IHD?
ď 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 âcoronary heart diseaseâ is often used to describe this syndrome.
IHD/CAD includes
ď Stable angina
ď Unstable angina
ď Myocardial infarction
ď Heart failure
ď Arrhythmia,
ď Sudden death
Davidson's Principles and Practice of Medicine,22rd Edition
Researchgate.net/publication/330840299
6.
Normal ECG
ď Standardizationâ 10 mm (2 boxes) = 1 mV
ď Double and half standardization if required
ď Sinus Rhythm â Each P followed by QRS, R-R constant
ď QRS positive in L1, L2, L3, aVF and aVL. â Neg in aVR
ď R wave progression from V1 to V6.
ď Axis normal â L1, L3, and aVF all will be positive
Be aware ofnormal ECG
ď§ Normal Resting ECG â cannot
exclude disease
ď§ Ischemia may be covert â
supply / demand equation
ď§ Changes of MI take some time
to develop in ECG
ď§ Some of the ECG abnormalities
are non specific
ď§ Single ECG cannot give
progress â Need serial ECGs
ď§ ECG changes not always
correlate with Angiographic
results
ď§ 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.
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
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
â physical activity
â emotional excitement
â cause of increased cardiac workload
⢠Relieved by rest, Nitrate
22.
Stable angina
ď Approximately50% of patients with angina pectoris have
normal findings after a resting ECG.
ď However, abnormalities such as evidence for prior MI,
intraventricular conduction delay, various degrees of
atrioventricular block, arrhythmias, or ST-Tâwave changes may
be seen.
ď Medscape.com/article/150215-workup#c12
23.
Stable anginaâŚ.
ď Duringan attack of angina pectoris, 50% of patients with
normal findings after resting ECG show abnormalities.
ď 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, Prinzmetalâs 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
ď Inferior wallMI â
ST segment elevation of > 1 mm in inferior leads
then look the following leads (Which coronary artery?)
ď ST segment elevation lead III> lead II-RCA
ď Reciprocal change in lead I & aVL-RCA
ď ST segment elevation lead II> lead III-LcX
ď If no reciprocal change in lead I & aVL- LcX
ď Signs of lateral infarction I,aVL,V5,V6-LcX
ď Look anterior lead âLAD
ECG -----
Clinical Examination in Cardiology, 2nd
B.N.Rao
40.
ď Then lookfor V1,V2,,V3,V4(Donât Missed)
ď In VI isoelectric/elevated
ď V2,V3, V4 ST segment depression
ď ST elevation in right sided chest lead(V3R/V4R)
----RV infarction
ECG -----
43.
Posterior wall MI
ďUsually caused by LCx occlusion but may also be seen in
dominant RCA occlusion.
ď 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:
ď Horizontal ST depression (i.e. reciprocal changes)
ď Tall, broad R waves (>30ms)
ď Prominent upright T waves, particularly in V2
ď Dominant R wave (R/S ratio > 1) in V2
Posterior MI :V7 â V9
Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall
46.
European Heart Journal(2018) 39, 119â177 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
ď ST elevation in V1 in association with IWMI (Lead
III>II)
ď ST elevation >1 mm in V4R with an upright T (most
sensitive sign of RVMI).
ď QS or QR in V3R and/or V4R (but less predictive than
ST elevation in these leads).
ď Occasionally, ST-segment elevation in V2 and V3
results from acute RVI, resembling anterior infarction.
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
Antero-apical MI: localization
Occlusion:More distally i.e. below Septal 1 and
D1
ď ST segment elevation more prominent in V3 â V6
than V2
ď Basal portion spared (ST vector directed
inferiorly)
ď ST segment not elevated in I, aVL/aVR
ď No depression in II, III, aVF
ď Indeed, ST segment elevation in II, III, aVF
when LAD is type IV vessel
LMCA stenosis
Typical ECGfindings in severe LMCA stenosis or
occlusion include:
ď ST-segment elevation in lead aVR more than V1
ď widespread ST-segment depression or anterior ST
elevation.
ď 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)
Wellenâs syndrome
â˘Type A= Biphasic, with initial positivity & terminal negativity (25% of cases)
â˘Type B = Deeply and symmetrically inverted (75% of cases)
67.
Wellens Syndrome
ď Thereare two patterns of T-wave abnormality in
Wellens syndrome:
ď Type A â Biphasic, with initial positivity and
terminal negativity (25% of cases)
ď Type B â Deeply and symmetrically inverted
(75% of cases)
https://litfl.com/wellens-syndrome-ecg-library/
de Winter Twave
ď 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
ď Key diagnostic features include ST depression and peaked T
waves in the precordial leads.
ď The de Winter pattern is seen in ~2% of acute LAD
occlusions and is under-recognised by clinicians.
ď 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------
ď Diagnostic Criteria
ď Tall, prominent, symmetric T waves in the precordial
leads
ď Upsloping ST segment depression >1mm at the J-
point in the precordial leads
ď Absence of ST elevation in the precordial leads
ď ST segment elevation (0.5mm-1mm) in aVR
ď âNormalâ STEMI morphology may precede or follow
the deWinter pattern
https://litfl.com/de-winter-t-wave-ecg-library/
73.
De Winterâs Twave
ď De Winter ECG pattern is an anterior STEMI equivalent
without obvious ST segment elevation, seen in ~2% of
acute LAD occlusions.
ď Key diagnostic features include ST depression and peaked T
waves in
precordial leads
ď Tall, prominent, symmetric T waves in the precordial leads
ď Upsloping ST segment depression >1mm at the J-point in the
precordial leads
ď Absence of ST elevation in the precordial leads
ď But, ST segment elevation (0.5mm-1mm) in aVR
74.
De Winterâs Twave
ď Upsloping ST depression in the precordial leads
(> 1mm at J-point).
ď Peaked anterior T waves (V2-6), with the
ascending limb of the T wave commencing below
the isoelectric baseline.
ď Subtle ST elevation in aVR > 0.5mm
â˘Upsloping ST depression in the precordial leads (> 1mm at J-point).
â˘Peaked anterior T waves (V2-6), with the ascending limb of the T wave commencing below
the isoelectric baseline.
â˘Subtle ST elevation in aVR > 0.5mm
75.
Diagnosing MI inLBBB
ď In patients with LBBB or ventricular paced rhythm,
infarct diagnosis based on the ECG is difficult.
ď The baseline ST segments and T waves tend to be
shifted in a discordant direction (âappropriate
discordanceâ) in LBBB
ď This can mask or mimic acute Mi.
ď Serial ECGs may show dynamic
ST segment changes during ischemia.
76.
Diagnosis of MIin presence of LBBB
OLD ANTERIOR MI WITH LBBB
ď Cabreraâs sign â 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
ď Chapmanâs sign â 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:
ď Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
ď Concordant ST depression > 1 mm in V1-V3 (score 3)
ď 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.
âĽ
LBBB satisfying SgarbossaCriteria
Left Bundle Branch Block Satisfying the First Sgarbossa Criterion: Concordant ST elevation 1 mm in any single le
âĽ
81.
LBBB with IHD
ďSgarbossa Criteria Overview
ď In patients with left bundle branch block(LBBB) or ventricular
paced rhythm, infarct diagnosis based on the ECG is difficult.
ď The baseline ST segments and T waves tend to be shifted in a
discordant direction (âappropriate discordanceâ), which can
mask or mimic acute myocardial infarction.
ď However, serial ECGs may show dynamic ST segment changes
during ischaemia.
ď A new LBBB is always pathological and can be a sign of
myocardial infarction.
ď First described by Elena B Sgarbossa in 1996
https://litfl.com/sgarbossa-criteria-history/
82.
LBBB with IHD----
ďThe original three criteria used to diagnose infarction in
patients with LBBB are:
ď Concordant ST elevation > 1mm in leads with a positive QRS
complex (score 5)
ď Concordant ST depression > 1 mm in V1-V3 (score 3)
ď Excessively discordant ST elevation > 5 mm in leads with a -ve
QRS complex (score 2).
ď These criteria are specific, but not sensitive for myocardial
infarction. A total score of ⼠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
ď MI diagnosis in RBBB is not very different from
normal MI diagnosis.
ď However, as repolarization in leads V1-V3 is
often abnormal in RBBB, these leads cannot
always be used for the diagnosis of ischemia.
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
Spodickâs 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
â˘ST elevationseen > 6 weeks following acute MI
â˘Most commonly seen in the precordial leads.
â˘May exhibit concave or convex morphology.
â˘Usually associated with well-formed Q- or QS waves.
â˘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
ď ECG identical to previous ECGs (if available).
ď Absence of dynamic ST segment changes.
ď Absence of reciprocal ST depression.
ď Well-formed Q waves.
ď Factors favouring acute STEMI
ď New ST changes compared with previous ECGs.
ď Dynamic / progressive ECG changes â the degree of ST elevation
increases on serial ECGs.
ď Reciprocal ST depression.
ď High clinical suspicion of STEMI â 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 (âsine-waveâ or âsinoventricularâ)
rhythm, and, ultimately, ventricular fibrillation
#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
#66Â Two types
Type I â 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 â 75%
deep symmetrical T wave inversion in I and aVL
chest leads: 1mm of ST elevation
#93Â 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), Spodickâs sign (downsloping TP segment in lead II), and PR segment depression (best seen in lead II).
#95Â Voltage criteria for left ventricular hypertrophy.
Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.