Step 3 — Cardiac axis. Step 4 — P-waves. Step 5 — P-R interval. Step 6 — QRS complex. Step 7 — ST segment. Step 8 — T waves. The ST Segment represents the interval between ventricular depolarization and repolarization. Bifid P waves known as P mitrale indicate left-atrial abnormality - e.
Absence of the P wave with a flat baseline may indicate: Fine atrial fibrillation. Sinoatrial arrest with a secondary escape rhythm. ST elevation refers to a finding on an electrocardiogram wherein the trace in the ST segment is abnormally high above the baseline. The placement of the electrodes for the standard limb leads is shown in this figure. Lead I is constructed by comparing the left arm as positive to the right arm's electrode as negative as shown in the next figure.
The zero point is in the center of the lead indicated by the hash mark. So the first electrical signal on a normal ECG originates from the atria and is known as the P wave. Although there is usually only one P wave in most leads of an ECG , the P wave is in fact the sum of the electrical signals from the two atria, which are usually superimposed. Technically, a Q wave indicates that the net direction of early ventricular depolarization QRS electrical forces projects toward the negative pole of the lead axis in question.
The QRS complex is ventricular depolarization. The T wave is ventricular repolarization. It is typically much wider than the ventricular depolarization that generates the QRS.
Sometimes it is upside down inverted. Sometimes half of it is upside down and the other half upright; this is called biphasic. The ' U ' wave is a wave on an electrocardiogram ECG. It comes after the T wave of ventricular repolarization and may not always be observed as a result of its small size. The ST segment must always be studied carefully since it is altered in a wide range of conditions.
Many of these conditions cause rather characteristic ST segment changes. The ST segment is of particular interest in the setting of acute myocardial ischemia because ischemia causes deviation of the ST segment ST segment deviation.
There are two types of ST segment deviations. ST segment depression implies that the ST segment is displaced, such that it is below the level of the PR segment. ST segment elevation implies that the ST segment is displaced, such that it is above the level of the PR segment. The J point is the point where the ST segment starts. If the baseline PR segment is difficult to discern, the TP interval may be used as the reference level. The T-wave reflects the rapid repolarization of contractile cells phase 3 and T-wave changes occur in a wide range of conditions.
T-wave changes are frequently misunderstood in clinical practice, which the discussion below will attempt to cure. The transition from the ST segment to the T-wave should be smooth and not abrupt. The normal T-wave is slightly asymmetric, with a steeper downward slope. The U-wave is seen occasionally. It is a positive wave occurring after the T-wave.
The U-wave is most frequently seen in leads V2—V4. Individuals with prominent T-waves, as well as those with slow heart rates, display U-waves more often.
The genesis of the U-wave remains elusive. QT duration reflects the total duration of ventricular depolarization and repolarization. It is measured from the onset of the QRS complex to the end of the T-wave. The QT duration is inversely related to heart rate; i. Therefore to determine whether the QT interval is within normal limits, it is necessary to adjust for the heart rate.
A long QTc interval increases the risk of ventricular arrhythmias. ECG interpretation usually starts with an assessment of the P-wave. The P-wave is a small, positive and smooth wave. It is small because the atria make a relatively small muscle mass. If the rhythm is sinus rhythm i. The P-wave is always positive in lead II during sinus rhythm.
This is rather easy to understand because lead II is angled alongside the P-wave vector, and the exploring electrode is located in front of the P-wave vector Figure 2, right-hand side. The P-wave vector is slightly curved in the horizontal plane. It is initially directed forward but then turns left to activate the left atrium Figure 2 , left-hand side.
Lead V1 might therefore display a biphasic diphasic P-wave , meaning that the greater portion of the P-wave is positive but the terminal portion is slightly negative the vector generated by left atrial activation heads away from V1. Occasionally, the negative deflection is also seen in lead V2.
Figure 2 above does not show that the P-wave in lead II might actually be slightly asymmetric by having two humps.
This is often but not always seen on ordinary ECG tracings and it is explained by the fact that the atria are depolarized sequentially, with the right atrium being depolarized before the left atrium.
The first half of the P-wave is therefore a reflection of right atrial depolarization and the second half is a reflection of left atrial depolarization. This is shown in Figure 3 upper panel. Recall that the P-wave in V1 is often biphasic, which is also shown in Figure 3. If an atrium becomes enlarged typically as a compensatory mechanism its contribution to the P-wave will be enhanced. Enlargement of the left and right atria causes typical P-wave changes in lead II and lead V1 Figure 3.
Enlargement of the right atrium is commonly a consequence of increased resistance to empty blood into the right ventricle. This may be due to pulmonary valve stenosis, increased pulmonary artery pressure etc. The right atrium must then enlarge hypertrophy in order to manage to pump blood into the right ventricle. Right atrial enlargement hypertrophy leads to stronger electrical currents and thus enhancement of the contribution of the right atrium to the P-wave. The P-wave will display higher amplitude in lead II and lead V1.
Such a P-wave is called P pulmonale because pulmonary diseases are the most common causes Figure 3, P-pulmonale. If the left atrium encounters increased resistance e. The second hump in lead II becomes larger and the negative deflection in V1 becomes deeper. This is called P mitrale , because mitral valve disease is a common cause Figure 25, P-mitrale. If the atria are depolarized by impulses generated by cells outside of the sinoatrial node i. If the ectopic focus is located close to the sinoatrial node, the P-wave will have a morphology similar to the P-wave in sinus rhythm.
However, an ectopic focus may be located anywhere. If it is located near the atrioventricular node, the activation of the atria will proceed in the opposite direction, which produces an inverted retrograde P-wave. It reflects the time interval from the start of atrial depolarization to the start of ventricular depolarization.
The PR interval is assessed in order to determine whether impulse conduction from the atria to the ventricles is normal in terms of speed. The PR interval must not be too long nor too short.
A normal PR interval ranges between 0. Numerous conditions can diminish the capacity of the atrioventricular node to conduct the atrial impulse to the ventricles.
As the conduction diminishes, the PR interval becomes longer. When the PR interval exceeds 0. The term block is somewhat misleading since it is actually a matter of abnormal delay and not a block per se. The most common cause of first-degree AV-block is degenerative age-related fibrosis in the conduction system. Note that the upper reference limit 0.
Refer to Figure 4 second panel. AV-blocks are discussed in detail later. The atrioventricular AV node is normally the only connection between the atria and the ventricles. The atria and the ventricles are electrically isolated from each other by the fibrous rings anulus fibrosus. However, it is not rare to have an additional — accessory — pathway between the atria and the ventricles. Such an accessory pathway is an embryological remnant that may be located almost anywhere between the atria and the ventricles.
It enables the atrial impulse to pass directly to the ventricles and start ventricular depolarization prematurely. The condition is referred to as pre-excitation because the ventricles are excited prematurely.
This is illustrated in Figure 4 third panel. As seen in Figure 4 third panel the initial depolarization of the ventricles starting where the accessory pathway inserts into the ventricular myocardium is slow because the impulse will not spread via the normal His-Purkinje pathway.
The slow initial depolarization is seen as a delta wave on the ECG Figure 4 , third panel. However, apart from the delta wave, the R-wave will appear normal because ventricular depolarization will be executed normally as soon as the atrioventricular node delivers the impulse to the His-Purkinje system. 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. The 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 generates 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 are 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 the activation of the basal parts of the ventricles.
The vector is directed backward 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 are more muscles and hence larger electrical potentials generated. However, the distance between the heart and the electrodes may have a significant impact on the 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 COPD often displays diminished QRS amplitudes due to hyperinflation of the 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 occasionally 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 dictate 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 the previous discussion.
Two small septal q-waves can actually be seen in V5—V6 in Figure 10 left-hand side. Beyond this frequency, unwanted signals due to muscle activity or from the mains supply must be filtered out.
Uniform frequency respose across the full range - Its frequency response should be even across the frequency range otherwise the output voltage from the amplifier will be distorted. High input impedance - A high input impedance is vital otherwise most of the input pd will be lost due to body and contact resistance where the electrodes are on the skin.
You should be aware that contact resistance is lowered as much as possible by using a conducting paste between the electrode surface and the skin. However, the remaining resistance due to body fluids can be as much as The input resistance of the amplifier and the patient's electrical resistance form a potential divider so the 'source' pd the pd from the biopotential between the L and R of the body will be split in the same ratio as the two resistances.
If the input resistance is not much higher than the patient's resistance, the input pd to the amplifier will be roughly half that of the source pd.
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