This chapter includes many ECG diagnoses that are important to know and understand but do not conveniently fit into any of the other chapters.
The Wolff-Parkinson-White syndrome (WPW) consists of three ECG findings that must all be present inn order to make the diagnosis. With WPW, there is an accessory pathway between the atrium and ventricle that conducts the atrial impulse to the ventricle bypassing the AV node. The accessory pathway is responsible for all three ECG findings: short PR interval, delta wave and widened QRS complex. The short PR interval is a result of the wave of propagation activating the ventricle at the site of the accessory pathway before normal conduction through the AV node. Similarly, the delta wave is the beginning of ventricular activation prior to the wave of propagation stimulating the ventricle through the AV node. After the wave of propagation is through the AV node, normal activation of the ventricle occurs down the His-Purkinje conducting system. The combination of early activation through the accessory pathway and normal activation through the His-Purkinje system results in a fusion complex with a wide QRS complex. If the delta wave is removed, there is normal atrial-AV node-ventricular activation and the entire syndrome resolves: the PR interval returns to normal and the QRS is no longer widened.
A short PR interval (<120 milliseconds) is only part of WPW and by itself is not diagnostic. The other causes of a short PR interval are listed below.
Early repolarization is a term used to describe an ECG phenomenon that has nothing to do with repolarization. The ECG has diffuse ST segment elevation with classic "fish hook" changes. This diagnosis is classically present in young males. The most important factor is differentiating early repolarization from myocardial injury and acute pericarditis. Early repolarization will not have reciprocal ST segment depression and is a more diffuse process than myocardial injury. The use of lead V6 has been used to differentiate early repolarization from acute pericarditis. If the ST segment elevation is less than 25% of the height of the T wave then early repolarization is more likely but if the ST segment elevation is greater than 25% of the height of the T wave then acute pericarditis is more likely. Early repolarization is considered a normal variant.
Juvenile T waves is a term used to describe persistently inverted T waves in leads V2 and V3 on the ECG. Children normally have inverted T waves in lead V3 and if this persists into adulthood, it is referred to as juvenile T waves. This finding is more common in young females and is considered a normal variant.
Acute pericarditis has two characteristic findings on ECG. First is diffuse ST segment elevation. Here, diffuse does not mean all leads but will involve most leads. Lead aVL is typically spared with ST segment deviation and lead aVR may have ST segment depression. As the ST segment elevations resolve, there may then be diffuse T wave inversions in the leads that had ST segment involvement. Depression of the PR segment can also be found in acute pericarditis and is frequently in the same leads with ST segment elevation. The one exception again is lead aVR where there can be PR segment elevation.
Differentiating acute pericarditis from acute myocardial injury and early repolarization can provide some challenge. Compared to an acute injury pattern, acute pericarditis will not have reciprocal changes and may have a more diffuse pattern. There are times when separating the diagnoses based on ECG alone are not possible. Compared to early repolarization, both will have diffuse ST segment elevation but lead V6 has been used to isolate the diagnosis. If the ST segment elevation in lead V6 is less than 25% of the height of the T wave, then early repolarization is suggested. If the ST segment elevation in lead V6 is greater than 25% of the T wave height, then acute pericarditis is suggested.
The measurement of the QT interval is simple but the interpretation of the ECG is somewhat more difficult. The interval varies with several factors including age, sex, diurnal variation and heart rate. Heart rate is the biggest variable making the same QT interval prolonged at a heart rate of 100 beats per minute but normal at a heart rate of 60 beats per minute. A formula to correct for heart rate provides the corrected QT interval (QTc) and is shown.
QTc = QT interval / (R to R interval)1/2
The QTc is considered prolonged if it is greater than 460 milliseconds. The formula is cumbersome, difficult to remember and hard to calculate on a regular basis. A "shortcut" formula is also available. In this calculation, the QT interval is considered prolonged if it is over half of the R to R interval. This calculation can be done with calipers and can provide a rough estimate of QT prolongation. The interpretation and management of a prolonged QT interval is covered in the Arryhthmia module. Common causes of a prolonged QT interval include various drugs (class Ia antiarrhythmics), electrolyte abnormalities, subarachnoid or intracranial hemorrhage and congenital long QT.
There have been many criteria proposed for the diagnosis of acute pulmonary embolus on ECG. The most commonly discussed criteria is the SIQIIITIII criteria. In this proposal, the presence of an S wave in lead I along with a Q wave in lead III and an inverted T wave in lead III suggests the diagnosis of acute pulmonary embolism and may represent right ventricular strain. Other ECG criteria suggestive of right ventricular strain have also been used to suggest acute pulmonary embolism. Unfortunately, the only criteria that has been shown to be more than 50% sensitive or specific for acute pulmonary embolism is incomplete right bundle branch block and sinus tachycardia.
As with many things in medicine, the more criteria available for any diagnosis, the poorer the tool for diagnosing the disease. This is an important concept to remember when considering acute pulmonary embolism clinically and the ECG should not be relied upon in this setting.
There are two patterns involved with atrial septal defects. An atrial septal defect secundum type is represented on the ECG by an incomplete right bundle branch block and right axis deviation. An atrial septal defect primum type is represented on the ECG by an incomplete right bundle branch block and left axis deviation.
The ECG changes associated with intracerebral hemorrhage and subarachnoid hemorrhage are the same. Both have wide, deep and inverted T waves that are asymmetric and fuse with inverted U waves. The T-U wave fusion provides the asymmetry and produces a prolonged QT inverval. The T wave changes are more prominent in the precordial leads. These changes are not associated with cerebral vascular accidents.
The pattern of chronic lung disease is a constellation of four diagnoses discussed in previous chapters. Prominent P waves are present in the inferior leads and are consistent with the right atrial enlargement that develops from pulmonary hypertension. There may be ST segment depression in the inferior leads as well which represents right ventricular strain again due to pulmonary hypertension. There is right axis deviation because the heart sits more vertically in the chest due to the hyperinflation of the surrounding lungs. There may be low voltage because of the hyperinflated lungs increasing the distance between the heart and the electrical leads. The low voltage is usually more pronounced in the precordial leads, especially the left precordial leads of V5 and V6.
In dextrocardia, the heart is on the right side of the chest. Because of the heart's position in the chest, the ECG is a mirror image of the normal ECG. The axis may appear as if there is limb lead reversal with a northwest or extreme right axis deviation. The clue to differentiating these two diagnoses is the precordial leads. If limb leads have been reversed, the R wave progression of the precordial leads is normal. If dextrocardia is present, there will be R wave regression across the precordial leads.
Changes in the ECG are not present until the core temperature is below 92 degrees Fahrenheit. As hypothermia progresses, all intervals begin to lengthen. The pathognomonic ECG finding of hypothermia is the presence of Osborne waves which appear at the end of the QRS complex. Atrial fibrillation will develop in 50% of patients whose core temperature is below 90 degress Fahrenheit.
Low voltage is a commonly overread diagnosis on ECG. Criteria for the diagnosis of low voltage include all QRS complexes in the limb leads to be less than 5 millimeters and all QRS complexes in the precordial leads to be less than 10 millimeters. If there is only criteria in either the limb leads or the precordial leads, the diagnosis of low voltage can be made but with much lower specificity than if the criteria are met in both sets of leads.
Many disease processes can lead to low voltage QRS complexes but the most common are listed below.
The ECG criteria for myxedema is poor but there are characteristic changes that may suggest the presence of the disorder. The criteria include low voltage QRS complexes, flattened or inverted T waves and bradycardia. There is also a prolonged QT interval but the flattened T waves may make the interpretation difficult.
Electrical alternans refers to the varying size of the QRS complex and is present on a complex to complex basis. The alternans may also occur with the T wave or U wave as well and on rare occasion involve the P wave. The most important diagnostic utility of electrical alternans is its relationship to pericardial effusion.
Criteria on the ECG suggestive of pericardial effusion include electrical alternans, low voltage QRS complexes and tachycardia. Total electrical alternans, the alternating of the P waves as well as the QRS complex, is pathognomonic for a malignant pericardial effusion.
On a normal ECG, the R wave in the precordial leads is expected to reach at least 3 millimeters in height by lead V3. If the R wave in V3 is less than 3 mm, it is considered poor R wave progression. This entity is associated with anterior wall myocardial infarction. If the R wave in lead I is less than 4 mm and the S wave in lead I is less than 1 mm, then anterior wall myocardial infarction can be diagnosed. If the R wave in lead I is greater than 4 mm or the S wave in lead I is more than 1 mm then no definitive diagnosis can be made and the generic term of poor R wave progression is used.