Organized electrical activity of the heart plays a significant role in cardiac function, and disruption of this activity in the form of arrythmias may result in clinical symptoms or even death. These arrythmias may be too fast - tachyarrythmias - or to slow - bradyarrhythmias.
Antiarrhytmic drugs work in two main ways. They may impact the ion channels that cause and regulate the heart beat, including sodium, potassium, and calcium. They may also modify the neuronal control of the heart, particularly the beta adrenergic innervation of the sympathetic nervous system.
Unfortunately, while antiarrythmic drugs are meant to bring normalcy to the heart beat, on occasion, the opposite may occur, and they may in fact cause arrythmias. This is particularly true for the sodium channel blocking drugs.
Antiarrhythmic medications have a number of uses, including:
There are many ways to classify antiarrhythmic medications.
One of the most common, to be used here, is the Vaughan-Williams classification, which is organized according to the mechanism of action. These mechanisms include:
However, this is an inexact classification, as many medications have numerous sites of action.
Class I medications, which block sodium channels, are further subdivided into three categories.
Class Ia medications slow the rise of phase 0 of the action potential, therefore slowing conduction velocity. They also prolong the ventricular refractory period, as well as slow the depolarization of phase 4 of pacemaker cells. Class Ia medications include:
Class Ib medications slow the conduction, and shorten the action potential, of healthy tissue. Class Ib medications include:
Class Ic medications slow the rise of phase 0 of the action potential, as well as shorten the refractory period of Purkinje fibres. Class Ic medications include:
Increase action pulse duration
Calcium channel blocker
Bradycardia due to a damaged SA node can be treated with:
Contains large amounts of iodine
Amiodarone is an atiarrhythmic drug, acting on sodium, potassium, and calcium channels, and with alpha- and beta-adrenergic blocking capacity. It comes with many substantial side effects, and should be used only in life-threatening situations by people well-versed in its use.
CCBs are used for
Calcium channel blockers are negative inotropes, blocking Ca2+ influx into vascular smooth muscle cells and cardiomyocytes. This leads to:
The two classes of CCBs are
can cause headaches, flushing, dizziness
bradycardia/heart block (verapamil, diltiaezm)
worsening heart failure
Digoxin is a cardiac glycoside used to increase cardiac contractility.
Digoxin is one of the few drugs whose levels can be monitored. Use low doses (0.0625 or 0.125) if necessary.
DIG trial (NEJM, 1997): no benefit for mortality; lower hospitalization rates. However, may be high levels of mortality in women.
Digoxin withdrawal has been shown be safe in many patients (PROVED study, RADIANCE study). However, patients do worse if they have: