What it is:Acute myocardial ischemia from a mismatch between oxygen demand and supply. A plaque ruptures, platelets pile onto the exposed collagen, thrombin builds a fibrin mesh around them, and blood flow abruptly drops.
Three flavors, split by ECG and troponin:STEMI (ST elevation + troponin), NSTEMI (troponin, no ST elevation), unstable angina (symptoms, no troponin).
The clock is the treatment.STEMI carries the highest short-term mortality and goes straight to reperfusion. Do not wait for troponin to come back before acting.
ST elevation → the artery is completely occluded → open it NOW(primary PCI, or fibrinolysis if PCI isn't reachable in time).
No ST elevation → the artery is partially occluded with residual flow → you have hours, not minutes.Risk-stratify, then choose early invasive or ischemia-guided.
Plaques that rupture typically have thin fibrous caps and are nonobstructive, occluding under 70% of the lumen. That's counterintuitive but important: because the narrowing is modest, autoregulation keeps flow adequate even during exertion, so many patients never had angina before the event. A surge of catecholamines during physical or emotional stress can be what tips a thinning cap into rupture.
Aspirinblocks thromboxane A₂. P2Y₁₂ inhibitorsblock the ADP receptor. GP IIb/IIIa inhibitorsblock the final common aggregation step. Heparins and bivalirudinblock thrombin. Four drug classes, four sequential points on one pathway - which is exactly why you use more than one at once.
This matters clinically: a Type 2 MI in a septic patientis treated by fixing the sepsis, not by cath lab activation.
SNS and RAAS activation compensate for reduced cardiac output acutely, but chronic hyperactivation causes ventricular hypertrophy and further impairs contractility. Inflammatory mediators and collagen deposition produce fibrosis and scarring, thinning the LV wall and potentially causing dilated cardiomyopathy. This is why ACE inhibitors and beta blockers are secondary prevention, not just BP drugs.
Classic:abrupt substernal chest pain or discomfort - squeezing, heaviness, tightness - persisting 10 minutes or longer. Radiates to arms and shoulders (especially left), back, abdomen, or jaw. Often with nausea, vomiting, diaphoresis, or shortness of breath.
Who:older adults, women, patients with diabetes, impaired renal function, or dementia.
What:epigastric pain, indigestion, pleuritic chest pain, increasing exertional dyspnea - withoutchest pain at all. Missing these is a major source of delayed diagnosis.
Physical exam:nothing is specific to ACS. Nonspecific findings include S4or paradoxical splitting of S2. Signs of acute decompensated HF include JVD, pulmonary edema, and S3. Patients may present with arrhythmias, heart block, hypertension, hypotension, or shock.
12-lead ECG within 10 minutes of presentation.Prehospital ECG if possible. This single step determines whether the patient goes to the cath lab immediately or gets risk-stratified.
| Diagnosis | ECG | Troponin |
|---|---|---|
| STEMI | ST elevation ≥1 mm in 2 contiguous leads, or new LBBB | Elevated, dynamic |
| NSTEMI | No ST elevation (may have depression or T inversion) | Elevated |
| Unstable angina | No ST elevation | Not elevated |
NSTEMI and unstable angina present identically. The onlything separating them is whether troponin rose. And STEMI is separated from both by the ECG, not the troponin - which is why you never delay reperfusion waiting for a troponin result.
Other baseline labs:renal function (identifies dose adjustments and high-risk patients), potassium and magnesium (rhythm), CBC, fasting lipid panel, and coagulation tests (aPTT or anti-Xa, INR) since nearly everyone gets antithrombotics.
| Intervention | Dose | Notes |
|---|---|---|
| Aspirin | 162–325 mg non-enteric-coated, chewed and swallowed | All ACS patients without contraindication, any type, any strategy. Chewing gets platelet inhibition in <30 min. Then 81 mg daily indefinitely |
| Nitroglycerin SL | 0.3–0.4 mg q5min × up to 3 doses PRN | For angina, uncontrolled HTN, acute HF |
| Nitroglycerin IV | Start 10 mcg/min, titrate to symptoms and BP | For persistent angina despite SL. Continue until symptoms resolve, BP controlled, HF subsided. Taper graduallyon discontinuation |
| Oxygen | 2–4 L/min, only if SaO₂ <90% | Routine use may harm- increases coronary vascular resistance and reduces coronary blood flow |
| Morphine | STEMI: 4–8 mg IV × 1 (lower if elderly), then 2–8 mg q5–15 min PRN NSTE-ACS: 1–5 mg q5–30 min, only if refractoryto other anti-ischemics | Role is uncertain - some studies show adverse outcomes |
| Beta blocker (oral) | Within first 24 hours | All patients without contraindications. Continue ≥3 yearsif normal LVEF; often lifelong if LVEF <40% |
Nitrates are contraindicatedin anyone who recently took a PDE-5 inhibitor (sildenafil, tadalafil, vardenafil). Ask directly - profound hypotension otherwise.
Aspirin contraindicationsare hypersensitivity and major GI intolerance. In those cases use clopidogrel with a loading dose instead.
The old mnemonic implies you give all four to everyone in that order. Reality: aspirinis the only one that's genuinely universal and outcome-improving. Oxygenis now restricted to SaO₂ <90% because routine use may cause harm. Morphinehas uncertain benefit and is second-line in NSTE-ACS. Nitratesrelieve symptoms but don't reduce mortality.
Anti-ischemic but no proven mortality benefit. Use non-dihydropyridines (diltiazem 120–360 mg/day, verapamil 240–480 mg/day)for angina in patients who are intolerant of, contraindicated to, or refractory to beta blockers - but onlyin the absence of LV dysfunction, cardiogenic shock risk, or AV conduction defects. Long-acting CCBs for known or suspected vasospasm (amlodipine 5–10 mg, nifedipine ER 30–120 mg, nicardipine 60–120 mg/day).
Why PCI wins:compared to fibrinolysis it improves survival, gives consistent revascularization of the infarct artery, reduces stroke and intracranial hemorrhage, and reduces reinfarction and recurrent ischemia.
| Agent | Dose |
|---|---|
| Alteplase | 15 mg IV bolus over 1–2 min → 0.75 mg/kg (max 50 mg) over 30 min → 0.5 mg/kg (max 35 mg) over 60 min. Max total 100 mg |
| Reteplase | 10 units IV over 2 min, repeat 10 units 30 min later |
| Tenecteplase | Single IV bolus over 5 sec by weight: <60 kg → 30 mg · 60–69.9 → 35 mg · 70–79.9 → 40 mg · 80–89.9 → 45 mg · ≥90 kg → 50 mg |
Fibrin-specific agents(alteplase, reteplase, tenecteplase) are preferred over streptokinasebecause of greater reperfusion success and less systemic bleeding.
Primary PCI is preferred in all of these situations.Between 12 and 24 hours after symptom onset, limit fibrinolysis to patients with ongoing clinical or ECG evidence of ischemia.
Fibrinolysis carries a 0.9–1.0%ICH rate. Predictors: advanced age, lower body weight, female sex, preexisting cerebrovascular disease, and systolic or diastolic hypertension at presentation.
These patients typically have a partially occludedartery with residual perfusion, so the urgency to open it is lower.
| Strategy | Who | What happens |
|---|---|---|
| Early invasive | Intermediate to high risk for death, MI, refractory angina, acute HF, cardiogenic shock, or arrhythmias | Diagnostic angiography within 24 hours, revascularize if appropriate |
| Ischemia-guided(medical management) | Select low-riskpatients | Antiplatelet + anticoagulant, no planned PCI. Noninvasive stress testing; angiography only if symptoms recur or instability develops |
Both antiplatelet andanticoagulant therapy are needed acutely, because platelets dominate arterial thrombosis while thrombin drives both platelet activation and coagulation. After discharge, most patients continue antiplatelet only.
| Agent | Loading dose | Maintenance | Notes |
|---|---|---|---|
| Clopidogrel | 600 mgbefore primary PCI 300 mgwith fibrinolysis or no reperfusion No loading dose if age ≥75 | 75 mg daily | The only agent studied in large trials with fibrinolysis |
| Prasugrel | Per protocol, at time of PCI | Daily | More potent. Avoid with prior stroke/TIA; caution age ≥75 and low body weight |
| Ticagrelor | Loading dose | Twice daily | Reversible. Dyspnea is a characteristic side effect |
| Cangrelor | IV | IV infusion | Adjunct to PCI in patients noton an oral P2Y₁₂ inhibitor or planned GP IIb/IIIa inhibitor |
1.With fibrinolysis, use clopidogrel- it's the only P2Y₁₂ inhibitor with large-trial evidence in that setting. Any of the four can be used with primary PCI.
2.No clopidogrel loading dose in patients ≥75 years old.Go straight to maintenance.
Considered during PCI when no P2Y₁₂ inhibitor was given beforehand, or in high-risk NSTE-ACS. They block the final common aggregation step, so bleeding risk is meaningful and they've become more selective in modern practice.
| Setting | Options |
|---|---|
| STEMI - primary PCI | UFHor bivalirudin; may switch to bivalirudin during PCI |
| STEMI - fibrinolysis | UFHor LMWH |
| NSTE-ACS - early invasive | UFHor LMWH, may switch to bivalirudin during PCI |
| NSTE-ACS - ischemia-guided | Fondaparinux, LMWH, or UFH |
It appears in the ischemia-guided NSTE-ACSpathway, not in the PCI pathways, because of catheter thrombosis risk when used alone during PCI. If a patient on fondaparinux goes to the cath lab, additional anticoagulation with anti-IIa activity is needed.
Every ACS patient should leave on this unless contraindicated. This is a very common exam and rotation question.
| Drug class | Why | Duration |
|---|---|---|
| Aspirin 81 mg daily | Antiplatelet | Indefinitely |
| P2Y₁₂ inhibitor | DAPT prevents stent thrombosis and recurrent events | Typically 12 months, individualized by bleeding vs ischemic risk |
| High-intensity statin | Established ASCVD = secondary prevention | Indefinitely. Atorvastatin 40–80 or rosuvastatin 20–40 |
| Beta blocker | Reduces angina, MI, arrhythmias; limits remodeling | ≥3 yearsif normal LVEF; often lifelong if LVEF <40% |
| ACE inhibitor / ARB | Blocks RAAS-driven remodeling | Especially with LV dysfunction, HF, diabetes, or CKD |
| Aldosterone antagonist | Post-MI with LVEF <40% plus HF or diabetes | Watch potassium and renal function |
| Sublingual NTG | PRN for breakthrough angina | Every patient goes home with it |
A-B-C-D-E:Aspirin + ACE inhibitor · Beta blocker · Clopidogrel (or other P2Y₁₂) + Cholesterol (high-intensity statin) · Diet and Diabetes control · Exercise / cardiac rehab. Add smoking cessation to every one of these.
Many ACS patients develop depression while recovering. It's listed in the complications for a reason. On rotations, a patient who "isn't taking their meds" after an MI is often depressed rather than noncompliant.
| Parameter | When | Watching for |
|---|---|---|
| Continuous multilead ECG | Throughout admission | Arrhythmias, ongoing or recurrent ischemia |
| Serial troponin | Presentation, 3–6 h, beyond 6 h if high risk with normal values | Dynamic rise/fall ≥20% confirms acute injury |
| Vital signs | Frequently | Hypotension limiting beta blocker, ACEi, nitrate titration |
| Renal function | Baseline and during admission | Drives anticoagulant dosing; contrast nephropathy after PCI |
| Potassium and magnesium | Baseline and periodically | Arrhythmia risk |
| CBC, aPTT/anti-Xa, INR | Baseline and during antithrombotic therapy | Bleeding, HIT |
| Lipid panel | Fasting, on admission | Confirms high-intensity statin need |
| LVEF (echo) | Before or shortly after discharge | Determines beta blocker duration, ACEi and MRA indication, ICD candidacy |