Ventricular extra-systoles: arrhythmia

2021-05-31 03:15 PM

People with frequent ventricular premature beats have a higher risk of fatal ventricular fibrillation caused by an episode of ventricular extrasystoles.

An early cardiac stroke is a contraction that occurs earlier than would normally be expected. This phenomenon is also known as extrasystoles, premature beats, or ectopic beats.

Figure. Ventricular extrasystoles (PVCs) are indicated by a large abnormal QRS-T complex (leads DII and DIII). The axes of the extrasystoles were plotted according to the principles of vector analysis and showed that the origin of the ventricular extrasystoles was near the base of the ventricles.

Pictured is each sequence of premature ventricular contractions (PVCs) alternating with a normal rhythm. Ventricular extrasystoles have the following typical electrocardiographic findings:

1. The QRS complex is prolonged. The reason for this prolongation is that the pulses conducted through the ventricles are slower than those conducted through the Purkinje lattice.

2. Higher QRS complex. When the normal pulse passes through the heart, it passes through both ventricles almost simultaneously, resulting in a normal heart, the depolarization waves of both sides, with two different depolarization directions, partially neutralizing the electrical current. cardiogram.

When ventricular extrasystoles occur, pulses are almost exclusively unidirectional and there will be no neutralization, one side will completely anteriorly depolarize the opposite side causing potential prolongation and presenting as a prolonged QRS interval. in the picture.

3. After most ventricular extrasystoles, the T wave is inversely related to the QRS complex. Because of slow conduction of the impulse through the myocardium, the first depolarized myocardium will repolarize first.

Some ventricular extrasystoles also have little effect on the total pumping capacity of the heart, and ventricular extrasystoles can be caused by smoking, coffee, lack of sleep, mild intoxication, and even emotional stimulation. In contrast, many ventricular extrasystoles are caused by impulses associated with myocardial infarction or ischemia. The appearance of such ventricular extrasystoles and their effects is not gentle.

People with frequent ventricular premature beats have a higher risk of fatal ventricular fibrillation caused by an episode of ventricular extrasystoles.

This progression is especially true when ventricular extrasystoles occur during a vulnerable period, immediately after the end of the T wave, when the ventricles are preparing to escape refractory, as will be explained later.

Analysing the direction of the ventricular ectopic origin, the important points of the direction analysis have been explained. By applying these points, it is possible to identify the source of the ventricular extrasystoles shown in the following figure. The upper ECG is in leads II or III. Determine the axis of the extrasystoles compared with the normal QRS, we see that the direction of the extrasystole is opposite, the peak is downward. Thus, the first part of the heart that is depolarized during extrasystoles is close to the base of the ventricles, which is where the beat originates.

Repolarization disorder - Long QT syndrome. Again, the Q wave is indicative of the ventricular depolarization phase, and the T wave is the ventricular polar tasiphaan wave. The QT interval is the interval from the beginning of Q to the end of T. This type of slow repolarization of the myocardium after depolarization causes a prolongation of the ventricular action potential and is indicated by a prolonged QT interval called prolonged QT syndrome. long. (LQTS: long QT syndrome).

The main reason for the long QT syndrome is related to delayed repolarization in hyposensitive patients progressing to ventricular arrhythmias called torsade de pointes, literally "twisting of points". This type of arrhythmia is characteristically characteristic. The shape of the QRS complex can change several times with the onset of arrhythmia usually after an extrasystole, a pause, followed by a pulse with a prolonged QT interval, which causes arrhythmia, tachycardia, and sometimes ventricular fibrillation.

Figure. Arrhythmia in long QT syndrome (LQTS). When the action potential of the ventricular myocardium is prolonged due to slow repolarization, early depolarization (dashed line in upper left image) may occur before complete repolarization. Repeated premature depolarization (top right) can lead to multiple depolarizations under certain conditions. In torsade de pointes (bottom image), ventricular extrasystoles lead to pauses, prolongation of the QT interval, and arrhythmias.

The repolarization disorder leading to long QT syndrome can be inherited or acquired. The congenital form of long QT syndrome is found and is caused by the alteration of Na-K channels. At least 10 mutations in these genes that cause varying degrees of QT prolongation have been identified.

The most common is the acquired type that is associated with electrolyte disturbances, such as hypomagnesaemia, hypokalaemia, hypocalcaemia, or an overdose of antiarrhythmic drugs such as quinidine or some antibiotics such as fluoroquinolones or erythromycin, which prolong QT interval.

Although some people with long QT syndrome have no symptoms (usually as QT prolongation), others have fainting and ventricular arrhythmias that may be apparent during physical activity, strong emotions such as anger or scared, startled. Ventricular dysrhythmias are associated with long QT syndrome, which, in some cases, worsens to ventricular fibrillation and sudden death.