Acute Coronary Syndromes

📘 1 · Washington Manual of Critical Care, 4th Ed

Washington Manual Summary

"Every minute of myocardial ischaemia results in approximately 1.7 additional deaths per 1000 treated patients. The most important principle in ACS management is rapid reperfusion — time is muscle, and time is life."

Washington Manual of Critical Care, 4th Ed. (Kollef & Witt, eds.) Wolters Kluwer 2023.

ACS Spectrum

Type	Troponin	ECG	Mechanism	Urgency
STEMI	Positive	ST elevation ≥1mm (≥2mm V1–V4)	Complete occlusion major coronary artery	Immediate — D2B <90 min
NSTEMI	Positive	ST depression / T-wave inversion / Normal	Partial/transient occlusion — subendocardial	Early — GRACE score guided
UA	Negative	ST depression / T-wave changes / Normal	Plaque rupture without necrosis	Urgent — risk-stratify with HEART score

ECG Localisation (STEMI)

Territory	Artery	ECG Leads	Watch For
Anterior	LAD (proximal)	V1–V4	Cardiogenic shock (large territory)
Inferior	RCA (80%) or LCx (20%)	II, III, aVF	RV infarction — always do right-sided leads
Lateral	LCx	I, aVL, V5–V6	MR from posteromedial PM rupture
RV Infarction	Proximal RCA	V3R–V4R (right-sided leads)	Hypotension + clear lungs + ↑JVP — AVOID nitrates

📗 2 · Marino's The ICU Book, 5th Edition (2025)

Marino Physiology — ACS

🔬 How acute coronary syndrome develops

TriggerAtheromatous plaque rupture or erosion in a coronary artery

Exposed collagen → platelet adhesion (GPIb–vWF) → activation (ADP, TXA₂, thrombin)

Aggregation (GPIIb/IIIa–fibrinogen) + thrombin→fibrin → coronary thrombus

Partial occlusion → UA / NSTEMIsubendocardial ischaemia

Complete occlusion → STEMItransmural wavefront over 6–12h

Myocyte death from ~20–40 min; reperfusion injury if prolonged

Pathological stateMyocardial infarction → pump failure · arrhythmia · cardiogenic shock

"The central event in the pathogenesis of most cases of ACS is disruption (rupture or erosion) of an atheromatous plaque in a coronary artery. This leads to thrombus formation and, in most cases, partial or complete obstruction of coronary blood flow."

Marino PL. The ICU Book, 5th Ed. Chapter 20: Acute Coronary Syndromes, p.356 (approx). Wolters Kluwer; 2025.

📗 Marino Ch.20 — ACS Pathophysiology

From the saved Marino Ch.20 content:

Plaque rupture exposes subendothelial collagen → platelet adhesion (GPIb-vWF) → activation (ADP, TXA₂, thrombin) → aggregation (GPIIb/IIIa-fibrinogen) → thrombus
Thrombin generated → fibrin → red clot → coronary occlusion → ischaemia → infarction if prolonged
Myocardial cells die within 20–40 minutes of complete ischaemia; wavefront progresses subendocardium → transmural over 6–12 hours
Reperfusion injury: paradoxical worsening on reopening blocked artery (reactive oxygen species, Ca²⁺ overload) — irreversible if >4–6h of ischaemia

📗 Marino Ch.20 — Why Oxygen is NOT Routinely Indicated

ACC/AHA 2025 and Marino: supplemental O₂ NOT recommended if SpO₂ ≥90%. High-flow O₂ in normoxic MI may increase infarct size (coronary vasoconstriction, oxidant stress) — Class III: Harm. Give O₂ only if SpO₂ <90%.

📋 3 · ACC/AHA/ACEP 2025 Guidelines

Key Recommendations — ACC/AHA 2025

Rao SV, O'Donoghue ML, Ruel M, et al. ACC/AHA/ACEP/NAEMSP/SCAI 2025 Guideline for Management of Patients with ACS. JACC 2025;85(9):e59–e161.

STEMI — Reperfusion Timing Strong · Class I

Primary PCI: First medical contact (FMC) to balloon (D2B) <90 min if PCI-capable centre | <120 min if transfer needed
Fibrinolysis: FMC to needle <30 min if PCI not available within 120 min and symptoms <12h
ECG within 10 min of FMC — STEMI is an ECG diagnosis, NOT troponin-dependent

NSTEMI — Risk Stratification Strong · Class I

GRACE score for risk stratification: >140 = High risk → invasive within 24h | 109–140 = Intermediate → 72h | <109 = Low → conservative or stress testing
Immediate (<2h): haemodynamic instability, refractory ischaemia, life-threatening arrhythmia, cardiogenic shock

Oxygen — Class III (Harm) Avoid in normoxic MI

Do NOT give supplemental O₂ if SpO₂ ≥90%. High-flow O₂ in normoxic ACS may increase infarct size (AVOID-HF, DETO2X-AMI trials). Titrate O₂ to maintain SpO₂ 90–96% only if hypoxic.

💊 4 · Drug Doses

Drug Doses in ACS

Drug	Dose	Timing	Notes
Aspirin	300 mg PO (chewed/crushed loading); then 75–100 mg OD	Immediately on diagnosis	Chew and swallow — faster absorption. Give even before transport.
Ticagrelor	180 mg PO loading; 90 mg BD maintenance	As early as possible	Preferred over clopidogrel for STEMI (PLATO trial). Avoid if prior ICH, active bleeding.
Clopidogrel	600 mg load (PCI); 300 mg (fibrinolysis); 75 mg OD maintenance	As early as possible	Use if ticagrelor unavailable; mandatory with fibrinolysis
Heparin (UFH)	60–70 IU/kg IV bolus (max 5000); then 12–15 IU/kg/hr (aPTT 50–70s)	Immediately	Standard anticoagulant for STEMI/NSTEMI; weight-based dosing
Enoxaparin	1 mg/kg SC q12h (NSTEMI); 30 mg IV bolus + 1 mg/kg SC (STEMI with fibrinolysis)	Immediately	Preferred over UFH for NSTEMI (Superior in ExTRACT-TIMI 25); reduce dose in renal failure
GTN (Nitroglycerin)	0.4 mg SL q5 min × 3; then IV 5–200 mcg/min infusion	For ongoing pain/hypertension	CONTRAINDICATED: SBP <90, RV infarction, PDE5 inhibitors within 24–48h, severe AS
Metoprolol	25–50 mg PO BD (or 5 mg IV q5 min × 3 if rate control needed)	Start within 24h if stable	CONTRAINDICATED: cardiogenic shock, acute HF, severe bronchospasm, HR <60, AV block
Atorvastatin	80 mg OD (high-intensity)	Within 24h	PROVE IT: atorvastatin 80 mg reduced recurrent events vs pravastatin 40 mg
Tenecteplase (TNK)	Weight-based single IV bolus: <60kg: 30 mg; 60–70 kg: 35 mg; 70–80 kg: 40 mg; 80–90 kg: 45 mg; >90 kg: 50 mg	Only if PCI unavailable in 120 min	Most convenient fibrinolytic (single bolus). Check weight before dosing.
Streptokinase	1.5 million IU in 100 ml NS over 60 min	Only if PCI/TNK unavailable	Widely available in India. Avoid if prior streptokinase within 6 months (antibodies). Cheaper.

🗺 5 · Clinical Flowchart

ACS Management — Step by Step

ECG within 10 Minutes — First Priority

Every patient with chest pain/dyspnoea/syncope: ECG within 10 min. STEMI on ECG → activate cath lab NOW. Do NOT wait for troponin. Troponin takes hours; ECG diagnosis is immediate.

STEMI — Reperfusion Decision

PCI available in <120 min → Primary PCI (D2B <90 min). PCI NOT available in 120 min AND symptoms <12h AND no contraindications → Fibrinolysis (Tenecteplase weight-based IV push OR Streptokinase 1.5 MIU in India). Then transfer for angiography within 24h.

Dual Antiplatelets + Anticoagulation

Aspirin 300 mg chewed + Ticagrelor 180 mg (preferred) or Clopidogrel 600 mg. UFH or Enoxaparin. Start before PCI/fibrinolysis. Withhold only if absolute contraindication to antiplatelet (active CNS bleed).

Inferior STEMI — Right-Sided Leads Mandatory

ST elevation V3R–V4R = RV infarction (30–50% of inferior STEMI). Management: IV fluids (NOT diuretics), AVOID nitrates (precipitate hypotension), inotropes if needed. Missing RV infarction = iatrogenic cardiac arrest.

NSTEMI/UA — GRACE Score Risk Stratification

GRACE >140 or haemodynamic instability/refractory ischaemia → angiography <2h (immediate). GRACE 109–140 → angiography <24h. GRACE <109 → conservative or stress testing. Medical: aspirin + ticagrelor + anticoagulation + high-intensity statin.

Cardiogenic Shock in ACS

Early revascularisation (SHOCK trial). Noradrenaline (MAP ≥65) + Dobutamine (↑CO). IABP: no mortality benefit (IABP-SHOCK II) — use as bridge only. VA-ECMO for refractory cardiogenic shock. Transfer early to ECMO/surgical centre.

⚠️ 6 · Common Mistakes

Common Mistakes

❌ Mistake 1 — Waiting for Troponin to Activate Cath Lab

STEMI is an ECG diagnosis. Do NOT wait for troponin results (takes 1–6h depending on assay). Activate cath lab immediately on ECG criteria. Every minute of delay = 1.7 additional deaths per 1000 treated patients.

❌ Mistake 2 — Not Doing Right-Sided ECG in Inferior STEMI

RV infarction complicates 30–50% of inferior STEMI. Diagnosis: ST elevation V3R–V4R. Nitrates in RV infarction = severe hypotension. Diuretics = worsens RV preload. Treatment: IV fluids. Missing RV infarction = preventable catastrophe.

❌ Mistake 3 — High-Flow O₂ in Normoxic ACS

ACC/AHA 2025: Class III (Harm) — supplemental O₂ NOT recommended if SpO₂ ≥90%. Hyperoxia may cause coronary vasoconstriction and increase infarct size. Titrate to SpO₂ 90–96% only if hypoxic.

❌ Mistake 4 — Nitrates in RV Infarction or With PDE5 Inhibitors

RV infarction = preload-dependent. Nitrates → ↓ venous return → ↓ RV filling → cardiovascular collapse. Also: sildenafil/tadalafil within 24–48h + nitrates = severe hypotension. Always ask about PDE5 inhibitors before giving GTN.

❌ Mistake 5 — Metoprolol in Acute Heart Failure or Cardiogenic Shock

Beta-blockers are contraindicated in acute decompensated heart failure and cardiogenic shock. Start within 24h ONLY if haemodynamically stable. Evidence (COMMIT trial): early IV beta-blocker in Killip class II–IV patients → harm.

🎓 7 · Exam Pearls — DrNB / PDCC / IFCCM

Exam Pearls

Q: ACC/AHA 2025 door-to-balloon time targets?
<90 min if patient presents to PCI-capable centre. <120 min if transfer is required. If PCI not available within 120 min AND symptoms <12h → fibrinolysis (Tenecteplase single IV bolus, weight-based) within 30 min of arrival (door-to-needle).

Q: Why avoid nitrates in inferior STEMI? When?
If right-sided leads (V3R–V4R) show ST elevation = RV infarction = preload-dependent. Nitrates → ↓ venous return → ↓ RV filling → haemodynamic collapse. Also contraindicated if PDE5 inhibitors used within 24–48h (sildenafil, tadalafil, vardenafil).

Q: GRACE score thresholds for angiography timing?
>140 OR haemodynamic instability/refractory ischaemia → Immediate (<2h) | 109–140 → Early (<24h) | <109 → Conservative or 72h. HEART score used for chest pain risk stratification in ED (low ≤3 = 2% MACE; high ≥7 = 65% MACE).

Q: Tenecteplase (TNK) dosing for STEMI?
Weight-based single IV bolus: <60 kg: 30 mg | 60–70 kg: 35 mg | 70–80 kg: 40 mg | 80–90 kg: 45 mg | >90 kg: 50 mg. Give over 10 seconds. Add aspirin 300 mg + clopidogrel 300 mg + enoxaparin or UFH simultaneously.

Q: What is the ACC/AHA 2025 recommendation on oxygen in ACS?
Class III (Harm): supplemental O₂ NOT recommended if SpO₂ ≥90%. Hyperoxia in normoxic MI may increase infarct size. Give O₂ only if SpO₂ <90%; titrate to maintain 90–96%.

📚 8 · References

References

Marino PL. Marino's The ICU Book, 5th edition. Chapter 20: Acute Coronary Syndromes (pp.356–389). Philadelphia, PA: Wolters Kluwer; 2025. ISBN: 978-1-975176-71-6.
Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients with Acute Coronary Syndromes. J Am Coll Cardiol. 2025;85(9):e59–e161.
Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the Management of Acute Coronary Syndromes. Eur Heart J. 2023;44(38):3720–3826.
Hochman JS, Sleeper LA, Webb JG, et al. (SHOCK trial). Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock. N Engl J Med. 1999;341(9):625–634.
Thiele H, Zeymer U, Neumann FJ, et al. (IABP-SHOCK II). Intraaortic Balloon Support in Myocardial Infarction with Cardiogenic Shock. N Engl J Med. 2012;367(14):1287–1296.
Stub D, Smith K, Bernard S, et al. (AVOID). Air versus Oxygen in ST-Segment Elevation Myocardial Infarction. Circulation. 2015;131(24):2143–2150.
Washington Manual of Critical Care, 4th Edition. Kollef MH, Witt CA (eds). Wolters Kluwer; 2023.
Oh TE (ed). Oh's Intensive Care Manual, 8th edition. Chapter: Acute Coronary Syndromes. Elsevier; 2018.