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In medicine, ischemia (Greek ισχαιμία, isch- is restriction, hema or haema is blood) is a restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue.[1] It may also be spelled ischaemia or ischæmia.

Mechanism

Rather than in hypoxia, a more general term denoting a shortage of oxygen (usually a result of lack of oxygen in the air being breathed), ischemia is an absolute or relative shortage of the blood supply to an organ, i.e. a shortage of oxygen, glucose and other blood-borne fuels. A relative shortage means the mismatch of blood supply (oxygen/fuel delivery) and blood request for adequate metabolism of tissue. Ischemia results in tissue damage because of a lack of oxygen and nutrients. Ultimately, this can cause severe damage because of the potential for a build-up of metabolic wastes.

Ischemia can also be described as an inadequate flow of blood to a part of the body, caused by constriction or blockage of the blood vessels supplying it. Ischemia of heart muscle produces angina pectoris.

This can be due to

Consequences

Since oxygen is mainly bound to hemoglobin in red blood cells, insufficient blood supply causes tissue to become hypoxic, or, if no oxygen is supplied at all, anoxic. This can cause oncosis (i.e. cell death by lysis). In very aerobic tissues such as heart and brain, at body temperature necrosis due to ischemia usually takes about 3-4 hours before becoming irreversible. This and typically some collateral circulation to the ischemic area accounts for the efficacy of "clot-buster" drugs such as Alteplase, given for stroke and heart attack within this time period. However, complete cessation of oxygenation of such organs for more than 20 minutes typically results in irreversible damage.

Ischemia is a feature of heart diseases, transient ischemic attacks, cerebrovascular accidents, ruptured arteriovenous malformations, and peripheral artery occlusive disease. The heart, the kidneys, and the brain are among the organs that are the most sensitive to inadequate blood supply. Ischemia in brain tissue, for example due to stroke or head injury, causes a process called the ischemic cascade to be unleashed, in which proteolytic enzymes, reactive oxygen species, and other harmful chemicals damage and may ultimately kill brain tissue.

Restoration of blood flow after a period of ischemia can actually be more damaging than the ischemia. Reintroduction of oxygen causes a greater production of damaging free radicals, resulting in reperfusion injury. With reperfusion injury, necrosis can be greatly accelerated. Low doses of hydrogen sulfide (H2S) have been found to protect against regional myocardial ischemia–reperfusion injury.[2]

Variations

The mechanism of ischemia depends on the type. One important type is cardiac ischemia, another is bowel ischemia.

Cardiac ischemia

Cardiac ischemia may cause chest pain, known as angina pectoris

Detection

Initial evaluation of chest-pain patients involves a 12 lead electrocardiogram (ECG) and cardiac markers such as troponins. These tests are highly specific but very insensitive and often leave the requirement for further testing to achieve an accurate diagnosis. Magnetocardiography (MCG) imaging utilises superconducting quantum interference devices (SQUIDs) to detect the weak magnetic fields generated by the heart's electrical fields. There is a direct correlation between abnormal cardiac depolarisation or repolarisation and abnormality in the magnetic field map. In July 2004, the Food and Drug Administration (FDA) approved the CardioMag Imaging MCG as a safe device for the non-invasive detection of ischemia.

Bowel ischemia

An ischemia in the large bowel caused by an inflammation results in ischemic colitis. An ischemia in the small bowel, on the other hand, caused by an inflammation results in mesenteric ischemia.

Cutaneous ischemia

Reduced blood flow to the skin layers may result in mottling or uneven, patchy discoloration of the skin.

See also

References


Notes

  • Oxford Reference: Concise Medical Dictionary (1990, 3rd ed.). Oxford University Press: Market House Books.



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