Electrocardiography

ECG
 INTRODUCTION

The heart is a vital link in the oxygen transport system, pumping blood
to the pulmonary and peripheral circulation systems to supply oxygen
and other nutrients required for metabolism in all tissues.
The beating heart generates rhythmic, electrical impulses that cause
mechanical contraction, or the pumping action, of cardiac muscle.
Some of the electrical current produced by these rhythmic impulses is
detectable by electrodes that may be placed on the surface of the skin.
Current flow during the cardiac cycle is then recorded as the
characteristic waveforms of the electrocardiogram(ECG).
Mechanical events such as contraction and relaxation of the
myocardium are inferred from the waveforms produced by the ECG.
 ECG

“An ECG is the recording (gram)

of the electrical activity (electro)
generated by the cells of the heart (cardio)
over time.”
Useful in diagnosis of…
 Cardiac Arrhythmias (gold standard)
 Myocardial ischemia and infarction
 Pericarditis
 Electrolyte disturbances
 Drug effects and toxicity
 non-cardiac diseases (e.g. pulmonary embolism)
The Normal ECG
Electrocardiogram (ECG/EKG)

 Is a recording
of electrical
activity of
heart
conducted
through ions
in body to
surface
 BASIC ELECTROPHYSIOLOGY

 At rest when the heart muscle is not contracting, the electrical

charge is positive on the outside of each cell membrane but
negative inside. (Cells are polarized).
 Depolarization occurs when ions move across the membrane
rendering the inner surface more positive thus causing
contraction.
 Depolarization – repolarization -------------contraction – relaxation
of heart muscle.
 The changing electrical status across the cell membranes causes
voltage changes within the heart muscle
 These voltage differences can be detected at skin level and
measured with electrodes placed on the skin.
 Normal conduction pathway:

 SA node -> atrial muscle -> AV node -> bundle of His -> Left and Right
Bundle Branches -> Ventricular muscle
 Recording the ECG

12 leads ECG include

 6 limb leads ( 3 standard leads, 3 unipolar leads)
 6 chest or precordial leads
 Each lead incorporates two electrodes measuring the
potential or voltage difference between them.
 The positive electrodes detects the electrical impulse
while neutral electrodes completes the circuit.
 The ECG monitor placed in the circuit detects electrical
activity.
 Standard limb leads

 LOCATION:
 Lead 1: the exploring electrode is attached to left arm and neutral to the
right arm
 Lead 2: exploring electrode to the left leg and the neutral electrode to the rt
arm
 Lead 3: exploring electrode to the left leg and the neutral electrode to the
left arm.
 ASSESSMENT:
 Lead 1: Anterior surface of the heart
 Lead 2: Inferior surface of the heart
 Lead 3: Inferior surface of the heart
 Unipolar limb leads

LOCATION:
Exploring electrode is on the rt leg and neutral electrode on all the other
limbs
 Lead AvR attached to right arm
 Lead AvL attached to left arm
 Lead AvF attached to left leg
Where “A” represents augmented.
 ASSESSMENT:
 AvR - (R) side of the heart
 AvL - (L) side of the heart
 AvF – Inferior aspect of the heart
 Chest leads

 LOCATION:
 V1 4th IC space (R)
 V2 4th IC space (L)
 V3 b/w V2 and V4
 V4 5th IC space mid-clavicular line
 V5 5th IC space anterior axillary line
 V6 5th IC space mid-axillary line
ASSESSMENT:
 V1 and V2 assess the right ventricle
 V3 and V4 interventricular septum
 V5 and V6 anterior and lateral aspect of the heart
 ECG
 3 distinct waves
are produced
during cardiac
cycle:
 P wave caused by
atrial
depolarization
 QRS complex
caused by
ventricular
depolarization
 T wave results
from ventricular
repolarization Fig 13.24
13-63
 COMPONENTS OF THE ECG

P – Wave:
 Represents atrial depolarization
 Duration: b/w 0.08 - 0.12 sec
QRS complex:
 Represents depolarization of ventricles
 Duration: b/w 0.08 - 0.10* sec
T – wave:
 Represents ventricular repolarization
U – wave:
 Represents late repolarization after the T – wave
 Of little importance but needs to be recognized so as not to confuse it
with other components
 COMPONENTS OF THE ECG

P – R interval:
 starts at the beginning of the P wave and ends at the onset of the QRS
 Represents the time lapse of the impulse travelling from the SA node
through the AV node on its way to the ventricles.
 No m/s contraction during this event.
 Duration: 0.12 and 0.2 sec
S – T segment:
 starts from the end of the QRS and terminates at the onset of the T
wave. 
 Following completion of ventricular depolarization, there is a period
of electrical inactivity represented by the S – T segment.
 HOW TO READ ECG PAPER
 1 small box represents 0.04 seconds or 1mm
 1 large box represents 0.2 seconds or 5mm
 5 large box  = 1 second 25mm
 30 large box = 6sec
 300 large box = 1 minute
 PR interval (0.20sec) = 1 big box
 QRS complex (0.12 sec*) = 3 small boxes
The normal running speed for recording an ECG is 25mm/sec
ECG PAPER
 Evaluating the ECG Strip

What is the rate and pattern (regularity) of the rhythm? If the R-R interval, that is,
the distance between successive R-waves, is inconsistent, is the pattern irregular?
Does a P-wave precede every QRS complex? This indicates appropriate atrial
activity.
Is there a QRS complex after every P-wave? This indicates appropriate conduction
of impulses from atria to ventricles.
What is the P-R interval? A P-R interval of greater than 0.20 seconds indicates delay
in conduction from atria to ventricles.
Is the QRS complex of normal duration and morphology (shape)? A QRS complex
greater than 0.12 seconds indicates either that an impulse arose within a ventricle
or was conducted abnormally through the ventricular conduction system.
By answering each of these questions, the tendency to "eyeball" the rhythm and
make a quick but inaccurate assessment is avoided.
 Determination of Heart Rate
Method 1

 Find an R-wave located on or near a heavy vertical line.

Proceeding to the left of that R wave, for each
subsequent heavy vertical line, assign the following
numbers: 300 for the first heavy line encountered, 150 for
the next followed by 100, 75, 60, 50, and 42 (Figure 11-5).

 In the following figure , the rate would be estimated as

falling between 100 and 75, or close to 80 beats per
minute (BPM).
Determination of Heart Rate
 Method 2

 Count the number of R-waves within the 6-second recording,

and multiply by lO.

 In Figure The rate of this irregular rhythm is estimated at 60

BPM.
 Summary

 SA node atrial depolarization slight delay in the A V node, 

ventricular depolarization normal sinus rhythm (Figure 1 1-8).
 P-wave precedes every QRS complex and every P-wave is, in turn,
succeeded by a QRS complex. This occurs within an interval of
0.20 seconds (one large box), as determined by the P-R interval.
 The QRS complexes occur within a range of 0.08 to 0.10 seconds
(3 small boxes), indicating that ventricular impulse conduction and
depolarization is occurring in a normal interval.
 The positively deflected T-wave indicates normal ventricular
repolarization.
Evaluation of Rhythms
 Sinus bradycardia

 Sinus bradycardia is a sinus rhythm occurring

at a rate of less than 60 BPM (Figure 11-10).
 This rhythm may significantly reduce cardiac
output, causing hemodynamic compromise,
manifested by hypotension or symptoms
such as dizziness, lightheadedness, or
syncope.
 Sinus tachycardia

 Sinus tachycardia is a sinus rhythm occuring at

a rate of greater than 100 BPM (Figure 11- 1 1).
 Sinus tachycardia, increases myocardial
oxygen demand and the workload on the
heart. This may initiate or exacerbate ischemia
in the presence of coronary artery disease
(CAD).
 Supraventricular tachycardia (SVT)

 Heart rate is rapid exceeding 150 BPM.

 The tachycardia may be sustained, lasting hours or even days, or may be
"paroxysmal" (PSVT), appearing abruptly and spontaneously reconverting to
the previous rhythm within seconds or minutes.
 The P-wave is often not visible and the duration of the QRS complexes occurs
within an appropriate interval. The R-R interval, however, is markedly
shortened.
 Symptoms associated with inadequate cardiac output, such as dizziness,
lightheadedness, and syncope may ensue.
 SVT

 P – waves not
identifiable.
 Duration of
QRS normal.

Figure 11-13 demonstrates supraventricular

tachycardia at a rate of 190 BPM.
 Atrial fibrillation

 Atrial fibrillation is characterized by inconsistent, irregular R-R intervals

with an absence of true P-waves.
 P-waves may be replaced by multiple, fibrillatory F waves of varying
configuration.
 The atria, are not pumping effectively which cause impair ventricular
contraction.
 Figure 11-7 illustrates atrial fibrillation with a "controlled," that is, less
than 100 BPM, ventricular response.
 Pulse monitoring of an individual in atrial fibrillation reveals an
irregularly irregular pattern.
Atrial Fibrillation
 Atrial flutter

 P-waves are replaced by F-waves that have a

distinctive morphology often referred to as a "saw
tooth" or "picket fence" appearance.

 Of clinical importance is the ratio of atrial to

ventricular conduction and whether or not the patient
is hemodynamically stable. 
Atrial Flutter
 Ventricular tachycardia

 This is a serious and potentially lethal arrhythmia that may require

emergency measures be undertaken.
 During v-tach all complexes are ventricular in origin.
 V –tach sometimes occurs in "runs" of three or more ectopic
complexes followed by reversion to the baseline rhythm, or it may be
sustained. Effective circulation may be preserved, or it may be seriously
compromised or absent in sustained v-tach.
 QRS duration greater then 0.12 s
 P and T waves are difficult to distinguish.
 PR interval is not measureable
VT
 Ventricular fibrillation

 (V-fib, VF) is a lethal arrhythmia accompanied by immediate loss of consciousness and

loss of circulation, that is, cardiac arrest.
 It is characterized by disorganized, simultaneous firing of multiple, ectopic
ventricular foci; there is no organized rhythm (Figure 11-21).
 Effective ventricular contraction ceases and cardiopulmonary resuscitation is
indicated until defibrillation is available.
 If not successfully treated, v-fib may further degenerate into asystole, which indicates
complete absence of ventricular electrical activity (Figure 11-21).
 Asystole may also occur as a primary event. This is known as "flat line" rhythm. Like
ventricular fibrillation, asystole requires that cardiopulmonary resuscitation begin
immediately to save the patient's life.
 Care must be taken to distinguish an apparent lethal arrhythmia from lead
disconnection or movement artifact.
 during activity or exercise, movement artifact may easily be mistaken for v-tach.
VF
 Conduction Blocks

 The propagation of a cardiac impulse may be inhibited or terminated

along the conduction pathway.
 Blockage can occur at the sinus node, between the atria and ventricles,
Or within the ventricular conduction system.
 Sinus block occurs if the impulse cannot propagate beyond the sinus
node. In this case, the AV junction usually takes over as the pacemaker,
and a junctional rhythm is seen with the absence of P-waves.
 More common are the AV blocks. They are ranked as first-, second, or
third-degree, depending on the extent of delay or obstruction of the
cardiac impulse between the atria and ventricles.
 First-degree A V block

 First-degree A V block is characterized by a prolongation of

the P-R interval beyond its normal 0.2 seconds (Figure I 1-22).
 Remember that the P-R interval is measured from the
beginning of the P-wave to the beginning of the QRS
complex.Each impulse is delayed between the atria and
ventricles but each eventually reaches the ventricular
conduction system resulting in a normal QRS complex. Thus
for each P wave, there is a QRS complex; therefore the
conduction ratio is 1: 1.
First-degree A V block
 Second-degree A V block

 If the ventricles do not respond to atrial stimuli

the P wave is not followed by QRS complex
 In 2nd degree AV block there is blocked atrial
conduction of varying frequency so not every P
wave is followed by a QRS
 If there is 2 P wave deflections to every
ventricular deflections this is known as 2:1 block. 
SECOND DEGREE AV BLOCK
 Third degree A V block

 Third degree A V block or complete heart block is also known as AV

dissociation.
 In this rhythm (Figure 11-25), P-waves are present, but there is no
relationship between P-waves or QRS complexes.
 P-waves may be superimposed on QRS complexes, but none of the
sinus impulses are conducted to the ventricles
 the atria and ventricles are contracting independently of each other.
 In most cases of third degree block, treatment now includes
implantation of an artificial pacemaker.
 In Figure 11-25, the needlelike spikes indicate that an artificial
pacemaker is depolarizing the ventricles at a rate of 60 BPM.
THIRD DEGREE AV BLOCK
 MYOCARDIAL ISCHEMIA OR INFARCTION

 During myocardial ischemia, blood flow to a portion of

myocardium is compromised, resulting in alteration of
myocardial metabolism.
 If full thickness of heart wall commonly of left ventricle
is depleted of its perfusion this is transmural
infarction,
 S-T segment shift has significant diagnostic value. For
example S-T segment elevation (Figure 11-26) is
associated with transmural Ml.
MYOCARDIAL ISCHEMIA OR
INFARCTION
MYOCARDIAL ISCHEMIA OR INFARCTION

 whereas S-T segment depression is associated with

non transmural or subendocardial MI where
percentage of wall is effected

 Onset of S-T segment depression during activity is

often considered diagnostic of myocardial ischemia.
Figure 11-27 is an example of exercise-induced S-T
segment depression observed in one lead during
exercise.
ST DEPRESSION
MYOCARDIAL ISCHEMIA OR INFARCTION

 A prominent, pathological Q-wave is indicative of a transmural MI (Lilly,

1993).
 "non-Q" is synonymous with nontransmural concerning MI.
 The presence of a prominent Q-wave (Figure 11-28) does not, however,
distinguish between an old or an acute event. 
 The T-wave may also undergo changes during myocardial ischemia or MI.
During ischemia, for example, the T-wave may invert as a result of
prolongation of repolarization (Guyton, 1991).
 Similarly, during MI, changes in the T - wave may "evolve" with the infarct,
at first becoming indistinguishable within an elevated S-T segment, then
inverting, then perhaps reverting to original configuration following the
passage of time.
Q – WAVE
 MI - ECG changes with time
The change that occur on the ECG depict the changing state of
myocardium:
 Within minutes or hours, the ST segment becomes elevated in the leads
facing the infarction.
 Within hours or days, there is development of broad deep Q –waves
with R wave reduction and an inverting T wave.
 Abnormal Q wave is the definitive diagnosis for transmural infarction.
 Within a week or more, there is return of S-T segment to baseline but
the other signs remain same.
 Months later, there is a possible gradual return of the T wave but
persistent abnormal Q waves.
 BUNDLE BRANCH BLOCK
 There is disturbance in the intraventricular conduction.
 QRS complex wide
 2 peaks on R – wave
 P – wave, P-R intervals and heart rate normal.
Depending on which leads demonstrates the changes, it can be
established if the block is a left or right bundle branch block
 Pulmonary embolus

In the acute stage of pul. embolism if the embolus is of

sufficient size to cause right heart strain there may be
 right bundle branch block or
 inverted T waves or
 ST depression in V1 to V3.
 Ventricular Hypertrophy

 In left ventricular hypertrophy there are abnormally

large R waves in V4 and V6
 In right ventricular hypertrophy large R waves in V1
and V2
 This may be accompanied by signs of heart muscle
strain such as ST depression and T wave inversion.
 Brain damage

 Cause of abnormalities in ecg is altered autonomous

tone to the heart.
 Typical findings:
Deep inverted or tall upright T waves and QT interval
prolongation with prominent U waves.
 COPD

 Patients with severe respiratory disease with

pulmonary hypertension may show ECG signs in
keeping with right sided heart strain similar to those
found in pulmonary embolism.