Electrocardiography

Dr Uwanuruochi Kelechukwu
 Defination
• Electrocardiography is the graphic display of
the hearts integrated current, as voltage
changes over time
• Or the process of producing a graphic record
of the electrical activity of the heart, voltage
versus time, using electrodes placed on the
skin.
 Introduction
• Membrane potential (also transmembrane
potential or membrane voltage) is the
difference in electric potential between the
interior and the exterior of a cell. With respect
to the exterior of the cell, typical values of
membrane potential ranges from –40 mV to
–80 mV.
• Action potential in a neuron, showing depolarization, in which the cell's
internal charge becomes less negative (more positive), and repolarization,
where the internal charge returns to a more negative value.
 Introduction
• Action potential occurs when the membrane
potential of a specific cell location rapidly rises
and falls: this depolarisation then causes
adjacent locations to similarly depolarise.
Action potentials occur in several types of
animal cells, called excitable cells, which
include neurons, muscle cells,
 Introduction
• Depolarization is a change within a cell, during
which the cell undergoes a shift in electric
charge distribution, resulting in less negative
charge inside the cell.
• Electrical depolarisation of myocardial tissue
produces a small current which can be
detected by electrode pairs on the body
surface
 Uses of Electrocardiogram
• The ECG is used to assess cardiac rhythm and
conduction.
• It provides information about chamber size
• Assesses for myocardial ischaemia and
infarction.
 The Electrocardiogram
• During sinus rhythm, the SA node triggers atrial
depolarisation, producing a P wave.
• Depolarisation proceeds slowly through the AV
node, which is too small to produce a depolarisation
wave detectable from the body surface.
• The bundle of His, bundle branches and Purkinje
system are then activated, initiating ventricular
myocardial depolarisation, which produces the QRS
complex.
 The Electrocardiogram
• The muscle mass of the ventricles is much
larger than that of the atria, so the QRS
complex is larger than the P wave.
• The interval between the onset of the P wave
and the onset of the QRS complex is termed
the ‘PR interval’ and largely reflects the
duration of AV nodal conduction
 Injury to fascicles
• Selective injury of one of the left fascicles
(hemiblock) affects the electrical axis.
 QRS Axis Determination:
• First look for an isoelectric lead if there is one;
it’s the lead with equal QRS forces in both
positive and negative direction. This is often the
lead with the smallest QRS complex.
• The correct QRS axis is perpendicular (i.e., right
angle or 90 degrees) to that lead's orientation.
Since there are two possible perpendiculars for
each isoelectric lead, one must chose the one
that best fits the direction of the QRS forces in
other ECG leads
 Axis Determination
• If there is no isoelectric lead, there are usually
two leads that are nearly isoelectric, and these
are usually always 30° apart.
• Find the perpendiculars for each lead and
chose an approximate QRS axis within the 30°
range.
Analysis
1.Lead aVR is the smallest and nearly isoelectric.
2.The two perpendiculars to aVR are -60° and +120°.
3.Note that Leads II and III are mostly negative
4.The axis, therefore, has to be-60° (LAD)
• Analysis
• 1.Lead aVR is closest to being isoelectric (but slightly more positive than negative)
• 2.The two perpendicularsto aVRare -60° and +120°.
• 3.Note that Lead Iis mostly negative; lead III is mostly positive.
• 4.Therefore the axis is close to +120°. Because aVR is slightly more positive, the axis is slightly
beyond +120° (i.e., closer to the positive right arm for aVR, ~ +125º)
 Injury to bundles
• Injury to the left or right bundle branch delays
ventricular depolarisation, widening the QRS
complex.
 The Electrocardiogram (contd)
• Repolarisation is a slower process that spreads
from the epicardium to the endocardium.
Atrial repolarisation does not cause a
detectable signal but ventricular repolarisation
produces the T wave.
• The QT interval represents the total duration
of ventricular depolarisation and
repolarisation.
 ECG conventions
• Depolarisation towards electrode: positive deflection
• Depolarisation away from electrode: negative
deflection
• Sensitivity: 10 mm = 1 mV
• Paper speed: 25 mm per second
• Each large (5 mm) square = 0.2 s
• Each small (1 mm) square = 0.04 s
• Heart rate = 1500/small squares in RR interval (i.e.
300 ÷ number of large squares between beats)
 The standard 12-lead ECG
• generated from ten electrodes that are attached to the skin
• Lead I records the signal between the right (-ve) and left (+ve)
arms. Lead II records the signal between the right arm (-ve) and
left leg (+ve). Lead III records the signal between the left arm (-ve)
and left leg (+ve).
• Leads aVR, aVL and aVF are the augmented voltage limb leads.
These record electrical activity between a limb electrode and a
modified central terminal.
• lead aVL records the signal between the left arm and a central
terminal formed by connecting the right arm and left leg
electrodes, aVR central terminal connects left arm and left leg,
aVF central terminal connects right arm and left arm.
• The average vector of ventricular
depolarisation is the axis. When the vector is
at right angles to a lead, the depolarisation in
that lead is equally negative and positive
(isoelectric).
• There are six chest leads, V1–V6. Leads V 1
and V2 lie approximately over the RV, V3 and
V4 over the interventricular septum, and V5
and V6 over the LV
 Precordial lead placement
• V1: 4th intercostal space (IS) adjacent to right
sternal border
• V2: 4th IS adjacent to left sternal border
• V3: Halfway between V2 and V4
• V4: 5th IS, midclavicular line
• V5: horizontal to V4; anterior axillary line
• V6: horizontal to V4-5; midaxillary line
• The LV contributes the major component of the
QRS complex.
• Depolarisation of the interventricular septum
occurs first and moves from left to right; this
generates a small initial negative deflection in lead
V6 (Q wave) and an initial positive deflection (R) in
lead V1.
• The second phase of depolarisation is activation of
the body of the LV, which creates a large positive
deflection (R) in V6 (with reciprocal changes in
V1).
• The final phase of depolarisation involves the RV
and produces a small negative deflection (S) in V 6.
• Activation of the septum occurs first (red arrows),
• followed by spreading of the impulse through the LV (blue arrows)
and then the RV (green arrows )
 ECG INTERPRETATION
• It is important to follow a standardized sequence of
steps in order to avoid missing abnormalities in the
ECG tracing. The 6 major sections are:
• 1. Measurements
• 2. Rhythm Analysis
• 3. Conduction Analysis
• 4. Waveform description
• 5. Final Interpretation
• 6. Comparison (if available) to previous ECG
 1. MEASUREMENTS
• Heart rate (state both atrial and ventricular
rates, if different)
• PR interval (from beginning of P to beginning
of QRS complex)
• QRS duration (width of most representative
QRS)
• QT interval (from beginning of QRS to end of T)
• QRS axis in frontal plane-limb leads
 2. RHYTHM ANALYSIS:

• State the basic rhythm (e.g., "normal sinus

rhythm", "atrial fibrillation", etc.)
• Identify additional rhythm events if present
(e.g., "PVC's", "PAC's", etc.)
• Remember that arrhythmias may originate in
the atria, AV junction, and ventricles
Afib with rapid ventricular response
1. Nonconducted (or blocked) PAC; i.e., no QRS complex because the early
PAC finds the AV node still refractory to conduction. (See PAC 'a' in the
diagram above, and the nonconducted PAC in ECG shown below (red arrow);
note that it’s hidden and slightly distorts the ST-T wave). Note also that the
last sinus P wave has been ‘reset’ by the PAC resulting in an incomplete
pause.
 • Ectopic Atrial Tachycardia and Rhythms
• Ectopic, discrete looking, unifocal P waves
with atrial rates <250/min.
• Ectopic P’ waves usually precede QRS
complexes with P'R interval < RP' interval.

• The above V1 strip begins with a sequence of 3 sinus

beats followed a PVC and one more sinus beat; after
this 4th sinus beat note the onset of an ectopic atrial
tachycardia (HR >100 bpm) and different, unifocal P
wave morphology).
• typical VT: 1) QRS morphology in lead V1: the
notch is on the downstroke of the R wave;
• 2) the QRS is mostly negative in lead V6;
• 3) bizarre northwest QRS axis of -180 degrees
-(QRS axis from +180 degrees to -90 degrees or NW quadrant)
suggests ventricular tachycardia )
 3. CONDUCTION ANALYSIS:

• "Normal" conduction implies normal sino-atrial

(SA), atrio-ventricular (AV), and intraventricular (IV)
conduction.
Conduction abnormalities may include
• 2nd degree SA ‘exit’ block (type I, type II, or
uncertain)
• 1st, 2nd (type I or type II), and 3rd degree AV block
• IV blocks: bundle branch, fascicular blocks
 Type II 2nd degree SA Block:
• PP intervals are fairly constant (unless sinus
arrhythmia present) until conduction failure
occurs.
• The pause is approximately twice the basic PP
interval
 CONDUCTION ABNORMALITIES
• 1st Degree AV Block: PR interval > 200 ms; all P
waves conduct and are followed by QRS
complexes.
• Type I (Wenckebach) 2nd degree AV block
• Type II (Mobitz) 2nd degree AV block
• In the lower strip (LBBB) there is 2:1 conduction and several
longer RR intervals where multiple P waves are nonconducted
 Complete (3rd Degree) AV Block:
• Usually there is complete AV dissociation
because the atria and ventricles are each
controlled by independent pacemakers
• 3rd degree AB block
• The sinus rhythm is ~85 bpm (arrows), but it is
often reset by nonconducted PAC’s (*).
The wide QRS rhythm (~48 bpm) is either
a junctional escape rhythm with RBBB or a left
ventricular escape rhythm. Complete AV
dissociation is present. The last QRS is a PVC.
 4. WAVEFORM DESCRIPTION:
• Carefully analyze each of the12-leads for abnormalities of the
waveforms in the order in which they appear: P-waves, QRS
complexes, ST segments, T waves, U waves.
• P waves: are they too wide, too tall, look abnormal (i.e., are they
ectopic), etc.?
• QRS complexes: look for pathologic Q waves, abnormal voltage, etc.
• ST segments: look for leads with abnormal ST elevation and/or
depression.
• T waves: look for abnormally inverted T waves or unusually tall T
waves (hyperk).
• U waves: look for prominent (hypok) or inverted U waves (Ischemia
of LAD).
• Acute anteroseptal MI; marked ST elevation in
V1-3 with poor R wave progression V1-4 (note
convex-up ST elevation in V1-2).
• ECG changes in AMI
• A. Normal ECG waveform prior to the onset
of plaque rupture
• B. Hyperacute T wave changes - increased T
wave amplitude and width; QT may prolong;
may also see early ST segment elevation
• C. Marked ST elevation with hyperacute T
waves (“tombstone” pattern)
• D. Pathologic Q waves appear (cell necrosis),
ST elevation decreases, T waves begin to
invert (this is also called the "fully evolved"
phase)
• E. Pathologic Q waves, T wave inversion
(necrosis and fibrosis)
• F. Pathologic Q waves, upright T waves
(fibrosis)
• (G). Q waves may get smaller or disappear
with time
 5. FINAL ECG INTERPRETATION:

• Interpret the ECG as "Normal", or "Abnormal".

Examples of "abnormal" statements are:
• Left ventricular hypertrophy (LVH)
• Right atrial enlargement (RAE)
• Nonspecific ST-T wave abnormalities
• Specific rhythm abnormalities such as atrial fibrillation
• Inferior MI, probably acute
• Old anteroseptal MI
• Left anterior fascicular block (LAFB)