Palpitation can be attributed to one of four main causes:

1. Extra-cardiac stimulation of the sympathetic nervous system (inappropriate stimulation of the sympathetic nervous system, particularly the vagus nerve (which innervates the heart), can be caused by anxiety and stress due to acute or chronic elevations in glucocorticoids and catecholamines. Gastrointestinal distress such as bloating or indigestion, along with muscular imbalances and poor posture, can also irritate the vagus nerve causing palpitations)

2. Sympathetic overdrive (panic disorders, low blood sugar, hypoxia, antihistamines (i.e. levocetirizine), low red blood cell count, heart failure, mitral valve prolapse).

3. Hyperdynamic circulation (valvular incompetence, thyrotoxicosis, hypercapnia, high body temperature, low red blood cell count, pregnancy).

4. Abnormal heart rhythms (ectopic beat, premature atrial contraction, junctional escape beat, premature ventricular contraction, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, ventricular fibrillation, heart block).

Anxiety and stress elevate the body's level of cortisol and adrenaline, which in turn can interfere with the normal functioning of the parasympathetic nervous system resulting in overstimulation of the vagus nerve. Vagus nerve induced palpitation is felt as a thud, a hollow fluttery sensation, or a skipped beat, depending on at what point during the heart's normal rhythm the vagus nerve fires. In many cases, the anxiety and panic of experiencing palpitations causes a sufferer to experience further anxiety and increased vagus nerve stimulation. The link between anxiety and palpitation may also explain why many panic attacks involve an impending sense of cardiac arrest. Similarly, physical and mental stress may contribute to the occurrence of palpitation, possibly due to the depletion of certain micronutrients involved in maintaining healthy psychological and physiological function. Gastrointestinal bloating, indigestion and hiccups have also been associated with overstimulation of the vagus nerve causing palpitations, due to branches of the vagus nerve innervating the GI tract, diaphragm, and lungs.

The following stimulants, conditions and triggers may increase your risk of the more frequent occurrence of premature ventricular contractions:

- Caffeine, tobacco and alcohol

- Exercise

- High blood pressure (hypertension)

- Anxiety

- Underlying heart disease, including congenital heart disease, coronary artery disease, heart attack, heart failure and a weakened heart muscle (cardiomyopathy)

- African American ethnicity- increased the risk of PVCs by 30% in comparison with the risk in white individuals

- Male sex

- Lower serum magnesium or potassium levels

- Faster sinus rates

- A bundle-branch block on 12-lead ECG

- Hypomagnesemia

- Hypokalemia

Paroxysmal supraventricular tachycardia (PSVT) is a type of supraventricular tachycardia. Often people have no symptoms. Otherwise symptoms may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.

The cause is not known. Risk factors include alcohol, caffeine, nicotine, psychological stress, and Wolff-Parkinson-White syndrome which often is inherited from a person's parents. The underlying mechanism typically involves an accessory pathway that results in re-entry. Diagnosis is typically by an electrocardiogram (ECG) which shows narrow QRS complexes and a fast heart rhythm typically between 150 and 240 beats per minute.

Vagal maneuvers, such as the valsalva maneuver, are often used as the initial treatment. If not effective and the person has a normal blood pressure the medication adenosine may be tried. If adenosine is not effective a calcium channel blockers or beta blocker may be used. Otherwise synchronized cardioversion is the treatment. Future episodes can be prevented by catheter ablation.

About 2.3 per 1000 people have paroxysmal supraventricular tachycardia. Problems typically begin in those 12 to 45 years old. Women are more often affected than men. Outcomes in those who otherwise have a normal heart are generally good. An ultrasound of the heart may be done to rule out underlying heart problems.

As an overall medical condition PVCs are normally not very harmful to patients that experience them, but frequent PVCs may put patients at increased risk of developing arrhythmias or cardiomyopathy, which can greatly impact the functioning of the heart over the span of that patient's life. On a more serious and severe scale, frequent PVCs can accompany underlying heart disease and lead to chaotic, dangerous heart rhythms and possibly sudden cardiac death.

Asymptomatic patients that do not have heart disease have long-term prognoses very similar to the general population, but asymptomatic patients that have ejection fractions greater than 40% have a 3.5% incidence of sustained ventricular tachycardia or cardiac arrest. One drawback comes from emerging data that suggests very frequent ventricular ectopy may be associated with cardiomyopathy through a mechanism thought to be similar to that of chronic right ventricular pacing associated cardiomyopathy. Patients that have underlying chronic structural heart disease and complex ectopy, mortality is significantly increased.

In meta-analysis of 11 studies, people with frequent PVC (≥1 time during a standard electrocardiographic recording or ≥30 times over a 1-hour recording) had risk of cardiac death 2 times higher than persons without frequent PVC. Although most studies made attempts to exclude high-risk subjects, such as those with histories of cardiovascular disease, they did not test participants for underlying structural heart disease.

In a study of 239 people with frequent PVCs (>1000 beats/day) and without structural heart disease (i.e. in the presence of normal heart function) there were no serious cardiac events through 5.6 years on average, but there was correlation between PVC prevalence and decrease of ejection fraction and increase of left ventricular diastolic dimension. In this study absence of heart of disease was excluded by echocardiography, cardiac magnetic resonance imaging in 63 persons and Holter monitoring.

Another study has suggested that in the absence of structural heart disease even frequent (> 60/h or 1/min) and complex PVCs are associated with a benign prognosis. It was study of 70 people followed by 6.5 years on average. Healthy status was confirmed by extensive noninvasive cardiologic examination, although cardiac catheterization of a subgroup disclosed serious coronary artery disease in 19%. Overall survival was better than expected.

On the other hand, the Framingham Heart Study reported that PVCs in apparently healthy people were associated with a twofold increase in the risk of all-cause mortality, myocardial infarction and cardiac death. In men with coronary heart disease and in women with or without coronary heart disease, complex or frequent arrhythmias were not associated with an increased risk. The at-risk people might have subclinical coronary disease. These Framingham results have been criticised for the lack of rigorous measures to exclude the potential confounder of underlying heart disease.

In the ARIC study of 14,783 people followed for 15 to 17 years those with detected PVC during 2 minute ECG, and without hypertension or diabetes on the beginning, had risk of stroke increased by 109%. Hypertension or diabetes, both risk factors for stroke, did not change significantly risk of stroke for people with PVC. It is possible that PVCs identified those at risk of stroke with blood pressure and impaired glucose tolerance on a continuum of risk below conventional diagnostic thresholds for hypertension and diabetes. Those in ARIC study with any PVC had risk of heart failure increased by 63% and were >2 times as likely to die due to coronary heart disease (CHD). Risk was also higher for people with or without baseline CHD.

In the Niigata study of 63,386 people with 10-year follow-up period those with PVC during a 10-second recording had risk of atrial fibrillation increased nearly 3 times independently from risk factors: age, male sex, body mass index, hypertension, systolic and diastolic blood pressure, and diabetes.

Reducing frequent PVC (>20%) by antiarrhythmic drugs or by catheter ablation significantly improves heart performance.

Recent studies have shown that those subjects who have an extremely high occurrence of PVCs (several thousand a day) can develop dilated cardiomyopathy. In these cases, if the PVCs are reduced or removed (for example, via ablation therapy) the cardiomyopathy usually regresses.

Also, PVCs can permanently cease without any treatment, in a material percentage of cases.

Atrial fibrillation increases the risk of heart failure by 11 per 1000, kidney problems by 6 per 1000, death by 4 per 1000, stroke by 3 per 1000, and coronary heart disease by 1 per 1000. Women have a worse outcome overall than men. Evidence increasingly suggests that atrial fibrillation is independently associated with a higher risk of developing dementia.

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

Orthostatic hypotension may cause accidental falls. It is also linked to an increased risk of cardiovascular disease, heart failure, and stroke. There is also observational data suggesting that orthostatic hypotension in middle age increases the risk of eventual dementia and reduced cognitive function.

If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.

Orthostatic hypotension may be caused by low blood volume, resulting from bleeding, the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest(immobility); as well as occurring in people with anemia.

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.

The cause of cardiomegaly is not well understood and many cases of cardiomegaly are idiopathic (having no known cause). Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let one's doctor know so that treatments can be implemented to help prevent worsening of the condition. In addition, prevention includes avoiding certain lifestyle risk factors such as tobacco use and controlling one's high cholesterol, high blood pressure, and diabetes. Non-lifestyle risk factors include family history of cardiomegaly, coronary artery disease (CAD), congenital heart failure, Atherosclerotic disease, valvular heart disease, exposure to cardiac toxins, sleep disordered breathing (such as sleep apnea), sustained cardiac arrhythmias, abnormal electrocardiograms, and cardiomegaly on chest X-ray. Lifestyle factors which can help prevent cardiomegaly include eating a healthy diet, controlling blood pressure, exercise, medications, and not abusing alcohol and cocaine. Current research and the evidence of previous cases link the following (below) as possible causes of cardiomegaly.

The most common causes of Cardiomegaly are congenital (patients are born with the condition based on a genetic inheritance), high blood pressure which can enlarge the left ventricle causing the heart muscle to weaken over time, and coronary artery disease that creates blockages in the heart's blood supply, which can bring on a cardiac infarction (heart attack) leading to tissue death which causes other areas of the heart to work harder, increasing the heart size.

Other possible causes include:

- Heart Valve Disease

- Cardiomyopathy (disease to the heart muscle)

- Pulmonary Hypertension

- Pericardial Effusion (fluid around the heart)

- Thyroid Disorders

- Hemochromatosis (excessive iron in the blood)

- Other rare diseases like Amyloidosis

- Viral infection of the heart

- Pregnancy, with enlarged heart developing around the time of delivery (peripartum cardiomyopathy)

- Kidney disease requiring dialysis

- Alcohol or cocaine abuse

- HIV infection

- Diabetes

A family history of AF may increase the risk of AF. A study of more than 2,200 people found an increased risk factor for AF of 1.85 for those that had at least one parent with AF. Various genetic mutations may be responsible.

Four types of genetic disorder are associated with atrial fibrillation:

- Familial AF as a monogenic disease

- Familial AF presenting in the setting of another inherited cardiac disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, familial amyloidosis)

- Inherited arrhythmic syndromes (congenital long QT syndrome, short QT syndrome, Brugada syndrome)

- Non-familial AF associated with genetic backgrounds (polymorphism in the ACE gene) that may predispose to atrial fibrillation

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.

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:

The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there were between 500,000 and 3,000,000 cases in the United States. POTS is more common in women, with a female-to-male ratio of 5:1. Most people with POTS are aged between 20 and 40, with an average onset of 30. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

Mechanically induced RS is characterized by pressure in the epigastric and left hypochondriac region. Often the pressure is in the fundus of the stomach, esophagus or distention of the bowel. It is believed this leads to elevation of the diaphragm, and secondary displacement of the heart. This reduces the heart's ability to fill and increases the contractility of the heart to maintain homeostasis.

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.

POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. About 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

The cranium dysfunction mechanical changes in the gut can compress the vagus nerve at any number of locations along the vagus, slowing the heart. As the heart slows, autonomic reflexes are triggered to increase blood pressure and heart rate.

This is complemented by gastro-coronary reflexes whereby the coronary arteries constrict with "functional cardiovascular symptoms" similar to chest-pain on the left side and radiation to the left shoulder, dyspnea, sweating, up to angina pectoris -like attacks with extrasystoles, drop of blood pressure, and tachycardia (high heart beat) or sinus bradycardia (heart beat below 60). Typically, there are no changes / abnormalities related in the EKG detected. This can actually trigger a heart attack for persons with cardiac structural abnormalities i.e. coronary bridge, missing coronary, and atherosclerosis.

If the heart rate drops too low for too long, catecholamines are released to counteract any lowering of blood pressure. Catecholamines bind to alpha receptors and beta receptors, decreasing vasodilation and increasing contractility of the heart. Sustaining this state causes heart fatigue which results in fatigue and chest pain.

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, or a heart attack.

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

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.

The true incidence of TIC is unclear. Some studies have noted the incidence of TIC in adults with irregular heart rhythms to range from 8% to 34%. Other studies of patients with atrial fibrillation and left ventricular dysfunction estimate that 25-50% of these study participants have some degree of TIC. TIC has been reported in all age groups.

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.