Ekg what do the waves mean

A lead composed of a single positive electrode and a reference point is called a Unipolar Lead. All leads of the ECG record the same electrical impulses of the heart muscle. Diagnosis of arrhythmias may be made easier by examination of different leads. The lead ECG tracing is standard. Six leads are recorded by placing wires on each limb. The other six leads are recorded by placing wires on the chest in six specific positions.

Chest Leads: , , , , ,. For diagnosis of most arrhythmias, lead II is most commonly used. Lead II and the chest leads most consistently show the most clear P Wave which can be diagnostic of many common arrhythmias. If changes in the ECG tracing are seen in a group of the above leads, the disease can be localized to a particular area of the heart. If the MD can thus localize the damage to the heart they can also diagnose other possible problems in the heart.

Valvular problems may show up as a specific change in one or more leads of the ECG tracing. Blockages in one of the major arteries of veins may also show up as an altered deflection in the ECG. Below is a diagram of the chest and the placement of leads of the chest so as to trace leads I and II.

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. U-wave inversion is rare but when seen, it is a strong indicator of pathology, particularly for ischemic heart disease and hypertension. The QT duration represents the total time for de- and repolarization. It is measured from the beginning of the QRS-complex to the end of the T-wave.

Prolonged QT duration predisposes to life-threatening ventricular arrhythmias and therefore QT duration must always be assessed. Prolonged QT duration may either be congenital genetic mutations, so-called long QT syndrome or acquired medications, electrolyte disorders. Fortunately, basic ECG interpretation can be rather straightforward, as long as you know the basics. An electrocardiogram is a tracing of the electrical activity that is taking place within the heart.

Under normal circumstances, an electrical impulse will travel from the sinoatrial node, spread across the atrium, to the atrioventricular node and through the ventricular septum of the heart. This electrical impulse causes the four chambers of the heart to contract and relax in a coordinated fashion. Studying these electrical impulses allows us to understand how the heart is functioning.

The P wave represents the depolarization of the left and right atrium and also corresponds to atrial contraction. Strictly speaking, the atria contract a split second after the P wave begins. Because it is so small, atrial repolarization is usually not visible on ECG. In most cases, the P wave will be smooth and rounded, no more than 2.

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.

Normal corrected Q-c intervals are 0. There is no distinctly visible wave representing atrial repolarization in the ECG because it occurs during ventricular depolarization. Because the wave of atrial repolarization is relatively small in amplitude i.

ECG tracings recorded simultaneous from different electrodes placed on the body produce different characteristic waveforms. Cardiovascular Physiology Concepts Richard E.