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.

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.

The underlying condition may be treated by medications to control hypertension or diabetes, if they are the primary underlying cause. If coronary arteries are blocked, an invasive coronary angioplasty may relieve the impending RBBB.

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.

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.

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.

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.

Pharmacologic management of ARVD involves arrhythmia suppression and prevention of thrombus formation.

Sotalol, a beta blocker and a class III antiarrhythmic agent, is the most effective antiarrhythmic agent in ARVD. Other antiarrhythmic agents used include amiodarone and conventional beta blockers (i.e.: metoprolol). If antiarrhythmic agents are used, their efficacy should be guided by series ambulatory holter monitoring, to show a reduction in arrhythmic events.

While angiotensin converting enzyme inhibitors (ACE Inhibitors) are well known for slowing progression in other cardiomyopathies, they have not been proven to be helpful in ARVD.

Individuals with decreased RV ejection fraction with dyskinetic portions of the right ventricle may benefit from long term anticoagulation with warfarin to prevent thrombus formation and subsequent pulmonary embolism.

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.

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.

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).

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.

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 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.

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.

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.

Premature atrial contractions are often benign, requiring no treatment. Occasionally, the patient having the PAC will find these symptoms bothersome, in which case the doctor may treat the PACs. Sometimes the PACs can indicate heart disease or an increased risk for other cardiac arrhythmias. In this case the underlying cause is treated. Often a beta blocker will be prescribed for symptomatic PACs.

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.

Catheter ablation may be used to treat intractable ventricular tachycardia.

It has a 60–90% success rate. Unfortunately, due to the progressive nature of the disease, recurrence is common (60% recurrence rate), with the creation of new arrhythmogenic foci. Indications for catheter ablation include drug-refractory VT and frequent recurrence of VT after ICD placement, causing frequent discharges of the ICD.

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.

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.

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

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).

The prognosis for TIC after treatment of the underlying tachyarrhythmia is generally good. Studies show that left ventricular function often improves within 1 month of treatment of the tachyarrhythmia, and normalization of the left ventricular ejection fraction occurs in the majority of patients by 3 to 4 months. In some patients however, recovery of this function can take greater than 1 year or be incomplete. In addition, despite improvement in the left ventricular ejection fraction, studies have demonstrated that patients with prior TIC continue to demonstrate signs of negative cardiac remodeling including increased left ventricular end-systolic dimension, end-systolic volume, and end-diastolic volume. Additionally, recurrence of the tachyarrhythmia in patients with a history of TIC has been associated with a rapid decline in left ventricular ejection fraction and more severe cardiomyopathy that their prior presentation, which may be a result of the negative cardiac remodeling. There have also been cases of sudden death in patients with a history of TIC, which may be associated with worse baseline left ventricular dysfunction. Given these risks, routine monitoring with clinic visits, ECG, and echocardiography is recommended.