Transcript Definition, leads, limb, augmented limb, precordial, Characteristics

This lecture was conducted during the Nephrology Unit Grand
Ground by Medical Student rotated under Nephrology Division
under the supervision and administration of Prof. Jamal Al
Wakeel, Head of Nephrology Unit, Department of Medicine and
Dr. Abdulkareem Al Suwaida, Chairman of the Department of
Medicine. Nephrology Division is not responsible for the content
of the presentation for it is intended for learning and /or
education purpose only.
ECG Changes in ischemic
disease
Presented by:
Aliaa Ali Al Saffar
Medical Student
December 17, 2008
definition

An electrocardiogram (ECG or EKG) is
a recording of the electrical activity of the
heart over time produced by an
electrocardiograph, usually in a
noninvasive recording via skin electrodes.
Leads

The word lead has two meanings in
electrocardiography: it refers to either the
wire that connects an electrode to the
electrocardiograph, or (more commonly)
to a combination of electrodes that form
an imaginary line in the body along which
the electrical signals are measured.
When a depolarization wavefront (or mean
electrical vector) moves toward a positive
electrode, it creates a positive deflection on the
ECG in the corresponding lead.
 When a depolarization wavefront (or mean
electrical vector) moves away from a positive
electrode, it creates a negative deflection on the
ECG in the corresponding lead.
 When a depolarization wavefront (or mean
electrical vector) moves perpendicular to a
positive electrode, it creates an equiphasic (or
isodiphasic) complex on the ECG.

limb
Leads I, II and III are the so-called limb leads
.
 Lead I is a dipole with the negative (white)
electrode on the right arm and the positive
(black) electrode on the left arm.
 Lead II is a dipole with the negative (white)
electrode on the right arm and the positive (red)
electrode on the left leg.
 Lead III is a dipole with the negative (black)
electrode on the left arm and the positive (red)
electrode on the left leg.

Augmented limb




Leads aVR, aVL, and aVF are augmented limb leads .
Lead aVR or "augmented vector right" has the positive electrode
(white) on the right arm. The negative electrode is a combination of
the left arm (black) electrode and the left leg (red) electrode, which
"augments" the signal strength of the positive electrode on the right
arm.
Lead aVL or "augmented vector left" has the positive (black)
electrode on the left arm. The negative electrode is a combination
of the right arm (white) electrode and the left leg (red) electrode,
which "augments" the signal strength of the positive electrode on
the left arm.
Lead aVF or "augmented vector foot" has the positive (red)
electrode on the left leg. The negative electrode is a combination of
the right arm (white) electrode and the left arm (black) electrode,
which "augments" the signal of the positive electrode on the left leg.
Diagram: Frontal Plane Leads
Precordial
The precordial leads V1, V2, V3, V4, V5,
and V6 are placed directly on the chest.
Because of their close proximity to the
heart, they do not require augmentation.
and these leads are considered to be
unipolar. The precordial leads view the
heart's electrical activity in the so-called
horizontal plane.


Leads V1, V2, and V3 are referred to as the right
precordial leads and V4, V5, and V6 are referred to as
the left precordial leads.

The QRS complex should be negative in lead V1 and
positive in lead V6. The QRS complex should show a
gradual transition from negative to positive between
leads V2 and V4. The equiphasic lead is referred to as
the transition lead. When the transition occurs earlier
than lead V3, it is referred to as an early transition.
When it occurs later than lead V3, it is referred to as a
late transition. There should also be a gradual
increase in the amplitude of the R wave between leads
V1 and V4. This is known as R wave progression.
Poor R wave progression is a nonspecific finding. It can
be caused by conduction abnormalities, myocardial
infarction, cardiomyopathy, and other pathological
conditions.
Characteristics of the Normal
ECG
1. Measurement
2. Rhythm
3. Conduction
4. Waveform Description
Measurements
Heart Rate: 60 - 100 bpm
 PR Interval: 0.12 - 0.20 sec
 QRS Duration: 0.06 - 0.10 sec
 QT Interval (QTc<0.40 sec)

2. Rhythm:
 Normal sinus rhythm
 The P waves in leads I and II must be
upright (positive) if the rhythm is coming
from the sinus node.
Conduction

Normal Sino-atrial (SA), Atrio-ventricular
(AV), and Intraventricular (IV) conduction
Waveform Description
P Wave
During normal atrial depolarization, the main
electrical vector is directed from the SA node
towards the AV node, and spreads from the
right atrium to the left atrium. This turns into
the P wave on the ECG, which is upright in II,
III, and aVF and inverted in aVR A P wave must
be upright in leads II and aVF and inverted in
lead aVR to designate a cardiac rhythm as
Sinus Rhythm .
 P duration < 0.12 sec
 P amplitude < 2.5 mm


P wave rate 60-100 pbm with <10%
variation.
 Rate <60= sinus bradycardia
 Rate >100= sinus tachycardia
 Variation> 10%= sinus arrhythmia

Abnormal P waves : Right atrail hypertrophy
 left atrail hypertrophy
 Atrial premature beat
 hyperkalaemia
Normal Sinus Rhythm
Sinus Bradycardia
SinusTachycardia
QRS Complex

The QRS complex is a structure on the ECG that corresponds to the
depolarization of the ventricles.

QRS duration < 0.10 sec
QRS amplitude is quite variable from lead to lead and from person
to person.

Two determinates of QRS voltages are:
1. Size of the ventricular chambers (i.e., the larger the chamber, the
larger the voltage)
2. Proximity of chest electrodes to ventricular chamber (the closer,
the larger the voltage)

For abnormally wide QRS:
 RBBB
 LBBB
 htperkalaemia
The electrical axis
both I and aVF +ve = normal axis
 both I and aVF -ve = axis in the extreme
right axis deviation
 lead I -ve and aVF +ve right axis
deviation
 lead I +ve and aVF -ve
 lead II +ve = normal axis
 lead II -ve left axis deviation.

causes of extreme right axis deviation.
 emphysema
 hyperkalaemia
 lead transposition
 artificial cardiac pacing
 ventricular tachycardia
causes of right axis deviation
 normal finding in children and tall thin adults
 right ventricular hypertrophy
 chronic lung disease even without pulmonary
hypertension
 anterolateral myocardial infarction
 left posterior hemiblock
 pulmonary embolus
 Wolff-Parkinson-White syndrome - left sided
accessory pathway
 atrial septal defect
 ventricular septal defect
causes of left axis deviation
 left anterior hemiblock
 Q waves of inferior myocardial infarction
 artificial cardiac pacing
 emphysema
 hyperkalaemia
 Wolff-Parkinson-White syndrome - right sided accessory
pathway
 tricuspid atresia
 ostium primum ASD
 injection of contrast into left coronary artery
QT interval
The QT interval is measured from the
beginning of the QRS complex to the end
of the T wave. Normal values for the QT
interval are between 0.30 and 0.44 (0.45
for women) seconds. The most commonly
used method for correcting the QT interval
by dividing the QT interval by sequare
root of preceeding R-R interval.

Causes of long QT interval:
 MI, myocarditis , diffuse myocardial
disease
 Hypocalcaemia, hypotgyrodism
 Subarachnoid haemorrhage, intracerebral
haemorrhage.
 Drugs (sotalol, amiodarone)
ST Segment and T wave
 The normal T wave is usually in the same
direction as the QRS except in the right
precordial leads. In the normal ECG
the T wave is always upright in leads I, II,
V3-6, and always inverted in lead aVR.
Causes of elevation of ST segment: MI( anterior, inferior)
 LBBB
 Normal varients (athletic heart)
 Acute pericarditis.
Causes of depression of ST segment:
 Myocardial ischaemia
 Digoxin effect.
 Ventricular hypertrophy
 Acute post. MI, pulmonary embolus
 LBBB
Causes of tall T waves: Hyperkalaemia.
 Hyperacute myocardial infarction.
 LBBB
Causes of flattened or inverted T waves:
 Age, race.
 hyperventilation
 Anxiety
 LVH
 PE
 Pericarditis, electrolyte imbalance.
The normal U Wave: (the most neglected of the
ECG waveforms)
 U wave amplitude is usually < 1/3 T wave
amplitude in same lead
 U wave direction is the same as T wave direction
in that lead
 U waves are more prominent at slow heart rates
and usually best seen in the right precordial
leads.
 Origin of the U wave is thought to be related to
after depolarizations which interrupt or follow
repolarization.
ECG changes in angina
Resting ECG typically shows ST segment
depression and T wave flattening or
inversion during an attacks.
 Exercise ECG testing is positive in about
75% of people with severe CAD; A normal
test does not exclude the diagnosis.

ECG changes in MI
MI's resulting from total coronary occlusion
result in more homogeneous tissue damage and
are usually reflected by a Q-wave MI pattern
on the ECG. MI's resulting from subtotal
occlusion
result in more heterogeneous damage, which may
be evidenced by a non Q-wave MI pattern
on the ECG. Two-thirds of MI's presenting to
emergency rooms evolve to non-Q wave
MI's, most having ST segment depression or
T wave inversion.


Most MI's are located in the left
ventricle. In the setting of a proximal
right coronary artery occlusion, however,
up to 50% may also have a component of
right ventricular infarctionas well. Rightsided chest leads are necessary to
recognize RV MI.
Acute anterior MI
ST elevation in the anterior leads V1-6,I and AVL
 Reciprocal ST depression in the inferior leads

Acute inferior MI
ST elevation in the inferior leads II, III and aVF.
 Reciprocal ST depression in the anterior leads.

Acute posterior MI
The mirror image of acute injery in leads V1-3
 Tall R rave, tall upright Twave in leads V1-3.
 Usually associated with inferior and/or lateral
wall MI.

Old Inferior MI
A Q wave in lead III wider than 1mm .
 A Q wave in lead AVF wider than 0.5 mm
 A Q wave of any size in lead II.

Anteroseptal MI
The QS complexes, resolving ST segment elevation and T
wave inversions in V1-2 are evidence for afully evolved
anteroseptal MI. The inverted T waves in V3-5, I, aVL
are also probably related to the MI.
Extensive Anterior/Anterolateral
MI
Significant pathologic Q-waves (V2-6, I, aVL) plus marked ST
segment elevation are evidence for this large
anterior/anterolateral MI. The exact age of the infarction
cannot be determined without clinical correlation and previous
ECGs, but this is likely a recent MI.
Postero-lateral MI
The "true" posterior MI is recognized by pathologic R waves in
leads V1-2. These are the posterior equivalent of pathologic Q
waves (seen from the perspective of the anterior leads). Tall
T waves in these same leads are the posterior equivalent of
inverted T waves in this fully evolved MI. The loss of forces in
V6, I, aVL suggest a lateral wall extension of this MI.
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