Electrolyte and Metabolic Abnormalities

In addition to the structural and functional cardiac conditions already discussed, numerous systemic metabolic aberrations affect the ECG, including electrolyte abnormalities and acid-base disorders, as well as systemic hypothermia.

CALCIUM

Hypercalcemia and hypocalcemia predominantly alter the action potential duration. An increased extracellular calcium concentration shortens the ventricular action potential duration by shortening phase 2 of the action potential. In contrast, hypocalcemia prolongs phase 2 of the action potential. These cellular changes correlate with abbreviation and prolongation of the QT interval (ST segment portion) with hypercalcemia and hypocalcemia, respectively. Severe hypercalcemia (e.g., serum Ca²⁺ ³15 mg/dl) can also be associated with decreased T wave amplitude, sometimes with T wave notching or inversion. Hypercalcemia sometimes produces a high takeoff of the ST segment in leads V₁ and V₂ and can thus simulate acute ischemia.

Prolongation of the QT interval (ST segment portion) is typical of hypocalcemia. Hypercalcemia may cause abbreviation of the ST segment and shortening of the QT interval.

POTASSIUM  

Hyperkalemia is associated with a distinctive sequence of ECG changes. The earliest effect is usually narrowing and peaking (tenting) of the T wave. The QT interval is shortened at this stage associated with decreased action potential duration. Progressive extracellular hyperkalemia reduces atrial and ventricular resting membrane potentials, thereby inactivating sodium channels, which decreases Vmax and conduction velocity. The QRS begins to widen and P wave amplitude decreases. PR interval prolongation can occur, followed sometimes by second- or third-degree AV block. Complete loss of P waves may be associated with a junctional escape rhythm or sinoventricular rhythm. In the latter instance, sinus rhythm persists with conduction between the SA and AV nodes and occurs without producing an overt P wave. Moderate to severe hyperkalemia occasionally induces ST elevations in the right precordial leads (V₁ and V₂) and simulates an ischemic current-of-injury pattern. However, even severe hyperkalemia can be associated with atypical or nondiagnostic ECG findings. Very marked hyperkalemia leads to eventual asystole, sometimes preceded by a slow undulatory (sine-wave) ventricular flutter-like pattern. The ECG triad of (1) peaked T waves (from hyperkalemia), (2) QT prolongation (from hypocalcemia), and (3) LVH (from hypertension) is strongly suggestive of chronic renal failure.

Electrocardiographic changes in hyperkalemia (A) and hypokalemia (B). A, On day 1, at a K⁺ level of 8.6 mEq/liter, the P wave is no longer recognizable and the QRS complex is diffusely prolonged. Initial and terminal QRS delay is characteristic of K⁺ -induced intraventricular conduction slowing and is best illustrated in leads V₂ and V₆. On day 2, at a K⁺ level of 5.8 mEq/liter, the P wave is recognizable with a PR interval of 0.24 seconds, the duration of the QRS complex is approximately 0.10 seconds, and the T waves are characteristically “tented.” B, On day 1, at a K⁺ level of 1.5 mEq/liter, the T and U waves are merged. The U wave is prominent and the QU interval prolonged. On day 4, at a K⁺ level of 3.7 mEq/liter, the tracing is normal.

The electrophysiological changes associated with hypokalemia, in contrast, include hyperpolarization of myocardial cell membranes and increased action potential duration. The major ECG manifestations are ST depression with flattened T waves and increased U wave prominence. The U waves can exceed the amplitude of T waves. Hypokalemia is an important cause of acquired long QT(U) syndrome that predisposes to torsades de pointes. Hypokalemia also predisposes to tachyarrhythmias from digitalis.

MAGNESIUM

Specific ECG effects of mild to moderate isolated abnormalities in magnesium ion concentration are not well characterized. Severe hypermagnesemia can cause AV and intraventricular conduction disturbances that may culminate in complete heart block and cardiac arrest (Mg²⁺ >15 mEq/L). Hypomagnesemia is usually associated with hypocalcemia or hypokalemia. Hypomagnesemia can potentiate certain digitalis toxic arrhythmias.

OTHER FACTORS

Isolated hypernatremia or hyponatremia does not produce consistent effects on the ECG. Acidemia and alkalemia are often associated with hyperkalemia and hypokalemia, respectively. Systemic hypothermia may be associated with the appearance of a distinctive convex elevation at the junction (J point) of the ST segment and QRS complex (J wave or Osborn wave). The cellular mechanism of this type of pathological J wave appears to be related to an epicardial-endocardial voltage gradient associated with the localized appearance of a prominent epicardial action potential notch.

Systemic hypothermia. The arrows (V₃ through V₆ ) point to the characteristic convex J waves, termed Osborn waves. Prominent sinus bradycardia is also present.

Nonspecific QRS and ST-T Changes

Low QRS voltage is said to be present when the total amplitude of the QRS complexes in each of the six extremity leads is 0.5 mV or less or 1.0 mV or less in leads V₁ through V₆. Low QRS voltage can relate to a variety of mechanisms, including increased insulation of the heart by air (chronic obstructive pulmonary disease) or adipose tissue (obesity); replacement of myocardium, for example, by fibrous tissue (ischemic or nonischemic cardiomyopathy), amyloid, or tumor; or short-circuiting effects (pericardial or pleural effusions). The combination of relatively low limb voltage (QRS voltage 0.8 mV in each of the limb leads), relatively prominent QRS voltage in the chest leads (SV₁ or SV₂+RV₅ or RV₆ ³3.5 mV), and poor R wave progression (R wave less than the S wave in V₁ through V₄) has been reported as a relatively specific, but not sensitive sign of dilated-type cardiomyopathies (ECG–congestive heart failure triad).

Multiple factors in addition to ischemia (e.g., postural changes, meals, drugs, hypertrophy, electrolyte and metabolic disorders, central nervous system lesions, infections, pulmonary diseases) can affect the ECG.Ventricular repolarization is particularly sensitive to these effects, which can lead to a variety of nonspecific ST-T changes. The term is usually applied to slight ST depression or T wave inversion or to T wave flattening without evident cause. Care must be taken to not overinterpret such changes, especially in subjects with a low prior probability of heart disease. At the same time, subtle repolarization abnormalities can be markers of coronary or hypertensive heart disease or other types of structural heart disease and probably account for the association of relatively minor but persistent nonspecific ST-T changes with increased cardiovascular mortality in middle-aged men.

Alternans Patterns

The term alternans applies to conditions characterized by the sudden appearance of a periodic beat-to-beat change in some aspect of cardiac electrical or mechanical behavior. These abrupt changes (AAAA ABAB pattern) are reminiscent of a generic class of subharmonic (period-doubling) bifurcation patterns, well described in perturbed nonlinear control systems. Many different examples of electrical alternans have been described clinically; a number of others have been reported in the laboratory. Most familiar is total electrical alternans with sinus tachycardia, a specific but not highly sensitive marker of pericardial effusion with tamponade physiology. This finding is associated with an abrupt transition from a 1:1 to a 2:1 pattern in the “to-fro” swinging motion of the heart in the effusion. Other alternans patterns are due to primary electrical rather than mechanical causes. ST-T alternans has long been recognized as a marker of electrical instability in acute ischemia, where it may precede ventricular tachyarrhythmia. Considerable interest has recently been shown in the detection of microvolt T wave (or ST-T) alternans as a noninvasive marker of the risk of ventricular tachyarrhythmia in patients with chronic heart disease. Similarly, TU wave alternans  may be a

marker of imminent risk of a ventricular tachyarrhythmia such as torsades de pointes in hereditary or acquired long QT syndromes.

Prinzmetal angina with ST segment and T wave alternans. B, ST segment and T wave alternans associated with nonsustained ventricular tachycardia

Total electrical alternans (P-QRS-T) caused by pericardial effusion with tamponade. This finding, particularly in concert with sinus tachycardia and relatively low voltage, is a highly specific, although not sensitive marker of cardiac tamponade.

The QT(U) interval is prolonged and measures approximately 600 milliseconds with TU wave alternans. The tracing was recorded in a patient with chronic renal disease shortly following dialysis. This type of repolarization alternans may be a precursor to torsades de pointes.