Mechanisms of Arrhythmias

Principles of Arrhythmias

Abnormal impulse formation

Abnormal impulse formation can result in an abnormal frequency, as in symptomatic sinusbradycardia, but oftenwise the problem is an abnormal location of impulse formation, as is the cause in an ectopic pacemaker.

Abnormal automaticity

The sinus node contains pacemaker cells that have spontaneous firing capacity, this is called normal automaticity. Abnormal automaticity occurs when other cells start firing spontaneously, resulting in premature heartbeats. All cardiac cells have spontaneous firing capacity, but at only at a very slow heartrate. Therefore, during a normal heart rate, they will never have the chance to show off their firing capacity. However in pathologic conditions, such as during extreme bradycardia other cells can take over and cause for example a AV-nodal heart rate.

Triggered activity

Triggered activity vuren cellen twee keer, terwijl ze maar één keer gestimuleerd zijn. Dit is meestal het gevolg van zogenaamde nadepolarisaties (early of delayed afterdepolarisations EAD's / DAD's) door electrische onstabiliteit in de hartcelmembraam. Een typisch voorbeeld hiervan is Torsade de pointes.

Abnormal conduction

Conduction delay

Conduction delay can cause a slow heart rate, as happens during AV conduction blocks. If conduction delay occurs more distally in the heart, i.e. within the ventricles, the QRS complex will widen and a left or right bundle branch block can be seen on the ECG.

Re-entry

Re-entry. Image A shows two pathways. The signal splits in two at arrival, but no arrhythmia is initiated as the slow signal extincts when in meets the fast signal. However, in image B re-entry is initiated by an extrasystole. The extrasystole follows shortly after the previous signal. The fast pathway is still in a refractory state and blocks the signal. The slow signal reaches the 'tail' of the fast path by the time that the fast path's refractory period is finished. The fast path conducts the signal towards the start (upwards) and the circle completes.

Re-entry is a common cause of arrhythmias. Ventricular tachycardia and AV-nodal re-entry are typical examples. Re-entry can occur when a conduction path is partly slowed down. As a result of this, the signal is conducted by both a fast and a slow pathway. During normal sinus rhythm this generally does not cause problems, but when an extrasystole follows rapidly upon the previous beat, the fast pathway is sometimes still refractory and cannot conduct the signal. Now the following sequence results in re-entry.

1. The atrial signal coming from above is conducted by the slow pathway
2. As the signal through the slow pathway reaches the end of the fast pathway, it finds this pathway willing to conduct.
3. The signal is conducted through the fast pathway up to the beginning of the slow pathway, which by that time is willing to conduct.
4. This circle is perpetuated and a signal generator is created. In the case of AV-nodal re-entry this will typically generate a signal at a frequency of 180-250 bpm.