Cardiovascular

Acute coronary syndrome: STEMI initial management and reperfusion timing

Clinical Overview and When to Suspect STEMI

— New ST elevation at the J point in ≥2 contiguous leads

— ≥1 mm in all leads except V2–V3

— V2–V3: ≥2 mm in men ≥40, ≥2.5 mm in men <40, ≥1.5 mm in women

— New LBBB alone is not STEMI — apply Sgarbossa criteria

— Crushing substernal chest pain >20 min, diaphoresis, dyspnea, radiation to jaw/left arm

— Anginal equivalents in elderly, diabetics, women, post-op: dyspnea, epigastric pain, syncope, new heart failure, delirium

— Hemodynamic instability or new arrhythmia in a patient with cardiac risk factors

— Posterior MI: ST depression V1–V3 with tall R waves; confirm with V7–V9 showing ≥0.5 mm elevation

— de Winter T waves: upsloping ST depression with tall symmetric T waves in precordials → proximal LAD occlusion

— Sgarbossa-positive LBBB or paced rhythm

— aVR ST elevation with diffuse ST depressions → left main or three-vessel disease

— IV access ×2, continuous telemetry, defibrillator at bedside, supplemental O2 only if SpO2 <90%

— Aspirin 162–325 mg chewed, sublingual nitroglycerin if SBP >90 and no RV infarct

— Activate cath lab before troponin returns if ECG is diagnostic

Step 3 management: Do not wait for troponin to activate PCI. The ECG is the decision. Time-to-reperfusion is the single most outcome-determining variable in STEMI.

Definition: ST-elevation myocardial infarction = acute transmural ischemia from complete epicardial coronary occlusion, almost always from atherothrombotic plaque rupture with overlying thrombus.

ECG criteria (Fourth Universal Definition of MI):

When to suspect on presentation:

Door-to-ECG goal: ≤10 minutes for any adult with chest pain or anginal equivalent.

STEMI "equivalents" that get the cath lab activated:

Initial bedside actions (parallel, not sequential):

Presentation Patterns and Key History

— Substernal pressure/heaviness >20 min, unrelieved by rest or nitro

— Diaphoresis, nausea, vomiting, sense of impending doom

— Radiation to left arm, jaw, neck, or back

— Often occurs in early morning hours (catecholamine surge)

— Women: fatigue, dyspnea, nausea, mid-back/jaw pain often without classic chest pain

— Diabetics: silent or painless MI from autonomic neuropathy; may present with hyperglycemia, DKA, or vague malaise

— Elderly (>75): confusion, syncope, dyspnea, falls, new-onset weakness

— Post-operative patients: hypotension, dyspnea, troponin bump on routine surveillance

— Cocaine/methamphetamine users: chest pain hours after use; coronary vasospasm + thrombosis

— Time of symptom onset — anchors the "ischemic time" clock

— Prior CAD, PCI, CABG, stents (and stent type/date — DAPT duration implications)

— Bleeding history, recent surgery, stroke, GI bleed — fibrinolytic contraindications

— Anticoagulant or antiplatelet use; last dose

— Cocaine/stimulant use in last 24h (changes management — favor benzos, nitrates, avoid β-blockers acutely)

— Allergies (especially contrast, aspirin)

— Tearing pain to back + pulse/BP differential → aortic dissection

— Pleuritic pain + recent immobilization → PE

— Positional pain relieved leaning forward → pericarditis

Board pearl: A diabetic with new-onset dyspnea and unexplained hyperglycemia in the ED gets an ECG before anything else — silent MI is the classic vignette trap.

Classic presentation:

Atypical and high-miss populations — anchor here on Step 3:

Targeted history (do not delay reperfusion):

Risk factor inventory: HTN, DM, dyslipidemia, smoking, family history of premature CAD (<55 men, <65 women), CKD, prior MI/PCI/CABG.

Red flags suggesting alternative dx during history:

Physical Exam Findings and Hemodynamic Assessment

— Tachycardia + hypotension → cardiogenic shock or RV infarct

— Bradycardia + hypotension → inferior MI with vagal tone or AV block

— Hypertension + tachycardia → anterior MI with sympathetic surge (target with β-blocker if no HF)

— S4 gallop (stiff ischemic ventricle) — common in acute MI

— S3 gallop → LV dysfunction, worse prognosis

— New holosystolic murmur:

— Apex radiating to axilla → acute mitral regurgitation (papillary muscle rupture/dysfunction)

— Left sternal border with thrill → ventricular septal rupture

— Pericardial friction rub (late, days 2–4) → post-infarct pericarditis

— Elevated JVP + clear lungs + hypotension = RV infarction triad

— Kussmaul sign (JVP rises with inspiration) supports RV involvement

— Cool, mottled extremities, narrow pulse pressure → cardiogenic shock

— I: no HF (mortality ~6%)

— II: rales, S3 (~17%)

— III: pulmonary edema (~38%)

— IV: cardiogenic shock (~67%)

Key distinction: Inferior STEMI (II, III, aVF) with hypotension that worsens after nitroglycerin = RV infarction. Treat with IV fluids, avoid nitrates/morphine/diuretics. Get right-sided ECG (V4R) — ≥1 mm elevation confirms RV involvement and changes preload management entirely.

General appearance: diaphoretic, anxious, ashen, clutching chest (Levine sign). Cool extremities suggest low cardiac output.

Vital signs — categorize hemodynamics immediately:

Cardiac exam:

Pulmonary exam: crackles → pulmonary edema; clear lungs with hypotension and elevated JVP → think RV infarct.

JVP and peripheral exam:

Killip classification (bedside prognosis in STEMI):

Diagnostic Workup — ECG, Biomarkers, and Initial Labs

— Anterior (V1–V4) → proximal LAD; high risk of pump failure, anterior wall rupture

— Lateral (I, aVL, V5–V6) → LCx or diagonal

— Inferior (II, III, aVF) → RCA (80%) or LCx; watch for AV block, RV infarct

— Posterior (V1–V3 ST depression, tall R) → RCA or LCx; confirm with V7–V9

— RV (V4R ST elevation) → proximal RCA; preload-dependent

— aVR elevation + diffuse depression → left main or LAD-equivalent

— High-sensitivity troponin I or T at 0 and 1–3 hr

— Rises 2–4 hr post-onset, peaks 12–24 hr, persists 7–14 days

— Do not delay PCI for troponin in diagnostic STEMI

— Troponin elevation interpretation matters: rise/fall pattern distinguishes MI from chronic elevation (CKD, HF, sepsis)

— CBC, BMP, magnesium, coags (PT/INR, PTT) — needed for anticoagulation dosing

— Lipid panel (fasting not required acutely)

— HbA1c, BNP, lactate if shock

— Type and screen

— β-hCG in reproductive-age women before contrast/radiation

— Portable CXR to evaluate pulmonary edema, mediastinum (dissection screen), pneumothorax — must not delay cath lab

— Bedside echo if hemodynamically unstable or dx uncertain: regional wall motion abnormality supports STEMI; rules in tamponade, dissection flap, RV strain

CCS pearl: Order ECG, aspirin, IV access, troponin, BMP, coags, CXR, and "activate cardiac catheterization lab" in the first clock advance. Holding orders to wait for results loses points and lives.

12-lead ECG within 10 minutes — repeat every 15–30 min if initial nondiagnostic but suspicion high.

Localize the infarct (predicts complications):

Cardiac biomarkers:

Initial labs (drawn concurrent with cath activation):

Imaging:

Diagnostic Workup — Advanced and Confirmatory Studies

— Pre-cath (if unstable or dx unclear): regional wall motion abnormality, EF, valve function, pericardial effusion

— Post-PCI (within 24–48 hr): baseline EF for ICD risk stratification and medication decisions

— Repeat at 40 days post-MI: if EF ≤35% on optimal medical therapy, evaluate for primary prevention ICD

— Reserved for diagnostic uncertainty, suspected myocarditis vs MINOCA, or assessment of viability

— Late gadolinium enhancement patterns differentiate ischemic (subendocardial → transmural) from non-ischemic (mid-wall, epicardial)

— Defined as MI criteria met but <50% stenosis on angiography

— Causes: plaque erosion, coronary spasm, SCAD (spontaneous coronary artery dissection), embolism, microvascular dysfunction, takotsubo

— Next steps: intravascular imaging (IVUS/OCT), provocation testing, cardiac MRI

— Right heart catheterization in cardiogenic shock to guide therapy

— CT coronary angiography is not appropriate for active STEMI (delays reperfusion)

— CT chest with contrast if dissection or PE seriously suspected — but only if it does not delay reperfusion in a clear STEMI

Board pearl: Young woman, peripartum or postpartum, with STEMI and minimal risk factors → think SCAD. Management is often conservative (medical) because PCI can extend the dissection. This is a classic Step 3 trap.

Coronary angiography is both diagnostic and therapeutic — it is the gold standard and the definitive study in STEMI. No additional confirmation needed before activation.

Echocardiography roles:

Cardiac MRI:

MINOCA workup (MI with Non-Obstructive Coronary Arteries):

Stress testing: Not used acutely in STEMI. May have role post-discharge for non-culprit lesion evaluation in stable patients.

Special advanced studies:

Risk Stratification and Reperfusion Strategy Logic

— First medical contact (FMC) to PCI ≤90 minutes if presenting to PCI-capable hospital

— FMC to PCI ≤120 minutes if transferring from non-PCI hospital

— If anticipated PCI delay >120 min from FMC → fibrinolysis within 30 min of arrival (door-to-needle ≤30 min)

— Symptom onset to reperfusion ideally <12 hours; PCI still beneficial up to 12 hr, and considered up to 24 hr if ongoing ischemia, shock, or instability

— Available within time window

— Cardiogenic shock or severe HF (Killip III–IV)

— Contraindication to fibrinolysis

— Diagnosis uncertain

— Late presentation (>3 hr from onset)

— Any prior intracranial hemorrhage

— Known cerebrovascular lesion (AVM, aneurysm)

— Known intracranial malignancy

— Ischemic stroke within 3 months (except acute <4.5 hr)

— Suspected aortic dissection

— Active bleeding or bleeding diathesis

— Significant closed head/facial trauma within 3 months

— Intracranial/spinal surgery within 2 months

— Severe uncontrolled HTN unresponsive to therapy

Step 3 management: Rural ED, STEMI, nearest PCI center 2.5 hours away by ground — give fibrinolytics now, then transfer (pharmacoinvasive strategy: cath within 3–24 hr post-lysis regardless of success).

The central STEMI decision: PCI vs fibrinolysis — driven by time and access.

Time targets (memorize cold):

PCI is preferred over lysis when:

Fibrinolysis absolute contraindications:

Relative contraindications: chronic severe HTN, SBP >180/DBP >110 on presentation, ischemic stroke >3 mo ago, traumatic CPR >10 min, major surgery <3 wk, recent internal bleeding <2–4 wk, noncompressible vascular puncture, pregnancy, active peptic ulcer, current anticoagulant use.

Pharmacotherapy — First-Line Regimen ("MONA-BASH" Reimagined)

— Aspirin 162–325 mg chewed immediately, then 81 mg daily indefinitely

— P2Y12 inhibitor loading dose:

— Ticagrelor 180 mg load, then 90 mg BID (preferred in most STEMI per ACC/AHA)

— Prasugrel 60 mg load, then 10 mg daily — only if going to PCI, avoid if age ≥75, weight <60 kg, or prior stroke/TIA

— Clopidogrel 600 mg load, then 75 mg daily — used with fibrinolysis (300 mg load if age >75) or when ticagrelor/prasugrel contraindicated

— Unfractionated heparin 60 U/kg bolus (max 4000), then 12 U/kg/hr — most common during PCI

— Bivalirudin alternative, especially with HIT history

— Enoxaparin if fibrinolysis chosen

— Nitroglycerin SL then IV if persistent pain, HTN, or pulmonary edema — avoid if SBP <90, RV infarct, or PDE-5 inhibitor use <24–48 hr

— β-blocker (oral) within 24 hr if no HF, no shock, no AV block, no active asthma — metoprolol tartrate 25–50 mg PO q6–12h. Avoid IV β-blockers acutely in patients at risk for shock

— Morphine only for refractory pain — may slow P2Y12 absorption and is associated with worse outcomes

— Atorvastatin 80 mg or rosuvastatin 40 mg on day 1, regardless of LDL

Board pearl: Prasugrel is contraindicated in any prior stroke/TIA — net harm exceeds benefit. This is a classic single-best-answer distractor.

Antiplatelets (dual therapy — DAPT):

Anticoagulation (during PCI or lysis):

Anti-ischemic therapy:

High-intensity statin:

Supplemental O2 only if SpO2 <90% — hyperoxia worsens outcomes.

Glycemic control: target glucose 140–180 mg/dL; avoid hypoglycemia.

Reperfusion — Primary PCI, Fibrinolysis, and CABG

— Radial access preferred (lower bleeding, mortality benefit)

— Culprit-only PCI vs complete revascularization: in stable multivessel STEMI, complete revascularization (staged or same-sitting) is now favored (COMPLETE trial) — reduces MI/death

— In cardiogenic shock: culprit vessel only acutely (CULPRIT-SHOCK), stage the rest

— Drug-eluting stents preferred over bare-metal

— Aspiration thrombectomy not routinely recommended

— Tenecteplase (TNK): single weight-based bolus, preferred for ease

— Alteplase (tPA): 15 mg bolus, then weight-based infusion over 90 min

— Reteplase: two 10-U boluses 30 min apart

— Streptokinase: rarely used in US

— Signs of successful reperfusion: ≥50% ST resolution at 60–90 min, reperfusion arrhythmias (AIVR), pain relief

— Rescue PCI immediately if lysis fails (persistent pain/ST elevation, hemodynamic instability)

— Even if successful, transfer for cath within 3–24 hr (routine early invasive strategy)

— Failed PCI with ongoing ischemia

— Coronary anatomy unsuitable for PCI (severe left main, three-vessel with diabetes, complex disease)

— Mechanical complications (VSR, papillary muscle rupture, free wall rupture)

— Cardiogenic shock with surgical anatomy

CCS pearl: After PPCI, transfer patient to CCU, continue heparin per protocol (often stopped post-PCI unless ongoing indication), DAPT, statin, β-blocker, ACEi — and order echo within 24–48 hr to assess EF and complications.

Primary PCI (PPCI) — the gold standard:

Fibrinolysis agents (give within 30 min of arrival if PCI unavailable):

Post-lysis management (pharmacoinvasive):

CABG indications in STEMI:

Mechanical circulatory support (IABP, Impella, VA-ECMO): selectively in cardiogenic shock — IABP no longer routine.

Special Populations — Elderly and Renal/Hepatic Impairment

— Present atypically: dyspnea, confusion, syncope, falls — anchor low threshold for ECG

— Higher mortality but also greater absolute benefit from reperfusion — do not withhold based on age alone

— Avoid prasugrel (net harm from bleeding)

— Clopidogrel load 300 mg (not 600) if pairing with fibrinolytics in age >75

— Reduce fibrinolytic dose? — tenecteplase dose is weight-based; no age adjustment, but bleeding risk is elevated

— Higher risk of contrast-induced AKI — pre-hydrate, minimize contrast volume

— Frailty assessment guides goals-of-care discussions, but does not automatically exclude PCI

— Pre-procedural IV isotonic saline hydration; hold nephrotoxins (NSAIDs, ACE inhibitors transiently if AKI)

— N-acetylcysteine and bicarbonate are NOT recommended (PRESERVE trial)

— Use minimum contrast volume; iso-osmolar contrast

— Hold metformin at time of contrast if eGFR <30 or AKI

— Enoxaparin dosing: reduce to 1 mg/kg daily if CrCl <30

— UFH preferred over enoxaparin in dialysis patients

— Eptifibatide/tirofiban dose-adjust; avoid if on dialysis or severe CKD

— Ticagrelor contraindicated in severe hepatic impairment

— Statins: monitor LFTs, but acute STEMI still warrants therapy

— Increased bleeding risk from coagulopathy — favor radial access, careful anticoagulation dosing

— Often present with atypical symptoms; troponin baseline is elevated — rely on delta (rise/fall pattern)

— PCI preferred; bleeding risk high — careful anticoagulation

Step 3 management: 82-year-old with STEMI and CrCl 35 — still activate cath lab. Use radial access, UFH (not enoxaparin standard dose), clopidogrel (not prasugrel), atorvastatin 80, low-dose β-blocker. Age is not a contraindication.

Elderly (≥75 years):

CKD (eGFR <60):

Hepatic impairment:

Dialysis patients:

Special Populations — Pregnancy, Cocaine, and Young Patients

— Incidence rising with maternal age; peak risk peripartum and early postpartum

— SCAD is the #1 cause of pregnancy-associated MI (especially postpartum) — not atherosclerosis

— Imaging: ECG safe; troponin reliable; echo first-line; CT/cath only when essential, with abdominal shielding

— Management:

— Aspirin (low-dose) safe throughout pregnancy

— Clopidogrel: limited data, use if needed

— Avoid ACE inhibitors, ARBs, statins during pregnancy (teratogenic)

— β-blockers (labetalol, metoprolol) acceptable

— Fibrinolytics relative contraindication in pregnancy (placental abruption, postpartum hemorrhage); PCI preferred

— SCAD often managed conservatively unless ongoing ischemia/instability — instrumentation can propagate dissection

— Multidisciplinary team: cardiology, OB, MFM, anesthesia

— Mechanism: vasospasm + platelet activation + accelerated atherosclerosis

— Benzodiazepines first for agitation, HTN, tachycardia

— Nitrates and CCBs for vasospasm

— Aspirin, heparin, PCI if STEMI confirmed

— Avoid β-blockers acutely (unopposed α-adrenergic stimulation → worsened vasospasm); labetalol/carvedilol may be safer if needed later

— Cocaine, SCAD, premature atherosclerosis (familial hypercholesterolemia), vasculitis, hypercoagulable states, anomalous coronary anatomy

— Workup: lipid panel, Lp(a), homocysteine, hypercoagulable panel if recurrent

Board pearl: A 32-year-old woman 2 weeks postpartum with chest pain and anterior STEMI: SCAD until proven otherwise. PCI only if hemodynamically unstable or ongoing ischemia — otherwise medical therapy and serial imaging.

Pregnancy-associated MI:

Cocaine/methamphetamine-induced MI:

Young patient (<45) with STEMI — broaden the differential:

Pediatrics: STEMI is extraordinarily rare; consider Kawasaki disease sequelae, congenital anomalous coronary, hypertrophic cardiomyopathy.

Complications and Adverse Outcomes

— VF/pulseless VT — leading cause of pre-hospital death; defibrillate immediately

— AIVR (40–100 bpm) — benign reperfusion rhythm, no treatment

— Sinus bradycardia/AV block: common in inferior MI (vagal, RCA supplies AV node) — atropine, transcutaneous pacing if symptomatic

— New BBB or Mobitz II/complete heart block in anterior MI — bad prognosis, often needs pacing

— AFib in 10–20%; rate control and anticoagulation

— Papillary muscle rupture (3–5 days): acute MR, flash pulmonary edema, new apical murmur → emergent surgery; posteromedial papillary muscle (single blood supply from PDA) most often involved in inferior MI

— Ventricular septal rupture (3–5 days): harsh holosystolic murmur at LSB with thrill, biventricular failure → surgery

— Free wall rupture (5–14 days): sudden hypotension, tamponade, PEA arrest → pericardiocentesis bridge, emergent surgery; high mortality

— LV aneurysm (weeks–months): persistent ST elevation >2 weeks, HF, thrombus risk

— Cardiogenic shock: SBP <90, end-organ hypoperfusion, lactate ↑ — high mortality; supports + revascularization

— Acute pulmonary edema: diuresis, NIPPV, vasodilators if BP allows

— Early post-MI pericarditis (days 2–4): pleuritic pain, friction rub — high-dose aspirin (not NSAIDs/steroids — impair healing)

— Dressler syndrome (weeks–months): autoimmune pericarditis, fever, pleuropericardial pain, effusion

Key distinction: New murmur day 3–5 post-MI: apex/axilla = papillary muscle rupture (MR); LSB with thrill = VSR. Both need surgery; echo confirms.

Arrhythmias (first 24–48 hr):

Mechanical complications (days 2–7, classic timeline):

Pump failure:

Pericardial:

LV thrombus in anterior STEMI with apical akinesis — anticoagulate ×3–6 months

Recurrent ischemia, stent thrombosis — emergent re-cath

When to Escalate — ICU, Consults, and Triage

— Mechanical complications (papillary muscle rupture, VSR, free wall rupture)

— Coronary anatomy unsuitable for PCI (left main, complex three-vessel)

— Failed PCI with ongoing ischemia

— Refractory cardiogenic shock despite vasopressors/inotropes → Impella, VA-ECMO

— Refractory VT/VF → consider ECMO + ablation

— Acute mechanical complications awaiting surgery → IABP or Impella as bridge

— EF severely reduced, persistent shock, transplant candidacy

— Recurrent VT, sustained VT >48 hr post-MI

— Persistent EF ≤35% at 40 days post-MI on GDMT → primary prevention ICD evaluation

— Hemodynamically stable, no recurrent ischemia, no significant arrhythmia >24 hr → step-down telemetry

— Mobilize early (ambulate day 1–2 post-PCI if uncomplicated)

— ≥24–48 hr post-PCI uncomplicated

— Stable vitals, no recurrent chest pain, no arrhythmia

— Tolerating GDMT

— Cardiac rehab referral, follow-up scheduled, medications reconciled

— Patient/family education on stent care, DAPT importance, when to return

CCS pearl: Do not discharge a STEMI patient without scheduling cardiology follow-up within 1–2 weeks, cardiac rehab referral, and explicit DAPT counseling. Premature DAPT discontinuation is a leading cause of stent thrombosis — a Step 3 favorite.

All STEMI patients → CCU/CICU post-reperfusion for at least 24 hr.

Immediate cardiology consultation at the moment of STEMI recognition — activate cath lab in parallel.

Cardiothoracic surgery consultation for:

Indications for advanced mechanical support / tertiary transfer:

Heart failure / advanced HF consult:

Electrophysiology consult:

Cardiac rehabilitation referral before discharge — Class I indication, reduces mortality and readmission.

Floor vs CCU step-down criteria:

Discharge readiness criteria:

Key Differentials — Same Category (Cardiac/Ischemic)

— Same pathophysiology spectrum but no ST elevation — ST depression, T-wave inversion, or normal ECG

— Positive troponin distinguishes from unstable angina

— Management: early invasive (within 24 hr) for high-risk (GRACE >140, dynamic ECG changes, hemodynamic instability, recurrent ischemia)

— Do not give fibrinolytics in NSTEMI — increases mortality

— Anginal symptoms at rest, crescendo, or new-onset severe

— Negative troponin

— Now rare with hs-troponin sensitivity

— Transient ST elevation, often at rest, often nocturnal

— Resolves with nitrates/CCBs

— Provocation testing (ergonovine, acetylcholine) confirms; treat with CCBs and long-acting nitrates

— Avoid β-blockers (unopposed α stimulation)

— Postmenopausal woman, emotional/physical stressor

— ECG mimics anterior STEMI (anterior ST elevation, T-wave inversions)

— Apical ballooning on echo with normal coronaries on cath

— Modest troponin elevation

— Management: supportive; usually recovers in weeks

— Troponin elevation from supply-demand mismatch (sepsis, tachyarrhythmia, hypotension, anemia)

— No acute plaque rupture

— Treat the underlying cause — not the cath lab

— May or may not have ST changes; rarely true STEMI pattern

— Young patient, viral prodrome, chest pain, troponin elevation

— ECG may mimic MI; MRI shows mid-wall/epicardial late gadolinium enhancement

Key distinction: Anterior ST elevation + apical ballooning + clean coronaries + recent emotional stressor in a 65-year-old woman = takotsubo, not STEMI from atherothrombosis. Both initially activate cath — cath defines the diagnosis.

NSTEMI:

Unstable angina:

Prinzmetal (variant) angina / coronary vasospasm:

Takotsubo (stress) cardiomyopathy:

MINOCA: discussed in chunk 5

Demand ischemia (Type 2 MI):

Myocarditis:

Key Differentials — Other Categories

— Tearing pain radiating to back, pulse/BP differential (>20 mmHg), widened mediastinum on CXR

— Critical: dissection can extend into a coronary ostium and cause STEMI (typically inferior/RCA) — giving fibrinolytics is catastrophic

— Screen with CTA chest if any feature suggests dissection before lytics

— Type A → emergent surgery; Type B → medical (β-blocker, BP control)

— Pleuritic chest pain, dyspnea, hypoxia, sinus tach, S1Q3T3, RV strain on echo

— Troponin can be positive from RV strain

— D-dimer, CTPA confirm

— Massive PE → thrombolysis (different agent doses than STEMI)

— Sharp, pleuritic, positional pain, relieved leaning forward, friction rub

— ECG: diffuse concave-up ST elevation, PR depression, no reciprocal changes

— Treat with high-dose NSAIDs (if not post-MI) + colchicine

— GERD, esophageal spasm — may mimic angina, even relieved by nitrates

— Boerhaave (esophageal rupture): vomiting, chest pain, subcutaneous emphysema, pneumomediastinum → surgical emergency

— Sudden pleuritic pain, dyspnea, unilateral decreased breath sounds, tracheal deviation → needle decompression

— Costochondritis, reproducible with palpation — diagnosis of exclusion

— Dermatomal pain preceding rash; consider in elderly with unilateral pain

— Panic disorder — diagnosis of exclusion only after ruling out cardiac

Board pearl: Hypertensive emergency + tearing back pain + inferior ST elevation = think dissection extending into RCA, not primary STEMI. CTA before any antithrombotic. Misdiagnosing dissection as STEMI and giving lytics is lethal — and a recurrent Step 3 vignette.

Aortic dissection:

Pulmonary embolism:

Pericarditis:

Esophageal:

Pneumothorax (tension):

Musculoskeletal:

Herpes zoster:

Psychiatric:

Secondary Prevention — Discharge Medications and Long-Term Plan

— Aspirin 81 mg daily — lifelong

— P2Y12 inhibitor (ticagrelor/prasugrel/clopidogrel) — DAPT for at least 12 months after STEMI regardless of stent type

— Shorter DAPT (1–6 mo) only in selected high-bleeding-risk patients

— Longer DAPT considered in low-bleeding-risk patients with high ischemic risk

— High-intensity statin: atorvastatin 80 or rosuvastatin 40 — target LDL <70 mg/dL (some advocate <55)

— Add ezetimibe if LDL not at goal

— Add PCSK9 inhibitor (evolocumab, alirocumab) if still not at goal

— β-blocker (metoprolol succinate, carvedilol, bisoprolol) — continue at least 1 year; indefinitely if EF ≤40%

— ACE inhibitor or ARB — especially if EF ≤40%, HTN, diabetes, CKD; lifelong

— Mineralocorticoid receptor antagonist (spironolactone, eplerenone) if EF ≤40% with HF symptoms or diabetes

— SGLT2 inhibitor (empagliflozin, dapagliflozin) — now Class I for HFrEF regardless of diabetes

— Consider sacubitril/valsartan if persistent HFrEF

— Smoking cessation — single largest mortality reduction; varenicline/NRT/bupropion + counseling

— BP target <130/80

— Diabetes: HbA1c <7%; prefer GLP-1 agonists and SGLT2 inhibitors for cardiovascular benefit

— Weight, Mediterranean diet, exercise

Step 3 management: Patient calls 6 months post-PCI saying he wants to stop "the expensive blood thinner" (ticagrelor) — counsel strongly against discontinuation; premature DAPT cessation carries high stent thrombosis risk. Coordinate with insurance/pharmacy for cost assistance, switch to generic clopidogrel only if necessary in consultation with cardiology.

The post-STEMI "Big 5" — all Class I unless contraindicated:

Add for HFrEF (EF ≤40%) post-MI:

Risk factor modification:

Influenza vaccine annually — reduces cardiovascular mortality post-MI (Class I).

ICD evaluation at 40 days post-MI if EF ≤35% on optimized GDMT.

Follow-Up, Monitoring, and Cardiac Rehabilitation

— 1–2 weeks post-discharge: PCP or cardiology — medication adherence, side effects, symptoms, BP, HR, wound check

— 4–6 weeks: cardiology — titrate β-blocker, ACEi to target doses

— 3 months: lipid panel — confirm LDL goal; intensify if needed

— 3 months and ongoing: every 3–6 months first year, then annually

— Class I recommendation — refer before discharge

— 36 sessions over 12 weeks: supervised exercise, risk factor education, psychosocial support, dietary counseling

— Reduces mortality ~20%, reduces readmission, improves QoL

— Underutilized — only ~30% of eligible patients attend; address barriers (transportation, cost, work)

— Lipids at 4–12 weeks post-statin initiation, then annually

— LFTs baseline and as indicated (not routine for statins)

— Renal function and potassium within 1–2 weeks of ACEi/ARB/MRA initiation

— HbA1c every 3–6 months if diabetic

— Repeat echo at 40 days post-MI to assess EF for ICD candidacy

— Light activity within days; gradual increase

— Driving: typically resume after 1 week (uncomplicated PCI); commercial drivers longer

— Sexual activity: safe to resume in 1–2 weeks if can climb 2 flights without symptoms

— Air travel: typically after 2 weeks if uncomplicated

— Return to work timing depends on job demands and recovery

Board pearl: Cardiac rehab is the single most underutilized Class I intervention post-MI. Step 3 loves a vignette where the "best next step" is referral to rehab, not another med.

Follow-up cadence:

Cardiac rehabilitation:

Monitoring parameters:

Activity and return-to-work counseling:

Depression screening (PHQ-9): post-MI depression is common and independently predicts mortality — treat with SSRIs (sertraline preferred — best cardiac safety data).

Vaccinations: influenza annually, pneumococcal, COVID-19, RSV per age.

Ethical, Legal, and Patient Safety Considerations

— In STEMI, implied consent applies when the patient is incapacitated or delay would cause harm

— If patient has capacity, brief verbal consent with discussion of risks (bleeding, contrast nephropathy, vascular complications, ~1% mortality) is appropriate — written consent should follow when feasible

— Family/surrogate involvement when patient lacks capacity

— A patient with capacity may refuse PCI even in active STEMI

— Confirm capacity (understanding, appreciation, reasoning, choice), document thoroughly, involve ethics/social work, offer second opinion, ensure no reversible factors (pain, hypoxia, delirium) impair decision-making

— Continue maximal medical therapy and palliative options

— Elderly, frail, or high-comorbidity patients — discuss prognosis, quality vs quantity, ICU thresholds

— Document code status before procedure

— Medication reconciliation at discharge — confirm DAPT, statin, β-blocker, ACEi, list discontinued meds

— Teach-back method for DAPT importance — never stop without cardiology approval, including before dental/elective surgery

— Coordinate early follow-up within 7–14 days

— Provide written instructions, warning signs (chest pain, bleeding, syncope), and 24/7 contact number

— Notify PCP via discharge summary within 48 hr

— Door-to-balloon delays are reportable quality metrics (CMS, ACC NCDR)

— Bleeding complications, contrast nephropathy, stent thrombosis trigger root-cause analysis

Step 3 management: Patient with capacity refuses PCI for active anterior STEMI. Do not override. Confirm capacity, exhaust persuasion, offer medical therapy, document the conversation, involve ethics. Autonomy trumps beneficence when capacity is intact.

Informed consent for emergent PCI:

Refusal of care:

Goals-of-care discussions:

Transition-of-care safety (huge Step 3 theme):

Patient safety events:

Disclosure of medical errors: if a complication arose from a system or human error, transparent disclosure is ethically and legally required.

Driving and occupational safety: commercial drivers, pilots, transit operators have regulated return-to-work requirements; document clearance carefully.

High-Yield Associations and Rapid-Fire Facts

— V1–V4 anterior → LAD → pump failure, anterior wall rupture, LV thrombus, BBB

— II, III, aVF inferior → RCA → AV block, RV infarct, bradyarrhythmias

— V1–V3 ST depression + tall R → posterior MI → confirm V7–V9

— V4R elevation → RV infarct → preload-dependent

— aVR elevation + diffuse depression → left main / proximal LAD / 3-vessel

— Hours–day 1: arrhythmias (VF, AIVR)

— Days 2–4: early pericarditis

— Days 3–5: papillary muscle rupture, VSR

— Days 5–14: free wall rupture

— Weeks–months: LV aneurysm, Dressler syndrome

— Prasugrel: avoid age ≥75, weight <60 kg, prior stroke/TIA

— Ticagrelor: causes dyspnea (~15%), increased uric acid, requires BID dosing

— Nitrates: avoid in RV infarct and recent PDE-5 inhibitor (sildenafil 24 hr, tadalafil 48 hr)

— Morphine: slows P2Y12 absorption — use sparingly

— β-blockers: avoid acutely in cocaine MI, shock, severe bradycardia, advanced AV block

— LBBB (use Sgarbossa), LVH with strain, early repolarization, pericarditis, hyperkalemia, Brugada, hypothermia (Osborn waves), takotsubo

Board pearl: "What is the most important factor predicting mortality in STEMI?" → Time to reperfusion. Not age, not EF, not Killip class — time.

Lead localization → artery → complication risk:

Mechanical complication timeline:

Drug "gotchas":

ECG mimics of STEMI:

Reperfusion arrhythmia: AIVR — benign, no treatment.

Anterior STEMI + apical akinesis → LV thrombus → anticoagulate × 3–6 months.

Single most important time metric: FMC-to-device ≤90 min (or ≤120 min with transfer).

Aspirin reduces post-MI mortality by ~25% — the largest absolute benefit of any single drug in cardiology.

Smoking cessation = single biggest modifiable mortality reducer post-MI.

Board Question Stem Patterns

— 58 y/o man, chest pain 1 hr, anterior ST elevations, presents to rural ED. Nearest PCI center 3 hr by ground. Next step? → Fibrinolytics within 30 min, then transfer for pharmacoinvasive PCI.

— Inferior STEMI, hypotension worsens after sublingual nitro. Next step? → IV normal saline bolus, obtain right-sided ECG (V4R), avoid nitrates/morphine/diuretics.

— STEMI patient with hemorrhagic stroke 2 years ago. Best management? → Transfer for primary PCI regardless of delay; absolute contraindication to lytics.

— Day 4 post-MI, new harsh holosystolic murmur at LSB with thrill, biventricular failure. Dx? → VSR; echo confirms; emergent surgical repair, IABP bridge.

— Day 3 post-MI, sharp pleuritic pain, friction rub. Treatment? → High-dose aspirin (NSAIDs and steroids impair myocardial healing).

— Patient stopped clopidogrel 2 weeks ago for elective surgery, now with recurrent STEMI. Lesson: never stop DAPT without cardiology input within 12 months post-DES.

— Young man, cocaine use 2 hr ago, ST elevations. Management? → Benzodiazepines, aspirin, nitrates, CCBs; avoid β-blockers acutely; PCI if STEMI persists.

— Patient 40 days post-anterior MI, EF 30% on GDMT. Next step? → Primary prevention ICD evaluation.

— 30 y/o woman, 1 week postpartum, anterior STEMI. Likely cause? → SCAD; consider conservative medical management if stable.

— Tearing back pain, inferior ST elevation, widened mediastinum. Next step? → CT angiography, not lytics; surgical/medical management of dissection.

Step 3 management: When stems give you a clock — symptom onset time, FMC time, transfer distance — they want you to calculate whether PCI vs lysis. Memorize 90/120/30 min thresholds.

Pattern 1 — The transfer dilemma:

Pattern 2 — RV infarction:

Pattern 3 — Contraindication to fibrinolysis:

Pattern 4 — Mechanical complication:

Pattern 5 — Post-MI pericarditis:

Pattern 6 — Stent thrombosis from premature DAPT discontinuation:

Pattern 7 — Cocaine chest pain:

Pattern 8 — Post-MI EF assessment:

Pattern 9 — Pregnancy-related MI:

Pattern 10 — Aortic dissection masquerade:

One-Line Recap

STEMI is a time-critical emergency: rapid ECG diagnosis, dual antiplatelet + anticoagulation, and reperfusion via primary PCI within 90 minutes (or fibrinolysis within 30 minutes if PCI unavailable within 120 minutes), followed by lifelong guideline-directed secondary prevention.

Board pearl: Every Step 3 STEMI vignette tests one of three axes — time-to-reperfusion decision, recognition of a complication (RV infarct, mechanical rupture, arrhythmia), or secondary prevention completeness. Master those three and you will own this topic on exam day.

Recognition: Door-to-ECG ≤10 min for any chest pain or anginal equivalent; ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V2–V3 for men); know STEMI equivalents (posterior MI, de Winter T waves, Sgarbossa+, aVR elevation).

Reperfusion timing: FMC-to-device ≤90 min at PCI hospital, ≤120 min with transfer, otherwise fibrinolytics within 30 min of arrival followed by transfer for pharmacoinvasive PCI within 3–24 hr. Time is muscle.

Acute pharmacotherapy: Aspirin 162–325 mg chewed, P2Y12 inhibitor (ticagrelor preferred; avoid prasugrel if age ≥75, weight <60 kg, or prior stroke), anticoagulation (UFH or bivalirudin), high-intensity statin, β-blocker within 24 hr if stable, ACEi/ARB especially if EF ≤40%; nitrates and β-blockers contraindicated in RV infarct and cocaine MI respectively.

Secondary prevention: Lifelong aspirin, DAPT ≥12 months, high-intensity statin to LDL <70, β-blocker, ACEi/ARB, smoking cessation, cardiac rehabilitation referral before discharge, repeat echo at 40 days for ICD evaluation if EF ≤35%, follow-up at 1–2 weeks, and aggressive risk factor modification.