Because multiple factors can affect ventricular repolarization in diseased hearts, the finding characteristic of a specific electrolyte abnormality may be modified, and even mimicked, by various pathologic processes and the effects of certain drugs. In practice, the major problem with the ECG diagnosis of electrolyte imbalance is not the negative ECG with abnormal serum values but the production of similar changes by other conditions in patients with normal serum values.122


The initial effect of acute hyperkalemia is the appearance of peaked T waves with a narrow base (&H0; Fig. 11-34, left). The diagnosis of hyperkalemia is almost certain when the duration of the base is 0.20 s or less (with rates between 60 and 110 beats per minute).122 As the degree of hyperkalemia increases, the QRS complex widens Fig. 11-35), with the electrical axis usually being deviated abnormally to the left and only rarely to the right. In addition, the PR interval prolongs, and the P wave flattens until it disappears.45,122 If untreated, death ensues either due to ventricular standstill or coarse, slow ventricular fibrillation. Death also can result if wide QRS complexes occurring at fast rates are diagnosed as ventricular tachycardia and the patient is treated with antiarrhythmic drugs. On the other hand, class IA, IC, and III drugs as well as large doses of tricyclic antidepressants (especially when ingested for suicidal purposes) also can produce marked QRS widening. These processes, however, do not coexist with narrow-based, peaked T waves. Rarely, hyperkalemia produces (in the absence of coronary artery disease) a degree of ST-segment elevation in the right chest leads capable of suggesting anteroseptal myocardial injury (see Fig. 11-35). These constitute the "dialyzable currents of injury in potassium intoxication" reported by Levine et al.123


The abnormal and delayed repolarization that occurs in hypokalemia is best expressed as QU, rather than QT, prolongation, since at times it can be difficult to differentiate between notchingof the T wave and T- and U-wave fusion.122 On the basis of the previously mentioned M cells, these U waves are part of notched T waves, suggesting that that term be used in place of U. As the serum potassium level falls, the ST segment becomes progressively more depressed, and there is a gradual blending of the T wave into what appears to be a tall U wave Fig. 11-36, top). An

ECG pattern similar to that of hypokalemia can be produced by some antiarrhythmic drugs, especially quinidine and, experimentally, DL-sotalol. In any case, when repolarization is greatly prolonged, ventricular arrhythmias, including the so-called torsades de pointes, can occur.


Hypomagnesemia does not produce QU prolongation unless the coexisting hypokalemia (with which it is almost invariably associated) is severe.122 Long-standing and very marked magnesium deficiency lowers the amplitude of the T wave and depresses the ST segment.122 It may be difficult to differentiate the changes produced by magnesium from those produced by potassium. For this reason, it has been stated that hypomagnesemia does not cause any changes in the ECG.45


Similarly, in clinical tracings, the effects of hypermagnesemia on the ECG are difficult to identify because the changes are dominated by calcium.!24 According to some authors, administration of intravenous magnesium to patients with normal ECGs may shorten the QT interval.45 Other authors found no effects on ventricular refractoriness that are reflected by changes in the QT interval.125 Intravenous magnesium given to patients with torsades de pointes controls the arrhythmia in a high percentage of patients without changing the prolonged QT interval significantly.126 The calcium-blocking activity of magnesium was suggested to be one of the mechanisms responsible for this antiarrhythmic activity.146


During sinus rhythm with normal rates, the QT interval is short (see Fig. 11-36, bottoni). In some cases, the Q-to-apex of T intervals is also short. If factors known to modify the QT interval are not present, it has been said that a reasonably accepted correlation exists between the duration of the interval and serum calcium levels.122 Occasionally, the ST segment disappears, and the T waves may become inverted in left and right chest leads. Digitalis also shortens the QT interval but produces its characteristic "effects" in leads where the R waves predominate. The classic upward concavity of the ST segment is seen in the left chest leads in patients with LV hypertrophy and in leads Vj and V2 when there is RV hypertrophy (with predominantly positive deflections in these leads).


The typical ECG pattern of hypocalcemia consists of QT prolongation at the expense of the ST segment.45,122 The T wave is usually of normal width but can be narrow if there is coexisting (moderate) hyperkalemia (see Fig. 11-34,5). A very marked injury (with the so-called hyperacute ST-T changes) can produce a similar pattern, but in such cases the T wave, though peaked, is not as narrow based. It has been said that hypocalcemia per se does not produce T-wave inversion. When present, the latter is usually a reflection of coexisting processes such as LV hypertrophy and incomplete LBBB. An ECG pattern similar to that of hypocalcemia can be produced by some organic abnormalities of the central nervous system and by congenitally prolonged QT intervals (see below).

QT Interval: Normal and Prolonged

The QT interval is measured from the beginning of the q wave to the end of the T wave.1!! The latter may be difficult to define. The point at which the maximal downslope of the T wave crosses the baseline helps to identify the end of this wave.45 The QT interval is affected by autonomic tone and cathecolamines and has day-night differences. It varies with heart rate and sex. Several formulas have been proposed to take these variables into account and provide a corrected measurement (QTc interval).127

In general, the unadjusted (noncorrected), usually resting QT interval decreases from ±0.42 s at rates of 50/min to ±0.32 s at 100/min to ±0.26 s at 150/min.911 During exercise, the rate becomes faster; the QTc first increases until reaching, approximately, a rate of 120/min, thereafter again decreasing.128 Although the value of the normal QTc is open to question, it is still used in routine computer interpretations. Because the 12-lead ECG shows a normal degree of QT and QTc dispersion, indexes have been used to quantify the extent of heterogeneity in ventricular repolarization. The difference between the longest and shortest QT interval is referred to as QT dispersion.129-134 Since 1990 it has been used as a prognostic marker not only in patients with prolonged QT intervals but also in those with acute MI.130-132 The upper limits of normal vary with different investigators; a value of 65 may be an acceptable compromise according to Antzelevitch.i4 Others may disagree. Coumel et al.133 emphasized that QT dispersion could be an illusion or a reality.!33 Inferred from the oncoming section on spatial vectorcardiography, the fact is that a truly spatial QRS-T loop cannot yield abnormal QT dispersion, for in planar projections of this spatial loop (as well as in the standard and unipolar extremity leads of the ECG) the shortest interval occurs because the terminal forces are perpendicular to the plane or derived lead. On the other hand, if precordial leads are considered scalar leads capable of recording (as stated in a previous section) local potentials with different durations, then QT dispersion is a reality.

The M-cell studies of Antzelevitch allow for the differentiation of this global "dispersion" (derived from multiple leads) from "local" transmural dispersion in single leads reflecting the time elapsing between the peak of the T wave (given by the end of the composite epicardial action potentials) and the end of the T wave (given by the end of the composite M-cell action potentials).!4

The QT intervals are shortened with hypercalcemia, pure hyperkalemia, digoxin, and acidosis.45 Prolongation of the QT interval may be congenital or acquired and is an important marker for malignant ventricular arrhythmias (see Chap. 24). A partial list of conditions causing a prolonged QT or, in some instances, prolonged QU intervals (delayed repolarization) is given in Table 118.45

Table 11-8: Acquired QT Prolongation Usually Bradycardia-and(or) Pause-Dependent

1. Electrolyte disturbances a. Hypokalemia b. Hypocalcemia c. Hypomagnesemia

2. Drugs a. Class IA antiarrhythmic agents (quinidine, disopyramide, procainamide)

b. Class III antiarrhythmic agents (amiodarone, sotalol)

c. Psychotropic drugs

3. Central nervous system diseases a. Subarachnoid hemorrhage b. Ruptured berry aneurysm c. Cryptococcal meningitis

4. Congenital syndromes

5. Electrocardiographic ischemia

6. Arrhythmias a. Posttachycardia syndrome b. Cardiac arrest of any etiology c. Chronic idioventricular rhythms

7. Hypothermia


Characteristic ECG changes develop when the body temperature drops to approximately 30°C.ii The QT interval becomes prolonged. In addition, a deflection, called an Osborn wave, appears in a place said to be located between the end of the QRS complex and the beginning of the ST segment435 Fig. 11-37). This deflection has been attributed to delayed depolarization, to a current of injury, or to "early" repolarization.!53 In leads facing the left ventricle, the deflection is positive, and its size is inversely related to body temperature. The role played by the intramyocardial M cells in its genesis has been discussed previously.44


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