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STEMI & NSTEMI: A Nurse's Guide to Reading & Managing Heart Attacks

William Kelly, MSN, FNP-C
Updated June 2026 · Medically reviewed for nurses
15 min read

A STEMI — ST-Segment Elevation Myocardial Infarction — is the most dangerous type of heart attack, and recognizing it fast on the 12-lead can save your patient's heart muscle and their life.

An NSTEMI (Non-STEMI) is still a heart attack, but without ST elevation on the ECG. Ruling out a STEMI is the whole reason 12-leads get ordered, and the sooner one is caught, the better the outcome. Providers should lay eyes on every ECG quickly, but that doesn't always happen on time. The faster a STEMI is identified, the more heart tissue survives — and that recognition often starts with the nurse.

Coronary Artery Anatomy

The coronary arteries lie on the surface of the heart (the epicardium) and deliver the blood and oxygen that keep the myocardium perfused and beating. The three main vessels are the left anterior descending (LAD), the circumflex (Cx), and the right coronary artery (RCA). Knowing what each one feeds tells you which wall is in trouble when you see changes on the ECG.

Right Coronary Artery (RCA)
Right atrium and ventricle, the inferior/posterior LV (~85%), the SA node (~60%), and the AV node (~85–90%).
Left anterior descending artery
Left Anterior Descending (LAD)
Anterior wall and part of the lateral LV, plus the anterior two-thirds of the interventricular septum.
Circumflex artery
Circumflex (Cx)
Left atrium and the lateral LV; the SA node (~40%) and AV node (~10–15%) in some people.
Posterior descending artery
Posterior Descending (PDA)
Branches off the RCA (most people) or the Cx. Whichever supplies it is the "dominant" coronary artery.

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the umbrella term for any condition that drops blood flow to the heart — ischemia. Prolonged ischemia leads to infarction, the death of heart tissue, which releases troponin into the bloodstream.

Most cardiac ischemia is caused by atherosclerosis — plaque buildup in the coronary arteries from factors like diet, obesity, sedentary lifestyle, hyperlipidemia, smoking, and genetics. When that plaque ruptures, it spills its contents, triggers local inflammation and a coagulation cascade, and the resulting clot can completely occlude the artery, causing infarction.

Coronary plaque rupture leading to clot formation and arterial occlusion
Plaque rupture triggering clot formation and occlusion.
STEMI vs NSTEMI in one line: a STEMI is a full-thickness (transmural) infarction with ST elevation in contiguous leads; an NSTEMI is a smaller, usually subendocardial infarction with a rising troponin but no ST elevation.

An NSTEMI often shows nonspecific changes — T-wave inversion or ST depression in contiguous leads, with or without inversion — and the ECG can even be completely normal. Troponin is elevated, confirming cell death. A STEMI, by contrast, shows ST elevation in at least 2 contiguous leads, and where that elevation appears tells you which wall is infarcting and which artery is occluded.

Want the lab side of this picture? See Cardiac Lab Interpretation (Troponin, CK, CK-MB, and BNP).

Ischemia & Infarction on the ECG

The ST-segment sits right after the QRS and before the T wave. It represents early ventricular repolarization and should rest at the isoelectric line. Use the TP segment as your baseline, or the PR segment if the TP is hard to see.

ST segment on the ECG
The ST-Segment
Should sit flat on the isoelectric line; deviation up or down is the key MI clue.
J point on the ECG
The J-Point
Where the QRS meets the ST segment — the reference point for measuring elevation or depression.

ST-Segment Depression

ST depression most often signals cardiac ischemia, and it can appear as a reciprocal change in an acute MI. It can also reflect strain, digitalis effect, hypokalemia, hypomagnesemia, or be rate-related — but those tend to be diffuse rather than localized to 2 contiguous leads.

It's defined as ≥0.5 mm (½ small box) below the isoelectric line, measured 80 ms (2 small boxes) after the J-point. Horizontal and down-sloping depression are more specific for ischemia; up-sloping is less concerning but can still indicate it.

Up-sloping, horizontal, and down-sloping ST-segment depression types
Up-sloping, horizontal, and down-sloping ST depression.

Don't Miss De Winter T Waves

In about 2% of acute LAD occlusions there's no obvious ST elevation. Instead you'll see up-sloping ST depression at the J-point with tall, symmetric T waves in the precordial leads (V1–V6). Treat it like a STEMI equivalent.

ST-Segment Elevation

ST elevation usually means myocardial infarction when it appears in at least 2 contiguous leads. Other causes exist — coronary vasospasm, pericarditis, benign early repolarization, LBBB, LV hypertrophy, ventricular aneurysm, Brugada, paced rhythms, raised ICP, blunt chest trauma, and hypothermia — so context matters.

It's defined as ≥1 mm (1 small box) above the isoelectric line at the J-point. Leads V2–V3 have higher thresholds: >1.5 mm in women, >2 mm in men ≥40, and >2.5 mm in men <40.

Concave Elevation
Less ominous; can reflect benign early repolarization, especially when diffuse.
Convex "Tombstoning"
Convex-upward elevation is almost always a large MI — a true red flag.
Concave versus convex ST-segment elevation morphology
Concave vs convex ("tombstone") ST elevation.

Q Waves

A Q wave is the initial negative deflection of the QRS complex, reflecting septal depolarization. Small Q waves are normal in many leads. Pathologic Q waves point to underlying pathology — usually a current or prior MI.

They're defined as >40 ms wide (1 small box) and >2 mm deep (2 small boxes). Any Q wave in V1–V3 is considered pathologic. Q waves can appear hours to days after an infarct begins and may persist for years.

Pathologic Q wave on the ECG
Pathologic Q wave.

LBBB or Ventricular Paced Rhythm

Spotting ST changes is tricky in a left bundle branch block (LBBB) or a ventricular paced rhythm, because both normally carry some ST elevation and discordant T waves. To suspect ischemia or infarction in these patients, look for the Sgarbossa-type findings:

Concordant ST elevation >1 mm in a lead with a positive QRS complex.
ST depression >1 mm in V1, V2, or V3.

New LBBB + Chest Pain = Concern

A new LBBB morphology with acute chest pain or shortness of breath should make you highly suspicious of an acute MI, even without classic ST elevation.

New to rhythm strips? Start with How to Read an EKG Rhythm Strip.

STEMI Progression

A STEMI tends to evolve through a recognizable sequence on the ECG. Knowing the stages helps you place where your patient is in the timeline.

1
Hyperacute T Waves

Tall, peaked, symmetric T waves in ≥2 contiguous leads. These last only minutes to about an hour.

2
ST Elevation

Elevation appears at the J-point in ≥2 contiguous leads, initially concave, then becoming convex/rounded upward.

3
Tombstone Pattern

The ST segment merges with the T wave until they're indistinguishable. Reciprocal ST depression may show in opposite leads.

4
Resolution & Q Waves

The ST segment drifts back to baseline over a week or so. Q waves develop over hours to days and deepen over time, followed by T-wave inversion that may be temporary.

Typical ECG progression of a STEMI over time
The typical ECG evolution of a STEMI.

STEMI Location

STEMIs are classified by where they sit — which leads are affected on the ECG. Contiguous leads are simply leads that look at the same anatomical region of the heart.

Anteroseptal
V1, V2
Anteroapical
V3, V4
Anterolateral
V5, V6
Lateral
I, aVL
Inferior
II, III, aVF
12-lead ECG map showing which leads correspond to each region of the heart
Which leads look at each region of the heart.

The precordial and lateral leads often light up together, since the infarct area isn't always precise. Here's an inferior wall STEMI as an example:

Inferior wall STEMI with ST elevation in II, III, aVF and reciprocal lateral changes
Inferior wall MI: ST elevation in II, III, and aVF with reciprocal changes in the lateral leads.

Acute Management of STEMI

STEMIs are true emergencies. The patient is at high risk for conduction disturbances, arrhythmias, and cardiac arrest, and every minute of delay means more dead heart cells and worse outcomes.

12-Lead Within 10 Minutes

Any patient with significant cardiac symptoms — chest pain or SOB — needs a 12-lead ECG within 10 minutes. Women, older adults, and diabetics may have atypical or even "silent" MIs with no chest pain at all.

A lot happens fast. Activate a code STEMI (or your facility's equivalent) to alert the interventional cardiologist and cath team immediately. Then work the bedside basics:

1
Monitor & Access

Place the patient on the monitor, get vitals, establish two IVs (ideally 18g), and apply defibrillation pads.

2
Labs

Draw and send labs including troponin and PT/PTT.

3
Stabilize

Address any abnormal vitals, and manage arrhythmias per ACLS guidelines.

Medications
Aspirinantiplatelet
324 mg chewed and swallowed. A 300 mg rectal suppository is an option if the patient can't take it by mouth.
P2Y12 Inhibitorclopidogrel · ticagrelor
A receptor blocker such as Plavix or Brilinta is given in addition to aspirin for dual antiplatelet therapy.
Nitroglycerinvasodilator
0.4 mg SL × 3, q5min for persistent chest discomfort, hypertension, or signs of heart failure. An IV nitro drip can be used for ongoing symptoms.

When NOT to Give Nitro

Avoid nitroglycerin with recent PDE5 inhibitor use (Viagra/Cialis within 24–48 hours), hypotension, severe aortic stenosis, or a suspected right ventricular infarct (can accompany inferior wall MIs). In these patients nitro can cause severe hypotension.

Anticoagulationheparin · enoxaparin
An unfractionated heparin drip is commonly used; Lovenox is another option.
High-Intensity Statinatorvastatin
Atorvastatin 80 mg PO ASAP, ideally before PCI. If the patient is already on a statin, increase to 80 mg.

Be Cautious with Morphine

Morphine 2–4 mg slow IVP q5–15min can be used for refractory chest pain or anxiety, but research links it to higher mortality in STEMI — likely because it blunts the antiplatelet effect of P2Y12 inhibitors. Reserve it for pain that can't be controlled otherwise.

Oxygen is given only to keep SpO2 >90% (routine oxygen in non-hypoxic patients isn't beneficial). If the patient has left heart failure, treat with nitro, a loop diuretic like Lasix, and consider BiPAP. Beta-blockers are started within 24 hours unless contraindicated (bradycardia, heart failure, severe reactive airway disease), usually after PCI.

STEMI medications quick reference for nurses
STEMI medication quick reference.
Reperfusion is the priority. Primary PCI in the cath lab (angiography + stent) is the preferred method and should happen ASAP. Fibrinolytics are the alternative when PCI isn't available within ~120 minutes, as long as symptoms began <12 hours ago and there are no bleeding contraindications.

NSTEMI Management

As the name says, an NSTEMI has no ST elevation on the ECG — but it's still a heart attack, marked by an elevated and rising troponin. The ECG may be normal or show nonspecific T-wave changes or ST depression in contiguous leads.

Medication management mirrors a STEMI, with two key differences: NSTEMI patients do not receive fibrinolytics and are not rushed emergently to the cath lab. Instead, medical therapy is maximized, the patient is monitored, and troponins are trended (typically every 6–8 hours). They may or may not get a cardiac cath during the admission.

STEMIs and NSTEMIs are high-stakes events every nurse will encounter. Recognizing a STEMI on the ECG is the first and most important step.

Clinical Pearls

1
Location maps to artery. Inferior (II, III, aVF) → usually RCA; anterior/septal (V1–V4) → LAD; lateral (I, aVL, V5–V6) → Cx or LAD. The leads tell you the vessel.
2
Inferior STEMI? Think right ventricle. A right-sided infarct makes the patient preload-dependent — hold the nitro and be ready with fluids if they drop their pressure.
3
New LBBB with chest pain is a STEMI until proven otherwise. Look for the Sgarbossa findings rather than waiting for textbook elevation.
4
Time is muscle. 12-lead within 10 minutes, activate the cath team early, and aim for the fastest possible reperfusion.
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Want to go deeper? ECG Rhythm Master is a complete video course built for nurses, covering rhythms, pathophysiology, and emergency procedures in real depth.

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References

Clinical Databases & Guidelines
  1. Reeder, G., & Kennedy, H. Overview of the acute management of ST-elevation myocardial infarction. UpToDate.
  2. ECG tutorial: Myocardial ischemia and infarction. UpToDate.
  3. American Heart Association. ACLS Algorithms.
Textbooks
  1. Aehlert, B. ECGs Made Easy (6th ed.).
  2. Davis, K. EKGs for the Nurse Practitioner and Physician Assistant.
Attribution
  1. "Coronary Blood Vessels" by OpenStax College, licensed under CC BY 3.0; changes were made.
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