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1. Introduction
• The ECG is considered an essential part of the diagnosis and initial
evaluation of patients with chest pain.
• The information that can be obtained from the admission ECG in
patients with STEMI,
• (1) prediction of infarct size,
(2) estimation of prognosis, and
(3) Various electrocardiographic patterns and the localisation of the
infarct and the underlying coronary anatomy.
• ECG without extra costs or time

3. • Non-ST-elevation acute coronary syndrome
(NSTEACS) encompasses two main entities:
• Non-ST-elevation myocardial infarction (NSTEMI).
• Unstable angina pectoris (UAP).
• The differentiation between these two conditions
is usually retrospective, based on the
presence/absence of raised cardiac enzymes at 8-
12 hours after the onset of chest pain.
• Both produce the same spectrum of ECG changes
and symptoms and are managed identically in the
Emergency Department.

4. • Two main ECG patterns associated with NSTEACS:
• ST segment depression
• T wave flattening or inversion
• While there are numerous conditions that may simulate myocardial
ischaemia (e.g. left ventricular hypertrophy, digoxin
effect), dynamic ST segment and T wave changes (i.e. different
from baseline ECG or changing over time) are strongly suggestive of
myocardial ischaemia.
• Other ECG patterns of ischaemia
• Hyperacute (peaked) T waves or pseudonormalisation of previously
inverted T waves (i.e. becoming upright) suggest hyperacute STEMI.
• Another, less well-known ECG feature of myocardial ischaemia is U-
wave inversion.

5. Morphology Of ST Depression
• ST depression can be either upsloping, downsloping, or
horizontal (see diagram below).
• Horizontal or downsloping ST depression ≥ 0.5 mm at the
J-point in ≥ 2 contiguous leads indicates myocardial
ischaemia (according to the 2007 Task Force Criteria).
• ST depression ≥ 1 mm is more specific and conveys a worse
prognosis.
• ST depression ≥ 2 mm in ≥ 3 leads is associated with a high
probability of NSTEMI and predicts significant mortality
(35% mortality at 30 days).
• Upsloping ST depression is non-specific for myocardial
ischaemia.

6. ST depression: upsloping (A), downsloping (B),
horizontal (C)

7. Distribution of ST segment depression
• ST depression due to myocardial ischaemia may be present in a
variable number of leads and with variable morphology:
• ST depression due to subendocardial ischaemia is usually
widespread — typically present in leads I, II, V4-6 and a variable
number of additional leads.
• A pattern of widespread ST depression plus ST elevation in aVR > 1
mm is suggestive of left main coronary artery occlusion.
• ST depression localised to a particular territory (esp. inferior or high
lateral leads only) is more likely to represent reciprocal change due
to STEMI. The corresponding ST elevation may be subtle and
difficult to see, but should be sought.
• This concept of ST depression failing to localise is further discussed
on Dr Smiths blog.
• Widespread subendocardial ischaemia due to LMCA occlusion

8. T wave inversion
• T wave inversion may be considered to be evidence of
myocardial ischaemia if:
• At least 1 mm deep
• Present in ≥ 2 continuous leads that have dominant R
waves (R/S ratio > 1)
• Dynamic — not present on old ECG or changing over time
• NB. T wave inversion is only significant if seen in leads with
upright QRS complexes (dominant R waves). T wave
inversion is a normal variant in leads III, aVR and V1.
• Widespread T wave inversion due to myocardial ischaemia
(most prominent in the lateral leads)

9. Wellens’ Syndrome
• Wellens’ syndrome is a pattern of inverted or biphasic T waves in
V2-4 (in patients presenting with ischaemic chest pain) that is highly
specific for critical stenosis of the left anterior descending artery.
• Patients may be pain free by the time the ECG is taken and have
normally or minimally elevated cardiac enzymes; however, they are
at extremely high risk for extensive anterior wall MI within the next
2-3 weeks.
• There are two patterns of T-wave abnormality in Wellens’
syndrome:
• Type 1 Wellens’ T-waves are deeply and symmetrically inverted
• Type 2 Wellens’ T-waves are biphasic, with the initial deflection
positive and the terminal deflection negative

10. Wellens’ Type 1

11. Wellens’ Type 2

12. Non-specific ST segment and T wave
changes
• The following changes may occur with
myocardial ischaemia but are relatively non-
specific:
• ST depression < 0.5 mm
• T wave inversion < 1 mm
• T wave flattening
• Upsloping ST depression

13. Subendocardial ischaemia:
The most striking abnormality is the widespread ST depression, seen in leads I, II and V5-6. This is consistent
with widespread subendocardial ischaemia.
There is also some subtle ST elevation in V1-2 and aVR with small Q waves in V1-2, suggesting that the cause of
the widespread ischaemia is a proximal LAD occlusion.

14. Inferior STEMI
• Inferior MIs account for 40-50% of all myocardial infarctions.
• Generally have a more favourable prognosis than anterior
myocardial infarction (in-hospital mortality only 2-9%), however
certain factors indicate a worse outcome.
• Up to 40% of patients with an inferior STEMI will have a
concomitant right ventricular infarction. These patients may
develop severe hypotension in response to nitrates and generally
have a worse prognosis.
• Up to 20% of patients with inferior STEMI will develop significant
bradycardia due to second- or third-degree AV block. These patients
have an increased in-hospital mortality (>20%).
• Inferior STEMI may also be associated with posterior infarction,
which confers a worse prognosis due to increased area of
myocardium at risk.

15. How to recognise an inferior STEMI
• ST elevation in leads II, III and aVF
• Progressive development of Q waves in II, III
and aVF
• Reciprocal ST depression in aVL (± lead I)

16. Which Artery Is the Culprit?
• Inferior STEMI can result from occlusion of all three coronary arteries:
• The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary
artery (RCA).
• Less commonly (around 18% of the time), the culprit vessel is a dominant left circumflex artery
(LCx).
• Occasionally, inferior STEMI may result from occlusion of a “type III” or “wraparound” left anterior
descending artery (LAD). This produces the unusual pattern of concomitant inferior and anterior ST
elevation.
• While both RCA and circumflex occlusion may cause infarction of the inferior wall, the precise area
of infarction in each case is slightly different:
• The RCA territory covers the medial part of the inferior wall, including the inferior septum.
• The LCx territory covers the lateral part of the inferior wall and the left posterobasal area.
• This produces subtly different patterns on the ECG:
• The injury current in RCA occlusion is directed inferiorly and rightward, producing ST elevation in
lead III > lead II (as lead III is more rightward facing).
• The injury current in LCx occlusion is directed inferiorly and leftward, producing ST elevation in the
lateral leads I and V5-6.
•

17. These differences allow for electrocardiographic
differentiation between RCA and LCx occlusion.
• RCA occlusion is suggested by:
• ST elevation in lead III > lead II
• Presence of reciprocal ST depression in lead I
• Signs of right ventricular infarction: STE in V1 and V4R
• Circumflex occlusion is suggested by:
• ST elevation in lead II = lead III
• Absence of reciprocal ST depression in lead I
• Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-
6
• (NB. Relative Q-wave depth in leads II and III is not useful in determining
the culprit artery. Both RCA and LCx occlusion produce a similar pattern of
Q wave changes, often with deeper Q waves seen in lead III)
•

18. Early inferior STEMI:
Hyperacute (peaked) T waves in II, III and aVF with relative loss of R wave height.
Early ST elevation and Q-wave formation in lead III.
Reciprocal ST depression and T wave inversion in aVL.
ST elevation in lead III > lead II suggests an RCA occlusion; the subtle ST elevation in V4R would
be consistent with this.

19. • Note how the ST segment
morphology in aVL is an exact
mirror image of lead III. This
reciprocal change occurs
because these two leads are
approximately opposite to one
another (150 degrees apart).
• The concept of reciprocal
change can be further
highlighted by taking lead aVL
and inverting it… see how the
ST morphology now looks
identical to lead III.

20. Bradycardia and AV Block in Inferior STEMI
• Up to 20% of patients with inferior STEMI will develop either second- or third
degree heart block. There are two presumed mechanisms for this:
• Ischaemia of the AV node due to impaired blood flow via the AV nodal artery. This
artery arises from the RCA 80% of the time, hence its involvement in inferior
STEMI due to RCA occlusion.
• Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.
• The conduction block may develop either as a step-wise progression from 1st
degree heart block via Wenckebach to complete heart block (in 50% of cases) or as
abrupt onset of second or third-degree heart block (in the remaining 50%).
• Patients may also manifest signs of sinus node dysfunction, such as sinus
bradycardia, sinus pauses, sinoatrial exit block and sinus arrest. Similarly to AV
node dysfunction, this may result from increased vagal tone or ischaemia of the SA
node (the SA nodal artery is supplied by the RCA in 60% of people).
• Bradyarrhythmias and AV block in the context of inferior STEMI are usually
transient (lasting hours to days), respond well to atropine and do not require
permanent pacing.

21. Anterior Myocardial Infarction
• Anterior STEMI results from occlusion of the left anterior
descending artery (LAD).
• Anterior myocardial infarction carries the worst prognosis of all
infarct locations, mostly due to larger infarct size.
• A study comparing outcomes from anterior and inferior infarctions
(STEMI + NSTEMI) found that on average, patients with anterior MI
had higher incidences of in-hospital mortality (11.9 vs 2.8%), total
mortality (27 vs 11%), heart failure (41 vs 15%) and significant
ventricular ectopic activity (70 vs 59%) and a lower ejection fraction
on admission (38 vs 55%) compared to patients with inferior MI.
• In addition to anterior STEMI, other high-risk presentations of
anterior ischaemia include left main coronary artery (LMCA)
occlusion, Wellens’ syndrome and De Winter’s T waves.

22. How to Recognise Anterior STEMI
• ST segment elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I
and aVL).
• Reciprocal ST depression in the inferior leads (mainly III and aVF).
• NB. The magnitude of the reciprocal change in the inferior leads is determined by the magnitude of
the ST elevation in I and aVL (as these leads are electrically opposite to III and aVF), hence may be
minimal or absent in anterior STEMIs that do not involve the high lateral leads.
• Patterns of Anterior Infarction
• The nomenclature of anterior infarction can be confusing, with multiple different terms used for
the various infarction patterns. The following is a simplified approach to naming the different types
of anterior MI.The precordial leads can be classified as follows:
• Septal leads = V1-2
• Anterior leads = V3-4
• Lateral leads = V5-6
• The different infarct patterns are named according to the leads with maximal ST elevation:
• Septal = V1-2
• Anterior = V2-5
• Anteroseptal = V1-4
• Anterolateral = V3-6, I + aVL
• Extensive anterior / anterolateral = V1-6, I + aVL

23. important ECG patterns to be aware
of
• Anterior-inferior STEMI due to occlusion of a “wraparound” LAD:
– simultaneous ST elevation in the precordial and inferior leads due to
occlusion of a variant (“type III”) LAD that wraps around the cardiac
apex to supply both the anterior and inferior walls of the left
ventricle.
• Left main coronary artery occlusion:
– widespread ST depression with ST elevation in aVR ≥ V1
• Wellens’ syndrome:
– deep precordial T wave inversions or biphasic T waves in V2-3,
indicating critical proximal LAD stenosis (a warning sign of imminent
anterior infarction)
• De Winter’s T waves:
– upsloping ST depression with symmetrically peaked T waves in the
precordial leads; a “STEMI equivalent” indicating acute LAD occlusion.

24. Hyperacute Anteroseptal STEMI
ST elevation is maximal in the anteroseptal leads (V1-4).
Q waves are present in the septal leads (V1-2).
There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in lead III.
There are hyperacute (peaked ) T waves in V2-4.
These features indicate a hyperacute anteroseptal STEMI

25. Prediction of the Site of LAD Occlusion
• The site of LAD occlusion
(proximal versus distal) predicts
both infarct size and prognosis.
• Proximal LAD / LMCA occlusion
has a significantly worse
prognosis due to larger infarct
size and more severe
haemodynamic disturbance.
• The site of occlusion can be
inferred from the pattern of ST
changes in leads corresponding to
the two most proximal branches
of the LAD: the first septal branch
(S1) and the first diagonal branch
(D1).

26. • Territories
• S1 supplies the basal part of the interventricular septum, including the bundle branches
(corresponding to leads aVR and V1)
• D1 supplies the high lateral region of the heart (leads I and aVL).
• Occlusion proximal to S1
Signs of basal septal involvement:
• ST elevation in aVR
• ST elevation in V1 > 2.5 mm
• Complete RBBB
• ST depression in V5
• Occlusion proximal to D1
Signs of high lateral involvement:
• ST elevation / Q-wave formation in aVL
• ST depression ≥ 1 mm in II, III or aVF (reciprocal to STE in aVL)
• ST elevation in aVR of any magnitude is 43% sensitive and 95% specific for LAD occlusion proximal
to S1. Right bundle branch block in anterior MI is an independent marker of poor prognosis; this is
due to the extensive myocardial damage involved rather than the conduction disorder itself.

27. Lateral STEMI
• The lateral wall of the LV is supplied by branches of the left anterior
descending (LAD) and left circumflex (LCx) arteries.
• Infarction of the lateral wall usually occurs as part of a larger
territory infarction, e.g. anterolateral STEMI.
• Isolated lateral STEMIs are less common, but may be produced by
occlusion of smaller branch arteries that supply the lateral wall, e.g.
the first diagonal branch (D1) of the LAD, the obtuse marginal
branch (OM) of the LCx, or the ramus intermedius.
• Lateral STEMI is a stand-alone indication for emergent reperfusion.
• Lateral extension of an anterior, inferior or posterior MI indicates a
larger territory of myocardium at risk with consequent worse
prognosis.

28. How to recognise a lateral STEMI
• ST elevation in the lateral leads (I, aVL, V5-6).
• Reciprocal ST depression in the inferior leads (III
and aVF).
• ST elevation primarily localised to leads I and aVL
is referred to as a high lateral STEMI.
• NB. Reciprocal change in the inferior leads is only
seen when there is ST elevation in leads I and aVL.
This reciprocal change may be obliterated when
there is concomitant inferior ST elevation (i.e an
inferolateral STEMI)

29. • There are three broad categories of lateral
infarction:
• Anterolateral STEMI due to LAD occlusion.
• Inferior-posterior-lateral STEMI due to LCx
occlusion.
• Isolated lateral infarction due to occlusion of
smaller branch arteries such as the D1, OM or
ramus intermedius.

30. High Lateral STEMI
ST elevation is present in the high lateral leads (I and aVL).
There is also subtle ST elevation with hyperacute T waves in V5-6.
There is reciprocal ST depression in the inferior leads (III and aVF) with associated ST depression in V1-3 (which could
represent anterior ischaemia or reciprocal change).
This pattern is consistent with an acute infarction localised to the superior portion of the lateral wall of the left ventricle
(high lateral STEMI).
The culprit vessel in this case was an occluded first diagonal branch of the LAD.

31. Anterolateral STEMI
ST elevation is present in the anterior (V2-4) and lateral leads (I, aVL, V5-6).
Q waves are present in both the anterior and lateral leads, most prominently in V2-4.
There is reciprocal ST depression in the inferior leads (III and aVF).
This pattern indicates an extensive infarction involving the anterior and lateral walls of the left ventricle.
ST elevation in the precordial leads plus the high lateral leads (I and aVL) is strongly suggestive of an acute
proximal LAD occlusion (this combination predicts a proximal LAD lesion 87% of the time).

32. Inferolateral STEMI
There is ST elevation in the inferior (II, III, aVF) and lateral (I, V5-6) leads.
The precordial ST elevation extends out as far as V4, however the maximal STE is in V6.
ST depression in V1-3 is suggestive of associated posterior infarction (the R/S ratio > 1 in V2 is consistent with this).
This is an acute inferolateral STEMI with probable posterior extension.
This constellation of ECG abnormalities is typically produced by occlusion of the proximal circumflex artery.

33. Inferoposterolateral STEMI
ST elevation is present in the inferior (II, III and aVF) and lateral leads (I, V5-6).
ST depression in V1-3 with tall, broad R waves and upright T waves and a R/S ratio > 1 in V2 indicate concomitant posterior
infarction (this patient also had ST elevation in the posterior leads V7-9).
These changes are consistent with a massive infarction involving the inferior, lateral and posterior walls of the left ventricle.
The culprit vessel is again very likely to be an occluded proximal circumflex artery.

34. Posterior Myocardial Infarction
• Posterior infarction accompanies 15-20% of STEMIs, usually
occurring in the context of an inferior or lateral infarction.
• Isolated posterior MI is less common (3-11% of infarcts).
• Posterior extension of an inferior or lateral infarct implies a
much larger area of myocardial damage, with an increased
risk of left ventricular dysfunction and death.
• Isolated posterior infarction is an indication for emergent
coronary reperfusion. However, the lack of obvious ST
elevation in this condition means that the diagnosis is often
missed.

35. How to spot posterior infarction
• As the posterior myocardium is not directly
visualised by the standard 12-lead ECG,
reciprocal changes of STEMI are sought in
the anteroseptal leads V1-3. Posterior MI is
suggested by the following changes in V1-3:
• Horizontal ST depression
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2
• In patients presenting with ischaemic
symptoms, horizontal ST depression in the
anteroseptal leads (V1-3) should raise the
suspicion of posterior MI.
• Typical appearance of posterior infarction in
V2
• Posterior infarction is confirmed by the
presence of ST elevation and Q waves in the
posterior leads (V7-9).

36. posterior MI
ST depression in V2-3
Tall, broad R waves (> 30ms) in V2-3
Dominant R wave (R/S ratio > 1) in V2
Upright terminal portions of the T waves in V2-3
(The ECG changes extend out as far as V4, which may reflect superior-medial misplacement of the V4 electrode
from its usual position).

37. Posterior infarction is diagnosed based on the presence of ST segment
elevation >0.5mm in leads V7-9.
Note that there is also some inferior STE in leads III and aVF (but no Q wave
formation) suggesting early inferior involvement.
The same patient, with posterior leads
recorded:

38. Right Ventricular Infarction
• Right ventricular infarction complicates up to 40% of
inferior STEMIs. Isolated RV infarction is extremely
uncommon.
• Patients with RV infarction are very preload
sensitive (due to poor RV contractility) and can
develop severe hypotension in response to nitrates or
other preload-reducing agents.
• Hypotension in right ventricular infarction is treated
with fluid loading, and nitrates are contraindicated.
• The ECG changes of RV infarction are subtle and easily
missed!

39. How to spot right ventricular infarction
• The first step to spotting RV infarction is to suspect it… in all patients with
inferior STEMI!
• In patients presenting with inferior STEMI, right ventricular infarction is
suggested by the presence of:
• ST elevation in V1 – the only standard ECG lead that looks directly at the
right ventricle.
• ST elevation in lead III > lead II – because lead III is more “rightward
facing” than lead II and hence more sensitive to the injury current
produced by the right ventricle.
• Other useful tips for spotting right ventricular MI:
• ST elevation in V1 > V2.
• ST elevation in V1 + ST depression in V2 (= highly specific for RV MI).
• Isoelectric ST segment in V1 with marked ST depression in V2.
• Right ventricular infarction is confirmed by the presence of ST elevation
in the right-sided leads (V3R-V6R).

40. Right-sided leads
• There are several different approaches to
recording a right-sided ECG:
• A complete set of right-sided leads is
obtained by placing leads V1-6 in a mirror-
image position on the right side of the chest
(see diagram, below).
• It may be simpler to leave V1 and V2 in their
usual positions and just transfer leads V3-6
to the right side of the chest (i.e. V3R to
V6R).
• The most useful lead is V4R, which is
obtained by placing the V4 electrode in the
5th right intercostal space in the
midclavicular line.
• ST elevation in V4R has a sensitivity of 88%,
specificity of 78% and diagnostic accuracy of
83% in the diagnosis of RV MI.
• ST elevation in the right-sided leads is a
transient phenomenon, lasting less than 10
hours in 50% of patients with RV infarction.