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MEDICINE II
AND ARRHYTHMIA
SEMESTER ECG RECOGNITION | DOC DAET

—» Specialized conduction tissue

OUTLINE — Heart muscle
I. REVIEW OF THE CONDUCTION SYSTEM
II. ECG LEADS . .
lnfeinoil )l
Tr icts >
Bundle
of His

III. ECG WAVEFORMS AND INTERVALS

Anteiioi
IV. INTERPRETATION AND APPROACH SA Node Fascicle
V. ISCHEMIA AND INFARCTION
VI. COMMON ARRHYTHMIAS
Puikiiije
Filieis

AV Node

Right Bundle Left Posteiioi

Branch Fascicle
i. REVIEW OF THE CONDUCTION SYSTEM .
Figure 1 Conduction system of the heart

A. ELECTROCARDIOGRAM (ECG ) >

SA node -> R and L atrial contraction -> AV node - Bundle of His - right >
and left bundle branch -> Purkinje fibers -> right and left ventricular
• Representation of the electrical events of the cardiac cycle
contraction
• A graphic recording of the electrical potentials produced
A. SA NODE
by the cardiac tissue. It is measured in millivolts ( mV).
— Records the complex spatial and temporal
*
• Collection of pacemaker cells where depolarization
stimulus for the normal heartbeat originates
summation of electrical potentials from multiple
Exhibits automaticity
myocardial fibers conducted to the surface of
the body • Main pacemaker of the heart
• Usually fires at 60-100bpm (AV node fires at 40-60bpm )
• Useful screening tool for a variety of cardiac abnormalities
—> If the patient has a problem with the SA node, the
• Most commonly performed cardiac test
AV node takes over, leads to lower bpm- needs a
• It does not record directly the electrical activity of the
pacemaker
source itself; it records only the depolarization
( stimulation ) and repolarization (recovery ) potentials
B . PACEMAKER ACTION POTENTIAL
generated by the atrial and ventricular myocardium.
Action potential results from highly coordinated,
• Since the cardiac depolarization and repolarization waves
sequential changes in ion conductance through gated
have direction and magnitude, they can be represented by
sarcolemma membrane channels
vectors
Pacemaker potential: change of mV of the pacemaker cells
• Vector analysis- central concept of electrocardiography
from approximately - 60mV to - 40mV ( aka slow
• Types of pathology Identified in ECG
depolarization, which is caused by influx of some Na+ ions)
—> Arrhythmias
—* Myocardial ischemia and infarction
—> Pericarditis •It

—» Chamber hypertrophy
—> Electrolyte disturbances (i.e. hyperkalemia, -It

i!:
i
hypokalemia )
—> Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
!~
• The electric currents that spread through the heart are
produced by three components
-
—>
f
Cardiac pacemaker cells
—> Specialized conduction tissue
—> Heart muscle cells
Tkiw (me)

.
Figure 2 Action potential of pacemaker cells
B. NORMAL CONDUCTION SYSTEM
• Depolarization (initiating event for cardiac contraction)
• SA depolarizes spontaneously
and repolarization are a result of movements of ions across
the plasma membrane of cardiomyocytes and the • At - 40 mV ( threshold potential ), Ca 2+ ions enter the cells - >
rapid depolarization phase
pacemaker cells
• The electrical currents that spread through the heart ae • Between 0 and +10 mV, the peak is reached, then
repolarization starts via K* efflux, until -60 mV is reached.
produced by three components
Then, a new cycle begins.
—> Cardiac pacemaker cells

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• Pacemaker cells has NO true resting membrane potential. —* One point on the body and a virtual reference
point with zero electrical potential, located in
.
C PHASES OF CARDIAC ELECTRICAL ACTIVATION the center of the heart (unipolar leads )
• Impulse stimulates pacemaker and specialized conduction Standard ECG has 12 leads:
tissues in the AV nodal and HI- bundle areas —» 3 Standard Limb Leads
• These two regions constitute the AV junction —* 3 Augmented Limb Leads
• AV node
—*
6 Precordial Leads
—* Conducts action potential more slowly The 12 conventional ECG leads are divided into two
—> Ensures ventricles receive signal to contract
after atria have contracted groups:

• The bundle of His bifurcates into two main branches, the

right and left bundles, which rapidly transmit
6 limb ( extremity ) leads : record potentials
transmitted onto the frontal plane
depolarization wavefronts to the right and left ventricular — 6 chest (precordial ) leads: record potentials
myocardium by way of Purkinje fibers transmitted onto the horizontal plane
• Depolarization wavefronts then spread through the Axis: viewpoint from which it looks at the heart
ventricular all, from endocardium, triggering ventricular
Upright deflection: wave of depolarization spreads toward
contraction
the positive pole
e Negative deflection: wave spreads toward the negative
> pole
E
0
I Biphasic deflection: mean orientation of the
i depolarization vector is at right angles to a particular lead
5 —25
1 axis ( equally positive and negative)
e - so
<12 A. ELECTRIDE PLACEMENT
I A. LIMB ELECTRODES
§ -75
• Right Arm ( RA ) - Red
-100 a Left Arm (LA) - Yellow
tt t t t t t m IH t
• Right Leg ( RL) - Black
Na* Ca2* K* Na* K* e Left Leg ( LL) - Green
influx influx efflux efflux Influx

.
Figure 3 Phases of the action potential of cardiomyocytes B. PRECORDIAL LEADS
Table 2. Precordial leads
Table 1. Phases of the action potential of cardiomyocytes
Precordial Leads Color Location
PHASE DESCRIPTION
VI Red 4th ICS RPSB
Phase 0 Rapid upstroke
V2 Yellow 4th ICS LPSB
Caused by the stimulus sent by the
V3 Green Midway between V2 & V4
pacemaker cells and Na+ influx
V4 Brown 5 th ICS LMCL
Phase 1 Notch
V5 Black LAAL lateral and horizontal to
Initial rapid repolarization phase
V4, 5th ICS
K* and Cl conductance
'

V6 Violet LMAL lateral and horizontal to

Phase 2 Plateau V4, 5th ICS
Results from a balance of inward Ca 2+ and To locate the 4 ICS (usually along the nipple line) palpate the jugular notch
th

outward K+ currents then downwards 3 centimeter where you will find the sternal notch. From
P Final rapid repolarization the angle of Louis, move your fingers to the right and you will feel a gap
hase 3 Restores resting potential between the ribs. This gap is the 2nd Intercostal space. From this position,

Caused by inactivation of the Ca 2+

current
.
run your fingers downward across the next rib, and the next one The space

and an increase in the outward K+ current

.
you are in is the 4th intercostal space

Phase 4 Slow, spontaneous diastolic depolarization

responsible for the property of automaticity Angle of
Louis

ECG LEADS
Leads are electrodes which measure the difference in
electrical potential between either: vi
—> Two different points on the body (bipolar leads)
Figure 4. Precordial Leads Location

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• Augmented Leads ( "a") ECG WAVEFORMS AND INTERVALS

—> Augmented means to increase in size - > ECG
A . ECG PAPER
machine amplifiesfby 50%) the signal to make it
more readable
"a” refers to augmented
"V" refers to voltage
"R" refers to right
"L" refers to left
"F” refers to foot
—* Three types:
aVR : looks down at the heart from the .
Figure 7 ECG Paper dimension
patients right shoulder
aVL: looks at the heart from the left Table 4. ECG Paper Dimension
shoulder Voltage Time
aVF: looks up at the heart from the left (height in mm) (in seconds)
leg 1small box 1mm 0.04 ( 40 ms)
• Difference in voltage between two extremities: 5 small boxes (1 5 mm 0.2 ( 200 ms)
—> Lead I: difference in voltage between L and R large square)
arm
—» Lead II: difference in voltage between L leg and Note: The y-axis in the ECG paper is represented as the "voltage" (1
R arm mV = 10 mm with standard calibration ) where the "amplitude" is
—» Lead III: difference in voltage between L leg and
reflected, while the x -axis is represented as the time in seconds. The
L arm ECG is recorded on to standard paper travelling at a rate of 25
mm/ sec .

B. WAVEFORMS AND INTERVALS

< -> K|•
R wave T wav U wav
complex
* *

Figure 5. Leads 1-3

PR Interval OX Interval

.
Figure 6 Precordial leads on the chest record potentials Figure 8. Waveforms of ECG and the corresponding process of heart
transmitted onto the horizontal plane. contraction
P wave
Table 3. Summary of Leads —> Represents atrial depolarization
Leads Type Limb Leads Precordial Leads —* Represents atrial contraction
Unipolar I, II, III —» Slow rounded wave
(standard limbs) —» Duration between 0.08 and O.llsecs ( 2 % small
Bipolar aVR , aVL , aVF VI to V6 squares)
(augmented limb —> Height less than 2.0 mm ( 2 small squares)
leads) • Higher - possible atrial enlargement
—* Upright in Lead I, II, avF and left precordial leads
(usual lead for a rhythm strip)
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—» Inverted in Avr
e T wave
—» For adults more than 30 years old: normally
inverted only in VI
—» Less than 30 yrs. old: normally inverted in VI to
V3
—> Represents ventricular relaxation
—* Rounded peak
Figure 9. P wave
—> Should be in the same direction as the main QRS
complex
— Abnormal if inverted seen in LVH, Bundle branch
• QRS complex
blocks & ischemia
—* Represents ventricular depolarization
—» Measured from the onset of the Q to the end of I
the S wave
—* Predominantly Upward in left sided leads
—» Negative in right sided leads
H
—» Between 0.08 and 0.12 secs in duration ( 3 small
squares)
Figure 13. T wave
• U wave
Prominent in V3
Not >1mm amplitude
Very prominent U waves : marker of T"
susceptibility to torsades de pointes
Figure 10. QRS Complex If prominent in all chest leads, possible
electrolyte abnormalities (hypokalemia )
• J point: junction between the end of the QRS complex Abnormal increase in U wave amplitude is most
and the beginning of the ST segment commonly due to:
Drugs ( e.g., dofetilide, amiodarone,
sotalol, quinidine)
• Hypokalemia
Normal U wave: small, rounded deflection (<1
mm) that follows the T wave and usually has the
same polarity as the T wave

Figure 11. J point (yellow arrow)

• ST- T-U complex

—* Combination of ST segment, T wave, and U wave
—» Ventricular repolarization

Figure 14. U wave

• ST segment
—» Isoelectric
• Four Major ECG Intervals
—> Normally deviate
—» RR Interval- from R wave to the next R wave
—* between -0.5 and +lmm from the baseline • Used to compute the rate and rhythm
—> Measured between the end of the QRS and the
—> PR Interval- from start of P wave to the QRS
beginning of the T wave complex
—> Should be no more than 1mm above or below
— t QRS Interval- end of PR interval to end of S
the baseline wave
—> QT Interval- end of PR interval to end of T wave
• Normal QT for rates 60-100 is 0.30-
0.40 seconds

Figure 12. ST segment

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Table 7. Sinus rhythms

6.1 mv I RR interva Normal Sinus 60-100 bpm
R Sinus Bradycardia < 60 bpm
Spmtnl TP.
sygffii Sinus Tachycardia > 100 bpm

1/ Note: Some can have a normal beats of 50 bpm, as long

I
^ .
PF inlei W
Q
S J Perl

?
A.
as there is no signs and symptoms in the patient.

DETERMINING THE HEART RATE

QT interval • R -R Interbeat ( Interval ) Technique
Time 0 04 See 0.2 Sec —> HR = 300 -r ( number of large squares)

.
Figure 15 ECG intervals —* Has to use ECG paper
— Applies the mnemonics: "300, 150, 100, 75, 60,
50"
Table 5. ECG intervals
300 is for 1 (large square), 150 is for 2 ( large squares ), 100 is for 3,
ECGINTERVAL DESCRIPTION
75 is for 4, 60 is for 5, and 50 is for 6.
RR • Time between beats ( used to calculate
HR )
• 0.6 to 1 sec (HR: 60 - 100 bpm)
PR AV nodal delay
Measured from the onset of the P wave
to the onset of the QRS complex.
No more than 5 small squares in
duration (0.20secs).
Prolonged PR interval >0.20secs is 1st
1. Determine and locate the R wave in the ECG paper.
degree heart block
The 2 R’s are the Interval, just choose 1 given interval.
QRS Ventricular depolarization
In this case, we’ll choose the green R to blue R.
QT Total duration of ventricular 2. From the green R, count the # of large squares (arrow)
depolarization ( all myocytes). to the blue R. We have 6 large squares from this
Normal QT for rates 60-100 = 0.30 - 0.40 interval.
seconds 3. Calculate 300 divided by the # of large squares.
Thereby, 300/ 6 = 50. So, the HR is 50 bpm.
L .
INTERPRETATION AND APPROACH

A. ANATOMIC GROUPS Rule of 300

Table 6. Anatomic groups of ECG leads o Basically the same principle with the R -R Interval
ANATOMIC ECG LEADS technique
GROUP o Regular rhythms
Septum VI and V2 o HR = 300 T (number of large squares of the R-R
Anterior wall V 3 and V4 Interval)
Lateral wall V 5, V6, Lead I, and aVL
Inferior Lead II, Lead III and aVF Example:

e
T. J
Figure 16. Anatomic groups of ECG leads

B. SINUS RHYTHM
A beat is considered as sinus if:
i

j
L
^ »

300 + 6 = 50 bpm
>

^
A » yv yv
0 MV.C J

—» P wave originated from the SA node

—> Impulses have normal conduction normal
PQRST complex
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1
^
300
- 1.5 = 200 bpm
1

Rule of 1500
—> In this technique, the small squares are the one
to be counted.
.
Figure 17 Atrial fibrillation
—> In 1large square there are 5 small squares in its
Count how many QRS complex then multiply it by 10 (because
width.
there are six ten seconds in 1 minute)
—> This is applied when the R- R is not exactly
located to a fixed demarcation. 9 QRS complex x 10 = 90 bpm
—> HR = 1500 -f (number of small squares ) -
I

Rill
.::
_ Example 2.
m S hi - ttrr
I
.
lAJUt lMI < r» r»i

tt 11| 13 16 17110' 21 +
— Number af «m«M iqMrw'

/ { 300 • <
H «1 rat # rnmuto
«64»• 9 m i
A « A _
AAjU
^Orv-rYYVW IMM TJ I1 J 11
AAA
.•- A / W \l
'
ia/
f

A - >» A n I
VWW
taoo 11 >

‘ 1600 * 13 • 11«

/ 1600 » 16
- A ICO

1600 • 17 a m A
isoo • ie m n A 1 Choose the ECG recording that has a better visual of the R
wave You need to use the R wave to count. So from this
ISOO •
*
1.71 A given example, we will choose the bottom ECG.
Why 1500? The ECG is recorded on to standard paper travelling at a 2 Count the total 3 of R waves in the chosen ECG. In this case,
rate of 25mm/ sec (25 x 60 = 1500 ) it has 33 R waves.
3. 33 x 10 = 330. So, the heart rate is 330 bpm.
Example:
C. QRS AXIS
• Represents the net overall direction of the heart' s
electrical activity
• Abnormalities of axis can suggest:
—* Ventricular enlargement ( if mas makapal yung L
side ng heart, ibig sabihin yung mean electrical
activity is leaning to L side of the chest -> visible
in lateral leads V5, V6 )
1. Determine and locate the chosen R-R interval. In this —» Conduction blocks (e.g. hemiblocks or fascicular
case, 0 to 1 interval. blocks )
2. Count the total # of small squares from 0 to 1 R-R interval.

-
In this case, it has 22 small squares.
Table 8. Electrogram
I 3. 1500 22 = 68 18 rounded off to 68 bpm
Upward A wave of
deflection depolarization spreads
e 10 Second Rule toward the positive pole
—> Most EKGs record 10 seconds of rhythm per of that lead (NEG
page POS)
—* Count the number of beats present on the EKG Downward A wave spreads toward
and multiply by 6 to get the number of beats per deflection the negative pole ( POS
60 seconds. -> NEG)
—» This method works well for irregular rhythms Biphasic Mean orientation of the
( e.g. Atrial fibrillation) deflection depolarization vector is
Example 1. right angles to a
at
particular lead axis

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• Normal QRS axis: -30° to +90°

• Left Axis Deviation ( LAD) : -30° to -90° W-iM"
. -

e Right Axis Deviation ( RAD): +90° to +180°

• Indeterminate Axis: -90° to +180°

in

AXIS- Negative in I, positive in aVF —> RAD

Example 2.

Figure 18. QRS Axis

D. DETERMINING THE AIXS

1

i
~
~
— 1 — ~

^ ~
T~

A. QUADRANT APPROACH
Easier to remember
n -4 -V'" ~ivT A —

‘Vr ’f
T

r
— Rate: 75 bpm
Predominantly Predominantly Equiphasic | Rhythm- Regular
positive negative I Positive in I, negative in aVF —*• LAD -> Predominantly
| positive in Lead II -<• Normal Axis ( non-pathologic LAD)
l_
STEPS IN USING THE QUADRANT APPROACH
1. Examine the QRS complex in leads I and aVF B. DETERMINING THE NUMBER OF MALL SQUARES
2. Determine if they are predominantly positive or R wave minus S wave
predominantly negative
Steps In using this kind of approach
3. In the event that LAD is present , examine lead II to
1. Count the number of small squares Leads I and aVF
determine if this deviation is pathologic.
2. Plot
a. QRS positive - NON PATHOLOGIC (it is likely
that the axis is in the range of 0 ° to -30°)
b. QRS negative - PATHOLOGIC
Easier way to remember:
Hold up your left and right hands and make a thumbs up/ thumbs
down position in the direction of the QRS in Leads I and aVF. Left hand
is Lead I and your right hand is Lead aVF. Do the thumbs up sign if
the value is positive and thumbs down if it is negative. For example,
yung Lead I mo is positive and yung Lead aVF mo ay negative. Check
mo kung ano yung naka-thumbs up mong kamay, left hand, so ibig Figure 19. L — Lead I, R — Lead aVF. Count the number of small squares.
sabihin LAD.

Lead aVF

Positive Negative

LEAD I Normal LAD

Axis
Lead I
Indeterminate
Negative RAD
Axis

Example 1.

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. .
Figure 20 After counting the number of small squares, plot In this example, it is seen
that the axis is 45° The Normal Sinus P Wate
C.
Lead V,
EQUIPHASIC APPROACH
Lead II

STEPS IN USING THE EQUIPHASIC APPROACH

1. Determine which lead contains the most equiphasic
QRS complex. The fact that the QRS complex in this Upright Up ricfit Eiiphaac lrri» red
lead is equally positive and negative indicates that the
net electrical vector is perpendicular to the axis of this
particular lead . Right Atrial Enlaigement
2. Examine the QRS complex in whichever lead lies 90°
away from the lead identified in step 1 Leads II, III oraVF Lead V ,
a. QRS complex Is predominantly positive —> axis of

I
this lead is approximately the same as the net
QRS axis
b. QRS complex is predominantly negative -> net
•P - piJmonale" Upright or Hphasic or hverfed P Waves
QRS axis lies 180° from the axis of this lead

Example 1. Lead VI with large biphasic P wave with tall initial

—JL nr-nr
component.
U
ii

JUJL-JUL 4
III

—ri— ^
BHHMt STIlPi II

—
25 M/ MCI I

J JJ J—J i—J i —
Equiphasic in aVF -> predominantly positive in I -> QRS axis = 0° Figure 21. Lead VI is located in the 4th ICS right parasternal line so kung
titingnan niyo kung may RAE mas affected ang VI
Example 2.
OlUriJUlWT ( t»

n. Example

m
I^ cic.1 II

•VL

1 III aVP
A

The height (or amplitude) of P wave seen in Lead II is 3 mm

A , which is more than the normal value (<2.5 mm).
, J
load V ,
Equiphasic in II -> predominantly negative in aVL -> QRS axis ~
+150°

E HYPERTROPHY .
A. RIGHT ATRIAL ENLARGEMENT ( RAE )

• P wave amplitude
The amplitude of the P wave in Lead V1 is also 3 mm which
—> >2.5 mm in Lead II and/or
is more than the normal value (<1.5 mm) This indicates right
—> >1.5 mm in VI atrial enlargement
( these criteria are not very specific or sensitive) L.

• Height
• Clinical implications
—> Usually seen in patients with COPD

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—» Patients with ECG change have more severe

pulmonary dysfunction and reduced survival D. CHAMBER ABNORMALITIES

B. LEFT ATRIAL ENLARGEMENT

>
Right atrial ( RA ) overload - tall, peaked P waves
Left atrial (LA) abnormality broad, often notched P
• Duration or length or lower waves in the limb leads and a biphasic P wave in lead VI
• P wave duration with a prominent negative component representing
—* > 0.12s ( more than 3 small squares ) in frontal delayed depolarization of the LA
plane (usually lead II)
e Notched P wave in limb leads with the inter -peak duration
> 0.04s Normal Right Left

• Terminal P negativity ( mas negative yung latter part ng P

wave orpababa ) in Lead VI (e.g., "P-terminal force")
—
> duration >0.04s
RA
\
LA
—» depth >1mm

Left Atrial Enlargement

,
RA

Leads I , II oraVF Lead V, V

LA

>2 V, mm
Figure 24. Right atrial ( RA ) overload may cause tall, peaked P waves in the limb
or precordial leads. Left atrial (LA ) abnormality may cause broad, often notched
P waves in the limb leads and a biphasic P wave in Lead I

“P- mitrale " Terminally inverted Totally Inverted

E. VENTRICULAR HYPERTROPHY
Figure 22. Left atrial enlargement
Leads VI and V 6
Criteria for diagnosing right or left ventricular hypertrophy
Clinical implications:
are very insensitive (i.e., sensitivity ~50%, which means
o Associated with more severe LV dysfunction in
that ~50% of patients with ventricular hypertrophy cannot
patients with ischemic heart disease
be recognized by ECG criteria).
o More severe valve damage with mitral or aortic valve
However, the criteria are very specific (i.e., specificity
disease
>90%, which means if the criteria are met, it is very likely
( RAE tingin sa height ng P wave, LAE sa length ng P wave)
that ventricular hypertrophy is present).

C. BI - ATRIAL ENLARGEMENT (BAE)

QRS In hypertrophy Main QRS vector
• Features of both RAE and LAE in same ECG
V , V6
• P wave
—* Lead II >2.5 mm tall and >0.12s in duration
—> Initial positive component of P wave in VI >1.5
mm tall and prominent P-terminal force (> 0.04
Normal
s, depth > 1mm)

Bi-atrial Enlargement J

LVH
Leads II . Ill or aVP
LV strain pattern

Figure 23. Bi-atrial enlargement

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Figure 25. Left ventricular hypertrophy ( LVH) increases the amplitude of Wide QRS (0.10 sec or more): 3 or more small
electrical forces directed to the left and posteriorly. Repolarization squares
abnormalities may cause ST-segment depression and T-wave inversion in
leads with a prominent R wave.
• Right ventricular hypertrophy
R wave greater than S wave in Lead VI
R wave gets progressively smaller from V1-V6
Left ventricular hypertrophy Prominent S waves in V5 & V 6
—» Sokolov -Lyon criteria RAD, +110 degrees or greater
• S wave depth in VI + tallest R wave R in VI 7 mm or greater
height in V5/ V6 = > 35 mm R /S ratio in VI is 1 or greater
R in VI + S in V6 10 mm or greater
• Compute the number of small squares ofS wave in VI
P pulmonale (tall pointed P taller in III than I)
(downward deflection ) and the R wave of Lead V5/ V6
S > R in V6
(whichever is higher )
Incomplete RBBB
ST segment depression and T wave inversion in
Example 1. right precordial leads is usually seen in severe
Lead V , RVH such as in pulmonary stenosis and
> abnormality
isssi
Left atrial pulmonary hypertension

-
fill : ::
Bits
i!
: iM
:
—Ir .
Deep S in V or V . V,
QRS In hypertrophy
V,
Main ORS vector

i
Delayed onset of
mtrinscoid deflection
EEIS
— ^ > 0.05 second
Normal
HE
rrrn if y TallRmVsorVe
t
ill
:: : : :3
B
I N N

inii *+ -- Slight widening of the

^ QRS complex R wave greater than
'S 3 S wave in Lead V1
Left ventricular strain

Lead V 5 or V 6
-
"P mitrale"

S wave in Lead V1 + R wave in Lead V5A/ 6 = 38 mm. It is

n
RVH 4~
more than the normal range so this suggests LV .
Figure 26 Right ventricular hypertrophy ( RVH) may shift the QRS
hypertrophy . vector to the right; this effect usually is associated with an R, RS,
L .
.
or QR complex in lead VI T- wave inversions may be present in

—> Another criteria for LV hypertrophy: right precordial leads.

• ST segment deviation which is
suggestive of a strain pattern
• R wave in Lead aVL is >11 mm and (+)
LAD >30°

Lead aVL

R wave in aVL
mm
> 11

Left axis
deviation >- 30°

Cornell voltage criteria for LVH (sensitivity =

22%, specificity = 95%)
• S in V3 + R in aVL > 24 mm (men)
• S in V3 + R in aVL > 20 mm (women)
—» LAD, -30° (often) - not sensitive

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From Harrison’s:
Major ECG abnormalities
1. Cardiac enlargement and hypertrophy
• Right atrial overload (“P-pulmonale”)
O Lead to increase in p-wave amplitude (>2.5 mm)
• Left atrial overioad (“P-mitrale”)
o Produces a biphasic P wave in V1 with a broad negative component or a broad (>120 ms), often notched P wave in one or more
limb leads
o May also occur with LA conduction delays in the absence of actual atrial enlargement —> LA abnormality
• RV hypertrophy
o Due to a sustained, severe pressure load
o Tall R wave in Lead V1 (R>S wave)
o Usually with R axis deviation
o qR pattern in V1 or V3R
o ST depression and T-wave inversion in the right-to-midprecordial leads (RV strain pattern, due to repolarization abnormalities in
acutely or chronically overloaded muscle)
• Acute cor pulmonale d/t pulmonary embolism
o Sinus tachycardia
o QRS axis may shift to the right
• Chronic cor pulmonale d/t obstructive lung disease
o Small R waves in right-to-midprecordial leads (slow R-wave progression
• LV hypertrophy
o Presence of tall left precordial R waves and deep right precordial S waves
o ST depression with T-wave inversions
o Often progresses to incomplete or complete left bundle branch block
2. Others: BBB, Ml, Metabolic factors and drug effects etc

Practice 1

fvJ/U/OJ." m 4

v-Ai
4
' W. V'iAJL/

4i
1 1a

II

Rate: 1500 4- 13 small squares = 115 bpm (sinus

tachycardia )
Rhythm: Regular
Axis: right axis deviation
Atrial enlargement: Height ng P wave ang problem -> P
wave height >2.5 mm RA enlargement
Ventricular enlargement: No hypertrophy

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Practice 2.
17 -OCT- mO ( 2S y )
Ciu»c u« A
*

1 I aYR
f
i wj -V
IV4
—

P II
-tVIJ
..
/V J vs

1 ;i

II> ymiiavi .
oi.ocT ivw 2i:i?

Rate: 75 bpm
Rhythm: Regular
Deviation: RAD
>
Atrial enlargement: height ang prominent - RAE
Ventricular hypertrophy: prominent R wave in VI >7mm - >
RVH
Possible valve problem: pulmonic stenosis, pulmonic
regurgitation, pulmonic hypertension ( mitral stenosis may
not be possible because there is no LAE or combined atrial
enlargement )

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Combined ventricular hypertrophy

RlfM Bundle E ranch Block
• Tall biphasic complexes in mid-precordial leads - Katz-
Wachtel phenomenon ( mataas na R wave and
• Wi<
o
*
V:
QRS completes measuring 20 12 second
,
sobrang deep ng S wave ) • Large terminal R ’ waves with rR' or rsR’ configuration
• Onset ofintnnacoal defection (R peak toe) »0 05 sec
a
F. BUNDE BRANCH BLOCKS
Intrinsic impairment of conduction in either the right or
• •,Wide
and leads oa
V side Wt
terminal S waves are presert
t ventrtcafer septan (laadaVLg

the left bundle system ( intraventricular conduction

• Septal q waves are preserved

disturbances) leads to prolongation of the QRS interval

* «m») *> V,( >o 05 sac)
,
Onsatof natnaond dttecton (Bpo is iMayrd
a Complete bundle branch blocks: the widest QRS interval
is >120 ms in duration ( >3 small squares ) fL ^
Tavnral

a Incomplete blocks : QRS interval is between 100 (in

Harrison's, 110) and 120 ms.
. .
PR
• The QRS vector usually is oriented in the direction of the
myocardial region where depolarization is delayed.
< fl«t«c or ( Pp»» vnanncnna rV ( fl) 0St«c)
O»»«« otr wyrol
* .
Right Bundle
Branch Block
Table 9. Bundle branch blocks
BUNDLE DESCRIPTION LEADS PATTERN
BRANCH
BLOCKS l.cft Bundle Branch Block
Right Bundle Wide QRS VI and V6 (I rSR in VI • Wide QRS complexes measuring 20.12 second
Branch Block complexes >0.12 and aVL) o V|t
seconds • QS or rS complexes
o Y „ and leads on left side of sentricular septum (I and aVL ):
• Septal q waves are absent
Delayed S wave • Monophcsic R. RR \ slurred R or M- shapcd R
• Onset of intrinsicoid deflection or R peak time is prolonged
Left Bundle Wide QRS VI, V 6 (I and RR' in V6 (>0.05 sec )
Branch Block complexes aVL)
-» Oraet o# mntcnd c *n*cson
3 i R PMI inw) noimai in V ,
measuring >0.12
second
rS OS OS

Normal

Lett Bundle
Branch Block

ISCHEMIA AND INFARCTION

A. ST Segment
e Isoelectric
e Normally deviate between -0.5 and +1 mm from the
baseline
e How to count ? Determine the J point.

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Rate: Normal
Rhythm: Regular
1*11 segment used os
basolino for ST soyrnont 80 msoc Deviation: Normal axis
Atrial enlargement: none
Ventricular enlargement: none
Bundle branch block- none
Ischemia: V2,V 3, V4- anteroseptal wall ischemia

J point
VI. COMMON ARRHYTHMIAS
In this example, there Is slightly more than t . 5 mm of horizontal • Arrhythmias are caused by
ST segment depression 80 msec from the J point .
—» Disturbances in automaticity
—» Disturbances in conduction
—» Combinations of altered automaticity and
conduction

Q Firing TACHYARRHYTHMIAS Firing

Automaticity
of SA Node
Abnormal Re-entry

/
Automaticity Physiologic
and Altered Altered
Triggered Imp ube *"*Imp ube
Activity / Pathologic
Formation Conduction

Downsloping ST Upsloping ST Horizontal ST Conduction

The J point occurs at Ihe end of the QRS comples . Automaticity
Blocks
The ST segment begins al the ] point and extends lo a user defined interval
ofSANode
ST Segment Depression |Firing BRADYARRHYTHMIAS Firing
The most specific or consistent in patients with ischemia are A. BRADYARHYTMIAS
downsloping and horizontal ST depressions. If downsloping or Table 10. Bradyarrhythmias
horizontal ST are considered ischemic changes . Pwede pang ABNORMALITY MECHANISM EXAMPLES
maconsider na normal ang upsloping Altered impulse Phase 4 Sinus Bradycardia
formation -> depolarization ( e.g.
What do you call the ST depression in Leads VI and V2 ? Septal wall DECREASED cholinergic
ischemia automaticity stimulation)
What do you call the ST depression in Leads VI -4 ? Anteroseptal wall
ischemia Altered impulse Ischemic, 1st, 2nd, 3rd degree
What do you call the ST depression in Leads Leads II, III and aVF? conduction - > anatomic, or drug- AV Blocks
Inferior wall ischemia Conduction blocks induced impaired
What do you call the ST depression in Leads V1-V6? Massive conduction
ischemia

From Harrison's:
Example
Bradyarrhythmia results from failure of either impulse initiation or
impulse conduction
• Failure of impulse initiation: caused by depressed
automaticity resulting from a slowing OR failure of phase 4
diastolic depolarization (due to a disease or exposure to
drug)
• Failure of conduction of an impulse from nodal to atrial or
ventricular myocardium -» exit blocks

SA node dysfunction and AV conduction block are the most

common causes of pathologic bradycardia

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B. TACHYARRHYTMIAS From Harrison's:

MECHANISMS OF TACHYARRHYTMIAS
Sinus tachycardia can either be physiologic or
• Altered Impulse Formation
nonphysiologic.
—> Enhanced automaticity o Physiologic: appropriate response to exercise, stress
Sinus node or illness
Ectopic focus o Nonphysiologic
—» Triggered activity Inappropriate: sinus rate increases spontaneously
Early after depolarization at rest or out of proportion to physiologic stress or
exertion and associated with autonomic
Delayed after depolarization
dysregulation; affects women (30-40 years old);
Altered impulse conduction: reentry fatigue, dizziness, syncope, palpitations
Increased phase 4 depolarization: sympathetic Postural orthostatic tachycardia syndrome
stimulation (POTS): symptomatic sinus tachycardia that occurs
Acquired phase 4 depolarization with postural change, sinus rate increases by 30
beats/ min or to >120 beats/min within 10 min of
Prolonged action potential: tissue damage or drug-
standing and in the absence of hypotension
induced
Intracellular calcium overload: digitalis toxicity D. SINUS BRADYCARDIA
Unidirectional block + slowed retrograde conduction • Normal looking QRS
Sinus tachycardia • Rate <60 bpm

Ectopic atrial tachycardia • Regular rhythm

Torsade de pointes • P waves upright in I, II, AVF
PAC,PVC, digitalis - induced SVT
Paroxysmal SVT, atrial flutter/fibrillation, Ventricular
tachycardia/fibrillation

C. SINUS TACHYCARDIA
JLA
. fj

• Normal looking QRS

Figure 28. Sinus bradycardia
• Atrial rate >100 bpm
• Regular rhythm E. SUPRAVENTICULAR TACHYCARDIA
• P waves upright in I, II, AVF
T
• Atrial Fibrillation
!
::
• Atrial Flutter

I • Paroxysmal Supraventricular Tachycardia ( PSVT)

rr —* Non paroxysmal atrial tachycardia
: —> Multifocal atrial tachycardia ( MAT)
m 1
. -
— — Junctional tachycardia
Figure 27. Sinus tachycardia
Table 11. Supraventricular arrhythmias
IRREGULAR RHYTHM REGULAR RHYTHM
• Atrial fibrillation Sinus Tachycardia
• Atrial flutter with varying AV conduction Atrial tachycardia
• Wandering atrial pacemaker Junctional/atrioventricular rhythm
• Multifocal atrial tachycardia Atrial flutter with fixed AV conduction
AV nodal reentrant tachycardia
AV reentrant tachycardia

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F. SUPRAVENTRICULAR ARRHYTHMIAS
SUPRAVENTRICULAR DESCRIPTION ECG
ARRHYTHMIAS
ATRIAL FIBRILLATION Results from multiple
areas of re-entry with in
the atria from multiple
ectopic foci
Atrial rate = 400 - 700/min
( ECG: fibrillatory waves ) NO DEFINITE P WAVES

©1P—F© T"—
Irregularly irregular R-R
interval
No organized atrial
r ir "

Heart Rhythm P Wave PR interval QRS

activity; no P waves Rate ( in seconds) ( in seconds )
A: 350-650 Irregular Fibrillatory N/ A <12
Management: bpm ( fine to course)
UNSTABLE: Cardiovert V: Slow
to rapid
• STABLE: Digoxin,
Verapamil, Diltiazem,
Rapid ventricular response: HR >100 bpm
Beta-blockers
Normal: HR 60-100 bpm
Slow ventricular response: HR <60 bpm Slow ventricular response: HR <60bpm
If the patient has a rapid ventricular response and symptomatic si patient, then
you have to give an IV medication

ATRIAL FLUTTER • Atrial rate 220-350/min

Ventricular rhythm may be
regular
P waves: flutter waves
resemble SAWTOOTH or
PICKET FENCE

Management:
UNSTABLE: Cardiovert Heart Rhythm P Wave PR interval QRS
Rate ( in seconds! ( in seconds )
• STABLE: Digoxin,
A: 220-430 Regular Sawtoothed N/ A <12
Verapamil, Diltiazem, bpm or variable appearance
Beta-blockers V: <300 bpm

LU>1
PAROXYSMAL Circus movement or
SUPRAVENTRICULAR reciprocating tachycardias
TACHYCARDIA Utilize the mechanism of

( less than 3 small

reentry
Sudden onset or cessation
A
squares ) Stops abruptly
Regular narrow QRS
complex tachycardia
Delayed P
without discernible P
waves In sinus tachycardia, PQRST PQRST PQRST. Meanwhile in PSVT, it' s like QRST
Regular R — R interval QRSTQRST.
Exceptions:
o Pre-existing
conduction
o Aberrant ventricular
conduction
o Pre-excitation

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G. VENTRICULAR TACHYCARDIA

Wide complex tachycardia ( more than 3 small squares ) Criteria for Ventricular Tachycardia :
At least 3 consecutive PVC's —» Rhythm: regular to slightly irregular
Rapid, bizarre, wide QRS complexes (> 0.10 sec) Rate: >100 bpm (130-170)
No P wave (ventricular impulse origin) —> Atrial conduction: P waves absent
Treatment ; amiodarone, lidocaine AV conduction: PR interval not measured
—> If unstable: electrical cardioversion or Ventricular conduction: wide QRS complex
defibrillation
Rale > 140 . min I

t
III
; i I

VENTRICULAR TACHYCARDIA DESCRIPTION ECG

Premature Ventricular Contraction Prematurely occurring complex
• Wide, bizarre looking QRS
aka Premature Ventricular complex ( parang abnormal
Depolarization beat )
Usually no preceding P wave
T wave opposite in deflection to
the QRS complex
• Complete compensatory pause
following every premature beat
Premature Ventricular Contraction Two premature ventricular
in Couplets contractions occurring
consecutively

Premature Ventricular Contraction Alternating normal sinus beat and

in Bigeminy a PVC

Normal - PVC - Normal - PVC

Premature Ventricular Contraction PVC's regularly occurring every
in Trigeminy third beat ( regularly irregular
pattern )

Normal - Normal - PVC - Normal —

Normal - PVC
Multifocal Premature Ventricular PVC's coming from different foci
Contraction in the ventricle
PVC's assuming different
polarities in a single lead
PVC's of different morphology
and coupling interval

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Premature Ventricular Contraction R or Q of the PVC occurring at lllllllllllllllllll

1111111111111111111
miiiiiiiipiiiiiiiiiii
. > : ' lllPllll
i iiiiiHiiiiiiiiiiii linn
mmi
rggk
R on T Phenomenon the T wave of the preceding lllllllllllllllllll linn ii iiiiiiiiiimimii
iiiip’miiiiiimi pi i
sinus beat
Most dangerous PVC in II
iiiiiiiniiiii
iiiiini
iiiimi ill
i Jimiimi miiiiiiiiiiiiniiii min
iiiimi
iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiin IIIIIIIIIHIIIIIIIIIIIIIIII

Idioventricular Rhythm ( IV) Impulse ventricular in origin < mill I

.
Rate < 401 min
I
Absence of ( N), upright P wave I
i
t
i
i i

associated with QRS complexes 4

QRS > 0.10 sec •
' ' ’
Tf *
• • •I
T wave opposite in direction to *
lv/
1 « I
• 4 i
QRS
Rate < 40 / min V
Wide UHS |)?.b smill boxes). No H waves.
Accelerated Idioventricular Impulse ventricular in origin |

Rhythm Absence of ( N), upright P wave *

associated with QRS complexes ••
**
R2le = 40 120 min
*

QRS > 0.10 sec

T wave opposite in direction to
QRS
Rate = 40-120 / min
I
Wldf OHS \ )U small boxes) , No P waves,
,
Pre- excitation Wolff Parkinson Rhythm is sinus except during
White pre-excited tachycardia
Short PR interval t —i-- r ' !
QRS distorted by delta wave
Can be seen in patients with
r 4->
-
congenital problems -
+ - •
-
Torsades de Pointes A form of polymorphic VT
Widened QRS, large amplitude

iw
May be due to low magnesium
level
Electrical tracing appears to be
twisted into a helix ( may
twisting, parang DNA)
Degenerates relatively often I *
into ventricular fibrillation
Treatment : magnesium sulfate,
+ j

overdrive pacing

H. SUPRAVENTICULAR TACHYCARDIA

Associated with coarse or fine chaotic undulations of the No organized ventricular depolarization
ECG baseline No EFFECTIVE cardiac output
No P wave May be coarse or fine
No true QRS complexes Management: only DEFIBRILLATION provides definitive
Indeterminate rate therapy
• Single most important rhythm for an ACLS provider to
recognize

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I. VENTRICULAR ASYSTOLE
Total absence of ventricular electrical activity
Sometimes p waves or ventricular escape beats ( agonal
beats) may occur
Flat line protocol:
Check 2 leads on the monitor perpendicular to each other
to make sure patient is in asystole
Check all connections of patient to monitor
—* Adjust gain/sensitivity
What is the difference between V fib and A fib? In Vfib, there is no —> Always remember to treat the patient, not the
definite P and QRS complex unlike in Afib which has no definite P monitor !
wove but has an irregularly irregular QRS complex. Treatment:
Epinephrine
What is the difference coarse fib and vtach ? In v tach, there is a Atropine
definite R - R interval. Search for reversible cause
CPR
"i

Coarse ventricular fibrillation: waves that are 3 or more mm high,

high probability of successful defibrillation, usually caused by R-on-T
phenomenon
Fine ventricular fibrillation: with low amplitude waves (less than 3
mm); heart muscle depletes its metabolic stores
Fine ventricular fibrillation is more dangerous than coarse ventricular
fibrillation, because there is even less contractility of the myocardium,
which results in a smaller amplitude Usually when a person
experiences ventricular fibrillation, it first starts off as coarse
ventricular fibrillation. If untreated, it then may progress to fine
ventricular fibrillation, which can then progress to asystole.

L.

J. BRADYCARDIAS: ATRIOVENTRICULAR BLOCKS

A. JUNCTIONAL COMPLEXES
Conducting tissue near AV node has taken over the pacemaker of the heart
Rate: 40-60 bpm
Usually with retrograde P waves (or no P wave)

Figure 29. Junctional complexes

B. ATRIOVENTRICULAR BLOCKS

AV BLOCK DESCRIPTION ECG

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• PR interval prolonged P-R interval: 7 small squares X 0.04 = 0.28

>0.20 sec ( more than 5 Parang LDR, kahit malayo sila may connection pa rin
small squares )
Second degree
Progressive Lengthening of P-R interval
Type I (Mobitz

XL
Type 1- Progressive prolongation of

—
Wenckebach ) PR interval until an impulse
is blocked
—\ --
’v '
200 ms \
240 ms
\
280 ms \
320 ms
\
No Conduction

Atrrium - P wave, ventricle - QRS complex

Una close kayo tapos habang tumatagal di na nagtetext then biglang nawala
Second degree No lengthening of PR
PR interval = 0.20 second throughout

I*1
Type II interval before a dropped
beat
AJ * II * II II II * IIr
\

Close kayo tapos close pa rin then biglang nawala (' ghosting' as per khadi haha). To compare
it with Type 1, ito kasi walang pasabi iniwan ka lang bigla.
Third degree Complete absence of
Slower R - R , narrow complex
conduction between
atria and ventricles
Atrial rate is always
equal to or more than
ventricular rate
JU 1
*JL/\
QRS may be narrow or Constant P- P intervals
wide depending on level
of block Level of AV node
r

1
QRS complexes are narrowed

Red circles - T wave (note the height of the first T wave, parang nagpeak so ibig sabihin may
ibang wave form doon )
Green circles - P wave

Ventricular level
-

/
f
K
/
3S -
'

.
/ PS——
{
K- f

—
L

QRS complexes are widened ( red arrows - P wave)

Sa relationship para itong divorce. May sariling mundo yung P wave, may sariling mundo yung
QRS complex.
Among the AV blocks, who needs the pacemaker ? 3 rd degree AV block because there is no regular PR conduction and widening of QRS complex
Which is more ideal to have a pacemaker ? Second degree type I or type II ? To remember the answer here, isipin mo raw kung ano mas masakit? Yung type II kasi yun
yung iniwan pagkatapos maging close kayo .

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—» Specialized conduction tissue

OUTLINE — Heart muscle
I. REVIEW OF THE CONDUCTION SYSTEM
II. ECG LEADS . .
lnfeinoil )l
Tr icts >
Bundle
of His

III. ECG WAVEFORMS AND INTERVALS

Anteiioi
IV. INTERPRETATION AND APPROACH SA Node Fascicle
V. ISCHEMIA AND INFARCTION
VI. COMMON ARRHYTHMIAS
Puikiiije
Filieis

AV Node

Right Bundle Left Posteiioi

Branch Fascicle
i. REVIEW OF THE CONDUCTION SYSTEM .
Figure 1 Conduction system of the heart

A. ELECTROCARDIOGRAM (ECG ) >

SA node -> R and L atrial contraction -> AV node - Bundle of His - right >
and left bundle branch -> Purkinje fibers -> right and left ventricular
• Representation of the electrical events of the cardiac cycle
contraction
• A graphic recording of the electrical potentials produced
A. SA NODE
by the cardiac tissue. It is measured in millivolts ( mV).
— Records the complex spatial and temporal
*
• Collection of pacemaker cells where depolarization
stimulus for the normal heartbeat originates
summation of electrical potentials from multiple
Exhibits automaticity
myocardial fibers conducted to the surface of
the body • Main pacemaker of the heart
• Usually fires at 60-100bpm (AV node fires at 40-60bpm )
• Useful screening tool for a variety of cardiac abnormalities
—> If the patient has a problem with the SA node, the
• Most commonly performed cardiac test
AV node takes over, leads to lower bpm- needs a
• It does not record directly the electrical activity of the
pacemaker
source itself; it records only the depolarization
( stimulation ) and repolarization (recovery ) potentials
B . PACEMAKER ACTION POTENTIAL
generated by the atrial and ventricular myocardium.
Action potential results from highly coordinated,
• Since the cardiac depolarization and repolarization waves
sequential changes in ion conductance through gated
have direction and magnitude, they can be represented by
sarcolemma membrane channels
vectors
Pacemaker potential: change of mV of the pacemaker cells
• Vector analysis- central concept of electrocardiography
from approximately - 60mV to - 40mV ( aka slow
• Types of pathology Identified in ECG
depolarization, which is caused by influx of some Na+ ions)
—> Arrhythmias
—* Myocardial ischemia and infarction
—> Pericarditis •It

—» Chamber hypertrophy
—> Electrolyte disturbances (i.e. hyperkalemia, -It

i!:
i
hypokalemia )
—> Drug toxicity (i.e. digoxin and drugs which
prolong the QT interval)
!~
• The electric currents that spread through the heart are
produced by three components
-
—>
f
Cardiac pacemaker cells
—> Specialized conduction tissue
—> Heart muscle cells
Tkiw (me)

.
Figure 2 Action potential of pacemaker cells
B. NORMAL CONDUCTION SYSTEM
• Depolarization (initiating event for cardiac contraction)
• SA depolarizes spontaneously
and repolarization are a result of movements of ions across
the plasma membrane of cardiomyocytes and the • At - 40 mV ( threshold potential ), Ca 2+ ions enter the cells - >
rapid depolarization phase
pacemaker cells
• The electrical currents that spread through the heart ae • Between 0 and +10 mV, the peak is reached, then
repolarization starts via K* efflux, until -60 mV is reached.
produced by three components
Then, a new cycle begins.
—> Cardiac pacemaker cells

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• Pacemaker cells has NO true resting membrane potential. —* One point on the body and a virtual reference
point with zero electrical potential, located in
.
C PHASES OF CARDIAC ELECTRICAL ACTIVATION the center of the heart (unipolar leads )
• Impulse stimulates pacemaker and specialized conduction Standard ECG has 12 leads:
tissues in the AV nodal and HI- bundle areas —» 3 Standard Limb Leads
• These two regions constitute the AV junction —* 3 Augmented Limb Leads
• AV node
—*
6 Precordial Leads
—* Conducts action potential more slowly The 12 conventional ECG leads are divided into two
—> Ensures ventricles receive signal to contract
after atria have contracted groups:

• The bundle of His bifurcates into two main branches, the

right and left bundles, which rapidly transmit
6 limb ( extremity ) leads : record potentials
transmitted onto the frontal plane
depolarization wavefronts to the right and left ventricular — 6 chest (precordial ) leads: record potentials
myocardium by way of Purkinje fibers transmitted onto the horizontal plane
• Depolarization wavefronts then spread through the Axis: viewpoint from which it looks at the heart
ventricular all, from endocardium, triggering ventricular
Upright deflection: wave of depolarization spreads toward
contraction
the positive pole
e Negative deflection: wave spreads toward the negative
> pole
E
0
I Biphasic deflection: mean orientation of the
i depolarization vector is at right angles to a particular lead
5 —25
1 axis ( equally positive and negative)
e - so
<12 A. ELECTRIDE PLACEMENT
I A. LIMB ELECTRODES
§ -75
• Right Arm ( RA ) - Red
-100 a Left Arm (LA) - Yellow
tt t t t t t m IH t
• Right Leg ( RL) - Black
Na* Ca2* K* Na* K* e Left Leg ( LL) - Green
influx influx efflux efflux Influx

.
Figure 3 Phases of the action potential of cardiomyocytes B. PRECORDIAL LEADS
Table 2. Precordial leads
Table 1. Phases of the action potential of cardiomyocytes
Precordial Leads Color Location
PHASE DESCRIPTION
VI Red 4th ICS RPSB
Phase 0 Rapid upstroke
V2 Yellow 4th ICS LPSB
Caused by the stimulus sent by the
V3 Green Midway between V2 & V4
pacemaker cells and Na+ influx
V4 Brown 5 th ICS LMCL
Phase 1 Notch
V5 Black LAAL lateral and horizontal to
Initial rapid repolarization phase
V4, 5th ICS
K* and Cl conductance
'

V6 Violet LMAL lateral and horizontal to

Phase 2 Plateau V4, 5th ICS
Results from a balance of inward Ca 2+ and To locate the 4 ICS (usually along the nipple line) palpate the jugular notch
th

outward K+ currents then downwards 3 centimeter where you will find the sternal notch. From
P Final rapid repolarization the angle of Louis, move your fingers to the right and you will feel a gap
hase 3 Restores resting potential between the ribs. This gap is the 2nd Intercostal space. From this position,

Caused by inactivation of the Ca 2+

current
.
run your fingers downward across the next rib, and the next one The space

and an increase in the outward K+ current

.
you are in is the 4th intercostal space

Phase 4 Slow, spontaneous diastolic depolarization

responsible for the property of automaticity Angle of
Louis

ECG LEADS
Leads are electrodes which measure the difference in
electrical potential between either: vi
—> Two different points on the body (bipolar leads)
Figure 4. Precordial Leads Location

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• Augmented Leads ( "a") ECG WAVEFORMS AND INTERVALS

—> Augmented means to increase in size - > ECG
A . ECG PAPER
machine amplifiesfby 50%) the signal to make it
more readable
"a” refers to augmented
"V" refers to voltage
"R" refers to right
"L" refers to left
"F” refers to foot
—* Three types:
aVR : looks down at the heart from the .
Figure 7 ECG Paper dimension
patients right shoulder
aVL: looks at the heart from the left Table 4. ECG Paper Dimension
shoulder Voltage Time
aVF: looks up at the heart from the left (height in mm) (in seconds)
leg 1small box 1mm 0.04 ( 40 ms)
• Difference in voltage between two extremities: 5 small boxes (1 5 mm 0.2 ( 200 ms)
—> Lead I: difference in voltage between L and R large square)
arm
—» Lead II: difference in voltage between L leg and Note: The y-axis in the ECG paper is represented as the "voltage" (1
R arm mV = 10 mm with standard calibration ) where the "amplitude" is
—» Lead III: difference in voltage between L leg and
reflected, while the x -axis is represented as the time in seconds. The
L arm ECG is recorded on to standard paper travelling at a rate of 25
mm/ sec .

B. WAVEFORMS AND INTERVALS

< -> K|•
R wave T wav U wav
complex
* *

Figure 5. Leads 1-3

PR Interval OX Interval

.
Figure 6 Precordial leads on the chest record potentials Figure 8. Waveforms of ECG and the corresponding process of heart
transmitted onto the horizontal plane. contraction
P wave
Table 3. Summary of Leads —> Represents atrial depolarization
Leads Type Limb Leads Precordial Leads —* Represents atrial contraction
Unipolar I, II, III —» Slow rounded wave
(standard limbs) —» Duration between 0.08 and O.llsecs ( 2 % small
Bipolar aVR , aVL , aVF VI to V6 squares)
(augmented limb —> Height less than 2.0 mm ( 2 small squares)
leads) • Higher - possible atrial enlargement
—* Upright in Lead I, II, avF and left precordial leads
(usual lead for a rhythm strip)
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—» Inverted in Avr
e T wave
—» For adults more than 30 years old: normally
inverted only in VI
—» Less than 30 yrs. old: normally inverted in VI to
V3
—> Represents ventricular relaxation
—* Rounded peak
Figure 9. P wave
—> Should be in the same direction as the main QRS
complex
— Abnormal if inverted seen in LVH, Bundle branch
• QRS complex
blocks & ischemia
—* Represents ventricular depolarization
—» Measured from the onset of the Q to the end of I
the S wave
—* Predominantly Upward in left sided leads
—» Negative in right sided leads
H
—» Between 0.08 and 0.12 secs in duration ( 3 small
squares)
Figure 13. T wave
• U wave
Prominent in V3
Not >1mm amplitude
Very prominent U waves : marker of T"
susceptibility to torsades de pointes
Figure 10. QRS Complex If prominent in all chest leads, possible
electrolyte abnormalities (hypokalemia )
• J point: junction between the end of the QRS complex Abnormal increase in U wave amplitude is most
and the beginning of the ST segment commonly due to:
Drugs ( e.g., dofetilide, amiodarone,
sotalol, quinidine)
• Hypokalemia
Normal U wave: small, rounded deflection (<1
mm) that follows the T wave and usually has the
same polarity as the T wave

Figure 11. J point (yellow arrow)

• ST- T-U complex

—* Combination of ST segment, T wave, and U wave
—» Ventricular repolarization

Figure 14. U wave

• ST segment
—» Isoelectric
• Four Major ECG Intervals
—> Normally deviate
—» RR Interval- from R wave to the next R wave
—* between -0.5 and +lmm from the baseline • Used to compute the rate and rhythm
—> Measured between the end of the QRS and the
—> PR Interval- from start of P wave to the QRS
beginning of the T wave complex
—> Should be no more than 1mm above or below
— t QRS Interval- end of PR interval to end of S
the baseline wave
—> QT Interval- end of PR interval to end of T wave
• Normal QT for rates 60-100 is 0.30-
0.40 seconds

Figure 12. ST segment

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Table 7. Sinus rhythms

6.1 mv I RR interva Normal Sinus 60-100 bpm
R Sinus Bradycardia < 60 bpm
Spmtnl TP.
sygffii Sinus Tachycardia > 100 bpm

1/ Note: Some can have a normal beats of 50 bpm, as long

I
^ .
PF inlei W
Q
S J Perl

?
A.
as there is no signs and symptoms in the patient.

DETERMINING THE HEART RATE

QT interval • R -R Interbeat ( Interval ) Technique
Time 0 04 See 0.2 Sec —> HR = 300 -r ( number of large squares)

.
Figure 15 ECG intervals —* Has to use ECG paper
— Applies the mnemonics: "300, 150, 100, 75, 60,
50"
Table 5. ECG intervals
300 is for 1 (large square), 150 is for 2 ( large squares ), 100 is for 3,
ECGINTERVAL DESCRIPTION
75 is for 4, 60 is for 5, and 50 is for 6.
RR • Time between beats ( used to calculate
HR )
• 0.6 to 1 sec (HR: 60 - 100 bpm)
PR AV nodal delay
Measured from the onset of the P wave
to the onset of the QRS complex.
No more than 5 small squares in
duration (0.20secs).
Prolonged PR interval >0.20secs is 1st
1. Determine and locate the R wave in the ECG paper.
degree heart block
The 2 R’s are the Interval, just choose 1 given interval.
QRS Ventricular depolarization
In this case, we’ll choose the green R to blue R.
QT Total duration of ventricular 2. From the green R, count the # of large squares (arrow)
depolarization ( all myocytes). to the blue R. We have 6 large squares from this
Normal QT for rates 60-100 = 0.30 - 0.40 interval.
seconds 3. Calculate 300 divided by the # of large squares.
Thereby, 300/ 6 = 50. So, the HR is 50 bpm.
L .
INTERPRETATION AND APPROACH

A. ANATOMIC GROUPS Rule of 300

Table 6. Anatomic groups of ECG leads o Basically the same principle with the R -R Interval
ANATOMIC ECG LEADS technique
GROUP o Regular rhythms
Septum VI and V2 o HR = 300 T (number of large squares of the R-R
Anterior wall V 3 and V4 Interval)
Lateral wall V 5, V6, Lead I, and aVL
Inferior Lead II, Lead III and aVF Example:

e
T. J
Figure 16. Anatomic groups of ECG leads

B. SINUS RHYTHM
A beat is considered as sinus if:
i

j
L
^ »

300 + 6 = 50 bpm
>

^
A » yv yv
0 MV.C J

—» P wave originated from the SA node

—> Impulses have normal conduction normal
PQRST complex
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1
^
300
- 1.5 = 200 bpm
1

Rule of 1500
—> In this technique, the small squares are the one
to be counted.
.
Figure 17 Atrial fibrillation
—> In 1large square there are 5 small squares in its
Count how many QRS complex then multiply it by 10 (because
width.
there are six ten seconds in 1 minute)
—> This is applied when the R- R is not exactly
located to a fixed demarcation. 9 QRS complex x 10 = 90 bpm
—> HR = 1500 -f (number of small squares ) -
I

Rill
.::
_ Example 2.
m S hi - ttrr
I
.
lAJUt lMI < r» r»i

tt 11| 13 16 17110' 21 +
— Number af «m«M iqMrw'

/ { 300 • <
H «1 rat # rnmuto
«64»• 9 m i
A « A _
AAjU
^Orv-rYYVW IMM TJ I1 J 11
AAA
.•- A / W \l
'
ia/
f

A - >» A n I
VWW
taoo 11 >

‘ 1600 * 13 • 11«

/ 1600 » 16
- A ICO

1600 • 17 a m A
isoo • ie m n A 1 Choose the ECG recording that has a better visual of the R
wave You need to use the R wave to count. So from this
ISOO •
*
1.71 A given example, we will choose the bottom ECG.
Why 1500? The ECG is recorded on to standard paper travelling at a 2 Count the total 3 of R waves in the chosen ECG. In this case,
rate of 25mm/ sec (25 x 60 = 1500 ) it has 33 R waves.
3. 33 x 10 = 330. So, the heart rate is 330 bpm.
Example:
C. QRS AXIS
• Represents the net overall direction of the heart' s
electrical activity
• Abnormalities of axis can suggest:
—* Ventricular enlargement ( if mas makapal yung L
side ng heart, ibig sabihin yung mean electrical
activity is leaning to L side of the chest -> visible
in lateral leads V5, V6 )
1. Determine and locate the chosen R-R interval. In this —» Conduction blocks (e.g. hemiblocks or fascicular
case, 0 to 1 interval. blocks )
2. Count the total # of small squares from 0 to 1 R-R interval.

-
In this case, it has 22 small squares.
Table 8. Electrogram
I 3. 1500 22 = 68 18 rounded off to 68 bpm
Upward A wave of
deflection depolarization spreads
e 10 Second Rule toward the positive pole
—> Most EKGs record 10 seconds of rhythm per of that lead (NEG
page POS)
—* Count the number of beats present on the EKG Downward A wave spreads toward
and multiply by 6 to get the number of beats per deflection the negative pole ( POS
60 seconds. -> NEG)
—» This method works well for irregular rhythms Biphasic Mean orientation of the
( e.g. Atrial fibrillation) deflection depolarization vector is
Example 1. right angles to a
at
particular lead axis

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• Normal QRS axis: -30° to +90°

• Left Axis Deviation ( LAD) : -30° to -90° W-iM"
. -

e Right Axis Deviation ( RAD): +90° to +180°

• Indeterminate Axis: -90° to +180°

in

AXIS- Negative in I, positive in aVF —> RAD

Example 2.

Figure 18. QRS Axis

D. DETERMINING THE AIXS

1

i
~
~
— 1 — ~

^ ~
T~

A. QUADRANT APPROACH
Easier to remember
n -4 -V'" ~ivT A —

‘Vr ’f
T

r
— Rate: 75 bpm
Predominantly Predominantly Equiphasic | Rhythm- Regular
positive negative I Positive in I, negative in aVF —*• LAD -> Predominantly
| positive in Lead II -<• Normal Axis ( non-pathologic LAD)
l_
STEPS IN USING THE QUADRANT APPROACH
1. Examine the QRS complex in leads I and aVF B. DETERMINING THE NUMBER OF MALL SQUARES
2. Determine if they are predominantly positive or R wave minus S wave
predominantly negative
Steps In using this kind of approach
3. In the event that LAD is present , examine lead II to
1. Count the number of small squares Leads I and aVF
determine if this deviation is pathologic.
2. Plot
a. QRS positive - NON PATHOLOGIC (it is likely
that the axis is in the range of 0 ° to -30°)
b. QRS negative - PATHOLOGIC
Easier way to remember:
Hold up your left and right hands and make a thumbs up/ thumbs
down position in the direction of the QRS in Leads I and aVF. Left hand
is Lead I and your right hand is Lead aVF. Do the thumbs up sign if
the value is positive and thumbs down if it is negative. For example,
yung Lead I mo is positive and yung Lead aVF mo ay negative. Check
mo kung ano yung naka-thumbs up mong kamay, left hand, so ibig Figure 19. L — Lead I, R — Lead aVF. Count the number of small squares.
sabihin LAD.

Lead aVF

Positive Negative

LEAD I Normal LAD

Axis
Lead I
Indeterminate
Negative RAD
Axis

Example 1.

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. .
Figure 20 After counting the number of small squares, plot In this example, it is seen
that the axis is 45° The Normal Sinus P Wate
C.
Lead V,
EQUIPHASIC APPROACH
Lead II

STEPS IN USING THE EQUIPHASIC APPROACH

1. Determine which lead contains the most equiphasic
QRS complex. The fact that the QRS complex in this Upright Up ricfit Eiiphaac lrri» red
lead is equally positive and negative indicates that the
net electrical vector is perpendicular to the axis of this
particular lead . Right Atrial Enlaigement
2. Examine the QRS complex in whichever lead lies 90°
away from the lead identified in step 1 Leads II, III oraVF Lead V ,
a. QRS complex Is predominantly positive —> axis of

I
this lead is approximately the same as the net
QRS axis
b. QRS complex is predominantly negative -> net
•P - piJmonale" Upright or Hphasic or hverfed P Waves
QRS axis lies 180° from the axis of this lead

Example 1. Lead VI with large biphasic P wave with tall initial

—JL nr-nr
component.
U
ii

JUJL-JUL 4
III

—ri— ^
BHHMt STIlPi II

—
25 M/ MCI I

J JJ J—J i—J i —
Equiphasic in aVF -> predominantly positive in I -> QRS axis = 0° Figure 21. Lead VI is located in the 4th ICS right parasternal line so kung
titingnan niyo kung may RAE mas affected ang VI
Example 2.
OlUriJUlWT ( t»

n. Example

m
I^ cic.1 II

•VL

1 III aVP
A

The height (or amplitude) of P wave seen in Lead II is 3 mm

A , which is more than the normal value (<2.5 mm).
, J
load V ,
Equiphasic in II -> predominantly negative in aVL -> QRS axis ~
+150°

E HYPERTROPHY .
A. RIGHT ATRIAL ENLARGEMENT ( RAE )

• P wave amplitude
The amplitude of the P wave in Lead V1 is also 3 mm which
—> >2.5 mm in Lead II and/or
is more than the normal value (<1.5 mm) This indicates right
—> >1.5 mm in VI atrial enlargement
( these criteria are not very specific or sensitive) L.

• Height
• Clinical implications
—> Usually seen in patients with COPD

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—» Patients with ECG change have more severe

pulmonary dysfunction and reduced survival D. CHAMBER ABNORMALITIES

B. LEFT ATRIAL ENLARGEMENT

>
Right atrial ( RA ) overload - tall, peaked P waves
Left atrial (LA) abnormality broad, often notched P
• Duration or length or lower waves in the limb leads and a biphasic P wave in lead VI
• P wave duration with a prominent negative component representing
—* > 0.12s ( more than 3 small squares ) in frontal delayed depolarization of the LA
plane (usually lead II)
e Notched P wave in limb leads with the inter -peak duration
> 0.04s Normal Right Left

• Terminal P negativity ( mas negative yung latter part ng P

wave orpababa ) in Lead VI (e.g., "P-terminal force")
—
> duration >0.04s
RA
\
LA
—» depth >1mm

Left Atrial Enlargement

,
RA

Leads I , II oraVF Lead V, V

LA

>2 V, mm
Figure 24. Right atrial ( RA ) overload may cause tall, peaked P waves in the limb
or precordial leads. Left atrial (LA ) abnormality may cause broad, often notched
P waves in the limb leads and a biphasic P wave in Lead I

“P- mitrale " Terminally inverted Totally Inverted

E. VENTRICULAR HYPERTROPHY
Figure 22. Left atrial enlargement
Leads VI and V 6
Criteria for diagnosing right or left ventricular hypertrophy
Clinical implications:
are very insensitive (i.e., sensitivity ~50%, which means
o Associated with more severe LV dysfunction in
that ~50% of patients with ventricular hypertrophy cannot
patients with ischemic heart disease
be recognized by ECG criteria).
o More severe valve damage with mitral or aortic valve
However, the criteria are very specific (i.e., specificity
disease
>90%, which means if the criteria are met, it is very likely
( RAE tingin sa height ng P wave, LAE sa length ng P wave)
that ventricular hypertrophy is present).

C. BI - ATRIAL ENLARGEMENT (BAE)

QRS In hypertrophy Main QRS vector
• Features of both RAE and LAE in same ECG
V , V6
• P wave
—* Lead II >2.5 mm tall and >0.12s in duration
—> Initial positive component of P wave in VI >1.5
mm tall and prominent P-terminal force (> 0.04
Normal
s, depth > 1mm)

Bi-atrial Enlargement J

LVH
Leads II . Ill or aVP
LV strain pattern

Figure 23. Bi-atrial enlargement

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Figure 25. Left ventricular hypertrophy ( LVH) increases the amplitude of Wide QRS (0.10 sec or more): 3 or more small
electrical forces directed to the left and posteriorly. Repolarization squares
abnormalities may cause ST-segment depression and T-wave inversion in
leads with a prominent R wave.
• Right ventricular hypertrophy
R wave greater than S wave in Lead VI
R wave gets progressively smaller from V1-V6
Left ventricular hypertrophy Prominent S waves in V5 & V 6
—» Sokolov -Lyon criteria RAD, +110 degrees or greater
• S wave depth in VI + tallest R wave R in VI 7 mm or greater
height in V5/ V6 = > 35 mm R /S ratio in VI is 1 or greater
R in VI + S in V6 10 mm or greater
• Compute the number of small squares ofS wave in VI
P pulmonale (tall pointed P taller in III than I)
(downward deflection ) and the R wave of Lead V5/ V6
S > R in V6
(whichever is higher )
Incomplete RBBB
ST segment depression and T wave inversion in
Example 1. right precordial leads is usually seen in severe
Lead V , RVH such as in pulmonary stenosis and
> abnormality
isssi
Left atrial pulmonary hypertension

-
fill : ::
Bits
i!
: iM
:
—Ir .
Deep S in V or V . V,
QRS In hypertrophy
V,
Main ORS vector

i
Delayed onset of
mtrinscoid deflection
EEIS
— ^ > 0.05 second
Normal
HE
rrrn if y TallRmVsorVe
t
ill
:: : : :3
B
I N N

inii *+ -- Slight widening of the

^ QRS complex R wave greater than
'S 3 S wave in Lead V1
Left ventricular strain

Lead V 5 or V 6
-
"P mitrale"

S wave in Lead V1 + R wave in Lead V5A/ 6 = 38 mm. It is

n
RVH 4~
more than the normal range so this suggests LV .
Figure 26 Right ventricular hypertrophy ( RVH) may shift the QRS
hypertrophy . vector to the right; this effect usually is associated with an R, RS,
L .
.
or QR complex in lead VI T- wave inversions may be present in

—> Another criteria for LV hypertrophy: right precordial leads.

• ST segment deviation which is
suggestive of a strain pattern
• R wave in Lead aVL is >11 mm and (+)
LAD >30°

Lead aVL

R wave in aVL
mm
> 11

Left axis
deviation >- 30°

Cornell voltage criteria for LVH (sensitivity =

22%, specificity = 95%)
• S in V3 + R in aVL > 24 mm (men)
• S in V3 + R in aVL > 20 mm (women)
—» LAD, -30° (often) - not sensitive

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From Harrison’s:
Major ECG abnormalities
1. Cardiac enlargement and hypertrophy
• Right atrial overload (“P-pulmonale”)
O Lead to increase in p-wave amplitude (>2.5 mm)
• Left atrial overioad (“P-mitrale”)
o Produces a biphasic P wave in V1 with a broad negative component or a broad (>120 ms), often notched P wave in one or more
limb leads
o May also occur with LA conduction delays in the absence of actual atrial enlargement —> LA abnormality
• RV hypertrophy
o Due to a sustained, severe pressure load
o Tall R wave in Lead V1 (R>S wave)
o Usually with R axis deviation
o qR pattern in V1 or V3R
o ST depression and T-wave inversion in the right-to-midprecordial leads (RV strain pattern, due to repolarization abnormalities in
acutely or chronically overloaded muscle)
• Acute cor pulmonale d/t pulmonary embolism
o Sinus tachycardia
o QRS axis may shift to the right
• Chronic cor pulmonale d/t obstructive lung disease
o Small R waves in right-to-midprecordial leads (slow R-wave progression
• LV hypertrophy
o Presence of tall left precordial R waves and deep right precordial S waves
o ST depression with T-wave inversions
o Often progresses to incomplete or complete left bundle branch block
2. Others: BBB, Ml, Metabolic factors and drug effects etc

Practice 1

fvJ/U/OJ." m 4

v-Ai
4
' W. V'iAJL/

4i
1 1a

II

Rate: 1500 4- 13 small squares = 115 bpm (sinus

tachycardia )
Rhythm: Regular
Axis: right axis deviation
Atrial enlargement: Height ng P wave ang problem -> P
wave height >2.5 mm RA enlargement
Ventricular enlargement: No hypertrophy

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Practice 2.
17 -OCT- mO ( 2S y )
Ciu»c u« A
*

1 I aYR
f
i wj -V
IV4
—

P II
-tVIJ
..
/V J vs

1 ;i

II> ymiiavi .
oi.ocT ivw 2i:i?

Rate: 75 bpm
Rhythm: Regular
Deviation: RAD
>
Atrial enlargement: height ang prominent - RAE
Ventricular hypertrophy: prominent R wave in VI >7mm - >
RVH
Possible valve problem: pulmonic stenosis, pulmonic
regurgitation, pulmonic hypertension ( mitral stenosis may
not be possible because there is no LAE or combined atrial
enlargement )

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Combined ventricular hypertrophy

RlfM Bundle E ranch Block
• Tall biphasic complexes in mid-precordial leads - Katz-
Wachtel phenomenon ( mataas na R wave and
• Wi<
o
*
V:
QRS completes measuring 20 12 second
,
sobrang deep ng S wave ) • Large terminal R ’ waves with rR' or rsR’ configuration
• Onset ofintnnacoal defection (R peak toe) »0 05 sec
a
F. BUNDE BRANCH BLOCKS
Intrinsic impairment of conduction in either the right or
• •,Wide
and leads oa
V side Wt
terminal S waves are presert
t ventrtcafer septan (laadaVLg

the left bundle system ( intraventricular conduction

• Septal q waves are preserved

disturbances) leads to prolongation of the QRS interval

* «m») *> V,( >o 05 sac)
,
Onsatof natnaond dttecton (Bpo is iMayrd
a Complete bundle branch blocks: the widest QRS interval
is >120 ms in duration ( >3 small squares ) fL ^
Tavnral

a Incomplete blocks : QRS interval is between 100 (in

Harrison's, 110) and 120 ms.
. .
PR
• The QRS vector usually is oriented in the direction of the
myocardial region where depolarization is delayed.
< fl«t«c or ( Pp»» vnanncnna rV ( fl) 0St«c)
O»»«« otr wyrol
* .
Right Bundle
Branch Block
Table 9. Bundle branch blocks
BUNDLE DESCRIPTION LEADS PATTERN
BRANCH
BLOCKS l.cft Bundle Branch Block
Right Bundle Wide QRS VI and V6 (I rSR in VI • Wide QRS complexes measuring 20.12 second
Branch Block complexes >0.12 and aVL) o V|t
seconds • QS or rS complexes
o Y „ and leads on left side of sentricular septum (I and aVL ):
• Septal q waves are absent
Delayed S wave • Monophcsic R. RR \ slurred R or M- shapcd R
• Onset of intrinsicoid deflection or R peak time is prolonged
Left Bundle Wide QRS VI, V 6 (I and RR' in V6 (>0.05 sec )
Branch Block complexes aVL)
-» Oraet o# mntcnd c *n*cson
3 i R PMI inw) noimai in V ,
measuring >0.12
second
rS OS OS

Normal

Lett Bundle
Branch Block

ISCHEMIA AND INFARCTION

A. ST Segment
e Isoelectric
e Normally deviate between -0.5 and +1 mm from the
baseline
e How to count ? Determine the J point.

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Rate: Normal
Rhythm: Regular
1*11 segment used os
basolino for ST soyrnont 80 msoc Deviation: Normal axis
Atrial enlargement: none
Ventricular enlargement: none
Bundle branch block- none
Ischemia: V2,V 3, V4- anteroseptal wall ischemia

J point
VI. COMMON ARRHYTHMIAS
In this example, there Is slightly more than t . 5 mm of horizontal • Arrhythmias are caused by
ST segment depression 80 msec from the J point .
—» Disturbances in automaticity
—» Disturbances in conduction
—» Combinations of altered automaticity and
conduction

Q Firing TACHYARRHYTHMIAS Firing

Automaticity
of SA Node
Abnormal Re-entry

/
Automaticity Physiologic
and Altered Altered
Triggered Imp ube *"*Imp ube
Activity / Pathologic
Formation Conduction

Downsloping ST Upsloping ST Horizontal ST Conduction

The J point occurs at Ihe end of the QRS comples . Automaticity
Blocks
The ST segment begins al the ] point and extends lo a user defined interval
ofSANode
ST Segment Depression |Firing BRADYARRHYTHMIAS Firing
The most specific or consistent in patients with ischemia are A. BRADYARHYTMIAS
downsloping and horizontal ST depressions. If downsloping or Table 10. Bradyarrhythmias
horizontal ST are considered ischemic changes . Pwede pang ABNORMALITY MECHANISM EXAMPLES
maconsider na normal ang upsloping Altered impulse Phase 4 Sinus Bradycardia
formation -> depolarization ( e.g.
What do you call the ST depression in Leads VI and V2 ? Septal wall DECREASED cholinergic
ischemia automaticity stimulation)
What do you call the ST depression in Leads VI -4 ? Anteroseptal wall
ischemia Altered impulse Ischemic, 1st, 2nd, 3rd degree
What do you call the ST depression in Leads Leads II, III and aVF? conduction - > anatomic, or drug- AV Blocks
Inferior wall ischemia Conduction blocks induced impaired
What do you call the ST depression in Leads V1-V6? Massive conduction
ischemia

From Harrison's:
Example
Bradyarrhythmia results from failure of either impulse initiation or
impulse conduction
• Failure of impulse initiation: caused by depressed
automaticity resulting from a slowing OR failure of phase 4
diastolic depolarization (due to a disease or exposure to
drug)
• Failure of conduction of an impulse from nodal to atrial or
ventricular myocardium -» exit blocks

SA node dysfunction and AV conduction block are the most

common causes of pathologic bradycardia

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B. TACHYARRHYTMIAS From Harrison's:

MECHANISMS OF TACHYARRHYTMIAS
Sinus tachycardia can either be physiologic or
• Altered Impulse Formation
nonphysiologic.
—> Enhanced automaticity o Physiologic: appropriate response to exercise, stress
Sinus node or illness
Ectopic focus o Nonphysiologic
—» Triggered activity Inappropriate: sinus rate increases spontaneously
Early after depolarization at rest or out of proportion to physiologic stress or
exertion and associated with autonomic
Delayed after depolarization
dysregulation; affects women (30-40 years old);
Altered impulse conduction: reentry fatigue, dizziness, syncope, palpitations
Increased phase 4 depolarization: sympathetic Postural orthostatic tachycardia syndrome
stimulation (POTS): symptomatic sinus tachycardia that occurs
Acquired phase 4 depolarization with postural change, sinus rate increases by 30
beats/ min or to >120 beats/min within 10 min of
Prolonged action potential: tissue damage or drug-
standing and in the absence of hypotension
induced
Intracellular calcium overload: digitalis toxicity D. SINUS BRADYCARDIA
Unidirectional block + slowed retrograde conduction • Normal looking QRS
Sinus tachycardia • Rate <60 bpm

Ectopic atrial tachycardia • Regular rhythm

Torsade de pointes • P waves upright in I, II, AVF
PAC,PVC, digitalis - induced SVT
Paroxysmal SVT, atrial flutter/fibrillation, Ventricular
tachycardia/fibrillation

C. SINUS TACHYCARDIA
JLA
. fj

• Normal looking QRS

Figure 28. Sinus bradycardia
• Atrial rate >100 bpm
• Regular rhythm E. SUPRAVENTICULAR TACHYCARDIA
• P waves upright in I, II, AVF
T
• Atrial Fibrillation
!
::
• Atrial Flutter

I • Paroxysmal Supraventricular Tachycardia ( PSVT)

rr —* Non paroxysmal atrial tachycardia
: —> Multifocal atrial tachycardia ( MAT)
m 1
. -
— — Junctional tachycardia
Figure 27. Sinus tachycardia
Table 11. Supraventricular arrhythmias
IRREGULAR RHYTHM REGULAR RHYTHM
• Atrial fibrillation Sinus Tachycardia
• Atrial flutter with varying AV conduction Atrial tachycardia
• Wandering atrial pacemaker Junctional/atrioventricular rhythm
• Multifocal atrial tachycardia Atrial flutter with fixed AV conduction
AV nodal reentrant tachycardia
AV reentrant tachycardia

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F. SUPRAVENTRICULAR ARRHYTHMIAS
SUPRAVENTRICULAR DESCRIPTION ECG
ARRHYTHMIAS
ATRIAL FIBRILLATION Results from multiple
areas of re-entry with in
the atria from multiple
ectopic foci
Atrial rate = 400 - 700/min
( ECG: fibrillatory waves ) NO DEFINITE P WAVES

©1P—F© T"—
Irregularly irregular R-R
interval
No organized atrial
r ir "

Heart Rhythm P Wave PR interval QRS

activity; no P waves Rate ( in seconds) ( in seconds )
A: 350-650 Irregular Fibrillatory N/ A <12
Management: bpm ( fine to course)
UNSTABLE: Cardiovert V: Slow
to rapid
• STABLE: Digoxin,
Verapamil, Diltiazem,
Rapid ventricular response: HR >100 bpm
Beta-blockers
Normal: HR 60-100 bpm
Slow ventricular response: HR <60 bpm Slow ventricular response: HR <60bpm
If the patient has a rapid ventricular response and symptomatic si patient, then
you have to give an IV medication

ATRIAL FLUTTER • Atrial rate 220-350/min

Ventricular rhythm may be
regular
P waves: flutter waves
resemble SAWTOOTH or
PICKET FENCE

Management:
UNSTABLE: Cardiovert Heart Rhythm P Wave PR interval QRS
Rate ( in seconds! ( in seconds )
• STABLE: Digoxin,
A: 220-430 Regular Sawtoothed N/ A <12
Verapamil, Diltiazem, bpm or variable appearance
Beta-blockers V: <300 bpm

LU>1
PAROXYSMAL Circus movement or
SUPRAVENTRICULAR reciprocating tachycardias
TACHYCARDIA Utilize the mechanism of

( less than 3 small

reentry
Sudden onset or cessation
A
squares ) Stops abruptly
Regular narrow QRS
complex tachycardia
Delayed P
without discernible P
waves In sinus tachycardia, PQRST PQRST PQRST. Meanwhile in PSVT, it' s like QRST
Regular R — R interval QRSTQRST.
Exceptions:
o Pre-existing
conduction
o Aberrant ventricular
conduction
o Pre-excitation

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G. VENTRICULAR TACHYCARDIA

Wide complex tachycardia ( more than 3 small squares ) Criteria for Ventricular Tachycardia :
At least 3 consecutive PVC's —» Rhythm: regular to slightly irregular
Rapid, bizarre, wide QRS complexes (> 0.10 sec) Rate: >100 bpm (130-170)
No P wave (ventricular impulse origin) —> Atrial conduction: P waves absent
Treatment ; amiodarone, lidocaine AV conduction: PR interval not measured
—> If unstable: electrical cardioversion or Ventricular conduction: wide QRS complex
defibrillation
Rale > 140 . min I

t
III
; i I

VENTRICULAR TACHYCARDIA DESCRIPTION ECG

Premature Ventricular Contraction Prematurely occurring complex
• Wide, bizarre looking QRS
aka Premature Ventricular complex ( parang abnormal
Depolarization beat )
Usually no preceding P wave
T wave opposite in deflection to
the QRS complex
• Complete compensatory pause
following every premature beat
Premature Ventricular Contraction Two premature ventricular
in Couplets contractions occurring
consecutively

Premature Ventricular Contraction Alternating normal sinus beat and

in Bigeminy a PVC

Normal - PVC - Normal - PVC

Premature Ventricular Contraction PVC's regularly occurring every
in Trigeminy third beat ( regularly irregular
pattern )

Normal - Normal - PVC - Normal —

Normal - PVC
Multifocal Premature Ventricular PVC's coming from different foci
Contraction in the ventricle
PVC's assuming different
polarities in a single lead
PVC's of different morphology
and coupling interval

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Premature Ventricular Contraction R or Q of the PVC occurring at lllllllllllllllllll

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. > : ' lllPllll
i iiiiiHiiiiiiiiiiii linn
mmi
rggk
R on T Phenomenon the T wave of the preceding lllllllllllllllllll linn ii iiiiiiiiiimimii
iiiip’miiiiiimi pi i
sinus beat
Most dangerous PVC in II
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i Jimiimi miiiiiiiiiiiiniiii min
iiiimi
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Idioventricular Rhythm ( IV) Impulse ventricular in origin < mill I

.
Rate < 401 min
I
Absence of ( N), upright P wave I
i
t
i
i i

associated with QRS complexes 4

QRS > 0.10 sec •
' ' ’
Tf *
• • •I
T wave opposite in direction to *
lv/
1 « I
• 4 i
QRS
Rate < 40 / min V
Wide UHS |)?.b smill boxes). No H waves.
Accelerated Idioventricular Impulse ventricular in origin |

Rhythm Absence of ( N), upright P wave *

associated with QRS complexes ••
**
R2le = 40 120 min
*

QRS > 0.10 sec

T wave opposite in direction to
QRS
Rate = 40-120 / min
I
Wldf OHS \ )U small boxes) , No P waves,
,
Pre- excitation Wolff Parkinson Rhythm is sinus except during
White pre-excited tachycardia
Short PR interval t —i-- r ' !
QRS distorted by delta wave
Can be seen in patients with
r 4->
-
congenital problems -
+ - •
-
Torsades de Pointes A form of polymorphic VT
Widened QRS, large amplitude

iw
May be due to low magnesium
level
Electrical tracing appears to be
twisted into a helix ( may
twisting, parang DNA)
Degenerates relatively often I *
into ventricular fibrillation
Treatment : magnesium sulfate,
+ j

overdrive pacing

H. SUPRAVENTICULAR TACHYCARDIA

Associated with coarse or fine chaotic undulations of the No organized ventricular depolarization
ECG baseline No EFFECTIVE cardiac output
No P wave May be coarse or fine
No true QRS complexes Management: only DEFIBRILLATION provides definitive
Indeterminate rate therapy
• Single most important rhythm for an ACLS provider to
recognize

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I. VENTRICULAR ASYSTOLE
Total absence of ventricular electrical activity
Sometimes p waves or ventricular escape beats ( agonal
beats) may occur
Flat line protocol:
Check 2 leads on the monitor perpendicular to each other
to make sure patient is in asystole
Check all connections of patient to monitor
—* Adjust gain/sensitivity
What is the difference between V fib and A fib? In Vfib, there is no —> Always remember to treat the patient, not the
definite P and QRS complex unlike in Afib which has no definite P monitor !
wove but has an irregularly irregular QRS complex. Treatment:
Epinephrine
What is the difference coarse fib and vtach ? In v tach, there is a Atropine
definite R - R interval. Search for reversible cause
dengue CPR
"i

Coarse ventricular fibrillation: waves that are 3 or more mm high,

high probability of successful defibrillation, usually caused by R-on-T
phenomenon
Fine ventricular fibrillation: with low amplitude waves (less than 3
mm); heart muscle depletes its metabolic stores
Fine ventricular fibrillation is more dangerous than coarse ventricular
fibrillation, because there is even less contractility of the myocardium,
which results in a smaller amplitude Usually when a person
experiences ventricular fibrillation, it first starts off as coarse
ventricular fibrillation. If untreated, it then may progress to fine
ventricular fibrillation, which can then progress to asystole.

L.

J. BRADYCARDIAS: ATRIOVENTRICULAR BLOCKS

A. JUNCTIONAL COMPLEXES
Conducting tissue near AV node has taken over the pacemaker of the heart
Rate: 40-60 bpm
Usually with retrograde P waves (or no P wave)

Figure 29. Junctional complexes

B. ATRIOVENTRICULAR BLOCKS

AV BLOCK DESCRIPTION ECG

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• PR interval prolonged P-R interval: 7 small squares X 0.04 = 0.28

>0.20 sec ( more than 5 Parang LDR, kahit malayo sila may connection pa rin
small squares )
Second degree
Progressive Lengthening of P-R interval
Type I (Mobitz

XL
Type 1- Progressive prolongation of

—
Wenckebach ) PR interval until an impulse
is blocked
—\ --
’v '
200 ms \
240 ms
\
280 ms \
320 ms
\
No Conduction

Atrrium - P wave, ventricle - QRS complex

Una close kayo tapos habang tumatagal di na nagtetext then biglang nawala
Second degree No lengthening of PR
PR interval = 0.20 second throughout

I*1
Type II interval before a dropped
beat
AJ * II * II II II * IIr
\

Close kayo tapos close pa rin then biglang nawala (' ghosting' as per khadi haha). To compare
it with Type 1, ito kasi walang pasabi iniwan ka lang bigla.
Third degree Complete absence of
Slower R - R , narrow complex
conduction between
atria and ventricles
Atrial rate is always
equal to or more than
ventricular rate
JU 1
*JL/\
QRS may be narrow or Constant P- P intervals
wide depending on level
of block Level of AV node
r

1
QRS complexes are narrowed

Red circles - T wave (note the height of the first T wave, parang nagpeak so ibig sabihin may
ibang wave form doon )
Green circles - P wave

Ventricular level
-

/
f
K
/
3S -
'

.
/ PS——
{
K- f

—
L

QRS complexes are widened ( red arrows - P wave)

Sa relationship para itong divorce. May sariling mundo yung P wave, may sariling mundo yung
QRS complex.
Among the AV blocks, who needs the pacemaker ? 3 rd degree AV block because there is no regular PR conduction and widening of QRS complex
Which is more ideal to have a pacemaker ? Second degree type I or type II ? To remember the answer here, isipin mo raw kung ano mas masakit? Yung type II kasi yun
yung iniwan pagkatapos maging close kayo .

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