Important Limitations of the ECG

The diagnostic accuracy of any test is determined by the percentages of false-positive and false-negative results. The sensitivity of a test is a measure of the percentage of patients with a particular abnormality that can be identified by an abnormal test result. For example, a test with 100% sensitivity has no false-negative results. The more false-negative results, the less sensitive is the test. The specificity of a test is a measure of the percentage of false-positive results. The more false-positive test results, the less specific is the test.

Like most clinical tests the ECG yields both false-positive and false-negative results, as previously defined. A false-positive result is exemplified by an apparently abnormal ECG in a normal subject. For example, prominent precordial voltage may occur in the absence of left ventricular hypertrophy (LVH) (see Chapter 6). Furthermore, Q waves may occur as a normal variant and therefore do not always indicate heart disease (see Chapters 8 and 9). In other cases, Q waves may be abnormal (e.g., due to hypertrophic cardiomyopathy) but lead to a mistaken diagnosis of myocardial infarction (MI).

False-negative results, on the other hand, occur when the ECG fails to show evidence of some cardiac abnormality. For example, some patients with acute MI may not show diagnostic ST-T changes, and patients with severe coronary artery disease may not show diagnostic ST segment depressions during stress testing (see Chapter 9).

As just noted, both the sensitivity and specificity of the ECG in diagnosing a variety of conditions, including MI, are limited. Clinicians need to be aware of these diagnostic limitations. The following are some important problems that cannot be excluded simply because the ECG is normal or shows only nondiagnostic abnormalities:

Utility of the ECG in Special Settings

Although the ECG has definite limitations, it often helps in the diagnosis of specific cardiac conditions and sometimes aids in the evaluation and management of general medical problems such as life-threatening electrolyte disorders (Box 23-1). Some particular areas in which the ECG may be helpful are described here:

Most patients with acute MI show diagnostic ECG changes (i.e., new Q waves or ST segment elevations, hyperacute T waves, ST depressions, or T wave inversions). However, in the weeks and months after an acute MI these changes may become less apparent and in some cases may disappear.

ST segment elevation in right chest precordial leads (e.g., V_4-6R) in a patient with acute inferior infarction indicates associated right ventricular ischemia or infarction (see Chapter 8).

Persistent ST elevations several weeks after an MI should suggest a ventricular aneurysm.

A new S₁Q₃T₃ pattern or right bundle branch block (RBBB) pattern, particularly in association with sinus tachycardia, should suggest the possibility of acute cor pulmonale resulting from, for example, pulmonary embolism (see Chapter 11).

Low QRS voltage in a patient with elevated central venous pressure (distended neck veins) and sinus tachycardia suggests possible pericardial tamponade. Sinus tachycardia with electrical alternans is virtually diagnostic of pericardial effusion with tamponade (see Chapter 11).

LVH is seen in most patients with severe aortic stenosis or severe aortic regurgitation.

ECG signs of left atrial enlargement (abnormality) with concomitant RVH strongly suggest mitral stenosis (Fig. 23-1).

Figure 23-1 This ECG from a 45-year-old woman with severe mitral stenosis (due to rheumatic heart disease) shows multiple abnormalities. The rhythm is sinus tachycardia. Right axis deviation and a tall R wave in lead V₁ indicate right ventricular hypertrophy. The prominent biphasic P wave in lead V₁ indicates left atrial enlargement. The tall P wave in lead II may indicate concomitant right atrial enlargement. Nonspecific ST-T changes and incomplete right bundle branch block (rSr’ in V₂) are also present. The combination of right ventricular hypertrophy and left atrial enlargement is highly suggestive of mitral stenosis.

Frequent premature beats may occur in association with mitral valve prolapse, especially with severe mitral regurgitation.

Most patients with a moderate to large atrial septal defect have an RBBB pattern.

Severe hyperkalemia, a life-threatening electrolyte abnormality, virtually always produces ECG changes, beginning with T wave peaking, loss of P waves, QRS widening, and finally asystole (see Chapter 10).

The triad of LVH (caused by hypertension), peaked T waves (caused by hyperkalemia), and prolonged QT interval (caused by hypocalcemia) should suggest chronic renal failure.

The combination of low voltage and sinus bradycardia should suggest possible hypothyroidism. (“Low and slow—think hypo.”)

Unexplained AF (or sinus tachycardia at rest) should prompt a search for hyperthyroidism.

The combination of low voltage and slow precordial R wave progression is commonly seen with chronic obstructive lung disease (see Chapter 11).

The ECG-CHF (chronic heart failure) triad of relatively low limb lead voltage, prominent precordial voltage, and slow R wave progression suggests an underlying dilated cardiomyopathy (see Chapter 11).

Common General Medical Applications of the ECG

The ECG may also provide important and immediately available clues in the evaluation of such major medical problems as syncope, coma, shock, and weakness.

Reducing Medical Errors: Common Pitfalls in ECG Interpretation

Reducing and eliminating preventable medical errors are central preoccupations of contemporary practice. ECG misinterpretations are an important source of such errors, which include under- and over-diagnosis. For example, failing to recognize AF can put your patient at risk for stroke and other thromboembolic events. Missing AF with an underlying pacemaker is a common mistake (see Chapter 21). At the same time, miscalling multifocal atrial tachycardia (MAT) or baseline artifact for AF can lead to inappropriate anticoagulation.

You can help minimize errors in interpreting ECGs by taking care to analyze all the points listed in the first section of Chapter 22. Many mistakes result from the failure to be systematic. Other mistakes result from confusing ECG patterns that are “look-alikes.” Important reminders are provided in Box 23-2. Some common pitfalls in ECG interpretation are discussed further here.

Unless recognized and corrected, inadvertent reversal of limb lead electrodes can cause diagnostic confusion. For example, reversal of the left and right arm electrodes usually causes an apparent rightward QRS axis shift as well as an abnormal P wave axis that simulates an ectopic atrial rhythm (Fig. 23-2). As a general rule, when lead I shows a negative P wave and a negative QRS, reversal of the left and right arm electrodes should be suspected.

Figure 23-2 Whenever the QRS axis is unusual, limb lead reversal may be the problem. Most commonly, the left and right arm electrodes become switched so that lead I shows a negative P wave and a negative QRS complex.

Voltage can appear abnormal if standardization is not checked. ECGs are sometimes mistakenly thought to show “high” or “low” voltage when the voltage is actually normal but the standardization marker is set at half standardization or two times normal gain.

Atrial flutter with 2:1 block is one of the most commonly missed diagnoses. The rhythm is often misdiagnosed as sinus tachycardia (mistaking part of a flutter wave for a true P wave) or PSVT. When you see a narrow complex tachycardia with a ventricular rate of about 150 beats/min, you should always consider atrial flutter (see Chapter 15).

Coarse AF and atrial flutter are sometimes confused. When the fibrillatory (f) waves are prominent (coarse), the rhythm is commonly mistaken for atrial flutter. However, with AF the ventricular rate is erratic, and the atrial waves are not exactly consistent from one segment to the next. With pure atrial flutter the atrial waves are identical from one moment to the next, even when the ventricular response is variable (see Chapter 15).

The Wolff-Parkinson-White (WPW) pattern is sometimes mistaken for bundle branch block, hypertrophy, or infarction because the preexcitation results in a wide QRS complex and may cause increased QRS voltage, T wave inversions, and pseudoinfarction Q waves (see Chapter 12).

Isorhythmic AV dissociation and complete heart block can be confused. With isorhythmic AV dissociation the SA and AV node pacemakers become “desynchronized,” and the QRS rate is the same as or slightly faster than the P wave rate (see Chapter 17). With complete heart block the atria and ventricles also beat independently, but the ventricular rate is much slower than the atrial (sinus) rate. Isorhythmic AV dissociation is usually a minor arrhythmia, although it may reflect conduction disease or drug toxicity (e.g., digitalis, diltiazem, verapamil, and beta blockers). Complete heart block is always a major arrhythmia and generally requires pacemaker therapy.

Normal variant and pathologic Q waves require special attention. Remember that Q waves may be a normal variant as part of QS waves in leads aVR, aVL, aVF, III, V₁, and occasionally V₂ (see Chapter 8). Small q waves (as part of qR waves) may occur in leads I, II, III, aVL, and aVF as well as in the left chest leads (V₄ to V₆). These “septal” Q waves are less than 0.04 sec in duration. On the other hand, small pathologic Q waves may be overlooked because they are not always very deep. In some cases it may not be possible to state definitively whether or not a Q wave is pathologic.

Mobitz type I (Wenckebach) AV block is a commonly missed diagnosis. “Group beating” is an important clue to the diagnosis of this problem (see Chapter 17). The QRS complexes become grouped in clusters because of the intermittent failure of AV nodal conduction. The PR interval after the nonconducted (“dropped”) P wave is shorter than the last one to conduct to the ventricles.

Hidden P waves may lead to mistakes in the diagnosis of a number of arrhythmias, including blocked atrial premature beats (APBs), paroxysmal AT with block, and second- or third-degree (complete) AV block. Therefore, you must search the ST segment and T wave for buried P waves (see Chapters 17 and 18).

MAT and AF are often confused because the ventricular response in both is usually rapid and irregular. With MAT, you need to look for multiple different P waves. With AF, you must be careful not to mistake the sometimes “coarse” f waves for actual P waves.

LBBB may be mistaken for infarction because it is associated with slow R wave progression and often ST segment elevation in the right chest leads.

U waves are sometimes overlooked. Small U waves are a physiologic finding, but large U waves (which may be apparent in only the chest leads) are sometimes an important marker of hypokalemia or drug toxicity (e.g., dofetilide). Large U waves may be associated with increased risk of torsades de pointes (see Chapter 16).

Severe hyperkalemia must be considered immediately in any patient with an unexplained wide QRS complex, particularly if P waves are not apparent. Delay in making this diagnosis can be fatal because severe hyperkalemia may lead to asystole and cardiac arrest while the clinician is waiting for the laboratory report (see Chapter 10).