagulation cascade.
- Thrombus partially obstructs the coronary lumen, causing unstable angina or NSTEMI; complete occlusion commonly produces STEMI.
- Reduced blood flow causes myocardial ischaemia. Within minutes, aerobic metabolism falls, ATP is depleted and contractility weakens.
- Persistent ischaemia causes membrane injury and irreversible myocyte necrosis. Necrosis generally begins in the subendocardium and can extend outward as a wavefront.
- Injured myocytes release troponin into the circulation. Inflammatory repair then produces scar tissue and can lead to ventricular remodelling.
- Infarct size and outcome depend on the artery involved, collateral circulation, duration of occlusion, reperfusion time and the patient’s baseline health.
Time matters: “Time is muscle.” Rapid recognition, a diagnostic ECG, safe transfer and reperfusion reduce infarct size and complications. Do not delay an emergency referral while waiting for a routine outpatient appointment or a non-essential test.
5. Clinical presentation
5.1 Typical symptoms
- Central or left-sided pressure, squeezing, heaviness, tightness or burning lasting more than a few minutes or recurring.
- Pain spreading to one or both arms, shoulder, neck, jaw, back or epigastrium.
- Breathlessness, sweating, nausea, vomiting, dizziness, palpitations or a feeling of impending death.
- Symptoms triggered by exertion but now occurring at rest or with progressively less activity.
- Persistent discomfort that is not relieved by rest or the patient’s usual prescribed nitrate.
5.2 Atypical, silent and high-risk presentations
Some patients do not describe chest pain. Women, older adults, people with diabetes or kidney disease, and patients with neuropathy may report shortness of breath, unusual fatigue, weakness, indigestion, nausea, faintness, sleep disturbance, confusion or collapse. An older patient may simply become less mobile or acutely confused. A patient with diabetes may have silent ischaemia. Atypical does not mean low risk.
5.3 Signs of a complicated or extensive infarction
- Hypotension, narrow pulse pressure, cold clammy skin, weak pulse, oliguria or altered consciousness suggesting shock.
- Severe dyspnoea, crackles, orthopnoea, hypoxaemia or pink frothy sputum suggesting acute left-ventricular failure.
- Raised JVP, clear lungs and hypotension suggesting right-ventricular infarction or obstructive physiology.
- Bradycardia, new irregular rhythm, palpitations, syncope or recurrent collapse suggesting conduction disease or dysrhythmia.
- Sudden new murmur, acute pulmonary oedema or refractory shock suggesting a mechanical complication.
6. Focused history: OPQRST and ACS questions
| Question | What to ask | Why it matters |
|---|---|---|
| Onset | Exact time, sudden or gradual, at rest or with activity, first episode or recurrent? | Establishes symptom-to-treatment time and helps recognise acute occlusion. |
| Provocation/palliation | Exertion, emotion, cold, meals, breathing, position, rest, nitrate or other medicine? | Helps distinguish patterns but cannot rule out MI from atypical symptoms. |
| Quality and region | Pressure, heaviness, squeezing, burning, tearing, pleuritic or sharp; central chest, jaw, back, arm or epigastrium? | Maps ischaemic features and important differentials. |
| Severity and duration | Pain score, minutes per episode, continuous or intermittent, improving or worsening? | Persistent severe symptoms increase urgency and may indicate extensive injury. |
| Associated symptoms | Dyspnoea, sweat, nausea, vomiting, faintness, palpitations, weakness or confusion? | Identifies ACS equivalents, shock, arrhythmia and heart failure. |
| Previous pattern | Known angina, previous MI, PCI/stent, CABG, heart failure, stroke or peripheral vascular disease? | Defines baseline risk and informs treatment decisions. |
| Medicine and allergy history | Aspirin/antiplatelets, anticoagulants, nitrates, PDE-5 inhibitors, beta-blockers, diabetes medicines, last doses and allergies? | Prevents contraindicated treatment and identifies bleeding or hypotension risk. |
| Precipitating conditions | Fever, infection, bleeding, anaemia, stimulant use, cocaine/amphetamines, severe stress, pregnancy or recent surgery? | May indicate type 2 MI or alter the differential and treatment. |
7. Initial assessment and emergency triage
- Ensure safety and call for help: bring the resuscitation trolley, defibrillator and senior clinician. Do not leave an unstable patient alone.
- Airway: assess patency, voice and protective reflexes. Prepare suction and airway support if consciousness is reduced.
- Breathing: inspect work of breathing, respiratory rate, saturation and chest movement. Give oxygen only for hypoxaemia or significant respiratory distress according to local protocol.
- Circulation: check pulse, BP, skin, capillary refill, cardiac rhythm, IV access and signs of shock. Take blood without delaying the ECG or transfer.
- Disability: assess mental status, glucose and new neurological signs. Hypoglycaemia, stroke and shock may coexist.
- Exposure: look for bleeding, medication patches, signs of infection, trauma, calf swelling and aortic-dissection clues while protecting dignity and warmth.
- Record the clock: document symptom onset, first medical contact, ECG time, aspirin/antiplatelet time, transfer request and reperfusion time.
- Obtain a 12-lead ECG urgently: repeat if symptoms persist or change; posterior or right-sided leads may be needed when clinically indicated.
- Activate the local ACS pathway: notify the emergency and cardiology/reperfusion team early. Arrange monitored transfer for suspected STEMI or unstable NSTEMI.
Never wait for troponin before treating an obvious STEMI. A diagnostic ECG is the time-critical test for a suspected occlusive MI; laboratory results should not delay reperfusion activation.
8. Differential diagnoses that must not be missed
| Condition | Clues | Immediate concern |
|---|---|---|
| Acute aortic dissection | Abrupt tearing pain to the back, pulse or BP difference, new neurological deficit or aortic regurgitation. | Anticoagulation or fibrinolysis may be dangerous; urgent senior assessment and imaging. |
| Pulmonary embolism | Sudden dyspnoea, pleuritic pain, tachycardia, hypoxaemia, haemoptysis or venous-thromboembolism risk. | Right-heart strain and shock may mimic MI. |
| Pericarditis/myocarditis | Positional or pleuritic pain, viral illness, diffuse ECG changes or inflammatory features. | Myocarditis can cause arrhythmia and acute pump failure. |
| Pneumothorax or pneumonia | Unilateral absent breath sounds, pleuritic pain, fever, cough or focal chest signs. | Tension pneumothorax is immediately life-threatening. |
| Oesophageal rupture or reflux | Vomiting followed by severe chest pain, dysphagia or burning post-meal discomfort. | Rupture causes sepsis and mediastinal contamination. |
| Hypoglycaemia, anaemia or sepsis | Weakness, sweating, confusion, tachycardia, fever or bleeding history. | May precipitate type 2 MI and must be corrected urgently. |
9. Diagnostic investigations
| Investigation | What it shows | Nursing considerations |
|---|---|---|
| 12-lead ECG | ST elevation/depression, T-wave changes, Q waves, conduction block, bradycardia or arrhythmia. | Apply leads correctly, record time and symptoms, compare with previous ECG and repeat after deterioration. |
| High-sensitivity cardiac troponin | Acute myocardial injury when interpreted as a rise/fall pattern with clinical evidence of ischaemia. | Follow the local serial protocol; do not dismiss a very early result or chronic elevation in renal disease. |
| Full blood count | Anaemia, infection and platelet count before antithrombotic therapy. | Report severe anaemia, thrombocytopenia, leukocytosis or bleeding risk. |
| Electrolytes and renal function | Potassium, magnesium, creatinine and renal clearance affecting arrhythmia and medicine safety. | Correct dangerous abnormalities and flag contrast or anticoagulant concerns. |
| Glucose and HbA1c | Hypoglycaemia, stress hyperglycaemia and previously unrecognised diabetes. | Monitor glucose; avoid both untreated hyperglycaemia and iatrogenic hypoglycaemia. |
| Chest radiograph | Pulmonary oedema, cardiomegaly, pneumonia, pneumothorax or another cause. | Use when clinically indicated; never delay reperfusion for a routine film. |
| Bedside echocardiography | Regional wall-motion abnormality, ejection fraction, valve disease, right-heart strain or pericardial effusion. | Monitor during positioning and escalate new deterioration. |
| Coronary angiography | Identifies the culprit lesion and allows PCI when indicated. | Check consent, allergies, renal function, access site, bleeding and post-procedure pulses. |
| Cardiac MRI or CT in selected cases | Helps distinguish myocarditis, Takotsubo syndrome, scar, infarction with non-obstructive arteries and other causes. | Prepare safely and follow specialist imaging requirements. |
10. Immediate and pre-hospital management
Management must follow the current facility and national protocol, the patient’s contraindications and the clinician’s orders. The following sequence helps nursing students organise a safe response.
- Stop activity and position safely: keep the patient at rest, usually semi-sitting unless hypotension or another condition requires a different position. Reassure without minimising the symptoms.
- Call emergency services and activate ACS: arrange a monitored ambulance or urgent transfer. Avoid private transport when the patient is unstable or has ongoing chest pain.
- Obtain ECG and monitoring: attach cardiac monitoring, pulse oximetry and frequent BP checks; obtain serial ECGs if the first is non-diagnostic.
- Aspirin when appropriate: if acute MI/ACS is suspected and there is no true allergy, active major bleeding or another contraindication, administer the locally authorised chewable loading dose according to protocol. Document dose and time.
- Other antiplatelet/anticoagulant medicines: prepare prescribed P2Y12 inhibitor and parenteral anticoagulant after the clinician considers bleeding, renal function, fibrinolysis, PCI and diagnosis. Do not self-prescribe or duplicate doses.
- Nitrates: administer only if prescribed and BP is adequate. Avoid in hypotension, suspected right-ventricular infarction, severe aortic stenosis or recent phosphodiesterase-5 inhibitor use unless the specialist protocol states otherwise.
- Analgesia and antiemetic treatment: use prescribed therapy for severe refractory pain and vomiting while monitoring respiratory rate, consciousness and BP. Opioids can cause hypotension and may delay oral antiplatelet absorption.
- Oxygen: do not give routine high-flow oxygen to a well-saturated patient. Give titrated oxygen for hypoxaemia, respiratory distress or shock according to local targets.
- Prepare reperfusion: transmit the ECG, obtain consent and arrange primary PCI for eligible STEMI patients when timely. If timely PCI is not available, the specialist team may consider fibrinolysis after a careful contraindication screen.
- Prevent avoidable delay: keep the patient nil by mouth if an invasive procedure may be required, but do not delay critical medicines or transfer. Send ECGs, observations, medicine chart, allergies, history and laboratory results.
11. Reperfusion and hospital management
11.1 STEMI
- Recognise the ECG pattern and activate a coordinated STEMI pathway immediately.
- Primary percutaneous coronary intervention (PCI) is generally preferred when it can be delivered within the service’s recommended time target.
- When timely PCI is not possible and symptom onset is appropriate, fibrinolysis may be considered by an authorised clinician after checking absolute and relative contraindications.
- After fibrinolysis, assess for reperfusion and arrange transfer to a PCI-capable facility; failed reperfusion or instability requires rescue PCI evaluation.
- Continue monitoring for ventricular fibrillation, cardiogenic shock, bleeding, stroke and recurrent pain.
11.2 NSTEMI
- Use symptoms, serial ECGs, troponin pattern, haemodynamic status and risk scores to determine urgency.
- Very-high-risk features such as shock, ongoing/refractory pain, life-threatening arrhythmia, acute heart failure or dynamic ECG changes require immediate senior/cardiology review.
- High-risk patients may need early invasive coronary angiography and revascularisation; timing depends on risk, bleeding, renal function and local capacity.
- Continue evidence-based antithrombotic and anti-ischaemic therapy while checking for bleeding, renal impairment and alternative diagnoses.
11.3 Fibrinolysis safety screen
Before thrombolysis, the clinician must check for active bleeding, previous intracranial haemorrhage, recent major surgery or trauma, suspected aortic dissection, severe uncontrolled hypertension, bleeding disorders, recent stroke and other protocol-defined contraindications. Nurses must ask directly, document clearly and escalate uncertainty rather than assuming eligibility.
11.4 Secondary hospital medicines
| Medicine group | Purpose | Monitoring and nursing teaching |
|---|---|---|
| Aspirin plus a P2Y12 inhibitor | Reduces platelet aggregation and stent thrombosis risk when indicated. | Check allergy, bleeding, bruising, haemoglobin, stool/vomit blood and adherence. Never stop a prescribed stent-protection plan without cardiology advice. |
| Parenteral anticoagulant | Reduces thrombin-mediated clot extension during ACS/PCI or selected NSTEMI care. | Check weight, renal function, platelet count, bleeding and dose timing; avoid duplicate anticoagulants. |
| High-intensity statin | Stabilises plaque and lowers recurrent cardiovascular risk. | Reinforce daily adherence; monitor liver or muscle symptoms and prescribed laboratory follow-up. |
| Beta-blocker | Reduces heart rate and myocardial oxygen demand in selected haemodynamically stable patients. | Check pulse, BP, conduction block, heart failure, bronchospasm and shock before administration; do not give reflexively to an unstable patient. |
| ACE inhibitor/ARB | Limits adverse remodelling and benefits selected patients with LV dysfunction, diabetes, hypertension or heart failure. | Monitor BP, creatinine, potassium, cough and angioedema. |
| Mineralocorticoid receptor antagonist | May benefit selected post-MI patients with reduced EF, heart failure or diabetes. | Check renal function and potassium; report hyperkalaemia or hypotension. |
| Diuretics and vasodilators | Relieve congestion in acute heart failure when prescribed. | Monitor respiratory status, urine output, weight, BP, electrolytes and renal function. |
12. Nursing management
12.1 Priority nursing assessment
- Assess chest discomfort and equivalents with OPQRST; record onset and every change in severity.
- Trend airway, respiratory effort, RR, oxygen saturation, pulse, rhythm, BP, temperature, mental status, urine output and peripheral perfusion.
- Review ECG rhythm continuously where available and report ST changes, ventricular ectopy, bradycardia, heart block or new atrial fibrillation.
- Assess heart-failure signs: crackles, JVP, oedema, orthopnoea, weight gain, fatigue and falling oxygen saturation.
- Check pain, bleeding and access sites after PCI or vascular procedures; compare distal pulses and limb colour.
- Review allergies, last medicines, anticoagulant use, diabetes, kidney disease, bleeding history and social support.
12.2 Nursing interventions and rationales
| Intervention | Rationale and practical actions |
|---|---|
| Reduce myocardial workload | Keep the patient at rest, minimise exertion, provide a calm environment and cluster care without delaying essential observations. |
| Maintain continuous surveillance | Use cardiac monitoring, pulse oximetry and frequent observations to detect dysrhythmia, shock or heart failure early. |
| Give medicines safely | Use the rights of medication administration, verify indication and contraindication, and document exact time, route, response and adverse effects. |
| Support reperfusion | Prepare ECG, IV access, bloods, consent, transfer documents and patient education. Communicate time-critical information using SBAR. |
| Prevent bleeding | Inspect gums, urine, stool, vomit, skin and vascular access sites; avoid unnecessary invasive procedures and report falling BP or haemoglobin. |
| Manage oxygenation and congestion | Position upright when pulmonary oedema is present, titrate oxygen only when indicated, measure urine output and prepare prescribed diuresis or ventilatory support. |
| Assess pain and anxiety | Reassess after every intervention; explain what is happening, listen to fears and avoid dismissing persistent or atypical symptoms. |
| Promote safe nutrition and glucose control | Follow procedure-related fasting instructions, prevent hypoglycaemia and coordinate dietetic advice without compromising urgent care. |
| Mobilise gradually | Begin activity according to haemodynamic stability and rehabilitation guidance. Stop for chest pain, dyspnoea, dizziness, arrhythmia or marked fatigue. |
| Prepare discharge early | Check medicine access, transport, follow-up, rehabilitation referral, smoking cessation, family support and understanding before leaving. |
13. Complications and their management priorities
| Complication | Warning signs | Priority response |
|---|---|---|
| Ventricular fibrillation or pulseless VT | Collapse, unresponsiveness, absent normal breathing or no pulse. | Call resuscitation team, start high-quality CPR, attach defibrillator and follow ALS protocol. |
| Bradyarrhythmia or heart block | Slow pulse, dizziness, syncope, hypotension or altered consciousness. | Continuous ECG, senior review, treat reversible causes and prepare pacing according to protocol. |
| Acute left-ventricular failure/pulmonary oedema | Severe breathlessness, crackles, orthopnoea, hypoxaemia and frothy sputum. | Upright position, urgent help, oxygen/ventilatory support if indicated, prescribed diuresis and close urine/BP monitoring. |
| Right-ventricular infarction | Hypotension, raised JVP, clear lungs and sensitivity to preload reduction. | Urgent ECG/right-sided leads, cautious fluid strategy and avoid uncritical nitrates or diuresis. |
| Cardiogenic shock | Persistent hypotension, cold clammy skin, confusion, oliguria, metabolic acidosis or weak pulse. | Immediate critical-care escalation, haemodynamic support, echo and urgent revascularisation assessment. |
| Papillary muscle rupture or acute mitral regurgitation | Sudden pulmonary oedema, new harsh systolic murmur and shock several days after MI. | Emergency echocardiography, cardiology/cardiothoracic review and stabilisation. |
| Ventricular septal rupture | New murmur, acute heart failure, shock and a step-up in oxygen saturation between chambers. | Urgent echo, cardiology and surgical/interventional management. |
| Free-wall rupture/tamponade | Sudden collapse, electromechanical dissociation, muffled sounds, JVP elevation or pulsus paradoxus. | Resuscitation, emergency echocardiography and immediate surgical response. |
| Pericarditis and post-MI syndrome | Pleuritic or positional pain, fever and a pericardial rub days to weeks later. | Notify clinician, exclude reinfarction and follow prescribed anti-inflammatory plan. |
| LV thrombus and embolism | Large anterior infarct, apical akinesis, stroke symptoms or acute limb ischaemia. | Urgent neurological/vascular assessment, echo and specialist anticoagulation decision. |
14. Discharge, rehabilitation and secondary prevention
- Explain the diagnosis, infarct type, procedure or stent, medicines, duration of dual antiplatelet therapy and what to do if a dose is missed.
- Teach the patient never to stop antiplatelets after stenting without specialist advice because stent thrombosis can be fatal.
- Provide a written warning-sign plan: recurrent or prolonged chest pain, breathlessness, syncope, palpitations, bleeding, unilateral weakness or sudden confusion require urgent help.
- Refer to cardiac rehabilitation or the most accessible equivalent. Rehabilitation includes monitored activity, education, psychosocial support and risk-factor control.
- Support tobacco cessation, healthy diet, BP control, diabetes management, lipid lowering, safe physical activity, sleep and healthy alcohol decisions.
- Assess depression, anxiety, health literacy, financial barriers, medication availability, transport and family caregiving needs.
- Arrange follow-up for cardiology/medical review, lipid and glucose monitoring, renal function, blood pressure, wound/access review and rehabilitation progress.
- Teach gradual return to work and sexual activity according to clinical advice; warn against sudden strenuous exertion before review.
Teach-back: Ask the patient to explain what happened, the purpose of each medicine, how to recognise recurrent ACS, whom to call, where to go and how family members should respond if collapse occurs.
15. Worked clinical scenarios
Scenario 1: STEMI at first contact
A 61-year-old develops crushing central chest pressure while walking, with sweating and nausea. The nurse stops activity, calls the emergency team, records onset, performs ABCDE, obtains a 12-lead ECG, attaches monitoring, checks contraindications and prepares the prescribed antiplatelet pathway. The ECG is transmitted and the catheter laboratory is activated without waiting for troponin.
Scenario 2: Atypical NSTEMI
A 74-year-old with diabetes presents with weakness, breathlessness and mild epigastric discomfort but denies chest pain. The nurse recognises an anginal equivalent, performs glucose and vital observations, obtains serial ECGs and troponin, and escalates when the troponin rises. Absence of classic pain does not make the presentation safe.
Scenario 3: Cardiogenic shock
After an anterior MI, a patient becomes pale, confused and hypotensive with cool extremities and low urine output. The nurse calls critical care, reassesses ABCDE, maintains monitoring, prepares vasoactive and revascularisation support as ordered, measures urine output and communicates deterioration using SBAR. This is not managed by repeated unmonitored fluid boluses.
Scenario 4: Bleeding after PCI
Two hours after femoral-access PCI, a patient reports back pain and becomes tachycardic. The nurse checks the access site and distal pulses, measures BP frequently, suspects concealed retroperitoneal bleeding, keeps the patient at rest, alerts the team, checks blood results and avoids removing prescribed antiplatelets without specialist direction.
HEART-MI
H – Hear the patient and identify the exact onset · E – ECG early and repeat when needed · A – ABCDE, aspirin/ACS pathway when appropriate · R – Reperfusion and risk-stratified treatment · T – Track rhythm, troponin, perfusion and complications · M – Medicines safely with contraindication checks · I – Information, rehabilitation and prevention.
H – Hear the patient and identify the exact onset · E – ECG early and repeat when needed · A – ABCDE, aspirin/ACS pathway when appropriate · R – Reperfusion and risk-stratified treatment · T – Track rhythm, troponin, perfusion and complications · M – Medicines safely with contraindication checks · I – Information, rehabilitation and prevention.
16. Examination and revision questions
- Define myocardial infarction and explain why an elevated troponin alone does not always equal type 1 MI.
- Differentiate STEMI, NSTEMI, unstable angina, type 1 MI, type 2 MI and MINOCA.
- Describe the pathophysiological sequence from plaque rupture to myocardial necrosis.
- List typical, atypical and silent symptoms of MI.
- Outline the ABCDE and ECG-based assessment of suspected ACS.
- Why must ECG and reperfusion activation not wait for troponin results in suspected STEMI?
- Discuss aspirin, P2Y12 inhibitors, anticoagulants, nitrates, oxygen, analgesics and statins in acute MI care.
- Compare primary PCI and fibrinolysis, including the importance of contraindication screening.
- Describe nursing monitoring after PCI and list signs of vascular bleeding.
- Explain the presentation and urgent management priorities of cardiogenic shock.
- Describe at least five mechanical complications of MI and the clues that should trigger urgent echocardiography.
- Prepare a teach-back discharge plan for a patient discharged after NSTEMI.
Key takeaways
- MI is acute myocardial necrosis from ischaemia; ACS is the emergency spectrum that includes unstable angina, NSTEMI and STEMI.
- Time-sensitive ECG, early activation and reperfusion save myocardium and lives.
- Women, older adults and people with diabetes may present with breathlessness, fatigue, nausea, weakness or confusion rather than chest pain.
- Troponin must be interpreted with its rise/fall pattern and clinical evidence of ischaemia.
- Safe nursing care combines monitoring, antithrombotic safety, bleeding surveillance, complication recognition, communication and prevention.
- Discharge is not the end of treatment: adherence, rehabilitation and risk-factor control reduce recurrent events.
Suggested references
- American Heart Association/American College of Cardiology. 2025 Guideline for the Management of Patients With Acute Coronary Syndromes.
- European Society of Cardiology. 2023 Guidelines for the Management of Acute Coronary Syndromes.
- American Heart Association. Acute Coronary Syndrome and Heart Attack resources.
- World Health Organization. Cardiovascular diseases and heart-attack warning symptoms.
- Use the current Uganda Ministry of Health, ambulance, emergency department and cardiology protocols for local drug availability, referral, transfer and reperfusion targets.