2. Electrocardiography (ECG)
Electrocardiography (ECG or EKG) is
the process of transthoracic recording of the
electrical activity of heart over a period of
time using electrodes placed on the skin that
detect the tiny electrical changes on the skin
arising from the heart muscle's electro-
physiologic pattern of depolarizing and
repolarizing during each heartbeat.
5. Electrodes and leads:
A "lead" is not the same as an “electrode”
Electrode: a conductive pad in contact with the body that makes an
electrical circuit with the electrocardiograph
Lead: a connector to an electrode. Leads can share the same electrode
Limb leads, "bipolar“ comparison between two electrodes
Precordial leads, "unipolar“ compared to a common lead
Leads are broken down into 3 sets:
Limb
augmented limb
Precordial or chest
The 12-lead EKG has
3 limb leads and 3 augmented limb leads arranged like spokes of a
wheel in the coronal plane (vertical)
6 precordial leads or chest leads that lie on the perpendicular
transverse plane (horizontal)
6.
7. Electrode Placement
RA Right arm
LA In the same location where RA was placed, but on the left arm.
RL On the right leg, lower end of medial aspect of calf muscle.
LL In the same location where RL was placed, but on the left leg.
V1
In the 4th intercostal space along the right sternal border
V2
In the 4th intercostal space along the left sternal border
V3
Between leads V2 and V4.
V4
In the 5th intercostal space in the mid clavicular line
V5
Horizontally even with V4, in the left anterior axillary line
V6
Horizontally even with V4 and V5 in the left mid-axillary line
8.
9. Each electrode consists of an electrically conductive electrolyte gel
(Potassium Chloride) and a silver chloride conductor to permit
electron conduction from the skin to the wire and to the
electrocardiogram.
The common lead, Wilson's central terminal VW
Average of the measurements from the electrodes RA, LA, and LL to
give an average potential across the body:
vW: 1/3 (RA+LA+LL)
Limb leads (Leads I, II and III )
The electrodes that form these signals are located on the
limbs—one on each arm and one on the left leg. The limb
leads form the points of what is known as Einthoven's triangle.
Lead I (LA-RA)
voltage between the (positive) LA electrode and RA electrode
Lead II (LL-RA)
voltage between the (positive) LL electrode and RA electrode
Lead III (LL-LA)
voltage between the (positive) LL electrode and LA electrode
10.
11.
12. Augmented limb leads (aVR, aVL, and aVF)
Derived from the same three electrodes as leads I, II, and III, but use Goldberger's central
terminal as their negative pole.
Goldberger's central terminal is a combination of inputs from two limb
electrodes, with a different combination for each augmented lead. It is referred to
immediately below as "the negative pole".
Lead aVR has the positive electrode on the right arm. The negative pole is a
combination of the left arm electrode and the left leg electrode:
Lead aVL has the positive electrode on the left arm. The negative pole is a combination
of the right arm electrode and the left leg electrode:
Lead aVF has the positive electrode on the left leg. The negative pole is a combination
of the right arm electrode and the left arm electrode:
Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis
of the hexaxial reference system, which is used to calculate the heart's electrical axis in the
frontal plane.
Precordial leads:
lie in the transverse (horizontal) plane, perpendicular to the other six leads.
13.
14.
15. Contiguity of leads:
Each of the 12 ECG leads records the electrical activity of the heart from a
different angle, and therefore align with different anatomical areas of the heart.
Two leads that look at neighboring anatomical areas are said to be contiguous.
Category Leads Activity
Inferior
Leads II, III and
aVF
Look at electrical activity from the vantage point
of the inferior surface
Lateral
I, aVL (High)
V5 and V6 (Low)
Look at the electrical activity from the vantage
point of the lateral wall of left ventricle
Septal V1 and V2
Look at electrical activity from the vantage point
of the septal surface of the heart
Anterior
V3 and V4
Look at electrical activity from the vantage point
of the anterior/ sternocostal surface
16.
17. Interpretation of ECG:
Depolarization of the
heart towards the positive
electrode produces a
positive deflection
Depolarization of the
heart away from the
positive electrode produces
a negative deflection
Repolarization of the
heart towards the positive
electrode produces a
negative deflection
Repolarization of the
heart away from the
positive electrode produces
a positive deflection
18.
19. Thus, the overall direction of depolarization and
repolarization produces a vector that produces
positive or negative deflection on the ECG
depending on which lead it points to.
Electrocardiogram grid
• The horizontal axis represents time and the
vertical axis represents voltage.
• A small box is 1 mm x 1 mm big and represents
0.1 mV x 0.04 seconds.
• A large box is 5 mm x 5mm big and represents 0.5
mV x 0.2 seconds wide.
20.
21. Interpretation of ECG:
Rate
Rhythm
Axis
Waves/ Amplitudes
Intervals & Segments
Heart Rate (Cycles/ minute):
SA Node, located in the postero-superior wall of the right atrium
the heart’s pacemaker & the dominant center of automaticity,
generates a sinus rhythm, pacing the heart at 60-100 beats/ minute
To look for: Sinus Bradycardia (<60/min)
Sinus Tachycardia (>100/min)
To find out heart rate, look at the R waves
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30. Normal Sinus Rhythm: Cycles of equal length
• Pacing of all automaticity foci with the consistent duration between
similar waves, maintaining the regular cadence of depolarization
stimuli for SA node pace-making at a constant, unvarying rate
• Cycles of equal length are produced
• The prototypical pattern of P wave, QRS complex, and T wave.
Generally, deviation from normal sinus rhythm is considered a
cardiac arrhythmia.
• A criterion for sinus rhythm is that P waves and QRS complexes
appear 1-to-1, thus implying that the P wave causes the QRS
complex.
31.
32. Cardiac Axis:
The heart has several
axes, but the most
common by far is the
axis of the QRS
complex
Beyond +105° is
right axis
deviation
Beyond −30° is
left axis deviation
The third quadrant
of −90° to −180°
is very rare and is
an indeterminate
axis
33. Classification Angle Notes
Normal −30° to 105° Normal
Left Axis Deviation −30° to −90°
• Left Ventricular
Hypertrophy
• Left anterior fascicular
block
• An old inferior q wave
myocardial infarction
Right Axis Deviation +105° to +180°
• Right ventricular
hypertrophy
• Left posterior
fascicular block
• An old lateral q wave
MI
Indeterminate axis +180° to −90° Rarely seen
34.
35. Amplitudes and intervals:
Each 1 mm (one small box on the standard EKG paper) represents
40 milliseconds of time on the x-axis, and 0.1 millivolts on the y-
axis.
P wave (<80 milliseconds)
2 or <2 small squares
• typically upright in most leads except for
aVR
• Unusually long duration represents atrial
enlargement.
• A large right atrium a tall, peaked p-wave
• A large left atrium Bifid p-wave
36.
37. PR Interval (120-200 ms)
3-5 small squares
measured from the beginning of the P
wave to the beginning of the QRS
complex.
• This interval reflects the time the
electrical impulse takes to travel
from the sinus node through the AV
node.
• <120 ms the electrical impulse is
bypassing the AV node, as in Wolf-
Parkinson-White syndrome
• Consistently >200 ms first
38. QRS Complex (80-100 ms/ <120ms)
<3 small squares
• represents the rapid depolarization of right & left
ventricles
• Large ventricular muscle mass compared to the atria
Much larger amplitude
• Wide (>120ms)Disruption of the heart's
conduction system, such as in LBBB, RBBB
• Unusually tall left ventricular hypertrophy
• Very low-amplitude QRS complex
pericardial effusion
Q waves can be normal or abnormal.
Abnormal indicate an ongoing or old MI.
Pathologic Q wave: duration of > 40 milliseconds (1 small box)
or size > 25% of the QRS complex amplitude.
39. J-point
• The point at which
the QRS complex
finishes and the ST
segment begins
• A separate J wave
or Osborn
wave at the J point
is pathognomonic of
hypothermia
or
hypercalcemia
ST Segment
• the period when the
ventricles are
depolarized
• May be depressed/
elevated with MI/
ischemia
• ST depression can
also be caused by
LVH or digoxin
toxicity
• ST elevation by
pericarditis, Brugada
syndrome, or can be
a normal variant (J-
point elevation)
40. T wave (160 ms)
• represents the
repolarization of
ventricles
• Upright in all leads
except avR & V1
• Inverted T waves can
be a sign of myocardial
ischemia, LVH, high
intracranial pressure
• Peaked T waves can
be a sign of hyperkalemia
or very early myocardial
infarction
Corrected QT interval
(QTc)
<440 ms
• from the beginning of the QRS
complex to the end of the T
wave.
• Variation with heart rate, so it
must be corrected to the QTc
by dividing by the square root
of the RR interval with QT
• Prolonged a risk factor for
ventricular tachyarrhythmias
and sudden death.
• Unusually short QTc severe
hypercalcemia
41. U wave:
• Hypothesized to be caused by the
repolarization of the interventricular
septum
• Normally low amplitude, and even
more often completely absent
• Very prominent suspect
hypokalemia, hypercalcemia or
hyperthyroidism
42.
43. Myocardial infarction (MI), commonly known as a heart attack,
occurs when blood flow decreases or stops to a part of the heart,
causing damage to the heart muscle
Diagnostic Criteria:
An acute myocardial infarction, according to current consensus, is
defined by an elevated cardiac biomarker and at least one of the
following:
• Symptoms relating to ischemia
• Changes on an electrocardiogram (ECG), such as ST segment
changes, or Q waves
• Changes in the motion of the heart wall on imaging
• Demonstration of a thrombus on angiogram or at autopsy
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51. Treatment:
Presumptive ACS are typically treated with aspirin, clopidogrel or ticagrelor,
nitroglycerin, and if the chest discomfort persists morphine.
Angiography is recommended in those who have either new ST elevation or a new
left bundle branch block on their ECG.
STEMI
If the ECG confirms changes suggestive of myocardial infarction
• Thrombolytics: medication is injected that stimulates fibrinolysis,
destroying blood clots obstructing the coronary arteries
• Primary Coronary Angioplasty: a flexible catheter is passed via the
femoral or radial arteries and advanced to the heart to identify occlusions. When
found, they can be intervened upon mechanically with angioplasty and usually
stent deployment.
• The time frame for door-to-needle thrombolytic administration according to
American College of Cardiology (ACC) guidelines should be within 30 minutes,
whereas the door-to-balloon Percutaneous Coronary Intervention (PCI) time
should be less than 90 minutes.
52. NSTEMI and NSTE-ACS:
If the ECG does not show typical changes, the term "non-ST
segment elevation ACS" is applied.
• The accepted management of unstable angina and NSTE acute
coronary syndrome is
• Empirical treatment with aspirin, a second platelet inhibitor such
as clopidogrel, prasugrel or ticagrelor, and heparin (usually a
low-molecular weight heparin), with intravenous glyceryl
trinitrate and opioids if the pain persists.
• A blood test is generally performed for cardiac troponins twelve
hours after onset of the pain. If this is positive, coronary
angiography is typically performed on an urgent basis, as this is
highly predictive of a heart attack in the near-future.
• If the troponin is negative, a treadmill exercise test or a thallium
scintigram may be requested.