A circulatory collapse is defined as a general or specific failure of the circulation, either cardiac or peripheral in nature. Although the mechanisms, causes and clinical syndromes are different, the pathogenesis is the same—the circulatory system fails to maintain the supply of oxygen and other nutrients to the tissues and to remove the carbon dioxide and other metabolites from them. The failure may be hypovolemic or distributive. A common cause of this could be shock or trauma from injury or surgery. Types
A general failure is one that occurs across a wide range of locations in the body, such as systemic shock after the loss of a large amount of blood collapsing all the circulatory systems in the legs. A specific failure can be traced to a particular point, such as a clot. Cardiac circulatory collapse affects the vessels of the heart such as the aorta and is almost always fatal. It is sometimes referred to as "acute" circulatory failure. Peripheral circulatory collapse involves outlying arteries and veins in the body and can result in gangrene, organ failure or other serious complications. This form is sometimes called peripheral vascular failure, shock or peripheral vascular shutdown. A milder or preliminary form of circulatory collapse is circulatory insufficiency. Causes
A very large range of medical conditions can cause circulatory collapse. These include, but are not limited to:
Hypovolemic shock
Trauma, especially those with massive hemorrhage
Surgery, particularly on patients who have lost blood
Hemorrhagic conditions, e.g. upper gastrointestinal bleeding (esophageal varices, Mallory–Weiss syndrome, aortoenteric fistula, etc.
Thyroid uptake measurements (I-123 or I-131), which are used to differentiate causes of hyperthyroidism, are generally unreliable in patients who have been taking amiodarone. Because of the high iodine content of amiodarone, the thyroid gland is effectively saturated, thus preventing further uptake of isotopes of iodine. However, a positive radioactive iodine can be used to rule in type 1AIT . Eye
Corneal micro-deposits (cornea verticillata, also called vortex or whorl keratopathy) are almost universally present (over 90%) in individuals taking amiodarone longer than 6 months, especially doses greater than 400 mg/day. These deposits typically do not cause any symptoms. About 1 in 10 individuals may complain of a bluish halo. Anterior subcapsular lens deposits are relatively common (50%) in higher doses (greater than 600 mg/day) after 6 months of treatment. Optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), occurs in 1–2% of people and is not dosage dependent. Bilateral optic disc swelling and mild and reversible visual field defects can also occur. Loss of eyelashes has been linked to amiodarone use. Liver
Abnormal liver enzyme results are common in people taking amiodarone. Much rarer are jaundice, hepatomegaly (liver enlargement), and hepatitis (inflammation of the liver).Low-dose amiodarone has been reported to cause pseudo-alcoholic cirrhosis. Skin
Long-term administration of amiodarone (usually more than eighteen months) is associated with a light-sensitive blue-grey discoloration of the skin, sometimes called ceruloderma; such patients should avoid exposure to the sun and use sunscreen that protects against ultraviolet-A  and -B.