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

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.

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.

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).

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

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.

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.

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.

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.

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

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.

It can be divided by the origin:

- supraventricular tachycardia

- ventricular 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.

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.

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.

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.

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.

The ECG tracing in torsades demonstrates a "polymorphic ventricular tachycardia" with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline (peaks, which are at first pointing up, appear to be pointing down for subsequent "beats" when looking at ECG traces of the "heartbeat"). It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and fainting. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate into ventricular fibrillation, leading to sudden death in the absence of prompt medical intervention. Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to an , wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization (represented by the latter half of the T-wave). An R-on-T can initiate torsades. Sometimes, pathologic T-U waves may be seen in the ECG before the initiation of torsades.

A "short-coupled variant of torsade de pointes", which presents without long QT syndrome, was also described in 1994 as having the following characteristics:

- Drastic rotation of the heart's electrical axis

- Prolonged QT interval (LQTS) - may not be present in the short-coupled variant of torsade de pointes

- Preceded by long and short RR-intervals - not present in the short-coupled variant of torsade de pointes

- Triggered by a premature ventricular contraction (R-on-T PVC)

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.

The main symptom of AVNRT is the sudden development of rapid regular palpitations. Often, no provoking factor is identified, although some people affected by AVNRT report developing symptoms in stressful situations, and following consumption of alcohol or caffeine.

In some cases, the onset of the fast heart is associated with a brief drop in blood pressure. When this happens, the patient may experience dizziness or rarely lose consciousness (faint). If the heart rate is very fast, and the patient has underlying coronary artery disease (obstruction of the arteries of the heart by atherosclerosis), chest pain similar to angina may be experienced; this pain is band- or pressure-like around the chest and often radiates to the left arm and angle of the left jaw. AVNRT is rarely life-threatening.

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.

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%.

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.

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".