Chest Pain & Acute Coronary Syndromes

Unstable, persistent ischemic symptoms, or diagnostic ST elevation? Activate the emergency reperfusion pathway while resuscitation and the differential continue. A normal first ECG or troponin does not close the case.

1 · StabilizeABCs, monitor, IV access, vitals in both arms if aortic concern. Treat shock, malignant rhythm, or severe hypoxemia in parallel.

2 · ECG ≤10 minCompare prior. Repeat with recurrent pain. Add right-sided leads for inferior MI/RV concern and posterior leads for reciprocal anterior ST depression.

3 · hs-cTn pathwayUse a validated 0/1-h, 0/2-h or High-STEACS pathway with exact assay thresholds and sampling times. The simple 99th-percentile 0/3-h rule-out is inferior and is not recommended.

Do not miss the other killers

test to the phenotype

Concern	Clues	Immediate next move
Aortic syndrome	Abrupt maximal pain, pulse/BP deficit, neuro finding, new AR, mediastinal widening	Avoid empiric antithrombotics if strongly suspected. Urgent aortic imaging/surgery pathway
Pulmonary embolism	Pleuritic pain, hypoxemia, tachycardia, DVT/risk context, RV strain	Probability-based D-dimer or CTPA, with POCUS if unstable
Tension PTX	Sudden pain/dyspnea, unilateral absent breath sounds, shock	Immediate decompression if unstable. Do not wait for formal imaging
Tamponade	Shock, JVP, narrow pulse pressure, electrical alternans, cancer/procedure context	Bedside echo and urgent drainage pathway
Esophageal rupture	Forceful emesis, severe chest pain, crepitus, sepsis	NPO, broad-spectrum antibiotics, urgent CT/esophageal/surgical evaluation

Injury is not automatically infarction

name what is established

Myocardial injury hs-cTn above the assay’s sex-specific 99th percentile upper reference limit.
Acute injury rise/fall with at least one value above that limit. A delta alone below the limit does not establish injury.

Myocardial infarction acute injury plus evidence of ischemia: symptoms, ischemic ECG, new ischemic regional dysfunction, or acute coronary pathology. Confirm the mechanism with imaging when feasible.
Shock, HF, tachyarrhythmia, PE, myocarditis, sepsis, and kidney disease can cause injury without an acute coronary lesion. See the 2026 MI classification on page 4.

Practice boundary: confirm the current STEMI/OMI activation criteria, assay-specific hs-cTn deltas, and emergency transfer process before applying this framework.

Three lanes

escalation is dynamic

Lane	Signals	Disposition
Immediate / emergent	STEMI/occlusion pattern, shock, refractory/recurrent ischemia, malignant ventricular rhythm, mechanical complication	Activate PCI/reperfusion and CICU pathway now. Bedside echo must not delay cath when diagnosis is clear
High-risk NSTE-ACS	Definite NSTEMI, dynamic ST/T changes, recurrent symptoms, HF, major arrhythmia, high clinical-risk score	Monitored admission and cardiology. Angiography within 24 h is reasonable for high-risk NSTE-ACS. Instability requires immediate evaluation
Low risk by validated CDP	Reassuring serial ECG/hs-cTn and clinical decision pathway, with no unstable alternative diagnosis	Discharge may be reasonable with clear follow-up, return precautions, and preventive-care ownership

Do not use a score to overrule instability. HEART/EDACS support ED disposition. GRACE estimates risk in established ACS. A nonischemic ECG plus rule-out by a validated hs-cTn pathway can permit discharge without another score.

ECG patterns that deserve a second look

call early

Posterior occlusion horizontal ST depression V1–V3 with tall R waves → V7–V9.
RV infarction inferior MI + hypotension/JVP/clear lungs → right-sided leads. Avoid preload-reducing drugs if shock.
Diffuse subendocardial ischemia widespread ST depression ± aVR elevation signals severe supply-demand imbalance or high-risk coronary disease, not a lesion by itself.

LBBB / paced rhythm apply validated concordance criteria and the whole clinical picture. New LBBB alone is not an automatic STEMI diagnosis.
Hyperacute or dynamic T waves repeat during symptoms and compare prior tracings.
Wellens-like pattern pain-free anterior biphasic/deep T inversion after symptoms warrants urgent cardiology evaluation and no exercise stress.

Testing after ACS is not established

match test to question

Clinical question	Useful direction	Avoid
Known CAD, new high-risk features	Cardiology-directed angiography or functional/anatomic strategy	Routine low-value duplicate testing
No known CAD, intermediate risk	CCTA or stress imaging based on age, calcification, rhythm, renal function, prior testing, and available expertise	Uninterpretable exercise ECG when baseline ECG cannot diagnose ischemia
Low risk after CDP	Often no urgent test. Prioritize follow-up and prevention	Automatic admission or testing solely because pain occurred

Disposition sentence: “Serial ECG/hs-cTn trajectory ___. Current lane ___ because ___. Lethal alternative assessment ___. Next decision/test ___. Owner and time ___.”

Initial ACS treatment

parallel, not sequential

Therapy	Use	Safety boundary
Aspirin	162–325 mg chewed promptly when ACS is likely and no contraindication, then 75–100 mg daily	Withhold when aortic dissection is strongly suspected or active major bleeding is present
P2Y12 inhibitor	Choose and time with planned invasive strategy, bleeding risk, stroke history, need for anticoagulation, and PCI plan	Do not reflexively pre-load every NSTE-ACS patient before anatomy. Coordinate with the interventional team and current pathway
Anticoagulant	UFH, enoxaparin, or other guideline-supported strategy based on ACS lane and invasive plan	Verify weight, kidney function, recent anticoagulant, bleeding, and procedure timing. Use the current dosing standard
Nitroglycerin	0.4 mg SL q5 min × up to 3 for ongoing ischemic pain if safe, with IV for selected persistent pain/HTN/edema	Avoid hypotension, suspected RV infarction with preload dependence, severe AS, or recent PDE-5 inhibitor
Oxygen	Give for hypoxemia (SpO₂ <90%), titrating to ≥90%	No routine supplemental oxygen when SpO₂ ≥90%. Evaluate respiratory distress and its cause
Beta-blocker	Selected stable patients without contraindication	Avoid acute HF, low output/shock risk, bradycardia/AV block, or severe active bronchospasm
High-intensity statin	Start/continue early unless contraindicated. Plan secondary-prevention intensification	Medication reconciliation, interaction and liver/muscle context

Reperfusion & revascularization

time is myocardium

Primary PCI STEMI targets: first medical contact to device ≤90 min for direct presentation and ≤120 min with transfer.
Fibrinolysis for eligible STEMI within 12 h when PCI will exceed 120 min. Screen exclusions, target lysis ≤30 min after arrival, and transfer immediately. Failed lysis or instability → rescue PCI.

Shock urgent culprit-vessel revascularization. Routine nonculprit PCI during the index shock procedure is generally avoided.
Multivessel disease plan complete revascularization according to stability, anatomy, LV function, complexity, and Heart Team input.

Before the patient leaves the acute lane

close the loops

Loop	Required handoff content
Diagnosis	STEMI/NSTEMI/unstable angina/acute or chronic injury/alternate cause, plus culprit and revascularization result if known
Antithrombotics	Exact agents, last doses, indication, intended duration, bleeding risk, and whether oral anticoagulation is also needed
Function/complications	LVEF, HF/shock, rhythm, mechanical complication, kidney/hemoglobin trajectory
Prevention	Lipid plan, smoking, BP/diabetes, cardiac rehab referral, activity/work advice, and follow-up date

Practice boundary: verify antithrombotic selection and dosing, fibrinolysis exclusions, and activation/transfer targets against current guidelines, labels, and the treating system.

Read the trajectory

value + delta + time

Pattern	Interpretation	Next question
Below rule-out threshold with reassuring delta	Low probability of acute MI only within the validated assay-specific pathway and correct symptom-time window	Is the clinical risk truly low, and has another serious cause been addressed?
Above 99th percentile, stable	Chronic injury is possible. A late-presenting MI can also have little change over a short interval	Compare prior values and symptoms, ECG and imaging. Kidney disease does not make the result benign
Rise/fall + value above URL	Acute myocardial injury. Use the sex-specific 99th-percentile upper reference limit (URL) and assay-specific delta	Ischemic or nonischemic? Which clinical setting?
Early / observation zone	A first low value may precede release. Single-draw rule-out needs the pathway’s very-low threshold, nonischemic ECG and symptoms ≥3 h	Repeat as specified. Intermediate-risk patients often need repeat hs-cTn at 3–6 h and further assessment

Reasoning sequence, not an elapsed-time model. Without evidence of ischemia, retain myocardial injury. In acute illness and after procedures, use objective imaging confirmation when feasible.

Classify the clinical setting

phenotype the cause

Primary MI spontaneous acute coronary disease: atherothrombosis, SCAD, embolism or spasm.
Secondary MI consider with acute injury and supply–demand ischemia from another acute illness. When feasible, confirm by obstructive CAD without acute coronary pathology and/or new ischemic regional dysfunction or viability loss.
Procedure-related MI a coronary complication within 30 days of a cardiac procedure. Confirmation uses coronary complication and/or new ischemic regional dysfunction or viability loss. Both are required during the index procedure or when the procedure treats acute MI.

Nonischemic injury myocarditis, acute HF, PE, sepsis, renal disease, catecholamine injury, cardiac contusion, infiltrative disease.
Terminology changed in 2026 “primary” includes more than former type 1. “Secondary” replaces only part of former type 2. Document the actual mechanism and diagnostic certainty.

Echo and angiography questions

test to change management

Tool	High-value use	Limit
Bedside echo	Shock, HF, suspected mechanical complication, RV infarct/PE, tamponade. New regional dysfunction can support ischemia	A normal study does not exclude ACS. Do not delay reperfusion in a clear STEMI
Formal TTE	LVEF, regional function, valve/mechanical complication, alternative structural diagnosis	Prior abnormalities need comparison
Coronary angiography	Emergent/high-risk ACS and anatomy-directed management	MINOCA is a working diagnosis of myocardial injury with nonobstructive coronary arteries in the Fifth UDMI. Resolve coronary and nonischemic causes with targeted imaging/testing
Cath-lab sequencing	When spasm/dynamic caliber change is plausible and BP permits, give intracoronary nitroglycerin before reaching for IVUS/OCT.	Improvement proves a dynamic component, not the only process. Extra instrumentation can propagate suspected SCAD. For CTO planning, acquire a stable run long enough to show late collateral filling while preserving dose/contrast discipline.

An open epicardial artery is a procedural result—not proof of tissue reperfusion. Persistent pain or ST elevation, no-reflow, ventricular arrhythmia, or shock means the microcirculation and myocardium may remain in trouble. Reopen the physiology and treatment plan.

Documentation: “hs-cTn ___→___ over ___ h using ___ assay/pathway. ECG ___. Ischemic evidence ___. Injury phenotype ___. Suspected cause ___. Planned confirmation/management ___.”

Occlusion blind spots

repeat and extend leads

Pattern	Actionable concern	Response
Posterior	ST depression V1–V3, tall R, upright T can be reciprocal posterior injury	Posterior V7–V9 and urgent cardiology/reperfusion assessment
Inferior + RV	Hypotension, JVP, clear lungs, AV block	Right-sided leads, cautious preload/vasodilator decisions, reperfusion
LBBB / paced	Concordant or excessively discordant changes with an ischemic syndrome	Apply validated criteria, compare prior, urgent expert review
Dynamic / transient	ECG normalizes when pain ends or evolves after the first tracing	Capture ECG during symptoms and repeat serially

Deterioration after MI

echo + cath/surgery early

Problem	Clues	Immediate direction
Cardiogenic shock	Hypotension/hypoperfusion, pulmonary or systemic congestion, rising lactate, oliguria	Shock team, urgent culprit revascularization, echo/hemodynamics, individualized vasoactive/MCS strategy
Papillary muscle rupture / acute MR	Flash edema/shock, new murmur may be soft, hyperdynamic LV	Urgent echo/TEE, afterload/support, cardiac surgery/interventional valve team
Ventricular septal rupture	Shock, new harsh murmur/thrill, RV oxygen step-up	Urgent echo, surgery/MCS planning
Free-wall rupture / tamponade	Sudden collapse, PEA, pericardial effusion or clot	Immediate echo and surgical rescue. Controlled drainage is a specialist bridge, not routine full evacuation
Recurrent ischemia / stent thrombosis	Recurrent pain/ST change, ventricular arrhythmia, shock	Repeat activation and urgent angiography

Arrhythmia & conduction

treat cause + rhythm

VF/pulseless VT: defibrillation/ACLS and immediate reperfusion assessment.
Sustained VT with pulse: instability determines cardioversion. Correct ischemia/electrolytes.
AF: control rate/rhythm according to stability, LV function and shock. Account for antithrombotic overlap.

Inferior MI AV block is often nodal/transient. Anterior MI block is more often infranodal and ominous.
Prepare temporary pacing when unstable high-grade block persists. Reperfusion remains central.
Avoid routine suppression of benign ventricular ectopy.

Practice boundary: shock-team activation, MCS selection, mechanical-complication transfer, temporary pacing, and cath-lab reactivation require the treating center’s current capabilities and escalation process.

Antithrombotic ledger

one source of truth

Field	Record explicitly
PCI / anatomy	Date, culprit, stent(s), residual disease, staged procedure, access complication
Antiplatelets	Aspirin + P2Y12 agent, load/maintenance. Default after ACS: ≥12 months if not at high bleeding risk. Record the reason and stop dates for a shorter or modified regimen
Oral anticoagulant	Indication, dose and renal method. After PCI with long-term OAC, generally stop aspirin at 1–4 weeks and continue OAC + P2Y12 (usually clopidogrel), tailored to ischemic/bleeding risk
Bleeding protection	Hemoglobin/bleeding course, GI protection where indicated, avoid NSAIDs, follow-up lab
Interruption warning	Who must be contacted before procedures or stopping therapy, plus an emergency plan for bleeding

Secondary prevention bundle

start before discharge

Lipids high-intensity statin, then add nonstatin therapy to reach the 2026 LDL-C goal: <55 mg/dL for very-high-risk ASCVD, <70 otherwise. Document the risk category.
LV protection LVEF and HF phenotype. ACEi/ARB and beta-blocker when indicated. MRA for LVEF ≤40% with HF or diabetes if kidney/K permit. ARNI/SGLT2i follow the HF indication, not MI alone.
Lifestyle tobacco treatment, nutrition, activity, weight, BP and diabetes care.

Cardiac rehabilitation place referral and address transportation/access.
Vaccination / prevention appropriate preventive care and medication adherence/affordability.
Psychosocial depression/anxiety, sleep, work/sexual activity questions, caregiver understanding.

PROMISE

Death/MI prevention and angina relief are different endpoints. ISCHEMIA did not show a lower primary composite with an initial invasive strategy in its enrolled stable population. ORBITA-2 showed symptom benefit from PCI in selected patients receiving little or no antianginal therapy. State which outcome the next procedure is meant to change, and retain anatomy, LV function, exclusions, symptom burden, medical therapy, risk, and preference.

Follow-up clocks

scheduled, not suggested

Clock	Close these loops
Before discharge	Rehab, medications in hand, ECG/echo result, return precautions, staged PCI/surgery plan
Early follow-up	Symptoms, BP/HR, bleeding, access site, adherence, kidney/K, HF status, work/activity and rehab entry
4–8 weeks	Recheck lipids 4–8 weeks after starting/changing therapy. Titrate prevention and HF treatment. Reassess LV function at the device-guideline interval after recovery/revascularization

Copy-ready summary: “___ ACS on ___. Culprit/anatomy ___. Revascularization ___. LVEF ___. Complications ___. Antithrombotic plan through ___. Prevention targets ___. Rehab/follow-up ___.”

Practice boundary: individualize DAPT/AF-PCI duration, lipid targets, post-MI HF therapies, device reassessment, and rehabilitation using current guidelines and patient factors.