Class II antiarrhythmics: beta-blockers | Medicines for heart rhythm disturbances

Class II antiarrhythmics: beta-blockers

The main targets of this class of antiarrhythmic drugs are the beta receptors of the excitatory and conduction system, mainly sinus nodes and AV nodes. The sinus node is located in the area of the atria and is the place where electrical activity in the heart normally occurs. The signal is then transmitted to the AV node.

This acts as a kind of filter and ensures the orderly transfer of excitation to the heart chambers. Beta blockers inhibit the excitability of the sinus node and reinforce the filtering function of the AV node.The faster the heart beats, the more pronounced the beta blockade. They are generally well tolerated and are particularly suitable for excessively fast heartbeats emanating from the atria (sinus tachycardia, supraventricular tachycardia) as well as for heartbeats that occur outside the basic rhythm and emanate from the ventricle (ventricular extrasystoles).

Class III antiarrhythmics: Potassium channel blocker

This class of antiarrhythmics (drugs for cardiac arrhythmia) are substances that block potassium channels. Potassium is important for the reduction of electrical activity. When these potassium channels are blocked, the ion can no longer flow out of the cell so easily.

The cells remain excited longer (absolute refractory phase is prolonged) and are better protected against new excitations that occur too early. Potassium channel blockers are less proarrhythmogenic than class – I – antiarrhythmics. They are used for severe, therapy-refractory rhythm disturbances.

They can also be used in case of cardiac insufficiency. Increasingly, they are also being used for atrial fibrillation. The lead substance in this class is amiodarone (Cordarex).

It blocks sodium, potassium and calcium channels, thus lowering the heart rate and protecting against excitation that occurs too early or is out of synch with the basic rhythm. When using it, the time until the amiodarone is broken down should be taken into account (elimination half-life of up to 100 days), because the substance accumulates in the tissue. Therapy therefore begins with an eight to ten-day intake of high doses (600 – 1000 mg per day).

A maintenance dose of 100 – 200 mg per day follows. After five days, a break of two days must be observed. This requires a high level of cooperation from the person concerned. In addition, the iodine atoms contained in amiodarone can trigger thyroid dysfunction.