teach me the blood supply of heart, ecg leads and how it is affected in MI (with LOCALISATION)

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Blood Supply of the Heart, ECG Leads & MI Localisation


PART 1: BLOOD SUPPLY OF THE HEART

The heart is supplied by two coronary arteries arising from the aortic sinuses (sinuses of Valsalva) just above the aortic valve cusps.

Sternocostal (Anterior) View

Sternocostal surface of the heart showing coronary arteries

Diaphragmatic (Posterior/Inferior) View

Diaphragmatic surface of the heart showing posterior coronary vessels

Left Coronary Artery (LCA)

Arises from the left aortic sinus and divides after a short left main trunk (~1-2 cm) into:
1. Left Anterior Descending (LAD) = Anterior Interventricular Artery
  • Runs in the anterior interventricular groove
  • Supplies:
    • Anterior wall of the left ventricle
    • Anterior 2/3 of the interventricular septum (via septal perforators)
    • Anterior right ventricular wall (small branches)
    • Apex of the heart
  • Key branches: Diagonal branches (D1, D2) - supply the anterolateral LV wall; Septal perforators
  • The "widow maker" - largest MI territory if occluded proximally
2. Left Circumflex (LCx)
  • Runs in the left atrioventricular groove
  • Supplies:
    • Left atrium
    • Lateral and posterior wall of the left ventricle
    • SA node (in ~40% of people)
  • Gives off: Obtuse marginal (OM) branches - numbered OM1, OM2
3. Ramus Intermedius (variant - present when LCA trifurcates)
  • Supplies the high lateral wall

Right Coronary Artery (RCA)

Arises from the right aortic sinus, runs in the right atrioventricular groove.
  • Supplies:
    • Right atrium and right ventricle
    • SA node (in ~60% of people via the SA nodal branch, the first branch)
    • AV node (in ~85-90% of people)
    • Posterior 1/3 of interventricular septum
  • Key branches:
    • Acute marginal branch - supplies the free wall of the RV
    • Posterior Descending Artery (PDA) - in right dominant systems, runs in the posterior interventricular groove, supplies the inferior LV wall and posterior septum
    • Posterolateral branches - supply the inferior-posterior LV

Coronary Dominance

Dominance is determined by which vessel gives rise to the Posterior Descending Artery (PDA):
DominancePDA OriginFrequency
Right dominantRCA~85%
Left dominantLCx~5%
CodominantBoth~10%
In right dominant circulation, the RCA supplies the AV node, the posterior wall, and the inferior septum.
  • Harrison's Principles of Internal Medicine 22E

Venous Drainage

Most venous blood returns via the coronary sinus (drains into the right atrium):
  • Great cardiac vein (alongside the LAD) - drains the anterior LV
  • Middle cardiac vein (posterior interventricular groove) - drains the inferior heart
  • Small cardiac vein (right atrioventricular groove) - drains the right heart
  • Posterior vein of the LV - drains the lateral LV
A small amount drains directly into the right heart via Thebesian veins.

Conduction System Supply

StructureArtery
SA nodeRCA (~60%), LCx (~40%)
AV nodeRCA (dominant ~90%), LCx (left dominant)
Bundle of HisDual: LAD septal perforators + AV nodal artery
Right bundle branchLAD (septal perforators)
Left anterior fascicleLAD (dual supply)
Left posterior fascicleRCA + LAD (most protected - dual supply)
  • Tintinalli's Emergency Medicine

PART 2: ECG LEADS - AN OVERVIEW

The standard 12-lead ECG records 12 different electrical "views" of the heart from 10 electrodes (4 limb + 6 chest).

Limb Leads (Frontal Plane)

Bipolar leads (record potential difference between two limbs):
LeadPositive PoleNegative PoleLooks at
ILeft armRight armLateral
IILeft legRight armInferior
IIILeft legLeft armInferior
Augmented Unipolar leads (compare one limb to a combined reference):
LeadPositive ElectrodeLooks at
aVRRight armCavity (normally negative)
aVLLeft armHigh lateral
aVFLeft footInferior
Because normal depolarisation moves from right-to-left and craniocaudally: P and QRS are positive in I, II, aVL, aVF and negative in aVR in sinus rhythm.

Precordial Leads (Horizontal/Transverse Plane)

Unipolar leads - compare chest electrode to the Wilson central terminal:
LeadPositionLooks at
V14th intercostal space, right sternal borderSeptum/RV
V24th intercostal space, left sternal borderSeptum/anterior
V3Between V2 and V4Anterior
V45th intercostal space, mid-clavicular lineAnterior/apex
V5Anterior axillary line (same level as V4)Lateral
V6Mid-axillary line (same level as V4)Lateral
Grouped by territory:
  • Inferior: II, III, aVF
  • Anterior/Septal: V1-V4
  • Lateral: I, aVL, V5, V6
  • Right ventricular: V3R-V6R (right-sided leads, placed mirror-image)
  • Posterior: V7-V9 (posterior axillary line, paraspinal) - or reciprocal changes in V1-V3
  • Goldman-Cecil Medicine, ELECTROCARDIOGRAPHIC LEADS section
Normal intervals to know:
ParameterNormal
Heart rate50-100 bpm
P wave duration< 120 ms
PR interval90-200 ms
QRS duration75-110 ms
QTcM: 390-450 ms; F: 390-460 ms
QRS axis-30° to +90°

PART 3: ECG CHANGES IN MI AND LOCALISATION

Mechanism of ECG Changes in MI

Three electrical changes occur in infarcted myocardium, all producing ST elevation in leads overlying the infarct:
  1. Rapid repolarisation (K+ channels open) - current flows out of infarct - ST elevation
  2. Decreased resting membrane potential (K+ loss from cells) - current flows into infarct during diastole - manifests as TQ depression, recorded as ST elevation due to the AC-coupled ECG
  3. Delayed depolarisation - infarcted area stays positive during repolarisation - current flows out of infarct - ST elevation
Leads on the opposite side of the heart show reciprocal ST depression (mirror image).
After days-weeks, the infarcted area becomes electrically silent (scar), producing pathological Q waves (the dead zone cannot contribute positivity to the QRS).
  • Ganong's Review of Medical Physiology, 26th Edition

ECG Sequence in STEMI

TimeECG change
MinutesTall, peaked "hyperacute" T waves (earliest sign)
HoursST elevation (injury current)
Hours-daysQ wave development (pathological necrosis)
DaysT wave inversion (evolving/reperfusion)
Weeks-monthsST normalises, Q waves may persist permanently
Pathological Q waves: width > 40 ms (1 small box) OR depth > 25% of the R wave amplitude.

MI Localisation Table (The Core of Your Exam)

Infarct LocationLeads with ChangesCoronary ArteryReciprocal Changes
AnteriorV1-V4LAD (mid-distal)II, III, aVF
SeptalV1-V2LAD (septal perforators)None specific
AnteroseptalV1-V3LAD (proximal-mid)Inferior leads
AnterolateralV1-V6, I, aVLLAD (proximal, before D1)II, III, aVF
High lateralI, aVLLCx or D1 (diagonal)III, aVF
LateralI, aVL, V5-V6LCx (OM1 or OM2)II, III, aVF
InferiorII, III, aVFRCA (85%) or LCx (15%)I, aVL
Right ventricularV3R-V4R (V1 sometimes)Proximal RCAAnterior leads
PosteriorTall R + ST depression V1-V3; ST elevation V7-V9RCA or LCx(V1-V3 are reciprocal)
Left main / MultivesselaVR elevation + widespread ST depressionLeft main or proximal LADGlobal ST depression
  • Rosen's Emergency Medicine, Table 64.4

Detailed Breakdown by Territory

Anterior STEMI (V1-V4)

ST elevation in V1-V4. The LAD supplies this territory. "Failure of R wave progression" in the precordials is a chronic marker. Reciprocal depression in II, III, aVF.
Anterior STEMI - V1 to V4 ST elevation
Anterior wall STEMI - ST elevation in leads V1-V4. LAD 90% stenosis confirmed on catheterisation. (Rosen's Emergency Medicine)

Inferior STEMI (II, III, aVF)

  • ST elevation in II, III, aVF
  • Usually RCA (right dominant, ~85%), occasionally LCx
  • Key tip: If III > II in elevation → RCA more likely; If II > III → LCx more likely
  • Reciprocal ST depression in I and aVL (very sensitive - if absent, reconsider diagnosis)
  • Always check right-sided leads (V3R-V4R) - ST elevation in V3R/V4R indicates right ventricular involvement (important because these patients should NOT receive nitrates - preload dependent)
  • AV nodal artery is often involved → watch for bradycardia, heart blocks

Right Ventricular MI

  • Occurs with proximal RCA occlusion (before the RV marginal branch)
  • ST elevation in right-sided leads V3R-V4R (V4R is most sensitive/specific)
  • Clinical triad: hypotension + elevated JVP + clear lungs (Kussmaul's sign may be present)
  • Avoid nitrates and diuretics (both reduce preload)

High Lateral STEMI (I, aVL)

  • Obstruction of the left circumflex or first diagonal (D1) branch of LAD
  • Reciprocal changes in inferior leads (III, aVF)
  • Can be "silent" - small territory, may produce subtle changes

Posterior MI

  • No standard ECG lead looks directly at the posterior wall
  • Reciprocal changes in V1-V3: tall broad R wave + horizontal ST depression + upright T wave
  • Confirm with posterior leads V7-V9: direct ST elevation
  • Associated with inferior STEMI (infero-posterior pattern)
  • Artery: RCA (right dominant) or LCx (left dominant)

Left Main / Proximal LAD (Massive Anterior)

  • ST elevation in aVR (>1 mm) + widespread ST depression in multiple leads
  • This represents diffuse subendocardial ischemia or very proximal LAD/LM occlusion
  • If aVR elevation > V1 elevation → left main more likely
  • If V1 elevation > aVR → proximal LAD more likely
  • Also consider de Winter pattern: J-point depression with tall hyperacute T waves in V1-V6 + aVR elevation (proximal LAD equivalent STEMI)

Special Patterns and Tips

Wellens Syndrome (critical LAD stenosis, seen between pain episodes):
  • Type A: Biphasic T waves in V2-V3
  • Type B: Deep symmetric T wave inversions in V2-V3
  • Does NOT show ST elevation - often asymptomatic on the ECG - DO NOT stress test
STEMI Criteria (Harrison's 22E):
  • Two contiguous leads with J-point ST elevation:
    • V2-V3: ≥2 mm in men, ≥1.5 mm in women
    • All other leads: ≥1 mm

Quick-Reference: Artery → Territory → Leads

RCA (proximal) ─── Inferior + RV + AV node
                   → II, III, aVF + V3R-V4R
                   → Heart blocks, bradycardia

RCA (mid-distal) ── Inferior + posterior
                    → II, III, aVF + reciprocal V1-V3

LAD (proximal) ─── Anteroseptal + lateral + septal
                   → V1-V6, I, aVL

LAD (mid) ────── Anterior
                 → V1-V4

LAD (diagonal) ── High lateral
                  → I, aVL

LCx ────────── Lateral / High lateral / Posterior
               → I, aVL, V5-V6 (or V7-V9)

Left Main ───── Massive anterior + aVR elevation
                → Widespread ST depression + aVR ST↑

Summary Table: ECG Findings vs. Location

FindingThink of
STE V1-V4Anterior MI (LAD)
STE V1-V4 + I, aVLAnterolateral MI (proximal LAD)
STE II, III, aVFInferior MI (RCA or LCx)
STE V3R-V4R (with inferior STE)Right ventricular MI (proximal RCA)
STD V1-V3 + tall RPosterior MI (RCA or LCx)
STE I, aVL onlyHigh lateral MI (D1 or LCx)
STE aVR + diffuse STDLeft main / proximal LAD / multivessel
Biphasic/deep T V2-V3 (no STE)Wellens syndrome (critical LAD stenosis)
STE V7-V9True posterior MI

Sources: Rosen's Emergency Medicine; Goldman-Cecil Medicine; Harrison's Principles of Internal Medicine 22E; Ganong's Review of Medical Physiology 26th Ed; Netter's Atlas of Human Anatomy

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Cardiac BloodSupply ECG MI

PDF Document · PDF


What's inside the PDF:
  • Cover page with title and source credits
  • Part 1 - Blood Supply - LCA (LAD + LCx), RCA, coronary dominance table, venous drainage, conduction system supply - with two Netter's Atlas anatomical images (sternocostal and diaphragmatic views)
  • Part 2 - ECG Leads - bipolar limb leads, augmented unipolar leads, precordial leads with positions and territories, additional leads (V3R-V9), lead grouping by territory, normal intervals table
  • Part 3 - MI ECG Changes - mechanism of ECG changes (Ganong's), temporal STEMI sequence, STEMI diagnostic criteria, master localisation table, territory-by-territory detail with clinical pearls, special patterns (Wellens, Sgarbossa/LBBB), plus the real Anterior STEMI ECG from Rosen's
  • Quick Reference Summary - artery-to-territory-to-leads table, ECG finding-to-diagnosis cheat sheet
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