Treating Arrhythmias: Quelling The Riot

To make the cardiac contractions hemodynamically effective and to avoid the dangerous consequences of arrhythmias, treatment is often necessary. Pharmacotherapy, electrical therapy using defibrillator, pacemaker implantation, radio-frequency ablation and even surgery are some methods that are available.

Bradyarrhythmias arising due to AV block (conduction disturbance) may be treated with vagolytics (parasympatholytics) like atropine, or sympathomimetics like isoproterenol (isoprenaline), given intravenously. These medications increase the heart rate. The heart is innervated by the vagus nerve, which secretes acetyl choline when stimulated. This chemical combines with a receptor molecule, called muscarinic receptor, type M2, on the cell membrane of the heart muscles. After combining, they give instructions to some other substances in the cell membranes called G proteins, to open the potassium channels. Potassium being more in the interior of the cell, leaks to the outside, along the gradient. This efflux of K+ ions make the cell more negative (hyper-polarized) and thus less excitable, lowering the speed of conduction. Atropine, an antimuscarinic drug, does not let this happen. Potassium channels are NOT opened and the cells are as more excitable. Impulse can pass easily now. Sympathetic nervous stimulation, through beta receptor stimulation, or drugs like isoprenaline also increase the speed of conduction.

A better way of tackling bradyarrhythmias is through the implantation of a pacemaker, an artificial one. These devices have a stimulating electrode which passes through some vein on the surface of the body straight to the right atrial appendage or the apex of the right ventricle. These pacemakers have a coding nomenclature (like the color coding of resistors or capacitors) that describe them. For example, in the usual VVIR type, the first letter 'V' indicates that it is the ventricle that is paced (i.e. stimulated); the second 'V' means that the pacemaker senses the ventricles to determine its action (described later); 'I' means that the action will be inhibitory (i.e. if it senses that an impulse is normally there in the ventricle, it will inhibit the next impulse from the artificial pacemaker); whereas R means that it is rate controlled. This protocol is much like the color coding of resistors in electronics. Pacemakers are also useful in the treatment of paroxysmal tachycardias (the implanted pacemaker depolarizes ahead of the ectopic signal and make aberrant conduction difficult through the now refractory tissue.)

Pharmacotherapy, using antiarrhythmics, is rather disappointing. In the CAST study (cardiac arrhythmia suppression trial), it was shown that patients treated with one of the drugs (moricizine or flecainide or encainide) had actually more mortality than the control group. In fact, antiarrhythmics are themselves arrythmogenic (proarrhythmic). However, amiodarone, beta blockers, adenosine and some other drugs do seem to confer some benefit.

Implantable cardioverter defibrillators (ICD) are very useful. They sense arrhythmias and send DC shock upto 40 W.s (Watt seconds), to tame the 'revolting rebels'. This 'recognize and treat' methodology based tool (picture shown) is very useful. Another useful approach is by using catheters with a probe electrode at their tips. They can virtually sniff out the abnormal focus by mapping (electrophysiology study or EPS), which are later burned, using radio frequency currents (RF ablation). Radio frequency ablation is very helpful in burning out the aberrant bundle of Kent in WPW syndrome, in atrial flutter, AV nodal reentrant tachycardias and others.

Role of surgery is very minimal. It is invoked only when other measures fail and in some recalcitrant cases. While the above information is important, one must never forget the immense significance of cardiopulmonary resuscitation (CPR) in this regard. This intelligent step consisting of pressing the sternum (breastbone) with the heel of the hand and giving artificial respiration through the mouth simultaneously, is life saving. Here in this case, the first part, i.e. pressing the sternum is particularly important as it will pump the heart from outside and result in a cardiac massage. In a suspected event of cardiac arrest where the heart has stopped (i.e. no effective cardiac output), do a CPR first, save a life!

Last modified: Mar20, 2009
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