Why does the isoelectric line read zero

This overall direction of travel of the electrical depolarisation through the heart is known as the electrical axis. A fundamental principle of ECG recording is that when the wave of depolarisation travels toward a recording lead this results in a positive or upward deflection. When it travels away from a recording lead this results in a negative or downward deflection. Six of these are recorded from the chest overlying the heart — the chest or precordial leads.

Four are recorded from the limbs — the limb leads. It is essential that each of the 10 recording electrodes is placed in its correct position, otherwise the appearance of the ECG will be changed significantly, preventing correct interpretation.

The limb leads record the ECG in the coronal plane, and so can be used to determine the electrical axis which is usually measured only in the coronal plane.

A horizontal line through the heart and directed to the left exactly in the direction of lead I is conventionally labelled as the reference point of 0 degrees 0 o. A detailed explanation of how to determine the axis is beyond the scope of this article but the principles mentioned here should help readers to understand the concepts involved. It is conventional to record the ECG using standard measures for amplitude of the electrical signal and for the speed at which the paper moves during the recording.

This allows:. The amplitude, or voltage, of the recorded electrical signal is expressed on an ECG in the vertical dimension and is measured in millivolts mV. On standard ECG paper 1mV is represented by a deflection of 10 mm. Cardiac axis represents the sum of depolarisation vectors generated by individual cardiac myocytes.

Clinically is is reflected by the ventricular axis, and interpretation relies on determining the relationship between the QRS axis and limb leads of the ECG below diagram. Since the left ventricle makes up most of the heart muscle under normal circumstances, normal cardiac axis is directed downward and slightly to the left:. This method allows a more precise estimation of QRS axis, using the axis diagram below.

Step 1: Find the isoelectric lead. The isoelectric equiphasic lead is the frontal lead with zero net amplitude. This can be either:. Step 2: Find the positive leads. Step 3: Calculate the QRS axis. This concept can be difficult to understand at first, and is best illustrated by some examples. Lead aVL is isoelectric , being biphasic with similarly sized positive and negative deflections no need to precisely measure this. This is an example of right axis deviation secondary to right ventricular hypertrophy.

This is an example of borderline left axis deviation due to inferior MI. This is an example of extreme axis deviation due to ventricular tachycardia. For a deeper understanding of axis determination, including a detailed explanation of the hexaxial reference system, check out this excellent series of articles from EMS lead. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation.

Hello, can I please clarify.. For this purpose, it is wise to subdivide ST-T changes into primary and secondary.

Primary ST-T changes are caused by abnormal repolarization. This is seen in ischemia, electrolyte disorders calcium, potassium , tachycardia, increased sympathetic tone, drug side effects etc. Secondary ST-T changes occur when abnormal depolarization causes abnormal repolarization. This is seen in bundle branch blocks left and right bundle branch block , pre-excitation, ventricular hypertrophy, premature ventricular complexes, pacemaker stimulated beats etc.

In each of these conditions, the depolarization is abnormal and this affects the repolarization so that it cannot be carried out normally. The next discussion will be devoted to characterizing important and common ST-T changes. ST segment depression is measured in the J point. The reference point is, as usual, the PR segment. ST segment depression less than 0. ST segment depression 0. Some expert consensus documents also note that any ST segment depression in V2—V3 should be considered abnormal because healthy individuals rarely display depressions in those leads.

Please note that every cause of ST segment depression discussed below is illustrated in Figure Study this figure carefully. Physiological ST segment depressions occur during physical exercise. Hyperventilation brings about the same ST segment depressions as physical exercise. Figure 15 A. Digoxin causes generalized ST segment depressions with a curved ST segment generalized implies that the depression can be seen in most ECG leads.

Figure 15 B. Heart failure may cause ST segment depression in the left lateral leads V5, V6, aVL and I and these depressions are generally horizontal or downsloping.

Supraventricular tachycardias also cause ST segment depressions which typically occur in V4—V6 with a horizontal or slightly upsloping ST segment. These ST segment depression should resolve within minutes after termination of the tachycardia.

Ischemic ST depressions display a horizontal or downsloping ST segment this is a requirement according to North American and European guidelines. The horizontal ST segment depression is most typical of ischemia Figure 15 C. ST segment depressions with upsloping ST segments are rarely caused by myocardial ischemia. However, there is one notable exception, when an upsloping ST segment is actually caused by ischemia and the condition is actually alarming.

Upsloping ST segment depressions which are accompanied by prominent T-waves in the majority of the precordial leads may be caused by acute occlusion of the left anterior descending coronary artery LAD.

This constellation — with upsloping ST depression and prominent T-waves in the precordial leads during chest discomfort — is referred to as de Winters sign Figure 15 C. These are all common conditions in which an abnormal depolarization altered QRS complex causes abnormalities in the repolarization altered ST-T segment.

For example, a block in the left bundle branch means that the left ventricle will not be depolarized via the Purkinje network, but rather via the spread of the depolarization from the right ventricle. The abnormal ventricular depolarization will cause abnormal repolarization. As evident from Figure 35 panel D these conditions are characterized by oppositely directed QRS- and ST-T-segments recall that this is referred to as discordance.

ST segment elevation is measured in the J-point. In the setting of chest discomfort or other symptoms suggestive of myocardial ischemia ST segment elevation is an alarming finding as it indicates that the ischemia is extensive and the risk of malignant arrhythmias is high.

However, there are many other causes of ST segment elevations and for obvious reasons, one must be able to differentiate these. Figure 16 displays characteristics of ischemic and non-ischemic ST segment elevations.

This figure must also be studied in detail. The straight ST segment can be either upsloping, horizontal or rarely downsloping. Non-ischemic ST segment elevations are typically concave Figure 16, panel B. Concave ST segment elevations are extremely common in any population; e.

There is no definite way to rule out myocardial ischemia by judging the appearance of the ST segment, which is why North American and European guidelines assert that the appearance of the ST segment cannot be used to rule out ischemia. Assessment of the T-wave represents a difficult but fundamental part of ECG interpretation. The normal T-wave in adults is positive in most precordial and limb leads. The T-wave amplitude is highest in V2—V3.

The amplitude diminishes with increasing age. As noted above, the transition from the ST segment to the T-wave should be smooth. The T-wave is normally slightly asymmetric since its downslope second half is steeper than its upslope first half. Women have a more symmetrical T-wave, a more distinct transition from ST segment to T-wave and lower T-wave amplitude. Otherwise, there is discordance opposite directions of QRS and T which might be due to pathology.

A negative T-wave is also called an inverted T-wave. T-wave changes are notoriously misinterpreted, particularly inverted T-waves. Below follows a discussion which aims to clarify some of the common misunderstandings. All T-waves are illustrated in Figure Positive T-waves are rarely higher than 6 mm in the limb leads typically highest in lead II.

In the chest leads the amplitude is highest in V2—V3, where it may occasionally reach 10 mm in men and 8 mm in women. Usually, though, the amplitude in V2—V3 is around 6 mm and 3 mm in men and women, respectively. T-waves that are higher than 10 mm and 8 mm, in men and women, respectively, should be considered abnormal.

A common cause of abnormally large T-waves is hyperkalemia, which results in high, pointed and slightly asymmetric T-waves. These must be differentiated from hyperacute T-waves seen in the very early phase of myocardial ischemia.

Hyperacute T-waves are broad-based, high and symmetric. Their duration is short; they typically disappear within minutes after a total occlusion in a coronary artery occurs then, of course, the ST segment will be elevated. T-wave inversion means that the T-wave is negative. The T-wave is negative if its terminal portion is below the baseline, regardless of whether its other parts are above the baseline. T-wave inversions are frequently misunderstood, particularly in the setting of ischemia.

An isolated single T-wave inversion in lead V1 is common and normal. It is generally concordant with the QRS complex which is negative in lead V1. In any instance, one must verify whether the inversion is isolated, because if there is T-wave inversion in two anatomically contiguous leads, then it is pathological.

Ischemia never causes isolated T-wave inversions. It is a general misunderstanding that T-wave inversions, without simultaneous ST-segment deviation, indicate acute ongoing myocardial ischemia. T-wave inversions without simultaneous ST-segment deviation are not ischemic! However, T-wave inversions that are accompanied by ST-segment deviation either depression or elevation is representative of ischemia but in that scenario, it is actually the ST-segment deviation that signals that the ischemia is ongoing.

Then one might wonder why T-wave inversions are included as criteria for myocardial infarction. This is explained by the fact that T-wave inversions do occur after an ischemic episode, and these T-wave inversions are referred to as post-ischemic T-waves.

Such T-waves are seen after periods of ischemia, after infarction and after successful reperfusion PCI. Post-ischemic T-wave inversion is caused by abnormal repolarization. These T-wave inversions are symmetric with varying depth.

They may be gigantic 10 mm or more or less than 1 mm. Negative U-waves may occur when post-ischemic T-wave inversions are present. T-wave inversions may actually become chronic after myocardial infarction. Normalization of T-wave inversion after myocardial infarction is a good prognostic indicator.

Please refer to Figure Secondary T-wave inversions — similar to secondary ST-segment depressions — are caused by bundle branch block, pre-excitation, hypertrophy, and ventricular pacemaker stimulation.

T-wave inversions that are secondary to these conditions are typically symmetric and there is simultaneous ST-segment depression. Note that the T-wave inversion may actually persist for a period after the normalization of the depolarization if it occurs. This is referred to as T-wave memory or cardiac memory. Secondary T-wave inversions are illustrated in Figure 19 as well as Figure 18 D.

T-waves with very low amplitude are common in the post-ischemic period. A biphasic T-wave has a positive and a negative deflection Figure 37, panel C. Thus, a biphasic T-wave should be classified accordingly. The T-wave vector is directed to the left, downwards and to the back in children and adolescents. This explains why these individuals display T-wave inversions in the chest leads.

T-wave inversions may be present in all chest leads. However, these inversions are normalized gradually during puberty. Some individuals may display persisting T-wave inversion in V1—V4, which is called persisting juvenile T-wave pattern. If all T-waves persist inverted into adulthood, the condition is referred to as idiopathic global T-wave inversion. T-wave progression follows the same rules as R-wave progression see earlier discussion.

A U-wave is occasionally seen after the T-wave. It is not known what engenders the U-wave. It is typically most prominent in leads V2—V3. Moreover, the U-wave is more prominent during slower heart rates. The height of the U-wave is typically one-third of the T-wave.

Its first half is steeper than its second half. Therefore, repolarization waves generally are oriented opposite of depolarization waves green versus red arrows in figure , and repolarization waves moving away from a postive recording electrode produce a positive voltage.

The T wave is longer in duration than the QRS complex that represents depolarization. The longer duration occurs because conduction of the repolarization wave is slower than the wave of depolarization. The reason for this is that the repolarization wave does not utilize the high-velocity bundle branch and purkinje system, and therefore primarily relies on cell-to-cell conduction.

Sometimes a small positive U wave may be seen following the T wave not shown in figure at top of page. This wave represents the last remnants of ventricular repolarization. Inverted T waves or prominent U waves indicates underlying pathology or conditions affecting repolarization.

The QT interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. This interval can range from 0. At high heart rates, ventricular action potentials shorten in duration, which decreases the QT interval.

Because prolonged QT intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias, it is important to determine if a given QT interval is excessively long. In practice, the QT interval is expressed as a "corrected QT QTc " by taking the QT interval and dividing it by the square root of the R-R interval interval between ventricular depolarizations.

This allows an assessment of the QT interval that is independent of heart rate.