Myocardial Infarction: What Actually Happens During a Heart Attack?
David is 62 and has been feeling unwell for about half an hour. He describes a heavy pressure across the centre of his chest that has started to spread into his jaw. He looks pale, his shirt is damp with sweat and he feels nauseated. His first instinct is to sit quietly and hope it passes.
For the nurse assessing David, the words myocardial infarction are only the end of a much longer story. Something has changed in the blood supply to his myocardium. Heart muscle is becoming ischaemic, cells are being injured, and the longer that process continues, the more myocardium may be lost.
A myocardial infarction (MI) is therefore more than “a blocked artery”. It is myocardial injury caused by ischaemia. Understanding that distinction helps make sense of the symptoms, the electrocardiogram (ECG), cardiac troponin, reperfusion and the complications nurses watch for afterwards.
From coronary plaque to injured myocardium
The myocardium has a high and continuous demand for oxygen. It receives this through the coronary arteries, which branch over the surface of the heart and supply the cardiac muscle. If coronary blood flow suddenly falls, the balance between myocardial oxygen supply and demand is disturbed.
In the familiar form of acute MI, the problem often begins with coronary atherosclerosis. Lipids, inflammatory cells and other material accumulate within the arterial wall and form an atherosclerotic plaque. The important point is that the artery does not necessarily have to become gradually narrower until it finally closes. An established plaque can become disrupted. Plaque rupture or erosion exposes thrombogenic material to circulating blood, promoting platelet activation, coagulation and formation of a thrombus. The thrombus can then markedly reduce or obstruct coronary blood flow. The British Heart Foundation describes this atheroma-to-thrombus process as the cause of most heart attacks, although it is not the only route to MI.
Downstream from the obstruction, cardiomyocytes receive less oxygen. Aerobic production of adenosine triphosphate (ATP) falls and cells increasingly depend on anaerobic metabolism. Cellular ion pumps begin to fail, metabolites accumulate and contractile function deteriorates. At first, ischaemic myocardium may still be salvageable. If severe ischaemia continues, however, cell injury becomes irreversible and cardiomyocytes die. This is why restoring coronary blood flow quickly can preserve myocardium rather than simply improve the patient's pain. The amount of muscle ultimately lost depends on factors including the artery involved, the site and duration of obstruction, collateral circulation and how quickly effective reperfusion occurs.
This also explains why an MI can affect far more than one patch of heart muscle. Damaged myocardium may contract poorly, reducing stroke volume and cardiac output. Ischaemic tissue can become electrically unstable, increasing the risk of dysrhythmias. A sufficiently large infarction can impair left ventricular function and lead to pulmonary oedema, acute heart failure or cardiogenic shock. Less commonly, structural damage after MI can contribute to serious mechanical complications such as ventricular septal rupture, free-wall rupture or acute mitral regurgitation associated with papillary muscle rupture. Modern reperfusion has made these mechanical complications less common, but sudden haemodynamic deterioration after MI still demands urgent assessment.
STEMI, NSTEMI and the changing definition of MI
Students often meet MI through two labels: ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). These remain clinically important because the ECG pattern helps determine the immediate management pathway. A STEMI usually reflects acute coronary occlusion producing a pattern of persistent ST-segment elevation in the appropriate clinical context and requires urgent consideration of reperfusion. NSTEMI does not produce the diagnostic ST-elevation pattern, but myocardial infarction has still occurred. The ECG may show ST depression, T-wave changes or other abnormalities, and sometimes the initial ECG is not diagnostic at all.
That last point is important at the bedside: a normal initial 12-lead ECG does not exclude an acute coronary syndrome. NICE recommends obtaining a resting 12-lead ECG as soon as possible when acute coronary syndrome (ACS) is suspected and considering serial ECGs when the diagnosis remains uncertain. NICE CG95 also advises that ECG recording should not delay transfer to hospital.
There is another classification students now need to know. In August 2026, the Fifth Universal Definition of Myocardial Infarction replaced the previous numbered MI types with three clinical categories: primary MI, secondary MI and procedure-related MI. The new universal definition was produced jointly by the European Society of Cardiology, American College of Cardiology, American Heart Association and World Heart Federation.
A primary MI arises spontaneously because of an acute coronary problem. Atherosclerotic plaque disruption with thrombosis is an important cause, but the category also recognises mechanisms such as spontaneous coronary artery dissection (SCAD), coronary vasospasm and coronary embolism. A secondary MI occurs when another acute condition creates a mismatch between the myocardium's oxygen supply and demand rather than an acute primary coronary process. Severe hypoxaemia, major haemodynamic disturbance or a marked tachyarrhythmia are examples of situations that can contribute to this kind of imbalance. Procedure-related MI occurs in association with a complication of a cardiac procedure or operation within the definition's specified time window.
These categories do not make STEMI and NSTEMI irrelevant. They answer a different question. STEMI and NSTEMI help describe the acute clinical presentation and guide management, while primary, secondary and procedure-related MI describe the setting and mechanism in which the infarction occurred. A student who keeps those two ideas separate is much less likely to become lost in the terminology.
Troponin tells you there is myocardial injury, not automatically why
Cardiac troponin is released into the circulation when cardiomyocytes are injured. High-sensitivity cardiac troponin I or T is therefore central to the investigation of suspected MI. But a raised troponin is not a diagnosis of MI on its own.
This distinction is one of the most useful things to understand about acute cardiac assessment. A patient can have myocardial injury without myocardial infarction. Troponin can be elevated in other clinical situations, including myocarditis, pulmonary embolism, renal disease, heart failure and critical illness. What turns myocardial injury into myocardial infarction is evidence that the acute injury occurred because of myocardial ischaemia.
In practice, clinicians interpret troponin alongside the patient's symptoms, ECG findings, timing, serial change and, where appropriate, imaging or coronary findings. NICE specifically warns that a detectable high-sensitivity troponin result does not necessarily mean the patient has had an MI. The 2026 universal definition also emphasises sex-specific 99th percentile upper reference limits for cardiac troponin, helping reduce systematic under-recognition of myocardial injury in females.
Go back to David. His chest pressure, radiation to the jaw, sweating and nausea make myocardial ischaemia a serious concern, but none of those symptoms confirms MI by itself. His ECG may provide immediate evidence of acute ischaemia. His troponin may initially be below the diagnostic threshold if he presents early, so the timing and pattern of serial results matter. Assessment is a process of putting the clinical picture together rather than waiting for one blood result to provide the answer.
Presentation can also be less recognisable than David's. ACS may present with discomfort in the chest, arms, back or jaw, breathlessness, nausea or vomiting, sweating or haemodynamic instability. Some people do not describe central chest pain as their predominant symptom. NICE advises against using different symptom criteria for men and women. The safer lesson is not to learn a separate “female heart attack” checklist, but to recognise that ACS presentation is variable in everyone and to assess the whole clinical picture.
What happens when MI is suspected?
Suspected MI is time-critical because ongoing ischaemia can mean ongoing myocardial loss. Nursing assessment begins at the same time as escalation and treatment, not after them. The patient needs an immediate structured assessment, observations, cardiac rhythm monitoring, oxygen saturation, a 12-lead ECG and appropriate blood sampling, including high-sensitivity troponin. Changes in pain, blood pressure, pulse, rhythm, oxygenation and clinical appearance can all alter the urgency of the situation.
The old image of every patient with chest pain automatically receiving oxygen is outdated. NICE advises against routine oxygen in suspected ACS. Oxygen saturation should be measured and supplemental oxygen used when indicated, with the target adjusted for people at risk of hypercapnic respiratory failure. NICE also recommends a 300 mg loading dose of aspirin as soon as possible in suspected ACS unless there is clear evidence of aspirin allergy. Pain relief may include glyceryl trinitrate (GTN) and, when appropriate, intravenous opioid analgesia. A response to GTN should not be used to decide whether chest pain is cardiac.
If David's ECG shows an acute STEMI, the priority is rapid reperfusion. NICE NG185 recommends coronary angiography with follow-on primary percutaneous coronary intervention (PCI), when indicated, as the preferred reperfusion strategy for eligible people with acute STEMI when it can be delivered within the recommended timeframe. PCI allows the coronary anatomy to be visualised and the culprit lesion treated, commonly using balloon angioplasty and a stent. Where timely primary PCI cannot be delivered and the person meets the relevant criteria, fibrinolysis may be considered according to the reperfusion pathway.
NSTEMI follows a different immediate pathway because there is no STEMI pattern demanding the same emergency reperfusion route, but it is not a “milder heart attack”. Patients are assessed for ischaemic and bleeding risk, receive appropriate antithrombotic treatment and may require early coronary angiography and revascularisation. NICE recommends formal risk assessment after NSTEMI or unstable angina using an established system such as the Global Registry of Acute Coronary Events (GRACE) score, alongside the history, examination, ECG and blood results.
For the nurse, treatment is only part of the story. Persistent or recurrent chest pain, new ST changes, ventricular dysrhythmias, bradyarrhythmias, falling blood pressure, cool peripheries, reduced urine output, increasing breathlessness, pulmonary crackles or a falling level of consciousness can signal continuing ischaemia or complications. A new murmur or sudden haemodynamic collapse after MI is particularly concerning because it may indicate a mechanical complication. The trend matters. A patient who looked stable twenty minutes ago may not be stable now.
After the artery is opened, the MI is not over
Successful reperfusion limits further ischaemic injury, but it does not instantly restore the heart to its pre-infarction state. Some myocardium may already have been irreversibly injured, while surrounding tissue can remain stunned or vulnerable. The patient may develop dysrhythmias, impaired ventricular function or heart failure, and the longer-term healing response replaces necrotic myocardium with scar tissue. The size and location of the infarction influence how much this affects future cardiac function.
Before discharge, attention therefore moves from immediate survival to reducing the risk of another event and helping the person recover. NICE recommends secondary-prevention treatment after MI including an angiotensin-converting enzyme (ACE) inhibitor, appropriate antiplatelet therapy, a beta-blocker and a statin, with treatment tailored to the person's clinical circumstances. Left ventricular function is assessed, medicines need explanation and monitoring, and risk factors such as smoking, blood pressure and lipids form part of longer-term cardiovascular care.
Cardiac rehabilitation is not an optional extra for the especially motivated patient. It is part of recovery after MI. NICE recommends that people are offered a cardiac rehabilitation programme with an exercise component, alongside health education, lifestyle support and stress management, with referral beginning during the hospital admission. For someone like David, this is also where questions that may not be asked during the acute emergency start to surface: Can I exercise? When can I return to work? Why am I taking so many tablets? Will this happen again? Is every twinge in my chest another heart attack?
Understanding the pathophysiology helps the nurse answer those questions without reducing the MI to a single blocked vessel. The useful chain to remember is reduced coronary blood flow → myocardial ischaemia → myocardial injury → irreversible cardiomyocyte death if severe ischaemia persists. The ECG helps show what the myocardium is doing electrically. Troponin provides evidence of myocardial injury. The clinical context helps establish whether that injury is an infarction. Reperfusion aims to save threatened myocardium, and everything that follows is about detecting complications, supporting recovery and reducing the chance of another event.
References
British Heart Foundation (2025) Heart attack: symptoms, causes and treatment.
Damluji, A.A. et al. (2021) ‘Mechanical complications of acute myocardial infarction: a scientific statement from the American Heart Association’, Circulation, 144(2), pp. e16–e35.
European Society of Cardiology (2023) 2023 ESC Guidelines for the management of acute coronary syndromes.
European Society of Cardiology, American College of Cardiology, American Heart Association and World Heart Federation (2026) Fifth Universal Definition of Myocardial Infarction.
National Institute for Health and Care Excellence (2016) Recent-onset chest pain of suspected cardiac origin: assessment and diagnosis. CG95.
National Institute for Health and Care Excellence (2020, updated 2024) Acute coronary syndromes. NICE guideline NG185.
Welt, F.G.P. et al. (2024) ‘Reperfusion injury in patients with acute myocardial infarction: JACC Scientific Statement’, Journal of the American College of Cardiology, 83(22).