Vectorial Analysis
vector - arrow that points in direction of electrical potential generated by current flow
length of the arrow is drawn proportional to the voltage
current flows between depolarized areas inside and nondepolarized - elliptical arrows
Some current flows inside the heart chambers
Overall current flows downward =summated vector =instantaneous mean
vector - exactly horizontal and directed toward the person’s left side- 0 degrees
vector extends from above and straight downward, it has a direction of +90 degrees
from left to right, it has a direction of +180 degrees;
straight upward, it has a direction of -90 (or +270)
normal - average direction of vector in spread of depolarization ventricles mean QRS vector
+59
during most of the depolarization -apex remains positive with respect to the base
Axis for Each Standard Bipolar Lead and Each Unipolar Limb Lead
direction from negative electrode to positive electrode is called the “axis” of the lead.
Lead I electrodes lie horizontal direction, axis of lead I is 0 degrees
lead II electrodes +60 degrees
lead III has an axis of about +120 degrees;
lead aVR, +210 degrees; aVF, +90 degrees; and aVL -30 degrees.
1
partially depolarized heart;
vector A represents -instantaneous mean direction of current flow in the ventricles +55 +2
how much of the voltage in vector A will be recorded in lead I
instantaneous recorded voltage = (B / A *)2 millivolts, or about 1 millivolt
almost perpendicular ->voltage recorded in the electrocardiogram of this lead is very low
Vectors That Occur at Successive Intervals During Depolarization of the Ventricles—The QRS
Complex
2
12–7A ventricular muscle just begun to depolarize 0.01 second after onset of depolarization
short - small portion of the ventricles—the septum—is depolarized
voltage in lead II is greater - heart vector extends in same direction as axis of lead II
In Figure 12–7B 0.02 ventricular muscle mass has become depolarized
12–7C, about 0.035 - vector shorter
the outside of heart apex is now electronegative, neutralizing much of the positivity on the
other epicardial surfaces of the heart.
axis of the vector is beginning to shift toward the left side of the
ratio of the voltage in lead I to that in lead III is increasing
12–7D 0.05 second
vector points toward the base of the left ventricle
short because only a minute portion of the ventricular muscle is still polarized positive
voltages recorded in leads II and III are both negative
voltage of lead I is still positive
12–7E 0.06
no current flows
Sometimes the QRS complex has a slight negative depression at its beginning in one or more
of the leads, which is not shown in Figure 12–7;
this depression is the Q wave.
initial depolarization of the left side of the septum before the right side
weak vector from left to right
The major positive deflection - R wave
negative deflection is the S wave
3
Electrocardiogram During Repolarization—The T Wave
0.15 second later, repolarization begins ->proceeds until complete at about 0.35 second T
wave
septum and other endocardial areas have a longer period of contraction than most of the
external surfaces of the heart
greatest portion of ventricular muscle mass to repolarize first is the entire outer surface of
the ventricles, especially near the apex of the heart
endocardial areas, conversely, normally repolarize last
caused by the high blood pressure inside the ventricles during contraction
reduces coronary blood flow to the endocardium
slowing repolarization in the endocardial areas.
positive end of overall ventricular vector during repolarization is toward heart apex
normal T wave in all three bipolar limb leads is positive
vector extends from base of heart toward apex until it disappears in last stage
0.15 second, the period of time required for the whole process to take place
Vectorcardiogram
vector of current flow through the heart changes rapidly as the impulse spreads through the
myocardium.
It changes in two aspects:
First increasing and decreasing voltage
4
Second average direction of the electrical potential from the heart
vectorcardiogram depicts these changes at different times during the cardiac cycle, as shown
in Figure 12–10.
In the large vectorcardiogram of Figure 12–10,
5 zero reference point, negative end of all successive vectors- no electrical potential
current begins to flow =the vector leaves the zero reference point
septum first becomes depolarized- vector extends downward toward the apex, but weak
2 state of depolarization of the ventricles about 0.02 second after vector 1
After another 0.02 second vector 3 represents the potential
4 occurs in another 0.01 second
vector becomes zero once again
elliptical figure = QRS vectorcardiogram
recorded on an oscilloscope
estimated from standard bipolar limb lead electrocardiograms rather than from vectorcardiogram.
recording the standard leads, net potential and polarity of the recordings in leads I and III.
and in lead III, the recording is mainly positive but negative during part of the cycle.
each net potential for leads I and III is plotted on the axes
intersection of the lead I and lead III -negative end of the mean vector
5
20 - 100 degrees
anatomical differences in the Purkinje distribution
Such shift occurs (1) deep expiration, (2) person lies down (3) fat
right (1) inspiration, (2) stands up (3) tall
axis shifts toward the hypertrophied ventricle more time is required for the depolarization wave
Vectorial Analysis of Left Axis Deviation Resulting from Hypertrophy of the Left Ventricle.
Vectorial Analysis of Right Axis Deviation Resulting from Hypertrophy of the Right Ventricle.
170 degrees, 111 degrees to the right of the normal 59-degree mean ventricular QRS axis.
hypertrophy of the right ventricle
congenital pulmonary valve stenosis
tetralogy of Fallot and interventricular septal defect
6
R=2-3xL
left ventricle remains polarized for 0.1 second after right ventricle become depolarized
right ventricle becomes electronegative, the left ventricle remains electropositive
strong vector projects from the right ventricle toward the left ventricle
-50 degrees
duration of the QRS complex is prolonged
voltages in the three standard bipolar limb leads peak R - bottom S vary 0.5 and 2.0 mV
lead III the lowest voltage and lead II the highest
sum of voltages of all QRS complexes of three standard leads > 4, t highvoltage ecg
increased muscle mass of the heart
right ventricle hypertrophies when it must pump blood through a stenotic pulmonary valve
left ventricle hypertrophies when a person has high blood pressure
7
Decreased Voltage Caused by Conditions Surrounding the Heart.
block of one of the bundle branches occurs, the duration of QRS complex 0.14 second
Current of Injury
damage heart muscle itself, part of heart remain partially or totally depolarized all time
current flows between pathologically depol and pol areas even between heartbeats
injured part of the heart is negative
Some abnormalities that can cause current of injury
mechanical trauma
8
makes the membranes remain permeable
infectious processes that damage the muscle membranes;
ischemia of local areas of heart muscle caused by local coronary occlusions
9
J point of each of these two electrocardiograms is not on the same line as the T-P segment
injury potential = difference between voltage before onset of P and zero voltage from J
I -recorded voltage of injury potential is above zero potential level and is, therefore, positive.
III, below the zero voltage level and, therefore, is negative.
-30 degrees
negative end of vector points toward permanently depolarized, “injured” area of ventricles
lateral wall of the right ventricle
lack of oxygen, (2) excess carbon dioxide, and (3) lack of sufficient food nutrients
repolarization of the muscle membrane cannot occur
heart muscle does not die because the blood flow is sufficient to maintain life of the muscle
injury potential continues to flow during the diastolic portion (the T-P portion)
diagnostic feature of this electrocardiogram is intense injury potential in chest lead V2.
negative injury potential during the T-P interval is found
chest electrode over the front of the heart is in an area of strongly negative potential
negative end of injury potential vector in this heart is against anterior chest wall
negative potential in lead I and a positive potential in lead III
resultant vector of the injury +150 degrees
injury is coming mainly from the left ventricle
thrombosis of the anterior descending branch of the left coronary artery
J point of this lead- T-P interval, the potential of the current of injury is positive
10
positive end of the vector is in the direction of the anterior chest wall, and the negative end
(injured end of the vector) points away from the chest wall.
II and III of Figure, injury potential is negative in both leads.
-95 degrees,
negative end pointing downward and the positive end pointing upward.
the apical portion of the heart
infarct is near the apex on the posterior wall of the left ventricle
positive end of the injury potential vector points toward the normal cardiac muscle, and the negative
end points toward the injured portion of the heart that is emitting the current of injury
injury potential strong immediately after acute attack (T-P positively from S-T).
the injury potential has diminished considerably, and after 3 weeks, it is gone
the new collateral coronary blood flow develops enough to re-establish appropriate nutrition
Q wave has developed at the beginning of the QRS complex in lead I in anterior infarction because of
loss of muscle mass in the anterior wall of the left ventricle,
posterior infarction, a Q wave has developed at the beginning of the QRS complex in lead III because
of loss of muscle in the posterior apical part of the ventricle.
T wave becomes abnormal when the normal sequence of repolarization does not occur
shortened action potential, repolarization of the ventricles would not begin at apex
base of the ventricles would repolarize ahead of the apex
Consequently, the T wave in all three standard leads would be negative
Mild ischemia is by far the most common cause
11