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Dr. Payawal
Classification for MI is divided into 2 types:
o transmural
o involves whole thickness of myocardium
o subendocardial
o only involve subendocardium (outer part; more prone to
ischemic insults)

has different management (of which will benefit from

thrombolytic agents)
STEMI has higher short term mortality (many may die on
admission) but after a year has equal mortality rate with
NSTEMI due to high rate of recurrence of NSTEMI. So
management is still aggressive though not whole muscle is
infarcted (only subendocardium).

represents ventricular repolarization

usually upright in LI, LII and diphasic or inverted in LIII, V1

however, leads to a lot of confusion (Some docs consider T

inversion as ischemia):
may be inverted up to V3 in young adults
where clinical correlation comes in
e.g. #1:
ECG of a young lady (steff :>
-doesnt smoke
-not hypertensive
-not diabetic
-no strong family history
--brother or father did not have any
cardiovascular event: unstable angina,
heart attack, bypass, angioplasty,
When you see st segment depression and not elevation, request for stroke, peripheral vascular disease,
cardiac enzymes (troponin, CK-MB). dialysis, did not die of cv event at age
55 and younger, etc.
If elevated: diagnose Px with NSTEMI. --mother and sister did not have those
If normal: it can be normal early (an hour before/after onset events mentiponed above at age of 65
and younger
chest pain). So repeat it after several hours. Initial negative
low risk to have ischemic heart disease]
cardiac enzyme does not rule out MI. read as NORMAL
If cardiac enzyme still negative 12 hrs after onset of chest e.g. #2:
pain: rule out MI. Px just have coronary artery disease without ECG of 60 y.o. man
infarction (Stable angina w/o infarct) -came in to the clinic complaining of
angina on effort
There should always be clinical correlation (presentation similar to heart -PE: high BP
attack) -workup: diabetic, smoker
Even in ECG, early on it can still be normal. Initial normal ECG does not ISCHEMIA
yet ecg of both examples look exactly the same
rule out MI. admit Px and repeat ECG.
[has inverted T wave up to V3.
When you depend on interpretation of ecg, e.g.
#1 will reflect as anteroseptal wall ischemia then
you will give nitrates and she will have headche
bec. of drugs and go to another doctor :D do noot
rely on the machine! Correlate clinically!
Problem is when you treat a wrong disease: Px
will not get better and might even die

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Dr. Payawal
a lot of non-cardiac conditons can make the T wave U WAVE
invertedm (Physiologic T wave):
o body position we dont usually see this; not always present in all ecg
-supine after doing threadmill test o but if we do see it, it should have the same polarity as
-in this condition, T wave inversion cannot be the T wave (if the T wave is upright, the u wave should also
used as a marker for ischemia be upright)
o fever if not:
o skeletal abnormalities (pectus excavatum) negative u wave: specific for heart disease (but
o hyperventilation will not tell what kind of heart disease, just tell if
T wave in V6 usually > V1 there is something wrong)
small deflection after the T wave
QT INTERVAL represents repolarization of the Purkinje fibers
tallest in V2 & V3
usually does not exceed >1mm in amplitude
Affected by heart rate increased amplitude in LVH, hypokalemia, drugs etc.
o The slower the HR, the longer the qt interval
o The faster the HR, the shorter the qt interval
represents electrical systole LEFT ATRIAL HYPERTROPHY
measured by counting number of small boxes
time required for ventricular depolarization and repolarization
varies with age sex and heart rate o P wave duration > 0.12s (3 small squares or more)
normal QT = 0.35-0.44s (adults) o Normal duration= 2 small squares (0.10 sec)
Corrected QT or QTc (correction factor) o Normally biphasic in V1 (has upright and negative portion)
*you need calculator with square root o Sinus node is in the right atrium (RA depolarized first)
o proximal half of the p wave represents right atrial
o terminal half represents left atrial
Biphasic P wave in V1 & V2 with negative terminal portion
-by measuring qt interval in seconds in the number of small having depth of >0.1 Mv
squares times 0.04, divided by square root of R-R interval in if you have wide p wave particularly in inferior leads
sec (# small squares times 0.04). ->*this is exactly what doc o 2 small squares or more
said, I was confused so pa-check nlng o terminal portion has depth of at least one small square
Prolonged QTc > 0.425s or more
o -prone to develop Malignant Arrhythmia (has o width atleast one small square or more
potential to kill) cardiac arrest o + things mentioned aboved
Many drugs can prolong Q-T interval like GI drugs and Cardiac left atrial hypertrophy or dilatation
Drugs -we cannot distinguish hypertrophy or dilatation just
E.g. 26 yo female: for elective thyroidectomy due to non-toxic by ecg
- at recovery room: 2-3 hrs after surgery went into
cardiac arrest (did resuscitation and cpr; took some
time to revive Px)
- at ICU: intubated, in respirator, comatosed, on
double inotropic support (Dopamine & Dobutamine:
these drugs cause tachycardia or hr)
Absolute qt may be normal but qtc was around 0.5
(Prolonged qt interval) LII
Ecg before surgery: qtc normal
-rules out congenital prolonged qtc
-signifies acquired prolonged Q-T syndrome
During surgey (caused prolongation of qtc)
request serum calcium stat very low (only 0.8; N=
1.2 and above)
-Request for serum calcium after thyroidectomy
(suspect that parathyroid gland has been V1
accidentally removed or damaged or vascular or
nerve supply cut off causing serum ca drop and
prolonged qt LII:
o P wave is more than 3 small squares (at least 0.12

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Dr. Payawal
V1 leads (II, III and aVF)
o P wave is more than 3 small squares Biphasic P wave in V1 with first component larger than the
o Prominent terminal portion which is >1 small second
square Leads
Depth and width is 2 small squares
meets criteria for left atrial

**Loud S1 Opening Snap = Mitral Stenosis 2 Enlarged RA

height: at least 2 small squares or more than

tall p waves (evidence of RAH on ecg)

ST elevation seen in all leads (massive MI)

Lead I is (+) and aVF is (-) = Left axis Deviation

12 lead ecg Tall peaked P wave at Lead II

What is the axis? Prox of P wave is taller in lead V1
-lead AVF is predominantly negative 12 lead ecg
-lead I (qrs) predominantly positive What is the axis?
P wave (particularly in inferior leads: II, III, AVF?) RIGHT
o Has 2 peaks -AVF predominantly positive (upright)
o Terminal half at least 1 square -Lead I (qrs) predominanty negative
Inferior lead:
p waves are tall and peak
No more terminal half in V1 (not biphasic)
just have proximal half which is predominantly upright
it is not the duration anymore but the blabla of p wave
o should be equal and more than 2 small squares in
inferior lead
o proximal half more prominent than terminal half in lead
criteria for right atrial enlargement or hypertrophy
P waves tall (> 0.25mV)(2.5 mm or more) & peaked in inferior

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Dr. Payawal


R/S ratio in V1 > 1

o R wave is smallest in V1 and V2; if R wave is very tall in V1,
taller than how deeps S wave is in V1 = RVH
S in V1 < 2mm
R wave is very tall in V1 (recall: R wave is smallest in V1)
RAD > 110 degrees
Similar ECG with Bundle Branch Block and Posterior Wall MI
Right Axis Deviation
Not all prominent R waves in V1 is RVH, there is always
differential diagnosis: right bundle branch block, posterior wall MI
PE: palpation of ?
o RV is relatively anterior chamber, when becomes
bigger, pushes chest wall forward

V4, V5 and V6: concomitant ST depression may be a part of LVH or due

to ischemia. (LVH and ST depression 2LVH or Ischemia)

***ECG cant distinguish hypertrophy from dilatation (basta malaki lang)

12 lead ecg
-Lead I (qrs) still predominantly positive or upright
-Lead AVF still predominantly positive

Left ventricular hypertrophy

o Count number of squares of S wave in V1 or V2
(whichever is deeper)
*here, V2 is deeper= 24 squares
o *V5 has taller R wave= 26
26+20= 46 (is more than 35 or 40)

Same ecg lead ST segment depression (very deep)

Right axis deviation o st segment depression on top of LVH: we can no longer
Right atrial enlargement distinguish if this is due to ischemia or LVH [blabla pattern
Chest leads: tall R (should be very small here) of LVH]
Shallow s waves o Unless Px complains of angina and has elevated cardiac
R/S ratio is >1 enzymes: st segment depression may be due to ischemic
RVH unless proven otherwise heart disease
o But you can have st segment changes secondary to
--Hypertrophied heart Is more prone to ischemia
because of increased muscle mass which needs
Sum of R wave in V5 or V6 (whichever is taller) + S wave in V1 more blood supply
or V2 (whichever is deeper) --small arterioles are more easily compressed by
o > 30 y.o. = > 35mm in adults very thick muscle
o Younger (20-30 y.o)= > 40mm
Impt to know the name, age, sex, date and time [Proverbs 12:25]

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