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Ekg1 PDF
Ekg1 PDF
During each cardiac cycle the Atria contract in Diastole to fill the Ventricles which then contract during Systole to supply
blood to the lungs and the systemic circulation.
Contraction of the atria and ventricles is tightly coordinated by a wave of depolarization spreading through the muscular
walls of these chambers. The depolarization wave reflects movement of charge across myocyte membranes and is in
effect an electrical current spreading through the heart. Following contraction, cardiac muscle returns to a resting state
and this is associated with reversal of the movement of charge across the myocyte membranes, this second wave of
electrical activity is termed cardiac repolarization.
The leads of the ECG machine are designed to detect and record these two waves of cardiac electrical activity. The
depolarization wave spreads through the heart in a highly predictable pattern and to understand the ECG readout, the
pattern of spread of cardiac depolarization needs to be understood.
Cardiac depolarization is triggered by an electrical pulse generated in the Sinoatrial node. This electrical pulse then
spreads through the atria triggering their depolarization and contraction late in diastole. The atria and ventricles, however,
are separated by a non-conducting fibrous septum. The depolarization wave cannot penetrate this barrier and in order to
activate ventricular contraction the wave must be transmitted into the ventricles by the specialized cardiac conducting
system. In a normal heart, the only route by which the depolarizing wave can enter the ventricular conducting system is
through the AV node. In order to allow the ventricles to fill with blood following atrial contraction, the AV node initially
delays the spread of the depolarization wave. After this short delay, the depolarizing signal is transmitted into the
ventricles via the Bundle of His.
The bundle of His lies in the Interventricular Septum and divides into right and left bundle branches. The right and left
bundle branches transmit the depolarizing signal into the muscle mass of the right and left ventricles respectively. The
interventricular septum is the first part of the ventricular muscle mass to depolarize and it does so by movement
of depolarization across the septum from the left towards the right bundle branch. This early left to right spread of
depolarization in the septum is crucial to understanding several important ECG abnormalities.
As septal depolarization is taking place, the depolarizing wave begins to spread rapidly through the bulk of the left and
right ventricles. In the walls of the ventricles, depolarization spreads from the terminal fibers of the conducting
system outwards from the endocardium towards the epicardial surface of the heart and also back along the
ventricular wall to the atrioventricular groove.
Cardiac repolarization is not truly propagated between cells. However, cardiac myocytes repolarise at different rates
depending on their anatomical location within the heart. Within the ventricular wall there is a gradient in the rate of cellular
repolarization, cells in the epicardial region have the fastest rate of repolarization and repolarise first following
ventricular contraction. The rate of cellular repolarization is then progressively slower as we move from the epicardium
towards the endocardium. Therefore, perhaps counter-intuitively, repolarization spreads through the ventricles in
the opposite direction to the depolarization wave. Following ventricular contraction, repolarization begins in the
epicardium and spreads backwards from the epicardial to the endocardial surface of the ventricles. This
retrograde spread of ventricular repolarization is important in understanding the normal ECG readout.
KEYPOINTS
1. The Interventricular septum is the first part of the ventricular muscle mass to depolarize by movement of depolarization
across the septum from the left towards the right bundle branch.
2. In the walls of the ventricles, depolarization spreads outwards from the endocardium towards the epicardial surface of
the heart.
3. Repolarization spreads through the ventricles in the opposite direction to the depolarization wave moving from the
epicardial to the endocardial surface of the chambers.
When ventricular depolarization is complete there is a brief period when no current is flowing and the recording returns to
the isoelectric line. This period ends with the onset of ventricular repolarization.
Remember, repolarising current has the opposite polarity to the depolarization wave and, therefore, when it is moving
towards a lead it produces a negative deflection on the ECG paper and a positive deflection when moving away from a
lead. Weve also learned that repolarization spreads through the ventricles in the opposite direction to the depolarization
wave beginning in the epicardium and spreading from the epicardial to the endocardial surface of the ventricles. The
deflection produced on an ECG by ventricular repolarization is again dominated by the signal from the left ventricle. As
this repolarising current is moving towards V1 the deflection produced is negative in this lead. In contrast, this repolarising
signal is moving away from lead V6 producing a positive deflection. The deflection produced by ventricular repolarization
is termed a T wave. Cardiac repolarization spreads relatively slowly through the muscle mass, outside the conducting
system. Hence, the T wave is considerably longer in duration and, therefore, broader on the ECG paper than the QRS
complex.
The fact that repolarising current moves through the ventricles in the opposite direction to the depolarization wave means
that in leads with an overall positive QRS complex that is the positive deflection is larger than the negative deflection, the
T wave also tends to be positive above the isoelectric line, while in leads with an overall negative QRS complex the T
waves tend also to be negative, inverted below the isoelectric line. To use the jargon, in non-diseased hearts the QRS
complexes and T waves tend to be concordant. There are important exceptions to this rule which well deal with shortly.
Just to tie up a loose end, atrial repolarization produces a relatively weak electrical signal which is buried in the QRS
complex and is generally not detectable on a standard 12 lead ECG.
KEYPOINTS
1. Depolarizing current moving towards a lead produces a positive deflection on the ECG paper, while depolarizing
current moving away from a lead produces a negative deflection.
2. Repolarising current moving towards a lead produces a negative deflection on the ECG paper, while repolarising
current moving away from the lead produces a positive deflection.
3. Early left to right septal depolarization may produce small physiological q waves in left sided leads
4. The left ventricle has a much greater muscle mass than the right and so dominates the electrical signal of ventricular
depolarization in all leads.
5. In young, non-diseased, hearts the QRS complexes and T waves tend to be concordant.
defines 00 in all further discussions of the frontal leads, lead II looks at the heart at an
angle 600 further clockwise while lead III is positioned a further 600 clockwise from II.
These angles will become important in the next section of this course. The readout
from the standard leads, Leads I, II and III are recorded down the right hand side of the
ECG paper. We are now left with three further leads to remember, the augmented
leads aVR, aVL and aVF, aVL looks at the heart from the left (L is for left) but at 30o
anticlockwise (or more to the left if you like) from lead I, aVR looks at the right side of
the heart (R is for right), and, just like aVL, it is 300 above the horizontal relative to lead
I. aVF looks straight up at the inferior surface of the heart and is therefore at 90o
clockwise from lead I, think of aVF as looking straight up at the heart from the feet (F is
for feet). On the ECG readout, recordings from the augmented leads are positioned
between the standard leads and the chest leads from aVR to aVL and down to aVF at
the foot of the page.
For the experienced practitioner, looking at different areas on the ECG readout is like
looking at different anatomical regions of the heart. Three of the vertical leads II, III and
aVF form a group examining the inferior or diaphragmatic surface of the ventricles, a
region supplied by the right coronary artery (RCA), you will (eventually) get into the
habit of seeing these so-called inferior leads as a single entity in the bottom right hand
corner of the ECG. The chest leads V1 to V4 examine the anterior surface of the
ventricles and the septum, a region supplied by the left anterior descending (LAD)
artery. While leads I, aVL, V5 and V6 examine the left lateral aspect of the left ventricle,
a region supplied by the left circumflex artery (LCA). In a subsequent section of this
course, well see the key role that these groupings of leads play in diagnosing
myocardial infarction and in identifying the vessel obstructed in this condition.
*V1 is applied to the chest in the 4th right intercostal space to the right of the sternum,
lead V2 in the fourth left intercostal space to the left of the sternum, lead V4 is placed
on the chest over the apex beat. Lead V3 is placed down from V2 midway between V2
and V4. V6 is placed horizontally and laterally from V4 in the midaxillary line. V5 is
placed at the midpoint between V4 and V6.
[endif]
1.5 TIME AND THE ECG - Part 1
If you look at the bottom of the ECG readout you will see a long run of recording from
lead II, this is called the rhythm strip. We use the rhythm strip to calculate the heart rate
and to diagnose abnormal cardiac rhythms (arrhythmias). Lead II is used as the rhythm
strip as it is usually the easiest lead in which to see P waves and, as well see in
subsequent sections, identification and analysis of P waves plays a key role in the
diagnosis of rhythm disturbances on an ECG. For now lets deal with the calculation of
heart rate. ECG recording paper is divided into large squares 5 mm wide and these
large squares are in turn further subdivided into small squares each of 1 mm width. For
our present purposes we can consider that in all ECG machines the recording needles
run at a constant speed over the ECG paper of 25 mm/sec. If you think about it you will
realise that this means that distance on the ECG paper equates to time. At a recording
rate of 25mm/sec, 5 large squares are covered in one second. So, 300 large squares
represents one minute. Therefore, the number of R waves in 300 large squares is the
heart rate in beats per minute. This gives us a simple method for calculating heart rate
from an ECG. Identify two consecutive R waves on the rhythm strip, count the
number of large squares between them, then, take this number and divide it into
300. Provided the heart rhythm is regular, this method gives you an accurate
heart rate in beats per minute.
You will also appreciate that as 300 large squares equates to one minute and as there
are 5 small squares in each large square, 1500 small squares also equates to one
minute. Therefore, we can also calculate the heart rate by counting the number of
small squares between two consecutive R waves and dividing this number into
1500. This is useful when the R waves do not fall on a set number of large squares.
When calculating the heart rate from an ECG in the presence of an irregular rhythm,
count out 30 large squares, now remembering that 5 large squares equates to one
second, 30 large squares corresponds to 6 seconds, count the number of R waves in
these thirty large squares and multiple this number by 10 to get the heart rate in beats
per minute.
In addition to calculating heart rate, the fact that distance on the ECG paper equates to
time allows us to use the readout to time the duration of the major events of the cardiac
cycle. At a standard recording speed of 25mm/sec, 5 large squares corresponds to one
second. Therefore, one large square corresponds to 0.2 seconds and one small square
to 0.04 seconds. (35) There are a few numbers coming up now which you simply must
learn. In a normal heart, the time between the onset of atrial depolarisation (the
beginning of the P wave) and the onset of ventricular depolarisation, (the
beginning of the qrs complex) varies between 0.12 and 0.2 seconds that is
between 3 and 5 small squares. This is the PR interval. Analysis of the PR interval
plays a central role in diagnosing many different disorders of the heart.
The PR interval ends with the release of current into the main muscle mass of the
septum and ventricles from the terminal branches of the intraventricular conducting
system. On the ECG, this point is marked by the onset of the qrs complex and the next
key value we need to learn is the duration of the qrs complex. The duration of the qrs
complex represents the time taken for ventricular depolarisation to be completed
following the release of depolarising current from the conducting system. It also
includes the time taken for the recording needle to return to baseline when the flow of
depolarising current has ceased. The conducting system of the ventricles is a highly
specialised tissue capable of transmitting the depolarisation wave rapidly around the
ventricles. Note, therefore, that with an intact conducting system depolarising
current is delivered to all sectors of the ventricles in a very short time period and
ventricular depolarisation of all regions of the chambers is complete within 0.12
seconds that is 3 small squares. A normal qrs complex is less than three small
squares in width (<0.12s in duration). You will learn later in this course that the width
of the qrs complex is absolutely central to the ECG interpretation of life-threatening
arrhythmias. You must remember this number.
It is important to realise that if a depolarisation or repolarisation wave is travelling at 90
degrees relative to a lead, it will not be recorded by that lead. As the ECG leads record
electrical events in the heart from different perspectives, one important consequence of
this is that, an electrical event in the heart may be recorded by some leads but missed
by others. For this and many other reasons, the duration of the major events of the
cardiac cycle appears to vary between leads. When analysed manually, the width of
the qrs complexes in the lead with the widest complexes defines the qrs duration on
the ECG.
Finally, the duration of ventricular repolarisation is crucially important in clinical
practice. The time between the onset of ventricular depolarisation and the end of
ventricular repolarisation (that is the beginning of the qrs complex and the end of
the T wave on the ECG) is termed the QT interval. When the heart rate is 60 beats
per minute, the upper limit of normal for the QT interval is 0.44 seconds or
eleven small squares. It is important to realise, however, that the measured QT
interval varies with heart rate, becoming shorter as the heart speeds up or longer when
the heart slows down. Therefore, particularly at higher heart rates it is possible to miss
an underlying prolonged QT interval. When faced with an ECG with a heart rate other
than 60 beats per minute, to calculate the true underlying QT interval referred to as the
corrected QT interval we use the following formula: QTc = QT/RR where QTc is the
corrected QT value, QT is the actual QT interval measured on the ECG and the RR
interval is the distance between consecutive R waves on the ECG measured in
seconds. To give you a rule of thumb, when looking at an ECG readout with a heart
rate other than 60 beats per minute, if the QT interval is more than half the distance
between consecutive R waves, at least consider the possibility of prolonged QT.
The importance of these normal values will become increasingly obvious as we
discuss the ECG in disease states. Memorise them. The PR interval; 3 to 5 small
squares, the QRS complex width; less than 3 small squares, the QT interval;
(approximately) less than half the RR interval.
KEYPOINTS
2. To calculate the heart rate in beats per minute from an ECG with a regular
rhythm, count the number of large squares between two consecutive R waves
and divide this number into 300.
3. To calculate the heart rate in beats per minute from an ECG with a regular
rhythm, count the number of small squares between two consecutive R waves
and divide this number into 1500.
4. To calculate the heart rate in beats per minute from an ECG with an irregular
rhythm count the number of R waves in 30 large squares and multiply this
number by 10.
6. The normal qrs duration is less than 0.12 seconds (<3 small squares).
*An (occasionally useful) extension of this rule. If 300 large squares is equivalent to
one minute, then, as each large square contains 5 small squares, 1500 small squares
is also equivalent to one minute. So the number of R waves in 1500 small squares is
the heart rate in bpm. Therefore, if you count the number of small squares
between two R waves on the rhythm strip and divide this number into 1500, this
also gives the heart rate in bpm. This is useful if the R waves dont match up to a nice
round number of large squares.
1.6 THE PREDICTED NORMAL ECG, SOME REFINEMENTS
There are a few aspects of the normal ECG which wed like to emphasise at this point,
the importance of which will become obvious to you in the later sections of this course.
In leads V1 to V6 the dominance of the left ventricle produces deep S waves in the
right sided chest leads and prominent R waves in those more to the left. The transition
from dominant S waves to dominant R waves in the chest leads occurs at or around
lead V3 or V4. The transition at this point from an overall negative QRS to a positive
QRS complex in the chest leads is termed normal R wave progression and reflects a
normal healthy left ventricle dominating QRS morphology with a normal pattern of flow
of depolarisation around this chamber.
Weve also learned that leads with overall positive QRS complexes tend to have
upright T waves, while those leads with overall negative QRS complexes have inverted
T waves. The perfect concordance between QRS complexes and T waves is indeed
observed in healthy young adults and when present in older individuals (middle-aged)
is often referred to a persistent juvenile pattern. However, for reasons which are not
fully understood, in older completely healthy adults it is quite usual to see upright T
waves in lead V1 and even lead V2 despite the dominant S waves in the QRS
complexes of these leads. As this is the age group with which we are most commonly
confronted in medical practice it is important to be aware of this. A normal T wave is
somewhat asymmetrical in shape and in a healthy heart in leads with dominant R
waves the T wave tends to be less than half the amplitude of the preceding R
wave in height. These may appear to be strange points to emphasise at this time but
their importance will become obvious when we go on to deal with disease diagnosis.
It is quite normal for P waves to differ in morphology between the 12 leads as each
lead has a different perspective on atrial depolarisation. For example, as atrial
depolarisation spreads away from lead aVR on the right, the P wave in this lead is
negative. As weve already mentioned, P waves are usually most prominent in lead II.
Small physiological q waves in the left lateral leads produced by septal depolarisation
are a normal finding on the ECG. Weve seen that the interventricular septum is the
first region of ventricular myocardium to depolarise and that it does so by movement of
depolarisation from left to right. This early left to right depolarisation wave is the key to
understanding the potential existence of small physiological q waves in any left lateral
lead. However, the interventricular septum is, of course, a three dimensional structure.
Depolarisation of the septum does indeed spread from left to right but this left to right
movement also travels upwards and somewhat backwards from the lower part of the
left side of the septum towards the upper part of the right. This early septal current is,
therefore, also moving away from leads II, III and aVF. For this reason it is also
perfectly acceptable to see physiological q waves in the inferior leads.
The square deflection at the end (or beginning) of each recording strip on the ECG
readout is the calibration box, an internal standard in the ECG machine. It should be
two large squares in height indicating that 1mV of electricity yields a 10 mm
vertical deflection on the ECG paper. This is the standardised sensitivity of ECG
machines. As well see in certain disease situations it is common for the height of R
waves and depth of S waves to be abnormal. This can give us useful clinical
information but always look to see if the machine calibration is correctly set before
deducing anything from the magnitude of deflections in the leads. The calibration box
should also be one large square in width this indicates that the machine is recording
at a needle speed of 25 mm/s. As weve seen, knowing the speed at which the ECG
recording needle is moving over the paper is critical as it allows us to time the events
of the cardiac cycle and to calculate the heart rate. Again well see later that it is
sometimes useful to alter the paper speed when analysing cardiac arrhythmias.
KEYPOINTS
1. The QRS complex and T waves are concordant in leads V1 and V2 in children
and young adults. However, upright T waves in leads V1 and V2 are a normal
finding in adults.
2. Physiological q waves may be seen in the left lateral and inferior leads.
3. A standard calibration box of two squares vertically and one box horizontally
indicates that the ECG machine is correctly calibrated.
2.1 The flat line recorded on the ECG when no current is flowing is called the
isoelectric line.
2.2 Atrial depolarisation produces a deflection called a P wave.
2.3 Ventricular depolarisation produces the qrs complex.
2.4 The diffuse deflection produced by ventricular repolarisation is termed a T wave.
2.5 Within the qrs complex, any positive deflection, that is a deflection above the
isoelectric line, is termed an R wave.
2.6 Any negative deflection which follows an R wave is termed an S wave.
2.7 However, if, and only if, the first deflection of the qrs complex is negative (i.e. below
the isoelectric line) this deflection is termed a q wave.
2.8 The section of the ECG recording connecting the end of the qrs complex and the
beginning of the T wave is termed the ST segment.
2.9 The junction between the ST segment and the end of the QRS complex is termed
the J point.
3.2 Repolarising current moving towards a lead produces a negative deflection on the
ECG paper, while repolarising current moving away from the lead produces a positive
deflection.
3.3 Early septal depolarisation may produce physiological q waves which may be seen
in the left lateral and inferior leads.
3.4 The left ventricle has a much greater muscle mass than the right and so dominates
the electrical signal of ventricular depolarisation in all leads.
3.5 In young, non-diseased, hearts the QRS complexes and T waves tend to be
concordant.
4.2 The frontal leads examine the heart in the vertical plane.
5.7 The normal QRS duration is less than 0.12 seconds (<3 small squares).
5.8 The QT interval varies with heart rate. The corrected (QTc) is given by QT/square
rootRR. Where QT is the QT interval measured on the ECG and RR is the distance
between R waves measured in seconds. The normal QT interval for a male is less than
0.45s, for a female it is less than 0.46s.
5.9 As a rule of thumb if the QT interval is more than half the RR interval, consider
prolonged QT.