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CARDIOLOGY
Versi
Dr. O. Payawal Jr.
Legend: 07.5&19.12
Comic Sans – Notes
Times New Roman – Original Trans

Electrocardiography
● graphic recording of electric potentials produced
by the heart
● signals detected by metal electrodes attached to
extremities and chest wall and recorded by the
- study of electrical activity of the heart (review the cardiac
cycle)
- electrical events preceding the contraction of the heart
- electrical events seen on ECG

Electrical activity
Originates from the pacemaker cells

ECG (1st slide)
- can see enlargement of heart cavities Resting or Polarized State (Phase 4)
- non invasive, inexpensive and readily available
- warning: interpretation of machine is not reliable
- R-leg is used only as a ground

ECG machine -
● noninvasive, inexpensive and readily available

Cardiac cycle – electrical events represented in the ECG

Depolarization-Repolarization Cycle
(Action Potential)

Phase 0 : Rapid depolarization

● Na moves rapidly into the cell
● Ca moves slowly into the cell
● Charge = (+)

Phase 1: Early repolarization

● Na channels close
● Transient efflux of K
● Charge = slight dip in charge

Phase 2: Plateau phase

● Ca continues to flow in
● K continues to flow out
● Charge = 0

Phase 3: Rapid repolarization

● Large amounts of K diffuse out as all K channels open
● Inactvation of Ca channels
● Charge = continuous to go down

Phase 4: Resting Phase

● Na-K pump restores Na out
● Cell membrane impermeable to Na ions
● Charge = -90

Page 1 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

Electrical events PRECEDE Mechanical events

Orientation of leads is important

Lead I - from R arm to L arm
Lead II – from R arm to L leg
Lead III – From L arm to L leg
Limb leads:
R arm – negative electrode
L arm – positive electrode
L leg - positive electrode
QRS complex – seen in all ECG (unless dead) R leg – used for grounding only
- occurs in phase 0/ represents phase 0 of both ventricles
• we cannot see electricity , we can only measure it
ST segment – used to diagnose heart attack or ischemia
- represents phase 2 of ventricles Einthoven Triangle Hypothesis

T wave – represents phase 3 of ventricles Assumptions:
● Roots of the LA, RA, LL form apices of a triangle.

● Electrical forces produced by the heart are represented by
P wave – represents atrial depolarization (atrial repolarization is
an equivalent dipole at the center of the triangle.
buried in the QRS complex) ● Body tissues and fluids in which triangle is located act as
homogenous conductor.
Absolute Refractory period – from phase 0 to peak of T wave ● Bipolar limb leads record potential variations of the heart in
(middle of phase 3) the frontal plane.
- heart cannot be re stimulated
Einthoven’s Law: Lead I + Lead III = Lead II
Relative refractory period Ø If Lead I is positive and Lead III is positive, Lead II should be
- needs a strong stimulus for ehart to respond and the taller
response is weaker Ø If Lead I is negative and Lead III is positive, Lead II should
- from peak T wave until the end of phase 3 be smaller
- vulnerable period during the cardiac cycle that can cuase
malignant dysrhytmias

Page 2 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

 HEXIAI ratio

Chest leads measure the horizontal plane

Limb leads measure the frontal plane
Total electrical axis of heart – Take note of Lead I and AVF. Normal
direction is going to the left between (+) 30 degrees and (+) 60
degrees

If patient has a big left ventricle, the electrical axis of the heart can
be directed more to the left.

Example: In Inferior wall MI, cardiac tissue becomes necrotic; no
electrical activity = direction of the total electrical axis is directed
towards the left

Example: big right ventricle = axis deviated to the right

Lead I and AVF: they should have a QRS that is predominantly ECG – gives you an idea where the pathology is.
positive which means axis is between 0-90 degrees which is normal - if it is ischemia, you know which coronary artery is
involved depending on the wall affected. This is important
IF Lead I is (+) and AVF is (-) = L axis deviation specially when doing angioplasty (need to canulate the
IF Lead I is (-) and AVF is (+) = R axis deviation artery first)
IF Lead I is (-) and AVF is (-) = R axis deviation - you’ll have an idea about the extent of the
pathology/prognosis. If there are multiple leads affected
Unipolar Precordial Leads
Leads View of Heart
V1 - 4th ICS right sternal margin LI Lateral wall
V2 - 4th ICS left sternal margin LII Inferior wall
V3 - midway between V2 and V4 LIII Inferior wall
V4 - 5th ICS MCL AVR No specific view
V5 - AAL same level as V4 AVL Lateral wall
V6 - MAL same level as V4 AVF Interior wall
V1 Anteroseptal wall
For male patients – V4 is usually under the L nipple V2 Anteroseptal wall
V3 Anterior wall
V4 Anterior wall
V5 Lateral wall
V6 Lateral wall

Know the pathway of electrical conduction system of the heart

SA node to atrium to AV node (has the longest refractory period)HIS
bundle to purkinje fibers to ventricles

AV node as the longest refractory period (good)

Page 3 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

 (if seen in many leads or as prominent 1/3 of QRS = old
infarct,); not seen very often
R wave -first upward deflection whether preceded by a Qwave or not
(smallest in V1 and V2 and becomes taller as you go to V6.
Highest in V4)
S wave - downward deflection following the R wave
(deepest in V1 and V2 and becomes shallower as you go to
V6)
QS wave - single negative deflection representing entire QRS
(prominent in SOB with LV infarct. If prominent from V1 to
V6 may indicate a big part of the heart has an infarct)
R’ wave - second upward deflection
(bundle branch block); Will be absent in patients with
heart attack. (You will only have a QS wave)

X axis – horizontal , Measurement of time

Normal standard ECG machine paper speed is 25 mm/sec
1 small square = 0.04 seconds
1 big square = 0.20 seconds (5 small squares)

Y axis = measurement of voltage
1 millivolt of electricity = 10 mm amplitude on ECG paper
10 mm = 10 squares
Bigger heart gives a bigger voltage = bigger QRS
If heart is too big ECG graph has QRS larger than the paper. - Label
ECG paper as half sensitivity

1 small square = 0.1 mv

P wave
● represents atrial depolarization ST Segment
● atrial conduction time ● represents period from end of ventricular depolarization to
● normal amplitude is 0.5 to 2.5 mm (increased in RA start of ventricular repolarization
enlargement) ● between end of QRS and start of T wave
● normal duration is up to 0.10s (2 ½ small squares) in adults ● clinically important if elevated or depressed as it may
(increased in LA enlargement or dilatation) represent infarction or ischemia
● usually biphasic (with upward and downward deflection) ● usually isoelectric (like the P wave) but may be depressed –
in V1 (1st prox. half – RA phenomenon; later ½ - LA 0.5 mm or elevated by 1mm.
phenomenon) ● Used to diagnose acute MI > Elevated in acute infarct
(higher risk if seen in more leads)
P-R Interval (or PQ interval) ● Elevated >1mm in acute MI (heart attack)
● represents time interval for impulse to reach ventricles from ● Elevated >0.5mm in ischemia
SA node ● Elevation should be convex upward (MI unless proven
● measured in limb lead with longest PR interval otherwise) (drawing is kamukha ng 1st 2 figures ng part A
● normal is 0.12-0.20s in adults (HR = 70-90/min) (increased sa next pic)
in AV block) ● If elevated but concave upward, could be a normal variant,
● Start of P to start of QRS electrolyte imbalance or pericarditis (not specific for
• 0.20 s = 5 small squares or 1 big square infarcts but suspicious for a coronary event). (seen on next
tracings)
● Ex. ST elevation in Lead II. III and aVF – acute Inferior Wall
infarct -> Thrombosed Right Coronary Artery (Blood Supply
of inferior wall)
● MI: heaviness, feeling of impending death b/c of pain, cold
clammy perspiration, SOB
● The more elevated the ST segment is, the bigger the
infarct (massive MI) which, if not treated, can cause
CARDIOGENIC SHOCK (80% mortality)
● Philippines – CVD #1 mortality (9 pinoys die/hour)
● 50% of deaths of CVD is 2˚ Sudden Cardiac Death (death
within 1 hour after onset of S/Sx.
● Prevention: #1 factor is early recognition (utmost
importance) - ECG
● Depression of more than 0.5mm is an ischemia.

Caution:
Pleuritic chest pain (pericarditis) and MI present both with
One figure of impulse: chest pain. Be sure to differentiate because treatment of
Normal duration = 0.5 sec pleuritic chest pain is NSAIDS. But
QRS Complex
Q wave - initial downward deflection If you give NSAID to a patient with MI, you can cause
myocardial rupture.

You will kill your patient!

Page 4 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

 Normal axis
St elev
Acute MI

Part A figures – high specificity especially if with clinical correlation

with the pt’s dse.
ST elevation in Lead II, III, aVR, aVF, V4-V6 (eto lang ata)
Q wave at lead II (old infarct)
Long lead II shows the Concave upward variant of ST elevation, but
since ST elevations are also seen in other leads, it is more probable
that it is MI than normal (tinanong ko kay doc)
ADMIT = MASSIVE MI

**Giving MI tx to a non-MI pt can cause death 2˚ hemorrhagic
bleeding

Ø 12-Lead ECG is more Expensive

Diffuse MI
ST elevation in Leads I, II, aVL, V2, V3, V4, V5 and V6 Normalaxis
St depression in Lead III and aVF (compensatory)
ADMIT: NEEDS IMMEDIATE TX

**initially, ECG doesn’t rule out MI so pt still needs to be admitted
**NSAIDs can complicate healing of heart (in MI) which can cause
myocardial rupture

STEMI – ST elevation, Normal cardiac enzymes

Non STEMI – ST is Normal or depressed, elevated cardiac enzymes
Ischemia (no MI) – ST elevation, normal cardiac enzymes

**Cardiac Enzymes: CK-MB, Troponins
**Troponins are more specific (but is elevated even in small infarcts
even without clinical manifestation or significance)

S-T depression

Page 5 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

 Stemi- can give anti thrombo
Nstemi - not yet

● varies with age sex and heart rate (dec HR = prolonged Q-

T; inc HR = shorter QT)
● normal QT is 0.35-0.44s in adults
● Corrected QT or QTc

● Prolonged QTc > 0.425s (prone to develop Malignant

Arrhythmia à cardiac arrest)
● Many drugs can prolong Q-T interval like GI drugs and
Cardiac Drugs
● Ex. 26 yo female, non-toxic goiter, for thyroidectomy. 4 hrs
post-op à cardiac arrest, coma, tchycardic bec of
dopa/dobutamine. Post-op ECG showed prolonged Q-T
interval (Q-Tc = 0.51), with normal ECG pre-op à signifies
acquired prolonged Q-T syndrome. Serum Ca is very low
which caused prolonged Q-T interval.
:::accidental removal / destruction of parathyroids

T wave
● represents ventricular repolarization
● usually upright in LI, LII and diphasic or inverted in LIII,
V1
U wave
● maybe inverted up to V3 in young adults
● small deflection after the T wave
● T wave in V6 usually > V1 ● represents repolarization of the Purkinje fibers
● Physiologic T wave changes may be seen in body position,
● tallest in V2 & V3
fever, skeletal abnormalities, hyperventilation, fever, etc.
● usually does not exceed >1mm in amplitude
● Cause a lot of confusion - Some docs consider T inversion
● same as T wave polarity
as ischemia ● increased amplitude in LVH, hypokalemia, drugs etc.
● Therefore, ECG should always be correlated w/ the pt. ● negative U wave specific for heart disease
● Ex.
T wave is a bit T wave inversion in V1-V3 in a young female, no strong
diff to interpret
Left Atrial Hypertrophy
becaus it can hereditary predisposition to HPN, no HPN, non-smoker = ● P wave duration > 0.12s (3 small squares or more)
change even in No ischemia, NORMAL Pero if yan din nakita mo sa isang health ● Biphasic P wave in V1 & V2 with negative terminal
normal changes person, yung interpretation mo nito is
such as position normal. Wala kasi risk factors ung normal portion having depth of >0.1 mV
T wave inversion in V1-V3 IN AN OLDER ADULT, W/ HPN,
smoker, diabetic = Ischemic anteroseptal wall

LII

V1
**Loud S1 Opening Snap = Mitral Stenosis 2˚ Enlarged RA

Q-T Interval
● represents electrical systole
● measured by counting number of small boxes
● time required for ventricular depolarization and
repolarization

Page 6 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-

ST elevation seen in all leads (massive MI)
Left Ventricular Hypertrophy
Lead I is (+) and aVF is (-) = Left axis Deviation
● Sum of R wave in V5 or V6 + S wave in V1 or V2 (choose
Right Atrial Enlargement deeper tracings) is > 35mm in adults > 30 years (>40 mm
in 20-30 years & >60 mm in 6-20years )
● P waves tall (> 0.25mV)(2.5 mm or more) & peaked in
inferior leads ● Impt to know the name, age, sex, date and time
● Biphasic P wave in V1 with first component larger than ● Prone to have ischemia bec muscles are hypertrophied
the second
● Leads II, III and aVF

V4, V5 and V6: concomitant ST depression – may be a part of

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

***ECG can’t distinguish hypertrophy from dilatation (basta
malaki lang)
-END OF LECTURE-

Orig trans from -jheyk-
Notes from Cathy, Joyce and Me =D
Thank You

Cardio Team
bam, cathy, erick, jhigz, jhoey, lar, rowel
###good4urheart =D
Tall peaked P wave at Lead II
Prox ½ of P wave is taller in lead V1
Right Ventricular Hypertrophy
● R/S ratio in V1 > 1
● 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

Page 7 of 7 “Generosity and sacrifice go hand in hand, though it is possible to be generous without making a sacrifice.” -jheyk-