Q-T interval prolongation

Introduction QT prolongationsyndrome refers to a group of syndromes with QT prolongation, ventricular arrhythmia, syncope and sudden death on the electrocardiogram, possibly with congenital deafness. Many of the symptoms are familial, and those with deafness are first described by Jervell and Lange-Nielsen, so they are also called Jalan syndrome; those who are not accompanied by deafness are also called Ward-Roy (Ward- Romano) syndrome. Familial individuals are autosomal recessive. However, in recent years, the disease may be considered as a chronic viral infection or a non-infectious degeneration (mainly poisoning), not just a hereditary disease. Such chronic viral infections can be transmitted from mother to child or from siblings.

Cause

Can be divided into two categories: First, acquired, imbalanced by electrolytes (hypokalemia, hypocalcemia, hypomagnesemia), drug effects (quinidine, diisopropylpyramine, amiodarone and other antiarrhythmic drugs , phenothiazine, tricyclic antidepressants), some strokes, mitral valve prolapse and so on; one is congenital or familial, or the cause is unknown, the narrow sense of QT interval prolongation syndrome only refers to this category.

There are three opinions about the cause of the latter category:

1 Due to dysfunction of the autonomic nervous system, it is found in the experiment that stimulation or excision of one side of the stellate ganglion can cause QT interval prolongation and T wave alternating voltage, and some cases that affect the sympathetic tone clinically can be induced in this disease. syncope.

2 due to neurodegeneration in the heart. Pathological examination revealed neurofibrosis in the sinus node and left ventricle, and most inflammatory cells infiltrated between nerve fibers and ganglion cells. This lesion is not only seen in the conduction system, but also in the nerves of the ventricular myocardium.

3 due to the lack of an enzyme in the congenital heart muscle caused by metabolic abnormalities.

Electrophysiological studies have found that the mechanism of ventricular arrhythmia may be:

1 fold back;

2 trigger activity.

The factors associated with it are:

1 adrenaline can be excited;

2 action potential time changes;

3 early or delayed depolarization;

4 fold back to the loop.

an examination

Related inspection

Electrocardiogram blood routine

Relying on clinical manifestations, patients with prolonged QT interval and ventricular arrhythmia should consider this disease. Secondly, the cause of the disease should be analyzed. The majority of the acquired patients can find the cause according to the history of medication and blood electrolyte determination. Family history, QT prolongation and history of fainting are not difficult to diagnose as primary, according to whether there is deafness and it is not difficult to distinguish it as Jia-Lan or Val-Roy syndrome. Pay attention to the process before and after the attack, distinguish it from adrenergic dependence, or rely on cardiac arrest to facilitate treatment.

ECG characteristics of QT interval prolongation syndrome.

The QT interval is extended and the T wave is wide and can be notched, biphasic or inverted. The QT interval and T wave morphology of the same patient may vary at different times. u waves are often larger. The QT interval has a tendency to shrink with age. The electrocardiogram is supraventricular tachycardia when fainting occurs, most of which are torsades of the tip, and may also have ventricular fibrillation or ventricular arrest. There may be alternating T wave voltages before and after the onset, and frequent ventricular premature beats. However, there are only chest pain and ST-T changes at the time of attack without fainting and ventricular arrhythmia.

Differential diagnosis

ECG characteristics of QT interval prolongation syndrome:

The QT interval is extended and the T wave is wide and can be notched, biphasic or inverted.

The QT interval and T wave morphology of the same patient may vary at different times. u waves are often larger.

The QT interval has a tendency to shrink with age. The electrocardiogram is supraventricular tachycardia when fainting occurs, most of which are torsades of the tip, and may also have ventricular fibrillation or ventricular arrest. There may be alternating T wave voltages before and after the onset, and frequent ventricular premature beats. However, there are only chest pain and ST-T changes at the time of attack without fainting and ventricular arrhythmia.

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