2.

02

PHYSIOLOGY

ELECTROCARDIOGRAPHY

PAMANTASAN NG LUNGSOD NG MAYNILA

JEREMIAS T. BALGUA JR., MD | SEPTEMBER 20, 2016

OUTLINE
I.
II.

III.

IV.

V.
VI.
VII.

VIII.

Electrocardiogram
a. Clinical Utility of ECG
Anatomy/physiology of the conducting system
a. ECG and membrane potential of
ventricular cell
b. Mechanism of sinus nodal rhythmicity
c. Normal cardiac depolarization and
repolarization
d. Normal cardiac conduction steps
The normal ECG
a. Components of an ECG tracing
b. Segments and Intervals
ECG leads
a. Limb leads
i. Standard bipolar limb leads
ii. Einthovens triangle/ law
iii. Augmented unipolar limb leads
b. Precordial/chest leads
c. Additional types of ECG leads
Flow of current around the heart during the
cardiac cycle
Currents of Injury
ECG interpretation and associated abnormalities
a. Rhythm
b. Rate
c. Axis
i.
Axis Deviations
d. P wave morphology and duration
e. P-R interval
i.
AV blocks (1st, 2nd, 3rd degree)
f. QRS morphology and duration
i.
Bundle Blocks (Left and right)
ii.
Abnormal Voltages of the QRS
Complex
iii.
Prolonged and Bizarre Patterns of
the QRS Complex
g. ST segment (depression and elevation)
h. T wave, U wave and QT interval
i.
Premature contractions
i.
Premature atrial contractions
ii.
Premature ventricular contractions
j. Paroxysmal tachycardia
i.
Atrial paroxysmal tachycardia / A-V
Nodal Paroxysmal Tachycardia /
supraventricular tachycardia
iii.
AV nodal re-entrant tachycardia
(AVNRT)/ atrioventricular nodal reentrant tachycardia
iv.
Ventricular
Paroxysmal
Tachycardia
k. Atrial fibrillation
l. Atrial flutter
m. Ventricular Tachycardia
n. Ventricular fibrillation
o. Agonal rhythm to asystole/Cardiac arrest
Anti-arrhythmic drugs
I. ELECTROCARDIOGRAM (ECG/EKG)

Is a test that records the electrical activity of the heart

as detected by electrodes attached to the outer

1D

COLLEGE OF MEDICINE 2020

surface of the skin and recorded by a device external

to the body.
Info about: pattern of depolarization, mass of
electrically active cardiac muscles, rate and
rhythm.
The waves produced by myocardial depolarization and
repolarization have three chief characteristics:
o Duration- measured in fractions of a second
o Amplitude- measured in millivolts (mV)
o Configuration- referring to the shape and
appearance of the wave

CLINICAL UTILITY OF ECG

Baseline or initial evaluation of all patients especially

40 years old and above

Patients on drug therapy (anti-arrhythmic drugs)

Patients on pacemaker, with heart failure, and with

myocardial ischemia (and other coronary artery
disease)

Patients who will undergo surgery

o Most of the time, any major or minor surgery is
accompanied by arrhythmia
II. ANATOMY / PHYSIOLOGY OF THE CONDUCTING
SYSTEM

Figure 1. Anatomy of the heart showing the

pacemakers.F
Lifted from 2019 1D trans:
SA node AV node AV bundle AV bundle
branches Purkinje fibers
Pacemakers of the heart:
1.

Sinoatrial Node (SA node)

located lateral to the sulcus terminalis of the right
atrium

composed of specialized spindle shaped cells

with almost no contractile muscle filaments

has an intrinsic automaticity (fires inherently: selfexcitation)

o faster discharge rate
o diastolic depolarization

RMP nearer to threshold

Leakiness to Na and Ca

the only one with IF channel (funny current)

Discharges at a rate of 60-100 beats per minute

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2.2 ELECTROCARDIOGRAPHY
*Why is the SA node the dominant pacemaker?

Because of its action potential

o Has the fastest rhythmical discharge rate
among the AV node and Purkinje Fibers

Has less negative RMP than ventricular muscle

fibers (faster to reach threshold)
o SA node RMP: -55 to -60 mV
o AV node RMP: -60 to -70 mV
2.

Phase 0
o Fast depolarization
o Abrupt upstroke
o Rapid entry of Na+ into the cell through the fast
Na+-channels.
o The fast Na+-influx causes phase 0 of atrial,
ventricular and Purkinje action potentials
o The fast Na+-channels are both voltage- and
time-dependent.
o Stops at about +30 mV, because the fast Na+channels become voltage-inactivated by closure
of inactivation gates. The potential difference
approaches the equilibrium potential for Na+ (+ 60
mV), but only reaches +30 mV. The conduction
velocity along the fast response fiber increases
with the AP-amplitude and especially with the
slope of phase 0.

Phase 1
o Early repolarization from the upstroke.
o K+-efflux.

Phase 2
o Plateau of the action potential
o Slow Ca2+-Na+-channels remain open for a long
period - up to 300 ms.
o The net influx of Ca2+ and Na+ is almost
balanced by a net efflux of K+, so the balance is
forming the plateau. Ca2+ activates the muscle
contractile process. When the slow Ca2+-Na+channels close at the end of the plateau, the
voltage-gated K+-channels are activated, and the
permeability for K+ increases rapidly.

Phase 3
o Terminal repolarization. With all the K+-channels
open, large amounts of K+ diffuse out of the
ventricular fiber. The equilibrium potential for K+ (94 mV) and the RMP is rapidly approached.

Phase 4
o The RMP of - 90 mV
o The Na+-K+ pump restores ionic concentrations
by exchanging Na+ for K+ in a ratio of 3:2.

Phase 5
o Relative refractory period (RR), and the T-wave in
the ECG. The long absolute refractory period (AR)
of the ventricular cells covers the whole
shortening phase of the contraction (blue curve).
In the absolute refractory period all fast Na+channels are voltage-inactivated and closed,
which prevents sustained tetanus. As a
consequence, no stimulus is sufficient to trigger
contraction regardless of size.
o In the relative refractory period, enough of the fast
Na+-channels are recovered, so that a sufficiently
large stimulus can break through and produce an
action potential although smaller than normal.
o The long absolute refractory period protects the
cardiac pump, as it is not possible to bring
ventricles into smooth tetanus.

Atrioventricular Node (A-V node)

receives impulse from SA node from intermodal
pathways (found in the atrium)

Discharges at a rate of 40-60 bpm

Also exhibits rhythmical excitation

3.

Purkinje Fibers
Discharges at a rate of 30-40 bpm
Also exhibits rhythmical excitation

A. ECG AND MEMBRANE POTENTIAL OF A

VENTRICULAR CELL

Figure 2. Recordings of ECG with intracellular

membrane potential (red curve) and contraction (blue
curve) of one heart cycle in a ventricular fibre.

Across the ventricular cell membrane there is a steady

potential difference of almost the same size as the
equilibrium potential for K+ (-94 mV), that is -90 mV.
This negative potential is referred to as the resting
membrane potential (RMP), because it represents the
potential difference across the cell membrane (inside
negative) at rest between successive action potentials.
Any process that reduce the absolute size of the RMP
(ie, depolarize the membrane) tends to activate (open)
fast Na+-channels. These channels contain fast
opening and fast closing gates (inactivation gates).
Electrochemical forces favor the abrupt influx of Na+
from neighboring regions. Hereby, the potential is
further diminished and more and more Na+-channels
are activated or opened. The threshold potential for
release of an action potential is a rise of 25 mV from 90 mV. The cardiac action potential is an all-or-none
response, which can be divided into five phases:

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2.2 ELECTROCARDIOGRAPHY

As described above, the cardiac muscle fiber has a

horizontal plateau because of the slow Ca2+-Na+channels (phase 2). Skeletal muscle fibers have no
plateau, because they do not open slow Ca2+-Na+channels for a long time.

B. MECHANISM OF SINUS NODAL RHYTHMICITY

Types of Membrane Ion Channels in the Cardiac
Muscles
1. Fast Na channels
2. Slow Na-Ca channels
3. K channels

Na+ currents Membrane potential (MP) begins to

spontaneously depolarize initiating Phase 4.

As the MP reaches about -50 mV, transient or T-type

Ca++ channel opens inward directed Ca++ currents
further depolarize the cellmembrane continues to
depolarizeL-type Ca++ channels opensmore
Ca++ to enter the cellfurther depolarize cell until AP
threshold is reached.

Figure 4. Purkinje Fiber and SA Node Action Potential

Figure 3. Membrane action potential.

Opening of fast channels influx of positive Na+ ions

rapid upstroke spike AP in ventricular muscle fiber
Plateau in ventricular muscle fiber is due to the slower
sodium calcium channels.
Opening of the K+ channels diffusion of many
positive K+ ions in the outward direction membrane
returns to the RMP.

In Sinus Nodal Fibers

Sinus node RMP is less negative than ventricular

muscle fibercell membranes of sinus fibers are
naturally leaky to Na+ and Ca++, and positive charges
of the entering Na+ and Ca++ ions neutralize some of
the intracellular activity.
At sinus fibers RMP, fast Na+ channels have already
been inactivated (blocked). Only the slow Na+-Ca++
channels can open and cause action potential.
S-A node AP is slower to develop that in ventricular
muscle.
After AP, the return of the potential to its negative
state occurs slow compared to the abrupt return in the
ventricular fibers.

SA Node Action Potential

Phase 4= slow decline in the outward movement of K+

as the K+ channels responsible for Phase 3 continue
to close.

Phase 0 = increased Ca++ conductance (gCa++) thru

the L-type Ca++ channels depolarization. Funny
currents and Ca++ currents close.

Phase 3 = Repolarization occurs K+ channels open

(increased gK+)increasing the outward directed,
hyperpolarizing K+ currents.
At the same time, the L-type Ca++ channels become
inactivated and close, which decreases gCa++ and the
inward depolarizing Ca++ currents.
C. NORMAL CARDIAC DEPOLARIZATION AND
REPOLARIZATION

Firing of SA node is the atrial depolarization (P wave)

General direction of electric current

o Base to apex

Polarity of the wave depends on the direction of the

AP conduction with respect to the polarity of the lead
o If impulse goes towards the electrode (same
polarity) positive deflection (R wave)
o If impulse goes away from the electrode (opposite
polarity) negative deflection (Q or S wave)

Phase 4 spontaneous depolarization (pacemaker

potential) triggers AP
Phase 0 depolarization phase at AP
Phase 3 repolarization

End of repolarization, ion channels ["funny" currents

("If")] open that conduct slow, inward (depolarizing)

1D

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2.2 ELECTROCARDIOGRAPHY

D. NORMAL CARDIAC CONDUCTION STEPS

R wave apical and early ventricular

depolarization
o Completion of septal depolarization
S wave late ventricular depolarization
o The last area of the heart to be
depolarized is the posterior wall at the
base of the heart
o Completes the ventricular depolarization
(base to apex)

Analogy of Dr. Balgua:

Dapat papunta ka sa Alabang, pero nag side trip ka sa

NAIA (away from the general direction = Q wave)

After NAIA, pupunta ka sa Paranaque, which is

papunta pa rin sa Alabang (general direction = R
wave)

Detour sa Asian Hospital (away from the general

direction = S wave)

Bumalik na sa bahay (depolarization is complete)

Figure 5. Normal sinus rhythm of the heart

1. Spread of Depolarization from SA node (P wave)

SA sending impulse - (P wave in Lead 1 and aVF

of
lead)

2. Conduction from SA node to AV node

Isoelectric AV node
No depolarization or repolarization happening

3. Ventricular Depolarization (QRS complex)

Q wave septal depolarization (from AV node)

o Depolarization of septum Right
ventricle
o Away from the general direction

1D

4. Repolarization (T wave)

Septum initially has a positive outside, negative

inside

Depolarized creates a different electric potential

From the field of negativity goes to
positivity (base to apex)
Creates a positive inside
Establishes direction of electric current

Repolarization- vector force of downward to L side

upward T wave in both Lead I and aVF
Current goes from electronegative apex
to electropositive base

T wave ventricular repolarization (ends to

epicardium)
o Always upright
Because the electric current goes to the
electropositive potential

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2.2 ELECTROCARDIOGRAPHY
3. T wave

T wave deflection should be in the same direction

as the QRS complex in at least 5 of the 6 limb
leads

normally rounded and asymmetrical, with a more

gradual ascent than descent

should be upright in leads V2 - V6, inverted in

aVR

amplitude of at least 0.2 mV in leads V3 and V4

and at least 0.1 mV in leads V5 and V6

isolated T wave inversion in an asymptomatic

adult is generally a normal variant
* Representation of ventricular repolarization
Is there an atrial repolarization? Where is it in the
graph? Atrial repolarization occurs a little bit earlier than
ventricular depolarization. Since the electrical force of QRS
is much higher than atrial repolarization, it is masked by
the complex.
III. THE NORMAL ECG

4. Equidistant r-r intervals

5. Regular

Rhythm is regular if it has a P wave)

6. Rate:

60-100 (rule of 300)

7. Axis

Look only at Lead I and aVF, if both upright, normal

axis
8. PR interval: Normally between 0.12 and 0.20 seconds.
9. ST segment

isoelectric, slanting upwards to the T wave in the

normal ECG

can be slightly elevated (up to 2.0 mm in some

precordial leads)

never normally depressed greater than 0.5 mm in

any lead
10. QT interval

Durations normally less than or equal to 0.40

seconds for males and 0.44 seconds for females.

Figure 6. Normal ECG tracing

1. P wave

upright in leads I, aVF and V3 - V6

normal duration of less than or equal to 0.11

seconds

polarity is positive in leads I, II, aVF and V4 - V6;

diphasic in leads V1 and V3; negative in aVR

shape is generally smooth, not notched or peaked

* Representation of atrial depolarization
2. QRS wave

Duration less than or equal to 0.12 seconds,

amplitude greater than 0.5 mV in at least one
standard lead, and greater than 1.0 mV in at least
one precordial lead. Upper limit of normal
amplitude is 2.5 - 3.0 mV.

Small septal Q waves in I, aVL, V5 and V6

(duration less than or equal to 0.04 seconds;
amplitude less than 1/3 of the amplitude of the R
wave in the same lead).

Represented by a positive deflection with a large,

upright R in leads I, II, V4 - V6 and a negative
deflection with a large, deep S in aVR, V1 and V2

In general, proceeding from V1 to V6, the R

waves get taller while the S waves get smaller. At
V3 or V4, these waves are usually equal. This is
called the transitional zone
* Representation of tubular depolarization

1D

Figure 6. Parts of ECG tracing

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2.2 ELECTROCARDIOGRAPHY
A. COMPONENTS OF AN ECG TRACING

Segment - straight line connecting two waves

Interval - encompasses at least one wave plus the
connecting line \

PR interval (normal is about 0.16 sec) time from

START of atrial depolarization to the START of
ventricular repolarization
PR segment time from the END of atrial
depolarization to the
Start of ventricular repolarization

Calibrations can be used to compute for the duration

of the different intervals and determine certain
abnormalities
Standard Calibration in ECG = 25 mm /second
1 second/ 50 mm = calibration used to better visualize
very fast heart rates
a. Horizontal axis measures time
o 1 small square = 1 mm = 0.04 sec
o 1 big square(5 small squares) = 5 mm = 0.2
sec

b. Vertical axis measures voltage

o 1 small square = 1 mm = 0.1 mV
o 10 small squares = 1 mV
o 1 big square = 5 mm = 0.5 mV
o
NORMAL TIME INTERVAL

P waves - < 3 small squares (0.08-0.12s)

PR interval - < 5 small squares (0.12-0.2s)

QRS complex 1.5-2 squares tall (0.08-0.12 sec)

ST segment end of ventricular depolarization to

start of ventricular repolarization
QT interval (normal is about 0.35 sec) START of
Ventricular depolarization to the END of Ventricular
repolarization
0.36-0.46s (males); 0.36-0.48s (females)
QRS interval duration of Ventricular depolarization
T wave depends on electrolyte; elevated in high K or
may be inverted
Note:
PQ and ST segments- isoelectric (same amplitude)
IV. ECG LEADS

B. SEGMENTS AND INTERVALS

Standard ECG use of 12 leads, with each lead determined

and placed by the placement and orientation of various
electrodes on the body. Each lead views the heart at a
unique angle, enhancing its sensitivity to a particular region
of the heart. The more views, the more information
provided.
Standard Chest Lead ECG
Normal: Left-side lead
Pediatrics: Right-side lead
12-lead ECG
Six limb leads - 3 standard; 3 augmented
Six precordial leads
composed of limb leads and chest leads
15- lead ECG

1D

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2.2 ELECTROCARDIOGRAPHY

paediatric patients are directed to the right (until

12 years old), so we need to get the right side v1,
v3, v4, v5 and v6
Electrocardiographic Leads (12-Lead ECG)
1. Limb Leads
i. Standard Bipolar Limb Leads
ii. Augemented Unipolar Limb Leads
2. Chest/Precordial Leads
A. LIMB LEADS
i. Standard Bipolar Limb leads
1.
I
- Right arm (-) -> Left arm (+);
0
2.
II
- Right arm (-) -> Left leg (+);
60
3.
III
- Left arm (-) -> Left leg (+);
120
Frontal plane activity

the ground lead, lahat ng wave forms nakapositive deflected upwards except aVR, aVR
reflects the electrical force in the posterior form of
the heart. So if aVR is upright, mali placement ng
leads.
2. aVR (Right)
Positive (+) terminal: Right Arm
Negative deflection
-150 normal
Electrode positioning opposite the flow of
depolarization from R atrium to R ventricle
3. aVL (Left)
Positive terminal: Left arm
No deflection
Electrode position perpendicular to flow of
depolarization
-30 normal
4. aVF (Foot)
Positive terminal: Left leg
Positive Deflection
Electrode parallel to depolarization flow from
L atrium to L ventricle
90 normal

ii.

Einthovens Triangle
Follows the direction of the three leads
mentioned; forming a triangle
Einthovens Law
o Voltage of I + III = Voltage of II
o Follows normal heart electrical courses
o Obtain electric potentials of two leads,
third one can be solved
o Can be used to check if electrodes
placed correctly

Flow:
o
o
o
o

Apex is electropositive;
Outside of heart is electropositive;
Inside is electronegative
Electronegative would be attracted to the
electropositive potentials going to the
apex
o Flow of circuit is towards the apex and
that is the normal impulse conduction of
the heart.
iii. Augmented Unipolar Limb Leads
Placing an electrode on the left arm, right arm,
and left foot with a ground lead on the box, will
produce an amplification of electrical potential.
Augmented unipolar leads aVR was known to be

1D

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B. CHEST/PRECORDIAL LEADS
Electrical activity at horizontal plane
records mainly the electrical potential of the cardiac
musculature immediately beneath the electrode.

V. FLOW OF CURRENT AROUND THE HEART

DURING CARDIAC CYCLE

C. ADDITIONAL LEADS
a. Posterior Lead ECG
Lungs and muscle barriers prevent anterior
ECG to detect posterior heart damage
Used to record myocardial damage on the
posterior part of the heart
b. Right-sided 12-Lead ECG
Maybe used to detect right-side heart damage
Mirror of the standard
Rversion of V3 to V6

Electrical current flows from depol area to polarized

area
First areas to be depol in left ventricular area:
o Anterior preseptal wall
o Posterior preseptal wall
o Center of Left septum
o These are the sites of insertions of the 3
branches of the Left Bundle Branch
Last area to be depol: Posterobasal areas of Left
ventricle
Septal activation: starts @ mid 3rd of left side, then
spreads across interventricular septum: left to right
and apex to base
Right ventricle depol:
o Starts at insertion of Right Bundle
Branch close to anterior papillary
muscle -> free wall -> pulmonary conus > posterobasal areas
o Sept Septal surface to anterior free walls
to the posterior and basal regions in an
apex to base direction

THUS,
o Leads I, II, III, aVL, and aVF upward (positive)
o aVR downward (downward)
o V3, V4- isoelectric
o V1, V2- small R, peak S
o V3-V6 increasing R wave; decreasing S wave
o V5, V6- well developed R wave

1st pic: Impulse from SA node to atrial walls

2nd pic: Impulse reach AV node, delay .1second
3rd pic: Bundle branches (R and L) carry impulses from
AV node to Apex
4th pic: Signal spread through the ventricles
VI. CURRENTS OF INJURY

1D

When part of the heart remains partially or completely

depol
Current flows between pathologically depol and
normally depol even between heartbeat

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2.2 ELECTROCARDIOGRAPHY

Injured part = negative since it is depolarized and

sends negative charges to surrounding muscles fibers

Causes:
o Trauma = inc. memb permeability = no full
repol
o Infection = damage muscle membranes
o Ischemia

*Current of injury effect on QRS complex

the left ventricle. Thus, repolarization causes a return

of the current of injury in each lead, as noted at the far
right.
VII. ECG INTERPRETATION AND ASSOCIATED
ABNORMALITIES
Guide:
1. Rhythm
2. Rate: atrial and ventricular
3. Axis
4. P wave morphology and duration
5. P-R interval
6. QRS morphology and duration
7. ST segment
8. T wave, U wave and QT interval
A. RHYTHM

Check for P-waves on LeadII, V1, V2

The P waves must be upright in leads II, III and

aVF. The P waves are upright because the
direction of the impulse is going toward the
inferior wall away from the SA node

Check for regularity of R-R interval (normal sinus

rhythm)

II, V1, and V2 since it is on the side of the atrium

In the figure above, a small area in the base of the left

ventricle is newly infarcted (loss of coronary blood
flow).
During the T-P interval (polarization) abnormal
negative current (125o) still flows from the infarcted
area at the base of the left ventricle and spreads
toward the rest of the ventricles. With the base of the
vector, the negative end, toward the injured muscle.
As shown in the lower portions of the figure, even
before the QRS complex begins, this vector causes an
initial record in lead I below the zero potential line,
because the projected vector of the current of injury in
lead I points toward the negative end of the lead I axis.
Lead II - the record is above the line because the
projected vector points more toward the positive
terminal of the lead.
Lead III - the projected vector points in the same
direction as the positive terminal of lead III so that the
record is positive. Furthermore, because the vector
lies almost exactly in the direction of the axis of lead
III, the voltage of the current of injury in lead III is
much greater than in either lead I or lead II.
By vectorial analysis, the successive stages of
electrocardiogram generation by the depolarization
wave traveling through the ventricles can be
constructed graphically, as demonstrated in the lower
part.
When the heart becomes totally depolarized, at the
end of the depolarization process (as noted by the
next-to-last stag), all the ventricular muscle is in a
negative state. Therefore, at this instant in the
electrocardiogram, no current flows from the ventricles
to the electrocardiographic electrodes because now
both the injured heart muscle and the contracting
muscle are depolarized. Next, as repolarization takes
place, all of the heart finally repolarizes, except the
area of permanent depolarization in the injured base of

1D

B. RATE

ECG grid:
o 1mm block (small)
= 1/25 of a
sec (.04)
o 5mm block (large)
= 1/5 of a sec
(.20)

Measure R-R interval

Rule of 300

For regular rhythms: Rate = 300 / number of

large squares in between each consecutive R
wave.

For very fast rhythms: Rate = 1500 / number of

small squares in between each consecutive R
wave.

For slow or irregular rhythms: Rate = number of

complexes on the rhythm strip x 6 (this gives the
average rate over a ten-second period).
C. AXIS
a. Hexaxial Reference System (plot method)

Normal:
-30 to 110

Right Axis Dev: 120 to 180

Left Axis Dev:

-90 to -20

Indeterminate Dev:
180 to -90

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2.2 ELECTROCARDIOGRAPHY
b.

Axis Isoelectric Method

Identify the lead where R and Q is most
isoelectric. (Isoelectric QRS has equal positive
and negative deflections)
Check the lead perpendicular to it (consult axis
graph below)
Check the perpendicular lead if the QRS is
deflecting positively or negatively; if negative,
reference point will be 180 from it
Example:
o Say, the lead with the most isoelectric
QRS (same R and Q height in ECG
trace; none shown here) is Lead III (120
as shown in axis graph below)
o Select the perpendicular lead, which is
aVR
o Check if aVRs QRS is deflecting
positively or negatively (in ECG trace;
none shown here)
o If positively deflecting = extreme RAD (150); if Negatively deflecting = normal
axis(30)

d.

1.
2.
3.
4.
5.
6.

Axis by Thumb Rule

Check QRS Complexes in lead I and AVF
Then Check intersection
Left thumb = lead I
Right thumb = avR
If both are up, normal
If right thumb up, right axis deviation
If left thumb up, left axis deviation
If both down, extreme right axis deviation

Causes of Axis Deviations

(with * = additional info)
1. Left shift axis
Expiration (flattens heart horizontally)
Lying down
Obese, sedentary (Fats push heart upwards)
2.

3.

c.

1D

Axis by Lead I and Lead II

if both (+)
= Normal
if lead II upward
= RAD
if lead II downward
= LAD
if both downward
= Extreme RAD

Right shift axis

Inspiration
Standing up
Tall lanky party people
*Hypertrophy

axis shifts on the same ventricle

the bigger would be the electrical force

supinating over the other ventricles

left ventricle create more electrical force

overpowering the right ventricle -> axis shifts
to left

When one ventricle greatly hypertrophies,

the axis of the heart shifts toward the
hypertrophied ventricle for two reasons.
First, a far greater quantity of muscle exists
on the hypertrophied side of the heart than on
the other side, and this allows generation of

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2.2 ELECTROCARDIOGRAPHY
greater electrical potential on that side.
Second, more time is required for the
depolarization wave to travel through the
hypertrophied ventricle than through the
normal ventricle. Consequently, the normal
ventricle becomes depolarized considerably
in advance of the hypertrophied ventricle, and
this causes a strong vector from the normal
side of the heart toward the hypertrophied
side, which remains strongly positively
charged. Thus, the axis deviates toward the
hypertrophied ventricle.
4. *Bundle Blocks
Ordinarily, the lateral walls of the two ventricles
depolarize at almost the same instant (both the left
and the right bundle branches of the Purkinje system
transmit the impulse almost the same instant).
Potentials generated by the two ventricles almost
neutralize each other. If only one of the major bundle
branches is blocked, the cardiac impulse spreads
through the normal ventricle long before it spreads
through the other. Therefore, depolarization of the two
ventricles does not occur even nearly simultaneously,
and the depolarization potentials do not neutralize
each other. As a result, axis deviation occurs.
a.

When the left bundle branch is blocked, cardiac

depolarization spreads through the right ventricle two to
three times as rapidly as through the left ventricle.
Consequently, much of the left ventricle remains polarized
for as long as 0.1 second after the right ventricle has
become totally depolarized. Thus, the right ventricle
becomes electronegative, whereas the left ventricle
remains electropositive during most of the depolarization
process, and a strong vector projects from the right
ventricle toward the left ventricle. In other words, there is
intense left axis deviation of about -50 degrees because
the positive end of the vector points toward the left
ventricle. This is demonstrated in figure below, which
shows typical left axis deviation resulting from left bundle
branch block.
The duration of the QRS complex is greatly prolonged
because of extreme slowness of depolarization in the
affected side of the heart. This extremely prolonged QRS
complex differentiates bundle branch block from axis
deviation caused by hypertrophy.

RBBB (Right Bundle Branch Block)

When the right bundle branch is blocked, the left
ventricle depolarizes far more rapidly than the
right ventricle, so the left side of the ventricles
becomes electronegative as long as 0.1 second
before the right. Therefore, a strong vector
develops, with its negative end toward the left
ventricle and its positive end toward the right
ventricle. In other words, intense right axis
deviation occurs. In the figure below, an axis of
about 105 degrees is shown instead of the
normal 59 degrees and a prolonged QRS
complex because of slow conduction.

D. P WAVE MORPHOLOGY AND DURATION

b.

CLBBB (Complete Left Bundle Branch Block)

1D

E. P-R INTERVAL

Conduction time from SA node to AV node

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2.2 ELECTROCARDIOGRAPHY

AV blocks
o 1st Degree prolonged conduction time;
prolonged PR interval
o 2nd Degree

Type 1 Progressive
prolonged time leading to drop
beat; can be a precursor for a
pacemaker implantation

Type 2 can lead to block at

bundle of His (type 3)
o 3rd Degree
Complete heart block
Block bundle of His onwards
No impulse to ventricles
AV dissociation

Left Bundle Brach Block

V1 Wide QRS complex;

inverted T wave

V6 Twin R-wave peaks

Signals acute MI

Abnormalities (voltage)
1. Increased Voltage
Hypertrophy (increase in muscle
quantity) causes generation of
increased quantity of electricity
conducted
2. Decreased Voltage
MI
Decreased muscle mass
Slower depol wave propagation
Prolonged QRS and lower voltage

F. QRS MORPHOLOGY AND DURATION

Only lasts for .1sec

Pulmonary Effusion
Pleural effusion (extracellular fluid),
to a lesser extent, also can "shortcircuit" the electricity around the
heart so that the voltages at the
surface of the body and in the
electrocardiograms are decreased.

Emphysema
conduction of electrical current
through the lungs is depressed
considerably because of excessive
quantity of air in the lungs.
chest cavity enlarges, and the
lungs tend to envelop the heart to a
greater extent than normally.
Therefore, the lungs act as an
insulator to prevent spread of
electrical voltage from the heart to
the surface of the body, and these
results
in
decreased

1D

V6 Inverted T wave; Wide S

terminal

Abnormalities (blocks)
o Right Bundle Branch Block

V1 batman(?)

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2.2 ELECTROCARDIOGRAPHY
electrocardiographic potentials in
the various leads.

Prolonged and Bizarre Patterns of QRS Complex

1. Prolonged QRS: Cardiac Hypertrophy,
Prolonged Conduction
o Hypertrophy -> longer pathway of
impulse to travel
o QRS lasts as long as depol spreads
through ventricles
o Prolonged up to .09 to .12 second

Hyperkalemia- peak T waves; ventricular

arrhythmia
Hypercalcemia-short QT
Hypocalcemia- slow contraction; prolonged QT
Hypokalemia- flattened T wave
Hypokalemia- U wave appear in severe
hypokalemia with flattened T and prominent U
PVC - Prolonged QT

2.

Prolonged QRS: Purkinje System Block

o Blocked Purkinje fibers -> Impulse
conducted by Ventricular Muscles
instead -> velocity decreased up to 1/3 of
original
o Prolonged up to .14or greater
*block below bundle of His requires
pacemakers since the ventricular muscles will
be dominant pacemaker by then, and will only
produce slow heart rates.
3.

Bizarre QRS
a. Destruction of cardiac muscles
b. Multiple small local blocks in Purkinje
system -> irregular cardiac impulse ->
rapid voltage shift and axis deviation ->
double or triple peaks in ECG

G. ST SEGMENT
ST Segment depression in myocardial ischemia
Downslope = 0.5mV is a significant depression
ST segment elevation->Myocardial infarction
Upslope=chair-like pattern

I.
PREMATURE CONTRACTION
also called extrasystole/premature beat/ectopic beat.
most result from ectopic foci in the heart
Causes:
1. Local areas of ischemia
2. Small calcified plaques at different points in the heart ,
which press against the adjacent cardiac muscle so that
some of the fibers are irritated;
3. Toxic irritation of the A-V node, Purkinje System, or
myocardium caused by drugs, nicotine or caffeine
4. Mechanical initiation of premature contractions is also
frequent during cardiac catheterization; large numbers of
premature contractions often occur when the catheter
enters the right ventricle and presses against the
endocardium

PREMATURE ATRIAL CONTRACTIONS

palpitations kapag nakikita niyo si crush

H.

1D

T wave, U wave and QT interval

P wave of this beat occurred early

P-R interval shortened (ectopic origin of the beat is in

the atria near the A-V node)

causes: ischemia vs. calcified plaques vs. toxic

irritation of the AV node, Purkinje system, or
myocardium, drugs

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2.2 ELECTROCARDIOGRAPHY

nicotine, caffeine
compensatory pause
interval between the premature contraction and the
next succeeding contraction is slightly prolonged
o Cause: premature contraction originated in
the atrium some distance from the sinus
node, and the impulse had to travel through
a considerable amount of atrial muscle
before it discharged the sinus node.
Consequently, the sinus node discharged
late in the premature cycle, and this made
the succeeding sinus node discharge also
late in appearing.
other causes: healthy people can have it; smoking,
puyat, sobrang starbucks, redbull, alcohol, milk tea
pulse deficit
o a deficit in the number of radial pulses occurs
when compared with the actual number of
contractions of the heart
o heart contracts early
ventricles will not
have filled with blood normally
stroke
volume output depressed/ almost absent
pulse wave passing to the peripheral
arteries is
weak
PREMATURE VENTRICULAR CONTRACTIONS

few seconds, a few minutes, a few hours, or much

longer. Then the paroxysm usually ends as suddenly as
it began, with the pacemaker of the heart instantly
shifting back to the sinus node.
can be stopped by eliciting a vagal reflex (pressing on the neck in
the regions of the carotid sinuses)
quinidine and lidocaine can used
ATRIAL PAROXYSMAL TACHYCARDIA/ A-V NODAL
PAROXYSMAL
TACHYCARDIA/SUPRAVENTRICULAR
TACHYCARDIA

Atrial or A-V nodal paroxysmal tachycardia, both of which are

called supraventricular

demonstrates in the middle of the record a sudden increase in

the heart rate from about 95 to about 150 beats per minute.

inverted P wave is seen before each QRS-T complex, and this P

wave is partially superimposed onto the normal T wave of the
preceding beat. This indicates that the origin of this paroxysmal
tachycardia is in the atrium, but because the P wave is
abnormal in shape, the origin is not near the sinus node.

PACs SVTs VTAC

Paroxysmal tachycardia often results from an aberrant rhythm

that involves the A-V node. This usually causes almost normal
QRS-T complexes but totally missing or obscured P waves.

tachycardias,

usually occurs in young, otherwise healthy people, and they

generally grow out of the predisposition to tachycardia after
adolescence.

In general, supraventricular tachycardia frightens a person

tremendously and may cause weakness during the paroxysm,
but only seldom does permanent harm come from the attack.

AV NODAL RE-ENTRANCT TACHYCARDIA/ ATRIOVENTRAL NODAL

RE-ENTRANT TACHYCARDIA

Bizarre QRS
Sunod sunod na PVCS
Vtac!!!
wide QRS: impulse conduction thru ventricle not through
Purkinje fibers
QRS high voltage: impulse travel only one direction (no
neutralization effect of depolarization waves): with one
entire single ventricle(common in left ventricle) is
depolarized ahead of the other
large electrical
potentials
T is opposite in direction: slow conduction of impulse
(causes the muscle fibers that depolarize first also to
repolarize first)

PAROXYSMAL TACHYCARDIA
Some abnormalities in different portions of the heart (
such as atria, the Purkinje system, or the ventricles) can
occasionally cause rapid rhythmical discharge of
impulses that spread in all directions throughout the
heart.
caused most frequently by re-entrant circus movement
feedback pathways that set up local repeated selfreexcitation. Because of the rapid rhythm in the irritable
focus, this focus becomes the pacemaker of the heart.
"paroxysmal" - heart rate becomes rapid in paroxysms,
with the paroxysm beginning suddenly and lasting for a

1D

most common regular supraventricular tachycardia

Originates from a location within the heart above the bundle of
His.

P wave comes after QRS

Drug of choice: Adenosin, Beta blockers (Short acting beta

blocker esmolol), Calcium channel blockers (verapamil,
diltiazem), Digoxin but is not given in acute paroxysmal
attacks because of its slow onset

Pathogenesis - /dual mechanism proposed for re-entry

From textbook of clinical electrocardiography, 3rd edition:
A dual concept mechanism consisting of fast and slow
conducting pathways within the AV node is the proposed
mechanism for its initiation. The prolonged P-R interval or
prolonged A-H interval on bundle of His electrocardiography
strengthens the concept of dual entry pathway within AV node.
Therefore the present concept is that the AV node is
functionally split into two longitudinal pathways:
1. Beta pathway (fast pathway) : exhibits rapid
conductions and has a long refractory period

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2.2 ELECTROCARDIOGRAPHY
2.

Alpha pathway (slow pathway) : conducts slowly

and has a short refractory period Sir Balgua:

Functional block on fast pathway impulses conducted to slow

pathway
Before reaching ventricles, fast pathway would
recover its refractoriness
would attract slow impulses to
retrogradely conduct to fast pathway
impulses go up to
activate atrium or travel to slow pathway
re-entry
mechanism
simultaneous action of atrium and ventricle
walang P wave (P wave nasa loob ni QRS)

VENTRICULAR PAROXYSMAL TACHYCARDIA

k.

series of ventricular premature beats occurring one

after another without any normal beats interspersed.
usually a serious condition o
usually does
not
occur
unless considerable
ischemic
damage is present in the ventricles.
o ventricular tachycardia frequently initiates the lethal
condition of ventricular fibrillation because of
rapid repeated stimulation of the ventricular
muscle.
Causes: digitalis intoxication (causes irritable foci that
lead to ventricular tachycardia
Drug: quinidine (increases the refractory period and
threshold for excitation of cardiac muscle blocking
irritable foci)
ATRIAL FIBRILLATION

1D

Cause: atrial enlargement prevent the atria from

emptying adequately into the ventricles, or from
ventricular failure with excess damming of blood in
the atria. The dilated atrial walls provide ideal
conditions of a long conductive pathway, as well as
slow conduction, both of which predispose to atrial
fibrillation
loss of atrial contraction
ECG: no P wave
QRS-T complexes are normal, but their timing is
irregular
When the atria are fibrillating, impulses arrive from
the atrial muscle at the A-V node rapidly but also
irregularly. Because the A-V node will not pass a
second impulse for about 0.35 second after a
previous one, at least 0.35 second must elapse
between one ventricular contraction and the next.
Then an additional but variable interval of 0 to 0.6

l.

second occurs before one of the irregular atrial

fibrillatory impulses happens to arrive at the A-V
node. Thus, the interval between successive
ventricular contractions varies from a minimum of
about 0.35 second to a maximum of about 0.95
second, causing a very irregular heartbeat.
125-160 beats (due rapid rate of the fibrillatory impulses in the
atria)
irregular ventricular rhythm: varied ventricular contractions 0.350.95 seconds
The mechanism of atrial fibrillation is identical to that of
ventricular fibrillation, except the location. Remember that the
atrial muscle mass is separated from the ventricular muscle
mass by fibrous tissue except for the conducting pathway
through the A-V bundle. Therefore, ventricular fibrillation often
occurs without atrial fibrillation.
Not as lethal as ventricular fibrillation because blood still flows
passively through the atria into the ventricles, and the efficiency
ofventricular pumping is decreased only 20 to 30 %.
Electroshock Treatment
ATRIAL FLUTTER

sawtooth / flutter waves

Different from atrial fibrillation in that impulse travels as a single
large wave always in one direction around and around the
atrial muscle mass
200-350 beats
2:1 or 3:2 AV conduction rhythm (2 flutter waves before it would
be conducted to generate 1 QRS) o Because one side of the
atria is contracting while the other side is relaxing, the amount of
blood pumped by the atria is slight. Furthermore, the signals
reach the A-V node too rapidly for all of them to be passed into
the ventricles, because the refractory periods of the A-V node
and A-V bundle are too long to pass more than a fraction of the
atrial signals. Therefore, there are usually two to three beats of
the atria for every single beat of the ventricles.
m. VENTRICULAR TACHYCARDIA

cause: ischemia
precedes ventricular fibrillation
drugs: quinidine: Class IA anti-arrhythmic
Anti-arrhythmic drugs
can
ventricular tachycardia

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cause

15 of 17

2.2 ELECTROCARDIOGRAPHY

Has
dual
edge

proarrhythmic
and antiarrhythmic
VENTRICULAR FIBRILLATION
Choogs to Go! (machuchugi na!)

n.

Lethal emergency, most serious of all cardiac arrhythmias

Ventricular fibrillation results from cardiac impulses that
have gone berserk within the ventricular muscle mass,
stimulating portion after portion of ventricular mass and
eventually feeding back onto itself to re-excite the same
ventricular muscle over and over-never stopping.

When this happens, many small portions of the

ventricular muscle will be contracting at the same time,
while equally as many other portions will be relaxing. The
ventricular chambers remain in an indeterminate stage of
partial contraction, pumping either no blood or negligible
amounts.

No repetitive electrocardiographic pattern can be

ascribed to ventricular fibrillation.

potentials change constantly and spasmodically because

the electrical currents in the heart flow first in one
direction and then in another and seldom repeat any
specific cycle.

The voltages of the waves: usually about 0.5 millivolt

initially, but they decay rapidly so that after 20 to 30
seconds, they are usually only 0.2 to
0.3 millivolt. Minute voltages of 0.1 millivolt or less
may be recorded for 10 minutes or longer after
ventricular fibrillation begins.
Causes:
1.
PVC vs. ischemia
2.
re-entry as a basis of VF: circus movement
o "circus movement cause an impulse to continue to
travel around circle, that is to cause re-entry of
impulse into that muscle that has already been
excited
o 3 conditions that can cause circus movement
o First, if the pathway around the circle is too long,
o Second, if the length of the pathway remains
constant but the velocity of conduction becomes
decreased enough
o Third, the refractory period of the muscle might
become greatly shortened. All these conditions occur
in different pathological states of the human heart, as
follows:
1. A long pathway typically occurs in
dilated hearts.
2. Decreased rate of conduction frequently
results from
a. blockage of the Purkinje system,
b. ischemia of the muscle,
c. high blood potassium levels, or
many other factors.
3. A shortened refractory period commonly
occurs in response to various drugs, such as

1D

epinephrine, or after repetitive electrical

stimulation. Thus, in many cardiac
disturbances, re-entry can cause abnormal
patterns of cardiac contraction or abnormal
cardiac rhythms that ignore the pace-setting
effects of the sinus node.
o The re-entrant impulses in fibrillation are not simply a single
impulse moving in a circle. Instead, they have degenerated into
a series of multiple wave fronts that have the appearance of a
"chain reaction."
3. long pathway of conduction (dilated hearts) vs. slow conduction
velocity (AV blocks/ischemia/hyperkalemia) vs. short refractory
period(epinephrine)
4. fibrillation caused by 60 cycle AC: REENTRY unidirectional flow
vs. slow conduction time vs.
short refractory period vs. division of impulses

a 60-cycle electrical stimulus is applied through a stimulating

electrode.

Heart A
o The first cycle of the electrical stimulus causes a
depolarization wave to spread in all directions, leaving
all the muscle beneath the electrode in a refractory
state. After about 0.25 second, part of this muscle
begins to come out of the refractory state. Some
portions come out of refractoriness before other
portions.
o many lighter patches, which represent excitable
cardiac muscle, and dark patches, which represent still
refractory muscle.
o certain impulses travel for short distances, until they
reach refractory areas of the heart, and then are
blocked. But other impulses pass between the
refractory areas and continue to travel in the excitable
areas. Then, several events transpire in rapid
succession, all occurring simultaneously and
eventuating in a state of fibrillation.
State of fibrillation
1. Transmission of some of the depolarization waves around the
heart in only some directions but not other directions (due to
blockage).
2. the rapid stimulation of the heart causes two changes
in the cardiac muscle itself, both of which predispose
to circus movement: (1) The velocity of conduction
through the heart muscle decreases, which allows a
longer time interval for the impulses to travel around

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2.2 ELECTROCARDIOGRAPHY

3.

4.

5.

the heart. (2) The refractory period of the muscle is

shortened, allowing re-entry of the impulse into
previously excited heart muscle within a much shorter
time than normally.
Third, one of the most important features of fibrillation
is the division of impulses, as demonstrated in heart
A. Progressive chain reactions many new wave
fronts many small depolarization waves traveling in
many directions at the same time.
Irregular pattern of impulse travel causes many
circuitous routes for the impulses to travel, greatly
lengthening the conductive pathway, which is one of
the conditions that sustains the fibrillation. It also
results in a continual irregular pattern of patchy
refractory areas in the heart.

One can readily see when a vicious circle has been

initiated: More and more impulses are formed, more
and more patches of refractory muscle, more and
more division of the impulses. Therefore, any time a
single area of cardiac muscle comes out of
refractoriness, an impulse is close at hand to re-enter
the area.
o Heart B
o the final state that develops in fibrillation o many
impulses traveling in all directions, o In fact, a single
electric shock during this vulnerable period frequently
can lead to an odd pattern of impulses spreading multi
directionally around refractory areas of muscle, which
will lead to fibrillation.
Treatment
Electroshock Defibrillation of the Ventricles

a strong high-voltage alternating electrical

current passed through the ventricles for a
fraction of a second can stop fibrillation by
throwing all the ventricular muscle into
refractoriness simultaneously.

However, the same re-entrant focus that had

originally thrown the ventricles into fibrillation
often is still present, in which case fibrillation
may begin again immediately.
When electrodes are applied directly to the two
sides of the heart, fibrillation can usually be
stopped using 110 volts of 60-cycle alternating
current applied for 0.1 second or 1000 volts of
direct current applied for a few thousandths of a
second. CPR

Unless defibrillated within 1 minute after

fibrillation begins, the heart is usually too
weak to be revived by defibrillation because
of the lack of nutrition from coronary blood
flow. However, it is still possible to revive the
heart by preliminarily pumping the heart by
hand (intermittent hand squeezing) and then
defibrillating the heart later.
Implanted cardioverter defibrillator
ACLS

1D

o.

AGONAL RYTYHM TO ASYSTOLE/CARDIAC ARREST

Ongoing choogs!

cessation of all electrical control signals in the heart.

That is, no spontaneous rhythm remains.
Cardiac arrest may occur during deep anesthesia,
In some patients,severe myocardial disease can
cause permanent or semi permanent cardiac arrest,
which can causedeath.
To treat the condition, implanted electronic cardiac
pacemaker have been used successfully to keep
patients alive for months to years.
ANTI-ARRYTHMIC DRUGS
can cause ventricular tachycardia
Has dual edge pro-arrhythmic and antiarrhythmic

Class I: Fast sodium (Na) channel blockers

Ia - Quinidine, procainamide, disopyramide (depress phase 0,

prolonging repolarization) Quezon Police District

Ib -phenytoin, Lidocaine, , mexiletine (depress phase 0

selectively in abnormal/ischemic tissue, shorten repolarization)
PLM

Ic -Flecainide, propafenone, moricizine (markedly depress

phase 0, minimal effect on repolarization)
President Ferdinand Marcos
Class II: Beta blockers

Propranolol , Esmolol Timolol , Metoprolol , Atenolol

Class III: Potassium (K) channel blockers

Amiodarone, Sotalol, Ibutilide, Dofetilide

Class IV: Slow calcium (Ca) channel blockers

Verapamil, Diltiazem

Class V: Variable mechanism

Digoxin, Adenosine, Magnesium sulfate,

wave and QT, U wave

and QT interval T wave, U wave and QT interval

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