The a form of cardiac arrhythmia in

 

 

The
reduction of dimensionality of the unit vector is achieved by projecting it on
to linearly independent basis vectors or Eigen vectors which represent the most
characteristic features of signals.

1.11 Eigen vectors

 

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac
rhythm frequently related to the electrical conduction system of the heart, in
which beats arise from fibre or group of fibres outside the region in the heart
muscle ordinarily responsible for impulse formation. It is a form of cardiac
arrhythmia in which ectopic foci within either ventricular or atrial
myocardium, or from finer branches of the electric transduction system, cause
additional beats of the heart. Some medication may worsen the condition. The effect of ectopy is estimated by analyzing an
unfiltered series (all natural cycles included) and a filtered series that
excluded ectopic beats and the 2 sinus beats that preceded and followed each
ectopic.

1.10 Effect of ectopy

 

MKLT
automatically learns individual characteristic or  “core” pattern of CCL and accommodates the
diversity of individual CCL.MKLT detect the  
presence of ectopy and changes in neurohormonal activity. It tracks
changes in CPCCL regardless of their linear or nonlinear properties.
Disturbances in CPCCL   indicate destabilization of cardiac rhythm
that precedes the onset of spontaneous sustained VTA.

1.9 MKLT (Modified Karhunen-Loeve Transform)

Figure 1-10 Cardiac cycle dynamic

 

 

Cardiac cycle reflects underlying
physiological changes and it can predict imminent arrhythmias.

1.8   Cardiac cycle dynamic

   

Figure 1-9 QRS Complex

The QT interval is measured from the beginning of
the QRS complex to the end of the T wave. The Q-T interval represents the time
for both ventricular depolarization and repolarisation to occur, and therefore
roughly estimates the duration of an average ventricular action
potential.  This interval can range from 0.2 to 0.4 seconds depending upon
heart rate.  At high heart rates, ventricular action potentials shorten in
duration, which decreases the Q-T interval.  Because prolonged Q-T
intervals can be diagnostic for vulnerability to certain types of tachyarrhythmia’s,
it is important to determine if a given Q-T interval is excessively long. 
In practice, the Q-T interval is expressed as a “corrected Q-T (QTc)”
by taking the Q-T interval and dividing it by the square root of the R-R
interval (interval between ventricular depolarizations).  This allows an
assessment of the Q-T interval that is independent of heart rate.  Normal
corrected Q-Tc intervals are less than 0.44 seconds.                      

1.7 QT interval

The PR interval is measured from the beginning of the P wave to
the beginning of the QRS complex. The P wave represents the wave of depolarization that
spreads from the SA node throughout the atria, and is usually 0.08 to 0.1
seconds (80-100 ms) in duration.  The brief isoelectric (zero voltage)
period after the P wave represents the time in which the impulse is travelling
within the AV node (where the conduction velocity is greatly retarded) and the
bundle of His. Atrial rate can be calculated by determining the time
interval between P waves. The period of time from the onset of the P wave to
the beginning of the QRS complex is termed the P-R interval,
which normally ranges from 0.12 to 0.20 seconds in duration.  This
interval represents the time between the onset of atria depolarization and the
onset of ventricular depolarization.  If the P-R interval is >0.2 sec,
there is an AV conduction block, which is also termed a first-degree heart
block if the impulse is still able to be conducted into the ventricles.

1.6   PR interval

Ventricles
contain more muscle mass than the atria, therefore the QRS complex is
considerably larger than the P wave

The
QRS complex is a recording of a single heartbeat on the ECG that corresponds to
the depolarization of the right and left ventricles significant changes in the QRS axis can be indicative of cardiac
problems.

 

Figure
1-8 Normal features of ECG

The
shape of the QRS complex in the above figure is idealized. In fact, the shape
changes depending on which recording electrodes are being used. The shape will
also change when there is abnormal conduction of electrical impulses within the
ventricles. The figure to the right summarizes the nomenclature used to define
the different components of the QRS complex

Figure
1-7 QRS complexes

Heart
rate variability (HRV) is a measure of variation in heart rate. This term has
become widely accepted though in practice, one usually measures the variation
in the beat-to-beat interval rather than the variation in the instantaneous
heart rate. The QRS complex represents ventricular
depolarization. Ventricular rate can be calculated by determining the time
interval between QRS complexes. The duration of the QRS complex is normally
0.06 to 0.1 seconds.  This relatively short duration indicates that ventricular
depolarization normally occurs very rapidly.  If the QRS complex is
prolonged (> 0.1 sec), conduction is impaired within the ventricles. 
This can occur with bundle branch blocks or whenever a ventricular foci
(abnormal pacemaker site) becomes the pacemaker driving the ventricle. Such an
ectopic foci nearly always results in impulses being conducted over slower
pathways within the heart, thereby increasing the time for depolarization and
the duration of the QRS complex.

The main feature for QRS
detection is R Peak and heart rate variability (hrv).

1.5 QRS complexes and R peak

Figure 1.6 comparison of normal and VTA defected heart

 

 

Medically
it is helpful to considered ventricular tachyarrhythmia as either being
associated with structural heart disease.

 

Because
VTA tends to recur and may be fatal, therapy is geared to managing episodes
when they occur and if possible, to preventing another episode. The Implantable
Cardioverter-Defibrillator (ICD) has become the treatment of choice for
patients with life-threatening VTA. The defibrillator is always present and
monitors continuously for VTA. If an episode of VTA commences, the ICD
automatically detects and terminates the VT without patient input. Some
patients require drug therapy in conjunction with the ICD in order to suppress
frequent VTA episodes. In general, drug therapy alone is restricted to patients
who have well-tolerated arrhythmias or to those whose life expectancy is poor
despite aggressive therapy for their arrhythmias.

Ventricular
tachycardia most often occurs in the presence of demonstrable structural heart
disease. However, in young patients with ventricular tachycardia it is common
no structural heart disease may be found. Two forms of ventricular tachycardia
are commonly found and they are right ventricular outflow tract and left
posterior septal fascicular ventricular tachycardia. Both of these tachycardias
are repetitive monomorphic ventricular tachycardia. These tachycardias are
generally well tolerated and the patients complain mainly of episodes of
palpitations or fast pulse. Unlike the VTA associated with coronary artery
disease, this VTA is not associated with an adverse prognosis. This VTA seldom
degenerates into ventricular fibrillation, and it is often responsive to drug
therapy or RF ablation.

1.4   Non structural heart disease:

Right ventricular dysplasia is a rare condition with
unclear etiology (cause) that produces VTA. It is most frequently found in
young adult males, but is seen in both sexes and at any age without overt heart
disease. With this condition a variable amount of ventricular myocardium is
replaced by fatty and fibrous tissue and contractions are abnormal. Symptoms
vary from palpitations (increase heart beat) to syncope (fainting). Some
individuals who are considered normal on physical examination experience
malaise or abrupt extreme weakness. This temporary incapacitation could lead to
create major risk for themselves and others. This VTA, more common than
thought, is emerging as a cause of sudden death in young otherwise healthy
adults.

VT
circuits can also form when patients develop heart disease that results in
altered ventricular muscle due scarring, atrophy (wasting away), or hypertrophy
(thickening). The likelihood of re-entrant arrhythmia is proportional to the
degree of myocardial involvement in the underlying disease process, although
the correlation is far from perfect.

VTA
associated with coronary artery disease is by far the most common form of VTA.
VTA can be associated with acute myocardial infarction or can also appear years
after the infarct has healed. In the case of acute myocardial infarction,
electrical changes associated with cell starvation and oxygen deprivation or
death can result in either ventricular tachycardia or ventricular fibrillation.
In the case of VTA associated with prior myocardial infarction, scar tissue
from the myocardial infarction serves as insulating boundaries that set up
anatomic areas where viable tissue can form the re-entrant pathway. Re-entry
within circuits involving or in the vicinity of a healed myocardial infarction
arises in response to metabolically-induced changes in impulse conduction or
appropriately timed premature beats in otherwise asymptomatic patients.

1.3    Structural heart disease:

Ventricular
tachycardia may give rise to symptoms such as palpitations, shortness of
breath, or light-headedness, depending upon the rate of the arrhythmia, its
duration, and the underlying heart disease. With faster heart rates and
underlying heart disease loss of consciousness (syncope) or sudden death may
occur. Episodes lasting only a few beats may produce no or minimal symptoms.
Tachycardia rates between 110 and 150 may be tolerated even if sustained for
minutes to hours. However, faster rates (>180 beats per minute) may cause
drops in arterial pressure and produce syncope. Very fast rates (>220) are
imminently dangerous because they rarely terminate spontaneously and invariably
cause drops in blood pressure and low cardiac output. Most commonly, sufferers
of ventricular tachycardia have underlying cardiac disease. In developed
countries, the majority of the patients suffer from coronary artery disease.
Although most patients having ventricular tachycardia will have underlying
coronary disease or severely depressed heart function some have no demonstrable
disease of the heart muscle or coronary arteries.

The
most dangerous rhythm is a form of polymorphic ventricular tachycardia called
ventricular fibrillation. The ECG is extremely disorganized and most often
leads to death if not corrected very quickly.

An
electrocardiogram (ECG) is a
test that records the electrical activity of the heart. An ECG is done on a person to help
diagnose heart disease. It may also be used to monitor how well different heart
muscles are working. The ECG is
used to record heart rhythms. The electrocardiogram (ECG) is a technique of
recording bioelectric currents generated by the heart. Doctors can evaluate the
conditions of a patient’s heart from the ECG and perform further diagnosis. ECG
records are obtained by sampling the bioelectric currents sensed by several
electrodes, known as leads. Ventricular tachyarrhythmia include a number of
different rhythms, which arise in a number of different situations. The
ventricular tachyarrhythmias are fast heart rhythms that arise entirely within
the ventricles. They are faster than 100 beats per minute. Generally, the
tachyarrhythmia’s can be characterized as either mono morphic ventricular
tachycardia or polymorphic ventricular tachycardia. Monomorphic ventricular
tachycardia would appear on an ECG record with a regular rate and rhythm and
fixed shape or morphology of the ECG trace. Each beat of the tachycardia would
look the same, hence the designation monomorphic. Polymorphic ventricular
tachycardia typically is irregular in rate and rhythm and has varying shapes or
morphologies on the ECG. A problem that starts as a monomorphic ventricular
tachycardia may deteriorate into polymorphic ventricular tachycardia.

1.2    View
of ECG Data:

The
series is initially sampled at unequally time points that correspond to the
times of occurrence of R peaks. Then series is resample at equal interval of
time of 500 m sec. The reason of resampling is to convert the series from time
domain to frequency domain using Fourier transform.  It is important because the power
consideration is based on the specific frequency range which are the indicators
of sympathetic and parasympathetic nervous system. The power in 0.15 – 0.4 Hz
range represents parasympathetic activity and range 0.04 Hz to 0.15 Hz
represents both sympathetic and parasympathetic effects. Linear interpolation
is used because it does not affect the low frequency components which contain
most of the energy of series.

Figure 1?5 Ventricular tachycardia

The
most dangerous rhythm is a form of polymorphic ventricular tachycardia called
ventricular fibrillation. The ECG is extremely disorganized and most often
leads to death if not corrected very quickly. There are many techniques for the
detection of VTA. The most common is MKLT which has been done using pattern
recognition method. Prediction of arrhythmias by applying pattern
recognition techniques on ECG data is an emerging and important task in
biomedical engineering. Cardiac cycle dynamics reflect underlying physiological
changes that could predict arrhythmias but are obscured by high complexity, no
stationary, and large inter individual differences. These problems can be
solved by using a pattern recognition technique called the modified
karhunen-Loeve transform (MKLT), that identifies an individual characteristic
pattern of cardiac cycle and then track the changes in the pattern by
projecting the signal on to characteristic Eigen vectors. When a disturbance is
created in core pattern, it indicated destabilization of cardiac rhythm, which
has predicted the onset of spontaneous sustained ventricular tachyarrhythmia’s
(VTA). MKLT provided greater
sensitivity and specificity. By the theoretical analysis of MKLT and describe
the effects of ectopy and slow changes in cardiac cycle on the disturbance in
the pattern, MKLT provides greater predictive accuracy than previous methods.

 

Figure 1?4 QRS Complex

                    

The
electrical activity results in P, QRS,
and T waves that have a myriad of
sizes and shapes. When viewed from multiple anatomic-electric perspectives
(that is, leads), these waves can show a wide range of abnormalities of both
the electrical conduction system and the muscle tissue of the heart’s four
pumping chambers.   

Interestingly,
the letters P, Q, R, S, and T are not abbreviations for any actual
words but were chosen many years ago for their position in the middle of the
alphabet.

The
third and last common wave in an ECG is the
T wave. This reflects the electrical activity produced when the ventricles
are recharging for the next contraction (repolarising).

Ventricular
contractions (both right and left) show as a series of 3 waves, Q-R-S, known as the QRS complex.

Atrial
contractions (both right and left) show up as the P wave.

The
ECG records the electrical activity that results when the heart muscle cells in
the atria and ventricles contract.

The
normal delay between the contraction of the atria and of the ventricles is 0.12
to 0.20 seconds. This delay is perfectly timed to account for the physical
passage of the blood from the atrium to the ventricle. Intervals shorter or
longer than this range indicate possible problems.

From
the AV node, an electrical wave travels to ventricles, causing them to contract
and pump blood.

The
AV node serves as a relay point to further propagate the electrical impulse.

Two
events occur with each discharge: (1) both atria contract, and (2) an
electrical impulse travels through the atria to reach another area of the heart
called the atrioventricular (AV) node, which lies in the wall between the 2
ventricles.

It
has “automaticity,” meaning it discharges all by itself without
control from the brain.

The
heart normally beats between 60 and 100 times per minute, with many normal
variations. For example, athletes at rest have slower heart rates than most
people. This rate is set by a small collection of specialized heart cells
called the sinoatrial (SA) or sinus node located in the right atrium, the sinus
node is the heart’s “natural pacemaker”.

 

1.1     Heart Function and the ECG:

Before describing
the ECG itself, let’s take a look at the heart’s electrical system.

Even in cases of severe brain damage,
the heart often beats normally.
An extensive network of nerves runs
throughout all 4 chambers of the heart. Electrical impulses course through
these nerves to trigger the chambers to contract with perfectly
synchronized timing much like the distributor and spark plugs of a car
make sure that an engine’s pistons fire in the right sequence.
The ECG records this electrical
activity and depicts it as a series of graph-like tracings, or waves. The
shapes and frequencies of these tracings reveal abnormalities in the
heart’s anatomy or function.

Nerves of the
heart: The heart’s function is so important to the body that it has its own
electrical system to keep it running independently of the rest of the body’s
nervous system.

This blood flows to the heart muscle
through a group of arteries that begins less than one-half inch from where
the aorta begins. These are known as the coronary arteries. These arteries
deliver oxygen to both the heart muscle and the nerves of the heart.
When something happens so that the
flow of blood through a coronary artery gets interrupted, then the part of
the heart muscle supplied by that artery begins to die. This is called
coronary heart disease, or coronary artery disease. If this condition is
not stopped, the heart itself starts to lose its strength to pump blood, a
condition known as heart failure.
When the interruption of coronary
blood flow lasts only a few minutes, the symptoms are called angina, and
there is no permanent damage to the heart. When the interruption lasts
longer, that part of the heart muscle dies. This is referred to as a heart
attack (myocardial infarction).

The heart, like
all tissues in the body, requires oxygen to function. Indeed, it is the only
muscle in the body that never rests. Thus, the heart has reserved for itself
its own blood supply.

 

Figure 1?3 blood flow in heart

The right atrium receives blood that
has completed a tour around the body and is depleted of oxygen and other
nutrients. This blood returns via 2 large veins: the superior vena cava returning
blood from the head, neck, arms, and upper portions of the chest, and the
inferior vena cava returning blood from the remainder of the body.
The right atrium pumps this blood into
the right ventricle, which, a fraction of a second later, pumps the blood
into the blood vessels of the lungs.
The lungs serve 2 functions: to
oxygenate the blood by exposing it to the air you breathe in (which is 20%
oxygen), and to eliminate the carbon dioxide that has accumulated in the
blood as a result of the body’s many metabolic functions.
Having passed through the lungs, the
blood enters the left atrium, which pumps it into the left ventricle.
The left ventricle then pumps the
blood back into the circulatory system of blood vessels (arteries and
veins). The blood leaves the left ventricle via the aorta, the largest
artery in the body. Because the left ventricle has to exert enough
pressure to keep the blood moving throughout all the blood vessels of the
body, it is a powerful pump. It is the pressure generated by the left
ventricle that gets measured when you have your blood pressure checked.

This sequence
also represents the direction of blood flow through the heart.

         Figure 1?2 human heart

                         

The heart is really 2 “half
hearts,” the right heart and the left heart, which beat
simultaneously.
Each of these 2 sides has 2 chambers:
a smaller upper chamber called the atrium (together, the 2 are called
atria), and a larger lower chamber called the ventricle.
Thus, the 4 chambers of the heart are
called the right atrium, right ventricle, left atrium, and left ventricle.

The heart is a 4-chambered muscle whose function is to pump
blood throughout the body.

To
fully understand how an ECG reveals useful information about the condition of
your heart requires a basic understanding of the anatomy (that is, the
structure) and physiology (that is, the function) of the heart.

This
is necessary because no single point (or even 2 or 3 points of view) provides a
complete picture of what is going on.

The standard 12-lead ECG that is
used throughout the world was introduced in 1942.
It is called a 12-lead ECG
because it examines the electrical activity of the heart from 12 points of
view.

The term
electrocardiogram was introduced by Willem Einthoven in 1893 at a meeting of
the Dutch Medical Society. In 1924, Einthoven received the Nobel Prize for his
life’s work in developing the ECG. The ECG has evolved over the years.

The
electrocardiogram (ECG or EKG) is a diagnostic tool that measures and records
the electrical activity of the heart in exquisite detail. Interpretation of these
details allows diagnosis in a wide range of heart conditions. These conditions
can vary from minor to life threatening.

 

Figure 1?1 ECG of a normal human
being

 

 

 

E.C.G stands for Electrocardiography. ECG is a transthoracic interpretation of the electrical activity of the
heart over time captured and externally recorded by skin electrodes. It is a
noninvasive recording produced by an electrocardiography device. Electrical impulses in the heart originate in
the senatorial node and travel through the intrinsic conducting system to the
heart muscle. The impulses stimulate the myocardial muscle fibers to contract
and thus induce systole. The electrical waves can be measured at selectively
placed electrodes on the skin. Electrodes on different sides of the heart
measure the activity of different parts of the heart muscle. An ECG displays
the voltage between pairs of these electrodes, and the muscle activity that
they measure, from different directions.

1   INTRODUCTION:

 

 

INTRODUCTION

CHAPTER# 1