There can be similar patterns depending on the frequency of abnormal beats. If every other beat is abnormal, it is described as bigeminal. If every third beat is aberrant, it is trigeminal; every fourth would be quadrigeminal. Typically, if every fifth or more beat is abnormal, the aberrant beat would be termed occasional.

Bigeminy is contrasted with couplets, which are paired abnormal beats. Groups of three abnormal beats are called triplets and are considered as a brief run of non-sustained ventricular tachycardia (NSVT) and if the grouping last for more than 30 seconds, it is ventricular tachycardia (VT).

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.

The diagnosis of ventricular tachycardia is made based on the rhythm seen on either a 12-lead ECG or a telemetry rhythm strip. It may be very difficult to differentiate between ventricular tachycardia and a wide-complex supraventricular tachycardia in some cases. In particular, supraventricular tachycardias with aberrant conduction from a pre-existing bundle branch block are commonly misdiagnosed as ventricular tachycardia. Other rarer phenomena include ashman beats and antedromic atrioventricular re-entry tachycardias.

Various diagnostic criteria have been developed to determine whether a wide complex tachycardia is ventricular tachycardia or a more benign rhythm. In addition to these diagnostic criteria, if the individual has a past history of a myocardial infarction, congestive heart failure, or recent angina, the wide complex tachycardia is much more likely to be ventricular tachycardia.

The proper diagnosis is important, as the misdiagnosis of supraventricular tachycardia when ventricular tachycardia is present is associated with worse prognosis. This is particularly true if calcium channel blockers, such as verapamil, are used to attempt to terminate a presumed supraventricular tachycardia. Therefore, it is wisest to assume that all wide complex tachycardia is VT until proven otherwise.

Ventricular tachycardia can be classified based on its "morphology":

- Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).

- Scar-related monomorphic ventricular tachycardia is the most common type and a frequent cause of death in patients having survived a heart attack or myocardial infarction, especially if they have a weak heart muscle.

- RVOT tachycardia is a type of monomorphic ventricular tachycardia originating in the right ventricular outflow tract. RVOT morphology refers to the characteristic pattern of this type of tachycardia on an ECG.

- The source of the re-entry circuit can be identified by evaluating the morphology of the QRS complex in the V1 lead of a surface ECG. If the R wave is dominant (consistent with a right bundle branch block morphology), this indicates the origin of the VT is the left ventricle. Conversely, if the S wave is dominant (consistent with a left bundle branch block morphology, this is consistent with VT originating from the right ventricle or interventricular septum.

- Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardiac axis, previously referred to by its French name "torsades de pointes" ("twisting of the spikes"). However, at the current time, the term torsades de pointes is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval.

Another way to classify ventricular tachycardias is the "duration of the episodes": Three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia.

- If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia.

- If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds).

A third way to classify ventricular tachycardia is on the basis of its "symptoms": Pulseless VT is associated with no effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest. In this circumstance, it is best treated the same way as ventricular fibrillation (VF), and is recognized as one of the shockable rhythms on the cardiac arrest protocol. Some VT is associated with reasonable cardiac output and may even be asymptomatic. The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to pulseless VT or to VF.

Less common is ventricular tachycardia that occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors.

Current research seeks to predict the event of rearrest after patients have already achieved ROSC. Biosignals, such as electrocardiogram (ECG), have the potential to predict the onset of rearrest and are currently being investigated to preemptively warn health care providers that rearrest could be imminent.

A stronger pulse detector would also contribute to lowering the rate of rearrest. If the resuscitator could accurately know when the patient has achieved ROSC, there would be less instances of chest compressions being provided when a native pulse is present.

A recent study by Salcido et al. (2010) ascertained rearrest in all initial and rearrest rhythms treated by any level of Emergency Medical Service (EMS), finding a rearrest rate of 36% and a lower but not significantly different rate of survival to hospital discharge in cases with rearrest compared to those without rearrest.

Ambulatory monitoring of the electrocardiogram (ECG) may be necessary because arrhythmias are transient. The ECG may show any of the following:

- Inappropriate sinus bradycardia

- Sinus arrest

- Sinoatrial block

- Tachy-Brady Syndrome

- Atrial fibrillation with slow ventricular response

- A prolonged asystolic period after a period of tachycardias

- Atrial flutter

- Ectopic atrial tachycardia

- Sinus node reentrant tachycardia

- Wolff-Parkinson-White syndrome

Electrophysiologic tests are no longer used for diagnostic purposes because of their low specificity and sensitivity. Cardioinhibitory and vasodepressor forms of sick sinus syndrome may be revealed by tilt table testing.

Treatment is based on risk stratification of the individual, which is performed to determine which individuals with WPW are at risk for sudden cardiac death (SCD). The medical history may infrequently point to previous episodes of unexplained syncope (fainting) or, more commonly, palpitations (sudden awareness of one's own, usually irregular, heartbeat). These may have been due to earlier episodes of a tachycardia associated with the accessory pathway.

If an individual's delta waves disappear with increases in the heart rate, he or she is considered to be at lower risk of SCD. This is because the loss of the delta wave shows that the accessory pathway cannot conduct electrical impulses at a high rate (in the anterograde direction). These individuals typically do not have fast conduction down the accessory pathway during episodes of atrial fibrillation.

Risk stratification is best performed via programmed electrical stimulation (PES) in the cardiac electrophysiology laboratory. This is an invasive but generally low-risk procedure during which the atria are stimulated to try to induce tachycardia. If a tachycardia involving the accessory pathway can be triggered, the cardiologist can then assess how rapidly the accessory pathway is able to conduct. The faster it can conduct, the higher the likelihood the accessory pathway can conduct fast enough to trigger a lethal tachycardia.

High-risk features that may be present during PES include an effective refractory period of the accessory pathway less than 250 ms, multiple pathways, septal location of pathway, and inducibility of supraventricular tachycardia (AVRT, atrial fibrillation). Individuals with any of these high-risk features are generally considered at increased risk for SCD or symptomatic tachycardia, and should be treated accordingly (i.e.: catheter ablation).

It is unclear whether invasive risk stratification (with PES) is necessary in the asymptomatic individual. While some groups advocate PES for risk stratification in all individuals under 35 years old, others only offer it to individuals who have history suggestive of a tachydysrhythmia, since the incidence of sudden cardiac death is so low (less than 0.6% in some reports).

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.

ECG characteristics

- Rate: Less than 60 beats per minute.

- Rhythm: Regular.

- P waves: Upright, consistent, and normal in morphology and duration.

- P-R Interval: Between 0.12 and 0.20 seconds in duration.

- QRS Complex: Less than 0.12 seconds in width, and consistent in morphology.

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.

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.

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.

When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis.

The Swan-Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics.

AIVR appears similar to ventricular tachycardia with wide QRS complexes (QRS >0.12s) and a regular rhythm. It can most easily be distinguished from VT in that the rate is less than 120 and usually less than 100 bpm. There may or may not be AV dissociation depending on whether it is due to ventricular escape or AV block.

It can be associated with digitalis toxicity. It may be also be due to onset of acute coronary syndrome, heart failure, conduction system diseases with enhanced automaticity, or administration of theophylline.

A junctional escape beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. It is a protective mechanism for the heart, to compensate for the SA node no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so.

Junctional tachycardia is a form of supraventricular tachycardia characterized by involvement of the AV node. It can be contrasted to atrial tachycardia. It is a tachycardia associated with the generation of impulses in a focus in the region of the atrioventricular node due to an A-V disassociation. In general, the AV junction's intrinsic rate is 40-60 bpm so an Accelerated Junctional rhythm is from 60-100bpm and then becomes junctional tachycardia at a rate of >100 bpm.

The decreased heart rate can cause a decreased cardiac output resulting in symptoms such as lightheadedness, dizziness, hypotension, vertigo, and syncope. The slow heart rate may also lead to atrial, junctional, or ventricular ectopic rhythms.

Bradycardia is not necessarily problematic. People who regularly practice sports may have sinus bradycardia, because their trained hearts can pump enough blood in each contraction to allow a low resting heart rate. Sinus bradycardia can also be an adaptive advantage; for example, diving seals may have a heart rate as low as 12 beats per minute, helping them to conserve oxygen during long dives.

Sinus bradycardia is a common condition found in both healthy individuals and those who are considered well conditioned athletes.

Heart rates considered bradycardic vary by species; for example, in the common housecat, a rate of under 120 beats per minute is abnormal. Generally, smaller species have higher heart rates while larger species have lower rates.

Accelerated idioventricular rhythm is a ventricular rhythm with a rate of between 40 and 120 beats per minute. Idioventricular means “relating to or affecting the cardiac ventricle alone” and refers to any ectopic ventricular arrhythmia. Accelerated idioventricular arrhythmias are distinguished from ventricular rhythms with rates less than 40 (ventricular escape) and those faster than 120 (ventricular tachycardia). Though some other references limit to between 60 and 100 beats per minute. It is also referred to as AIVR and "slow ventricular tachycardia."

It can be present at birth. However, it is more commonly associated with reperfusion after myocardial injury.

MAT usually arises because of an underlying medical condition. Its prevalence has been estimated at about 3 per 1000 in adult hospital inpatients and is much rarer in paediatric practice; it is more common in the elderly, and its management and prognosis are both those of the underlying diagnosis.

It is mostly common in patients with lung disorders, but it can occur after acute myocardial infarction and can also occur in the setting of low blood potassium or low blood magnesium.

It is sometimes associated with digitalis toxicity in patients with heart disease.

It is most commonly associated with hypoxia and COPD. Additionally, it can be caused by theophylline toxicity, a drug with a narrow therapeutic index commonly used to treat COPD. Theophylline can cause a number of different abnormal heart rhythms when in excess, and thus further predisposes COPD patients to MAT. Theophylline toxicity often occurs following acute or chronic overtreatment or factors lowering its clearance from the body.

A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node (e.g. digoxin toxicity), a pathological slowing of the SA discharge, or a complete AV block.

An automatic tachycardia is a cardiac arrhythmia which involves an area of the heart generating an abnormally fast rhythm, sometimes also called enhanced automaticity. These tachycardias, or fast heart rhythms, differ from reentrant tachycardias (AVRT and AVNRT) in which there is an abnormal electrical pathway which gives rise to the pathology. Most automatic tachycardias are supraventricular tachycardias (SVT). It is important to recognise an automatic tachycardia because the treatment will be different to that for a reentrant tachycardia. The most useful clue will be the presence of 'warm up' and 'cool down'. This means that whereas a reentrant tachycardia will both begin and end abruptly as cardiac conduction utilises then ceases to utilise the accessory pathway, an automatic tachycardia will rise and fall gradually in rate as the automatic focus increases and decreases its automatic rate of electrical discharge.

Asystole (1860, from Modern Latin, from Greek privative a "not, without" + "systolē" "contraction") is the absence of ventricular contractions lasting longer than the maximum time sustainable for life, which is about 2 seconds for human life. Asystole is the most serious form of cardiac arrest and is usually irreversible. A cardiac flatline is the state of total cessation of electrical activity from the heart, which means no tissue contraction from the heart muscle and therefore no blood flow to the rest of the body.

Asystole should not be confused with very brief pauses in the heart's electrical activity, even those that produce a temporary flat line, in electrical activity that can occur in certain less severe abnormal rhythms. Asystole is different from very fine occurrences of ventricular fibrillation, though both have a poor prognosis, and untreated fine VF will lead to asystole. Faulty wiring, disconnection of electrodes and leads, and power disruptions should be ruled out.

Asystolic patients (as opposed to those with a "shockable rhythm" such as ventricular fibrillation or ventricular tachycardia, which can be potentially treated with defibrillation) usually present with a very poor prognosis: asystole is found initially in only about 28% of cardiac arrest cases, but only 15% of these patients ever leave the hospital alive, even with the benefit of an intensive care unit, with the rate being lower (only 6%) for those already prescribed drugs for high blood pressure.

Asystole is treated by cardiopulmonary resuscitation (CPR) combined with an intravenous vasopressor such as epinephrine (a.k.a. adrenaline). Sometimes an underlying reversible cause can be detected and treated (the so-called 'Hs and Ts', an example of which is hypokalaemia). Several interventions previously recommended—such as defibrillation (known to be ineffective on asystole, but previously performed in case the rhythm was actually very fine ventricular fibrillation) and intravenous atropine—are no longer part of the routine protocols recommended by most major international bodies. Asystole may be treated with 1 mg epinephrine by IV every 3–5 minutes as needed. Vasopressin 40 units by IV every 3–5 minutes may be used in place of the first and/or second doses of epinephrine, but doing so does not enhance outcomes.

Survival rates in a cardiac arrest patient with asystole are much lower than a patient with a rhythm amenable to defibrillation; asystole is itself not a "shockable" rhythm. Out-of-hospital survival rates (even with emergency intervention) are less than 2 percent.