It is not always visible on an ECG because it is a very small wave in comparison to the others. During ventricular fibrillation, the heart beats extremely fast and irregularly and can no longer pump blood, acting as a mass of quivering, disorganized muscle movements. Ventricular fibrillation will cause sudden cardiac death within minutes unless electrical resuscitation with an AED is performed immediately. It generally occurs with myocardial infarcations and heart failure, and is thought to be caused by action potentials that re-enter the AV nodes from the muscle tissue and induce rapid, irregular, weak contractions of the heart that fail to pump blood.
Learning Objectives Describe electrocardiograms and their correlation with systole. Key Points An ECG is used to measure the rate and regularity of heartbeats as well as the size and position of the chambers, the presence of damage to the heart, and the effects of drugs or devices used to regulate the heart, such as a pacemaker.
The ECG device detects and amplifies the tiny electrical changes on the skin that are caused when the heart muscle depolarizes during each heartbeat, and then translates the electrical pulses of the heart into a graphic representation.
A typical ECG tracing of the cardiac cycle heartbeat consists of a P wave atrial depolarization , a QRS complex ventricular depolarization , and a T wave ventricular repolarization. An additional wave, the U wave Purkinje repolarization , is often visible, but not always. The ST complex is usually elevated during a myocardial infarction.
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. These three waves occur in rapid succession.
The QRS complex represents the electrical impulse as it spreads through the ventricles and indicates ventricular depolarization. As with the P wave, the QRS complex starts just before ventricular contraction. The convention is that the Q wave is always negative and that the R wave is the first positive wave of the complex. If the QRS complex only includes an upward positive deflection, then it is an R wave. The S wave is the first negative deflection after an R wave. 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. 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.
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