ECG tutorial: Miscellaneous diagnoses

INTRODUCTION — Cardiac or systemic diseases may have electrocardiographic (ECG) manifestations that do not fit into standard categories.

LOW VOLTAGE — Low voltage of the limb leads is present when the amplitude of the QRS complex in each of the three standard limb leads (I, II, and III) is <5 mm (waveform 1). Low voltage of all leads is diagnosed when the average voltage in the limb leads is <5 mm and the average voltage in the chest leads is <10 mm. This may be due to underlying myocardial disease (particularly amyloidosis), pericardial effusion, lung disease, severe hypothyroidism, obesity, or anasarca, in which the low voltage correlates with weight gain [1].

EARLY REPOLARIZATION — The term early repolarization (ER) has long been used to characterize a QRS-T variant on the ECG. Most literature defines ER as being present on the ECG when there is J-point elevation of ≥0.1 mV in two adjacent leads with either a slurred or notched morphology but there has been disagreement across published studies. Early repolarization is discussed in greater detail separately. (See "Early repolarization".)

ELECTRICAL ALTERNANS — Electrical alternans is recognized by alternating amplitude of the QRS complexes in any or all leads, though it is more frequently seen in the precordial leads (waveform 2).

Electrical alternans with sinus tachycardia is a highly specific sign of pericardial effusion, usually with cardiac tamponade, but it is only modestly sensitive. As a result, its absence does not exclude cardiac tamponade. It is thought that the alternating amplitude is the result of a pendulum motion of the heart as it "swings" from beat to beat within the pericardial fluid (see "Pericardial effusion: Approach to diagnosis", section on 'ECG findings'). Electrical alternans may also be seen with severe cardiomegaly, left ventricular dysfunction, or aortic regurgitation.

Another setting associated with electrical alternans is supraventricular tachycardia (SVT), especially when the rate is rapid. Although it has been suggested that electrical alternans during SVT is indicative of atrioventricular reentrant tachycardia, this finding can be seen in any rapid SVT.

There may also be macrovolt alternans of the T waves, although this is infrequently present (waveform 3). It is most often seen with long QT syndrome and is a warning sign of impending polymorphic ventricular tachycardia. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations".)

U wave alternans is very uncommon and is associated with electrolyte disorders.

EARLY OR LATE TRANSITION — The R wave height normally becomes progressively taller from leads V1 through V6. The usual transition zone, where the R and S wave are equal in amplitude in the precordial leads, usually occurs between V3 and V4. Early or late transition may occur due to a variety of circumstances.

Early transition — The so-called "counterclockwise rotation" pattern is present when there is early transition of the R wave amplitude across the precordium (waveform 4). The right ventricle is anterior, and the left ventricle is leftward and slightly posterior. If the electrical axis of the heart is rotated in a counterclockwise direction around a central axis, the left ventricle is shifted more anteriorly. A partial list of causes include:

●Normal variant

●Lead placement

●Wolff-Parkinson-White pattern

●Muscular dystrophy

●Right ventricular hypertrophy

●Right bundle branch block or right ventricular conduction delay

●True posterior wall myocardial infarction (MI).

Q waves and ST segment changes in leads V7 to V9 are helpful in diagnosing a posterior wall MI. (See "ECG tutorial: Myocardial ischemia and infarction" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

LATE TRANSITION — When the R wave height does not become progressively taller from leads V1 to V3 or V4, or even remains at low amplitude across the entire precordium, slow or poor R wave progression (PRWP) is present (waveform 5). Several sets of criteria have been proposed to define PRWP more precisely [2].

There are many etiologies for PRWP:

●Normal variant

●Lead placement

●Anteroseptal or anterior wall myocardial infarction

●Left ventricular hypertrophy

●Left anterior fascicular block

●Left bundle branch block

●Infiltrative or dilated cardiomyopathy

●Wolff-Parkinson-White pattern

●Chronic lung disease

Poor R wave progression may be more frequently seen in females. Because there are so many different causes of PRWP, this finding alone is not useful in identifying patients with a prior anterior myocardial infarction [2].

DIGITALIS EFFECT — A digitalis effect is manifested as changes of the ST segment and T wave that may be similar to those due to ischemia. The J point is occasionally depressed, but more commonly seen is depression or sagging of the ST segment, which is concave in an upward direction (waveform 6). These changes are more apparent in the lateral precordial leads, although they may also be seen in the limb leads.

Other changes associated with digitalis include the following:

●The T waves are often flattened and the QT interval (ST segment) shortened.

●Usually, the PR interval is slightly prolonged as a result of an enhanced vagal effect upon the atrioventricular node.

●In some cases, there are abnormalities of the U wave (prominent or inverted), which may be due to digitalis itself, or can be secondary to hypokalemia.

DIGITALIS TOXICITY — Digitalis toxicity may have various ECG manifestations. (See "Cardiac arrhythmias due to digoxin toxicity".)

ELECTROLYTE ABNORMALITIES — A variety of electrolyte abnormalities may be associated with changes on the ECG.

Hyperkalemia — A tall peaked and symmetrical T wave is the first change seen on the ECG in a patient with hyperkalemia (waveform 7). (See "Clinical manifestations of hyperkalemia in adults", section on 'Clinical manifestations'.)

There is progressive slowing of impulse conduction through the myocardium as the hyperkalemia becomes more severe, with several consequences:

●The PR interval lengthens and the QRS duration increases. A variety of conduction disturbances, including right bundle branch block, left bundle branch block, bifascicular block, and advanced atrioventricular (AV) block, may be seen [3].

●The P wave may flatten or disappear as a result of atrial standstill or arrest.

●ST elevation in the leads V1 to V2 may occur, mimicking a type 1 Brugada pattern or myocardial infarction. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

●Ultimately the QRS widens further due to a severe conduction delay and may become "sine wave," resulting in ventricular standstill and a flat line on the ECG with complete absence of electrical activity.

The progression and severity of ECG changes do not correlate well with the serum potassium concentration.

Hypokalemia — Similar to hyperkalemia, hypokalemia produces changes on the ECG that are not necessarily related to the serum potassium level (waveform 8). (See "Clinical manifestations and treatment of hypokalemia in adults", section on 'Cardiac arrhythmias and ECG abnormalities'.)

Other findings associated with hypokalemia include the following:

●The U wave and T wave merge in some cases to form a T-U wave, which may be misdiagnosed as a prolonged QT interval.

●The P wave can become larger and wider and the PR interval may prolong slightly.

●The QRS duration may increase when the hypokalemia is more severe; in addition, the ST segment becomes markedly depressed, and T waves are inverted.

Hypocalcemia — Hypocalcemia causes prolongation of the QT interval (waveform 9). This is due to prolongation of phase 2 of the ventricular action potential and lengthening of the ST segment, while the T wave (which correlates with the time for repolarization) remains unaltered.

Hypercalcemia — Hypercalcemia causes shortening of the QT interval, primarily due to a decrease in phase 2 of the ventricular action potential and resultant decrease in the ST segment duration. There is also a decrease in duration of the proximal portion of the T wave, or upstroke, measured from the beginning of the T wave to its apex; thus, the initial portion of the T wave has an abrupt upslope (waveform 10). Other findings in some patients include PR prolongation, a diffuse increase in the amplitude of the QRS complex, ST elevation in V1 to V2, and flattened, inverted, or biphasic T waves.

DEXTROCARDIA — Dextrocardia is a condition in which the heart is located on the right side of the chest. Thus, the left ventricular apex is at the right midclavicular line. The resultant changes on the ECG often include a negative P wave and QRS complex in lead I, since atrial and ventricular depolarization begin on the left and spread to the right. There is also reverse R wave progression across the precordium; the R wave is tallest in V1 and progressively decreases in amplitude in leads V2 to V6 (waveform 11). The diagnosis may be confirmed by obtaining right-sided chest leads that demonstrate the normal progression of R wave amplitude.

HYPOTHERMIA — Hypothermia, defined as a temperature of less than 93 degrees (F) or 34 degrees (C), slows impulse conduction through all cardiac tissue, resulting in prolongation of all the ECG intervals, including the RR, PR, QRS, and QT. There is also elevation of the J point (only if the ST segment is unaltered), producing a characteristic J or Osborne wave, which represents distortion of the earliest phase of membrane repolarization (waveform 12). The height of the Osborne wave is roughly proportional to the degree of hypothermia. These findings are most prominent in the precordial leads V2 to V5.

ARTIFACT DUE TO TREMOR — Tremors can cause a rhythmic irregularity of the ECG baseline and occasionally the QRS complex (waveform 13). They may mimic atrial tachycardia, atrial flutter, or ventricular tachycardia. This abnormality is commonly seen in Parkinson disease or hypothermia. Counting the peaks of the artifact helps determine the periodicity of the muscle tremor.

LEAD SWITCH OR MISPLACEMENT — Placement of the ECG leads on the wrong limbs or incorrect positioning of the precordial leads may cause an abnormal P wave and QRS axis in the frontal plane or unusual R wave progression (waveform 14A-B). This may be confused with dextrocardia, a pathologic left or rightward axis, or myocardial infarction.

FUSION AND CAPTURE BEATS — Ventricular fusion and/or capture beats, when identified on the surface ECG in a patient with wide complex tachycardia (WCT), are diagnostic for VT. (See "Wide QRS complex tachycardias: Approach to the diagnosis".)

●Fusion beats occur when one impulse originating from the ventricle and a second supraventricular impulse simultaneously activate the ventricular myocardium. The resulting QRS complex has a morphology intermediate between that of a sinus beat and a purely ventricular complex (waveform 15). Intermittent fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT.

●Capture beats, or Dressler beats, are QRS complexes during a WCT that are identical to the sinus QRS complex (waveform 15). The term "capture beat" implies that the normal conduction system has momentarily "captured" control of ventricular activation from the VT focus.

RECIPROCAL (ECHO) COMPLEXES — Reciprocal or echo beats occur when a premature ventricular contraction is conducted retrogradely to the atrium through the AV node or a bypass pathway and then back down to the ventricle via a normal AV node conduction pathway (waveform 16).

If echo beats are able to continue conduction up or down two pathways, supraventricular tachycardia occurs. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

SUMMARY

●Early repolarization is present when there is J-point elevation of ≥0.1 mV in two adjacent leads with either a slurred or notched morphology. (See 'Early repolarization' above.)

●Low voltage is defined as a voltage in the limb leads <5mm and chest leads <10mm.

●Electrical alternans is most concerning for pericardial effusion, but may also be seen in severe left ventricular dysfunction or supraventricular tachycardia.

●Digitalis toxicity may lead to both tachyarrhythmias and bradyarrhythmias.

●Hyperkalemia may have peaked T waves, PR interval and QRS duration increases, atrial standstill, ST elevation in V1 to V2, or sine wave.

●Hypokalemia may cause ST-segment depression, decrease in T wave amplitude or T wave inversion, increase in U wave amplitude, merging of the T and U waves, increase in P wave size and duration, PR interval prolongation, and widening of the QRS complex.