Ischemia causes not only insufficiency of oxygen but also reduced availability ofnutrients and inadequate removal ofmetabolic wastes.[7] Ischemia can be partial (poorperfusion) or total blockage. The inadequate delivery of oxygenated blood to the organs must be resolved either by treating the cause of the inadequate delivery or reducing the oxygen demand of the system that needs it. For example, patients with myocardial ischemia have a decreased blood flow to the heart and are prescribed with medications that reducechronotropic andinotropic effect to meet the new level of blood delivery supplied by thestenosed vasculature so that it is adequate.
The signs and symptoms of ischemia vary, as they can occur anywhere in the body and depend on the degree to which blood flow is interrupted.[4] For example, clinical manifestations ofacute limb ischemia (which can be summarized as the"six P's") includepain,pallor,pulseless,paresthesia,paralysis, andpoikilothermia.[8]
Without immediate intervention, ischemia may progress quickly to tissuenecrosis andgangrene within a few hours.Paralysis is a very late sign of acute arterial ischemia and signals the death ofnerves supplying the extremity.Foot drop may occur as a result ofnerve damage. Because nerves are extremely sensitive tohypoxia, limbparalysis or ischemicneuropathy may persist afterrevascularization and may be permanent.[9]
Cardiac ischemia may be asymptomatic or may cause chest pain, known asangina pectoris. It occurs when the heart muscle, ormyocardium, receives insufficient blood flow.[10] This most frequently results fromatherosclerosis, which is the long-term accumulation of cholesterol-rich plaques in thecoronary arteries. In most Western countries,Ischemic heart disease is the most common cause of death in both men and women, and a major cause of hospital admissions.[11][12]
Brain ischemia is insufficient blood flow to thebrain, and can beacute orchronic. Acuteischemic stroke is a neurological emergency typically caused by a blood clot blocking blood flow in a vessel in the brain.[15] Chronic ischemia of the brain may result in a form ofdementia calledvascular dementia.[16] A sudden, brief episode (symptoms lasting only minutes) of ischemia affecting the brain is called atransient ischemic attack (TIA), often called a mini-stroke.[17] TIAs can be a warning of future strokes, with approximately 1/3 of TIA patients having a serious stroke within one year.[17][18]
Anemia vasoconstricts the periphery so that red blood cells cannot work internally on vital organs such as the heart, brain, etc., thus causing lack of oxygen to the periphery.
Premature discontinuation of any oral anticoagulant.
Unconsciousness, such as due to the ingestion of excessive doses ofcentral depressants likealcohol oropioids, can result in ischemia of the extremities due to unusual body positions that prevent normal circulation
Native records of contractile activity of the left ventricle of isolated rat heart perfused underLangendorff technique. Curve A - contractile function of the heart is greatly depressed after ischemia-reperfusion. Curve B - a set of short ischemic episodes (ischemic preconditioning) before prolonged ischemia provides functional recovery of contractile activity of the heart at reperfusion.
Restoration of blood supply to ischemic tissues can cause additional damage known asreperfusion injury that can be more damaging than the initial ischemia. Reintroduction of blood flow brings oxygen back to the tissues, causing a greater production offree radicals andreactive oxygen species that damage cells. It also brings more calcium ions to the tissues causing further calcium overloading and can result in potentially fatalcardiac arrhythmias and also accelerates cellularself-destruction. The restored blood flow also exaggerates theinflammation response of damaged tissues, causingwhite blood cells to destroy damaged cells that may otherwise still be viable.[27]
Early treatment is essential to keep the affected organ viable. The treatment options include injection of ananticoagulant,thrombolysis,embolectomy, surgical revascularization, or partial amputation. Anticoagulant therapy is initiated to prevent further enlargement of thethrombus. Continuous IVunfractionated heparin has been the traditional agent of choice.[9]
Directarteriotomy may be necessary to remove the clot. Surgicalrevascularization may be used in the setting of trauma (e.g., laceration of the artery).Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of furtherembolization from some persistent source, such as chronicatrial fibrillation, treatment includes long-term oralanticoagulation to prevent further acute arterial ischemic episodes.[9]
Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects ofhypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reducereperfusion injury.
Ischemic stroke is at times treated with various levels ofstatin therapy at hospital discharge, followed by home time, in an attempt to lower the risk of adverse events.[28][29]
^Merck & Co.Occlusive Peripheral Arterial Disease, The Merck Manual Home Health Handbook website, revised and updated March 2010. Retrieved March 4, 2012.
^Zhai Y, Petrowsky H, Hong JC, et al: Ischaemia-reperfusion injury in liver transplantation—From bench to bedside. Nat Rev Gastroenterol Hepatol 2013; 10:79–89
^Perico N, Cattaneo D, Sayegh MH, et al: Delayed graft function in kidney transplantation. Lancet 2004; 364:1814–1827
^Smith, David A.; Lilie, Craig J. (2021),"Acute Arterial Occlusion",StatPearls, Treasure Island (FL): StatPearls Publishing,PMID28722881, retrieved2021-10-27
^abcdefgLewis. S.L (2008).Medical-Surgical Nursing (7th ed.). Vascular disorder. pp. 907–908.
^World Health Organization Department of Health Statistics and Informatics in the Information, Evidence and Research Cluster (2004).The global burden of disease 2004 update. Geneva: WHO.ISBN92-4-156371-0.
