2. BLOOD SUPPLY OF THE HEART
Supplied by two coronary arteries :
right coronary artery and left
coronary artery.
Right coronary artery arises from
the right coronary sinus located
anteriorly.
Left coronary artery arises from
the left coronary sinus located
posteriorly and to the left.
3. Right coronary artery
The RCA arises from the right sinus of
Valsalva, inferior to the origin of the
LCA.
It courses anteriorly and inferiorly
under the right atrial appendage
along the right atrioventricular (AV)
groove, toward the acute margin of
the heart, where it turns posteriorly
and inferiorly toward the crux of the
heart and divides into the posterior
descending coronary artery (PDA) and
the posterolateral ventricular branch
(PLB)
5. Conus branch – 1st branch supplies the RVOT
Sinus node artery – 2nd branch - SA node.(40% originates from LCA)
Acute marginal arteries-Arise at acute angle and runs along the margin of
the right ventricle above the diaphragm.
Branch to AV node
Posterior descending artery : Supply lower part of ventricular septum &
adjacent ventricular walls. Arises from RCA in 85% of case.
6. AREAS SUPPLIED BY RIGHT CORONARY ARTERY
1. Right atrium
2. Ventricles
a) Greater part of right ventricle except the area adjoining the anterior IV
groove.
b) A small part of the left ventricle adjoining posterior IV groove.
c) Posterior part of the IV septum
7. Clinical division of RCA
Proximal - Ostium to 1st main RV
branch
Mid - 1st RV branch to acute
marginal branch
Distal - acute margin to the
crux
8. Left Main Coronary Artery
Arises from the left sinus of
Valsalva
Courses to the left, beneath the
left atrial appendage and
posterior to the right ventricular
outflow tract, before branching
into the LAD and the LCX.
A normal variation in the anatomy
is a true trifurcation of the LMCA,
when the middle branch between
the LAD and LCX is called the
ramus intermedius (RI)
9. Left Anterior Descending Artery
The LAD runs anteriorly and inferiorly
in the anterior interventricular groove
to the apex of the heart
Branches : diagonal branches (D1, D2)
and Septal branches.
• Anterior wall by diagonals
• Anterior Septum by septal branches.
• RBB by 1st septal
• Apex
• In some cases the LAD curves around
the cardiac apex to supply part of the
inferior wall of the left ventricle.
10. Clinical division of LAD
Proximal - Ostium to 1st major septal
perforator
Mid - 1st perforator to D2 (90
degree angle)
Distal - D2 to end
11. Left circumflex artery
The LCX runs posteriorly and to the left in the left AV groove, giving rise
to obtuse marginal branches ( OM 1, OM 2)
Supplies:
1. Anterior lateral wall
2. Inferior lateral wall and posterolateral wall of LV
3. Part of inferior wall
4. Part of inferior septum if dominant
12. Dominance
Coronary artery that supplies PDA determines the dominance
Dominant artery also gives rise to the AV nodal branch
RCA - 70%
LCX - 10%
Co - dominant – 20%
14. ECG LOCALIZATION
ST VECTOR :
Direction and displacement of the ST segment- sum of direction and
magnitude of all ST vectors
Resulting main vector point in the direction of most pronounced ischemia-ST
elevation in that area.
Opposite area record reciprocal ST depression
Lead perpendicular to dominant vector will record an isoelectrical ST segment
15. STEMI
ECG changes evolve over a period of time
1. Hyperacute phase ( over minute – hours )
2. Evolved phase ( over hours )
3. Chronic stable phase ( over days – weeks )
16. HYPERACUTE PHASE OF MI
In the leads oriented to the infarcted surface
1. tall, symmetrical , peaked and widened T waves ->0.5 in limb leads,>1 mv in
precordial
2. Slope elevation of ST segment
3. Increased amplitude of the R wave /changes in terminal ORS complexes
-J point elevation >50% R in leads with qR complexes
-disappearance of s vave in leads with Rs complexes
4.Increased ventricular activation time-intrinsicoid deflection >40 ms
17. ST SEGMENT ELEVATION
> 1MM in more than 2 anatomically consecutive leads
EXCEPTION V2 V3 > 1.5mm In females
> 2 mm in males > 40 yrs
> 2.5 mm in males < 40 yrs
TP segment is the isoelectric line
18. EVOLVED PHASE OF MI
1. Appearance of new q waves
2. Changes in ST segment
3. T wave inversion
4. Increased ventricular activation time and . appearance of new conduction
blocks due to slow conduction and delayed depolarisation in the affected
region
19. APPEARANCE OF A NEW Q WAVE
Appearance of new q waves is considered pathognomonic of myocardial necrosis
Small q waves are normal in most leads ,
deeper q waves (> 2mm) may be seen in leads 3 & aVR as normal
Pathological q waves :
≥ 20 ms in wide in v1-v4,>30 ms in other leads
> 25% depth of ensuing R wave
≥ 2 mm deep
20. EVOLVED PHASE OF MI
ST elevation of hyper-acute phase decreases.
Convexity decreases , demarcation from QRS complex and T wave becomes
evident as T wave inversions develop.
Persistent ST elevation signifies
a) Ongoing injury
b) Evolving aneurysm
c) Associated pericarditis
21. CHRONIC STABILISED PHASE
1. Changes in QRS
q wave evolves maximally in QS , QR or qR patterns
2. Changes in ST segment
elevated J point and ST segment returns to baseline
3. Changes in T waves
inverted T waves regain positivity
Persistent t wave inversion-ischemia,aneurysm
22. ANTERIOR WALL MI
Precordial lead (V1-V6) ST-segment elevation in patients with symptoms
suggestive of ACS indicates STEMI due to LAD occlusion.
ST segment changes in other precordial and frontal leads depends on the
presence of ischaemia in three vectorially opposite areas:
(i) basal septal area perfused by proximal septal branch;
(ii) basolateral area perfused by 1st diagonal
(iii) inferoapical area, when distal LAD wraps around apex
23.
24. ANTERIOR WALL MI
mainly to differentiate proximal lad or distal lad occlusion
30. INFARCT SITE ARTERY AFFECTED ST ELEVATION ST
DEPRESSION
(RECIPROCA
L)
Antero septal LAD before septal branch ,after
diagonal branch
V1-v4 , qRBBB ⅡⅢ
Antero lateral LAD before diagonal branch , after
septal branch
I, avL ,V2-V4 V5 , V6
Antero apical Distal LAD ,after diagonal and septal
branch
V4-V6 , OCASIONALLY
ⅡⅢavf
Avl
Extensive anterior
wall
PROXIMAL LAD , before septal and
diagonal branch
I , avL ,V1- V6 , ⅡⅢ,avF
Lateral wall Large obtuse marginal branch / large
diagonal
I, avL ,V5 –V6
Extensive
anterolateral
LMCA I , avL ,V1-V6 ,avR>V1
31. INFERIOR WALL MI
STANDARD LEADS TO LOOK are leads ⅡⅢ,Avf in ECG
85% -90% culprit vessel is RCA
10 % - 15% culprit vessel is LCX
32. RCA OCCLUSION LEADING TO IWMI
1.ST elevation in Lead Ⅲ> avF>Ⅱ
2.ST depression in Lead Ⅰ and avL
3. Sum of ST depression in v1-v3 /sum of ST elevation in Ⅱ,Ⅲ, Avf <1
4.S:R RATIO in lead avL >3
5.ST depression in v3/ST elevation in Ⅲ< 0.5 suggests proximal RCA occlusion and ratio 0.5 to 1.2
suggests distal RCA occlusion
SIGNS OF RV INFARCTION : STE IN V1 AND V4R
35. LEFT CIRCUMFLEX ARTERY OCCLUSION IN
IWMI
ST elevation leads Ⅱ> aVF> Ⅲ
NO ST depression OR sometimes ST
ELEVATION in leads Ⅰ,avl
ST elevation in v5,v6
ST depression in v3/ST elevation in Ⅲ >1.2
Sum of ST depression in V1-v3/ ST ELEVATION in lead ⅡⅢ avf > 1
S: R ratio in lead aVL < 3
ST DEPRESSION IN avR SUGGETS LCX
36.
37. LATERAL WALL MI
LCX
D 1
BRANCH
OF LAD
LEADS V5 –V6
ELEVATION
LEADS Ⅰ ,avL
elevation and
reciprocal ST
depression in inf
leads
ONLY ELEVATION IN
LEADS Ⅰ, aVL
38. PATTERNS OF LATERAL INFARCTION
ANTERO LATERAL – LAD OCCLUSION
INFERO-POSTERO LATERAL ----- LCX
ISOLATED LATERAL – D1/ OM of LCX / RAMUS INTERMEDIUS
43. POSTERIOR WALL STEMI
Posterior extension of an inferior or lateral infarct implies a much larger area
of myocardial damage .
As the posterior myocardium is not directly visualized by standard12 – ECG ,,
RECIPROCAL changes are seen in antero septal leads V1-V3
RCA
(RARE)
LCX
44. POSTERIOR MI IS SUGGESTED BY FOLLOWING CHANGES IN V1-V3
1) Horizontal ST depression
2) tall broad R waves (>30ms)
3) Upright T Waves
4)dominant R Waves (R/S RATIO >1 ) IN V2
45.
46.
47. RIGHT VENTRICULAR STEMI
RV infarction complicates upto 40% of inferior stemi . Isolated is uncommon
48. HOW TO SPOT RV INFARCTION
The first step to spotting RV infarction is to suspect it……..in all patients with
inferior STEMI
ST ELEVATION IN V1 – Only lead that looks directly RV
ST ELEVATION IN LEAD 3 > LEAD 2- BECAUSE LEAD 3 IS more rightward facing and
hence more sensitive to the injury current produced by right ventricle
confirmed by presence of st elevation in the
right sided leads (V3R-V6R )
AS ST segment which is highest in V4R than in
leads v1 to v3 offers high specificty and
efficiency in diagnosis.