Clinical course on ECG interpretation:

1. Myocardial Infarction
2. Pericarditis
3. Hypertrophy
4. Electrolyte imbalance

Dr Md Nazmul Hasan
MBBS(CMC),MRCP(UK)
MCPS(Medicine)
MD(Cardiology),FESC
ECG
MI types based on ECG

STEMI: Hyperacute T wave, ST elevation, Q waves.

NSTEMI: Have ST depression, T inversion etc.
: Have ST depression, T inversion etc.
ST elevation in MI

If 2mm/2 small box ST elevation or new LBBB (wide, flat QRS) in chest
leads.
More than 1 mm ST elevation in limb leads.
But!!! Patient presentation (typical chest pain) is the most important
thing!!!
!!! Patient presentation (typical chest pain) is the most
important thing!!!
ECG in STEMI
Acute phase:
ST segment elevations and tall positive (hyperacute) T waves in multiple
(usually two or more) leads within minutes
Q wave forms later (24 hours).
Evolving phase:
Occurs hours or days later and is characterized by deep T wave inversions in
the leads that previously showed ST elevation.
Persistent ST elevation ~1 month later + Systolic MR murmur+ LVF?=
Ventricular aneurysm.
ST elevation ~1 month later + Systolic MR murmur+ LVF?=
Ventricular aneurysm.
Clinical case
A 50 y/o diabetic, hypertensive, smoker male presented to the CCU of DMCH with
constricting heavy central chest pain for last 2 hours. The pain radiates to left arm
and jaw and did not relieve after taking 2 SL GTN spray. He also vomited twice and
has some breathlessness.
An ECG was taken.
was taken.
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
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
Coronary anatomy
The nomenclature of anterior
infarction infarction
anterior /Extensive anterolateral = V1-6, I + aVL
HHow to Recognize Anterior STEMIoSTEMI?

▪ 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 ).
ST depression in the inferior leads (mainly III and
aVF).
There is progressive ST elevation and Q wave formation in V2-5 ST elevation is now also
present in I and aVL.
There is some reciprocal ST depression in lead III.
This is an acute anterior STEMI
Extensive Anterolateral STEMI (acute) ST elevation in V2-6 , I and aVL.
Reciprocal ST depression in III and AVF
LMCA O
LMCA Occlusion Overviewn Overview

Typical ECG findings with left main coronary artery ( LMCA) occlusion :
▪ Widespread horizontal ST depression, most prominent in leads I, II and
V4-6
▪ ST elevation in aVR ≥ 1mm
▪ ST elevation in aVR ≥ V1
ST elevation in aVR ≥ V1
LMCA occlusion
Clinical Case

A 34 y/o diabetic male presents to the Emergency Department of DMCH with the
complaints of chest heaviness that radiates to the epigastric region. On examination
his BP was 110/80 but it dropped to 90/60 after taking sublingual GTN.

His ECG is shown in the next slide

His ECG is shown in the next slide
Ho
How to recognize an inferior STEMI
w to recognize 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)
ST depression in aVL (± lead I)
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
STE in V1 and V4R
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.
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
of lateral infarction: ST elevation in the lateral leads I
and aVL or V5-6
ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion in aVL
STelevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggest a
circumflex artery occlusion
How to recognize a lateral STEMIl
STEMI
▪ ST elevation in the lateral leads (I, aVL,
V5-6).
▪ Reciprocal ST depression in the inferior
leads (III and aVF).
▪ ST elevation primarily localized to leads I
and aVL is referred to as a high lateral
STEMI.
ST elevation primarily
Patterns of lateral infarctionterns

There are three broad categories of lateral infarction:

▪ Anterolateral STEMI due to LAD occlusion.

▪ Inferior-posterior-lateral STEMI due to Dominant LCX occlusion.
▪ Isolated lateral infarction due to occlusion of smaller branch
arteries such as the D1, OM or ramus intermedius.
Isolated lateral infarction due to occlusion of smaller
branch arteries such as the D1, OM or ramus intermedius.
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.
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).
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.
Posterior MIe MI

▪ Usually occur in the context of an

inferior or lateral infarction.
▪ Be vigilant for evidence of posterior MI
in any patient with an inferior or lateral
STEMI.
vigilant for evidence of
posterior MI in any patient
with an inferior or lateral
STEMI.
How to interpret posterior
infarctionw to spot posterior
infarction
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.
patients presenting with
ischaemic symptoms, horizontal
ST
Typical Posterior MI in
V2
 Confirmation of Posterior MI
Posterior infarction is confirmed by the presence of ST
elevation and Q waves in the posterior leads (V7-9).
Inferolateral STEMI with Posterior extension is suggested by:
Horizontal ST depression in V1-3
Tall, broad R waves (> 30ms) in V2-3
Dominant R wave (R/S ratio > 1) in V2
Upright T waves in V2-3
Right Ventricular Infarctionht
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.
ECG changes of RV infarction are subtle and easily missed!
How to recognize right ventricular
infarction
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.
Right ventricular infarction is confirmed by the presence of ST
elevation in the right-sided leads (V3R-V6R).
Right ventricular infarction is confirmed by the presence of ST
elevation in the right-sided leads (V3R-V6R).
RV leads
Right ventricular infarction is suggested by:
ST elevation in V1
ST elevation in lead III > lead II
Repeat ECG of the same patient with V4R electrode position: There is ST
elevation in V4R consistent with RV infarction
Extensive anterolateral (V1-V6, I, AVL) STEMI
Inferior STEMI with concave ST
Clinical case

A 25 y/o young male presents to a General Physician with the complaints of chest
pain of 2 days duration and cough with runny nose for last 7 days. He also has
fever. On auscultation of precordium there is a scratchy sound.
The ECG is shown in the next slide
ECG is shown in the next slide
ST elevation in all leads. (except V1, aVR and sometimes III), PR depression (depression between the end of the P wave
and the beginning of the QRS- complex)
Concave ST elevation and PR
depression in Pericarditis
Widespread ST elevation and PR depression
Clinical Case

A 45 y/o male comes to the hospital with complaints of uncontrolled

hypertension for last 3 years. He also has some occasional palpitation. On exam
his BP is 170/100 mm. Precordium examination reveals a visible apical impulse
which has a heaving quality.
An ECG is done and shown in the next slide
An ECG is done and shown in the next slide
Criteria for Diagnosing LVH

▪ There are numerous criteria for diagnosing LVH, some of which are
summarized below.
▪ The most commonly used are the Sokolov-Lyon criteria
(S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm).
▪ Voltage criteria must be accompanied by non-voltage criteria to be
considered diagnostic of LVH.
Voltage criteria must be accompanied by non-voltage
criteria to be considered diagnostic of LVH.
LVH voltage criteria

Limb Leads
R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
Precordial Leads
R wave in V5 or V6 > 26 mm
R wave in V5/V6 plus S wave in V1/V2 > 35 mm
Largest R wave plus largest S wave in precordial leads > 45 mmLargest R wave
plus largest S wave in precordial leads > 45 mm
LVH Non Voltage Criteria

▪ Increased R wave peak time >

50 ms in leads V5 or V6
▪ ST segment depression and T
wave inversion in the left-sided
leads: the left ventricular
‘strain’ pattern
LVH by voltage criteria: S wave in V2 + R wave in V5 >
35 mm
LV strain pattern: ST depression and T inversion
LVH (Measure the criteria)
Clinical case

A 56 y/o man with history COPD comes with complaints of weakness,

abdominal and leg swelling.
An ECG is done and shown in the next slide
An ECG is done and shown in the next slide
 Right Ventricular Hypertrophy

Diagnostic criteria:
▪ Dominant R wave in V1 (>7mm
tall or R/S ratio >1)
▪ Dominant S wave in V5/V6 (>7
mm deep or R/S ratio <1)
▪ Right axis deviation
RVH!!
 ECG features of hyperkalemia
> 5.5 mEq/L: Peaked T waves
> 6.5 mEq/L:
P wave widens and flattens and eventually disappear
> 7.0 mEq/L:
Prolonged QRS interval with bizarre QRS morphology
>9.0 mEq/L causes cardiac arrest
Asystole
Ventricular fibrillation
PEA with bizarre, wide complex rhythm
Clinical case
A 45 y/o man with h/o DM, HTN and CKD comes with a history of fatigue for last 1 day. His urine
volume has been low for the last 2 days. He is taking multiple medications including Losartan.
Here is his ECG!
What do you think??
Absent P and Broad QRS :
Hyperkalemia
ECG changes in hypokalemia
Hypokalaemia < 3.5 mmol/L
Moderate hypokalaemia < 3.0 mmol/L
Severe hypokalaemia < 2.5 mmol/L
 ECG changes in hypokalemia
Common changes are:
Increased amplitude and width of the P wave
T wave flattening and inversion
ST depression
Prominent U waves (best seen in the precordial
leads)
Apparent long QT interval due to fusion of the T
and U waves (= long QU interval)
U waves in hypokalemia
Prominent U waves: Hypokalemia

U
Hypocalcemia
Normal serum corrected calcium = 8.5 – 10.4 mg/dl.
Mild-moderate hypocalcaemia = 7.6– 8.5 mg/dl.
Severe hypocalcaemia = < 7.6 mg/dl
Causes QTc prolongation primarily by prolonging the ST segment
Normal QTc values
QTc is prolonged if > 440ms/11 small box>2 large box in men or > 460ms/11+small box >2 large
box in women
QTc > 500 is associated with increased risk of torsades de pointes
QTc is abnormally short if < 350ms
A useful rule of thumb is that a normal QT is less than half the preceding RR interval