Atrial fibrillation increases the risk of heart failure by 11 per 1000, kidney problems by 6 per 1000, death by 4 per 1000, stroke by 3 per 1000, and coronary heart disease by 1 per 1000. Women have a worse outcome overall than men. Evidence increasingly suggests that atrial fibrillation is independently associated with a higher risk of developing dementia.

Determining the risk of an embolism causing a stroke is important for guiding the use of anticoagulants. The most accurate clinical prediction rules are:

- CHADS2

- CHA2DS2-VASc

Both the CHADS2 and the CHA2DS2-VASc score predict future stroke risk in people with a-fib with CHA2DS2-VASc being more accurate. Some that had a CHADS2 score of 0 had a CHA2DS2-VASc score of 3, with a 3.2% annual risk of stroke. Thus a CHA2DS2-VASc score of 0 is considered very low risk.

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 The gastrokinetic drug cisapride (Propulsid) was withdrawn from the US market in 2000 after it was linked to deaths caused by long QT syndrome-induced torsades de pointes.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.

Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack". During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

The following is a list of factors associated with an increased tendency towards developing torsades de pointes:

- Hypokalemia (low blood potassium)

- Hypomagnesemia (low blood magnesium)

- Hypocalcemia (low blood calcium)

- Bradycardia (slow heartbeat)

- Heart failure

- Left ventricular hypertrophy

- Hypothermia

- Subarachnoid hemorrhage

- Hypothyroidism

Although often regarded as a relatively benign heart rhythm problem, atrial flutter shares the same complications as the related condition atrial fibrillation. There is paucity of published data directly comparing the two, but overall mortality in these conditions appears to be very similar.

Some causes of tachycardia include:

- Adrenergic storm

- Alcohol

- Amphetamine

- Anaemia

- Antiarrhythmic agents

- Anxiety

- Atrial fibrillation

- Atrial flutter

- Atrial tachycardia

- AV nodal reentrant tachycardia

- Brugada syndrome

- Caffeine

- Cocaine

- Exercise

- Fear

- Fever

- Hypoglycemia

- Hypovolemia

- Hyperthyroidism

- Hyperventilation

- Infection

- Junctional tachycardia

- Methamphetamine

- Multifocal atrial tachycardia

- Nicotine

- Pacemaker mediated

- Pain

- Pheochromocytoma

- Sinus tachycardia

- Tricyclic antidepressants

- Wolff–Parkinson–White syndrome

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, or a heart attack.

Arrhythmia may be classified by rate (tachycardia, bradycardia), mechanism (automaticity, re-entry, triggered) or duration (isolated premature beats; couplets; runs, that is 3 or more beats; non-sustained= less than 30 seconds or sustained= over 30 seconds).

It is also appropriate to classify by site of origin:

Congenital heart defects are structural or electrical pathway problems in the heart that are present at birth. Anyone can be affected with this because overall health does not play a role in the problem. Problems with the electrical pathway of the heart can cause very fast or even deadly arrhythmias. Wolff–Parkinson–White syndrome is due to an extra pathway in the heart that is made up of electrical muscle tissue. This tissue allows the electrical impulse, which stimulates the heartbeat, to happen very rapidly. Right Ventricular outflow tract Tachycardia is the most common type of ventricular tachycardia in otherwise healthy individuals. This defect is due to an electrical node in the right ventricle just before the pulmonary artery. When the node is stimulated, the patient will go into ventricular tachycardia, which does not allow the heart to fill with blood before beating again. Long QT Syndrome is another complex problem in the heart and has been labeled as an independent factor in mortality. There are multiple methods of treatment for these including cardiac ablations, medication treatment, or altering your lifestyle to have less stress and exercise. It is possible to live a full and happy life with these conditions.

Sudden death is not directly associated with atrial flutter. However, in individuals with a pre-existing accessory conduction pathway, such as the bundle of Kent in Wolff-Parkinson-White syndrome, the accessory pathway "may" conduct activity from the atria to the ventricles at a rate that the AV node would usually block. Bypassing the AV node, the atrial rate of 300 beats/minute leads to a ventricular rate of 300 beats/minute (1:1 conduction). Even if the ventricles are able to sustain a cardiac output at such a high rates, 1:1 flutter with time may degenerate into ventricular fibrillation, causing hemodynamic collapse and death.

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

In otherwise healthy patients, occasional premature atrial contractions are a common and normal finding and do not indicate any particular health risk. Rarely, in patients with other underlying structural heart problems, PACs can trigger a more serious arrhythmia such as atrial flutter or atrial fibrillation. In otherwise healthy people, PACs usually disappear with adolescence.

The true incidence of TIC is unclear. Some studies have noted the incidence of TIC in adults with irregular heart rhythms to range from 8% to 34%. Other studies of patients with atrial fibrillation and left ventricular dysfunction estimate that 25-50% of these study participants have some degree of TIC. TIC has been reported in all age groups.

Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".

Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other heart pathologies. In addition, it is seen with electrolyte imbalance, overdoses of cardiotoxic drugs, and following near drowning or major trauma. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40. It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death.

The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.

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

Rearrest may reduce the likelihood of survival when compared to patients who have had just one episode of cardiac arrest. Overall resuscitation rates have been estimated to be about 34%, however survival to hospital discharge rates are as low as 7%. This phenomenon may be contributed to rearrest.

Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include:

- Pain

- Fever

- Anxiety

- Dehydration

- Malignant hyperthermia

- Hypovolemia with hypotension and shock

- Anemia

- Heart failure

- Hyperthyroidism

- Mercury poisoning

- Kawasaki disease

- Pheochromocytoma

- Sepsis

- Pulmonary embolism

- Acute coronary ischemia and myocardial infarction

- Chronic obstructive pulmonary disease

- Hypoxia

- Intake of stimulants such as caffeine, theophylline, nicotine, cocaine, or amphetamines

- Hyperdynamic circulation

- Electric shock

- Drug withdrawal

- Porphyria

- Acute inflammatory demyelinating polyradiculoneuropathy

- Postural orthostatic tachycardia syndrome

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.

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.

They start from either the atria or atrioventricular node. They are generally due to one of two mechanisms: re-entry or increased automaticity. The other type of fast heart rhythm is ventricular arrhythmias—rapid rhythms that start within the ventricle. Diagnosis is typically by electrocardiogram (ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes such as hyperthyroidism or electrolyte abnormalities.

Specific treatments depend on the type of SVT. They can include medications, medical procedures, or surgery. Vagal maneuvers or a procedure known as catheter ablation may be effective in certain types. For atrial fibrillation calcium channel blockers or beta blockers may be used. Long term some people benefit from blood thinners such as aspirin or warfarin. Atrial fibrillation affects about 25 per 1000 people, paroxysmal supraventricular tachycardia 2.3 per 1000, Wolff-Parkinson-White syndrome 2 per 1000, and atrial flutter 0.8 per 1000.

Hypertension, or abnormally high blood pressure, often signifies an elevated level of both psychological and physiological stress. Often, hypertension goes hand in hand with various atrial fibrillations including premature atrial contractions (PACs). Additional factors that may contribute to spontaneous premature atrial contractions could be:

- Increased age

- Abnormal body height

- History of cardiovascular disease (CV)

- Abnormal ANP levels

- Elevated cholesterol

In the human heart the sinoatrial node is located at the top of the right atrium. The sinoatrial node is the first area of the heart to depolarize and to generate the action potential that leads to depolarization of the rest of the myocardium. Sinoatrial depolarization and subsequent propagation of the electrical impulse suppress the action of the lower natural pacemakers of the heart, which have slower intrinsic rates.

The accelerated idioventricular rhythm occurs when depolarization rate of a normally suppressed focus increases to above that of the "higher order" focuses (the sinoatrial node and the atrioventricular node). This most commonly occurs in the setting of a sinus bradycardia.

Accelerated idioventricular rhythm is the most common reperfusion arrhythmia in humans. However, ventricular tachycardia and ventricular fibrillation remain the most important causes of sudden death following spontaneous restoration of antegrade flow. Prior to the modern practice of percutaneous coronary intervention for acute coronary syndrome, pharmacologic thrombolysis was more common and accelerated idioventricular rhythms were used as a sign of successful reperfusion. It is considered a benign arrhythmia that does not require intervention, though atrioventricular dyssynchrony can cause hemodynamic instability, which can be treated through overdrive pacing or atropine.

Ventricular tachycardia (VT or V-tach) is a potentially life-threatening cardiac arrhythmia that originates in the ventricles. It is usually a regular, wide complex tachycardia with a rate between 120 and 250 beats per minute.

Both of these rhythms normally last for only a few seconds to minutes" (paroxysmal tachycardia)", but if VT persists it is extremely dangerous, often leading to ventricular fibrillation.

Atrial bradycardias are divided into three types. The first, respiratory sinus arrhythmia, is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation. This is thought to be caused by changes in the vagal tone during respiration. If the decrease during exhalation drops the heart rate below 60 bpm on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone.

The second, sinus bradycardia, is a sinus rhythm of less than 60 BPM. It is a common condition found in both healthy individuals and those considered well-conditioned athletes. Studies have found that 50–85% of conditioned athletes have benign sinus bradycardia, as compared to 23% of the general population studied. The heart muscle of athletes has become conditioned to have a higher stroke volume, so requires fewer contractions to circulate the same volume of blood.

The third, sick sinus syndrome, covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardia-tachycardia syndrome (atrial fibrillation, flutter, and paroxysmal supraventricular tachycardia).

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.