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.

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.

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

Determining the risk of an embolism causing a stroke is important for guiding the use of anticoagulants. The most accurate clinical prediction rules are:

- CHADS2

- CHA2DS2-VASc

Both the CHADS2 and the CHA2DS2-VASc score predict future stroke risk in people with a-fib with CHA2DS2-VASc being more accurate. Some that had a CHADS2 score of 0 had a CHA2DS2-VASc score of 3, with a 3.2% annual risk of stroke. Thus a CHA2DS2-VASc score of 0 is considered very low risk.

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.

Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2%. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack". During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

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 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

In otherwise healthy patients, occasional premature atrial contractions are a common and normal finding and do not indicate any particular health risk. Rarely, in patients with other underlying structural heart problems, PACs can trigger a more serious arrhythmia such as atrial flutter or atrial fibrillation. In otherwise healthy people, PACs usually disappear with adolescence.

Although often regarded as a relatively benign heart rhythm problem, atrial flutter shares the same complications as the related condition atrial fibrillation. There is paucity of published data directly comparing the two, but overall mortality in these conditions appears to be very similar.

Hypertension, or abnormally high blood pressure, often signifies an elevated level of both psychological and physiological stress. Often, hypertension goes hand in hand with various atrial fibrillations including premature atrial contractions (PACs). Additional factors that may contribute to spontaneous premature atrial contractions could be:

- Increased age

- Abnormal body height

- History of cardiovascular disease (CV)

- Abnormal ANP levels

- Elevated cholesterol

Due to the reentrant nature of atrial flutter, it is often possible to ablate the circuit that causes atrial flutter with radiofrequency catheter ablation. Catheter ablation is considered to be a first-line treatment method for many people with typical atrial flutter due to its high rate of success (>90%) and low incidence of complications. This is done in the cardiac electrophysiology lab by causing a ridge of scar tissue in the cavotricuspid isthmus that crosses the path of the circuit that causes atrial flutter. Eliminating conduction through the isthmus prevents reentry, and if successful, prevents the recurrence of the atrial flutter. Atrial fibrillation often occurs (30% within 5 years) after catheter ablation for atrial flutter.

Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" (Moe et al. 1964). A more complete definition is that ventricular fibrillation is a "turbulent, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction".

Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other heart pathologies. In addition, it is seen with electrolyte imbalance, overdoses of cardiotoxic drugs, and following near drowning or major trauma. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.

Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40. It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death.

The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work that we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease.

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.

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.

There are several potential challenges associated with routine screening for HCM in the United States. First, the U.S. athlete population of 15 million is almost twice as large as Italy's estimated athlete population. Second, these events are rare, with fewer than 100 deaths in the U.S. due to HCM in competitive athletes per year, or about 1 death per 220,000 athletes. Lastly, genetic testing would provide a definitive diagnosis; however, due to the numerous HCM-causing mutations, this method of screening is complex and is not cost-effective. Therefore, genetic testing in the United States is limited to individuals who exhibit clear symptoms of HCM, and their family members. This ensures that the test is not wasted on detecting other causes of ventricular hypertrophy (due to its low sensitivity), and that family members of the individual are educated on the potential risk of being carriers of the mutant gene(s).

Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia.

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.

Possible underlying causes, which may be treatable and reversible in certain cases, include the Hs and Ts.

- Hypovolemia

- Hypoxia

- Hydrogen ions (acidosis)

- Hypothermia

- Hyperkalemia or Hypokalemia

- Hypoglycemia

- Tablets or Toxins (drug overdose)

- Electric shock

- Tachycardia

- Cardiac Tamponade

- Tension pneumothorax

- Thrombosis (myocardial infarction or pulmonary embolism)

- Trauma (hypovolemia from blood loss)

While the heart is asystolic, there is no blood flow to the brain unless CPR or internal cardiac massage (when the chest is opened and the heart is manually compressed) is performed, and even then it is a small amount. After many emergency treatments have been applied but the heart is still unresponsive, it is time to consider pronouncing the patient dead. Even in the rare case that a rhythm reappears, if asystole has persisted for fifteen minutes or more, the brain will have been deprived of oxygen long enough to cause brain death.

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.

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.

These possible causes are remembered as the 6 Hs and the 6 Ts. See Hs and Ts

- Hypovolemia

- Hypoxia

- Hydrogen ions (Acidosis)

- Hyperkalemia or Hypokalemia

- Hypoglycemia

- Hypothermia

- Tablets or Toxins (Drug overdose)

- Cardiac Tamponade

- Tension pneumothorax

- Thrombosis (e.g., myocardial infarction, pulmonary embolism)

- Tachycardia

- Trauma (e.g., hypovolemia from blood loss)

This list is not fully comprehensive. Most notably, it does not include anaphylaxis. Pressure effects associated with artificial ventilation may also contribute to significant reduction in cardiac output, resulting in a clinical diagnosis of PEA.

The possible mechanisms by which the above conditions can cause pulseless in PEA or the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.

The overall chance of survival among those who have cardiac arrest outside hospital is 10%. Among those who have an out-of-hospital cardiac arrest, 70% occur at home and have a survival rate of 6%. For those who have an in-hospital cardiac arrest, survival rate is estimated to be 24%. Among children rates of survival is 3 to 16% in North America. For in hospital cardiac arrest survival to discharge is around 22% with many having a good neurological outcome.

Prognosis is typically assessed 72 hours or more after cardiac arrest. Rates of survival are better in those who someone saw collapse, got bystander CPR, or had either ventricular tachycardia or ventricular fibrillation when assessed. Survival among those with Vfib or Vtach is 15 to 23%. Women are more likely to survive cardiac arrest and leave hospital than men.

A 1997 review found rates of survival to discharge of 14% although different studies varied from 0-28%. In those over the age of 70 who have a cardiac arrest while in hospital, survival to hospital discharge is less than 20%. How well these individuals are able to manage after leaving hospital is not clear.

A study of survival rates from out-of-hospital cardiac arrest found that 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to hospital. Of these, 59% died during admission, half of these within the first 24 hours, while 46% survived until discharge from hospital. This reflects an overall survival following cardiac arrest of 6.8%. Of these 89% had normal brain function or mild neurological disability, 8.5% had moderate impairment, and 2% had major neurological disability. Of those who were discharged from hospital, 70% were still alive four years later.

The cause is poorly understood. However several risk factors are associated with pacemaker syndrome.

When an entire chamber of the heart is involved in multiple micro-reentry circuits and is therefore quivering with chaotic electrical impulses, it is said to be in fibrillation.

Fibrillation can affect the atrium (atrial fibrillation) or the ventricle (ventricular fibrillation): ventricular fibrillation is imminently life-threatening.

- Atrial fibrillation affects the upper chambers of the heart, known as the atria. Atrial fibrillation may be due to serious underlying medical conditions and should be evaluated by a physician. It is not typically a medical emergency.

- Ventricular fibrillation occurs in the ventricles (lower chambers) of the heart; it is always a medical emergency. If left untreated, ventricular fibrillation (VF, or V-fib) can lead to death within minutes. When a heart goes into V-fib, effective pumping of the blood stops. V-fib is considered a form of cardiac arrest. An individual suffering from it will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.

CPR can prolong the survival of the brain in the lack of a normal pulse, but defibrillation is the only intervention that can restore a healthy heart rhythm. Defibrillation is performed by applying an electric shock to the heart, which resets the cells, permitting a normal beat to re-establish itself.