In this chapter, we address the basic notions of electrolytes disturbances and QT interval abnormalities. The most important abnormality of the QT interval is long QT syndrome, which provokes inhomogeneity of repolarisation with a marked tendency to induce severe ventricular arrhythmias (torsades de pointes). This long QT syndrome can be found in several clinical settings. The Jervell and Lange-Nielsen syndrome is an autosomal recessive form of long QT syndrome with associated congenital deafness and the Romano-Ward syndrome is an autosomal dominant form of long QT syndrome that is not associated with deafness. QT prolongation is associated with syncope (fainting) and sudden death due to ventricular arrhythmias (torsades de pointes). Arrhythmias are often associated with exercise or excitement. LQTS is associated with the rare, ventricular arrhythmia torsades de pointes, which can deteriorate into ventricular fibrillation and ultimately death. Several genetic mutations have been described. Syncope is usually the first manifestation of the syndrome. The acquired long QT syndrome is most often iatrogenic or associated with the following clinical situations: ischemia, subarachnoid hemorrhage, thyroid disease, electrolyte disturbances (hypocalcemia), side effects of drugs like antiarrhythmic agents (class IA, like quinidine, or class III like sotalol or amiodarone), antidepressant agents, some antihistamine drugs or even some other substances. Short congenital QT syndrome is a newly described disease characterized by a shortened QT interval, QTc, < 340 ms associated with episodes of syncope, paroxysmal atrial fibrillation or life-threatening cardiac arrhythmias. Hyperkalemia is the most dramatic and life-threatening electrolyte disorder. There appears to be a direct effect of elevated potassium on some of the potassium channels by increasing their activity and speeding up membrane repolarisation. Also, hyperkalemia causes an overall membrane depolarisation that inactivates sodium channels. The faster repolarisation of the cardiac action potential causes tenting of the T waves, and the inactivation of sodium channels causes sluggish cardiac conduction, which leads to smaller P waves and widening of the QRS complex. Hypokalemia Electrocardiographic findings associated with Hypokalemia are flattened T waves, ST segment depression and prolongation of the QT interval. U wave amplitude is slightly increased. It is rarely associated with arrhythmia. Hypercalcemia is associated with a shortening of the ST segment and consequently the QT interval. A very high Ca level broadens the T wave and may normalize the QT interval. Hypocalcemia prolongs the ST segment and the QT interval. Many drugs, especially antiarrhythmic drugs, can be implicated in QT interval prolongation. Class 1a antiarrhythmics significantly prolong the QT interval and may be responsible for ventricular arrhythmias like ``torsades de pointes''. Class 1c, mainly flecainide broadens the QRS complex by slowing conduction in the Purkinje fibres. Antidepressants may be responsible for severe arrhythmias and conduction abnormalities. Common adverse effects of digoxin include severe arrhythmias like ventricular tachycardia (fascicular origin). Conduction abnormalities and atrial tachycardia are also observed. The combination of increased (atrial) arrhythmogenesis and inhibited A-V conduction (like
atrial tachycardia with A-V block) is said to be pathognomonic of digoxin toxicity, like fascicular ventricular tachycardia.
Keywords: QT interval, QT interval prolongation, hyperkalemia, hypokalemia, hypercalcemia, hypocalcemia, electrolytes disturbances, long QT syndrome, short QT syndrome, hypothermia, bidirectionnal tachycardia.
