13.01.3 Mechanisms of Arrhythmia

There are several mechanisms of arrhythmias (Figure 13.2). The most important cause of cardiac arrhythmias is cardiac injury, which includes the acute injury associated with a heart attack, and the chronic injury due to the ischemic heart disease associated with angina. Other factors can also contribute to arrhythmias including hypoxia, acidosis, and increases in extracellular K⁺ and/or Ca²⁺. Stress induced increase in the activity of sympathetic nervous system, with an increased release of noradrenaline and adrenaline and activation of cardiac b-adrenoceptors, can also precipitate cardiac arrhythmias.

Figure 13.2 Mechanisms of cardiac arrhythmias (Copyright QUT, Sheila Doggrell)

Cardiac arrhythmias are either disorders of impulse formation or disorders of impulse conduction. Disorders of impulse are of 3 types. Firstly, there is a heart block, where injury to sino-atrio node or atrio-ventricular node causing heart to stop. Usually, to start with this is only for short period, during which the person collapses, and then regains consciousness when the heart starts to beat again, but heart blocks do tend to be progressive; occurring more often and for longer. The treatment for advanced heart blocks is a pacemaker. The second disorder of impulse is an increased firing rate originating in the pacemaker region. Drugs that inhibit the SLOW response i.e. the calcium channel, at the sino-atrio node are useful in this condition. Thirdly, there is the development of ectopic pacemaker, a pacemaker outside of sino-atrial node. Ectopic pacemaker usually develops in the specialised His Purkinje conduction system of the atria or ventricles. Drugs that inhibit the FAST response of the specialised conducting system are useful in treating ectopic pacemakers.

Disorders of conduction are due to damage in the Purkinje conducting system. In the normal heart, impulses arise in the sino-atrial node (pacemaker) and spread around with atria to the atrio-ventricular node, and then around the ventricles to they meet and die out. Impulses leave in their wake refractory tissue, and refractory tissue cannot be re-excited for 200-500 msec. When the last part of heart is excited X, the impulses are surrounded by refractory tissue, and the impulses die out, and there is a period of electrical quiescence. Each of these impulse cycles is associated with a heart beat, and the process is repeated 60 to 80 per min to give a heart rate of 60 to 80 beats per min.

The most common disorder of impulse conduction is functionally defined re-entry. In this there is damage leading to a unidirectional functional block, the impulse can go through one way, but not the other. Thus, the impulse dies out at the damage area. The impulses coming from the other area does not meet one at the bottom of the heart, and just keeps going (Figure 13.3). The impulse can re-enter the ventricular circuit, and cause further activation with quivers of the heart muscle.

Figure 13.3 Functional defined re-entry (Copyright QUT, Sheila Doggrell)

Treatment for unidirectional blocks is most commonly, to turn a unidirectional block into a bidirectional block. With this approach, the impulses will die out at the damaged area rather than the apex of the heart. The benefit is due to preventing the impulse from re-entering. The other approach is to increase excitability or conduction to overcome block, and this returns to near normal function, with the impulses dying out at the apex. The problem with this approach is that if you increase excitability too much, and ectopic centre will develop in the conduction system giving an extra beat. Thus, although not the best method, turning a unidirectional block into a complete block is the safest approach with drug intervention.

Anti-arrhythmic drugs are divided into 4 classes.