Download 3. ECG ANALYSIS 3.1. Heartbeat

3. ECG ANALYSIS
The following parameters are assessed on ECG (in undermentioned sequence):
1.
Heartbeat
2.
Heart rate
3.
Rhythm
4.
Electric axis
5.
Description of waves, intervals and segments on ECG.
The advanced electrocardiographs evaluate some parameters automatically (for
example heart rate). A useful tool for ECG assessment is a special ruler shown in
Figure 3.1.).
Fig. 3.1. EGG ruler
Zdroj:http://www.pharmainsight.ca/pharmaceutical-images/slcardiac%20ruler.gif
3.1. Heartbeat
The heartbeat can be regular or irregular. Regularity or irregularity is determined
by analyzing the time intervals between two identical successive components of the
electrocardiogram, usually R-R intervals. If durations of these intervals are constant,
the heartbeat is regular (Fig. 3.2). If the durations of R-R intervals differ significantly,
the heartbeat is irregular (Fig. 3.3.).
R-R interval
Fig. 3.2. Regular heartbeat
R-R interval
R-R interval
R-R interval
Fig. 3.3. Irregular heartbeat
The irregular heart beat is called arrhythmia (or dysrhythmia). The arrhythmia
can occur in healthy person (so-called physiological arrhythmia) or can be induced by
some pathological cause. The most common physiological arrhythmia is respiratory
arrhythmia that is usually present in young persons. It is characterized by an
increase in the heart rate during inspiration and a decrease in the heart rate during
expiration (Fig. 3.4).
The cause of respiratory arrhythmia is a tone fluctuation of vagus nerve nuclei (the decrease in
tone during inspiration and the increase in tone during expiration). These nuclei are located close to a
respiratory center in brainstem. Respiratory arrhythmia probably positively influences a gas exchange
between alveolar air and the blood in pulmonary capillaries (the inspiration increases the pulmonary
blood supply and thereby stimulates the gas exchange). The heartbeat variability provides the
optimum ventilation-perfusion ratio during the entire respiratory cycle.
Fig. 3.4. Respiratory arrhythmia
VT – tidal volume
3.2. Heart rate
Heart rate is the number of ventricular systoles per one minute. Normal heart rate
(in adult person under resting conditions) is 60 - 90 beats per minute (BPM). A
decreased heart rate is called bradycardia, an increased heart rate is tachycardia.
Since many healthy individuals have the heart rate out of abovementioned interval,
the optimum heart rate is the value ensuring a sufficient cardiac output. For example
in endurance sportsmen having a stroke volume higher compared to the common
population the resting heart rate is markedly lower whereas the resting cardiac output
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is comparable to untrained people (cardiac output is equal to stroke volume multiplied
by heart rate). The method of heart rate determination depends on regularity or
irregularity of the heartbeat.
3.2.1 Regular heartbeat
At the regular heartbeat the heart rate is calculated by means of following
formulas:
BPM =
60
R − R ( s)
R-R (s) is a time interval of two successive R waves expressed in second (Fig. 3.5).
0,75 s
Fig. 3.5. Heart rate determination at the regular heartbeat
R-R interval has duration 0.75 s. The heart rate according the abovementioned
formula is
60
= 80 BPM.
0.75
At a standard paper movement the following formula can be used:
BPM =
150
R − R (cm)
R-R (cm) is a distance of two successive R waves expressed in centimeters; 150
cm corresponds to 1 minute at the paper speed of 2.5 cm/s (Fig. 3.6).
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2 cm
Fig. 3.6. Heart rate determination at the regular heartbeat
The distance of two successive R waves is 2 cm. The heart rate is
150
= 75 BPM.
2
3.2.2. Irregular heartbeat
At the irregular heartbeat the following procedure is recommended (Fig. 3.7):
¾ To count number of R waves in the definite time interval.
¾ To transform the accounted value into minute interval.
10 s
Fig 3.7. Heart rate determination at the irregular heartbeat
10-sec interval contains 12 R waves. Number of R waves is multiplicated by 6 (six
10-sec intervals in 1 minute) to calculate the heart rate, i.e. 72 BPM.
3.3. Rhythm
The rhythm of the heart is determined by a pacemaker region spontaneously
producing electric impulses. Under physiological conditions the source of cardiac
rhythm is usually the fastest pacemaker, i.e. sino-atrial (SA) node – sinus rhythm. If
the spontaneous activity of SA node is disturbed its function is replaced by the
activity of atrioventricular (AV) node – nodal rhythm. The complete failure of
conduction between the atria and ventricles leads to the complete independence of
the atrial and ventricular electric activity. The atria are controlled by SA node whereas
the ventricular impulses are produced by Purkyne fibers – idioventricular rhythm.
The frequency of produced impulses is the highest in SA node (60 – 90 BPM), lower
in AV node (46 – 60 BPM) and the lowest in Purkyne fibers (30 BPM).
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Under pathological conditions the source of pacemaker activity can be a tissue area located
outside the conductive system. If the frequency of thus produced impulses is high enough to take a
control over the whole heart an arrhythmia arises. The areas elsewhere than in SA node producing
electric impulses are called ectopic (ectopicus - occurring in an abnormal position or place, displaced).
Criteria for the sinus rhythm are:
1. P wave appears before QRS complex (the atrial depolarization precedes the
ventricular depolarization).
2. PQ interval has normal duration, i.e. from 0.12 to 0.2 s (transmission of the
electric signal from the atria to ventricles is normal).
3. Heart rate ranges between 60 and 90 BPM. This condition cannot be applied to
everybody. As mentioned above, although the resting heart rate of trained person
is lower compared to untrained population the trained person can have the sinus
rhythm.
The nodal rhythm is characterized by a change in shape and position of P wave. Three types of nodal
rhythm are distinguished according to the pacemaker location:
1. Upper nodal rhythm originates in the atrial part of AV node. P wave precedes QRS complex but
the duration of PQ interval is shorter (transmission of the electric signal from place of origin to
ventricles is faster due to a shorter distance). P wave is negative in leads II, III, aVF, V5 and V6
(Fig. 3.8a).
2. Middle nodal rhythm originates in the middle part of AV node. The electric impulse spreads
towards the atria and ventricles simultaneously to initiate atrial and ventricular depolarization at
the same time. Since the ventricular myocardium is thicker then atrial one, P wave is covered by
QRS complex being invisible on ECG recording (Fig. 3.8b).
3. Lower nodal rhythm originates in the ventricular part of AV node. The ventricular depolarization
precedes the atrial depolarization hence P wave comes after QRS complex (Fig. 3.8c).
The idioventricular rhythm is characterized by a very slow frequency. This rhythm results from a
block of atrioventricular transmission when the atria are controlled by the sinus rhythm and the
ventricles by the idioventricular rhythm. P waves and QRS complexes are visible on
electrocardiogram without any time relationship.
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AV node
a
b
c
Fig. 3.8. Nodal rhythm
The cells of AV node form the source of pacemaker activity in the nodal rhythm. a – upper nodal
rhythm, b – middle nodal rhythm, c – lower nodal rhythm.
3.4. Electric heart axis
The electric heart axis is the direction and size of vector of the electric heart field.
As explained earlier, the changes of the electric heart field are detectable only during
propagation of depolarization or repolarization, i.e. during atrial depolarization (P
wave), ventricular depolarization (QRS complex) or ventricular repolarization (T
wave). The direction of an average vector of QRS complex is the most important for
diagnosis of cardiac diseases, and usually, as the electrical heart axis, the mean
QRS vector is understood.
In most healthy persons the direction of electric heart axis corresponds to the
direction of the anatomic heart axis which is oriented forward, leftward and
downward. It is evident, that the vector of the electric heart field is defined in threedimensional space (3D). But ECG recording of limb leads makes possible projection
of vector only in the frontal plane (2D). The direction of the heart electric axis in
healthy people ranges between -30° and 105° (Fig. 3.9). Shift of the electric axis to
the right is called right axis deviation or vertical axis (more than 105°, Fig. 3.10).
Shift the electric axis to the left is called left axis deviation or horizontal axis (less
than -30°, Fig. 3.11).
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Fig. 3.9. Normal electric heart axis
Shaded area defines the direction of the normal heart axis.
lead I
lead I
lead III
lead II
lead III
lead II
Fig. 3.10. The heart axis deviation
Left – the black area defines the left axis deviation, right – the black area defines the
right axis deviation.
The deviation of the heart electric axis is usually caused by hypertrophy of cardiac chamber,
conduction abnormalities or deviations of the heart position in the thorax. The right axis deviation can
be induced by the right ventricle hypertrophy, left anterior hemiblock or by extreme slimness (the
diaphragm in a slim person is moved downwards and consequently the cardiac apex leaning on the
diaphragm is shifted downwards as well). On the other hand, the left axis deviation is caused by the
left ventricle hypertrophy, left posterior hemiblock, obesity or by advanced pregnancy (the diaphragm
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in obese people or in pregnant women is shifted upwards to push the cardiac apex up). The direction
of the electric heart axis is also influenced by deep breathing – the right axis deviation during deep
inspiration due to the diaphragm movement downwards and the left axis deviation during deep
expiration due the diaphragm movement upwards.
3.4.1. Determination of the electric heart axis
The electric axis can be determined by many methods. Two techniques will be
explained in the following text:
1. Estimate based on leads I and III.
2. Determination by means of Einthoven’s triangle.
Estimate of the electric axis based on leads I and III
Based on the QRS complex shape in bipolar leads I and III the heart electric axis
may be estimated:
•
The maximum positive QRS deflection in lead I and the maximum negative
QRS deflection in lead III → the left axis deviation.
•
The maximum negative QRS deflection in lead I and the maximum positive
QRS deflection in lead III → the right axis deviation.
•
Either the maximum positive QRS deflection in both lead or the maximum
negative QRS ones in both leads → normal heart axis (Fig. 3.11).
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Fig. 3. 11. Estimate of the electric heart axis by means with limb leads
Determination the electric heart axis by means of Einthoven’s triangle
The Einthoven’s triangle is an equilateral triangle whose sides are formed by
leads I, II and III. The polarity of triangle’s sides (i.e. ECG electrodes) is given by a
convention (Fig. 3.12).
Fig. 3.12. Einthoven’s triangle
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The procedure of the axis determination is following:
1. Draw an equilateral triangle and mark the polarity of sides. Plot three
perpendiculars in the midpoints of the triangle’s sides. The cross point of
perpendiculars forms the onset of the heart electric axis (Fig 3.13a).
2. Measure the amplitude of positive wave (R) and the maximum negative wave
(Q or S) in any two bipolar leads*. Calculate the difference of both measured
amplitudes as the absolute value of positive wave amplitude minus the
absolute value of the negative wave amplitude (Fig. 3.13b).
3. Mark out the calculated difference on an appropriate lead (lead I – upper side,
lead II – left side, lead III – right side). The direction of vector is towards
positive electrode if the difference of amplitudes is positive. Conversely, the
vector of negative difference directs towards the negative electrode (Fig.
3.13c).
4. Plot perpendiculars in the end points of coordinates (Fig. 3.13d).
5. Mark the cross point of perpendiculars. The electric heart axis directs towards
the found cross point. Determine the axis direction by means of protractor (Fig.
3.13e).
* Einthoven’s rule is stated as follows: Lead I – Lead III = Lead II. In other words, if any two
leads are known at a given time, the third lead can be determined mathematically.
10
+8
a
I
-
+
-
b
- -
II
II
/8/ - /2/ = 6
0
-2
I
-
+
II
II
c
-
-
I
-
+
6
-
-7
+3
0
II
II
-10
heart axis
beginning
+ +
d
-
/3/ - /10/ = - 7
+ +
I
-
+
6
e
-
-
I
-
+
6
-
-7
-7
II
II
+ +
II
II
heart axis
+ +
+ +
Fig. 3.13. Determination of the electric heart axis by means of Einthoven’s
triangle
3.5. Description of waves, intervals and segments on ECG
The individual waves, segments and intervals on ECG should be assessed in all
leads. It is necessary to point out that lead aVR is the least useful.
3.5.1. P wave
P wave caused by the atrial depolarization has maximum amplitude of 0.25 mV
and its duration is up 0.1 s (Fig 3.14). This wave is positive in most leads, it can be
positive or negative in lead III, usually biphasic in lead V1 (i.e. positive in the first
phase and negative in the second phase) and always negative in lead aVR.
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max. 0.25 mV
P
max. 0.1 s
Fig. 3.14. P wave
P wave caused by atrial depolarization precedes QRS complex under physiological
conditions.
3.5.2. PQ (PR) interval
The time interval from the beginning of P wave to the onset of QRS complex is
called PQ interval (if QRS complex starts with Q wave) or PR interval (ORS complex
starts with R wave). PQ (PR) interval representing the period from the beginning of
atrial depolarization to the beginning of ventricular one normally lasts 0.12 – 0.2 s
(Fig. 3.15). The duration of PQ interval is inversely proportional to the heart rate (it
shortens with increasing heart rate and prolongs with decreasing heart rate). The
prolongation of PQ interval can be physiological (in sportsmen with resting
bradycardia) or pathological (due to an abnormal conduction in AV node).
0,1 s
PQ
PR
Fig. 3.15. PQ and PR intervals
PQ (PR) interval comprises the isoelectric PQ (PR) segment (Fig 3.16). During
this segment all atrial cells are completely depolarized and simultaneously neither
atrial repolarization nor ventricular depolarization has started thus no deflection is
present on ECG.
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0,1 s
PQ segment
PR segment
Fig. 3.16. PQ a PR segments
3.5.3. QRS complex
QRS complex is produced by the ventricular depolarization. The sequence of the
ventricular depolarization is following: AV node – interventricular septum (from the left
to the right) – cardiac apex – free ventricular walls – atrioventricular groove.
Depolarization in the free walls travels from endocardium to epicardium. Normal
duration of QRS complex ranges between 0.06 and 0.11 s.
QRS complex consists of three waves (Q, R and S). But all three waves are not
ordinarily found in each lead. R wave is always positive. Q and S waves are always
negative, Q wave precedes R wave whereas S wave follows R wave. The complex
formed by only one negative wave is called QS (the absence of R wave makes the
exact designation impossible). The other positive waves in QRS complex are
specified by apostrophe R, R´, R´´ …). The various forms of QRS complex are shown
in the picture 3.17.
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R
R
R
r
q
q
s
S
S
R
R
0,1 s
R
R´
r
S
QS
Fig 3.17. Various forms of QRS complex
Small and capital letters determine the wave height – small letters (q, r, s) for waves
bellow 5 mm and capital letters (Q, R, S) for waves above 5 mm.
3.5.4. Q wave
The Q wave is caused by the depolarization of the ventricular septum and
papillary muscles. Its duration should be less than 0.03 s and the amplitude
maximum ¼ of R wave amplitude (in the same lead). The wave with parameters
outside these ranges is called pathological Q. Q wave is usually found in leads
located above the surface of the left ventricle (V5 and V6).
3.5.5. R wave
Always positive R wave is produced by free ventricular walls depolarization. The
maximum R wave amplitude in the limb leads is 10 mm. In the chest leads R wave
amplitude increases from V1 to V5 to reach the same or smaller amplitude in V6
compared to V5 (Fig. 3.18).
The time interval from the onset of Q wave to the peak of R wave called the ventricular
activation time corresponds to the depolarization of the whole ventricular walls. The ventricular
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activation time measured in V1 shows the activation of the right ventricle (normally up to 0.03 s)
whereas in V6 the left ventricular activation (up to 0.04 s). An extended ventricular activation time is
usually an indication of the ventricular hypertrophy.
R
S
V1
V2
V3
V4
V5
V6
Fig 3.18 . R and S waves in chest leads
The amplitude of R wave increases from lead V1 to V5 (rarely V6), S wave decreases.
3.5.6. S wave
The amplitude of S wave in chest leads decreases from V1 to V6. In lead V6 this
wave is usually not present (Fig. 3.18).
3.5.7. ST segment
The ST segment represents the period from the end of ventricular depolarization
to the beginning of ventricular repolarization. The normally isoelectric ST segment
lies between the end of the QRS complex and the initial deflection of the T wave. The
point marking the end of the QRS complex and the beginning of the ST segment is
called J point. This point should be at the same level as beginning of Q wave (i.e. on
the isoelectric line).
The shift of ST segment above the baseline is called ST elevation. The tolerated elevation is 0.1
mV in the limb leads and 0.2 mV in the chest leads. The shift of ST segment below the baseline is
called ST depression; the tolerated depression is 0.1 mV. A variation of ST segment can result from a
lot of causes both trivial (e.g. an activation of sympathetic nervous system due to fear, angriness or
physical effort) and severe (angina pectoris, myocardial infarction, ion imbalance or cardiotonics
overdose).
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3.5.8. T wave
The ventricular repolarization spreads from the atrioventricular groove through the
cardiac apex to the ventricular septum to produce T wave on ECG. The direction of
the ventricular repolarization is opposite to the depolarization. In the free ventricular
walls the repolarization travels from epicardium to endocardium hence the polarity of
T wave corresponds to the polarity of the QRS wave with the highest amplitude (if R
wave has the highest amplitude T wave is positive; if S or Q wave is maximum T
wave is negative). Under physiological conditions negative T wave is found in leads
aVR, III, V1 and V2.
T wave duration is about 0.2 s, its amplitude ranges between 0.2 and 0.8 mV.
3.5.9. U wave
U wave is a small positive wave sometimes visible after T wave (Fig. 3.19). It can
be normally present in young people and sportsmen. The pathological appearance of
U wave is due to hypokalemia (a decrease in plasmatic concentration of potassium).
U wave probably results from the delayed repolarization of Purkyne fibers or some
areas of the ventricular myocardium.
U wave
Fig 3.19. U wave
3.2.10. QT Interval
QT interval is defined by the onset of QRS complex and the end of T wave. This
interval comprises the depolarization and repolarization of ventricles (so-called an
electric systole of ventricles). Duration of QT interval is significantly influenced by
changes in heart rate (shortening due to tachycardia and prolongation due to
bradycardia). Therefore the duration of QT interval is corrected for the heart rate and
the corrected value is marked QTc. (Various formulas are used for the correction but
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their explanation is beyond the scope of this study material). A normal value of QTc is
from 0.32 to 0.42 s.
The most important time intervals for remembering are shown in the following
table:
PQ interval
0.12 – 0.2 s
QRS complex
0.06 – 0.11 s
QT interval
0.32 – 0.42 s
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