<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hypopnea and can you explain it in depth? [/INST] Hypopnea is overly shallow breathing or an abnormally low respiratory rate. Hypopnea is defined by some to be less severe than apnea (the complete cessation of breathing), while other researchers have discovered hypopnea to have a "similar if not indistinguishable impact" on the negative outcomes of sleep breathing disorders. In sleep clinics, obstructive sleep apnea syndrome or obstructive sleep apnea–hypopnea syndrome is normally diagnosed based on the frequent presence of apneas and/or hypopneas rather than differentiating between the two phenomena. Hypopnea is typically defined by a decreased amount of air movement into the lungs and can cause oxygen levels in the blood to drop. It commonly is due to partial obstruction of the upper airway.
Hypopnea during sleep is classed as a sleep disorder. With moderate to severe hypopnea, sleep is disturbed such that patients may get a full nights sleep but still not feel rested because they did not get the right kind of sleep.  The disruption in breathing causes a drop in blood oxygen level, which may in turn disrupt the stages of sleep.
Daytime hypopnea events, however, are mostly limited to those with severely compromised respiratory muscles, as occurs in certain neuromuscular diseases or compromised central respiratory drive, as occurs in conditions such as acquired or congenital central hypoventilation syndrome (ACHS or CCHS). Daytime hypopnea can also cause a drop in blood oxygen level.

Symptoms
The most common hypopnea symptom is excessive sleepiness, which results from constant sleep interruption. People with hypopnea due to airflow obstruction often have loud, heavy snoring that is interrupted with choking sounds or loud snorts followed by periods of silence, because not enough air can flow into the lungs through the mouth and nose. The periods of silence can last 20 seconds or longer and can happen many times each hour, resulting in poor sleep and reduced levels of oxygen in the blood.
Other symptoms of hypopnea may include depression, forgetfulness, mood or behaviour changes, trouble concentrating, loss of energy, nervousness, and morning headaches. Not all people with hypopnea experience all of these symptoms and not everyone who has these symptoms has hypopnea.

Consequences
Hypopnea is a disorder that may result in excessive daytime sleepiness and compromised quality of life, including traffic accidents, diminished productivity in the workplace, and emotional problems.
Cardiovascular consequences of hypopnea may include myocardial infarction, hypertension, coronary heart disease as well other problems such as stroke, psychiatric problems, impotence, cognitive dysfunction and memory loss.

Causes
Among the causes of hypopnea are:

anatomical defects such as nasal septum deformation or congenital narrowness of nasal meatus and the gullet
acute tonsillitis and/or adenoiditis
obesity or being overweight
neuromuscular disease or any condition that entails weakened respiratory muscles
hypoventilation syndromes involving compromised or failed respiratory drive
use of sedatives, for example sleeping pills
hazardous alcohol use
smoking
aging
others, most of which are also typical causes of airway obstruction, snoring and sleep apnea

Diagnosis
In the context of diagnosis and treatment of sleep disorders, a hypopnea is not considered to be clinically significant unless there is a 30% or greater reduction in flow lasting for 10 seconds or longer and an associated 4% or greater desaturation in the persons O2 levels, or if it results in arousal or fragmentation of sleep.
The direct consequence of hypopnea (as well as apnea) is that the CO2 in the blood increases and the oxygen level in the patients blood decrease is proportionate to the severity of the airway obstruction. This disruptive pattern of breathing generates disruptive sleep patterns, the consequences of which being that those individuals may exhibit increased fatigability, lethargy, decreased ability to concentrate, increased irritability, and morning headaches. Basically, those individuals are extremely tired due to their inability to get a good nights sleep.
Hypopneas can be either central i.e., as part of a waxing and waning in breathing effort, or obstructive in origin. During an obstructive hypopnea, in comparison to an obstructive apnea, the airway is only partially closed. However, this closure is still enough to cause a physiological effect i.e., an oxygen desaturation and/or an increase in breathing effort terminating in arousal.
A Hypopnea Index (HI) can be calculated by dividing the number of hypopnea events during the sleep period by the number of hours of sleep. The Apnea-Hypopnea Index (AHI) is an index of severity that combines apneas and hypopneas. Combining them both gives an overall severity of sleep apnea including sleep disruptions and desaturations (a low level of oxygen in the blood). The apnea-hypopnea index, like the apnea index and hypopnea index, is calculated by dividing the number of apneas and hypopneas by the number of hours of sleep. Another index that is used to measure sleep apnea is the Respiratory Disturbance Index (RDI). The RDI is similar to the AHI, however, RDI also includes respiratory events that do not technically meet the definitions of apneas or hypopneas, such as a Respiratory Effort Related Arousal (RERA), but do disrupt sleep.

Treatment
Obstructive hypopnea
One treatment for obstructive hypopnea is continuous positive airway pressure (CPAP). CPAP is a treatment in which the patient wears a mask over the nose and/or mouth. An air blower forces air through the upper airway </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pseudofolliculitis barbae and can you explain it in depth? [/INST] Pseudofolliculitis barbae (PFB) is a persistent irritation caused by shaving. It was first described in 1956.

Signs and symptoms
Related conditions
Razor burn is a less serious condition caused by shaving, characterized by mild to moderate redness and irritation on the surface of the skin. Unlike PFB, it is usually transient and there is no infection involved.
There is also a condition called folliculitis barbae. The difference between the two is the cause of the inflammation in the hair follicles. Where folliculitis barbae is caused by viral or bacterial infections, pseudofolliculitis is created by irritation from shaving and ingrown hairs.
Pseudofolliculitis nuchae, a related condition, occurs on the back of the neck, often along the posterior hairline, when curved hairs are cut short and allowed to grow back into the skin. Left untreated, this can develop into acne keloidalis nuchae, a condition in which hard, dark keloid-like bumps form on the neck. Both occur frequently in black men in the military. Here it is so common that services often have known protocols for management.

Cause
Pseudofolliculitis barbae (PFB) is most common on the face, but it can also happen on other parts of the body where hair is shaved or plucked, especially areas where hair is curly and the skin is sensitive, such as genital shaving (more properly termed pseudofolliculitis pubis or PFP).After a hair has been shaved, it begins to grow back. Curly hair tends to curl into the skin instead of straight out of the follicle, leading to an inflammation reaction. PFB can make the skin look itchy and red, and in some cases, it can even look like pimples. These inflamed papules or pustules can form especially if the area becomes infected.This is especially a problem for some men who have naturally coarse or tightly curling thick hair. Curly hair increases the likelihood of PFB by a factor of 50. If left untreated over time, this can cause keloid scarring in the beard area.Pseudofolliculitis barbae can further be divided into two types of ingrown hairs:  transfollicular and extrafollicular.  The extrafollicular hair is a hair that has exited the follicle and reentered the skin.  The transfollicular hair never exits the follicle, but because of its naturally curly nature curls back into the follicle causing fluid build-up and irritation.A common polymorphism in a keratin gene (K6hf) has been linked to PFB, suggesting that it may be a genetic risk factor. This sequence change leads to an amino acid substitution in the highly conserved helix initiation motif of the K6hf rod domain. Carriers of the A12T polymorphism are six times more likely to develop PFB compared with people homozygous for the wild-type K6hf sequence. This suggests K6hf mutation structurally weakens the companion layer separating the inner and outer root sheath and increases the chances that a beard hair will in-grow.

Prevention
The most efficient prevention is to grow a beard. For men who are required to, or simply prefer to shave, studies show the optimal length to be about 0.5 mm to 1 mm to prevent the hair growing back into the skin. Using a beard trimmer at the lowest setting (0.5mm or 1mm) instead of shaving is an efficient alternative.  The resulting faint stubble can be shaped using a standard electric razor on non-problematic areas (cheeks, lower neck).For most cases, completely avoiding shaving for three to four weeks allows all lesions to subside, and most extrafollicular hairs will resolve themselves within at least ten days. Permanent removal of the hair follicle is the only definitive treatment for PFB. Electrolysis is effective but limited by its slow pace, pain and expense. Laser-assisted hair removal is effective. There is a risk of skin discoloration and a very small risk of scarring.Some men use electric razors to control PFB.  Those who use a razor should use a single blade or special wire-wrapped blade to avoid shaving too closely, with a new blade each shave. Shaving in the direction of hair growth every other day, rather than daily, may improve pseudofolliculitis barbae. If one must use a blade, softening the beard first with a hot, wet washcloth for five minutes or shave while showering in hot water can be helpful. Some use shaving powders (a kind of chemical depilatory) to avoid the irritation of using a blade. Barium sulfide-based depilatories are most efficient, but produce an unpleasant smell.

Treatment
The simplest treatment for PFB is to let the beard grow. Complete removal of the hair from its follicle is not recommended </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Colitis and can you explain it in depth? [/INST] Colitis is an inflammation of the colon. Colitis may be acute and self-limited or long-term. It broadly fits into the category of digestive diseases.
In a medical context, the label colitis (without qualification) is used if:

The cause of the inflammation in the colon is undetermined; for example, colitis may be applied to Crohns disease at a time when the diagnosis is unknown, or
The context is clear; for example, an individual with ulcerative colitis is talking about their disease with a physician who knows the diagnosis.

Signs and symptoms
The signs and symptoms of colitis are quite variable and dependent on the cause of the given colitis and factors that modify its course and severity.Common symptoms of colitis may include: mild to severe abdominal pains and tenderness (depending on the stage of the disease), persistent hemorrhagic diarrhea with pus either present or absent in the stools, fecal incontinence, flatulence, fatigue, loss of appetite and unexplained weight loss.More severe symptoms may include: shortness of breath, a fast or irregular heartbeat and fever.Other less common or rare non-specific symptoms that may accompany colitis include: arthritis, mouth ulcers, painful, red and swollen skin and irritated, bloodshot eyes.Signs seen on colonoscopy include: colonic mucosal erythema (redness of the colons inner surface), ulcerations and hemorrhage.

Diagnosis
Symptoms suggestive of colitis are worked-up by obtaining the medical history, a physical examination and laboratory tests (CBC, electrolytes, stool culture and sensitivity, stool ova and parasites et cetera).  Additional tests may include medical imaging (e.g. abdominal computed tomography, abdominal X-rays) and an examination with a camera inserted into the rectum (sigmoidoscopy, colonoscopy).An important investigation in the assessment of colitis is biopsy. A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. It can provide important information regarding the cause of the disease and the extent of bowel damage.

Types
There are many types of colitis. They are usually classified by the cause.
Types of colitis include:

Autoimmune
Inflammatory bowel disease (IBD) – a group of chronic colitides.
Ulcerative colitis (UC) – a chronic colitis that affects the large intestine.
Crohns disease (CD) – another type of IBD that often leads to colitis.

Unknown
Microscopic colitis – a colitis diagnosed by microscopic examination of colonic tissue; macroscopically ("to the eye") it appears normal.
Lymphocytic colitis
Collagenous colitis

Treatment-caused
Diversion colitis
Chemical colitis
Chemotherapy-induced colitis
Radiation colitis
Checkpoint inhibitor induced colitis

Vascular disease
Ischemic colitis

Infectious
Infectious colitisA subtype of infectious colitis is Clostridioides difficile colitis, which is informally abbreviated as "C-diff colitis". It classically forms pseudomembranes and is often referred to as pseudomembranous colitis, which is its (nonspecific) histomorphologic description.
Enterohemorrhagic colitis may be caused by Shiga toxin in Shigella dysenteriae or Shigatoxigenic group of Escherichia coli (STEC), which includes serotype O157:H7 and other enterohemorrhagic E. coli.Parasitic infections, like those caused by Entamoeba histolytica, can also cause colitis.

Unclassifiable colitides
Indeterminate colitis is the classification for colitis that has features of both Crohns disease and ulcerative colitis.  Indeterminate colitis behaviour is usually closer to ulcerative colitis than Crohns disease.Atypical colitis is a phrase that is occasionally used by physicians for a colitis that does not conform to criteria for accepted types of colitis.  It is not an accepted diagnosis per se and, as such, a colitis that cannot be definitively classified.

Treatment
Some people may be admitted into the hospital following the colonoscopy depending on results.  It is sometimes necessary to get the patient started on a steroid to speed up the healing of the colon. It may also be necessary to get the patient hydrated from the fluid loss and iron replaced from the loss of blood.  After a hospital stay, the patient may be put on a daily medication to manage their  chronic colitis </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cardiac arrest and can you explain it in depth? [/INST] Cardiac arrest is when the heart suddenly and unexpectedly stops beating. It is a medical emergency that without immediate medical intervention will result within minutes in sudden cardiac death. Cardiopulmonary resuscitation (CPR), and possibly defibrillation are needed until further treatment can be provided. Cardiac arrest results in a rapid loss of consciousness, and breathing may be abnormal or absent.While cardiac arrest may be caused by heart attack or heart failure, these are not the same, and in 15 to 25% of cases there is a non-cardiac cause. Some individuals may experience chest pain, shortness of breath, nausea, an elevated heart rate and feeling light-headed immediately before entering cardiac arrest.The most common cause of cardiac arrest is an underlying heart problem like coronary artery disease which decreases the amount of oxygenated blood supplying the heart muscle. This, in turn, damages the structure of the muscle, which can alter its function. These changes can over time cause ventricular fibrillation (V-fib) which most commonly precedes cardiac arrest. Less common causes include major blood loss, lack of oxygen, very low potassium, electrical injury, heart failure, inherited heart arrhythmias and intense physical exercise. Cardiac arrest is diagnosed by the inability to find a pulse.CPR and defibrillation can reverse a cardiac arrest, leading to return of spontaneous circulation, but without such intervention it will prove fatal. In some cases, cardiac arrest is an anticipated outcome of serious illnesses where death is expected. Treatment for cardiac arrest includes immediate CPR and, if a shockable rhythm is present, defibrillation. Two protocols have been established for CPR: basic life support (BLS) and advanced cardiac life support (ACLS). Among those whose pulses are reestablished, targeted temperature management may improve outcomes. In addition, the care team may initiate measures to protect the patient from brain injury and preserve brain function. In post-resuscitation care, an implantable cardiac defibrillator may be considered to reduce the chance of death from recurrence.In the United States, approximately 535,000 cases occur a year (about 13 per 10,000 people). Of these, 326,000 (61%) experience cardiac arrest outside of a hospital setting, while 209,000 (39%) occur within a hospital. Cardiac arrest becomes more common with age and affects males more often than females.The percentage of people who survive out-of-hospital cardiac arrest with treatment by emergency medical services is about 8%. However, fictional media in the U.S. has often portrayed the immediate survival rate of cardiac arrest to be unreasonably high. This may contribute to misinformed expectations of the resuscitative efforts from the general public with many studies showing the expected survival rate of resuscitative efforts after cardiac arrest exceeding 40–50%. These portrayals may also contribute to a patients or medical decision makers desire to pursue aggressive measures. However, it has been shown that many of the critically ill are less likely to choose resuscitation when given accurate information about its limitations.In the event that cardiopulmonary resuscitation is successful, complete recovery is not guaranteed as many survivors experience an array of disability including partial paralysis, seizures, difficulty with walking, speaking, or memory, limited consciousness, or persistent vegetative state and brain death.

Signs and symptoms
Cardiac arrest is not preceded by any warning symptoms in approximately 50 percent of people. For individuals who do experience symptoms, the symptoms are usually nonspecific to the cardiac arrest. This can present in the form of new or worsening:

chest pain
fatigue
blackouts
dizziness
shortness of breath
weakness
vomitingWhen cardiac arrest is suspected due to signs of unconsciousness or abnormal breathing, a bystander should attempt to feel a pulse for 10 seconds; if no pulse is felt, it should be assumed the victim is in cardiac arrest. As a result of loss of cerebral perfusion (blood flow to the brain), the person will rapidly lose consciousness and can stop breathing. Near-death experiences are reported by 10 to 20 percent of people who survived cardiac arrest, which demonstrates a certain level of cognitive processes that are still active during resuscitation.

Risk factors
The risk factors for sudden cardiac arrest (SCA) are similar to those of coronary artery disease and include age, cigarette smoking, high blood pressure, high cholesterol, lack of physical exercise, obesity, diabetes, and family history of cardiac disease. A prior episode of sudden cardiac arrest also increases the likelihood of future episodes. A statistical analysis of many of these risk factors determined that approximately 50% of all cardiac arrests occur in 10% of the population perceived to be at greatest risk due to aggregate harm of multiple risk factors demonstrating that cumulative risk of multiple comorbidities exceeds the sum of each risk individually.Previous adverse cardiac events, non-sustained ventricular tachycardia (NSVT), syncope, and left ventricular hypertrophy (LVT) have been shown to predict sudden cardiac death in children. Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers risk was closer to that of those who had never smoked.Functional changes in the heart such as reduced ejection fraction or cardiac arrhythmia have been shown to increase the risk of cardiac arrest and act independently from the risk factors previously mentioned. Conditions that produce these functional changes can be acquired following previous cardiac injury, or inherited through familial history of arrhythmogenic disorders.: 828

Causes and mechanisms
Sudden cardiac arrest (SCA), or 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 hearts 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 sudden cardiac arrest are ventricular tachycardia and ventricular fibrillation. Less common causes of dysrhythmias in cardiac arrest include pulseless electrical activity (PEA), bradyarrhythmias or asystole. Such rhythms are seen when there is prolonged cardiac arrest, progression of ventricular fibrillation, or efforts such as defibrillation executed to resuscitate the person. The rhythm changes also appear to have a correlation to the underlying cause of cardiac injury when present (ischemic vs. nonischemic causes).: 831 Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

Cardiac causes
Coronary artery disease
Coronary artery disease (CAD), also known as ischemic heart disease, is responsible for 62 to 70 percent of all sudden cardiac deaths. CAD is a much less frequent cause of sudden cardiac death in people under the age of 40. Cases have shown that the most common finding at postmortem examination of sudden cardiac death is chronic high-grade stenosis of at least one segment of a major coronary artery, the arteries that supply the heart muscle with its blood supply. This stenosis is often the result of narrowing and hardening of the arteries following deposition of cholesterol plaques and inflammation over several years. This accumulation and remodeling of the coronary vessels along with other systemic blood vessels characterizes the progression of Atherosclerotic Cardiovascular Disease. When a stable plaque ruptures, it can block the flow of blood and oxygen through small arteries resulting in ischemic injury as a result. The injury to tissue following ischemia can lead to structural and functional changes preventing the heart from continuing normal conduction cycles and altering heart rate.: 829 : 829

Non-atherosclerotic coronary artery abnormalities
Abnormalities of the coronary arteries not related to atherosclerosis include congenital coronary artery anomalies (most commonly anomalous origin of left coronary artery from the pulmonary artery), inflammation known as coronary arteritis, embolism, vasospasm, and mechanical abnormalities related to connective tissue diseases or trauma. These conditions account for 10-15% of cardiac arrest and sudden cardiac death.: 829
Coronary arteritis commonly results from a pediatric febrile inflammatory condition known as Kawasaki disease. Other vasculitides can also contribute to increased risk of sudden cardiac death.
Embolism, or clotting, of the coronary arteries most commonly occurs from septic emboli secondary to endocarditis with involvement of the aortic valve, tricuspid valve, or prosthetic valves.
Coronary vasospasm may result in cardiac arrhythmias, altering the electrical conduction of the heart with a risk of complete cardiac arrest from severe or prolonged rhythm changes.
Mechanical abnormalities with associated risk of cardiac arrest may arise from coronary artery dissection which can be attributed to Marfan Syndrome or trauma.: 829

Structural heart disease
Structural heart diseases not related to coronary artery disease account for 10% of all sudden cardiac deaths. Examples of these include:  cardiomyopathies (hypertrophic, dilated, or arrythmogenic), cardiac rhythm disturbances, myocarditis, hypertensive heart disease, and congestive heart failure.

Left ventricular hypertrophy is thought to be a leading cause of sudden cardiac deaths in the adult population. This is most commonly the result of longstanding high blood pressure, or hypertension, which has caused a maladaptive change to the wall of the main pumping chamber of the heart, the left ventricle. Increased blood pressure means that the heart must pump even harder to adequately circulate blood throughout the body. If the heart does this for a prolonged period of time due to uncontrolled hypertension, the left ventricle can hypertrophy (grow larger) in a way that decreases the effectiveness of the heart. Left ventricular hypertrophy can be demonstrated on echocardiogram and electrocardiogram (EKG).A 1999 review of sudden cardiac deaths in the United States found that structural heart diseases accounted for over 30% of sudden cardiac arrests for those under 30 years. A study of military recruits age 18-35 found that this accounted for over 40% of sudden cardiac deaths.Congestive heart failure increases the risk of sudden cardiac death fivefold.Structural abnormalities of the cardiac conduction system (notably the Atrioventricular Node and His-Purkinje system) may predispose an individual to arrhythmias with risk of progressing to sudden cardiac arrest, albeit this risk remains low. Many of these conduction blocks can be treated with internal cardiac defibrillators for those determined to be at high risk due to severity of fibrosis or severe electrophysiologic disturbances.: 833

Inherited arrhythmia syndromes
Arrhythmias that are not due to structural heart disease account for 5 to 10% of sudden cardiac arrests. These are frequently caused by genetic disorders that lead to abnormal heart rhythms. The genetic mutations often affect specialized proteins known as ion channels that conduct electrically charged particles across the cell membrane, and this group of conditions are therefore often referred to as channelopathies. Examples of these inherited arrhythmia syndromes include Long QT syndrome (LQTS), Brugada Syndrome, Catecholaminergic polymorphic ventricular tachycardia, and Short QT syndrome. Many are also associated with environmental or neurogenic triggers such as response to loud sounds that can initiate lethal arrhythmias.: 833  Other conditions that promote arrhythmias but are not caused by genetic mutations include Wolff-Parkinson-White syndrome.Long QT syndrome, a condition often mentioned in young peoples deaths, occurs in one of every 5000 to 7000 newborns and is estimated to be responsible for 3000 deaths each year compared to the approximately 300,000 cardiac arrests seen by emergency services. These conditions are a fraction of the overall deaths related to cardiac arrest but represent conditions which may be detected prior to arrest and may be treatable. The symptomatic expression of Long-QT syndrome is quite broad and more often presents with syncope rather than cardiac arrest. However, the risk of cardiac arrest is still present and individuals with family history of sudden cardiac arrests should be screened for LQTS and other treatable causes of lethal arrhythmia. Higher levels of risk for cardiac arrest are associated with female sex, more significant QT prolongation, history of unexplained syncope (fainting spells) or premature sudden cardiac death.: 833  Additionally, individuals with LQTS should avoid certain medications that carry the risk of increasing the severity of this conduction abnormality such as certain anti-arrhythmic, anti-depressant, and quinolone or macrolide antibiotics.

Non-cardiac causes
Non-cardiac causes accounts for 15 to 25% of cardiac arrests. The most common non-cardiac causes are trauma, major bleeding (gastrointestinal bleeding, aortic rupture, or intracranial hemorrhage), hypovolemic shock, overdose, drowning, and pulmonary embolism. Cardiac arrest can also be caused by poisoning like the stings of certain jellyfish, or through electrocution, like lightning.

Reversible causes
Other non-cardiac causes of cardiac arrest may result from temporary disturbances in the bodies homeostasis. This may be the result from changes in electrolyte ratios, oxygen saturation, or alterations of other ions influencing the bodys pH.

Mnemonic for reversible causes
"Hs and Ts" is the name for a mnemonic used to remember the treatable or reversible causes of cardiac arrest. Note: This mnemonic includes causes of cardiac and non-cardiac origin, but all are reversible with appropriate and time-sensitive treatment.

HsHypovolemia – A lack of blood volume
Hypoxia – A lack of oxygen
Hydrogen ions (acidosis) – An abnormal pH in the body
Hyperkalemia or hypokalemia – Both increased and decreased potassium can be life-threatening
Hypothermia – A low core body temperature
Hypoglycemia or hyperglycemia – A low or high blood glucoseTsTablets or toxins such as drug overdose
Cardiac tamponade – Fluid building up around the heart
Tension pneumothorax – A collapsed lung
Thrombosis (myocardial infarction) – A heart attack
Thromboembolism (pulmonary embolism) – A blood clot in the lung
Traumatic cardiac arrest

Children
In children, the most common cause of cardiopulmonary arrest is shock or respiratory failure that has not been treated. Heart arrhythmia is not the most common cause in children. When there is a cardiac arrhythmia, it is most often asystole or bradycardia, in contrast to ventricular fibrillation or tachycardia as seen in adults. Other causes can include drugs such as cocaine, methamphetamine, or overdose of medications such as antidepressants in a child who was previously healthy but is now presenting with a dysrhythmia that has progressed to cardiac arrest. Common causes of sudden unexplained cardiac arrest in children include hypertrophic cardiomyopathy, coronary artery abnormalities, and arrhythmias.

Mechanism
The definitive electrical mechanisms of cardiac arrest, which may arise from any of the functional, structural or physiologic abnormalities mentioned above are characterized by tachyarrhythmic or bradyarrhythmic events that do not result in systole.: 837–838  The tachyarrhythmias can be further classified as Ventricular fibrillation (V-fib) and pulseless or sustained Ventricular tachycardia (V-tach), both of which are rapid and erratic arrhythmias that alter the circulatory pathway such that adequate blood flow cannot be sustained and is inadequate to meet the bodys needs.: 837–838 The mechanism responsible for the majority of sudden cardiac deaths is ventricular fibrillation.  Ventricular fibrillation is a tachyarrhythmia characterized by turbulent electrical activity in the ventricular myocardium leading to a heart rate too disorganized and rapid to produce any meaningful cardiac output, thus resulting in insufficient perfusion of the brain and essential organs. In ventricular tacycardia, the heart also beats faster than normal, which may  prevent the heart chambers from properly filling with blood. Some of the electrophysiologic mechanisms underpinning ventricular fibrillations include ectopic automaticity, re- entry, and triggered activity. Structural changes in the diseased heart as a result of inherited factors (mutations in ion-channel coding genes for example) cannot explain the suddenness of sudden cardiac death.Both ventricular fibrillation and ventricular tachycardia can result in the heart ineffectively pumping blood to the body. Ventricular tachycardia is characterized by an altered QRS complex and a heart rate greater than 100 beats per minute. When V-tach is sustained (lasts for at least 30 seconds), inadequate blood flow to heart tissue can lead to cardiac arrest.Bradyarrhthmias occur following dissociation of spontaneous electrical conduction and the mechanical function of the heart resulting in pulseless electrical activity (PEA) or through complete absence of electrical activity of the heart resulting in asystole. Similar to the result of tachyarrhthmias, these conditions lead to an inability to sustain adequate blood flow as well, though in the case of bradyarrhthmias, the underlying cause is absence mechanical activity and not rapid beats leading to disorganization.: 837–838

Diagnosis
Cardiac arrest is synonymous with clinical death. Historical information and a physical exam can diagnose cardiac arrest and provide information regarding the potential cause and the prognosis. The provider taking the persons clinical history should aim to determine if the episode was observed by anyone else, what time the episode took place, what the person was doing (in particular if there was any trauma), and if there were involvement of drugs. The physical examination portion of diagnosing cardiac arrest focuses on the absence of a pulse. In many cases, lack of a carotid pulse is the gold standard for diagnosing cardiac arrest. Lack of a pulse in the periphery (radial/pedal) may also result from other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers may often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals or lay persons.Point-of-care ultrasound (POCUS) is a tool that can be used to examine the movement of the heart and its force of contraction at the person experiencing cardiac arrests bedside. POCUS can accurately diagnose cardiac arrest in hospital settings, overcoming some of the shortcomings of diagnosis through checking the central pulse (carotid arteries or subclavian arteries), as well as detecting movement and contractions of the heart.Using POCUS, clinicians can have limited, two-dimensional views of different parts of the heart during arrest. These images can help clinicians determine whether electrical activity within the heart is pulseless or pseudo-pulseless, as well as help them diagnose the potentially reversible causes of an arrest. Published guidelines from the American Society of Echocardiography, American College of Emergency Physicians, European Resuscitation Council, and the American Heart Association, as well as the 2018 preoperative Advanced Cardiac Life Support guidelines, have recognized the potential benefits of using POCUS in diagnosing and managing cardiac arrest.Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. Instead, the current guidelines prompt  individuals to begin CPR on any unconscious person who has absent or abnormal breathing. The Resuscitation Council in the United Kingdom stand in line with the ERCs recommendations and those of the American Heart Association. They have suggested that the technique to check carotid pulses should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.Various other methods for detecting circulation, and therefore diagnosing cardiac arrest have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse. These signs included coughing, gasping, colour, twitching, and movement. However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally, a similar protocol that of which the European Resuscitation Council has adopted. In a non-acute setting where the patient is expired, diagnosis of cardiac arrest can be done via molecular autopsy or postmortem molecular testing which uses a set of molecular techniques to find the ion channels that are cardiac defective. This could help elucidate the cause of death in the patient.
Other physical signs or symptoms can help determine the potential cause of the cardiac arrest. Below is a chart of the clinical findings and signs/symptoms a person may have and a potential cause associated with it.

Classifications
Clinicians classify cardiac arrest into "shockable" versus "non-shockable", as determined by the EKG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using defibrillation. The two "shockable" rhythms are ventricular fibrillation and pulseless ventricular tachycardia, while the two "non-shockable" rhythms are asystole and pulseless electrical activity.

Prevention
With the lack of positive outcomes following cardiac arrest, efforts have been spent finding effective strategies to prevent cardiac arrest. With the prime causes of cardiac arrest being ischemic heart disease, efforts to promote a healthy diet, exercise, and smoking cessation are important. For people at risk of heart disease, measures such as blood pressure control, cholesterol lowering, and other medico-therapeutic interventions are used.[1] Of note, however, a Cochrane review published in 2016 found moderate-quality evidence to show that blood pressure-lowering drugs do not actually reduce the risk of sudden cardiac death. Exercise is an effective preventative measure for cardiac arrest in the general population but may be risky for those with pre-existing conditions. The risk of a transient catastrophic cardiac event increases in individuals with heart disease during and immediately after exercise. However, both the lifetime and acute risk of cardiac arrest are decreased in individuals with heart disease that perform regular exercise, suggesting the risks of exercise are outweighed by the benefits.

Diet
According to a study published in the Journal of the American Heart Association in 2021, diet may be a modifiable risk factor that leads to a lower incidence of sudden cardiac death. The study found that those who fell under the category of having "Southern diets" representing those of "added fats, fried food, eggs, organ and processed meats, and sugar‐sweetened beverages" had a positive association with an increased risk of cardiac arrest, while those deemed following the "Mediterranean diets" of  had an inverse relationship regarding the risk of cardiac arrest. The American Heart Association also has diet recommendations here that is aimed to prevent cardiovascular disease. Here, the readers may find broad information regarding healthy eating and some tips on what to look for and what to avoid from grocery stores to restaurant dining.Additionally, marine-derived omega-3 polyunsaturated fatty acids (PUFAs) have been promoted for the prevention of sudden cardiac death due to their postulated ability to lower triglyceride levels, prevent arrhythmias, decrease platelet aggregation, and lower blood pressure. However, according to a systematic review published in 2012, omega-3 PUFA supplementation are not being associated with a lower risk of sudden cardiac death.

Code teams
In medical parlance, cardiac arrest is referred to as a "code" or a "crash". This typically refers to "code blue" on the hospital emergency codes. A dramatic drop in vital sign measurements is referred to as "coding" or "crashing", though coding is usually used when it results in cardiac arrest, while crashing might not. Treatment for cardiac arrest is sometimes referred to as "calling a code".
People in general wards often deteriorate for several hours or even days before a cardiac arrest occurs. This has been attributed to a lack of knowledge and skill amongst ward-based staff, in particular, a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward-based staff. A number of "early warning" systems also exist which aim to quantify the persons risk of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being used more effectively in order to augment the work already being done at ward level. These include:

Crash teams (or code teams) – These are designated staff members with particular expertise in resuscitation who are called to the scene of all arrests within the hospital. This usually involves a specialized cart of equipment (including defibrillator) and drugs called a "crash cart" or "crash trolley".
Medical emergency teams – These teams respond to all emergencies, with the aim of treating the people in the acute phase of their illness in order to prevent a cardiac arrest. These teams have been found to decrease the rates of in-hospital cardiac arrest and improve survival.
Critical care outreach – As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted; the outreach team offers support to ward staff to prevent this from happening.

Implantable cardioverter defibrillator
An implantable cardioverter defibrillator (ICD) is a battery-powered device that monitors electrical activity in the heart and when an arrhythmia is detected is able to deliver an electrical shock to terminate the abnormal rhythm. ICDs are used to prevent sudden cardiac death (SCD) in those that have survived a prior episode of sudden cardiac arrest (SCA) due to ventricular fibrillation or ventricular tachycardia (secondary prevention). ICDs are also used prophylactically to prevent sudden cardiac death in certain high risk patient populations (primary prevention).Numerous studies have been conducted on the use of ICDs for the secondary prevention of SCD. These studies have shown improved survival with ICDs compared to the use of anti-arrhythmic drugs. ICD therapy is associated with a 50% relative risk reduction in death caused by an arrhythmia and a 25% relative risk reduction in all cause mortality.Primary prevention of SCD with ICD therapy for high-risk patient populations has similarly shown improved survival rates in a number of large studies. The high-risk patient populations in these studies were defined as those with severe ischemic cardiomyopathy (determined by a reduced left ventricular ejection fraction (LVEF)). The LVEF criteria used in these trials ranged from less than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT.

Management
Sudden cardiac arrest may be treated via attempts at resuscitation. This is usually carried out based upon basic life support, advanced cardiac life support (ACLS), pediatric advanced life support (PALS), or neonatal resuscitation program (NRP) guidelines.

Cardiopulmonary resuscitation
Early cardiopulmonary resuscitation (CPR) is essential to surviving cardiac arrest with good neurological function. It is recommended that it be started as soon as possible with minimal interruptions once begun. The components of CPR that make the greatest difference in survival are chest compressions and defibrillating shockable rhythms. After defibrillation, chest compressions should be continued for two minutes before a rhythm check is again done. This is based on a compression rate of 100-120 compressions per minute, a compression depth of 5–6 centimeters into the chest, full chest recoil, and a ventilation rate of 10 breath ventilations per minute. Correctly performed bystander CPR has been shown to increase survival; however, it is performed in less than 30% of out of hospital arrests as of 2007. If high-quality CPR has not resulted in return of spontaneous circulation and the persons heart rhythm is in asystole, discontinuing CPR and pronouncing the persons death is reasonable after 20 minutes. Exceptions to this include certain cases with hypothermia or who have drowned. Some of these cases should have longer and more sustained CPR until they are nearly normothermic. Longer durations of CPR may be reasonable in those who have cardiac arrest while in hospital. Bystander CPR, by the lay public, before the arrival of EMS also improves outcomes.Either a bag valve mask or an advanced airway may be used to help with breathing particularly since vomiting and regurgitation are common, particularly in out-of-hospital cardiac arrest (OHCA). If this occurs, then modification to existing oropharyngeal suction may be required, such as the use of Suction Assisted Laryngoscopy Airway Decontamination. High levels of oxygen are generally given during CPR. Tracheal intubation has not been found to improve survival rates or neurological outcome in cardiac arrest and in the prehospital environment may worsen it. Endotracheal tube and supraglottic airways appear equally useful. When done by EMS 30 compressions followed by two breaths appear better than continuous chest compressions and breaths being given while compressions are ongoing.For bystanders, CPR which involves only chest compressions results in better outcomes as compared to standard CPR for those who have gone into cardiac arrest due to heart issues. Mouth-to-mouth as a means of providing respirations to the patient has been phased out due to the risk of contracting infectious diseases from the patient. Mechanical chest compressions (as performed by a machine) are no better than chest compressions performed by hand. It is unclear if a few minutes of CPR before defibrillation results in different outcomes than immediate defibrillation. If cardiac arrest occurs after 20 weeks of pregnancy someone should pull or push the uterus to the left during CPR. If a pulse has not returned by four minutes emergency Cesarean section is recommended.

Defibrillation
Defibrillation is indicated if an electric-shockable heart rhythm is present. The two shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia. In children 2 to 4 J/Kg is recommended.The defibrillation is made by an automated external defibrillator (AED), a portable machine that can be used even by any user because it produces voice instructions that guide the process, automatically checks the victims condition, and applies the correct electric shocks. Some defibrillators even provide feedback on the quality of CPR compressions, encouraging the lay rescuer to press the persons chest hard enough to circulate blood.In addition, there is increasing use of public access defibrillation. This involves placing an automated external defibrillator in public places, and training staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services and has been shown to lead to increased chances of survival. It has been shown that those who have arrests in remote locations have worse outcomes following cardiac arrest.

Medications
As of 2016, medications other than epinephrine (adrenaline), while included in guidelines, have not been shown to improve survival to hospital discharge following out-of-hospital cardiac arrest. This includes the use of atropine, lidocaine, and amiodarone. Epinephrine in adults, as of 2019, appears to improve survival but does not appear to improve neurologically normal survival. It is generally recommended every five minutes. Epinephrine acts on the alpha-1 receptor, which in turn increases the blood flow that supplies the heart. This would assist with providing more oxygen to the heart. Based on 2019 guidelines, 1 mg of epinephrine may be administered to patients every 3–5 minutes, but doses higher than 1 mg epinephrine are not recommended for routine use in cardiac arrest. If the patient has a non-shockable rhythm, the epinephrine should be administered as soon as possible. For a shockable rhythm, epinephrine should only be administered after initial defibrillation attempts have failed. Vasopressin overall does not improve or worsen outcomes compared to epinephrine. The combination of epinephrine, vasopressin, and methylprednisolone appears to improve outcomes. Some of the lack of long-term benefit may be related to delays in epinephrine use. While evidence does not support its use in children, guidelines state its use is reasonable. Lidocaine and amiodarone are also deemed reasonable in children with cardiac arrest who have a shockable rhythm. The general use of sodium bicarbonate or calcium is not recommended. The use of calcium in children has been associated with poor neurological function as well as decreased survival. Correct dosing of medications in children is dependent on weight. To minimize time spent calculating medication doses, the use of a Broselow tape is recommended.The 2010 guidelines from the American Heart Association no longer contain the recommendation for using atropine in pulseless electrical activity and asystole for want of evidence for its use. Neither lidocaine nor amiodarone, in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation, improves survival to hospital discharge but both equally improve survival to hospital admission.Thrombolytics when used generally may cause harm but may be of benefit in those with a confirmed pulmonary embolism as the cause of arrest. Evidence for use of naloxone in those with cardiac arrest due to opioids is unclear but it may still be used. In those with cardiac arrest due to local anesthetic, lipid emulsion may be used.

Targeted temperature management
Current international guidelines suggest cooling adults after cardiac arrest using targeted temperature management (TTM), which was previously known as therapeutic hypothermia. People are typically cooled for a 24-hour period, with a target temperature of 32–36 °C (90–97 °F).  There are a number of methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body, or infusing cold saline. This is followed by gradual rewarming over the next 12 to 24 hrs.Effectiveness of TTM after out-of-hospital cardiac arrest is an area of ongoing study. Pre-hospital TTM after out-of-hospital cardiac arrest has been shown to increase the risk of adverse outcomes. The rates of re-arrest may be higher in people who were treated with pre-hospital TTM, however, more research is needed on the effectiveness and risks of TTM. TTM in post-arrest care has not been found to improve mortality or neurological outcomes. Moreover, TTM may have adverse neurological effects in people who survive post cardiac arrest.

Do not resuscitate
Some people choose to avoid aggressive measures at the end of life. A do not resuscitate order (DNR) in the form of an advance health care directive makes it clear that in the event of cardiac arrest, the person does not wish to receive cardiopulmonary resuscitation. Other directives may be made to stipulate the desire for intubation in the event of respiratory failure or, if comfort measures are all that are desired, by stipulating that healthcare providers should "allow natural death".

Chain of survival
Several organizations promote the idea of a chain of survival.  The chain consists of the following "links":

Early recognition If possible, recognition of illness before the person develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival for every minute a patient stays in cardiac arrest, their chances of survival drop by roughly 10%.
Early CPR improves the flow of blood and of oxygen to vital organs, an essential component of treating a cardiac arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
Early defibrillation is effective for the management of ventricular fibrillation and pulseless ventricular tachycardia
Early advanced care
Early post-resuscitation care which may include percutaneous coronary interventionIf one or more links in the chain are missing or delayed, then the chances of survival drop significantly.
These protocols are often initiated by a code blue, which usually denotes impending or acute onset of cardiac arrest or respiratory failure, although in practice, code blue is often called in less life-threatening situations that require immediate attention from a physician.

Other
Resuscitation with extracorporeal membrane oxygenation devices has been attempted with better results for in-hospital cardiac arrest (29% survival) than out-of-hospital cardiac arrest (4% survival) in populations selected to benefit most. Cardiac catheterization in those who have survived an out-of-hospital cardiac arrest appears to improve outcomes although high quality evidence is lacking. It is recommended that it is done as soon as possible in those who have had a cardiac arrest with ST elevation due to underlying heart problems.The precordial thump may be considered in those with witnessed, monitored, unstable ventricular tachycardia (including pulseless VT) if a defibrillator is not immediately ready for use, but it should not delay CPR and shock delivery or be used in those with unwitnessed out of hospital arrest.

Prognosis
The overall chance of survival among those who have cardiac arrest outside hospital is poor, at 10%. Among those who have an out-of-hospital cardiac arrest, 70% occur at home and their survival rate is 6%. For those who have an in-hospital cardiac arrest, the survival rate one year from at least the occurrence of cardiac arrest is estimated to be 13%. One year survival is estimated to be higher in people with cardiac admission diagnoses (39%), when compared to those with non-cardiac admission diagnoses (11%). Among children rates of survival are 3 to 16% in North America. For in hospital cardiac arrest survival to discharge is around 22%. Those who survive to Return-of-Spontaneous-Circulation (ROSC) and hospital admission frequently present with Post-Cardiac Arrest Syndrome which usually presents with neurological injury that can range from mild memory problems to coma.Hypoxic ischemic brain injury is the most detrimental outcome for people suffering a cardiac arrest. Poor neurological outcomes following cardiac arrest are much more prevalent in countries that do not use withdrawal of life support (~50%) as compared to those that do (less than 10%). Most improvements in cognition occur during the first three months following cardiac arrest, with some individuals reporting improvement up to one-year post cardiac arrest. 50 – 70% of cardiac arrest survivors report fatigue as a symptom, making fatigue the most prevalent patient-reported symptom.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 to 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.The global rate of people who were able to recover from out-of-hospital cardiac arrest after receiving CPR has been found to be approximately 30%, and the rate of survival to discharge from the hospital has been estimated at 9%. Survival to discharge from the hospital is more likely among people whose cardiac arrest was witnessed by a bystander or emergency medical services, who received bystander CPR and among those living in Europe and North America. Relatively lower survival to hospital discharge rates have been observed in Asian countries.

Epidemiology
The risk of cardiac arrest varies with geographical region, age, and gender. The lifetime risk is three times greater in men (12.3%) than women (4.2%) based on analysis of the Framingham Heart Study.  However this gender difference disappeared beyond 85 years of age. Around half of these individuals are younger than 65 years of age.

North America
Based on death certificates, sudden cardiac death accounts for about 20% of all deaths in the United States. In the United States, approximately 326,000 cases of out-of-hospital and 209,000 cases of in-hospital cardiac arrest occur among adults a year, which works out to be an incidence of approximately 110.8 per 100,000 adults a year. In the United States, during-pregnancy cardiac arrest occurs in about one in twelve-thousand deliveries or 1.8 per 10,000 live births. Rates are lower in Canada.

Other regions
Non-Western regions of the world have differing incidences </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Intravascular hemolysis and can you explain it in depth? [/INST] Intravascular hemolysis describes hemolysis that happens mainly inside the vasculature. As a result, the contents of the red blood cell are released into the general circulation, leading to hemoglobinemia and increasing the risk of ensuing hyperbilirubinemia.

Mechanism
Intravascular hemolysis is the state when the red blood cell ruptures as a result of the complex of complement autoantibodies attached (fixed) on the surfaces of RBCs attack and rupture RBCs membranes, or a parasite such as Babesia exits the cell that ruptures the RBCs membrane as it goes.Upon RBCs rupture, components of which are released and circulating in the blood plasma.These components comprise hemoglobin and others. At this stage, the hemoglobin is called free hemoglobin. Free hemoglobin (also called naked hemoglobin) is the un-bound hemoglobin that is not enclosed in the red blood cell. The naked hemoglobin is devoid of its anti-oxidant sentries that are normally available within the RBC. Free hemoglobin is thus vulnerable to be oxidized.When the serum concentration of free hemoglobin is within the physiologic range of haptoglobin, the potential deleterious effects of free hemoglobin are prevented because haptoglobin will bind to "free hemoglobin" forming a complex of "free hemoglobin-haptoglobin" evidenced by reduced amount of haptoglobin. However, during hyper-hemolytic conditions or with chronic hemolysis, haptoglobin is depleted so the remaining free hemoglobin readily distribute to tissues where it might be exposed to oxidative conditions, thus some of the ferrous heme (FeII), the oxygen-binding component of hemoglobin, of the free hemoglobin are oxidized and becoming met-hemoglobin (ferric hemoglobin). In such conditions, heme along with globin chains can be released from further oxidization of met-hemoglobin (ferric Hb). In which, the free heme can then accelerate tissue damage by promoting peroxidative reactions and activation of inflammatory cascades. At this time, hemopexin, another plasma glycoprotein come to bind with heme with its privilege of high heme affinity, forming a complex of heme-hemopexin, which is non-toxic, and travel together to a receptor on hepatocytes and macrophages within the spleen, liver and bone marrow </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fibrosing colonopathy and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Peliosis hepatis and can you explain it in depth? [/INST] Peliosis hepatis is an uncommon vascular condition characterised by multiple, randomly distributed, blood-filled cavities throughout the liver. The size of the cavities usually ranges between a few millimetres and 3 cm in diameter. In the past, it was a mere histological curiosity  occasionally found at autopsies, but has been increasingly recognised with wide-ranging conditions from AIDS to the use of anabolic steroids </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Dysuria and can you explain it in depth? [/INST] Dysuria refers to painful or uncomfortable urination.It is one of a constellation of irritative bladder symptoms (also sometimes referred to as lower urinary tract symptoms), which includes nocturia and urinary frequency.

Diagnosis
The clinician should also look for physical findings of fever, rash, direct tenderness over the bladder area, and joint pain. Physical findings of increased temperature, increased pulse, low blood pressure in the presence of dysuria can indicate systemic infection. Urological obstruction due to stone or tumor can result in findings of hematuria, decreased urination, and bladder spasms. All these physical findings should be looked for carefully while obtaining history. History regarding recent sexual activity is crucial.Urinalysis is the most useful test to start the work up in a patient of dysuria. Urinalysis positive for nitrite carries a high predictive value of a positive urine culture </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Apnea and can you explain it in depth? [/INST] Apnea (BrE: apnoea) is the temporal cessation of breathing. During apnea, there is no movement of the muscles of inhalation, and the volume of the lungs initially remains unchanged. Depending on how blocked the airways are (patency), there may or may not be a flow of gas between the lungs and the environment, but if theres sufficient flow, gas exchange within the lungs and cellular respiration wouldnt be severely affected. Voluntarily doing this is called holding ones breath.
Apnea may first be diagnosed in childhood, and it is recommended to consult an ENT specialist, allergist or sleep physician to discuss symptoms when noticed; malformation and/or malfunctioning of the upper airways may be observed by an orthodontist.

Cause
Apnea can be involuntary—for example, drug-induced (such as by opiate toxicity), mechanically / physiologically induced (for example, by strangulation or choking), or a consequence of neurological disease or trauma. During sleep, people with severe sleep apnea can have over thirty episodes of intermittent apnea per hour every night.Apnea can also be observed during periods of heightened emotion, such as during crying or accompanied by the Valsalva maneuver when a person laughs. Apnea is a common feature of sobbing while crying, characterised by slow but deep and erratic breathing followed by brief periods of breath holding when crying.
Another example of apnea are breath-holding spells; these are sometimes emotional in cause and are usually observed in children as a result of frustration, emotional stress and other psychological extremes.
Voluntary apnea can be achieved by closing the vocal cords, simultaneously keeping the mouth closed and blocking the nasal vestibule, or constantly activating expiratory muscles, not allowing any inspiration.

Complications
Under normal conditions, humans cannot store much oxygen in the body. Prolonged apnea leads to severe lack of oxygen in the blood circulation, leading to dysfunction of organ systems. Permanent brain damage can occur after as little as three minutes and death will inevitably ensue after a few more minutes unless ventilation is restored. However, under special circumstances such as hypothermia, hyperbaric oxygenation, apneic oxygenation (see below), or extracorporeal membrane oxygenation, much longer periods of apnea may be tolerated without severe detrimental consequences.
Untrained humans usually cannot sustain voluntary apnea for more than one or two minutes, since the urge to breathe becomes unbearable. The reason for the time limit of voluntary apnea is that the rate of breathing and the volume of each breath are tightly regulated to maintain constant values of CO2 tension and pH of the blood more than oxygen levels. In apnea, CO2 is not removed through the lungs and accumulates in the blood. The consequent rise in CO2 tension and drop in pH result in stimulation of the respiratory centre in the brain which eventually cannot be overcome voluntarily. The accumulation of carbon dioxide in the lungs will eventually irritate and trigger impulses from the respiratory center part of the brain and the phrenic nerve. Rising levels of carbon dioxide signal the body to breathe and resume unconscious respiration forcibly. The lungs start to feel as if they are burning, and the signals the body receives from the brain when CO2 levels are too high include strong, painful, and involuntary contractions or spasms of the diaphragm and the muscles in between the ribs. At some point, the spasms become so frequent, intense and unbearable that continued holding of the breath is nearly impossible.When a person is immersed in water, physiological changes due to the mammalian diving reflex enable somewhat longer tolerance of apnea even in untrained persons as breathing isnt possible underwater. Tolerance can in addition be trained. The ancient technique of free-diving requires breath-holding, and world-class free-divers can hold their breath underwater up to depths of 214 metres (702 ft) and for more than four minutes. Apneists, in this context, are people who can hold their breath for a long time.

Hyperventilation
Voluntary hyperventilation before beginning voluntary apnea is commonly believed to allow the person involved to safely hold their breath for a longer period. In reality, it will give the impression that one does not need to breathe, while the body is actually experiencing a blood-oxygen level that would normally, and indirectly, invoke a strong dyspnea and eventually involuntary breathing. Some have incorrectly attributed the effect of hyperventilation to increased oxygen in the blood, not realizing that it is actually due to a decrease in CO2 in the blood and lungs. Blood leaving the lungs is normally fully saturated with oxygen, so hyperventilation of normal air cannot increase the amount of oxygen available, as oxygen in blood is the direct factor. Lowering the CO2 concentration increases the pH of the blood, thus increasing the time before blood becomes acidic enough so the respiratory center becomes stimulated, as described above. While hyperventilation will yield slightly longer breath-holding times, any small time increase is at the expense of possible hypoxia, though it might not be felt as easily. One using this method can suddenly lose consciousness unnoticed—a shallow water blackout—as a result. If a person loses consciousness underwater, there is considerable danger that they will drown. An alert diving partner or nearby lifeguard would be in the best position to rescue such a person. Static apnea blackout occurs at the surface when a motionless diver holds their breath long enough for the circulating oxygen in blood to fall below that required for the brain to maintain consciousness. It involves no pressure changes in the body and is usually performed to enhance breath-hold time. It should never be practiced alone, but under strict safety protocols with a safety guard or equipment beside the diver.

Apneic oxygenation
Because the exchange of gases between the blood and airspace of the lungs is independent of the movement of gas to and from the lungs, enough oxygen can be delivered to the circulation even if a person is apneic, even if the diaphragm doesnt move. With the onset of apnea, low pressure develops in the airspace of the lungs because more oxygen is absorbed than CO2 is released. With the airways closed or obstructed, this will lead to a gradual collapse of the lungs and suffocation. However, if the airways are open, any gas supplied to the upper airways will follow the pressure gradient and flow into the lungs to replace the oxygen consumed. If pure oxygen is supplied, this process will serve to replenish the oxygen stored in the lungs and resume sufficient ventilation. The uptake of oxygen into the blood will then remain at the usual level, and the normal functioning of the organs will not be affected. A detriment to this hyperoxygenation is the occurrence of nitrogen washout, which can lead to absorption atelectasis.However, no CO2 is removed during apnea. The partial pressure of CO2 in the airspace of the lungs will quickly equilibrate with that of the blood. As the blood is loaded with CO2 from the metabolism without a way to remove it, more and more CO2 will accumulate and eventually displace oxygen and other gases from the airspace. CO2 will also accumulate in the tissues of the body, resulting in respiratory acidosis.
Under ideal conditions (i.e., if pure oxygen is breathed before onset of apnea to remove all nitrogen from the lungs, and pure supplemental oxygen is insufflated), apneic oxygenation could theoretically be sufficient to provide enough oxygen for survival of more than one hours duration in a healthy adult. However, accumulation of carbon dioxide (described above) would remain the limiting factor.
Apneic oxygenation is more than a physiologic curiosity. It can be employed to provide a sufficient amount of oxygen in thoracic surgery when apnea cannot be avoided, and during manipulations of the airways such as bronchoscopy, intubation, and surgery of the upper airways. However, because of the limitations described above, apneic oxygenation is inferior to extracorporal circulation using a heart-lung machine and is therefore used only in emergencies, short procedures, or where extracorporal circulation cant be accessed. Use of PEEP valves is also an accepted alternative (5 cm H2O in average weight patients and 10 cm H2O significantly improved lung and chest wall compliance in morbidly obese patients).In 1959, Frumin described the use of apneic oxygenation during anesthesia and surgery. Of the eight test subjects in this landmark study, the highest recorded PaCO2 was 250 millimeters of mercury, and the lowest arterial pH was 6.72 after 53 minutes of apnea.

Apnea scientific studies
Studies found spleen volume is slightly reduced during short breath-hold apnea in healthy adults.

Apnea test in determining brain death
A recommended practice for the clinical diagnosis of brain death formulated by the American Academy of Neurology hinges on the conjunction of three diagnostic criteria: a coma, absence of brainstem reflexes, and apnea (defined as the inability of the patient to breathe unaided: that is, with no life support systems like ventilators) </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Coarse facial features and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Reflex bradycardia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Cyanosis and can you explain it in depth? [/INST] Cyanosis is the change of body tissue color to a bluish-purple hue as a result of having decreased amounts of oxygen bound to the hemoglobin in the red blood cells of the capillary bed. Body tissues that reflect cyanosis are usually in locations where the skin is thinner, including the mucous membranes, lips, nail beds, and ear lobes. Some medications containing amiodarone or silver, Mongolian spots, large birth marks, and the consumption of food products with blue or purple dyes can also result in the bluish skin tissue discoloration and may be mistaken for cyanosis.Cyanosis is further classified into central cyanosis vs. peripheral cyanosis.

Pathophysiology
The mechanism behind cyanosis is different depending on whether it is central or peripheral.

Central cyanosis
Central cyanosis is caused by a decrease in arterial oxygen saturation (SaO2) and begins to show once the concentration of deoxyhemoglobin in the blood reaches a concentration of ≥ 5.0 g/dL (≥ 3.1 mmol/L or oxygen saturation of ≤ 85 %). Causes of central cyanosis are discussed below.

Peripheral cyanosis
Peripheral cyanosis happens when there is increased concentration of deoxyhemoglobin on the venous side of the peripheral circulation. In other words, cyanosis is dependent on the concentration of deoxyhemoglobin. Patients with severe anemia may appear normal despite higher than normal concentrations of deoxyhemoglobin. On the other hand, patients with increased amounts of red blood cells (e.g. polycythemia vera) can appear cyanotic even with lower concentrations of deoxyhemoglobin.

Causes
Central cyanosis
Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor blood oxygenation in the lungs. It develops when arterial oxygen saturation drops below 85% or 75%.Acute cyanosis can be a result of asphyxiation or choking and is one of the definite signs that ventilation is being blocked.

Central cyanosis may be due to the following causes:

Central nervous system (impairing normal ventilation):Intracranial hemorrhage
Drug overdose (e.g. heroin)
Generalized tonic–clonic seizure (GTCS)
Respiratory system:Pneumonia
Bronchiolitis
Bronchospasm (e.g. asthma)
Pulmonary hypertension
Pulmonary embolism
Hypoventilation
Chronic obstructive pulmonary disease, or COPD (emphysema)
Cardiovascular system:Congenital heart disease (e.g. Tetralogy of Fallot, right to left shunts in heart or great vessels)
Heart failure
Valvular heart disease
Myocardial infarction
Hemoglobinopathies:Methemoglobinemia
Sulfhemoglobinemia
Polycythemia
Congenital cyanosis (HbM Boston) arises from a mutation in the α-codon which results in a change of primary sequence, H → Y. Tyrosine stabilises the Fe(III) form (oxyhaemoglobin) creating a permanent T-state of Hb.
Others:
High altitude, cyanosis may develop in ascents to altitudes >2400 m.
Hypothermia
Frostbite
Obstructive sleep apnea

Peripheral cyanosis
Peripheral cyanosis is the blue tint in fingers or extremities, due to an inadequate or obstructed circulation. The blood reaching the extremities is not oxygen-rich and when viewed through the skin a combination of factors can lead to the appearance of a blue color. All factors contributing to central cyanosis can also cause peripheral symptoms to appear but peripheral cyanosis can be observed in the absence of heart or lung failures. Small blood vessels may be restricted and can be treated by increasing the normal oxygenation level of the blood.

Peripheral cyanosis may be due to the following causes:
All common causes of central cyanosis
Reduced cardiac output (e.g. heart failure or hypovolemia)
Cold exposure
Chronic obstructive pulmonary disease (COPD)
Arterial obstruction (e.g. peripheral vascular disease, Raynaud phenomenon)
Venous obstruction (e.g. deep vein thrombosis)

Differential cyanosis
Differential cyanosis is the bluish coloration of the lower but not the upper extremity and the head. This is seen in patients with a patent ductus arteriosus. Patients with a large ductus develop progressive pulmonary vascular disease, and pressure overload of the right ventricle occurs. As soon as pulmonary pressure exceeds aortic pressure, shunt reversal (right-to-left shunt) occurs. The upper extremity remains pink because deoxygenated blood flows through the patent duct and directly into the descending aorta while sparing the brachiocephalic trunk, left common carotid, and left subclavian arteries.

Evaluation
A detailed history and physical examination (particularly focusing on the cardiopulmonary system) can guide further management and help determine the choice of testing to be performed. Tests that can be performed include pulse oximetry, arterial blood gas, complete blood count, methemoglobin level,  electrocardiogram, echocardiogram, X-Ray, CT scan, cardiac catheterization, and hemoglobin electrophoresis.
In newborns, peripheral cyanosis typically presents in the distal extremities, circumoral, and periorbital areas. Of note, mucous membranes remain pink in peripheral cyanosis as compared to central cyanosis where the mucous membranes are cyanotic.

It is important to note that skin pigmentation and hemoglobin concentration can affect the evaluation of cyanosis. Cyanosis may be more difficult to detect on people with darker skin pigmentation </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Eczema vaccinatum and can you explain it in depth? [/INST] Eczema vaccinatum is a rare severe adverse reaction to smallpox vaccination.
It is characterized by serious local or disseminated, umbilicated, vesicular, crusting skin rashes in the face, neck, chest, abdomen, upper limbs and hands, caused by widespread infection of the skin in people with previous diagnosed skin conditions such as eczema or atopic dermatitis, even if the conditions are not active at the time. Other signs and symptoms include fever and facial and supraglottic edema. The condition may be fatal if severe and left untreated </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hyperalgesia and can you explain it in depth? [/INST] Hyperalgesia ( or ; hyper from  Greek ὑπέρ (huper, “over”), -algesia from Greek  algos, ἄλγος (pain)) is an abnormally increased sensitivity to   pain, which may be caused by damage to nociceptors or peripheral nerves and can cause hypersensitivity to stimulus.
Prostaglandins E and F are largely responsible for sensitizing the nociceptors.  Temporary increased sensitivity to pain also occurs as part of sickness behavior, the evolved response to infection.

Types
Hyperalgesia can be experienced in focal, discrete areas, or as a more diffuse, body-wide form. Conditioning studies have established that it is possible to experience a learned hyperalgesia of the latter, diffuse form.
The focal form is typically associated with injury, and is divided into two subtypes:

Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues.
Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.Opioid-induced hyperalgesia may develop as a result of long-term opioid use in the treatment of chronic pain. Various studies of humans and animals have demonstrated that primary or secondary hyperalgesia can develop in response to both chronic and acute exposure to opioids. This side effect can be severe enough to warrant discontinuation of opioid treatment.

Causes
Hyperalgesia is induced by platelet-activating factor (PAF) which comes about in an inflammatory or an allergic response. This seems to occur via immune cells interacting with the peripheral nervous system and releasing pain-producing chemicals (cytokines and chemokines).One unusual cause of focal hyperalgesia is platypus venom.Long-term opioid (e.g. heroin, morphine) users and those on high-dose opioid medications for the treatment of chronic pain, may experience hyperalgesia and experience pain out of proportion to physical findings, which is a common cause for loss of efficacy of these medications over time </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Thoracic outlet syndrome and can you explain it in depth? [/INST] Thoracic outlet syndrome (TOS) is a condition in which there is compression of the nerves, arteries, or veins in the passageway from the lower neck to the armpit. There are three main types: neurogenic, venous, and arterial. The neurogenic type is the most common and presents with pain, weakness, paraesthesia, and occasionally loss of muscle at the base of the thumb. The venous type results in swelling, pain, and possibly a bluish coloration of the arm. The arterial type results in pain, coldness, and pallor of the arm.TOS may result from trauma, repetitive arm movements, tumors, pregnancy, or anatomical variations such as a cervical rib. The diagnosis may be supported by nerve conduction studies and medical imaging.  TOS is difficult to diagnose and there are many potential differential diagnoses as well as other diseases that are often co-occurrent with TOS.Initial treatment for the neurogenic type is with exercises to strengthen the chest muscles and improve posture. NSAIDs such as naproxen may be used for pain. Surgery is typically done for the arterial and venous types and for the neurogenic type if it does not improve with other treatments. Blood thinners may be used to treat or prevent blood clots. The condition affects about 1% of the population. It is more common in women than men and it occurs most commonly between 20 and 50 years of age. The condition was first described in 1818 and the current term "thoracic outlet syndrome" first used in 1956.

Signs and symptoms
TOS affects mainly the upper limbs, with signs and symptoms manifesting in the shoulders, neck, arms and hands. Pain can be present on an intermittent or permanent basis. It can be sharp/stabbing, burning, or aching. TOS can involve only part of the hand (as in the pinky and adjacent half of the ring finger), all of the hand, or the inner aspect of the forearm and upper arm. Pain can also be in the side of the neck, the pectoral area below the clavicle, the armpit/axillary area, and the upper back (i.e., the trapezius and rhomboid area). Discoloration of the hands, one hand colder than the other hand, weakness of the hand and arm muscles, and tingling are commonly present.Only 1% of people with carpal tunnel syndrome have concomitant TOS.Repetitive motions can cause enlargement of muscles which causes compression of veins. Besides, overuse injury of the upper limbs causes swellings, small bleeding, and subsequent fibrosis which would cause the thrombosis of the subclavian vein, leading to Paget–Schroetter disease or effort-induced thrombosis.TOS can be related to cerebrovascular arterial insufficiency when affecting the subclavian artery. It also can affect the vertebral artery, in which case it could produce vision disturbances, including transient blindness, and embolic cerebral infarction.TOS can also lead to eye problems and vision loss as a circumstance of vertebral artery compression. Although very rare, if compression of the brain stem is also involved in an individual presentation of TOS, transient blindness may occur while the head is held in certain positions.
If left untreated, TOS can lead to neurological deficits as a result of the hypoperfusion and hypometabolism of certain areas of the brain and cerebellum.TOS has similar symptoms to pectoralis minor syndrome (PMS), which usually results from compression of the braxial plexus beneath the pectoralis minor muscle (while neurogenic TOS is caused by compression of the same nerves above the clavicle). Unlike TOS there is typically few headaches or neck pain in patients with PMS only, instead with pain in the chest area. Initially, it was believed that 95 percent of patients with TOS had nerve compression in the scalene area, but in the twenty-first century it is now recognized that the majority have nerve compression under the pectoralis minor, either by itself or in addition to the scalene area. One study of 100 patients diagnosed with neurogenic TOS found that 75 percent had neurogenic PMS and 30 percent in fact had PMS without TOS.

Causes
TOS can be attributed to one or more of the following factors:
Congenital abnormalities are frequently found in persons with TOS. These include cervical rib, prolonged transverse process, and muscular abnormalities (e.g., in the scalenus anterior muscle, a sickle-shaped scalenus medius) or fibrous connective tissue anomalies.
Trauma (e.g., whiplash injuries) or repetitive strain is frequently implicated.
Rarer acquired causes include tumors (especially pancoast tumor), hyperostosis, and osteomyelitis

Diagnosis
Adsons sign and the costoclavicular maneuver lack specificity and sensitivity and should make up only a small part of the mandatory comprehensive history and physical examination undertaken with a patient suspected of having TOS. There is currently no single clinical sign that makes the diagnosis of TOS with any degree of certainty.Additional maneuvers that may be abnormal in TOS include Wrights Test, which involves hyperabducting the arms over the head with some extension and evaluating for loss of radial pulses or signs of blanching of the skin in the hands indicating a decrease in blood flow with the maneuver. The "compression test" is also used, exerting pressure between the clavicle and medial humeral head causes radiation of pain and/or numbness into the affected arm.Doppler arteriography, with probes at the fingertips and arms, tests the force and "smoothness" of the blood flow through the radial arteries, with and without having the patient perform various arm maneuvers (which causes compression of the subclavian artery at the thoracic outlet). The movements can elicit symptoms of pain and numbness and produce graphs with diminished arterial blood flow to the fingertips, providing strong evidence of impingement of the subclavian artery at the thoracic outlet. Doppler arteriography does not utilize probes at the fingertips and arms, and in this case is likely being confused with plethysmography, which is a different method that utilizes ultrasound without direct visualization of the affected vessels. Doppler ultrasound (not really arteriography) would not be used at the radial artery in order to make the diagnosis of TOS. Finally, even if a Doppler study of the appropriate artery were to be positive, it would not diagnose neurogenic TOS, by far the most common subtype of TOS. There is plenty of evidence in the medical literature to show that arterial compression does not equate to brachial plexus compression, although they may occur together, in varying degrees. Additionally, arterial compression by itself does not make the diagnosis of arterial TOS (the rarest form of TOS). Lesser degrees of arterial compression have been shown in normal individuals in various arm positions and are thought to be of little significance without the other criteria for arterial TOS.MRI scan can show the anatomy of the thoracic outlet, the soft tissues causing compression, and can show directly the brachial plexus compression.

Classification
By structures affected and symptomatology
There are three main types of TOS, named according to the cause of the symptoms; however, these three classifications have been coming into disfavor because TOS can involve all three types of compression to various degrees. The compression can occur in three anatomical structures (arteries, veins and nerves), it can be isolated, or, more commonly, two or three of the structures are compressed to greater or lesser degrees. In addition, the compressive forces can be of different magnitude in each affected structure. Therefore, symptoms can be variable.
Neurogenic TOS includes disorders produced by compression of components of the brachial plexus nerves. The neurogenic form of TOS accounts for 95% of all cases of TOS.
Arterial TOS is due to compression of the subclavian artery. This is less than one percent of cases.
Venous TOS is due to compression of the subclavian vein. This makes up about 4% of cases.

By event
There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast-paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving much lifting of the arms and repetitive use of the wrists and arms.
One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.The two groups of people most likely to develop TOS are those with neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments.

By structure causing constriction
It is also possible to classify TOS by the location of the obstruction:
Anterior scalene syndrome (compression on brachial plexus and/or subclavian artery caused by muscle growth).
Cervical rib syndrome (compression on brachial plexus and/or subclavian artery caused by bone growth).
Costoclavicular syndrome (narrowing between the clavicle and the first rib) – diagnosed with the costoclavicular maneuver.Some people are born with an extra incomplete and very small rib above their first rib, which protrudes out into the superior thoracic outlet space. This rudimentary rib causes fibrous changes around the brachial plexus nerves, inducing compression and causing the symptoms and signs of TOS. This is called a "cervical rib" because of its attachment to C-7 (the seventh cervical vertebra), and its surgical removal is almost always recommended. The symptoms of TOS can first appear in the early teen years as a child is becoming more athletic.

Treatment
Evidence for the treatment of thoracic outlet syndrome as of 2014 is poor.

Physical measures
Stretching, occupational and physical therapy are common non-invasive approaches used in the treatment of TOS. The goal of stretching is to relieve compression in the thoracic cavity, reduce blood vessel and nerve impingement, and realign the bones, muscles, ligaments, or tendons that are causing the problem.
One commonly prescribed set of stretches includes moving the shoulders anteriorly (forward – called "hunching"), then back to a neutral position, then extending them posteriorly (backward, called "arching"), then back to neutral, followed by lifting the shoulders up as high as possible, and then back down to neutral, repeated in cycles as tolerated.
Another set of stretches involves tilting and extending the neck opposite to the side of the injury while keeping the injured arm down or wrapped around the back.
Occupational or Physical therapy can include passive or active range of motion exercises, working up to weighted or restricted sets (as tolerated).TOS is rapidly aggravated by poor posture. Active breathing exercises and ergonomic desk setup and motion practices can help maintain active posture. Often the muscles in the back become weak due to prolonged (years of) "hunching" and other poor postures.Ice can be used to decrease inflammation of sore or injured muscles. Heat can also aid in relieving sore muscles by improving blood circulation to them. While the whole arm generally feels painful in TOS, some relief can be seen when ice or heat is intermittently applied to the thoracic region (collar bone, armpit, or shoulder blades).

Medications
In a review, botox was compared to a placebo injected into the scalene muscles. No effect in terms of pain relief or improved movement was noted. However, in a six-months follow-up, paresthesia (abnormal sensations such as in pins and needles) was seen to be significantly improved.

Surgery
Surgical approaches have also been used successfully in TOS. Microsurgery can be used approaching the area from above the collar bone (supraclavicular) followed by neurolysis of the brachial plexus, removal of the scalene muscle (scalenectomy), and the release of the underlying (subclavicular) blood vessels. This approach avoids the use of resection, and has been found to be an effective treatment. In cases where the first rib (or a fibrous band extending from the first rib) is compressing a vein, artery, or the nerve bundle, part of the first rib and any compressive fibrous tissue, can be removed in a first rib resection and thoracic outlet decompression surgical procedure; scalene muscles may also need to be removed (scalenectomy). This allows increased blood flow and the reduction of nerve compression. In some cases there may be a rudimentary rib or a cervical rib that can be causing the compression, which can be removed using the same technique.Physical therapy is often used before and after the operation to improve recovery time and outcomes </s>