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7. Diagnostic of the Electrolyte disorders
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7. Diagnostic of the Electrolyte disorders

Hyperkalemia is associated with a distinctive sequence of ECG changes. The relationship between the degree of hyperkalemia and the ECG changes, however, is variable, and in rare cases of severe hyperkalemia the ECG may even be normal or near normal. The earliest changes are the appearance of high, narrow T waves and a shortened QT interval, which reflect abnormally rapid repolarization. The next changes of the ECG occur if plasma K+ concentration increase more than 7.5 mEq/l and develop due to delayed depolarization: prolonged duration of the QRS complex, low and wide P wave. PR prolongation can also occur, followed sometimes by second-degree or third-degree AV block. ST-segment elevation in leads V1 and V2, mimicking acute myocardial infarction and has been reported in severe hyperkalemia.

 

Figure 65 — ECG signs of hyperkalemia

Hypokalemia can commonly result from the loss of potassium through dehydration, vomiting, gastric suction, or excessive diuretic use. The thiazides and loop diuretics are most commonly implicated in the development of hypokalemia. Hypokalemia produces non-specific changes in the ECG due to delayed ventricular repolarization. The result is ST-segment depression with decreased amplitude or inversion of the T wave and increased U wave prominence. In severe hypokalemia, an increase in amplitude of the P wave, widening of the PR interval, and widening of the QRS complex may also occur.

 

Figure 66 — ECG signs of hypokalemia depend of potassium level. A – normal K+ -level. B – about 3 mEq/L. C – about 2 mEq/L. D – less than 1 mEq/L

Hypocalcemia and hypercalcemia predominantly alter the action potential duration, which results in either shortening (hypercalcemia) or prolongation (hypocalcemia) of the QT interval. The influence on the QT interval is entirely due to a modification of the ST-segment duration. Both conditions can affect T-wave morphology. In next stages of hypercalcemia, QRS complex and PR intervals often are prolonged, and AV block has been detected. When large amounts of Ca2+ are infused into experimental animals, the heart relaxes less during diastole and eventually stops in systole. However, in clinical conditions associated with hypercalcemia, the plasma calcium level is rarely if ever high enough to affect the heart.

 

Figure 67 — ECG changes in hypercalcemia (B) and hypocalcemia (C), a – normal ECG complexes

The combination of hypocalcemia and hyperkalemia, as seen in patients with renal insufficiency, produces a characteristic ST-segment prolongation with inverted T wave. Changes in plasma Ca2+ and K+ levels cause relatively noticeable changes in the sensitivity of the heart to some treats and toxins (as digitalis or antiarrhythmics). Hypercalcemia augments digitalis toxicity, and hyperkalemia counteracts it. Doctors must keep in mind this fact because treatment of digitalis intoxication in this case is very difficult. Increases in extracellular Ca2+ concentration enhance myocardial contractility.

The ECG changes of hypomagnesemia are equal to those of hypokalemia.  Hypomagnesemia is often seen in association with other electrolyte abnormalities (low sodium, potassium, calcium, or phosphorus), acute MI, cardiac arrest, digoxin or diuretic therapy, alcohol abuse, renal impairment.



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