In order to address these obstacles, we propose novel signal processing techniques that seek to not only establish the status of the ECG as an indisputable fixture in biometric research, but also reinforce its versatile utility, such as in alleviating the resource consumption in certain communication networks.
ECG signals reflect the variations in electrical potential of the heart over time. The change in voltage is due to the action potentials of cardiac cells. The electrical activity is initiated when the sinoatrial SA node, the pacemaker of the heart, depolarizes. This electrical signal then travels rhythmically until it reaches the atrioventricular AV node, which is responsible for delaying the conduction rate, to properly pump blood from the atria into the ventricles.
The P wave describes the depolarization of the right and left atria. The amplitude of this wave is relatively small, because the atrial muscle mass is limited. The QRS complex corresponds to the largest wave, since it represents the depolarization of the right and left ventricles, being the heart chambers with substantial mass.
Finally, the T wave depicts the ventricular repolarization. It has a smaller amplitude, compared to the QRS complex, and is usually observed ms after this larger complex. However, its precise position depends on the heart rate, e. However, this is highly dependent on emotional factors, such as stress, anxiety, and shock, as well as on cardiovascular activities, such as running and exercising. One of the main problems in biometric signal processing is the high degree of noise and variations.
In many cases, a reliable acquisition is only possible with sufficient knowledge of the spectral content, the dynamic range and other characteristics of not only the desired signal components, but also of the noise sources involved. This is so that the appropriate filters and quantizers can be accordingly constructed to extract the desired signals, and reject the noise sources. Based on the salient characteristics of ECG signal components, the P wave is a lower-amplitude and lower-frequency signal, while the QRS complex exhibits larger-amplitude and higher-frequency variations.
In addition, the following sources of noise and artifacts are relevant to ECG. However, all three waves may not be visible and there is always variation between the leads.
Some leads may display all waves, whereas others might only display one of the waves. Regardless of which waves are visible, the wave s that reflect ventricular depolarization is always referred to as the QRS complex. Naming of the waves in the QRS complex is easy but frequently misunderstood.
The following rules apply when naming the waves:. The QRS complex can be classified as net positive or net negative, referring to its net direction. The QRS complex is net positive if the sum of the positive areas above baseline exceeds that of the negative areas below baseline.
Refer to Figure 6 , panel A. These calculations are approximated simply by eyeballing. Panel B in Figure 6 shows a net negative QRS complex, because the negative areas are greater than the positive area. Depolarization of the ventricles generate three large vectors, which explains why the QRS complex is composed of three waves. It is fundamental to understand the genesis of these waves and although it has been discussed previously a brief rehearsal is warranted.
Figure 7 illustrates the vectors in the horizontal plane. Study Figure 7 carefully, as it illustrates how the P-wave and QRS complex are generated by the electrical vectors. Note that the first vector in Figure 7 is not discussed here as it belongs to atrial activity. The ventricular septum receives Purkinje fibers from the left bundle branch and therefore depolarization proceeds from its left side towards its right side. The vector is directed forward and to the right.
The ventricular septum is relatively small, which is why V1 displays a small positive wave r-wave and V5 displays a small negative wave q-wave. Thus, it is the same electrical vector that results in an r-wave in V1 and q-wave in V5. The vectors resulting from activation of the ventricular free walls is directed to the left and downwards Figure 7.
The explanation for this is as follows:. As evident from Figure 7 , the vector of the ventricular free wall is directed to the left and downwards.
Lead V5 detects a very large vector heading towards it and therefore displays a large R-wave. Lead V1 records the opposite, and therefore displays a large negative wave called S-wave.
The final vector stems from activation of the basal parts of the ventricles. The vector is directed backwards and upwards. It heads away from V5 which records a negative wave s-wave. Lead V1 does not detect this vector. Prolongation of QRS duration implies that ventricular depolarization is slower than normal.
This is very common and a significant finding. The reason for wide QRS complexes must always be clarified. Clinicians often perceive this as a difficult task despite the fact that the list of differential diagnoses is rather short.
The following causes of wide QRS complexes must be familiar to all clinicians:. A QRS complex with large amplitudes may be explained by ventricular hypertrophy or enlargement or a combination of both. The electrical currents generated by the ventricular myocardium are proportional to the ventricular muscle mass.
Hypertrophy means that there is more muscle and hence larger electrical potentials generated. However, the distance between the heart and the electrodes may have a significant impact on amplitudes of the QRS complex. For example, slender individuals generally have a shorter distance between the heart and the electrodes, as compared with obese individuals. Therefore, the slender individual may present with much larger QRS amplitudes. Similarly, a person with chronic obstructive pulmonary disease often display diminished QRS amplitudes due to hyperinflation of thorax increased distance to electrodes.
Low amplitudes may also be caused by hypothyreosis. In the setting of circulatory collapse, low amplitudes should raise suspicion of cardiac tamponade. It is important to assess the amplitude of the R-waves. High amplitudes may be due to ventricular enlargement or hypertrophy.
To determine whether the amplitudes are enlarged, the following references are at hand:. R-wave peak time Figure 9 is the interval from the beginning of the QRS-complex to the apex of the R-wave. This interval reflects the time elapsed for the depolarization to spread from the endocardium to the epicardium. R-wave peak time is prolonged in hypertrophy and conduction disturbances. R-wave progression is assessed in the chest precordial leads. Normal R-wave progression implies that the R-wave gradually increases in amplitude from V1 to V5 and then diminishes in amplitude from V5 to V6 Figure 10 , left hand side.
The S-wave undergoes the opposite development. Abnormal R-wave progression is a common finding which may be explained by any of the following conditions:.
Note that the R-wave is occassionally missing in V1 may be due to misplacement of the electrode. This is considered a normal finding provided that an R-wave is seen in V2. It is crucial to differentiate normal from pathological Q-waves, particularly because pathological Q-waves are rather firm evidence of previous myocardial infarction. However, there are numerous other causes of Q-waves, both normal and pathological and it is important to differentiate these.
The amplitude depth and the duration width of the Q-wave dictates whether it is abnormal or not. Pathological Q-waves must exist in at least two anatomically contiguous leads i. The existence of pathological Q-waves in two contiguous leads is sufficient for a diagnosis of Q-wave infarction. This is illustrated in Figure They are due to the normal depolarization of the ventricular septum see previous discussion. Two small septal q-waves can actually be seen in V5—V6 in Figure 10 left hand side.
An isolated and often large Q-wave is occasionally seen in lead III. The amplitude of this Q-wave typically varies with ventilation and it is therefore referred to as a respiratory Q-wave. Note that the Q-wave must be isolated to lead III i. This is considered a normal finding provided that lead V2 shows an r-wave.
If the R-wave is missing in lead V2 as well, then criteria for pathology is fulfilled two QS-complexes. Small Q-waves which do not fulfill criteria for pathology may be seen in all limb leads as well as V4—V6. If these Q-waves do not fulfill criteria for pathology, then they should be accepted.
Leads V1—V3, on the other hand, should never display Q-waves regardless of their size. The most common cause of pathological Q-waves is myocardial infarction. If myocardial infarction leaves pathological Q-waves, it is referred to as Q-wave infarction. Criteria for such Q-waves are presented in Figure Note that pathological Q-waves must exist in two anatomically contiguous leads.
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