Interpreting the Electrocardiogram

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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 thorax increased distance to electrodes. Low amplitudes may also be caused by hypothyreosis.

Interpreting the Electrocardiogram

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. 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 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 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 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.

New recommendations on interpreting athletes' ECG results prepared by Stanford team

Myocardial cells which depolarized at the beginning of the QRS complex will not be in the exact same phase as cells which 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.

ECG Learning Center - An introduction to clinical electrocardiography

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.

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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 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 my 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 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.

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  4. 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. QT duration is inversely related to heart rate; QT duration increases at low heart rate and vice versa.

    The formula follows all variables in seconds :. QTc duration is calculated automatically in all modern ECG machines. First-degree atrioventricular block is defined as a PR interval of more than ms, with every P wave being conducted Fig. Second-degree atrioventricular block Fig. In Mobitz type I block, the PR interval is progressively prolonged, eventually resulting in a dropped beat. Third-degree atrioventricular block is known as complete heart block, with the P wave failing to conduct into the ventricle, thus resulting in atrioventricular dissociation Fig. The ventricular rhythm is usually taken over by a slower junctional rhythm.

    A conduction defect in the bundle branches, such as right or left bundle branch block, causes the QRS complex to widen. Left bundle branch block is important because the widened QRS is also associated with ST change, which may be mistaken for ischemia. B Rhythm strip demonstrating second-degree atrioventricular block with progressive lengthening of PR interval and 2 P waves per R—R interval arrows.

    C Rhythm strip demonstrating third-degree atrioventricular block. Atrioventricular dissociation results in no QRS but prominent P wave. Absence of Q wave allows visualization of repolarization of atria arrow.

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    There are 3 main types of supraventricular tachyarrhythmias: those of sinoatrial origin sinoatrial node reentrant tachycardia , those of atrial origin atrial tachycardia [unifocal or multifocal], atrial fibrillation, or atrial flutter , and those of atrioventricular junctional origin atrioventricular junctional reentrant tachycardia or accessory atrioventricular reentrant tachycardia, including Wolff-Parkinson-White syndrome.

    Atrial fibrillation is characterized by chaotic electrical activity in the atrium, with the loss of synchronized atrial contraction. A ventricular rate of less than bpm during atrial fibrillation is considered well controlled. A Atrial fibrillation with rapid ventricular response. No P waves are seen, and ventricular rate is irregular and rapid. QRS complex is narrow. B Atrial flutter with sawtooth flutter wave arrows.

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    D Ventricular ectopic beats. E Ventricular pacing spikes arrow and QRS morphology associated with left bundle branch block. The electrocardiogram may show the sawtooth flutter wave, with the QRS conduction ratio varying from to Fig. Atrial tachycardia is a relatively uncommon form of atrial arrhythmia. The impulse comes from within the atrium but not from the sinoatrial node. Atrial tachycardia may be associated with drug toxicity such as digoxin overdose. More rarely, atrial tachycardia can be due to a reentrant mechanism. Atrial ectopic beats are associated with premature atrial contraction and manifest quite differently from premature ventricular contraction.

    They result from premature depolarization that produces a normal QRS because atrioventricular node conduction is normal. There may be atrioventricular dissociation during tachycardia, with the P wave bearing no relation to the QRS complex. VT is usually due to reentrance within the ventricle associated with ischemic heart disease or some types of cardiomyopathy.

    There are also hereditary forms of VT with normal cardiac structures, but these are relatively uncommon. VT is a life-threatening arrhythmia that leads to hemodynamic compromise and may degenerate into ventricular fibrillation VF , a form of chaotic ventricular electrical activity Fig. This is the most common type of cardiac arrest. Ventricular ectopic beats are associated with premature ventricular contraction.

    Typically, the electrocardiogram has a wide QRS complex that occurs earlier than expected and with a higher voltage amplitude and has an inverted T wave that obscures the P wave Fig. Depolarization of the ventricles occurs prematurely outside the usual conduction pathway and, consequently, is slower, producing the wide and unusually shaped QRS.

    This also results in less efficient ventricular contraction. Junctional tachycardia caused by a reentrant mechanism from a pathway close to the atrioventricular node is known as atrioventricular junctional reentrant tachycardia. Reentrance through an additional pathway outside the atrioventricular node—an accessory pathway—may also cause junctional tachycardia.

    The ventricular rate during junctional reentrant tachycardia is usually rapid, at more than bpm. The P wave may not be visible or may follow closely behind the QRS complex. In electrocardiogram interpretation, one should first check the heart rate for bradycardia or tachycardia and then determine whether the rhythm is sinus by checking for the P wave.

    The presence of the P wave does not always mean sinus rhythm. If the P wave is upright in aVR and inverted in aVL, it is traveling from left to right, which is the opposite of the normal P vector. The limb lead placement should then be checked, as misplacement of the leads is the most common cause of this pattern. If the rhythm is sinus, the relationship between the P wave and the QRS should be checked. Atrioventricular block is present if the P wave is not entirely conducted.

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    If the rhythm is not sinus and the P wave is absent, one should check whether the QRS rate is irregular, as would be the case in atrial fibrillation. One should also check the width of the QRS complex, for the sawtooth appearance of atrial flutter, and for right and left bundle branch block morphology. In cases of a widened QRS complex with a normal heart rate, one should check for ventricular pacing spikes because ventricular pacing causes a wide QRS complex with left bundle branch block morphology Fig.

    When the electrocardiogram shows a nonsinus tachyarrhythmia with a narrow and regular QRS complex, the main differential diagnoses are junctional reentrant tachycardia and atrial flutter. Wide-QRS-complex tachycardia is much more serious, as it can represent VT, which is life-threatening. Junctional reentrant tachycardia with aberrant conduction leading to wide-QRS-complex tachycardia may masquerade as VT.

    Distinguishing between VT and junctional reentrant tachycardia with aberrant conduction requires considerable experience. If in doubt, one should consider the tachyarrhythmia to represent VT until proven otherwise. Other than cardiac arrhythmia, the electrocardiogram is a key diagnostic test for myocardial ischemia and acute myocardial infarction. The electrocardiogram ECG is one of the most common, enduring, and important tests in all of medicine. It's easy to perform, noninvasive, produces results right away, and is useful in diagnosing dozens of heart conditions.

    The ECG has taken on even more importance lately because a particular ECG pattern, called ST elevation, is a strong indication that a serious heart attack has occurred, and there's more emphasis than ever on treating heart attacks as soon as possible. An ECG isn't necessarily going to be part of a routine physical, but if you need medical attention because you have chest pain, sudden unexplained shortness of breath, or other symptoms that suggest a possible heart attack, you will almost certainly get an ECG.

    The ECG is a reading of the electrical impulses in the heart that activate the heart muscle and its blood-pumping action. Twelve electrodes affixed to the skin on the chest, arms, and legs sense those impulses from various vantage points. Part of the reason the ECG has had such staying power is that the output is visual: a line graph with peaks and valleys, not a stream of numbers. As a result, reading an ECG is a matter of pattern recognition, not computation.

    There are many permutations, but someone can be trained to recognize the most common patterns relatively quickly.

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