Knowledge that TdP may occur in patients taking certain prescription drugs has been both a major liability and reason for retirement of these medications from the marketplace. Examples of compounds linked to clinical observations of TdP include amiodarone, fluoroquinolones, methadone, lithium, chloroquine, erythromycin, amphetamine, ephedrine, pseudoephedrine, methylphenidate, and phenothiazines. It has also been shown as a side effect of certain anti-arrhythmic medications, such as sotalol, procainamide, and quinidine. The gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes. In many cases, this effect can be directly linked to QT prolongation mediated predominantly by inhibition of the hERG channel.

In September 2011 (subsequently updated in March 2012 and February 2013), the FDA issued a warning concerning increased incidence of QT prolongation in patients prescribed doses of the antidepressant Celexa (citalopram) above 40 mg per day, considered the maximum allowable dosage, thereby increasing the risk of Torsades. However, a study, "Evaluation of the FDA Warning Against Prescribing Citalopram at Doses Exceeding 40 mg," reported no increased risk of abnormal arrhythmias, thus questioning the validity of the FDA's warning.

The management includes identifying and correcting electrolyte imbalances and withholding any offending medications. This condition does not require admission unless there is an associated myocardial infarction. Even though it usually does not progress to higher forms of heart block, it may require outpatient follow-up and monitoring of the ECG, especially if there is a comorbid bundle branch block. If there is a need for treatment of an unrelated condition, care should be taken not to introduce any medication that may slow AV conduction. If this is not feasible, clinicians should be very cautious when introducing any drug that may slow conduction; and regular monitoring of the ECG is indicated.

Sinoatrial blocks are typically well-tolerated. They are not as serious as an AV block and most often do not require treatment. In some people, they can cause fainting, altered mental status, chest pain, hypoperfusion, and signs of shock. They can also lead to cessation of the SA node and more serious dysrhythmias. Emergency treatment, if deemed necessary, consists of administration of atropine sulfate or transcutaneous pacing.

Treatment in emergency situations ultimately involves electrical pacing. Pharmacological management of suspected beta-blocker overdose might be treated with glucagon, calcium channel blocker overdose treated with calcium chloride and digitalis toxicity treated with the digoxin immune Fab.

Third-degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node via lead in the right atrium and sends a pulse via a lead to the right ventricle at an appropriate delay, driving both the right and left ventricles. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third-degree AV block. Since pacemaker correction of third-degree block requires full-time pacing of the ventricles, a potential side effect is pacemaker syndrome, and may necessitate use of a biventricular pacemaker, which has an additional 3rd lead placed in a vein in the left ventricle, providing a more coordinated pacing of both ventricles.

The 2005 Joint European Resuscitation and Resuscitation Council (UK) guidelines state that atropine is the first line treatment especially if there were any adverse signs, namely: 1) heart rate 3 seconds. Mobitz Type 2 AV block is another indication for pacing.

As with other forms of heart block, secondary prevention may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.

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.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.

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).

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.

The treatment for diffuse distal conduction system disease is insertion of a pacemaker. If the PR prolongation is due to AV nodal disease, a case may be made for observation, as it may never progress to complete heart block with life threateningly low heart rates.

Regardless of where in the conduction system the block is, if the block is believed to be the cause of syncope in an individual, a pacemaker is an appropriate treatment.

Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia.

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.

Treatment depends on the origin of the automatic tachycardia, however the mainstay of treatment is either antidysrhythmic medication or cardiac pacing. Specifically overdrive pacing may be used for all forms of automatic tachycardia; a pacemaker assumes control of the heart rhythm in overdrive pacing. In some cases ablation of the ectopic focus may be necessary.

Isolated first-degree heart block has no direct clinical consequences. There are no symptoms or signs associated with it. It was originally thought of as having a benign prognosis. In the Framingham Heart Study, however, the presence of a prolonged PR interval or first degree AV block doubled the risk of developing atrial fibrillation (irregular heart beat), tripled the risk of requiring an artificial pacemaker, and was associated with a small increase in mortality. This risk was proportional to the degree of PR prolongation.

A subset of individuals with the triad of first-degree heart block, right bundle branch block, and either left anterior fascicular block or left posterior fascicular block (known as trifascicular block) may be at an increased risk of progression to complete heart block.

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.

Arrhythmias due to medications have been reported since the 1920s with the use of quinine. In the 1960s and 1970s problems with antihistamines and antipsychotics were discovered. It was not until the 1980s that the underlying issue, QTc prolongation was determined.

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 an affected individual begins to experience severe TDBBB, then medical intervention is often advised. Suggested therapy for the treatment of TDBBB can include the prescription of certain medications or the implantation of a pacemaker device. Advised medications would possess anti-coagulant mechanisms to reduce the risk of blood clot formation ensuring that no further restriction of arteries would deprive the heart of oxygen and further damage the bundle branches. The use of a pacemaker would ensure that the heart receives a constant rhythmic electrical input that never changes in frequency. While this would effectively eliminate the occurrence of TDBBB, the pacemaker would restrict the patient's heart to a permanent rhythm, eliminating the ability of patients to perform physical activity. Future pacemakers that adaptively respond to physiological requirements are being developed in order to negate the limitations observed with their current use.

Treatment is directed towards the withdrawal of the offending agent, infusion of magnesium sulfate, antiarrhythmic drugs, and electrical therapy, such as a temporary pacemaker, as needed.

Because of the polymorphic nature of torsades de pointes, synchronized cardioversion may not be possible, and the patient may require an unsynchronized shock (or defibrillation).

Some people with bundle branch blocks are born with this condition. Many other acquire it as a consequence of heart disease. People with bundle branch blocks may still be quite active, and may have nothing more remarkable than an abnormal appearance to their ECG. However, when bundle blocks are complex and diffuse in the bundle systems, or associated with additional and significant ventricular muscle damage, they may be a sign of serious underlying heart disease. In more severe cases, a pacemaker may be required to restore an optimal electrical supply to the heart muscle.

The prognosis of patients with complete heart block is generally poor without therapy. Patients with 1st and 2nd degree heart block are usually asymptomatic.

Pacemaker failure is the inability of an implanted artificial pacemaker to perform its intended function of regulating the beating of the heart. A pacemaker uses electrical impulses delivered by electrodes in order to contract the heart muscles. Failure of a pacemaker is defined by the requirement of repeat surgical pacemaker-related procedures after the initial implantation. Most implanted pacemakers are dual chambered and have two leads, causing the implantation time to take longer because of this more complicated pacemaker system. These factors can contribute to an increased rate of complications which can lead to pacemaker failure.

Approximately 2.25 million pacemakers were implanted in the United States between 1990 and 2002, and of those pacemakers, about 8,834 were removed from patients because of device malfunction most commonly connected to generator abnormalities. In the 1970s, results of an Oregon study indicated that 10% of implanted pacemakers failed within the first month. Another study found that more than half of pacemaker complications occurred during the first 3 months after implantation. Causes of pacemaker failure include lead related failure, unit malfunction, problems at the insertion site, failures related to exposure to high voltage electricity or high intensity microwaves, and a miscellaneous category (one patient had ventricular tachycardia when using his electric razor and another patient had persistent pacing of the diaphragm muscle). Pacemaker malfunction has the ability to cause serious injury or death, but if detected early enough, patients can continue with their needed therapy once complications are resolved.

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.

No specific drugs are used to treat pacemaker syndrome directly because treatment consists of upgrading or reprogramming the pacemaker.

Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate

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.