The most common symptom is dizziness or syncope which often occurs during exercise or as a response to emotional stress.

Stokes-Adams attacks may be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic. The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.

Typically an attack occurs without warning leading to sudden loss of consciousness. Prior to an attack, a patient may be pale with hypoperfusion. Normal periods of unconsciousness last approximately thirty seconds; if abnormal movements are present, they will consist of twitching after 15–20 seconds (The movements, which are not seizures occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities). Breathing continues normally throughout the attack, and upon recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation, which has become dilated due to hypoxia.

As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient's position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.

It can be divided by the origin:

- supraventricular tachycardia

- ventricular tachycardia

CPVT typically start manifesting during the first or second decade of life. The majority of events occur during childhood with more than 60% of affected individuals having their first episode of syncope or cardiac arrest by age 12-20.

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

No specific set of criteria has been developed for diagnosis of pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly documented in patients history, classified according to cause:

- Neurological - Dizziness, near syncope, and confusion.

- Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

- Hypotension - Seizure, mental status change, diaphoresis, and signs of orthostatic hypotension and shock.

- Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.

- Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds, and headache.

- Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should look for the following in the physical examination, as these are frequent findings at the time of admission:

- Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

- Pulse amplitude may vary, and blood pressure may fluctuate.

- Look for neck vein distension and cannon waves in the neck veins.

- Lungs may exhibit crackles.

- Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

- Liver may be pulsatile, and the RUQ may be tender to palpation. Ascites may be present in severe cases.

- The lower extremities may be edematous.

- Neurologic examination may reveal confusion, dizziness, or altered mental status.

Paroxysmal tachycardia is a form of tachycardia which begins and ends in an acute (or paroxysmal) manner.

It is also known as "Bouveret-Hoffmann syndrome".

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).

Symptoms can be as follows. They are periodic, and occur only during an "episode", usually after eating.

- Sinus bradycardia

- Difficulty inhaling

- Angina pectoris

- Left ventricular discomfort

- Fatigue

- Anxiety

- Uncomfortable breathing

- Poor perfusion

- Muscle pain (crampiness)

- Burst or sustained vertigo or dizziness

- Sleep disturbance (particularly when sleeping within a few hours of eating, or lying on the left side)

- Extrasystoles

- Hot flashes

LGL syndrome is diagnosed on the basis of the surface EKG in a symptomatic individual with a PR interval less than or equal to 0.12 second (120 ms) with normal QRS complex configuration and duration. It can be distinguished from WPW syndrome because the delta waves seen in WPW syndrome are not seen in LGL syndrome. It is a clinical diagnosis that came about before the advent of electrophysiology studies. Be aware, however, that not all WPW EKG's have a delta wave; the absence of a delta wave does not conclusively rule out WPW.

An episode of SVT may present with palpitations, dizziness, shortness of breath, or losing consciousness (fainting). The electrocardiogram (ECG) would appear as a narrow-complex SVT. Between episodes of tachycardia the affected person is likely to be asymptomatic, however, the ECG would demonstrate the classic delta wave in Wolff–Parkinson–White syndrome.

Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.

Roemheld syndrome (RS), also known as Roemheld-Techlenburg-Ceconi-Syndrome or gastric-cardia, is a complex of gastrocardiac symptoms first described by Ludwig von Roemheld (1871–1938). It is a syndrome where maladies in the gastrointestinal tract or abdomen are found to be associated with cardiac symptoms like arrhythmias and benign palpitations. There is rarely a traceable cardiac source to the symptoms which may lead to a lengthy period of misdiagnosis.

Torsades de pointes or torsade depointes (TdP or simply torsade(s)) (, translated as "twisting of the points"), is a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG). It was described by Dessertenne in 1966. Prolongation of the QT interval can increase a person's risk of developing this abnormal heart rhythm.

Wolff–Parkinson–White syndrome (WPW) is a disorder due to a specific type of problem with the electrical system of the heart which has resulted in symptoms. About 40% of people with the electrical problem never develop symptoms. Symptoms can include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely cardiac arrest may occur. The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.

The cause of WPW is typically unknown. A small number of cases are due to a mutation of the PRKAG2 gene which may be inherited from a person's parents in an autosomal dominant fashion. The underlying mechanism involves an accessory electrical conduction pathway between the atria and the ventricles. It is associated with other conditions such as Ebstein anomaly and hypokalemic periodic paralysis. Diagnosis is typically when an electrocardiogram (ECG) show a short PR interval and a delta wave. It is a type of pre-excitation syndromes.

WPW syndrome is treated with either medications or radiofrequency catheter ablation. It affects between 0.1 and 0.3% in the population. The risk of death in those without symptoms is about 0.5% per year in children and 0.1% per year in adults. In those without symptoms ongoing observation may be reasonable. In those with WPW complicated by atrial fibrillation, cardioversion or the medication procainamide may be used. The condition is named after Louis Wolff, John Parkinson, and Paul Dudley White who described the ECG findings in 1930.

Lown–Ganong–Levine syndrome (LGL) is a pre-excitation syndrome of the heart due to abnormal electrical communication between the atria and the ventricles. Once thought to involve an accessory conduction pathway, it is grouped with Wolff–Parkinson–White syndrome as an atrioventricular re-entrant tachycardia (AVRT). Individuals with LGL syndrome have a short PR interval with normal QRS complexes and paroxysms of clinically-significant tachycardia. The syndrome is named after Bernard Lown, William Francis Ganong, Jr., and Samuel A. Levine.

Individuals with a short PR interval found incidentally on EKG were once thought to have LGL syndrome. However, subsequent studies have shown that a short PR interval in the absence of symptomatic tachycardia is simply a benign EKG variant.

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after pacemaker implantation.

It is an iatrogenic disease—an adverse effect resulting from medical treatment—that is often underdiagnosed. In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of total peripheral resistance response, and nonphysiologic pressure waves.

Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart (atrium) contracts as the second chamber (ventricle) is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. Patients who develop pacemaker syndrome may require adjustment of the pacemaker, or fitting of another lead to better coordinate the timing of atrial and ventricular contraction.

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

Atrioventricular reentrant tachycardia, atrioventricular reciprocating tachycardia or AVRT, is a type of abnormal fast heart rhythm and is classified as a type of supraventricular tachycardia (SVT). AVRT is most commonly associated with Wolff-Parkinson-White syndrome, in which an accessory pathway allows electrical signals from the heart's ventricles to enter the atria and cause earlier than normal contraction, which leads to repeated stimulation of the atrioventricular node.

Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart. Afterdepolarizations may lead to cardiac arrhythmias.

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.

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.

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node (AV node). In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia.

Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time. Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.