There are many classes of antiarrhythmic medications, with different mechanisms of action and many different individual drugs within these classes. Although the goal of drug therapy is to prevent arrhythmia, nearly every anti arrhythmic drug has the potential to act as a pro-arrhythmic, and so must be carefully selected and used under medical supervision.

A number of other drugs can be useful in cardiac arrhythmias.

Several groups of drugs slow conduction through the heart, without actually preventing an arrhythmia. These drugs can be used to "rate control" a fast rhythm and make it physically tolerable for the patient.

Some arrhythmias promote blood clotting within the heart, and increase risk of embolus and stroke. Anticoagulant medications such as warfarin and heparins, and anti-platelet drugs such as aspirin can reduce the risk of clotting.

For those who are stable with a monomorphic waveform the medications procainamide or sotalol may be used and are better than lidocaine. Evidence does not show that amiodarone is better than procainamide.

As a low magnesium level in the blood is a common cause of VT, magnesium sulfate can be given for torsades de pointes or if a low blood magnesium level is found/suspected.

Long-term anti-arrhythmic therapy may be indicated to prevent recurrence of VT. Beta-blockers and a number of class III anti-arrhythmics are commonly used, such as the beta-blockers carvedilol, metoprolol, and bisoprolol, and the Potassium-Channel-Blockers amiodarone, dronedarone,bretylium, sotalol, ibutilide, and dofetilide. Angiotensin-converting-eynsyme (ACE) inhibitors and aldostrone antatagonists are also sometimes used in this setting.

A person with pulseless VT is treated the same as ventricular fibrillation with high-energy (360J with a monophasic defibrillator, or 200J with a biphasic defibrillator) unsynchronised cardioversion (defibrillation). They will be unconscious.

The shock may be delivered to the outside of the chest using the two pads of an external defibrillator, or internally to the heart by an implantable cardioverter-defibrillator (ICD) if one has previously been inserted.

An ICD may also be set to attempt to overdrive pace the ventricle. Pacing the ventricle at a rate faster than the underlying tachycardia can sometimes be effective in terminating the rhythm. If this fails after a short trial, the ICD will usually stop pacing, charge up and deliver a defibrillation grade shock.

Medical therapy can be initiated with medications that slow electrical conduction through the AV node of the heart such as adenosine (which is a form of pharmacologic cardioversion), beta blockers, or non-dihydropyridine calcium channel blockers (such as verapamil or diltiazem). Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma.

Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective. If unsuccessful or the PSVT recurs diltiazem or verapamil are recommended. Adenosine may be safely used during pregnancy.

SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such as sotalol or amiodarone.

In general, atrial flutter should be managed the same as atrial fibrillation. Because both rhythms can lead to the formation of a blood clot in the atrium, individuals with atrial flutter usually require some form of anticoagulation or antiplatelet agent. Both rhythms can be associated with dangerously fast heart rates and thus require medication to control the heart rate (such as beta blockers or calcium channel blockers) and/or rhythm control with class III antiarrhythmics (such as ibutilide or dofetilide). However, atrial flutter is more resistant to correction with such medications than atrial fibrillation. For example, although the class III antiarrhythmic agent ibutilide is an effective treatment for atrial flutter, rates of recurrence after treatment are quite high (70-90%). Additionally, there are some specific considerations particular to treatment of atrial flutter.

Most SVTs are unpleasant rather than life-threatening, although very fast heart rates can be problematic for those with underlying ischemic heart disease or the elderly. Episodes require treatment when they occur, but interval therapy may also be used to prevent or reduce recurrence. While some treatment modalities can be applied to all SVTs, there are specific therapies available to treat some sub-types. Effective treatment consequently requires knowledge of how and where the arrhythmia is initiated and its mode of spread.

SVTs can be classified by whether the AV node is involved in maintaining the rhythm. If so, slowing conduction through the AV node will terminate it. If not, AV nodal blocking maneuvers will not work, although transient AV block is still useful as it may unmask an underlying abnormal rhythm.

If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.

In very rare instances, cardioversion (the electrical restoration of a normal heart rhythm) is needed in the treatment of AVNRT. This would normally only happen if all other treatments have been ineffective, or if the fast heart rate is poorly tolerated (e.g. the development of heart failure symptoms, low blood pressure or coma).

People with atrial fibrillation and rapid ventricular response are often treated with amiodarone or procainamide to stabilize their heart rate. Procainamide and cardioversion are now accepted treatments for conversion of tachycardia found with WPW. Amiodarone was previously thought to be safe in atrial fibrillation with WPW, but after several cases of ventricular fibrillation, it is no longer recommended in this clinical scenario.

AV node blockers should be avoided in atrial fibrillation and atrial flutter with WPW or history of it; this includes adenosine, diltiazem, verapamil, other calcium channel blockers, and beta blockers. They can exacerbate the syndrome by blocking the heart's normal electrical pathway (therefore favoring 1:1 atrial to ventricle conduction through the pre-excitation pathway, potentially leading to unstable ventricular arrhythmias).

People with WPW who are experiencing tachydysrhythmias may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, medication may be used.

Acute management is as for SVT in general. The aim is to interrupt the circuit. In the shocked patient, DC cardioversion may be necessary. In the absence of shock, inhibition at the AV node is attempted. This is achieved first by a trial of specific physical maneuvers such as holding a breath in or bearing down. If these maneuvers fail, using intravenous adenosine; causes complete electrical blockade at the AV node and interrupts the reentrant electrical circuit. Long-term management includes beta blocker therapy and radiofrequency ablation of the accessory pathway.

Once an acute arrhythmia has been terminated, ongoing treatment may be indicated to prevent recurrence. However, those that have an isolated episode, or infrequent and minimally symptomatic episodes, usually do not warrant any treatment other than observation.

In general, patients with more frequent or disabling symptoms warrant some form of prevention. A variety of drugs including simple AV nodal blocking agents such as beta-blockers and verapamil, as well as anti-arrhythmics may be used, usually with good effect, although the risks of these therapies need to be weighed against potential benefits.

Radiofrequency ablation has revolutionized the treatment of tachycardia caused by a re-entrant pathway. This is a low-risk procedure that uses a catheter inside the heart to deliver radio frequency energy to locate and destroy the abnormal electrical pathways. Ablation has been shown to be highly effective: around 90% in the case of AVNRT. Similar high rates of success are achieved with AVRT and typical atrial flutter.

Cryoablation is a newer treatment for SVT involving the AV node directly. SVT involving the AV node is often a contraindication for using radiofrequency ablation due to the small (1%) incidence of injuring the AV node, requiring a permanent pacemaker. Cryoablation uses a catheter supercooled by nitrous oxide gas freezing the tissue to −10 °C. This provides the same result as radiofrequency ablation but does not carry the same risk. If you freeze the tissue and then realize you are in a dangerous spot, you can halt freezing the tissue and allow the tissue to spontaneously rewarm and the tissue is the same as if you never touched it. If after freezing the tissue to −10 °C you get the desired result, then you freeze the tissue down to a temperature of −73 °C and you permanently ablate the tissue.

This therapy has further improved the treatment options for people with AVNRT (and other SVTs with pathways close to the AV node), widening the application of curative ablation to young patients with relatively mild but still troublesome symptoms who would not have accepted the risk of requiring a pacemaker.

If a person is unstable, the initial recommended treatment is intravenous atropine. Doses less than 0.5 mg should not be used, as this may further decrease the rate. If this is not effective, intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used. Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.

In children, giving oxygen, supporting their breathing, and chest compressions are recommended.

Emergency treatment is not needed if the person is asymptomatic or minimally symptomatic.

Atrial flutter is considerably more sensitive to electrical direct current cardioversion than atrial fibrillation, with a shock of only (20 to 50) J commonly being enough to cause a return to a normal heart rhythm (sinus rhythm). Exact placement of the pads does not appear important.

Artificial pacemakers have been used in the treatment of sick sinus syndrome.

Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias respond well to medical therapy.

However, because both bradyarrhythmias and tachyarrhythmias may be present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia. Therefore, a pacemaker is implanted before drug therapy is begun for the tachyarrhythmia.

Management of multifocal atrial tachycardia consists mainly of the treatment of the underlying cause, but if clinically judged necessary, the rate may in some cases be reduced by administering the calcium channel blocker verapamil or the beta blocker metoprolol.

Administration of oxygen may play a role in the treatment of some patients.

Treatment is aimed at slowing the rate by correcting acidosis, correcting electrolytes (especially magnesium and calcium), cooling the patient, and antiarrhythmic medications. Occasionally pacing of the atrium at a rate higher than the JET may allow improved cardiac function by allowing atrial and ventricular synchrony.

A 1994 study at the Adolph Basser Institute of Cardiology found that amiodarone, an antiarrhythmic agent, could be used safely and relatively effectively.

JET occurring after the first six months of life is somewhat more variable, but may still be difficult to control. Treatment of non-post-operative JET is typically with antiarrhythmic medications or a cardiac catheterization with ablation (removal of affected tissue). A cardiac catheterization may be performed to isolate and ablate (burn or freeze) the source of the arrhythmia. This can be curative in the majority of cases. The use of radiofrequency energy is infrequently associated with damage to the normal conduction due to the close proximity to the AV node, the normal conduction tissue. The use of cryotherapy (cold energy) appears to be somewhat safer, and can also be effective for the treatment of JET.

IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.

Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node I channel inhibitors (ivabradine), calcium channel blockers and antiarrhythmic agents. Some SSRI drugs are also occasionally tried and also treatments more commonly used to treat postural orthostatic tachycardia syndrome such as fludrocortisone. This approach is very much "trial-and-error". Patients with IST are often intolerant to beta blockers. A new selective sinus node inhibitor ivabradine is also being used to treat IST.

Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker) and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker).

However invasive treatments can also make the symptoms worse, not cure it. Treatment should be chosen with care as the patient could become in need of a pacemaker or have more extensive symptoms.

Treatment of TIC involves treating both the tachyarrhythmia and the heart failure with the goal of adequate rate control or restoration of the normal heart rhythm (aka. normal sinus rhythm) to reverse the cardiomyopathy. The treatment of the tachyarrhythmia depends on the specific arrhythmia, but possible treatment modalities include rate control, rhythm control with antiarrhythmic agents and cardioversion, radiofrequency (RF) catheter ablation, or AV node ablation with permanent pacemaker implantation.

For TIC due to atrial fibrillation, rate control, rhythm control, and RF catheter ablation can be effective to control the tachyarrhythmia and improve left ventricular systolic function. For TIC due to atrial flutter, rate control is often difficult to achieve, and RF catheter ablation has a relatively high success rate with a low risk of complications. In patients with TIC due to other types of SVT, RF catheter ablation is recommended as a first-line treatment. In patients with TIC due to VT or PVCs, both antiarrhythmics and RF catheter ablation can be used. However, the options for antiarrhythmic agents are limited because certain agents can be proarrhythmic in the setting of myocardial dysfunction in TIC. Therefore, RF catheter ablation is often a safe and effective choice for treatment VT and PVCs causing TIC. In cases where other treatment strategies fail, AV node ablation with permanent pacemaker implantation can also be used to treat the tachyarrhythmia.

The treatment of heart failure commonly involves neurohormonal blockade with beta-blockers and angiotensin convertase inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) along with symptomatic management with diuretics. Beta-blockers and ACE inhibitors can inhibit and potentially reverse the negative cardiac remodeling, which refers to structural changes in the heart, that occurs in TIC. However, the need to continue these agents after treatment of the tacharrhythmia and resolution of left ventricular systolic dysfunction remains controversial.

In people without underlying heart disease and who do not have any symptoms, bigeminy in itself does not require any treatment. If it does become symptomatic, beta-blockers can be used to try and suppress ventricular ectopy. Class I and III agents are generally avoided as they can provoke more serious arrhythmias.

Medications to treat CPVT include beta blockers and verapamil.

Flecainide inhibits the release of the cardiac ryanodine receptor–mediated Ca, and is therefore believed to medicate the underlying molecular cause of CPVT in both mice and humans.

Implantable cardioverter-defibrillators are used to prevent sudden death.