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Biomedical Signal and Image Processing
9.4.3 VENTRICULAR TACHYCARDIA
A rhythm of ventricular origin may be a consequence of a slower conduction in ischemic ventricular muscle that leads to circular activation (reentry). This results in the
activation of ventricular muscles at a high rate (over 120 beats per minute), causing rapid
and wide QRS complexes. Such an arrhythmia is called ventricular tachycardia (VT).
VT is often a consequence of ischemia and myocardial infarction. The main
change in ECG that indicates the occurrence of VT is the very fast heart rate that can
be easily detected in the Fourier domain using discrete Fourier transform, or DFT.
9.4.4 VENTRICULAR FIBRILLATION
When ventricular depolarization occurs chaotically, the situation is called ventricular
fibrillation. This is reflected in the ECG, which demonstrates coarse irregular undulations without QRS complex. The cause of fibrillation is the establishment of multiple reentry loops usually involving diseased heart muscle. In this type of arrhythmia,
the contraction of the ventricular muscle is also irregular, and, therefore, the timing
is ineffective at pumping blood. The lack of blood circulation leads to almost immediate loss of consciousness and even death within minutes. The ventricular fibrillation may be stopped with an external defibrillator pulse and appropriate medication.
9.4.5 MYOCARDIAL INFARCTION
If a coronary artery is occluded, the transport of oxygen to the cardiac muscle is
decreased, causing an oxygen debt in the muscle, which is called ischemia. Ischemia
causes changes in the resting potential and in the repolarization of the muscle cells.
This abnormality is observed in ECG as changes in the shape of the T wave. If the
oxygen transport is terminated in a certain area, the heart muscle dies in that region.
This is called a myocardial infarction or heart attack. After a blockage in the blood
vessels supplying the heart muscle with oxygen and nutrients, the muscle cells in the
region are severely compromised. Some cells may die while others will suffer severe
damage, all resulting in a decreased ability to conduct impulses by generating its
own depolarization. The dead cells will eventually be replaced by collagen since the
heart does not have the ability to regenerate.
An infarct area is electrically silent since it has lost its excitability. According
to the solid angle theorem described in Chapter 8, the loss of this outward dipole is
equivalent to an electric force pointing inward. With this principle, it is possible to
locate the infarction. The compromised cells will generate an action potential in a
much slower fashion, causing a localized delay in the depolarization wave front. If
this delay is enough to emerge at the time that healthy cells have already been repolarized, a subsequent delayed depolarization wave front may pass through the region
of the heart that had just contracted. This generates a chaotic electric pattern and a
disorganized contraction agreement.
Figure 9.11 shows nine sections of a recording in combined Einthoven and Wilson
electrode placement of an inferior myocardial infarction. A heart attack can result in
various deviating ECG patterns. In many heart attack cases, due to the existence of
Biomedical Signal and Image Processing
9.4.3 VENTRICULAR TACHYCARDIA
A rhythm of ventricular origin may be a consequence of a slower conduction in ischemic ventricular muscle that leads to circular activation (reentry). This results in the
activation of ventricular muscles at a high rate (over 120 beats per minute), causing rapid
and wide QRS complexes. Such an arrhythmia is called ventricular tachycardia (VT).
VT is often a consequence of ischemia and myocardial infarction. The main
change in ECG that indicates the occurrence of VT is the very fast heart rate that can
be easily detected in the Fourier domain using discrete Fourier transform, or DFT.
9.4.4 VENTRICULAR FIBRILLATION
When ventricular depolarization occurs chaotically, the situation is called ventricular
fibrillation. This is reflected in the ECG, which demonstrates coarse irregular undulations without QRS complex. The cause of fibrillation is the establishment of multiple reentry loops usually involving diseased heart muscle. In this type of arrhythmia,
the contraction of the ventricular muscle is also irregular, and, therefore, the timing
is ineffective at pumping blood. The lack of blood circulation leads to almost immediate loss of consciousness and even death within minutes. The ventricular fibrillation may be stopped with an external defibrillator pulse and appropriate medication.
9.4.5 MYOCARDIAL INFARCTION
If a coronary artery is occluded, the transport of oxygen to the cardiac muscle is
decreased, causing an oxygen debt in the muscle, which is called ischemia. Ischemia
causes changes in the resting potential and in the repolarization of the muscle cells.
This abnormality is observed in ECG as changes in the shape of the T wave. If the
oxygen transport is terminated in a certain area, the heart muscle dies in that region.
This is called a myocardial infarction or heart attack. After a blockage in the blood
vessels supplying the heart muscle with oxygen and nutrients, the muscle cells in the
region are severely compromised. Some cells may die while others will suffer severe
damage, all resulting in a decreased ability to conduct impulses by generating its
own depolarization. The dead cells will eventually be replaced by collagen since the
heart does not have the ability to regenerate.
An infarct area is electrically silent since it has lost its excitability. According
to the solid angle theorem described in Chapter 8, the loss of this outward dipole is
equivalent to an electric force pointing inward. With this principle, it is possible to
locate the infarction. The compromised cells will generate an action potential in a
much slower fashion, causing a localized delay in the depolarization wave front. If
this delay is enough to emerge at the time that healthy cells have already been repolarized, a subsequent delayed depolarization wave front may pass through the region
of the heart that had just contracted. This generates a chaotic electric pattern and a
disorganized contraction agreement.
Figure 9.11 shows nine sections of a recording in combined Einthoven and Wilson
electrode placement of an inferior myocardial infarction. A heart attack can result in
various deviating ECG patterns. In many heart attack cases, due to the existence of