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

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).

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.

This cardiac arrhythmia can be underlain by several causes, which are best divided into cardiac and noncardiac causes.

Noncardiac causes are usually secondary, and can involve recreational drug use or abuse; metabolic or endocrine issues, especially in the thyroid; an electrolyte imbalance; factors; autonomic reflexes; situational factors such as prolonged bed rest; and autoimmunity.

Cardiac causes include acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.

In general, two types of problems result in bradycardias: disorders of the sinoatrial node (SA node), and disorders of the atrioventricular node (AV node).

With sinus node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the sinus node into the surrounding atrial tissue (an "exit block"). Second-degree sinoatrial blocks can be detected only by use of a 12-lead EKG. It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.

Atrioventricular conduction disturbances (AV block; primary AV block, secondary type I AV block, secondary type II AV block, tertiary AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the bundle of His. The clinical relevance pertaining to AV blocks is greater than that of sinoatrial blocks.

Patients with bradycardia have likely acquired it, as opposed to having it congenitally. Bradycardia is more common in older patients.

Beta-blocker medicines also can slow the heart rate and decrease how forcefully the heart contracts. Beta blockers may slow the heart rate to a dangerous level if prescribed with calcium channel blocker-type medications.

Bradycardia is also part of the mammalian diving reflex.

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

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.

Also known as chronic nonparoxysmal sinus tachycardia, patients have elevated resting heart rate and/or exaggerated heart rate in response to exercise. These patients have no apparent heart disease or other causes of sinus tachycardia. IST is thought to be due to abnormal autonomic control.

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.

It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.

Sick sinus syndrome is a relatively uncommon syndrome in the young and middle age population. Sick sinus syndrome is more common in elderly adults, where the cause is often a non-specific, scar-like degeneration of the cardiac conduction system. Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

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.

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.

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.

Inappropriate Sinus Tachycardia (IST) is a rare type of cardiac arrhythmia, within the category of supraventricular tachycardia (SVT). IST may be caused by the sinus node itself having an abnormal structure or function, or it may be part of a problem called dysautonomia, a disturbance and/or failure of the autonomic nervous system. Research into the mechanism and etiology (cause) of Inappropriate Sinus Tachycardia is ongoing.

IST is viewed by most to be a benign condition in the long-term. Symptoms of IST however, may be distracting and warrant treatment. The heart is a strong muscle and typically can sustain the higher-than-normal heart rhythm, though monitoring the condition is generally recommended.

The mechanism and primary etiology of Inappropriate Sinus Tachycardia has not been fully elucidated. An autoimmune mechanism has been suggested as several studies have detected autoantibodies that activate beta adrenoreceptors in a portion of patients. The mechanism of the arrhythmia primarily involves the sinus node and peri-nodal tissue and does not require the AV node for maintenance. Treatments in the form of pharmacological therapy or catheter ablation are available, although it is currently difficult to treat successfully.

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.

Sinus bradycardia is a sinus rhythm with a rate that is lower than normal. In humans, bradycardia is generally defined to be a rate of under 60 beats per minute.

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.

Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.

Sinoatrial arrest (also known as sinus arrest or sinus pause) is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. This condition is sometimes confused with sinoatrial block, a condition in which the pacing impulse is generated, but fails to conduct through the myocardium. Differential diagnosis of the two conditions is possible by examining the exact length of the interruption of cardiac activity.

If the next available pacemaker takes over, it is in the following order:

1. Atrial escape (rate 60–80): originates within atria, not sinus node (normal P morphology is lost).

2. Junctional escape (rate 40–60): originates near the AV node; a normal P wave is not seen, may occasionally see a retrograde P wave.

3. Ventricular escape (rate 20–40): originates in ventricular conduction system; no P wave, wide, abnormal QRS.

Treatment includes stop medications that suppress the sinus node (beta blocker, Calcium channel blocker, digitalis); may need pacing.

Bigeminy is a heart rhythm problem in which there is a continuous alternation of long and short heart beats. Most often this is due to ectopic beats occurring so frequently that there is one after each sinus beat. The two beats are figuratively two twins (hence "" + ""). The ectopic beat is typically a premature ventricular contraction (PVC). For example, in ventricular bigeminy, a sinus beat is shortly followed by a PVC, a pause, another normal beat, and then another PVC. In atrial bigeminy, the other "twin" is a premature atrial contraction (PAC).

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

Many conditions can cause third-degree heart block, but the most common cause is coronary ischemia. Progressive degeneration of the electrical conduction system of the heart can lead to third-degree heart block. This may be preceded by first-degree AV block, second-degree AV block, bundle branch block, or bifascicular block. In addition, acute myocardial infarction may present with third-degree AV block.

An "inferior wall myocardial infarction" may cause damage to the AV node, causing third-degree heart block. In this case, the damage is usually transitory. Studies have shown that third-degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. The escape rhythm typically originates in the AV junction, producing a narrow complex escape rhythm.

An "anterior wall myocardial infarction" may damage the distal conduction system of the heart, causing third-degree heart block. This is typically extensive, permanent damage to the conduction system, necessitating a permanent pacemaker to be placed. The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.

Third-degree heart block may also be congenital and has been linked to the presence of lupus in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third-degree heart block in many patients is unknown. Studies suggest that the prevalence of congenital third-degree heart block is between 1 in 15,000 and 1 in 22,000 live births.

Hyperkalemia in those with previous cardiac disease and Lyme disease can also result in third-degree heart block.

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.

Symptoms reported by patients vary in frequency and severity.

Symptoms associated with IST include:

- Frequent or sustained palpitations

- Dyspnea (shortness of breath) and palpitations on exertion

- Pre-syncope (feeling as if about to faint)

- Fatigue (physical)

- Dizziness

- Exercise intolerance

- Occasional paresthesia and cramping

- Symptoms associated with autonomic nervous system disturbance, including GI disturbance