Case Study — Cardiac
Acute MI NGN Case Study
A Next Gen NCLEX-style unfolding case. Read each step, commit to your own answer — out loud or on paper — and only then reveal ours. The six steps mirror the NCSBN Clinical Judgment Measurement Model exactly as the exam tests it.
15 min activity · Cardiac
Educational use only. This case is a learning exercise with simplified values, not a treatment protocol — real ACS care follows provider orders, your facility’s chest-pain pathway, and current ACLS guidelines. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
The Scenario
1845, ED triage: Mr. Delgado, 58, walks in saying he has had “bad indigestion” for the past two hours that antacids didn’t touch. History: type 2 diabetes, hypertension, hyperlipidemia, smokes half a pack a day. His wife adds that he “looks gray” and made her drive him in — he wanted to wait it out.
Triage Assessment
- HR 96 · BP 148/92 · RR 20 · SpO₂ 96% RA · Temp 36.8°C
- Describes a “pressure” mid-chest, 6/10, radiating to the left jaw; worse with exertion in the parking lot
- Diaphoretic, pale, nauseated; one episode of vomiting at home
- Skin cool and clammy; no chest wall tenderness; lungs clear
- Took two antacid tablets and one of his wife’s “heart pills” (unknown) at home — no relief
Step 1 — Recognize Cues
Which findings are most relevant — and which matter most right now? List the cues you would flag before revealing.
▸Reveal answer
Most concerning cues: pressure-type chest discomfort radiating to the jaw, diaphoresis with cool clammy skin, nausea/vomiting, pallor, symptoms unrelieved by antacids, and a risk-factor stack (diabetes, hypertension, hyperlipidemia, smoking, male, 58).
The diabetes wrinkle: diabetic patients often present atypically — “indigestion,” fatigue, or dyspnea instead of crushing pain — because neuropathy blunts cardiac pain. A diabetic with new epigastric symptoms and diaphoresis is cardiac until proven otherwise.
The trap: the word “indigestion” and the normal-ish vitals. Stable vital signs do not rule out an MI in progress — the 12-lead does the sorting, not the blood pressure.
Step 2 — Analyze Cues
What conditions could explain this picture? The 12-lead EKG is done within 10 minutes of arrival: ST elevation in leads II, III, and aVF. Connect the cues before revealing.
▸Reveal answer
STEMI — inferior wall (most supported): ST elevation in II, III, aVF is the inferior pattern, usually a right coronary artery occlusion. The clinical picture (pressure, radiation, diaphoresis, nausea — vagal symptoms are classic with inferior MIs) fits completely.
GERD/dyspepsia: the patient’s own theory — but reflux doesn’t cause diaphoresis, pallor, and ST elevation. Antacid non-response was already a clue.
Unstable angina/NSTEMI: were on the list until the EKG declared itself. With ST elevation, troponin confirmation is NOT required to act — the EKG alone activates the cath lab.
One more thing to check: inferior MIs involve the right ventricle in a substantial minority — anticipate a right-sided EKG (V4R), because RV involvement changes the nitroglycerin calculus.
Step 3 — Prioritize Hypotheses
Rank your hypotheses. Which one drives your next actions, and why?
▸Reveal answer
1. Inferior STEMI with possible RV involvement — confirmed by EKG, lethal, and on a clock: “time is muscle.” Every minute of occlusion kills myocardium, so reperfusion (door-to-balloon goal ≤90 minutes) outranks everything.
2. Dysrhythmia risk — the ischemic heart is electrically irritable; inferior MIs particularly favor bradycardia and AV blocks (the RCA usually feeds the AV node). Continuous monitoring with pads nearby is part of the priority, not an afterthought.
NGN logic: a confirmed, time-critical diagnosis collapses the differential. The work now is speed and safety, not further sorting.
Step 4 — Generate Solutions
What should happen in the next 30 minutes? Draft your action list — include what you anticipate the provider will order.
▸Reveal answer
Immediate: STEMI/cath lab activation per protocol; continuous cardiac monitoring with defibrillator pads available; two large-bore IVs; chewable aspirin 162–325 mg (unless truly contraindicated); oxygen only if SpO₂ <90% — routine O₂ in normoxic MI patients is no longer recommended.
Labs and lines without delaying transport: troponin, CBC, BMP, coags — drawn, not waited on. The cath lab does not wait for a troponin result when the EKG shows STEMI.
Anticipated orders: antiplatelet loading (P2Y12 inhibitor), anticoagulation (heparin) per cath-lab protocol, nitroglycerin cautiously, analgesia per orders.
Also reasonable: right-sided EKG to assess RV involvement, brief targeted history (bleeding risk, recent surgery — PCI candidacy), keep NPO, and keep the wife informed — she got him here.
Step 5 — Take Action
Sequencing question: the protocol order set includes sublingual nitroglycerin PRN for chest pain. Before you give it, the repeat BP is 92/58 and the right-sided EKG suggests RV involvement. What do you do?
▸Reveal answer
Hold the nitroglycerin and notify the provider. An RV-involved inferior MI is preload-dependent — the failing right ventricle needs venous return to fill the left side. Nitroglycerin dumps preload and can crash this patient’s pressure. The same caution applies to morphine and diuretics.
Instead anticipate: IV fluids to support preload if hypotension worsens, and rapid transport to the cath lab — reperfusion fixes the underlying problem. Also screen any chest-pain patient for recent PDE-5 inhibitor use (sildenafil and friends) before nitrates, every time.
While preparing for transport: pads on, aspirin chewed and documented, IVs patent, family updated, SBAR to the cath-lab team.
Step 6 — Evaluate Outcomes
2120, post-PCI: a drug-eluting stent opened the RCA. Mr. Delgado returns with a radial access band, pain 0/10, BP 118/72, HR 78 in sinus rhythm with occasional PVCs. Which findings show success, and what still needs watching?
▸Reveal answer
Improving: pain resolved (reperfusion achieved), hemodynamics stable, rhythm organized — the artery is open.
Still watching: the access site (bleeding, hematoma, distal pulses — radial band deflation per protocol), reperfusion dysrhythmias (PVCs and accelerated idioventricular rhythm are common and usually benign — sustained VT is not), repeat troponins (expected to peak, then fall), urine output and renal function after contrast, and bleeding risk on dual antiplatelet therapy plus anticoagulation.
Not resolved: the disease that built the clot. Discharge work starts now — dual antiplatelet adherence (“never miss, never stop without the cardiologist”), smoking cessation, diabetes and BP control, statin, cardiac rehab referral.
Debrief — The Pattern to Keep
- ✦"Indigestion" + diaphoresis + risk factors = 12-lead within 10 minutes — diabetics and women present atypically.
- ✦ST elevation activates the cath lab; you do not wait for troponin to treat a STEMI.
- ✦Inferior MI (II, III, aVF): think RCA, bradycardia/AV blocks, and RV involvement — hold nitrates and preload-droppers if the RV is in.
- ✦Oxygen only for SpO₂ <90%; aspirin is chewed, early, and almost never skipped.
- ✦Post-PCI: access site, reperfusion rhythms, contrast nephropathy, and DAPT teaching — the case isn't over when the artery opens.