2. Outline
• Objectives
• Overview
• Electrocardiogram (ECG) waves
• Types of ECG Leads
• Application of ECG
– Vectorial Analysis of Potentials Recorded in Different
Leads
• Interpretation of abnormal ECG tracing
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3. Objectives
At the end of this session the students will able to:
• Explain the way electrocardiogram (ECG) is recorded.
• Discuss the normal waves, segments & intervals of the
ECG.
• Describe the relationship of the ECG to the electrical
axis of the heart.
• Differentiate normal and abnormal ECG tracing.
3
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4. 4
Electrocardiography Overview
The technique was developed by the Dutch physiologist
named Willem Einthoven.
Electrocardiogram (ECG) is the record of electrical
activity of the heart that is conducted through the body
fluid.
It is recorded from the surface of the body using highly
sensitive electrodes.
It is the algebraic sum of the action potentials of cardiac
muscle fibers during each cardiac cycle.
ECG provides events about arrhythmia, hypertrophy,
myocardial damage (ischemia and necrosis).
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5. Electrocardiography Overview…
ECG Conventions
• Each mm in the horizontal
direction is 0.04 second.
• 1mV input→10mm
deflection (vertical)
• Paper speed =25mm/sec.
• Recording points =wrist,
ankle, skin on chest
– Right leg = ground (earth)
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6. Electrocardiography Overview…
• The direction of deflection of the ECG trace indicates
the relationship between the direction of the vector of
the electrical current flow and the axis of the lead.
– An upward deflection on an ECG means the current flow
vector is toward the positive electrode
– A downward deflection means the current flow vector is
toward the negative electrode.
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7. Electrocardiogram
• There are two major components of
an ECG:
– Waves &
– Segments
• Waves appear as deflections above
or below the baseline.
• Segments are sections of baseline
between two waves.
• Intervals are combinations of
waves and segments.
• Different waves of the ECG reflect
depolarization or repolarization of
the atria and ventricles.
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8. Electrocardiogram...
• The P-wave is produced by atrial
depolarization.
• The QRS-complex by ventricular
depolarization.
• The T-wave by ventricular
repolarization.
• The U wave is due to slow
repolarization of the papillary
muscles.
• Atrial repolarization is masked by
QRS complex.
• PR interval: The time between the
beginning of the P wave and the QRS
complex.
– Atrial depolarization and conduction
through AV node & bundle.
• QT Interval: depolarization and
repolarization of the ventricle. 8
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Normal Durations in seconds
Intervals/waves Average Range Events in the Heart during Interval
P-Wave duration 0.08-0.1 Complete Atrial Depolarization
PR interval 0.18 0.12–0.20 Atrial depolarization and conduction through
AV node
QRS duration 0.08 0.06 - 0.1 Ventricular depolarization and atrial
repolarization
QT interval 0.40 0.35-0.43 Ventricular depolarization plus ventricular
repolarization
ST interval (QT
minus QRS)
0.32 0.30 - 0.33 Ventricular repolarization
ECG Waves & Intervals durations
Electrocardiogram...
11. Electrocardiogram...
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During atrial
depolarization current
spreads from the right
atrium downward toward
the atrioventricular (AV)
junction and left leg.
During ventricular depolarization
• Spread of ventricular depolarization
consists of two major sequential
phases:
Septal depolarization (left to right)
Spread of depolarization from apex
to base in to out
12. Electrocardiographic Leads
• Electrocardiographic lead is a combination of two wires
and their electrodes to make a complete circuit between
the body and the electrocardiograph.
• Twelve leads are used for ECG tracing:
– Three bipolar leads
– Nine unipolar leads
A. Bipolar Leads
• The standard limb leads—leads I, II, and III—each
record the differences in potential between two limbs.
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13. Electrocardiographic Leads...
Lead I
• In lead I, the negative terminal of
the electrocardiograph is
connected to the right arm and
the positive terminal to the left
arm.
• An upward deflection is recorded
when the left arm becomes
positive relative to the right.
Lead II
• In lead II, the electrodes are on
the right arm and left leg, with
the leg positive. 13
14. Electrocardiographic Leads...
• When the right arm is
negative with respect to
the left leg, the
electrocardiograph
records positively.
Lead III
• In lead III, the electrodes
are on the left arm and left
leg, with the leg positive.
• The electrocardiograph
records positively when
the left arm is negative
with respect to the left leg.
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15. Electrocardiographic Leads...
• Normal electrocardiograms recorded from the three
standard electrocardiographic leads:-
– The P-wave is up ward
– The QRS-complex is mainly up ward in all the three leads.
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16. Electrocardiographic Leads...
Einthoven’s Triangle:
• The bipolar standard limb
leads form equilateral
triangle of Einthoven drawn
around the heart.
• Einthoven’s law: If
electrical potentials of any
two of the three leads are
given, the 3rd one can be
determined by:
– Lead II = Lead I+ Lead III,
can estimate electric potential
of each of the leads.
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17. Electrocardiographic Leads...
B. Unipolar (V) Leads
• There are additional nine
unipolar leads that record the
potential difference b/n an
exploring electrode and an
indifferent electrodes.
Chest Leads (Precordial
Leads)
• There are six unipolar
chest leads designated
V1–V6.
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18. Electrocardiographic Leads...
• Chest lead records mainly the electrical potential of
the cardiac musculature immediately beneath the
electrode.
• In leads V1 and V2, the QRS recordings of the
normal heart are mainly negative (down ward).
Conversely, the QRS complexes in leads V4,V5, and V6 are mainly positive
(upward) b/c the chest electrode in these leads is nearer the heart apex.
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19. Electrocardiographic Leads...
Augmented limb leads
• There are three unipolar limb leads.
• In this type of recording, two of the limbs are connected
to the negative terminal of the electrocardiograph and
the third limb is connected to the positive terminal.
• When the positive terminal is on the right arm:
– The lead is known as the aVR lead;
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20. Electrocardiographic Leads...
– When on the left arm, the aVL lead;
– When on the left leg, the aVF lead
• Normal recordings of the augmented unipolar limb
leads are all similar to the standard limb lead
recordings, except that the recording from the aVR
lead is inverted.
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22. Acceptable Variations in Normal ECG
P wave
• The P wave is normally upright in all leads except aVR.
• When the QRS complex is predominantly downward in
lead V1, the P wave may also be inverted.
QRS complex
• In most people the QRS complex is tallest in lead II, but
in leads I and III the QRS complex is also predominantly
upright.
• It is common for the S wave to be greater than the R wave
in lead III, and the cardiac axis can still be considered
normal when the S wave equals the R wave in lead II.
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23. Acceptable Variations in Normal ECG…
The size of R and S waves in the chest leads
• In lead V1 there should be a small R wave and a deep
S wave, and the balance between the two should
change progressively from V1-V6.
• In lead V6 there should be a tall R wave and no S
wave.
– Balance between R wave and S wave is significant for
identifying a degree of cardiac axis deviation.
Q waves
• Is the normal depolarization of the interventricular
septum from left to right.
• Seen in any of leads I, II, aVL, or V4-V6.
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24. Acceptable Variations in Normal ECG…
• Septal Q waves are usually less than 2 mm deep and
less than 1 mm across.
The ST segment
• Should be horizontal and 'isoelectric‘
• But occasionally slopes upwards in leads V2-V5 after
deep S wave.
The T wave
• In a normal ECG the T wave is always inverted in
lead aVR & V1 but is usually upright in all the other
leads.
• The T wave is the most variable part of the ECG.
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25. Acceptable Variations in Normal ECG…
• U waves are commonly seen in the anterior chest
leads of normal ECGs.
• It is thought to represent repolarization of the
papillary muscles.
• A U wave is probably only important if it follows a
flat T wave.
– Which is the characteristic of hypokalaemia.
Variations in ECG pattern in athletes:
– Tall P waves (>2.5mm)
– Tall R waves and deep S waves
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26. Acceptable Variations in Normal ECG…
• Prominent septal Q waves
• Slight ST segment elevation
• Tall symmetrical T waves
• T wave inversion, especially in lateral leads
• Prominent U waves
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27. Application of ECG
• By analyzing electrical potential fluctuations in
ECG record, one can gate some insight into:
– Heart rate determination.
– Anatomical orientation of the heart.
– Relative size of heart chambers (Hypertrophy).
– A variety of disturbances of rhythm and
conduction block.
– Extent, location and progress of ischaemic heart
disease (e.g. myocardial infarction).
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28. Vectorial Analysis of Potentials Recorded in Different
Leads
• During ventricular
depolarization, current
flows mainly downward
from the base of the
ventricles toward the
apex than in the upward
direction.
• This is shown by the
summated vector of the
potential generated.
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29. Vectorial Analysis of Potentials Recorded in
Different Leads...
• Axes of the three bipolar
and three unipolar limb leads
are placed with their relative
axis and angles.
• The direction from negative
to positive electrode is called
axis of the lead.
• In lead I, the electrodes lie in
the horizontal direction with
the positive electrode to the
left; the axis of lead I is,
therefore, 0 degree.
• From this zero reference point,
the scale of vectors rotates
clockwise.
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30. Vectorial Analysis of Potentials Recorded in
Different Leads...
Mean electrical axis of the
heart
• Mean electrical axis of the
ventricles [vector showing
current flows from base of
ventricles (-ve) toward
apex (+ve)].
• It is determined from
standard limb leads
• Normal mean electrical
axis of the heart is about
59-60o.
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31. Vectorial Analysis of Potentials Recorded in
Different Leads...
• The normal mean QRS vector in the frontal plane is b/n
-30o and +110o.
• Mean QRS vectors greater than +110o are said to
represent right axis deviation.
– Right axis deviation suggests right ventricular hypertrophy
– Right bundle branch block
• Right ward angulation of the heart:
– At the end of deep inspiration,
– Normally in tall, lanky people whose hearts hang downward.
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33. Vectorial Analysis of Potentials Recorded in
Different Leads...
• Those less than -30o are designated as left axis
deviation.
– Left axis deviation may be due to left ventricular
hypertrophy
– Left bundle branch block
• Left side shift of the heart itself cause left axis
deviation.
• Such shift occurs:
– At the end of deep expiration
– Common in obese people
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36. ECG manifestation of Atrial
Enlargement
• Right atrium (RA)
enlargement may cause tall,
peaked P waves in the
extremity or chest leads.
• Left atrium (LA)
enlargement may cause
broad, often notched P waves
in the extremity leads and a
biphasic P wave in lead V1
with a prominent negative
component representing
delayed depolarization of
the left atrium.
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37. ECG manifestation of hypertrophied
ventricles
• Left ventricular
hypertrophy causes deeper
right precordial S-waves
and taller left precordial
R- waves.
• By contrast, right
ventricular hypertrophy
shifts the QRS vector to
the right, causing
increased right precordial
R waves.
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38. Rhythm and Conduction abnormalities
of the heart
Conduction Block
• This may occur anywhere between the S.A node and
the ventricles.
• A block between the SA node and the AV node occurs
very rarely.
• One of the more common sites of block is A-V node.
• Three degrees of heart block are usually
distinguished:
1. First degree heart block
– PR interval prolonged, >0.21 sec
– Usually due to A-V nodal delay
• May be caused by increased vagal tone or systemic
diseases.
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39. Conduction Block
• Has no effect on the pumping ability of the ventricles
2. Second Degree Heart Block
• Associated with organic heart disease
• Not all P waves are followed by QRS complexes.
a. Partial progressive AV block.
PR interval increases progressively leading to
dropped beat, 2:1 block)
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40. Conduction Block
b. Constant block: PR interval relatively fixed; the
atrio-ventricular rate is a constant small number ratio,
e.g. 2:1, 3:1
3. Third Degree (complete) Heart Block
• Impulses completely interrupted between atria and
ventricles:
QRS complexes dissociated from P waves
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41. Conduction Block
Results either from His bundle disease or from bilateral
bundle branch block
Ventricular rate much slowed (35-40 beats/min)
Fainting often occurs due to cerebral ischaemia
• Cause: organic heart disease is often the cause.
• Significance: May be associated with prolonged
ventricular stand still.
• If cardiac arrest prolonged, can lead to cerebral
ischemia, syncope, or death.
• This condition is termed Stokes-Adams Syndrome.
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42. Arrhythmias
• Abnormal impulse initiation or impulse propagation.
Disturbances of impulse initiation include:
– Those arise from the SA node
• SA node dysfunction bradycardia
• Sympathetic stimulation of SA node tachycardia
– Those originate from various ectopic foci
Possible causes of ectopic foci are:
1. Local areas of ischemia
2. Toxic irritation of the A-V node, Purkinje system, or
myocardium caused by drugs, nicotine, or caffeine.
3. Mechanical initiation of premature contractions
during cardiac catheterization.
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43. Arrhythmias…
Disturbances of impulse propagation:
– Conduction blocks and
– Reentrant rhythms
• Additional aberrant muscular or nodal tissue connection
(bundle of Kent) b/n the atria and ventricles.
– This conducts more rapidly than the slowly conducting AV
node, and one ventricle is excited early.
• Circus movements can also established in the atrial or
ventricular muscle fibers.
• Ectopic foci & re-entrant are the most common cause
of tachyarrhythmia.
• Tachy-arrhythmias can be classified as supra-
ventricular or ventricular tachycardia.
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44. Type Conditions of Heart
1. Extra systole (premature
beat)
•Abnormal contraction produced during diastole
•Caused by an ectopic foci
•It could be atrial, nodal or ventricular extra systole
•Absence of pulse (may not cause 2nd heart sounds)
•Have no pathologic significance
1.1. Atrial extra systoles •Abnormal P wave but normal QRS complex
•Absence of pulse
•Atrial premature beats often interrupt and "reset" the
normal rhythm.
1.2. Ventricular extra systole •The QRS complex of the extra systole is usually
considerably prolonged.
• After almost all extra systole, the T wave has an
electrical potential polarity exactly opposite to that of
the QRS complex.
Arrhythmias…
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46. Arrhythmias…
2. Paroxysmal atrial
tachycardia (PAT)
•Atrial beat >160 beats/min
•Caused by ectopic focus
•May be associated with ventricular tachycardia
that pumping capacity of the heart.
3. Paroxysmal ventricular
tachycardia (PVT)
•Ventricular beat =200 beats/min,
• Caused by ectopic focus
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47. 47
4. Atrial flutter
• Fast and regular atrial beats (200-400 b/min).
• Different parts contracting
• Caused by re-entry –a wave of excitation
propagating continuously within a closed circuit-a
ring-like pathway around ends of vena cavae
• 3:2, 3:1 AV block (AV node cannot conduct more
than about 230 impulses per minute)
5. Atrial fibrillation
• Fast and irregular uncoordinated atrial beats (400-
600 b/min), dissociated from ventricular beat
• Small and numerous waves in ECG.
• Caused by multiple re-entry.
• May be caused by: mitral valve disease, coronary
atherosclerosis, thyrotoxicosis, etc.
6. Ventricular
fibrillation
• Fast and irregular uncoordinated QRS and
ventricular beats (400-600b/min)
• Caused by multiple re-entry
• Circulation stops
• May lead to death if defibrillation was not performed
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50. Voltage Abnormalities
• Determined by making use of the convention for
voltage calibration.
Increased voltage
• If the sum of QRS of 3 standard leads is greater than
4mV, then the heart is said to be hypertrophic.
• Caused by pressure and volume overload
hypertrophy.
• Decreased voltage
Caused by:
• Muscle abnormalities-like myocardial infarction
• Conduction problem like 1st to 3rd degree heart
block
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51. Myocardial Ischemia and Infarction
• ECG findings of ischemic heart disease vary
considerably, depending on four major factors:
1. The duration of the ischemic process (acute versus
chronic);
2. Its extent (large versus small);
3. Its topography (anterior versus posterior and right
ventricular); and
4. The presence of other underlying abnormalities (e.g.
BBB) that can mask or alter the classic patterns.
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52. Myocardial Infarction
• A sudden, irreversible,
ischemic injury due to
coronary arterial
narrowing or occlusion
with sustained damage
to a portion of the
myocardium.
Elevation of the ST
segment at early stage
return to normal on
overlaying leads.
Leads on the opposite
side of the heart show
ST segment depression.
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Hours few days days to weeks Very late
pattern
53. Myocardial Infarction…
• Profound ST elevation or depression in multiple leads
usually indicates very severe ischemia.
• Prompt resolution of ST elevation is a specific marker
of successful reperfusion.
• Within a period ranging from hours to days T wave
inversion appear.
– T wave inversion correlates with increased ventricular
depolarization duration.
• Other common changes in infarcted area include the
appearance of a Q wave in some of the leads in which
it was not previously present and an increase in the
size of the normal Q wave in some of the other leads.
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55. Myocardial Infarction…
• The electrocardiographic leads are more helpful in
localizing regions of transmural than subendocardial
ischemia.
• For examples, ST elevation can be seen in the following:
One or more of the precordial leads (V1 through V6) and
in leads I and aVL with acute transmural anterior or
anterolateral wall ischemia;
Leads V1 to V3 with anteroseptal or apical ischemia
Leads V4 to V6 with apical or lateral ischemia;
Leads II, III, and aVF with inferior wall ischemia; and
Right sided precordial lead with right ventricular
ischemia.
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57. Effects of Ionic imbalance on ECG tracing
• Changes in ECF Na+ and K+ concentration would be
expected to affect the potentials of the myocardial
fibers.
• Fall in the plasma level of Na+ may be associated
with low-voltage electrocardiographic complexes.
• Changes in the plasma K+ level produce severe
cardiac abnormalities.
• In K+ level, the first change in the ECG is the
appearance of tall peaked T waves.
– At higher K+ levels, paralysis of the atria and prolongation
of the QRS complexes occur.
– Ventricular arrhythmias may develop
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58. Effects of Ionic imbalance on ECG tracing...
– The RMP of the muscle fibers decreases as the
extracellular K+ conc. increases.
– The fibers eventually become unexcitable, and the
heart stops in diastole.
• A decrease in the plasma K+ level causes:
– Prolongation of the PR interval,
– Prominent U waves, and,
– Late T wave inversion in the precordial leads
Hypokalemia is a serious condition, but it is not as rapidly
fatal as hyperkalemia.
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59. Effects of Ionic imbalance on ECG tracing...
• Increases in
extracellular Ca2+
conc. enhance
myocardial
contractility.
• When large amounts
of Ca2+ are infused
into experimental
animals, the heart
relaxes less during
diastole and
eventually stops in
systole (calcium
rigor).
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This electrode is connected to the positive Terminal of the electrocardiograph, and the negative electrode, indifferent electrode, is connected through equal electrical resistances to the right arm, left arm, and left leg all at the same time
hexagonal reference system, coordinate system
It can be calculated by summing the depolarization during the QRS complex in any two leads.
Ventricles averages about 59 degrees, this axis can swing even in the normal heart from about 20 degrees to about 100 degrees. The causes of the normal variations are mainly anatomical differences in the Purkinje distribution system or in the musculature itself of different hearts.
systemic diseases –diphtheria or rheumatic fever
carotid sinus syndrome. In these patients, the pressure receptors (baroreceptors) in the carotid sinus region of the carotid artery walls are excessively sensitive. Therefore, even mild external pressure on the neck elicits a strong baroreceptor reflex, causing intense vagal-acetylcholine effects on the heart, including extreme bradycardia
the brain cannot remain active for more than 4 to 7 seconds without blood supply, most patients faint a few seconds after complete block occurs because the heart does not pump any blood for 5 to 30 seconds, until the ventricles “escape.”
Bizarre- unusual Atrial and ventricular premature beats are not strong enough to produce a pulse at the wrist if they occur early in diastole, when the ventricles have not had time to fill with blood and the ventricular musculature is still in its relatively refractory period. They may not even open the aortic and pulmonary valves, in which case there is, in addition, no second heart sound.
This produces a characteristic saw tooth pattern of flutter waves due to atrial contractions.
It is almost always associated with 2:1 or greater AV block, because in adults the AV node cannot conduct more than about 230 impulses per minute.
Highvoltage 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. This is accomplished by passing intense current through large electrodes placed on two sides of the heart.
Depolarization reverberates round the pathway,
causing a tachycardia. The anatomical requirement for this is the branching and rejoining of a conduction pathway. Normally, conduction is anterograde (forward) in both limbs of such a pathway, but an anterograde impulse may pass normally down one branch and be blocked in the other. From the point at which the pathways rejoin, the depolarization wave can spread retrogradely (backwards) up the abnormal branch.
When the acute ischemia is transmural, the ST vector is usually shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction
Rapid repolarization –Elevation of the ST segment, The manifestations of this positivity , appearance of a Q wave in some of the leads in which it was not previously present and an increase in the size of the normal Q wave in some of the other leads, direction of repolarization cause inverted T
The intracellular to extracellular potassium ratio is the primary determinate of the cardiac resting membrane potential because the potassium channels are mostly open at rest.1,7 The concentration gradient of potassium across the cardiac cell membrane is reduced when serum potassium levels increase resulting in a less negative resting membrane potential.14 This change in resting membrane potential should increase the cell membrane excitability because it decreases the difference between the resting and threshold potentials.
However, this is not the only change that occurs when extracellular potassium levels are increased. Elevated serum potassium concentrations inactivate the sodium–potassium channels that are integral to allowing potassium efflux during the resting phase, so cells are much slower in reaching threshold potential.
The decreased permeability of potassium will also slow the efflux of potassium out of the cell during phase 3 of repolarization, prolonging the muscle’s recovery.
These changes depress upstroke velocity and progressively prolong duration of the cardiac action potential as extracellular potassium concentration increases, and they explain the ECG alterations in experimentally derived hyperkalemia.