Maintenance of a consistent rhythm is central to efficient cardiac function. The electrical conductance system is designed to only allow electrical waves to travel in one direction and to prevent their arriving too close together, making for inefficient contraction of cardiac muscle. However, an injury to the heart muscle for example, by a heart attack, results in the death of a discrete area of the heart muscle, as defined by the location of the thrombus of the coronary artery that led to the heart attack. The infracted area is dominated by scar tissue, which alters the electrical conduction properties of that region. The site of the infarct has serious implications for the efficient transmission of the electrical activity across the heart and can lead to potentially fatal changes in heart rhythm- so-called arrhythmias.
Causes of Arrhythmias
1. Abnormal pace-maker activity: The heart rate is normally determined by the pacemaker cells in the sino-atrial node, but other cells in the heart can undertake pacemaker activity during or after the ischaemic damage. The cellular mechanisms have not been fully elucidated but may involve a decrease in Na+/K+-ATPase pump activity leading to membrane depolarization and pain-mediated adrenaline release might play a part during a heart attack.
2. Heart Block: If an infarct encompasses the AV node, the wave of activity may not be properly transmitted from the atria to the ventricles. The atria will continue to beat at the rate set by the SA node; the ventricles will beat independently, at a rate set by ventricular pacemaker cells. Sequential contraction of the atria, followed by the ventricles, is crucial for efficient pumping of blood and ‘heart block’ is best treated by artificial pacemaker.
3. Re-entry: The refractory nature of the cardiac muscle immediately after depolarization normally ensures that the impulse wave only travels in one direction. Re-entry implies a ring of a cardiac tissue, which can be anatomically distinct from the surrounding tissue, but is more commonly only functionally distinct. The concept indicates that the impulse arising from any one point in the ring will propagate in both directions, until the waves of depolarization meet and both the waves are cancelled out. However if a part of the ring is damaged, the impulse is not transmitted in the normal direction but will still propagate in the retrograde direction, so that the impulse can cycle around the ring continuously, if the time taken for each cycle exceeds the refractory period. Drugs that are useful in treating the re-entry prolong the refractory period.
Bradycardia and Atrial fibrillation
Bradycardia is an unusually slow heart rate that can be brought on by the sinus dysfunction or hypothyroidism and exacerbated by heart-slowing drugs such as Beta blockers. Severe cases can lead to cardiac arrest, atrial fibrillation or thromboembolism. Mild cases can effectively be treated drugs which prevent the slowing effect of the vagal stimulation of the heart. More serious cases may require temporary or permanent implantation of the pace-maker devices.
Atrial fibrillation is defines as irregular and extremely rapid contractions of the atria. The cause is often Myocardial Infarction. The main risk is thromboembolism which is prevented by anticoagulants. The key to treatment of AF is to deal with the underlying cause, if possible, and to use drugs to slow the atrial contractions.
Treatment of arrhythmias
Some arrhythmias are best treated by implantation of artificial pace-maker, by surgical intervention to ablate re-entry circuits or by cardioversion in acute cases.
Drug therapies are primarily aimed at the electrophysiological events of cardiac contractility.
