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Why is qrs negative in v1?

3 Answer(s) Available
Answer # 1 #

The R wave is the first upward deflection after the P wave. The R wave represents early ventricular depolarisation

There are three key R wave abnormalities:

This ECG shows all the classic features of dextrocardia:

The most common cause of a dominant R wave in aVR is incorrect limb lead placement, with reversal of the left and right arm electrodes. This produces a similar pattern to dextrocardia in the limb leads but with normal R-wave progression in the chest leads. With LA/RA lead reversal:

Poor R wave progression is described with an R wave ≤ 3 mm inV3 and is caused by:

Note that absent R wave progression is characteristically seen in dextrocardia (see previous ECG).

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[5]
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Amory Stoppard
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Answer # 2 #

A complete QRS complex consists of a Q-, R- and S-wave. 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:

Figure 5 shows examples of naming of the QRS-complex.

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. The QRS duration is generally <0,10 seconds but must be <0,12 seconds. If QRS duration is ≥ 0,12 seconds (120 milliseconds) then the QRS complex is abnormally wide (broad). 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:

Figure 8 (below) shows examples of normal and abnormally wide QRS complexes at 25 mm/s and 50 mm/s paper speed.

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:

(1 mm corresponds to 0.1 mV on standard ECG grid).

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.

Normal values for R-wave peak time follow:

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.

As seen in Figure 10 (left hand side) the R-wave in V1–V2 is considerably smaller than the S-wave in V1–V2. Dominant R-wave in V1/V2 implies that the R-wave is larger than the S-wave, and this may be pathological. If the R-wave is larger than the S-wave, the R-wave should be <5 mm, otherwise the R-wave is abnormally large. This may be explained by right bundle branch block, right ventricular hypertrophy, hypertrophic cardiomyopathy, posterolateral ischemia/infarction (if the patient experiences chest pain), pre-excitation, dextrocardia or misplacement of chest electrodes.

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 have duration ≥0,03 sec and/or amplitude ≥25% of the R-wave amplitude. Pathological Q-waves must exist in at least two anatomically contiguous leads (i.e neighbouring leads, such as aVF and III, or V4 and V5) in order to reflect an actual morphological abnormality. The existence of pathological Q-waves in two contiguous leads is sufficient for a diagnosis of Q-wave infarction. This is illustrated in Figure 11.

Septal q-waves are small q-waves frequently seen in the lateral leads (V5, V6, aVL, I). 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.e the neighbouring lead, which is aVF, must not display a pathological Q-wave).

As noted above, the small r-wave in V1 is occasionally missing, which leaves a QS-complex in V1 (a QRS complex consisting of only a Q-wave is referred to as a QS-complex). 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 11. Note that pathological Q-waves must exist in two anatomically contiguous leads.

Other causes of abnormal Q-waves are as follows:

To differentiate these causes of abnormal Q-waves from Q-wave infarction, the following can be advised:

Examples of normal and pathological Q-waves (after acute myocardial infarction) are presented in Figure 12 below.

[3]
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Dardano Lloyd
Natural Science
Answer # 3 #

In right chest leads V1 and V2, the QRS complexes are predominantly negative with small R waves and relatively deep S waves because the more muscular left ventricle produces depolarization current flowing away from these leads.

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Kaushalya Gupta
ORNAMENT SETTER