Cyanosis in the context of Congenital heart defects

Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). For those who survive, a decreased quality of life is common.

Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide. Adult diagnosis is based on a PaO₂/FiO₂ ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H₂O. Cardiogenic pulmonary edema, as the cause, must be excluded.

A congenital heart defect (CHD), also known as a congenital heart anomaly, congenital cardiovascular malformation, and congenital heart disease, is a defect in the structure of the heart or great vessels that is present at birth. A congenital heart defect is classed as a cardiovascular disease. Signs and symptoms depend on the specific type of defect. Symptoms can vary from none to life-threatening. When present, symptoms are variable and may include rapid breathing, bluish skin (cyanosis), poor weight gain, and feeling tired. CHD does not cause chest pain. Most congenital heart defects are not associated with other diseases. A complication of CHD is heart failure. Due to recent advances in the management of patients with CHD, an increased number of patients may develop heart failure and might even require heart transplantation in future.

Congenital heart defects are the most common birth defect. In 2015, they were present in 48.9 million people globally. They affect between 4 and 75 per 1,000 live births, depending upon how they are diagnosed. In about 6 to 19 per 1,000 they cause a moderate to severe degree of problems. Congenital heart defects are the leading cause of birth defect-related deaths: in 2015, they resulted in 303,300 deaths, down from 366,000 deaths in 1990.The cause of a congenital heart defect is often unknown. Risk factors include certain infections during pregnancy such as rubella, use of certain medications or drugs such as alcohol or tobacco, parents being closely related, or poor nutritional status or obesity in the mother. Having a parent with a congenital heart defect is also a risk factor. A number of genetic conditions are associated with heart defects, including Down syndrome, Turner syndrome, and Marfan syndrome. Congenital heart defects are divided into two main groups: cyanotic heart defects and non-cyanotic heart defects, depending on whether the child has the potential to turn bluish in color. The defects may involve the interior walls of the heart, the heart valves, or the large blood vessels that lead to and from the heart.

Methemoglobinemia, or methaemoglobinaemia, is a condition of elevated methemoglobin in the blood. Symptoms may include headache, dizziness, shortness of breath, nausea, poor muscle coordination, and blue-colored skin (cyanosis). Complications may include seizures and heart arrhythmias.

Methemoglobinemia can be due to certain medications, chemicals, or food, or it can be inherited. Substances involved may include benzocaine, nitrites, or dapsone. The underlying mechanism involves some of the iron in hemoglobin being converted from the ferrous [Fe] to the ferric [Fe] form. The diagnosis is often suspected based on symptoms and a low blood oxygen that does not improve with oxygen therapy. Diagnosis is confirmed by a blood gas analysis.

Raynaud syndrome, also known as Raynaud's phenomenon, is a medical condition in which the spasm of small arteries causes episodes of reduced blood flow to end arterioles. Typically the fingers, and, less commonly, the toes, are involved. Rarely, the nose, ears, nipples, or lips are affected. The episodes classically result in the affected part turning white and then blue. Often, numbness or pain occurs. As blood flow returns, the area turns red and burns. The episodes typically last minutes but can last several hours. The condition is named after the physician Auguste Gabriel Maurice Raynaud, who first described it in his doctoral thesis in 1862.

Episodes are typically triggered by cold or emotional stress. Primary Raynaud's is idiopathic (spontaneous and of unknown cause) and not correlated with another disease. Secondary Raynaud's is diagnosed given the presence of an underlying condition and is associated with an older age of onset. In comparison to primary Raynaud's, episodes are more likely to be painful, asymmetric and progress to digital ulcerations. Secondary Raynaud's can occur due to a connective-tissue disorder such as scleroderma or lupus, injuries to the hands, prolonged vibration, smoking, thyroid problems, and certain medications, such as birth control pills and stimulants. Diagnosis is typically based on the symptoms.

Epiglottitis is the inflammation of the epiglottis—the flap at the base of the tongue that prevents food entering the trachea (windpipe). Symptoms are usually rapid in onset and include trouble swallowing which can result in drooling, changes to the voice, fever, and an increased breathing rate. As the epiglottis is in the upper airway, swelling can interfere with breathing. People may lean forward in an effort to open the airway. As the condition worsens, stridor and bluish skin may occur.

Epiglottitis was historically mostly caused by infection by H. influenzae type b (commonly referred to as "Hib"). Following the introduction of the Hib vaccine, pediatric cases of epiglottitis fell from 3.47 cases per 100,000 children in 1980 to 0.63 cases in 1990 such that it is now more often caused by other bacteria, most commonly Streptococcus pneumoniae, Streptococcus pyogenes, or Staphylococcus aureus. Predisposing factors include burns and trauma to the area. The most accurate way to make the diagnosis is to look directly at the epiglottis. X-rays of the neck from the side may show a "thumbprint sign" but the lack of this sign does not mean the condition is absent.

High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). HAPE is a severe presentation of altitude sickness. Cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in people who are at a higher risk or are more vulnerable to the effects of high altitude.

Classically, HAPE occurs in people normally living at low altitude who travel to an altitude above 2,500 meters (8,200 feet). Re-entry HAPE has been described in people who normally live at high altitude but who develop pulmonary edema after returning from a stay at low altitude. Symptoms include crackling sounds when breathing, dyspnea (at rest), and cyanosis. The primary treatment is descent to a lower altitude, with oxygen therapy and medication as alternatives. If HAPE is not treated, there is a 50% risk of mortality.

Chronic mountain sickness (CMS) is a disease in which the proportion of blood volume that is occupied by red blood cells increases (polycythaemia) and there is an abnormally low level of oxygen in the blood (hypoxemia). CMS typically develops after extended time living at high altitude (over 2,500 metres (8,200 ft)). It is most common amongst native populations of high altitude nations. The most frequent symptoms of CMS are headache, dizziness, tinnitus, breathlessness, palpitations, sleep disturbance, fatigue, loss of appetite, confusion, cyanosis, and dilation of veins.

CMS was first described in 1925 by Carlos Monge Medrano, a Peruvian doctor who specialised in diseases of high altitude. While acute mountain sickness is experienced shortly after ascent to high altitude, chronic mountain sickness may develop only after many years of living at high altitude. In medicine, high altitude is defined as over 2,500 metres (8,200 ft), but most cases of CMS occur at over 3,000 metres (9,800 ft).