The thrombi may dislodge and may travel anywhere in the circulatory system, where they may lead to pulmonary embolus, an acute arterial occlusion causing the oxygen and blood supply distal to the embolus to decrease suddenly. The degree and extent of symptoms depend on the size and location of the obstruction, the occurrence of clot fragmentation with embolism to smaller vessels, and the degree of peripheral arterial disease (PAD).

- Thromboembolism (blood clots)

- Embolism (foreign bodies in the circulation, e.g. amniotic fluid embolism)

Traumatic injury to an extremity may produce partial or total occlusion of a vessel from compression, shearing or laceration. Acute arterial occlusion may develop as a result of arterial dissection in the carotid artery or aorta or as a result of iatrogenic arterial injury (e.g., after angiography).

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia. The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke. The AHA/ASA guidelines also provide information on how to prevent stroke if someone has more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.

The major cause of acute limb ischaemia is arterial thrombosis (85%), while embolic occlusion is responsible for 15% of cases. In rare instances, arterial aneurysm of the popliteal artery has been found to create a thrombosis or embolism resulting in ischaemia.

Risk factors contributing to PAD are the same as those for atherosclerosis:

- Smoking – tobacco use in any form is the single most important modifiable cause of PAD internationally. Smokers have up to a tenfold increase in relative risk for PAD in a dose-response relationship. Exposure to second-hand smoke from environmental exposure has also been shown to promote changes in blood vessel lining (endothelium) which is a precursor to atherosclerosis. Smokers are 2 to 3 times more likely to have lower extremity peripheral arterial disease than coronary artery disease. More than 80%-90% of patients with lower extremity peripheral arterial disease are current or former smokers. The risk of PAD increases with the number of cigarettes smoked per day and the number of years smoked.

- Diabetes mellitus – causes between two and four times increased risk of PAD by causing endothelial and smooth muscle cell dysfunction in peripheral arteries. The risk of developing lower extremity peripheral arterial disease is proportional to the severity and duration of diabetes.

- Dyslipidemia – a high level of low-density lipoprotein (LDL cholesterol) and a low level of high-density lipoprotein (HDL cholesterol) in the blood) - elevation of total cholesterol, LDL cholesterol, and triglyceride levels each have been correlated with accelerated PAD. Correction of dyslipidemia by diet and/or medication is associated with a major improvement in rates of heart attack and stroke.

- Hypertension – elevated blood pressure is correlated with an increase in the risk of developing PAD, as well as in associated coronary and cerebrovascular events (heart attack and stroke). Hypertension increased the risk of intermittent claudication 2.5- to 4-fold in men and women, respectively.

- Risk of PAD also increases in individuals who are over the age of 50, male, obese, heart attack, or stroke or with a family history of vascular disease.

- Other risk factors which are being studied include levels of various inflammatory mediators such as C-reactive protein, fibrinogen, hyperviscosity, hypercoagulable state.

Non-occlusive disease has a poor prognosis with survival rate between 40-50%.

The prognosis depends on prompt diagnosis (less than 12–24 hours and before gangrene) and the underlying cause:

- venous thrombosis: 32% mortality

- arterial embolism: 54% mortality

- arterial thrombosis: 77% mortality

- non-occlusive ischemia: 73% mortality.

In the case of prompt diagnosis and therapy, acute mesenteric ischemia can be reversible.

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

Whether a cerebral infarction is thrombotic or embolic based, its pathophysiology, or the observed conditions and underlying mechanisms of the disease. In thrombotic ischemic stroke, a thrombus forms and blocks blood flow. A thrombus forms when the endothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet plug. This platelet plug grows into a thrombus, resulting in a stenotic artery. Thrombotic ischemia can occur in large or small blood vessels. In large vessels, the most common causes of thrombi are atherosclerosis and vasoconstriction. In small vessels, the most common cause is lipohyalinosis. Lipohyalinosis is when high blood pressure and aging causes a build-up of fatty hyaline matter in blood vessels. Atheroma formation can also cause small vessel thrombotic ischemic stroke.

An embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). The embolus may be of cardiac origin due to Atrial fibrillation, Patent foramen ovale or from atherosclerotic plaque of another (or the same) large artery. Cerebral artery gas embolism (e.g. during ascent from a SCUBA dive) is also a possible cause of infarction (Levvett & Millar, 2008)

Peripheral arterial disease is more common in the following populations of people:

- All people who have leg symptoms with exertion (suggestive of claudication) or ischemic rest pain.

- All people aged 65 years and over regardless of risk factor status.

- All people between the age of 50 to 69 and who have a cardiovascular risk factor (particularly diabetes or smoking).

- Age less than 50 years, with diabetes and one other atherosclerosis risk factor (smoking, dyslipidemia, hypertension, or hyperhomocysteinemia).

- Individuals with an abnormal lower extremity pulse examination.

- Those with known atherosclerotic coronary, carotid, or renal artery disease.

- All people with a Framingham risk score 10%-20%

- All people who have previously experienced chest pain

Mesenteric ischemia is a medical condition in which injury of the small intestine occurs due to not enough blood supply. It can come on suddenly, known as acute mesenteric ischemia, or gradually, known as chronic mesenteric ischemia. Acute disease often presents with sudden severe pain. Symptoms may come on more slowly in those with acute on chronic disease. Signs and symptoms of chronic disease include abdominal pain after eating, unintentional weight loss, vomiting, and being afraid of eating.

Risk factors include atrial fibrillation, heart failure, chronic renal failure, being prone to forming blood clots, and previous myocardial infarction. There are four mechanisms by which poor blood flow occurs: a blood clot from elsewhere getting lodged in an artery, a new blood clot forming in an artery, a blood clot forming in the superior mesenteric vein, and insufficient blood flow due to low blood pressure or spasms of arteries. Chronic disease is a risk factor for acute disease. The best method of diagnosis is angiography, with computer tomography (CT) being used when that is not available.

Treatment of acute ischemia may include stenting or medications to break down the clot provided at the site of obstruction by interventional radiology. Open surgery may also be used to remove or bypass the obstruction and may be required to remove any intestines that may have died. If not rapidly treated outcomes are often poor. Among those affected even with treatment the risk of death is 70% to 90%. In those with chronic disease bypass surgery is the treatment of choice. Those who have thrombosis of the vein may be treated with anticoagulation such as heparin and warfarin, with surgery used if they do not improve.

Acute mesenteric ischemia affects about five per hundred thousand people per year in the developed world. Chronic mesenteric ischemia affects about one per hundred thousand people. Most people affected are over 60 years old. Rates are about equal in males and females of the same age. Mesenteric ischemia was first described in 1895.

When a limb is ischemic in the non-acute (chronic) setting, the condition is alternatively called peripheral artery disease or critical limb ischemia, rather than ALI. In addition to limb ischemia, other organs can become ischemic, causing:

- Renal ischemia (nephric ischemia)

- Mesenteric ischemia

- Cerebral ischemia

- Cardiac ischemia

CT angiography would be helpful in differentiating occlusive from non-occlusive causes of mesenteric ischaemia.

Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognised cause of stroke that preferentially affects the middle-aged.

The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.

Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. IgG4-related disease involving the carotid artery has also been observed as a cause.

However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.

Internal carotid artery dissection can also be associated with an elongated styloid process (known as Eagle syndrome when the elongated styloid process causes symptoms).

A study of aortic cross-clamping, a common procedure in cardiac surgery, demonstrated a strong potential benefit with further research ongoing.

An intriguing area of research demonstrates the ability of a reduction in body temperature to limit ischemic injuries. This procedure is called therapeutic hypothermia, and it has been shown by a number of large, high-quality randomised trials to significantly improve survival and reduce brain damage after birth asphyxia in newborn infants, almost doubling the chance of normal survival. For a full review see Hypothermia therapy for neonatal encephalopathy.

However, the therapeutic effect of hypothermia does not confine itself to metabolism and membrane stability. Another school of thought focuses on hypothermia’s ability to prevent the injuries that occur after circulation returns to the brain, or what is termed injuries. In fact an individual suffering from an ischemic insult continues suffering injuries well after circulation is restored. In rats it has been shown that neurons often die a full 24 hours after blood flow returns. Some theorize that this delayed reaction derives from the various inflammatory immune responses that occur during reperfusion. These inflammatory responses cause intracranial pressure, pressure which leads to cell injury and in some situations cell death. Hypothermia has been shown to help moderate intracranial pressure and therefore to minimize the harmful effect of a patient’s inflammatory immune responses during reperfusion. Beyond this, reperfusion also increases free radical production. Hypothermia too has been shown to minimize a patient’s production of deadly free radicals during reperfusion. Many now suspect it is because hypothermia reduces both intracranial pressure and free radical production that hypothermia improves patient outcome following a blockage of blood flow to the brain.

Thrombosis prevention is initiated with assessing the risk for its development. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. Some of these risk factors are related to inflammation. "Virchow's triad" has been suggested to describe the three factors necessary for the formation of thrombosis: stasis of blood, vessel wall injury, and altered blood coagulation. Some risk factors predispose for venous thrombosis while others increase the risk of arterial thrombosis.

The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow.

Trauma to the lung can also cause an air embolism. This may happen after a patient is placed on a ventilator and air is forced into an injured vein or artery, causing sudden death. Breath-holding while ascending from scuba diving may also force lung air into pulmonary arteries or veins in a similar manner, due to the pressure difference.

Functional hyperaemia is an increase in blood flow to a tissue due to the presence of metabolites and a change in general conditions. When a tissue increases activity there is a well-characterized fall in the partial pressure of oxygen and pH, an increase in partial pressure of carbon dioxide, and a rise in temperature and the concentration of potassium ions. The mechanisms of vasodilation are predominantly local metabolites and myogenic effects. Increased metabolic activity of the tissue leads to a local increase in the extracellular concentration of such chemicals as adenosine, carbon dioxide, and lactic acid, and a decrease in oxygen and pH. These changes cause significant vasodilation. The reverse occurs when metabolic activity is slowed and these substances wash out of the tissues. The myogenic effect refers to the inherent attempt of vascular smooth muscle surrounding arterioles and arteries to maintain the tension in the wall of these blood vessels by dilating when internal pressure is reduced and to constrict when wall tension increases.

Hyperaemia, hyperæmia, or hyperemia (Greek ὑπέρ (hupér, "over") + αἷμα (haîma, “blood”)) is the increase of blood flow to different tissues in the body. It can have medical implications but is also a regulatory response, allowing change in blood supply to different tissues through vasodilation. Clinically, hyperaemia in tissues manifest as erythema (redness of the skin) because of the engorgement of vessels with oxygenated blood. Hyperaemia can also occur due to a fall in atmospheric pressure outside the body.

Air can be injected directly into a vein or artery accidentally during clinical procedures. Misuse of a syringe to meticulously remove air from the vascular tubing of a hemodialysis circuit can allow air into the vascular system. Venous air embolism is a rare complication of diagnostic and therapeutic procedures requiring catheterization of a vein or artery. If a significant embolism occurs, the cardiovascular, pulmonary, or central nervous system may be affected. Interventions to remove or mitigate the embolism may include procedures to reduce bubble size, or withdrawal of air from the right atrium.

Cavernous sinus thrombosis has a mortality rate of less than 20% in areas with access to antibiotics. Before antibiotics were available, the mortality was 80–100%. Morbidity rates also dropped from 70% to 22% due to earlier diagnosis and treatment.

Renal ischemia also known as"nephric ischaemia", is the deficiency of blood in one or both kidneys or nephrons, usually due to functional constriction or actual obstruction of a blood vessel.

Cavernous sinus thrombosis (CST) is the formation of a blood clot within the cavernous sinus, a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. The cause is usually from a spreading infection in the nose, sinuses, ears, or teeth. "Staphylococcus aureus" and "Streptococcus" are often the associated bacteria. Cavernous sinus thrombosis symptoms include: decrease or loss of vision, chemosis, exophthalmos (bulging eyes), headaches, and paralysis of the cranial nerves which course through the cavernous sinus. This infection is life-threatening and requires immediate treatment, which usually includes antibiotics and sometimes surgical drainage.