AF is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations or exercise intolerance and occasionally may produce anginal chest pain (if the high heart rate causes ischemia). Other possible symptoms include congestive symptoms such as shortness of breath or swelling. The arrhythmia is sometimes only identified with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon for a patient to first become aware of AF from a routine physical examination or ECG, as it often does not cause symptoms.

Since most cases of AF are secondary to other medical problems, the presence of chest pain or angina, signs and symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease can indicate an underlying cause. A history of stroke or TIA, as well as high blood pressure, diabetes, heart failure, or rheumatic fever may indicate whether someone with AF is at a higher risk of complications. The risk of a blood clot forming in the left atrium, breaking off, and then traveling in the bloodstream can be assessed using the CHADS2 score or CHA2DS2-VASc score.

Presentation is similar to other forms of rapid heart rate and may be asymptomatic. Palpitations and chest discomfort are common complaints. The rapid uncoordinated heart rate may result in reduced cardiac output, with the heart being unable to provide adequate blood flow and therefore oxygen delivery to the rest of the body. Common symptoms of uncontrolled atrial fibrillation may include shortness of breath, shortness of breath when lying flat, dizziness, and sudden onset of shortness of breath during the night. This may progress to swelling of the lower extremities, a manifestation of congestive heart failure. Due to inadequate cardiac output, individuals with AF may also complain of light-headedness, may feel like they are about to faint, or may actually lose consciousness.

AF can cause respiratory distress due to congestion in the lungs. By definition, the heart rate will be greater than 100 beats per minute. Blood pressure may be variable, and often difficult to measure as the beat-by-beat variability causes problems for most digital (oscillometric) non-invasive blood pressure monitors. For this reason, when determining heart rate in AF, direct cardiac auscultation is recommended. Low blood pressure is most concerning and a sign that immediate treatment is required. Many of the symptoms associated with uncontrolled atrial fibrillation are a manifestation of congestive heart failure due to the reduced cardiac output. Respiratory rate will be increased in the presence of respiratory distress. Pulse oximetry may confirm the presence of hypoxia related to any precipitating factors such as pneumonia. Examination of the jugular veins may reveal elevated pressure (jugular venous distention). Lung exam may reveal crackles, which are suggestive of pulmonary edema. Heart exam will reveal a rapid irregular rhythm.

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body - because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to the layperson can look like normal spontaneous breathing, but it is in fact a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain. Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

A slow rhythm (less than 60 beats/min), is labelled bradycardia. This may be caused by a slowed signal from the sinus node (sinus bradycardia), a pause in the normal activity of the sinus node (sinus arrest), or by blocking of the electrical impulse on its way from the atria to the ventricles (AV block or heart block). Heart block comes in varying degrees and severity. It may be caused by reversible poisoning of the AV node (with drugs that impair conduction) or by irreversible damage to the node. Bradycardias may also be present in the normally functioning heart of endurance athletes or other well-conditioned persons. Bradycardia may also occur in some types of seizures.

While atrial flutter can sometimes go unnoticed, its onset is often marked by characteristic sensations of the heart feeling like it is beating too fast or hard. Such sensations usually last until the episode resolves, or until the heart rate is controlled.

Atrial flutter is usually well tolerated initially (a high heart rate is for most people just a normal response to exercise), however, people with other underlying heart disease (such as coronary artery disease) or poor exercise tolerance may rapidly develop symptoms, such as shortness of breath, chest pain, lightheadedness or dizziness, nausea and, in some patients, nervousness and feelings of impending doom.

Prolonged atrial flutter with fast heart rates may lead to decompensation with loss of normal heart function (heart failure). This may manifest as exercise intolerance (exertional breathlessness), difficulty breathing at night, or swelling of the legs and/or abdomen.

Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or Sino-atrial node or SA node. The impulse initially causes both atria to contract, then activates the atrioventricular (or AV) node, which is normally the only electrical connection between the atria and the ventricles (main pumping chambers). The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of the heart muscle and, thus, the pulse.

In adults the normal resting heart rate ranges from 60 to 90 beats per minute. The resting heart rate in children is much faster. In athletes, however, the resting heart rate can be as slow as 40 beats per minute, and be considered as normal.

The term sinus arrhythmia refers to a normal phenomenon of alternating mild acceleration and slowing of the heart rate that occurs with breathing in and out. It is usually quite pronounced in children and steadily decreases with age. This can also be present during meditation breathing exercises that involve deep inhaling and breath holding patterns.

Although there are many signs and symptoms associated with PVCs, PVCs may have no symptoms at all. An isolated PVC is hard to catch without the use of a Holter monitor. PVCs may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a potentially fatal abnormal heart rhythm. Overall it has been seen that the symptom felt most by patients experiencing a PVC is the mere perception of a skipped heartbeat. The more frequently these contractions occur, the more likely there are to be symptoms, despite the fact that these beats have little effect of the pumping action of the heart and therefore cause minimal if any symptoms.

Some other possible signs and symptoms of PVCs:

- Abnormal ECG

- Irregular heart beat

- Dyspnea

- Dizziness

- Feeling your heart beat (palpitations)

- Feeling of occasional, forceful beats

- Increased awareness of your heart beat

- Perception of a skipped heartbeat

Signs and symptoms can arise suddenly and may resolve without treatment. Stress, exercise, and emotion can all result in a normal or physiological increase in heart rate, but can also, more rarely, precipitate SVT. Episodes can last from a few minutes to one or two days, sometimes persisting until treated. The rapid heart rate reduces the opportunity for the "pump" to fill between beats decreasing cardiac output and as a consequence blood pressure. The following symptoms are typical with a rate of 150–270 or more beats per minute:

- Pounding heart

- Shortness of breath

- Chest pain

- Rapid breathing

- Dizziness

- Loss of consciousness (in only the most serious cases)

For infants and toddlers, symptoms of heart arrhythmias such as SVT are more difficult to assess because of limited ability to communicate. Caregivers should watch for lack of interest in feeding, shallow breathing, and lethargy. These symptoms may be subtle and may be accompanied by vomiting and/or a decrease in responsiveness.

Rapid heart rates may produce significant symptoms in patients with pre-existing heart disease and can lead to inadequate blood flow to the heart muscle and even a heart attack. In rare situations, atrial flutter associated with a fast heart rate persists for an extended period of time without being corrected to a normal heart rhythm and leads to a tachycardia-induced cardiomyopathy. Even in individuals with a normal heart, if the heart beats too quickly for a prolonged period of time, this can lead to ventricular decompensation and heart failure.

While a few seconds may not result in problems longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation.

Ventricular fibrillation (V-fib or VF) is when the heart quivers instead of pumping due to disorganized electrical activity in the ventricles. It is a type of cardiac arrhythmia. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by death in the absence of treatment. Ventricular fibrillation is found initially in about 10% of people in cardiac arrest.

Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, electric shock, or intracranial hemorrhage. Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves. An important differential diagnosis is torsades de pointes.

Treatment is with cardiopulmonary resuscitation (CPR) and defibrillation. Biphasic defibrillation may be better than monophasic. The medication epinephrine or amiodarone may be given if initial treatments are not effective. Rates of survival among those who are out of hospital when the arrhythmia is detected is about 17% while in hospital it is about 46%.

People with WPW are usually asymptomatic when not having a fast heart rate. However, individuals may experience palpitations, dizziness, shortness of breath, or infrequently syncope (fainting or near fainting) during episodes of supraventricular tachycardia. The telltale "delta wave" may sometimes be seen on an electrocardiogram (ECG/EKG).

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

Ventricular tachycardia (V-tach or VT) is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart. Although a few seconds may not result in problems, longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation. Ventricular tachycardia is found initially in about 7% of people in cardiac arrest.

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems, or a heart attack. Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 bpm and at least three wide QRS complexes in a row. It is classified as non-sustained versus sustained based on whether or not it lasts less than or more than 30 seconds. The term "ventricular tachycardias" refers to the group of irregular heartbeats that includes ventricular tachycardia, ventricular fibrillation, and torsades de pointes.

In those who have a normal blood pressure and strong pulse, the antiarrhythmic medication procainamide may be used. Otherwise immediate cardioversion is recommended. In those in cardiac arrest due to ventricular tachycardia cardiopulmonary resuscitation (CPR) and defibrillation is recommended. Biphasic defibrillation may be better than monophasic. While waiting for a defibrillator, a precordial thump may be attempted in those on a heart monitor who are seen going into an unstable ventricular tachycardia. In those with cardiac arrest due to ventricular tachycardia survival is about 45%. An implantable cardiac defibrillator or medications such as calcium channel blockers or amiodarone may be used to prevent recurrence.

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.

The following types of supraventricular tachycardias are more precisely classified by their specific site of origin. While each belongs to the broad classification of SVT, the specific term/diagnosis is preferred when possible:

Sinoatrial origin:

- Sinoatrial nodal reentrant tachycardia (SNRT)

Atrial origin:

- Ectopic (unifocal) atrial tachycardia (EAT)

- Multifocal atrial tachycardia (MAT)

- Atrial fibrillation with rapid ventricular response

- Atrial flutter with rapid ventricular response

Atrioventricular origin (junctional tachycardia):

- AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating tachycardia (JRT)

- Permanent (or persistent) junctional reciprocating tachycardia (PJRT), a form of JRT that occurs predominantly in infants and children but can occasionally occur in adults

- AV reciprocating tachycardia (AVRT) – visible or concealed (including Wolff-Parkinson-White syndrome)

- Junctional ectopic tachycardia (JET)

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:

- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation

- Dizziness or light-headedness

- Palpitations

- Chest pain or angina

- Shortness of breath

- Fatigue

- Headache

- Nausea

A premature ventricular contraction (PVC)—also known as a premature ventricular complex, ventricular premature contraction (or complex or complexes) (VPC), ventricular premature beat (VPB), or ventricular extrasystole (VES)—is a relatively common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator. The electrical events of the heart detected by the electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. Although a PVC can be a sign of decreased oxygenation to the heart muscle, often PVCs are benign and may even be found in otherwise healthy hearts.

A PVC may be perceived as a "skipped beat" or felt as palpitations in the chest. In a normal heartbeat, the ventricles contract after the atria have helped to fill them by contracting; in this way the ventricles can pump a maximized amount of blood both to the lungs and to the rest of the body. In a PVC, the ventricles contract first and before the atria have optimally filled the ventricles with blood, which means that circulation is inefficient. However, single beat PVC abnormal heart rhythms do not usually pose a danger and can be asymptomatic in healthy individuals.

A PVC is a type of ectopic beat.

Premature atrial contractions (PACs), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a common cardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, PACs occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat. The exact cause of PACs is unclear; while several predisposing conditions exist, PACs commonly occur in healthy young and elderly people. Elderly people that get PACs usually don't need any further attention besides follow ups due to unclear evidence. PACs are often completely asymptomatic and may be noted only with Holter monitoring, but occasionally they can be perceived as a skipped beat or a jolt in the chest. In most cases, no treatment other than reassurance is needed for PACs, although medications such as beta blockers can reduce the frequency of symptomatic PACs.

An electrocardiogram (ECG) is used to classify the type of tachycardia. They may be classified into narrow and wide complex based on the QRS complex. Presented order of most to least common, they are:

- Narrow complex

- Sinus tachycardia, which originates from the sino-atrial (SA) node, near the base of the superior vena cava

- Atrial fibrillation

- Atrial flutter

- AV nodal reentrant tachycardia

- Accessory pathway mediated tachycardia

- Atrial tachycardia

- Multifocal atrial tachycardia

- Junctional tachycardia

- Wide complex

- Ventricular tachycardia, any tachycardia that originates in the ventricles

- Any narrow complex tachycardia combined with a problem with the conduction system of the heart, often termed "supraventricular tachycardia with aberrancy"

- A narrow complex tachycardia with an accessory conduction pathway, often termed "supraventricular tachycardia with pre-excitation" (e.g. Wolff–Parkinson–White syndrome)

- Pacemaker-tracked or pacemaker-mediated tachycardia

Tachycardias may be classified as either narrow complex tachycardias (supraventricular tachycardias) or wide complex tachycardias. Narrow and wide refer to the width of the QRS complex on the ECG. Narrow complex tachycardias tend to originate in the atria, while wide complex tachycardias tend to originate in the ventricles. Tachycardias can be further classified as either regular or irregular.

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.

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.

Atrial tachycardia is a type of heart rhythm problem in which the heart's electrical impulse comes from an ectopic pacemaker (that is, an abnormally located cardiac pacemaker) in the upper chambers (atria) of the heart, rather than from the sinoatrial node, the normal origin of the heart's electrical activity. Atrial tachycardias can exhibit very regular (consistent) heart rates ranging typically from 140 to 220 beats per minute.

As with any other form of tachycardia (rapid heart beat), the underlying mechanism can be either the rapid discharge of an abnormal focus, the presence of a ring of cardiac tissue that gives rise to a circle movement (reentry), or a triggered rapid rhythm due to other pathological circumstances (as would be the case with some drug toxicities, such as digoxin toxicity). Atrial tachycardia is a risk factor for atrial fibrillation, as the rapid rhythm can trigger or degrade into the lack of a rhythm. All atrial tachycardias are by definition supraventricular tachycardias.

Forms of atrial tachycardia (ATach) include multifocal atrial tachycardia (MAT), ectopic atrial tachycardia (EAT), unifocal atrial tachycardia (UAT), and paroxysmal atrial tachycardia (PAT). The taxonomy varies somewhat between users (regarding names that mean the same versus those that label subsets). The codification of the terms "first detected", "paroxysmal", "persistent", and "permanent" in the classification of atrial fibrillation should be compared for reference.

Premature atrial contractions are typically diagnosed with an electrocardiogram, Holter monitor, or cardiac event monitor.