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.

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.

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.

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.

Type II (atypical) atrial flutter follows a significantly different re-entry pathway to type I flutter, and is typically faster, usually 340-440 beats/minute. Atypical atrial flutter rarely occurs in people who have not undergone previous heart surgery or previous catheter ablation procedures. Left atrial flutter is considered atypical and is common after incomplete left atrial ablation procedures. Atypical atrial flutter originating from the right atrium and heart's septum have also been described.

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.

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.

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.

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.

On an EKG, Junctional Tachycardia exhibits the following classic criteria:

- P-Waves: The p-wave may be inverted in leads II, III and V or not visible

- Narrow QRS complexes (which is consistent with non-ventricular rhythms)

It can coexist with other superventricular tachycardias due to the disassociation between the SA node and the AV node. Junctional Tachycardia can appear similar to atrioventricular nodal reentrant tachycardia.

One form is junctional ectopic tachycardia.

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)

Third-degree atrioventricular block (AV block), also known as complete heart block, is a medical condition in which the impulse generated in the sinoatrial node (SA node) in the atrium of the heart does not propagate to the ventricles.

Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an "escape rhythm". Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG).

- The P waves with a regular P-to-P interval (in other words, a sinus rhythm) represent the first rhythm.

- The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is lack of any apparent relationship between P waves and QRS complexes.

Patients with third-degree AV block typically experience severe bradycardia (an abnormally-low measured heart rate), hypotension, and at times, hemodynamic instability.

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.

In cardiology a ventricular escape beat is a self-generated electrical discharge initiated by, and causing contraction of, the ventricles of the heart; normally the heart rhythm is begun in the atria of the heart and is subsequently transmitted to the ventricles. The ventricular escape beat follows a long pause in ventricular rhythm and acts to prevent cardiac arrest. It indicates a failure of the electrical conduction system of the heart to stimulate the ventricles (which would lead to the absence of heartbeats, unless ventricular escape beats occur).

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.

Multifocal atrial tachycardia is characterized by an electrocardiogram (ECG) strip with 3 or more P-waves of variable morphology and varying P–R intervals, plus tachycardia, which is a heart rate exceeding 100 beats per minute. Narrow QRS complexes are visible as well.

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.

Most people with Wenckebach (Type I Mobitz) do not show symptoms. However, those that do usually display one or more of the following:

- Light-headedness

- Dizziness

- Syncope (fainting)

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.

Normally, the pacemaker of the heart that is responsible for triggering each heart beat (ventricular contraction) is the SA (Sino Atrial) node. However, if the ventricle does not receive triggering signals at a rate high enough from either the SA node or the AV (Atrioventricular) node, the ventricular myocardium itself becomes the pacemaker (escape rhythm). This is called Idioventricular Rhythm. Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes(> 0.12 sec). The rate is usually 20-40 bpm. If the rate is >40 bpm, it is called accelerated idioventricular rhythm. The rate of 20-40 is the "intrinsic automaticity" of the ventricular myocardium. It can be regarded as a physiological redundancy of the cardiac electrical system.

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).

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation ("i.e.", the sinoatrial node). An ectopic beat can be further classified as either a premature ventricular contraction, or a premature atrial contraction.

Some patients describe this experience as a 'flip' or a 'jolt' in the chest, or a 'heart hiccups', while others report dropped or missed beats. Ectopic beats are more common during periods of stress, exercise or debility; they may also be triggered by consumption of some food like alcohol, strong cheese, or chocolate.

It is a form of cardiac arrhythmia in which ectopic foci within either ventricular or atrial , or from finer branches of the electric transduction system, cause additional beats of the heart. Some medications may worsen the phenomenon.

Ectopic beats are considered normal and are not indicative of cardiac pathology. Ectopic beats often remain undetected and occur as part of minor errors in the heart conduction system. They are rarely indicative of cardiac pathology, although may occur more frequently or be more noticeable in those with existing cardiac abnormalities. Ectopic beats are a type of cardiac arrhythmias, which is a variety of cardiac abnormalities relating to rate or rhythm of the cardiac cycle.

Ectopic beats may become more frequent during anxiety, panic attack, and the fight-or-flight response due to the increase in sympathetic nervous activity, stimulating more frequent contractions and increasing stroke volume. The consumption of nicotine, alcohol, epinephrine and caffeine may also increase the incidences of ectopic beats, due to their influence on the action of cardiomyocytes.

Symptoms may include palpitations, feeling faint, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.

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.

An electrocardiogram can be used to identify a ventricular escape beat. The QRS portion of the electrocardiogram represents the ventricular depolarisation; in normal circumstances the QRS complex forms a sharp sudden peak. For a patient with a ventricular escape beat, the shape of the QRS complex is broader as the impulse can not travel quickly via the normal electrical conduction system.

Ventricular escape beats differ from ventricular extrasystoles (or premature ventricular contractions), which are spontaneous electrical discharges of the ventricles. These are not preceded by a pause; on the contrary they are often followed by a compensatory pause.