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Hub / Organ Systems / Cardiovascular Medicine
COMLEX Level 1 • Level 2-CE • COMAT • 14–18% Blueprint Weight

Cardiovascular Medicine Command Center

High-yield cardiovascular pathophysiology, ACS biomarker kinetics, 12-lead ECG localization, physical exam maneuver dynamics on murmurs, GDMT heart failure guidelines, and pediatric congenital cyanotic defect matrices.

Ischemic Heart Disease Spectrum

Acute Coronary Syndromes (ACS) Triad

ECG • Biomarkers • Plaque Pathology
Incomplete Occlusion No Necrosis

Unstable Angina (UA)

New-onset angina at rest, worsening frequency/duration, or post-infarction angina. Subtotal thrombotic occlusion over ruptured atheromatous plaque.

ECG: Normal or transient ST depression / T-wave inversion
Troponin: Negative
Management: Medical anti-ischemic + DAPT
Subendocardial Infarct Partial Occlusion

NSTEMI

Persistent ischemia causing subendocardial myocyte necrosis without transmural ST elevations. Subendocardium is most vulnerable to ischemic hypoperfusion.

ECG: ST depression (>0.5 mm) or T-wave inversion
Troponin: Positive (Elevated)
Management: DAPT, Heparin, early invasive angiography (<24h)
Transmural Infarct Full Occlusion

STEMI

Complete, acute thrombotic occlusion of epicardial coronary artery leading to full-thickness transmural necrosis of myocardium. Immediate time-critical emergency!

ECG: Convex-up ST elevation ≥1 mm in ≥2 contiguous leads (or new LBBB)
Troponin: Markedly Elevated
Target Door-to-Balloon: ≤90 minutes (or tPA ≤30 min if no PCI facility)
Coronary Angiography • 12-Lead Map

Coronary Territory & Infarction Localization

LAD • LCx • RCA • Reciprocal Shifts
Infarct Location ECG Leads with ST Elevation Occluded Coronary Artery Reciprocal ST Depression Key Board Exam Correlates
Anteroseptal V1, V2 LAD (Proximal / Septal Branches) None or minimal II, III, aVF Supplies IV septum and Bundle of His; high risk of Mobitz II and complete AV block.
Anteroapical V3, V4 LAD (Distal) Inferior leads (II, III, aVF) Most common STEMI location. Risk of true left ventricular apical aneurysm and mural thrombus.
Anterolateral / Extensive Anterior V1–V6, I, aVL LAD Mainstem ("Widowmaker") Inferior leads (II, III, aVF) Massive anterior wall necrosis; severe cardiogenic shock; acute pulmonary edema.
Lateral I, aVL, V5, V6 LCx (Left Circumflex Artery) Inferior leads (II, III, aVF) Supplies lateral left ventricle; perfused from diagonal or obtuse marginal branches.
Inferior II, III, aVF RCA (Right Coronary Artery) in 90% Leads I and aVL Supplies AV node in right-dominant circulation; risk of sinus bradycardia, Wenckebach AV block. Contraindicated: Nitrates/Morphine if RV involvement!
Right Ventricular (RV) V4R (Right-sided leads), V1 RCA (Acute Marginal Branches) Varies Clinical Triad: Hypotension, Clear lung fields, Elevated JVP. Highly preload-dependent → treat with IV Normal Saline boluses, avoid nitrates/diuretics.
Posterior V7–V9 (≥0.5 mm STE) PDA (from RCA or LCx) Tall R waves & ST depression in V1–V3 Mirror-image changes in standard V1–V3 leads (horizontal ST depression, upright tall T waves, tall R waves).
Clinical 12-Lead Diagnostic Exhibits

Anterior STEMI ("Tombstone") vs. Inferior STEMI

12-Lead Strip Verification
LAD Occlusion • Anteroseptal

Anterior STEMI: Massive "Tombstone" ST Elevations

Anterior STEMI Tombstone ST Elevations 12-Lead ECG

Marked convex-up ST elevations spanning V1–V4 with hyperacute T waves ("tombstoning"). Indicates proximal LAD occlusion with massive anterior wall necrosis.

RCA Occlusion • Diaphragmatic Wall

Inferior STEMI: Leads II, III, aVF with Reciprocal Changes

Inferior STEMI Leads II III aVF 12-Lead ECG

Prominent ST elevation in inferior leads (II, III, aVF) paired with classic reciprocal ST depression in high lateral leads (I, aVL). Indicates RCA occlusion.

High-Yield Board Pathology Timeline

Post-Myocardial Infarction Complications Timeline

0 Hours to >2 Weeks
0–24 Hours

Lethal Arrhythmias & Heart Failure

Ventricular Fibrillation (VF) and Ventricular Tachycardia (VT) from electrical re-entry around ischemic margins. Primary cause of pre-hospital death.

Histology: Early waviness of myofibers (0–4h), contraction bands (reperfusion), early coagulation necrosis, and edema.
1–3 Days

Fibrinous Pericarditis

Localized inflammation over transmural infarct area. Pleuritic chest pain worse supine, relieved sitting forward. Audible pericardial friction rub.

Histology: Dense neutrophil infiltration with extensive coagulation necrosis and loss of myocyte nuclei.
3–14 Days

Mechanical Rupture Triad

• Free Wall Rupture: Hemopericardium → rapid Cardiac Tamponade (Beck's triad).
• Papillary Muscle Rupture: Posteromedial papillary muscle (single blood supply from PDA) → acute severe Mitral Regurgitation & pulmonary edema.
• Interventricular Septum Rupture: Macrophage lysis of IV septum → left-to-right shunt with harsh new holosystolic murmur at LLSB.
Histology: Macrophage phagocytosis of necrotic tissue, granulation tissue formation, and neo-vascularization. Wall is softest and most vulnerable!
>2 Weeks

Dressler Syndrome & Aneurysm

Dressler Syndrome: Autoimmune pericarditis (Type III/IV hypersensitivity to exposed cardiac antigens) weeks after MI. Fever, pleurisy, leukocytosis. Treated with NSAIDs/colchicine.

Ventricular Aneurysm: Thin, fibrous scar bulges outward during systole (dyskinesis). Persistent ST elevation months post-MI; risk of mural thrombus and embolic stroke.