ECG Basics
Dr. Md. Ahsanul Hoque
Registrar (Cardiology)
Dhaka Medical College
Older ECG machine
Modern ECG machine
IHD?
 Ischemic heart disease (IHD) is the result of a limited blood supply to the
heart muscle. In more than 95% of cases, the cause of IHD is coronary
blood flow reduction caused by coronary artery atherosclerosis, therefore
the term “coronary heart disease” is often used to describe this syndrome.
IHD/CAD includes
 Stable angina
 Unstable angina
 Myocardial infarction
 Heart failure
 Arrhythmia,
 Sudden death
Davidson's Principles and Practice of Medicine,22rd Edition
Researchgate.net/publication/330840299
Normal ECG
 Standardization – 10 mm (2 boxes) = 1 mV
 Double and half standardization if required
 Sinus Rhythm – Each P followed by QRS, R-R constant
 QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR
 R wave progression from V1 to V6.
 Axis normal – L1, L3, and aVF all will be positive
Normal ECG
Be aware of normal ECG
 Normal Resting ECG – cannot
exclude disease
 Ischemia may be covert –
supply / demand equation
 Changes of MI take some time
to develop in ECG
 Some of the ECG abnormalities
are non specific
 Single ECG cannot give
progress – Need serial ECGs
 ECG changes not always
correlate with Angiographic
results
 Paroxysmal events will be
missed in single ECG
Normal ECG
Normal is defined as no significant Q waves, ST segment at
the isoelectric line, and normal T waves in all 12 leads.
Small Q waves (ie, <0.04 second wide and <25% the height
of the QRS complex) can be normal in all leads except V1,
V2, and V3; and lead AVR is often a QS complex normally. T
waves can be slightly inverted in the right precordial leads
(V1 and V2), and should be inverted in AVR in normal ECGs.
ECG Manifestations of Myocardial
Ischemia
The most familiar ECG patterns of ischemia are
horizontal or down sloping ST segment depression
of 1 mm or more and T-wave inversion.
ST segment elevation or depression
• More than one millimeter (one small box)
• Present in two anatomically contiguous leads
There is a correlation between the number of ECG
leads that show ST deviation and the extent and
severity of coronary artery disease.4 If ST segment
depression occurs in 8 or more leads along with ST
elevation in AVR and V1, there is a high risk of
either left main coronary artery disease or severe
triple vessel disease
Post-ischemic T wave changes
Post-ischemic T wave changes
Presentation of coronary
heart disease
Asymptomatic Chronic stable
angina
Acute coronary
syndrome (ACS) Death
Unstable angina
Non ST elevation MI
ST elevation MI
(
M
Heart failure
Stable angina
• Also called exertional angina
• The lumen of coronary artery is narrowed and hard; thus,
dilation in response to increased demand is impossible
Stable angina
• Initiated by known amount of activity
• Same activity tends to produce same symptoms
• Produced by
– physical activity
– emotional excitement
– cause of increased cardiac workload
• Relieved by rest, Nitrate
Stable angina
 Approximately 50% of patients with angina pectoris have
normal findings after a resting ECG.
 However, abnormalities such as evidence for prior MI,
intraventricular conduction delay, various degrees of
atrioventricular block, arrhythmias, or ST-T–wave changes may
be seen.
 Medscape.com/article/150215-workup#c12
Stable angina….
 During an attack of angina pectoris, 50% of patients with
normal findings after resting ECG show abnormalities.
 Exercise with ECG monitoring alone is the initial procedure of
choice in patients without baseline ST-segment abnormalities
or in whom anatomic localization of ischemia is not a
consideration
Medscape.com/article/150215-workup#c12
Printzmetal angina
• Also called variant angina, Prinzmetal’s variant angina
• An uncommon pattern of episodic angina that occurs at
rest
• Due to coronary artery spasm.
Printzmetal angina
• Occurs without a precipitating event, usually at the same
time of day
• Often awakens patient from sleep
• Unpredictable, occurs most often at rest
ECG changes of AMI
NSTEMI: ECG changes
Localization of territory
Inferior MI
Artery involved in Inferior MI
 RCA(Right dominant)
 LCX(left dominant)
 Type 4 LAD
Clinical Examination in Cardiology, 2nd
B.N.Rao
Clinical Examination in Cardiology, 2nd
B.N.Rao
 Inferior wall MI –
ST segment elevation of > 1 mm in inferior leads
then look the following leads (Which coronary artery?)
 ST segment elevation lead III> lead II-RCA
 Reciprocal change in lead I & aVL-RCA
 ST segment elevation lead II> lead III-LcX
 If no reciprocal change in lead I & aVL- LcX
 Signs of lateral infarction I,aVL,V5,V6-LcX
 Look anterior lead –LAD
ECG -----
Clinical Examination in Cardiology, 2nd
B.N.Rao
 Then look for V1,V2,,V3,V4(Don’t Missed)
 In VI isoelectric/elevated
 V2,V3, V4 ST segment depression
 ST elevation in right sided chest lead(V3R/V4R)
----RV infarction
ECG -----
Posterior wall MI
 Usually caused by LCx occlusion but may also be seen in
dominant RCA occlusion.
 ST-segment elevation in the posterior chest leads V7
through V9: > 0.5 mm in a case of IWMI
Posterior MI is suggested by the following changes in V1-3:
 Horizontal ST depression (i.e. reciprocal changes)
 Tall, broad R waves (>30ms)
 Prominent upright T waves, particularly in V2
 Dominant R wave (R/S ratio > 1) in V2
Posterior MI
Posterior MI : V7 – V9
Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall
European Heart Journal (2018) 39, 119–177 ESC GUIDELINES
doi:10.1093/eurheartj/ehx393
Recommendation for Post and RV
infarction
RV MI
Occlusion of proximal RCA (proximal to RV branch)
Identified by
 ST elevation in V1 in association with IWMI (Lead
III>II)
 ST elevation >1 mm in V4R with an upright T (most
sensitive sign of RVMI).
 QS or QR in V3R and/or V4R (but less predictive than
ST elevation in these leads).
 Occasionally, ST-segment elevation in V2 and V3
results from acute RVI, resembling anterior infarction.
V4R
Leads Sensitivity (%) Specificity (%)
V3 R 69 97
V4 R 93 95
V1 28 92
Clinical Examination in Cardiology, 2nd
B.N.Rao
Extensive Anterior wall MI: localization
Occlusion above D1 and S1
ST elevation ST depression
lead I, aVL, V1-V4 Âą V5-V6, often
in aVR
II, III, aVF (Inferior)
aVL > aVR III > II
Antero-septal MI: localization
Occlusion before S1
ST elevation ST depression
V1-V4, RBBB II, III, aVF
aVL > aVR III > II
High lateral MI
Occlusion in diagonal
ST elevation ST depression
I, aVL V5-V6
aVL > aVR III > II
Antero-apical MI: localization
Occlusion: More distally i.e. below Septal 1 and
D1
 ST segment elevation more prominent in V3 – V6
than V2
 Basal portion spared (ST vector directed
inferiorly)
 ST segment not elevated in I, aVL/aVR
 No depression in II, III, aVF
 Indeed, ST segment elevation in II, III, aVF
when LAD is type IV vessel
Anterior wall MI: localization
LMCA stenosis
Typical ECG findings in severe LMCA stenosis or
occlusion include:
 ST-segment elevation in lead aVR more than V1
 widespread ST-segment depression or anterior ST
elevation.
 ST-segment of >0.05 mV elevation in aVR present in
88% of the LMCA obstruction group compared with
46% of proximal LAD occlusion. (Yamaji, et al., 2001)
LMCA stenosis
Suspected LMD/TVD
LMD/TVD with IHD
https://doi.org/10.1161/01.CIR.23.3.331
Infarction…
Atrial infarction:
 https://doi.org/10.1161/01.CIR.23.3.331Circulation. 1961;23:331–338
Atrial infarction:
Atrial infarction
PR
depression
in inferior
STEMI
indicating
concomita
nt atrial
infarction
Wellen’s syndrome
•Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
•Type B = Deeply and symmetrically inverted (75% of cases)
Wellens Syndrome
 There are two patterns of T-wave abnormality in
Wellens syndrome:
 Type A – Biphasic, with initial positivity and
terminal negativity (25% of cases)
 Type B – Deeply and symmetrically inverted
(75% of cases)
https://litfl.com/wellens-syndrome-ecg-library/
Type-A Type- B
https://litfl.com/wellens-syndrome-ecg-library/
Wellens Syndrome,Type A
Wellens syndrome,Type B
de Winter T wave
 The de Winter ECG pattern is an anterior STEMI
equivalent that presents without obvious ST segment
elevation. First reported by first reported de Winter in 2008
 Key diagnostic features include ST depression and peaked T
waves in the precordial leads.
 The de Winter pattern is seen in ~2% of acute LAD
occlusions and is under-recognised by clinicians.
 Unfamiliarity with this high-risk ECG pattern may lead to
under-treatment (e.g. failure of cath lab activation), with
attendant negative effects on morbidity and mortality.
https://litfl.com/de-winter-t-wave-ecg-library/
de Winter T wave------
 Diagnostic Criteria
 Tall, prominent, symmetric T waves in the precordial
leads
 Upsloping ST segment depression >1mm at the J-
point in the precordial leads
 Absence of ST elevation in the precordial leads
 ST segment elevation (0.5mm-1mm) in aVR
 “Normal” STEMI morphology may precede or follow
the deWinter pattern
https://litfl.com/de-winter-t-wave-ecg-library/
De Winter’s T wave
 De Winter ECG pattern is an anterior STEMI equivalent
without obvious ST segment elevation, seen in ~2% of
acute LAD occlusions.
 Key diagnostic features include ST depression and peaked T
waves in
precordial leads
 Tall, prominent, symmetric T waves in the precordial leads
 Upsloping ST segment depression >1mm at the J-point in the
precordial leads
 Absence of ST elevation in the precordial leads
 But, ST segment elevation (0.5mm-1mm) in aVR
De Winter’s T wave
 Upsloping ST depression in the precordial leads
(> 1mm at J-point).
 Peaked anterior T waves (V2-6), with the
ascending limb of the T wave commencing below
the isoelectric baseline.
 Subtle ST elevation in aVR > 0.5mm
•Upsloping ST depression in the precordial leads (> 1mm at J-point).
•Peaked anterior T waves (V2-6), with the ascending limb of the T wave commencing below
the isoelectric baseline.
•Subtle ST elevation in aVR > 0.5mm
Diagnosing MI in LBBB
 In patients with LBBB or ventricular paced rhythm,
infarct diagnosis based on the ECG is difficult.
 The baseline ST segments and T waves tend to be
shifted in a discordant direction (“appropriate
discordance”) in LBBB
 This can mask or mimic acute Mi.
 Serial ECGs may show dynamic
ST segment changes during ischemia.
Diagnosis of MI in presence of LBBB
OLD ANTERIOR MI WITH LBBB
 Cabrera’s sign – notching of 50ms in ascending
limb of S wave in leads V3-V5
Diagnosis of MI in presence of LBBB
OLD ANTERIOR MI WITH LBBB
 Chapman’s sign – notching in the upstroke of R
wave in I, aVL, V6
Acute MI in presence of LBBB: Original Sgarbossa
Criteria
The original three criteria used to diagnose infarction in
patients with LBBB are:
 Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
 Concordant ST depression > 1 mm in V1-V3 (score 3)
 Excessively discordant ST elevation > 5 mm in leads with a -
ve QRS complex (score 2).
These criteria are specific, but not sensitive for myocardial
infarction.
A total score of 3 has specificity of 90% for diagnosing MI.
≥
Usual LBBB
LBBB satisfying Sgarbossa Criteria
Left Bundle Branch Block Satisfying the First Sgarbossa Criterion: Concordant ST elevation 1 mm in any single le
≥
LBBB with IHD
 Sgarbossa Criteria Overview
 In patients with left bundle branch block(LBBB) or ventricular
paced rhythm, infarct diagnosis based on the ECG is difficult.
 The baseline ST segments and T waves tend to be shifted in a
discordant direction (“appropriate discordance”), which can
mask or mimic acute myocardial infarction.
 However, serial ECGs may show dynamic ST segment changes
during ischaemia.
 A new LBBB is always pathological and can be a sign of
myocardial infarction.
 First described by Elena B Sgarbossa in 1996
https://litfl.com/sgarbossa-criteria-history/
LBBB with IHD----
 The original three criteria used to diagnose infarction in
patients with LBBB are:
 Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
 Concordant ST depression > 1 mm in V1-V3 (score 3)
 Excessively discordant ST elevation > 5 mm in leads with a -ve
QRS complex (score 2).
 These criteria are specific, but not sensitive for myocardial
infarction. A total score of ≥ 3 is reported to have a specificity
of 90% for diagnosing myocardial infarction.
https://litfl.com/sgarbossa-criteria-history/
Diagnosing MI in presence of RBBB
 MI diagnosis in RBBB is not very different from
normal MI diagnosis.
 However, as repolarization in leads V1-V3 is
often abnormal in RBBB, these leads cannot
always be used for the diagnosis of ischemia.
MI with RBBB: before MI
MI with RBBB: after STEMI anterior
MI with RBBB: before MI
MI with RBBB: after MI: Inferior
STEMI
When MI is not MI: mimickers
 LBBB
 Pacing ECG
 Non-Thrombotic Vasospasm
 Hypertrophic Cardiomyopathy
 Acute pericarditis
 LV aneurysm
 Early repolarization
 Hyperkalaemia
 Hypercalcaemia
 Brugada syndrome
 Osborn waves
Early repolarization
Early repolarization showing J-point elevation in multiple contiguous leads and slurring and/or
notching on the downstroke of the R wave in leads II, III, aVF, V5, and V6.
Pericarditis
Diffuse ST elevation most prominent in leads I, II, and V4-V6, without reciprocal cha
Spodick’s sign (downsloping TP segment in lead II)
PR segment depression (best seen in lead II).
28 year old male presented with chest pain for 8 hours.. Troponin I: 0.14 ng/ml.
a) What is the diagnosis?
Hypertrophic Cardiomyopathy
• Voltage criteria for left ventricular hypertrophy.
• Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.
• Giant T wave inversions in the precordial leads
• Inverted T waves are also seen in the inferior and lateral leads.
LV aneurysm
•ST elevation seen > 6 weeks following acute MI
•Most commonly seen in the precordial leads.
•May exhibit concave or convex morphology.
•Usually associated with well-formed Q- or QS waves.
•T-waves have a relatively small amplitude in
comparison to the QRS complex
(unlike the hyperacute T-waves of acute STEMI).
Differentiation of LV aneurysm from acute STEMI
Factors favouring left ventricular aneurysm
 ECG identical to previous ECGs (if available).
 Absence of dynamic ST segment changes.
 Absence of reciprocal ST depression.
 Well-formed Q waves.
 Factors favouring acute STEMI
 New ST changes compared with previous ECGs.
 Dynamic / progressive ECG changes — the degree of ST elevation
increases on serial ECGs.
 Reciprocal ST depression.
 High clinical suspicion of STEMI — ongoing ischaemic chest pain
Hyperkalaemia
Frequently results in ST elevation, especially in leads V1 and V2, but occasionally in other
leads
Symmetric peaking of the T waves.
Other ECG changes : shortening of the QT interval and PR interval, flattening of P waves,
loss of sinoatrial conduction resulting in a wide-complex (“sine-wave” or “sinoventricular”)
rhythm, and, ultimately, ventricular fibrillation
Hyperkalaemia
Sine wave ECG

ECG in IHD THE CONTEMORARY CHANGES IN SURFACE ECG

  • 1.
    ECG Basics Dr. Md.Ahsanul Hoque Registrar (Cardiology) Dhaka Medical College
  • 2.
  • 3.
  • 4.
    IHD?  Ischemic heartdisease (IHD) is the result of a limited blood supply to the heart muscle. In more than 95% of cases, the cause of IHD is coronary blood flow reduction caused by coronary artery atherosclerosis, therefore the term “coronary heart disease” is often used to describe this syndrome. IHD/CAD includes  Stable angina  Unstable angina  Myocardial infarction  Heart failure  Arrhythmia,  Sudden death Davidson's Principles and Practice of Medicine,22rd Edition Researchgate.net/publication/330840299
  • 6.
    Normal ECG  Standardization– 10 mm (2 boxes) = 1 mV  Double and half standardization if required  Sinus Rhythm – Each P followed by QRS, R-R constant  QRS positive in L1, L2, L3, aVF and aVL. – Neg in aVR  R wave progression from V1 to V6.  Axis normal – L1, L3, and aVF all will be positive
  • 7.
  • 8.
    Be aware ofnormal ECG  Normal Resting ECG – cannot exclude disease  Ischemia may be covert – supply / demand equation  Changes of MI take some time to develop in ECG  Some of the ECG abnormalities are non specific  Single ECG cannot give progress – Need serial ECGs  ECG changes not always correlate with Angiographic results  Paroxysmal events will be missed in single ECG
  • 9.
    Normal ECG Normal isdefined as no significant Q waves, ST segment at the isoelectric line, and normal T waves in all 12 leads. Small Q waves (ie, <0.04 second wide and <25% the height of the QRS complex) can be normal in all leads except V1, V2, and V3; and lead AVR is often a QS complex normally. T waves can be slightly inverted in the right precordial leads (V1 and V2), and should be inverted in AVR in normal ECGs.
  • 10.
    ECG Manifestations ofMyocardial Ischemia
  • 13.
    The most familiarECG patterns of ischemia are horizontal or down sloping ST segment depression of 1 mm or more and T-wave inversion. ST segment elevation or depression • More than one millimeter (one small box) • Present in two anatomically contiguous leads
  • 14.
    There is acorrelation between the number of ECG leads that show ST deviation and the extent and severity of coronary artery disease.4 If ST segment depression occurs in 8 or more leads along with ST elevation in AVR and V1, there is a high risk of either left main coronary artery disease or severe triple vessel disease
  • 17.
  • 18.
  • 19.
    Presentation of coronary heartdisease Asymptomatic Chronic stable angina Acute coronary syndrome (ACS) Death Unstable angina Non ST elevation MI ST elevation MI ( M Heart failure
  • 20.
    Stable angina • Alsocalled exertional angina • The lumen of coronary artery is narrowed and hard; thus, dilation in response to increased demand is impossible
  • 21.
    Stable angina • Initiatedby known amount of activity • Same activity tends to produce same symptoms • Produced by – physical activity – emotional excitement – cause of increased cardiac workload • Relieved by rest, Nitrate
  • 22.
    Stable angina  Approximately50% of patients with angina pectoris have normal findings after a resting ECG.  However, abnormalities such as evidence for prior MI, intraventricular conduction delay, various degrees of atrioventricular block, arrhythmias, or ST-T–wave changes may be seen.  Medscape.com/article/150215-workup#c12
  • 23.
    Stable angina….  Duringan attack of angina pectoris, 50% of patients with normal findings after resting ECG show abnormalities.  Exercise with ECG monitoring alone is the initial procedure of choice in patients without baseline ST-segment abnormalities or in whom anatomic localization of ischemia is not a consideration Medscape.com/article/150215-workup#c12
  • 24.
    Printzmetal angina • Alsocalled variant angina, Prinzmetal’s variant angina • An uncommon pattern of episodic angina that occurs at rest • Due to coronary artery spasm.
  • 25.
    Printzmetal angina • Occurswithout a precipitating event, usually at the same time of day • Often awakens patient from sleep • Unpredictable, occurs most often at rest
  • 26.
  • 27.
  • 29.
  • 36.
    Inferior MI Artery involvedin Inferior MI  RCA(Right dominant)  LCX(left dominant)  Type 4 LAD
  • 37.
    Clinical Examination inCardiology, 2nd B.N.Rao
  • 38.
    Clinical Examination inCardiology, 2nd B.N.Rao
  • 39.
     Inferior wallMI – ST segment elevation of > 1 mm in inferior leads then look the following leads (Which coronary artery?)  ST segment elevation lead III> lead II-RCA  Reciprocal change in lead I & aVL-RCA  ST segment elevation lead II> lead III-LcX  If no reciprocal change in lead I & aVL- LcX  Signs of lateral infarction I,aVL,V5,V6-LcX  Look anterior lead –LAD ECG ----- Clinical Examination in Cardiology, 2nd B.N.Rao
  • 40.
     Then lookfor V1,V2,,V3,V4(Don’t Missed)  In VI isoelectric/elevated  V2,V3, V4 ST segment depression  ST elevation in right sided chest lead(V3R/V4R) ----RV infarction ECG -----
  • 43.
    Posterior wall MI Usually caused by LCx occlusion but may also be seen in dominant RCA occlusion.  ST-segment elevation in the posterior chest leads V7 through V9: > 0.5 mm in a case of IWMI Posterior MI is suggested by the following changes in V1-3:  Horizontal ST depression (i.e. reciprocal changes)  Tall, broad R waves (>30ms)  Prominent upright T waves, particularly in V2  Dominant R wave (R/S ratio > 1) in V2
  • 44.
  • 45.
    Posterior MI :V7 – V9 Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall
  • 46.
    European Heart Journal(2018) 39, 119–177 ESC GUIDELINES doi:10.1093/eurheartj/ehx393 Recommendation for Post and RV infarction
  • 47.
    RV MI Occlusion ofproximal RCA (proximal to RV branch) Identified by  ST elevation in V1 in association with IWMI (Lead III>II)  ST elevation >1 mm in V4R with an upright T (most sensitive sign of RVMI).  QS or QR in V3R and/or V4R (but less predictive than ST elevation in these leads).  Occasionally, ST-segment elevation in V2 and V3 results from acute RVI, resembling anterior infarction.
  • 48.
  • 49.
    Leads Sensitivity (%)Specificity (%) V3 R 69 97 V4 R 93 95 V1 28 92 Clinical Examination in Cardiology, 2nd B.N.Rao
  • 53.
    Extensive Anterior wallMI: localization Occlusion above D1 and S1 ST elevation ST depression lead I, aVL, V1-V4 Âą V5-V6, often in aVR II, III, aVF (Inferior) aVL > aVR III > II
  • 54.
    Antero-septal MI: localization Occlusionbefore S1 ST elevation ST depression V1-V4, RBBB II, III, aVF aVL > aVR III > II
  • 55.
    High lateral MI Occlusionin diagonal ST elevation ST depression I, aVL V5-V6 aVL > aVR III > II
  • 56.
    Antero-apical MI: localization Occlusion:More distally i.e. below Septal 1 and D1  ST segment elevation more prominent in V3 – V6 than V2  Basal portion spared (ST vector directed inferiorly)  ST segment not elevated in I, aVL/aVR  No depression in II, III, aVF  Indeed, ST segment elevation in II, III, aVF when LAD is type IV vessel
  • 57.
    Anterior wall MI:localization
  • 58.
    LMCA stenosis Typical ECGfindings in severe LMCA stenosis or occlusion include:  ST-segment elevation in lead aVR more than V1  widespread ST-segment depression or anterior ST elevation.  ST-segment of >0.05 mV elevation in aVR present in 88% of the LMCA obstruction group compared with 46% of proximal LAD occlusion. (Yamaji, et al., 2001)
  • 59.
  • 60.
  • 61.
  • 62.
  • 63.
  • 64.
  • 65.
  • 66.
    Wellen’s syndrome •Type A= Biphasic, with initial positivity & terminal negativity (25% of cases) •Type B = Deeply and symmetrically inverted (75% of cases)
  • 67.
    Wellens Syndrome  Thereare two patterns of T-wave abnormality in Wellens syndrome:  Type A – Biphasic, with initial positivity and terminal negativity (25% of cases)  Type B – Deeply and symmetrically inverted (75% of cases) https://litfl.com/wellens-syndrome-ecg-library/
  • 68.
  • 69.
  • 70.
  • 71.
    de Winter Twave  The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation. First reported by first reported de Winter in 2008  Key diagnostic features include ST depression and peaked T waves in the precordial leads.  The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-recognised by clinicians.  Unfamiliarity with this high-risk ECG pattern may lead to under-treatment (e.g. failure of cath lab activation), with attendant negative effects on morbidity and mortality. https://litfl.com/de-winter-t-wave-ecg-library/
  • 72.
    de Winter Twave------  Diagnostic Criteria  Tall, prominent, symmetric T waves in the precordial leads  Upsloping ST segment depression >1mm at the J- point in the precordial leads  Absence of ST elevation in the precordial leads  ST segment elevation (0.5mm-1mm) in aVR  “Normal” STEMI morphology may precede or follow the deWinter pattern https://litfl.com/de-winter-t-wave-ecg-library/
  • 73.
    De Winter’s Twave  De Winter ECG pattern is an anterior STEMI equivalent without obvious ST segment elevation, seen in ~2% of acute LAD occlusions.  Key diagnostic features include ST depression and peaked T waves in precordial leads  Tall, prominent, symmetric T waves in the precordial leads  Upsloping ST segment depression >1mm at the J-point in the precordial leads  Absence of ST elevation in the precordial leads  But, ST segment elevation (0.5mm-1mm) in aVR
  • 74.
    De Winter’s Twave  Upsloping ST depression in the precordial leads (> 1mm at J-point).  Peaked anterior T waves (V2-6), with the ascending limb of the T wave commencing below the isoelectric baseline.  Subtle ST elevation in aVR > 0.5mm •Upsloping ST depression in the precordial leads (> 1mm at J-point). •Peaked anterior T waves (V2-6), with the ascending limb of the T wave commencing below the isoelectric baseline. •Subtle ST elevation in aVR > 0.5mm
  • 75.
    Diagnosing MI inLBBB  In patients with LBBB or ventricular paced rhythm, infarct diagnosis based on the ECG is difficult.  The baseline ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”) in LBBB  This can mask or mimic acute Mi.  Serial ECGs may show dynamic ST segment changes during ischemia.
  • 76.
    Diagnosis of MIin presence of LBBB OLD ANTERIOR MI WITH LBBB  Cabrera’s sign – notching of 50ms in ascending limb of S wave in leads V3-V5
  • 77.
    Diagnosis of MIin presence of LBBB OLD ANTERIOR MI WITH LBBB  Chapman’s sign – notching in the upstroke of R wave in I, aVL, V6
  • 78.
    Acute MI inpresence of LBBB: Original Sgarbossa Criteria The original three criteria used to diagnose infarction in patients with LBBB are:  Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)  Concordant ST depression > 1 mm in V1-V3 (score 3)  Excessively discordant ST elevation > 5 mm in leads with a - ve QRS complex (score 2). These criteria are specific, but not sensitive for myocardial infarction. A total score of 3 has specificity of 90% for diagnosing MI. ≥
  • 79.
  • 80.
    LBBB satisfying SgarbossaCriteria Left Bundle Branch Block Satisfying the First Sgarbossa Criterion: Concordant ST elevation 1 mm in any single le ≥
  • 81.
    LBBB with IHD Sgarbossa Criteria Overview  In patients with left bundle branch block(LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG is difficult.  The baseline ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”), which can mask or mimic acute myocardial infarction.  However, serial ECGs may show dynamic ST segment changes during ischaemia.  A new LBBB is always pathological and can be a sign of myocardial infarction.  First described by Elena B Sgarbossa in 1996 https://litfl.com/sgarbossa-criteria-history/
  • 82.
    LBBB with IHD---- The original three criteria used to diagnose infarction in patients with LBBB are:  Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)  Concordant ST depression > 1 mm in V1-V3 (score 3)  Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2).  These criteria are specific, but not sensitive for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction. https://litfl.com/sgarbossa-criteria-history/
  • 84.
    Diagnosing MI inpresence of RBBB  MI diagnosis in RBBB is not very different from normal MI diagnosis.  However, as repolarization in leads V1-V3 is often abnormal in RBBB, these leads cannot always be used for the diagnosis of ischemia.
  • 85.
    MI with RBBB:before MI
  • 86.
    MI with RBBB:after STEMI anterior
  • 87.
    MI with RBBB:before MI
  • 88.
    MI with RBBB:after MI: Inferior STEMI
  • 89.
    When MI isnot MI: mimickers  LBBB  Pacing ECG  Non-Thrombotic Vasospasm  Hypertrophic Cardiomyopathy  Acute pericarditis  LV aneurysm  Early repolarization  Hyperkalaemia  Hypercalcaemia  Brugada syndrome  Osborn waves
  • 92.
    Early repolarization Early repolarizationshowing J-point elevation in multiple contiguous leads and slurring and/or notching on the downstroke of the R wave in leads II, III, aVF, V5, and V6.
  • 93.
    Pericarditis Diffuse ST elevationmost prominent in leads I, II, and V4-V6, without reciprocal cha Spodick’s sign (downsloping TP segment in lead II) PR segment depression (best seen in lead II).
  • 94.
    28 year oldmale presented with chest pain for 8 hours.. Troponin I: 0.14 ng/ml. a) What is the diagnosis?
  • 95.
    Hypertrophic Cardiomyopathy • Voltagecriteria for left ventricular hypertrophy. • Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6. • Giant T wave inversions in the precordial leads • Inverted T waves are also seen in the inferior and lateral leads.
  • 96.
    LV aneurysm •ST elevationseen > 6 weeks following acute MI •Most commonly seen in the precordial leads. •May exhibit concave or convex morphology. •Usually associated with well-formed Q- or QS waves. •T-waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI).
  • 97.
    Differentiation of LVaneurysm from acute STEMI Factors favouring left ventricular aneurysm  ECG identical to previous ECGs (if available).  Absence of dynamic ST segment changes.  Absence of reciprocal ST depression.  Well-formed Q waves.  Factors favouring acute STEMI  New ST changes compared with previous ECGs.  Dynamic / progressive ECG changes — the degree of ST elevation increases on serial ECGs.  Reciprocal ST depression.  High clinical suspicion of STEMI — ongoing ischaemic chest pain
  • 98.
    Hyperkalaemia Frequently results inST elevation, especially in leads V1 and V2, but occasionally in other leads Symmetric peaking of the T waves. Other ECG changes : shortening of the QT interval and PR interval, flattening of P waves, loss of sinoatrial conduction resulting in a wide-complex (“sine-wave” or “sinoventricular”) rhythm, and, ultimately, ventricular fibrillation
  • 99.

Editor's Notes

  • #43 s 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 Abnormal R in V1 (0.04 in duration and/or R/S ratio > 1 in the absence of preexcitation or RVH), with inferior or lateral Q waves, isolated - occlusion of a dominant LCx
  • #66 Two types Type I – 25% pain free: biphasic T waves in the anterior leads during pain: paradoxical pseudonormalisation of ST segments needs to be recognized because it will cause anterior MI within 9 days (if not dealt to by PCI or CABG) Type II – 75% deep symmetrical T wave inversion in I and aVL chest leads: 1mm of ST elevation
  • #93 Diffuse ST elevation most prominent in leads I1, II, and V4-V6, without reciprocal changes (ST segment depression in leads opposite those with ST segment elevation), Spodick’s sign (downsloping TP segment in lead II), and PR segment depression (best seen in lead II).
  • #95 Voltage criteria for left ventricular hypertrophy. Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.