What does qrs represent

The point where the T Wave returns to the baseline marks the end of the T Wave. Often the onset and end of the T Wave are difficult to determine with certainty. The U Wave probably represents repolarization of a small segment of the ventricles, such as the papillary muscles or ventricular septum, after most of the right and left ventricles have been repolarized.

Although uncommon, and not easily identified, the U Wave can best be seen when the heart rate is slow. A U Wave indicates that the repolarization of the ventricles has occurred. An abnormally tall U wave may be present in hypokalemia, cardiomyopathy, left ventricle hypertrophy, diabetes, and may follow administration of digitalis and quinidine.

The lead EKG will be discussed in greater detail later in this course. However, at this time we will present an introduction to the EKG leads simply to help explain the basics of EKG interpretation that will follow. Later, the specifics of leads and lead placement will be discussed. An EKG lead consists of two surface electrodes of opposite polarity positive and negative or one positive surface electrode and one reference point. A lead composed of two electrodes of opposite polarity is called a Bipolar Lead.

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: , , , , ,. 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. 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 the 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 the 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. 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.

The ST segment corresponds to the plateau phase of the action potential Figure The ST segment extends from the J point to the onset of the T-wave. Because of the long duration of the plateau phase most contractile cells are in this phase at the same time more or less. Moreover, the membrane potential is relatively unchanged during the plateau phase.

These two factors are the reason why the ST segment is flat and isoelectric i. Displacement of the ST segment is of fundamental importance, particularly in acute myocardial ischemia. The electrical potential difference exists between ischemic and normal myocardium and it results in the displacement of the ST segment. The term ST segment deviation refers to elevation and depression of the ST segment. The magnitude of ST segment deviation is measured as the height difference in millimeters between the J point and the PR segment.

Refer to Figure 13 for examples. It must also be noted that the J point is occasionally suboptimal for measuring ST segment deviation.

This is explained by the fact that the J point is not always isoelectric; this occurs if there are electrical potential differences in the myocardium by the end of the QRS complex it typically causes J point depression. The reason for such electrical potential difference is that not all ventricular myocardial cells will finish their action potential simultaneously.

Myocardial cells which depolarized at the beginning of the QRS complex will not be in the exact same phase as cells that depolarized during the end of the QRS complex. At the time of J and J, there is minimal chance that there are any electrical potential differences in the myocardium. Current guidelines, however, still recommend the use of the J point for assessing acute ischemia Third Universal Definition of Myocardial Infarction, Thygesen et al, Circulation. A notable exception to this rule is the exercise stress test, in which the J or J is always used because exercise frequently causes J point depression.

As mentioned above there are numerous other conditions that affect the ST-T segment and it is fundamental to be able to differentiate these. 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. In sinus rhythm when the SA node is the pacemaker, the mean direction of atrial depolarization the P wave axis points downward and to the left, in the general direction of lead II within a coordinate between 15 o and 75 o and away from lead aVR.

On this count the P wave is always positive in lead II and always negative in lead aVR during sinus rhythm. Conversely, a P wave that is positive in lead II and negative in lead aVR indicates normal P wave axis and sinus rhythm. The second wave is the QRS complex. Typically this complex has a series of 3 deflections that reflect the current associated with right and left ventricular depolarization. By convention the first deflection in the complex, if it is negative, is called a Q wave.

The first positive deflection in the complex is called an R wave. A negative deflection after an R wave is called an S wave. Some QRS complexes do not have all three deflections. But irrespective of the number of waves present, they are all QRS complexes:. NB: The first wave of the last complex is a negative deflection.