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Cardiovascular

Acute Coronary Syndrome & MI

ACS High-yield Verified · Sep 2026

Acute coronary syndrome (ACS) is a spectrum of presentations caused by acute myocardial ischemia — unstable angina, NSTEMI, and STEMI — most often when a disrupted atherosclerotic plaque triggers platelet aggregation and thrombus formation in a coronary artery.

Every 40 seconds, someone in the United States has a heart attack. This page teaches the fork every nurse must make fast — unstable angina vs NSTEMI vs STEMI — plus the 10-minute ECG, the 90-minute balloon, and what actually replaced MONA.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 A plaque breaks, a clot grows

The event that starts almost every ACS is mechanical: an atherosclerotic plaque in a coronary artery ruptures (or, less often, erodes), exposing thrombogenic material beneath the endothelium. Platelets land on it, activate, aggregate, and build a thrombus — and from that moment the muscle downstream is living on whatever blood squeezes past the clot. Myocardial infarction is what follows when the deprivation lasts: myocardial cell death from prolonged inadequate oxygen supply.

Not every ACS starts with a plaque. Coronary vasospasm (Prinzmetal angina) can strangle a vessel without any thrombus — cocaine and methamphetamine are classic triggers, especially in younger patients. The universal definition captures this split: type 1 MI is the plaque-rupture-plus-thrombus event; type 2 MI is a supply–demand mismatch without atherothrombosis (vasospasm, embolism, spontaneous dissection). And MINOCA — MI with nonobstructive coronaries — accounts for 6–10% of MIs and is more prevalent in women.

02 One mechanism, three diagnoses

What the clot does to the lumen decides the diagnosis. Complete occlusion starves the full thickness of the wall — transmural ischemia — and lifts the ST segments: STEMI. Partial or transient occlusion starves only the vulnerable inner layer — subendocardial ischemia — producing NSTEMI or unstable angina, which present identically and are separated by one lab value: NSTEMI has a troponin rise above the 99th percentile with a rise/fall pattern; unstable angina does not.

Unstable angina is ischemia without necrosis — troponin stays normal — and it announces itself three classic ways: angina at rest, new-onset angina, or a crescendo pattern of previously stable angina. Treat it as an emergency anyway: it signals an unstable plaque and impending MI, with lower mortality than NSTEMI but a comparable risk of nonfatal infarction. The two questions that sort the whole spectrum — what does the ECG show, and what does the troponin do? — are the same two the nurse’s first hour is built around.

The ACS fork: how completely the thrombus occludes the artery decides transmural vs subendocardial ischemia — and the ECG plus troponin name the diagnosis.

03 Time is muscle

Ischemic injury is not instantaneous — it is a wavefront. Ultrastructural damage begins within 10–15 minutes of ischemia, and necrosis then advances from the subendocardium outward toward the epicardium over several hours. That window is the entire logic of ACS care: muscle not yet dead can still be saved, so every target on this page is a clock. The 12-lead ECG is obtained and interpreted within 10 minutes of first medical contact. For STEMI, primary PCI with a drug-eluting stent is the preferred reperfusion, with a first-medical-contact-to-device target of ≤ 90 minutes (≤ 120 minutes when transfer is required) — and every 10-minute reduction in door-to-balloon time is independently associated with lower in-hospital mortality.

When PCI cannot happen within 120 minutes, fibrinolysis substitutes — door-to-needle within 30 minutes, only for symptom onset under 12 hours, followed by transfer for angiography within 3–24 hours. Fibrinolytics are never used in NSTEMI or unstable angina: the artery is not fully occluded, so the bleeding risk buys nothing — those patients get antithrombotic therapy and catheterization on a risk-stratified timeline instead.

The STEMI reperfusion decision and its 2025 ACC/AHA time targets: PCI if achievable within 120 minutes; otherwise fibrinolysis inside 30 minutes, then a pharmacoinvasive transfer.

04 After the infarct — the complication timeline

Surviving the occlusion is not the end of the story; dead and dying muscle fails in a predictable order. Lethal ventricular arrhythmias (VF, sustained VT) dominate the first minutes to hours — along with bradycardia and high-degree AV block — which is why at least one-third of MI deaths happen before the hospital and why continuous ECG monitoring is non-negotiable. In the first days, a large infarct can fail as a pump: cardiogenic shock complicates about 10% of MIs. In days 2–7, necrotic wall softens and can tear — the mechanical complications: free wall rupture, septal rupture, papillary muscle rupture. And 2–6 weeks out, an immune-mediated pericarditis — Dressler syndrome — can appear.

The nurse’s job in each phase is to know its heralding cue: a new rhythm on the monitor early; hypotension in a patient who arrived hypertensive; a sudden loud systolic murmur in the first week; pleuritic pain with fever weeks later. Each cue is covered under Complications below.

The post-MI complication timeline: arrhythmias kill first, then pump failure, then mechanical rupture in the first week, then Dressler syndrome weeks later.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Abnormal lipids — modifiable factors like these account for ~90% of MI risk modifiable Smoking modifiable Hypertension modifiable Diabetes modifiable Abdominal obesity modifiable Physical inactivity modifiable Psychosocial stress modifiable Low fruit & vegetable intake modifiable Excessive alcohol modifiable Cocaine / methamphetamine use (vasospasm, especially in younger patients) modifiable Advancing age Male sex Family history of premature coronary disease Chronic kidney disease Autoimmune disorders

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Substernal chest pressure or heaviness — band-like, lasting ≥ 10 minutes Report immediately
Why: A thrombus on a disrupted plaque is starving myocardium of oxygen. Ischemic cardiac pain is pressure-like and poorly localized — patients often call it discomfort rather than pain — and it may radiate to the jaw, neck, either shoulder, one or both arms, the back, or the upper abdomen.
Diaphoresis, nausea, dyspnea, lightheadedness, palpitations, anxiety accompanying the pain Expected
Why: The classic autonomic accompaniment of myocardial ischemia — sweating and nausea alongside chest pressure make the ischemic story more convincing, not less.
Atypical presentation — isolated dyspnea, epigastric pain, fatigue, dizziness, or no chest pain at all Report immediately
Why: Women, older adults, and patients with diabetes or renal insufficiency infarct without the textbook script: women often present with abdominal pain or dizziness, elderly patients with shortness of breath. The nurse who waits for crushing chest pain in these patients misses the MI.
Angina at rest, new-onset angina, or a crescendo pattern (more severe, more frequent, longer) early Report immediately
Why: The three classic faces of unstable angina — a plaque has destabilized, and progression to infarction may be imminent even while troponin is still normal.
Chest pain unrelieved after 3 sublingual nitroglycerin doses (q5 min) Report immediately
Why: Pain that outlasts maximal venodilation means the occlusion is not yielding — the teaching line is “no relief after 3 doses: call 911.”
Silent MI — infarction discovered later with no recognized acute event
Why: MIs can go entirely undetected, most often in the same populations that present atypically — one more reason a new ECG finding or troponin rise is never dismissed as “no symptoms, no problem.”
Pleuritic pain, pain reproducible by palpation, or pain lasting only seconds Expected
Why: These features suggest a non-ischemic cause — useful for pattern-building, though the workup still rules ACS out rather than assuming.
New arrhythmia on the monitor — VT/VF, tachycardia, bradycardia, or high-degree AV block Report immediately
Why: Ischemic and infarcting myocardium is electrically unstable; lethal ventricular arrhythmias dominate the acute phase and are the reason for continuous ECG monitoring.
Hypotension in a patient who presented hypertensive late Report immediately
Why: The heralding cue of cardiogenic shock — the infarcted ventricle is failing as a pump and can no longer hold the pressure it arrived with.
Sudden loud systolic murmur (new) late Report immediately
Why: Think mechanical catastrophe: papillary muscle rupture causing acute mitral regurgitation, or ventricular septal rupture — first-week emergencies that need the surgeon, not the next scheduled assessment.
Crackles/rales, wheezing, or JVD after the infarct late Hold & notify
Why: Pump failure declaring itself: rales mean the left side is congesting the lungs (pulmonary edema); JVD suggests right ventricular failure.
Sudden loss of a distal leg pulse late Report immediately
Why: A mural thrombus formed on the infarcted wall has embolized — or output has fallen critically. Either way it is on the report-immediately list.

Diagnostics

Test In this disorder Normal
12-lead ECG (within 10 minutes) Obtained and interpreted within 10 minutes of first medical contact. A normal ECG never rules out MI (one nursing review puts sensitivity near 30% despite 95–97% specificity) — repeat serial ECGs if the first is nondiagnostic with ongoing symptoms STEMI: new ST elevation at the J point in ≥ 2 contiguous leads — ≥ 1 mm in most leads; in V2–V3, men ≥ 40 y need ≥ 2 mm, men < 40 y ≥ 2.5 mm, women ≥ 1.5 mm — often with reciprocal ST depressions. NSTE-ACS: ST depression, T-wave inversion, transient elevation — or a normal tracing 2025 ACC/AHA ACS guideline No acute ST-segment or T-wave changes
High-sensitivity cardiac troponin (hs-cTn) The biomarker of choice — order troponin only, not multi-marker panels. Serial hs-cTn algorithms (0/1 h, 0/3 h) can rule in or out within 1–3 h; a negative troponin at 6 h effectively excludes infarction in most cases. Elevated troponin = myocardial injury, not automatically MI — it also rises in myocarditis, HF, PE, sepsis, and end-stage renal disease MI = a rise and/or fall with ≥ 1 value above the 99th-percentile upper reference limit plus evidence of ischemia. Kinetics: begins rising 3–4 h after symptom onset, peaks 24–48 h; troponin I stays up 7–10 days, troponin T up to 14 days Fourth Universal Definition of MI Below the assay’s 99th-percentile upper reference limit
CK-MB Its fast clearance made it the historical marker for detecting reinfarction while troponin is still elevated from the first event Rises ~4 h post-injury, peaks ~24 h, normalizes by 48–72 h —
Risk scores — TIMI · GRACE · HEART They stratify who needs an early invasive strategy — but no score definitively beats clinician judgment TIMI predicts 14-day adverse events from 4.7% (score 0–1) to 40.9% (score 6–7); GRACE predicts in-hospital and 6-month mortality; HEART was built specifically for ED chest-pain patients —
Cardiac catheterization Radial access is now preferred over femoral (less bleeding, fewer vascular complications, lower mortality). Post-cath nursing: check the access site for hematoma and palpate distal pulses The gold standard for NSTE-ACS — defines the anatomy and delivers PCI; early PCI is recommended for elevated-risk patients 2025 ACC/AHA ACS guideline —

Complications

Warning: Ventricular fibrillation & sudden cardiac death — the early killer Report immediately
VF and sustained VT dominate the first minutes to hours; bradycardia and high-degree AV block also occur. At least one-third of MI deaths happen before the hospital.
This is why the patient goes on a continuous monitor immediately and stays on it — early CPR and defibrillation are the major determinants of surviving an arrest. Sudden-death risk stays highest through the first months post-MI.
Warning: Cardiogenic shock Report immediately
Complicates ~10% of acute MIs with early mortality of 40–50%. The cue: hypotension in a previously hypertensive presentation, with cool skin, falling urine output, and confusion.
Emergency revascularization of the culprit vessel is indicated; a microaxial flow pump is considered in selected patients. The nurse’s move is recognizing the pressure trend early and escalating — not chasing it with fluids on autopilot.
Warning: Mechanical complications — the first-week ruptures Report immediately
Necrotic wall tears in days 2–7: free wall rupture (→ tamponade, > 80% mortality), ventricular septal rupture (new loud holosystolic murmur radiating to the sternum), papillary muscle rupture (sudden loud systolic murmur + flash pulmonary edema).
Each needs emergent surgery. The bedside cue that buys the patient a chance is auscultation: a sudden new loud murmur in the first week post-MI is a call-now finding, never a “note for rounds.”
Caution: Dressler syndrome — the late pericarditis Hold & notify
Immune-mediated secondary pericarditis appearing ~3–4 days to 2–6 weeks post-injury (occasionally months): fever, malaise, pleuritic chest pain, friction rub, diffuse ST elevation on ECG, elevated WBC/ESR/CRP.
Treated with NSAIDs tapered over 4–6 weeks (corticosteroids if refractory); echo is the imaging gold standard. Watch for tamponade — Beck triad (hypotension, JVD, muffled heart sounds); as little as ~200 mL accumulating rapidly can tamponade.
Caution: LV thrombus, embolism & heart failure Hold & notify
Blood pooling against an akinetic infarcted wall forms a mural thrombus that can embolize (cue: sudden loss of a distal pulse); scarred myocardium can also aneurysm, reinfarct, or fail as a pump.
Reduced LVEF is the strongest negative prognostic predictor after MI — the reason echo, remodeling-blocking drugs, and rehab all follow the acute event.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Antiplatelets First-line
Cardiovascular · clopidogrel

The first drug in the door: aspirin 162–325 mg chewed (non–enteric-coated), immediately, for every suspected ACS — it blunts the platelet aggregation building the culprit thrombus. Then DAPT (aspirin + a P2Y12 inhibitor) for all ACS, continued ≥ 12 months in low-bleeding-risk patients (2025 ACC/AHA, Class 1); ticagrelor or prasugrel is preferred over clopidogrel for PCI patients — but with fibrinolysis, clopidogrel is the only P2Y12 used.
Anticoagulants First-line High-alert
Cardiovascular · heparin

Parenteral anticoagulation (unfractionated heparin, enoxaparin, fondaparinux, or bivalirudin) for all ACS at presentation: the antiplatelet stops new platelets from joining the clot; the anticoagulant halts propagation of the thrombus already there while the patient awaits — or undergoes — revascularization.
Nitrates
Cardiovascular · nitroglycerin

SL nitroglycerin 0.4 mg every 5 min, up to 3 doses, venodilates to drop preload and oxygen demand and relieve ischemic pain (IV is more effective for ongoing symptoms). Three hard stops: SBP < 90 mm Hg, suspected right-ventricular (inferior) infarction — an RV infarct is preload-dependent, and nitrates can collapse the pressure — and a PDE5 inhibitor within 48 h.
Opioid Analgesics High-alert
Nervous · morphine

Morphine is deliberately not routine: IV morphine only for severe ischemic pain unresponsive to nitrates, and only with adequate blood pressure. Pain relief does reduce sympathetic drive — but the old “M for everyone” MONA reflex is gone, and RV infarction is another reason to hold it.
Beta-Blockers
Cardiovascular · metoprolol

Cuts myocardial oxygen consumption in muscle fighting for supply — started orally within 24 h in hemodynamically stable patients, with the clearest benefit when LVEF is reduced. Contraindicated in cocaine-associated ACS or suspected vasospasm.
Statins First-line
Cardiovascular · atorvastatin

A high-intensity statin (atorvastatin 80 mg or rosuvastatin 20–40 mg) for all ACS patients (Class 1, Level A): plaque stabilization now, LDL lowering for life. LDL-C still ≥ 70 mg/dL on a maximally tolerated statin means adding a nonstatin (ezetimibe, evolocumab, alirocumab, inclisiran, or bempedoic acid).
ACE Inhibitors
Cardiovascular · lisinopril

Post-ACS for patients with LVEF ≤ 40%, hypertension, diabetes, CKD, or an anterior STEMI: blocking angiotensin limits the adverse remodeling that turns an infarct into chronic heart failure.

Beyond medications

  • Primary PCI with a drug-eluting stent — the preferred STEMI reperfusion: first-medical-contact-to-device ≤ 90 min (≤ 120 min with transfer), radial access preferred, and intracoronary imaging recommended to guide PCI of complex lesions.
  • Fibrinolysis when PCI is out of reach within 120 min: door-to-needle ≤ 30 min, symptoms < 12 h only, tenecteplase preferred (half-dose at age ≥ 75), then transfer for angiography in 3–24 h. Absolute contraindications include any prior intracranial hemorrhage, ischemic stroke within 3 months, suspected aortic dissection, and active bleeding. Never for NSTEMI or UA.
  • Early invasive strategy for elevated-risk NSTE-ACS — catheterization ± PCI on a risk-stratified timeline rather than a reperfusion clock.
  • Cardiac rehabilitation referral (strongly recommended) — participation is associated with reduced mortality and rehospitalization.
  • Graded activity — walking can usually start right away, building back to normal activities over a few weeks if there is no chest pain; cardiac rehab teaches safe progression.
  • Risk-factor overhaul — complete smoking cessation, a healthy diet, abstaining from alcohol, weight, cholesterol and glucose control, and treatment adherence.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Keep the patient on continuous cardiac monitoring with a daily 12-lead ECG; treat any new rhythm — VT/VF, tachycardia, bradycardia, heart block — as report-now.
Why: Lethal ventricular arrhythmias dominate the acute phase; the monitor plus early defibrillation is what converts an arrest into a survivable event.
Draw serial cardiac enzymes as ordered and track the trend, not the single value.
Why: MI diagnosis rests on a rise and/or fall of troponin above the 99th percentile; troponin rises 3–4 h after onset, so an early normal proves nothing.
Track vitals, daily weight, urine output, pulse oximetry, and chest-pain intensity with every set.
Why: Falling BP, falling urine output, or returning pain are the earliest signals of shock, reinfarction, or extension — trends the monitor alone won’t name.
Auscultate every shift for rales and new murmurs; palpate leg pulses.
Why: A sudden loud murmur heralds papillary muscle or septal rupture; rales mean pump failure congesting the lungs; a lost distal pulse means embolism from a mural thrombus.
After catheterization, check the access site for hematoma and palpate distal pulses on schedule.
Why: Bleeding and vascular occlusion are the signature post-PCI complications — part of why radial access is now preferred over femoral.
Report immediately: hypotension, continuing chest pain, nausea/vomiting, lost leg pulses, sudden mental-status change, continuing desaturation, new arrhythmia, or a sudden loud murmur.
Why: Each item on this list is the heralding cue of a specific post-MI catastrophe — shock, reinfarction, embolism, rupture.
The first hour — suspected ACS
Get the 12-lead ECG obtained and interpreted within 10 minutes of first contact — before anything that can wait.
Why: The ECG makes the STEMI/NSTE-ACS fork, and everything downstream — cath-lab activation, fibrinolysis eligibility — hangs on it. Necrosis is advancing as a wavefront while it waits.
Give aspirin 162–325 mg, chewed, non–enteric-coated, immediately for suspected ACS (unless unsafe).
Why: The single first-hour drug for every ACS subtype — it attacks the platelet aggregation building the culprit thrombus.
Establish 2 large-bore IVs and keep the patient on the monitor; give heparin and expedite cardiology evaluation as ordered.
Why: Anticoagulation halts thrombus propagation, and the IVs must exist before the emergency that needs them. Reperfusion is a race: every 10 minutes off door-to-balloon time lowers mortality.
Apply oxygen only when SpO₂ < 90% (or PaO₂ < 60 mm Hg) — not routinely.
Why: Studies show possible harm from supplemental oxygen in normoxic patients; the “O for everyone” of old MONA is obsolete.
Give SL nitroglycerin 0.4 mg q5 min (max 3) for ischemic pain — but hold and clarify for SBP < 90, suspected RV/inferior infarction, or PDE5-inhibitor use within 48 h.
Why: An RV infarct lives on preload; nitrates (and morphine and diuretics) can crash it — volume expansion is the initial strategy there instead.
Reserve IV morphine for severe pain unresponsive to nitrates, with adequate blood pressure.
Why: Morphine is explicitly non-routine in modern ACS care — analgesia for refractory pain, not a default line item.
Patient teaching (before the next event)
Chest pressure at home: call 911 — do not drive yourself, do not wait. If prescribed nitroglycerin gives no relief after 3 doses 5 minutes apart, call 911.
Why: Most MI deaths occur before the hospital, from arrhythmias EMS can treat; the 3-dose rule marks the moment “angina” becomes “possible infarction.”
Never stop cardiac medications suddenly — especially the antiplatelets.
Why: Abrupt discontinuation is a classic precipitant of a new event; the stent and the healing plaque are still thrombus-prone.
Report the warning signs: chest, arm, back, neck, or jaw pain or pressure, shortness of breath, heavy sweating, nausea, unusual fatigue, lightheadedness — a second heart attack may not feel like the first — and any change in angina pattern (new, worsening, or at rest).
Why: A changing pattern is the signature of unstable angina — the plaque destabilizing again — and it warrants evaluation before the troponin ever rises.
Progress activity gradually — cardiac rehab teaches how — and stop for chest pain, breathlessness, dizziness, or any other warning sign.
Why: Gradual, supervised progression rebuilds capacity without outrunning a healing myocardium.
Attend cardiac rehab — make sure the referral has been made.
Why: Rehab is associated with reduced mortality and rehospitalization; it is strongly recommended, not a nicety.
Sexual activity: agree a safe timeline with the provider, as for other activity. Never combine erectile-dysfunction drugs (PDE5 inhibitors) with nitrates.
Why: The PDE5-plus-nitrate combination can cause profound hypotension — the same 48-hour window that holds nitroglycerin in the ED.
Healthy diet, no alcohol, complete smoking cessation, and every medicine taken exactly as prescribed — no skipped or changed doses without the provider.
Why: The discharge bundle targets the modifiable factors that account for ~90% of MI risk — and the nonadherence that undermines the regimen.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter: band-like substernal pressure ≥ 10 minutes radiating to arm and jaw, at rest, with diaphoresis and nausea — and the headline, ST elevation in ≥ 2 contiguous leads (V2–V4) with reciprocal depressions. In a 58-year-old man, 3 mm in V2–V3 clears the ≥ 2 mm threshold decisively. The mildly elevated BP, normal temperature, and SpO₂ of 96% are background.

  2. 2
    Analyze cues

    The pattern is a complete coronary occlusion: transmural ischemia lifting the anterior ST segments — STEMI. The diagnosis stands on the ECG alone; troponin doesn’t begin rising until 3–4 hours after onset, so the pending (or even normal) first draw changes nothing. Necrosis is advancing as a wavefront from the subendocardium outward — muscle is being lost by the minute.

  3. 3
    Prioritize

    The reperfusion clock outranks everything: first-medical-contact-to-device ≤ 90 minutes, and every 10-minute reduction in door-to-balloon time lowers in-hospital mortality. The ECG beat the 10-minute standard (7 minutes); now the sequence is aspirin → cath-lab activation → the rest. Nothing on the chart competes with those two.

  4. 4
    Generate solutions

    Give aspirin 324 mg chewed now; activate the STEMI pathway so the lab is mobilizing; keep the monitor on with the defibrillator near — VF is the early killer; anticipate heparin per order; nitroglycerin for pain is reasonable here (SBP 152, anterior not inferior pattern, no PDE5-inhibitor use) — confirm before dosing; no oxygen at SpO₂ 96%; reserve morphine unless pain proves nitrate-refractory.

  5. 5
    Take action

    Aspirin chewed at 14:16, STEMI activation called, heparin started per order, SL nitroglycerin given with BP rechecked at each dose. Oxygen is deliberately withheld — supplemental O₂ in a normoxic patient shows possible harm. The trap is the old MONA reflex: morphine and oxygen for everyone. Modern care is ECG in 10 minutes, aspirin chewed, reperfusion triage — the rest is conditional.

  6. 6
    Evaluate

    Success: wheels to the cath lab well inside 90 minutes of first contact. Post-PCI (radial access), evaluation continues — access site for hematoma, distal pulses, pain resolved, ST segments settling, and the report-now list in force: hypotension, returning pain, new arrhythmia, or a sudden loud murmur. Before discharge: cardiac rehab referral, DAPT teaching, and the 911/3-dose nitroglycerin rule.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Emergency department · 14:05, triage

A 58-year-old man walks into the ED with 45 minutes of substernal chest pressure that began at rest — “a heavy pressure right in the middle of my chest,” radiating to his left arm and jaw. History: hypertension, type 2 diabetes, 30 pack-years of smoking. Home meds: lisinopril, metformin. No prior cardiac events.

14:05 triage — pain 8/10, pressure-type, radiating to left arm and jaw · nauseated · pale and diaphoretic
Vitals — HR 98 · BP 152/90 · RR 20 · SpO₂ 96% on room air · T 37.1 °C
14:12 ECG (7 min after arrival) — 3 mm ST elevation in V2–V4, reciprocal ST depressions in II, III, aVF
14:15 — 2 large-bore IVs placed, continuous monitor on, first troponin drawn (pending)
Standing chest-pain orders — aspirin 324 mg chewed · SL nitroglycerin 0.4 mg q5 min × 3 PRN · O₂ per protocol
Q1 Select all that apply
At 14:12 the nurse reviews the triage data and the ECG. Which cues require immediate action? Select all that apply.
  1. A. Band-like substernal pressure, 45 minutes, radiating to the left arm and jaw
  2. B. Diaphoresis and nausea accompanying the pain
  3. C. Blood pressure 152/90 mm Hg
  4. D. Temperature 37.1 °C
  5. E. ST elevation of 3 mm in V2–V4 with reciprocal inferior depressions
Reveal answer & rationale
Answer: A, B, E
Pressure-type pain ≥ 10 minutes radiating to arm and jaw is the hallmark ischemic story (A), and the autonomic accompaniment of diaphoresis + nausea strengthens it (B). ST elevation in ≥ 2 contiguous leads (E) is the finding that names it STEMI and starts the reperfusion clock. The BP (C) is mildly elevated but is not what drives the next 10 minutes, and 37.1 °C (D) is normal — neither is an action cue here.
Q2 Multiple choice
At 14:40 the first troponin returns normal. The best interpretation is:
  1. A. MI has been ruled out; the ST changes likely reflect early repolarization
  2. B. The result is expected — troponin rises 3–4 hours after onset, and STEMI is diagnosed from the ECG, so reperfusion proceeds now
  3. C. The diagnosis is unstable angina, which does not require emergent reperfusion
  4. D. The cath-lab activation should be paused until a second troponin confirms infarction
Reveal answer & rationale
Answer: B
Pain began ~80 minutes ago, and troponin does not begin rising until 3–4 hours after symptom onset — an early normal proves nothing (B). STEMI is an ECG diagnosis; waiting on any biomarker (D) burns the myocardium the 90-minute target exists to save. A single early negative cannot rule out MI (A) — that takes serial values (a negative at 6 h effectively excludes it in most cases). Unstable angina (C) requires a normal troponin over time and no ST elevation — this patient has 3 mm of elevation in contiguous leads.
Q3 Multiple choice
A nurse orienting to the ED asks, “Shouldn’t we put oxygen on him? He’s having a heart attack.” The best response is:
  1. A. “Yes — 2 L by nasal cannula is standard for all chest pain.”
  2. B. “Yes — use a non-rebreather to maximize delivery to the ischemic muscle.”
  3. C. “No — his SpO₂ is 96%; oxygen is given only when SpO₂ falls below 90%, because it shows possible harm in normoxic patients.”
  4. D. “Only if he reports feeling short of breath.”
Reveal answer & rationale
Answer: C
Oxygen is not routine in ACS: the threshold is SpO₂ < 90% (or PaO₂ < 60 mm Hg), and studies show possible harm in normoxic patients (C). Options A and B are the old “O in MONA for everyone” reflex — obsolete. Symptom-triggered dosing (D) is also wrong: the number that drives oxygen is the saturation, not dyspnea, which in ACS is an ischemia cue rather than an oxygen order.
Q4 Put in order
Put the nurse’s first four actions after the 14:12 ECG in priority order:
  1. A. Follow up on the pending troponin result
  2. B. Give aspirin 324 mg, chewed, non–enteric-coated
  3. C. Confirm STEMI activation so the cath lab is mobilizing toward the ≤ 90-minute device target
  4. D. Recheck BP, then give SL nitroglycerin 0.4 mg for pain per the standing order
Reveal answer & rationale
Correct order: B → C → D → A
Chewed aspirin is the first drug for every suspected ACS and takes seconds (B). Cath-lab activation is next — reperfusion is the definitive treatment and its clock is already running (C). Nitroglycerin then treats pain once the BP check confirms it’s safe — SBP is 152, this is an anterior (not inferior/RV) pattern (D). The troponin (A) is last: in a confirmed STEMI its result changes neither the diagnosis nor the plan, so chasing it before the interventions sequences a lab above the muscle.
Q5 Multiple choice
The patient returns from primary PCI (radial access) at 17:30. Which finding on the 20:00 assessment does the nurse report immediately?
  1. A. The radial access site is tender with a stable dressing and a palpable radial pulse
  2. B. The patient rates chest pain 0/10 and asks for dinner
  3. C. A sudden loud holosystolic murmur that was not present at 18:00
  4. D. Heart rate 88 and regular on the monitor
Reveal answer & rationale
Answer: C
A sudden loud murmur after an MI heralds mechanical catastrophe — papillary muscle rupture with acute mitral regurgitation or ventricular septal rupture, the first-week complications that need emergent surgery (C). Mild access-site tenderness with an intact pulse and stable dressing (A) is an expected post-cath finding to keep monitoring — it becomes reportable if a hematoma expands or the pulse disappears. Resolved pain with appetite (B) and a regular HR of 88 (D) are the success picture, not problems.

Common questions

What causes acute coronary syndrome & mi?
Common causes and risk factors include abnormal lipids — modifiable factors like these account for ~90% of mi risk, smoking, hypertension, diabetes, abdominal obesity, and others.
What are the early signs of acute coronary syndrome & mi?
Early findings include Angina at rest, new-onset angina, or a crescendo pattern (more severe, more frequent, longer).
Which findings should a nurse report immediately in acute coronary syndrome & mi?
Report immediately: Substernal chest pressure or heaviness — band-like, lasting ≥ 10 minutes, Atypical presentation — isolated dyspnea, epigastric pain, fatigue, dizziness, or no chest pain at all, Angina at rest, new-onset angina, or a crescendo pattern (more severe, more frequent, longer), Chest pain unrelieved after 3 sublingual nitroglycerin doses (q5 min), New arrhythmia on the monitor — VT/VF, tachycardia, bradycardia, or high-degree AV block, and others. These signal deterioration that needs rapid intervention.
What is the difference between unstable angina, NSTEMI, and STEMI?
All three are ACS — the same disrupted plaque and thrombus. STEMI is complete occlusion: transmural ischemia with ST elevation and elevated troponin. NSTEMI and unstable angina come from partial or transient occlusion and present identically; the split is the troponin — elevated with a rise/fall in NSTEMI, normal in unstable angina. UA is still an emergency: it signals an unstable plaque and impending infarction.
Is MONA still used for heart attacks?
Not as taught. Modern initial care is a 12-lead ECG within 10 minutes, aspirin 162–325 mg chewed, and rapid reperfusion triage. Oxygen is given only when SpO₂ < 90% (possible harm in normoxic patients), morphine is reserved for nitrate-refractory pain, and nitroglycerin has hard stops (SBP < 90, RV infarction, PDE5 inhibitors within 48 h). The mnemonic survives on flashcards, not in guidelines.
How long does troponin stay elevated after an MI?
Troponin begins rising 3–4 hours after symptom onset, peaks at 24–48 hours, and stays elevated for days — 7–10 days for troponin I, up to 14 days for troponin T. That long tail is why CK-MB, which normalizes by 48–72 hours, was historically used to catch reinfarction while troponin was still up from the first event.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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