Yunnan sudden death syndrome is a label used to define unexplained cases of cardiac arrest, which afflicted significant numbers of rural villagers in Yunnan province, in southwest China. Cases occurred almost always during the midsummer rainy season (from June to August), at an altitude of . The cause turned out to be a mushroom now blamed for an estimated 400 deaths in the past three decades.

The mysterious fatalities were recorded for decades before researchers from the Chinese Center for Disease Control and Prevention isolated a significant factor common in every case: a tiny unknown mushroom which was unintentionally gathered and consumed during wild mushroom harvests in the region. Previously the syndrome was thought to be caused by Keshan disease, caused by the Coxsackie virus.

The mushroom, "Trogia venenata", is also known as 'Little White'. It has been determined that families collecting fungi to sell have been eating these Little White mushrooms as they have no commercial value. Three amino acids present in the mushrooms have been shown to be toxic. The mushrooms have also been shown to contain very high quantities of barium, and it may be that some of the deaths are simply from barium poisoning.

In the hours before death, about two-thirds of the victims had such symptoms as nausea, dizziness, heart palpitations, seizures and fatigue.

However, in December 2012 it was announced that Dr Xu Jianping (徐建平) has been collecting samples of "Trogia venenata" in Yunnan for the past three years, and his research now shows that barium levels in the wild mushroom are no higher than those of common foods such as poultry and fish. Nonetheless, it appears the mushroom will still likely play a role. Since publication of the widely circulated 2010 "Science" article, no instances of Yunnan sudden death syndrome have been reported.

Holiday heart syndrome is an irregular heartbeat pattern presented in individuals who are otherwise healthy. Coined in 1978 the term is defined as "abnormal heart rhythms sometimes following excessive alcohol consumption; usually temporary".

Holiday heart syndrome can be the result of stress, dehydration, and drinking alcohol. It is sometimes associated with "binge drinking" common during the holiday season. The condition can also occur when individuals consume only moderate amounts of alcohol.

Irregular heartbeats can be serious. If palpitations continue for longer than a few hours patients should seek medical attention. Some arrhythmias associated with HHS after binge drinking can lead to sudden death, which may explain some of the sudden death cases commonly reported in alcoholics. Atrial fibrillation is the most common arrhythmia in holiday heart syndrome. Symptoms usually resolve themselves within 24 hours.

Holiday heart can also cause abnormal burning sensation whilst urinating and/or the feeling of passing blood similar to a kidney stone. This generally subsides in days or weeks.

Sudden infant death syndrome (SIDS), also known as cot death or crib death, is the sudden unexplained death of a child less than one year of age. Diagnosis requires that the death remains unexplained even after a thorough autopsy and detailed death scene investigation. SIDS usually occurs during sleep. Typically death occurs between the hours of 00:00 and 09:00. There is usually no evidence of struggle and no noise produced.

The exact cause of SIDS is unknown. The requirement of a combination of factors including a specific underlying susceptibility, a specific time in development, and an environmental stressor has been proposed. These environmental stressors may include sleeping on the stomach or side, overheating, and exposure to tobacco smoke. Accidental suffocation from bed sharing (also known as co-sleeping) or soft objects may also play a role. Another risk factor is being born before 39 weeks of gestation. SIDS makes up about 80% of sudden and unexpected infant deaths (SUIDs). Other causes include infections, genetic disorders, and heart problems. While child abuse in the form of intentional suffocation may be misdiagnosed as SIDS, this is believed to make up less than 5% of cases.

The most effective method of reducing the risk of SIDS is putting a child less than one year old on their back to sleep. Other measures include a firm mattress separate from but close to caregivers, no loose bedding, a relatively cool sleeping environment, using a pacifier, and avoiding exposure to tobacco smoke. Breastfeeding and immunization may also be preventive. Measures not shown to be useful include positioning devices and baby monitors. Evidence is not sufficient for the use of fans. Grief support for families affected by SIDS is important, as the death of the infant is sudden, without witnesses, and often associated with an investigation.

Rates of SIDS vary nearly tenfold in developed countries from one in a thousand to one in ten thousand. Globally it resulted in about 19,200 deaths in 2015 down from 22,000 deaths in 1990. SIDS was the third leading cause of death in children less than one year old in the United States in 2011. It is the most common cause of death between one month and one year of age. About 90% of cases happen before six months of age, with it being most frequent between two months and four months of age. It is more common in boys than girls.

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

Porcine stress syndrome, also known as malignant hyperthermia or PSS, is a condition in pigs. It is characterised by hyperthermia triggered by stress, anaesthesia with halothane or intense exercise. PSS may appear as sudden death in pigs, often after transport. It is an inherited, autosomal recessive disorder due to a defective ryanodine receptor leading to huge calcium influx, muscle contracture and increase in metabolism.

PSS can manifest itself in the abattoir as the production of Pale, Soft and Exudative meat due to a rapid fall in muscle pH and degradation of muscle proteins and structure. This meat is usually rejected after inspection.

This disorder is most common in Landrace, Piétrain and crossbreeds of these breeds of pig. The genes may have been favoured in the past due to a larger muscle bulk in these breeds. However this is not standard protocol in developed countries these days.

SIDS is a diagnosis of exclusion and should be applied to only those cases in which an infant's death is sudden and unexpected, and remains unexplained after the performance of an adequate postmortem investigation, including:

1. an autopsy (by an experienced pediatric pathologist, if possible);

2. investigation of the death scene and circumstances of the death;

3. exploration of the medical history of the infant and family.

After investigation, some of these infant deaths are found to be caused by accidental suffocation, hyperthermia or hypothermia, neglect or some other defined cause.

Australia and New Zealand are shifting to the term "sudden unexpected death in infancy" (SUDI) for professional, scientific, and coronial clarity.

The term SUDI is now often used instead of sudden infant death syndrome (SIDS) because some coroners prefer to use the term 'undetermined' for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data. In addition, the U.S. Centers for Disease Control and Prevention (CDC) has recently proposed that such deaths be called "sudden unexpected infant deaths" (SUID) and that SIDS is a subset of SUID.

Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is a type of non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart. This weakening may be triggered by emotional stress, such as the death of a loved one, a break-up, rejection from a partner or constant anxiety. This leads to one of the common names, broken heart syndrome. Stress cardiomyopathy is now a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.

The name "takotsubo syndrome" comes from the Japanese word for a kind of octopus trap: , because the left ventricle takes on a shape resembling a fishing pot.

The typical presentation of takotsubo cardiomyopathy is a sudden onset of chest pain associated with ECG changes mimicking a myocardial infarction of the anterior wall. During the course of evaluation of the patient, a bulging out of the left ventricular apex with a hypercontractile base of the left ventricle is often noted. It is the hallmark bulging out of the apex of the heart with preserved function of the base that earned the syndrome its name "tako tsubo", or octopus pot in Japan, where it was first described.

Stress is the main factor in takotsubo cardiomyopathy, with more than 85% of cases set in motion by either a physically or emotionally stressful event that prefaces the start of symptoms. Examples of emotional stressors include grief from the death of a loved one, fear of public speaking, arguing with a spouse, relationship disagreements, betrayal, and financial problems. Acute asthma, surgery, chemotherapy, and stroke are examples of physical stressors. In a few cases, the stress may be a happy event, such as a wedding, winning a jackpot, a sporting triumph, or a birthday.

Takotsubo cardiomyopathy is more commonly seen in postmenopausal women. Often there is a history of a recent severe (usually negative, sometimes happy) emotional or physical stress.

Sudden cardiac death occurs in approximately one per 200,000 young athletes per year, usually triggered during competition or practice. The victim is usually male and associated with soccer, basketball, ice hockey, or American football, reflecting the large number of athletes participating in these sustained and strenuous sports. For a normally healthy age group, the risk appears to be particularly magnified in competitive basketball, with sudden cardiac death rates as high as one per 3,000 annually for male basketball players in NCAA Division I. This is still far below the rate for the general population, estimated as one per 1,300–1,600 and dominated by the elderly. However, a population as large as the United States will experience the sudden cardiac death of a competitive athlete at the average rate of one every three days, often with significant local media coverage heightening public attention.

The sudden cardiac deaths of 387 young American athletes (under age 35) were analyzed in a 2003 medical review:

While most causes of sudden cardiac death relate to congenital or acquired cardiovascular disease, an exception is commotio cordis, in which the heart is structurally normal but a potentially fatal loss of rhythm occurs because of the accident of timing of a blow to the chest. Its fatality rate is about 65% even with prompt CPR and defibrillation, and more than 80% without.

Age 35 serves as an approximate borderline for the likely cause of sudden cardiac death. Before age 35, congenital abnormalities of the heart and blood vessels predominate. These are usually asymptomatic prior to the fatal event, although not invariably so. Congenital cardiovascular deaths are reported to occur disproportionately in African-American athletes.

After age 35, acquired coronary artery disease predominates (80%), and this is true regardless of the athlete's former level of fitness.

Short QT syndrome is a genetic disease of the electrical system of the heart. It consists of a constellation of signs and symptoms, consisting of a short QT interval on an EKG (≤ 300 ms) that does not significantly change with heart rate, tall and peaked T waves, and a structurally normal heart. Short QT syndrome appears to be inherited in an autosomal dominant pattern, and a few affected families have been identified.

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) occur when the heart abruptly begins to beat in an abnormal or irregular rhythm (arrhythmia). Without organized electrical activity in the heart muscle, there is no consistent contraction of the ventricles, which results in the heart's inability to generate an adequate cardiac output (forward pumping of blood from heart to rest of the body). There are many different types of arrhythmias, but the ones most frequently recorded in SCA and SCD are ventricular tachycardia (VT) or ventricular fibrillation (VF).

Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

Truckloads or railcar loads of PSS-susceptible pigs may be found with a higher-than-average percentage dead on arrival after stressful events such as transport.

Initial signs of the onset of PSS are pyrexia, panting, sweating, tachycardia and arrhythmias. Chronic cases may show muscle atrophy.

Under halothane anaesthesia, pigs will suddenly become rigid and pyrexic.

The halothane challenge was the historical method of diagnosis.

Genetic testing via a PCR enables affected and carrier animals to be found.

Psychologist Melanie Joy has likened PSS to post-traumatic stress disorder in humans.

Brugada syndrome (BrS) is a genetic condition that results in abnormal electrical activity within the heart, increasing the risk of sudden cardiac death. Those affected may have episodes of passing out. Typically this occurs when a person is at rest.

It is often inherited from a person's parent with about a quarter of people having a family history. Some cases may be due to a new mutation or certain medications. The abnormal heart rhythms can be triggered by a fever or increased vagal tone. Diagnosis is typically by electrocardiogram (ECG), however, the abnormalities may not be consistently present.

Treatment may be with an implantable cardioverter defibrillator (ICD). Isoproterenol may be used in those who are acutely unstable. In those without symptoms the risk of death is much lower, and how to treat this group is unclear. Testing people's family members may be recommended.

Between 1 and 30 per 10,000 people are affected. Onset of symptoms is usually in adulthood. It is more common in people of Asian descent. Males are more commonly affected than females. It is named after the Spanish cardiologists Pedro and Josep Brugada who described the condition in 1992. Their brother Ramon Brugada described the underlying genetics in 1998.

Romano–Ward syndrome presents the following in an affected individual:

- Ventricular fibrillation

- Syncope

- Torsade de pointes

- Abnormality of ear

Romano–Ward syndrome is the major variant of "long QT syndrome". It is a condition that causes a disruption of the heart's normal rhythm. This disorder is a form of long QT syndrome, which is a heart condition that causes the cardiac muscle to take longer than usual to recharge between beats; if untreated, the irregular heartbeats can lead to fainting, seizures, or sudden death

Many people with long QT syndrome have no signs or symptoms.

Some people may experience the following symptoms:

- Fainting (or syncope). This may occur when the patient is emotionally or physically stressed. It is unusual in QT syndrome to have any signs before the person actually faints.

- Seizures

- Sudden death. If there is sudden death, and doctors suspect long QT syndrome as the cause, they may recommend that the family members of the deceased get tested for the disease.

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.

Jervell and Lange-Nielsen syndrome (JLNS) is a type of long QT syndrome associated with severe, bilateral sensorineural hearing loss. Long QT syndrome causes the cardiac muscle to take longer than usual to recharge between beats. If untreated, the irregular heartbeats, called arrhythmias, can lead to fainting, seizures, or sudden death. It was first described by Anton Jervell and Fred Lange-Nielsen in 1957.

Athletic heart syndrome (AHS), also known as athlete's heart, athletic bradycardia, or exercise-induced cardiomegaly is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting heart rate is lower than normal.

The athlete's heart is associated with physiological remodeling as a consequence of repetitive cardiac loading. Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one.

Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete's heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in higher cardiac output, which also allows it to beat more slowly, as more blood is pumped out with each beat.

Another sign of athlete's heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as the diastolic pressure of the irregularly shaped heart creates a disordered blood flow. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition.

Individuals with LGL syndrome do not carry an increased risk of sudden death. The only morbidity associated with the syndrome is the occurrence of paroxysmal episodes of tachycardia which may be of several types, including sinus tachycardia, supraventricular tachycardia, atrial fibrillation, atrial flutter, or even ventricular tachycardia.

Some individuals with short QT syndrome frequently complain of palpitations and may have unexplained syncope (loss of consciousness). Mutations in the "KCNH2", "KCNJ2", and "KCNQ1" genes cause short QT syndrome. These genes provide instructions for making proteins that act as channels across the cell membrane. These channels transport positively charged atoms (ions) of potassium into and out of cells. In cardiac muscle, these ion channels play critical roles in maintaining the heart's normal rhythm. Mutations in the "KCNH2", "KCNJ2", or "KCNQ1" gene increase the activity of the channels, which changes the flow of potassium ions between cells. This disruption in ion transport alters the way the heart beats, leading to the abnormal heart rhythm characteristic of short QT syndrome. Short QT syndrome appears to have an autosomal dominant pattern of inheritance.

Short QT syndrome is associated with an increased risk of sudden cardiac death, most likely due to ventricular fibrillation.

Genetic testing for Brugada syndrome is clinically available and may help confirm a diagnosis, as well as differentiate between relatives who are at risk for the disease and those who are not. Some symptoms when pinpointing this disease include fainting, irregular heartbeats, and chaotic heartbeats. However, just detecting the irregular heartbeat may be a sign of another disease, so the doctor must detect another symptom as well.

Sudden unexpected death in epilepsy (SUDEP) is a fatal complication of epilepsy. It is defined as the sudden and unexpected, non-traumatic and non-drowning death of a person with epilepsy, without a toxicological or anatomical cause of death detected during the post-mortem examination.

While the mechanisms underlying SUDEP are still poorly understood, it is possibly the most common cause of death as a result of complications from epilepsy, accounting for between 7.5 and 17% of all epilepsy-related deaths and 50% of all deaths in refractory epilepsy. The causes of SUDEP seem to be multifactorial and include respiratory, cardiac and cerebral factors, as well as the severity of epilepsy and seizures. Proposed pathophysiological mechanisms include seizure-induced cardiac and respiratory arrests.

SUDEP occurs in about 1 in 1,000 adults and 1 in 4,500 children with epilepsy a year. Rates of death as a result of prolonged seizures (status epilepticus) are not classified as SUDEP.

The risk of PVF during acute myocardial infarction is related to the amount of ST elevation, the presence of hypokalemia, the absence of pre-infarction angina, the size of the infarction, and the presence of a blocked left coronary artery. Other risk factors could include younger age, male gender, and history of sudden cardiac death in first degree relatives.