Blood squirt (blood spurt, blood spray, blood gush, or blood jet) is the effect when an artery, a blood vessel in the human body (or other organism's body) is cut. Blood pressure causes the blood to bleed out at a rapid, intermittent rate, in a spray or jet, coinciding with the beating of the heart, rather than the slower, but steady flow of venous bleeding. Also known as arterial bleeding, arterial spurting, or arterial gushing, the amount of blood loss can be copious, occur very rapidly, and can lead to death.

In cut carotid arteries with 100 mL of blood through the heart at each beat (at 65 beats a minute), a completely severed artery will spurt blood for about 30 seconds and the blood will not spurt much higher than the human head. If the artery is just nicked, on the other hand, the blood will spurt longer but will be coming out under pressure and spraying much further.

To prevent hand ischemia, there is a "squirt test" that involves squirting blood from the radial artery, which is used in intraoperative assessment of collateral arm blood flow before radial artery harvest.

In 1933, a murder trial prompted a testimony from Dr. Clement Harrisse Arnold about how far blood could spurt from the neck: 6 inches (ca. 15 cm) vertically and 18 inches (ca. 46 cm) laterally.

Effect on the body is weakness and mild to moderate dehydration from the severe anxiety and both blood and sweat loss.

The condition is very rare but there are reports in medical literature of successful treatment with beta blockers (propranolol 10 mg) with significant reduction in the frequency of spontaneous blood oozing. The successful use of beta blockers supports the theory that the condition is induced by stress and anxiety yet this etiology is not established yet as the high prevalence of stress and anxiety in the modern era did not change the incidence of this extremely rare disease, suggesting that other co-abnormality also play a key role in this disease. Atropine sulfate transdermal patches have also been used successfully.

Favorable results with psychiatric counselling to reduce stress highlight the relationship between psychogenic causes and hematohidrosis.

Hematidrosis is a condition in which capillary blood vessels that feed the sweat glands rupture, causing them to exude blood, occurring under conditions of extreme physical or emotional stress. Severe mental anxiety activates the sympathetic nervous system to invoke the stress-fight or flight reaction to such a degree as to cause hemorrhage of the vessels supplying the sweat glands into the ducts of the sweat glands. It has been suggested that acute fear and extreme stress can cause hematidrosis.

Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply. This intervention can be life-saving.

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can; however, blood substitutes are being developed which can. Infusion of colloid or crystalloid IV fluids will also dilute clotting factors within the blood, increasing the risk of bleeding. It is current best practice to allow permissive hypotension in patients suffering from hypovolemic shock, both to ensure clotting factors are not overly diluted and also to stop blood pressure being artificially raised to a point where it "blows off" clots that have formed.

Hypovolemia is a state of decreased blood volume; more specifically, decrease in volume of blood plasma. It is thus the intravascular component of volume contraction (or loss of blood volume due to things such as bleeding or dehydration), but, as it also is the most essential one, "hypovolemia" and volume contraction are sometimes used synonymously.

Hypovolemia is characterized by sodium depletion (salt depletion) and thus differs from dehydration, which is defined as excessive loss of body water.

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas. Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe. It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.

White coat hypertension, more commonly known as white coat syndrome, is a phenomenon in which patients exhibit a blood pressure level above the normal range, in a clinical setting, though they don't exhibit it in other settings. It is believed that the phenomenon is due to anxiety that those afflicted experience during a clinic visit.

The patient's daytime ambulatory blood pressure is used as a reference as it takes into account ordinary levels of daily stress. Many problems have been incurred in the diagnosis and treatment of white coat hypertension.

The term "masked hypertension" can be used to describe the contrasting phenomenon, where a patient's blood pressure is above the normal range during daily living, although it isn't above the normal range when the patient is in a clinic setting.

Circulatory shock, commonly known as shock, is a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function. The typical signs of shock are low blood pressure, rapid heart rate, signs of poor end-organ perfusion (i.e., low urine output, confusion, or loss of consciousness), and weak pulses.

The shock index (SI), defined as heart rate divided by systolic blood pressure, is an accurate diagnostic measure that is more useful than hypotension and tachycardia in isolation. Under normal conditions, a number between 0.5 and 0.8 is typically seen. Should that number increase, so does suspicion of an underlying state of shock. Blood pressure alone may not be a reliable sign for shock, as there are times when a person is in circulatory shock but has a stable blood pressure.

Circulatory shock is not related to the emotional state of shock. Circulatory shock is a life-threatening medical emergency and one of the most common causes of death for critically ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac and/or respiratory arrest.

One of the key dangers of shock is that it progresses by a positive feedback mechanism. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. This is normally very useful to match up blood supply level with tissue demand for nutrients. However, if enough tissue causes this, it will deprive vital nutrients from other parts of the body. Additionally, the ability of the circulatory system to meet this increase in demand causes saturation, and this is a major result, of which other parts of the body begin to respond in a similar way; thus, exacerbating the problem. Due to this chain of events, immediate treatment of shock is critical for survival.

Medium-term (and less well-demonstrated) treatments of hypotension include:

- Blood sugar control (80–150 by one study)

- Early nutrition (by mouth or by tube to prevent ileus)

- Steroid support

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. A morning dose of caffeine can also be effective. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs increases venous return, thus making more blood available to critical organs in the chest and head. The Trendelenburg position, though used historically, is no longer recommended.

Hypotensive shock treatment always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed that hypotension is corrected. Still-debated methods are in parentheses, as are benchmarks for evaluating progress in correcting hypotension. A study on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

Orthostatic hypotension may cause accidental falls. It is also linked to an increased risk of cardiovascular disease, heart failure, and stroke. There is also observational data suggesting that orthostatic hypotension in middle age increases the risk of eventual dementia and reduced cognitive function.

In general, individuals with white coat hypertension have lower morbidity than patients with sustained hypertension, but higher morbidity than the clinically normotensive.

However, it should be remembered that all the established published trials on the consequences of high blood pressure and the benefits of treating are based on one-time measurement in clinical settings rather than the generally slightly lower readings obtained from ambulatory recordings.

The debate and conflicting ideas revolve around whether or not it would be feasible to treat white coat hypertension, as there still is no conclusive evidence that a temporary rise in blood pressure during office visits has an adverse effect on health.

In fact, many cross sectional studies have shown that "target-organ damage (as exemplified by left ventricular hypertrophy) is less in white-coat hypertensive patients than in sustained hypertensive patients even after the allowance has been made for differences in clinic pressure". Many believe that patients with "white coat" hypertension do not require even very small doses of antihypertensive therapy as it may result in hypotension, but must still be careful as patients may show signs of vascular changes and may eventually develop hypertension. Even patients with established hypertension that is well-controlled based on home blood pressure monitoring may experience elevated readings during office visits.

There are several methods of healing blood blisters, including elevation of the wound, application of a cold pack, and application of padded dressings or splints.

Although this hypothesis is well known among clinicians and individuals with diabetes, there is little scientific evidence to support it. Clinical studies indicate that a high fasting glucose in the morning is more likely because the insulin given on the previous evening fails to last long enough. Studies from 2007 onwards using continuous glucose monitoring show that a high glucose in the morning is not preceded by a low glucose during the night. Furthermore, many individuals with hypoglycemic episodes during the night don't wake due to a failure of release of epinephrine during nocturnal hypoglycemia. Thus, Somogyi's theory is not assured and may be refuted.

Blood phobia is often caused by direct or vicarious trauma in childhood or adolescence. Though some have suggested a possible genetic link, a study of twins suggests that social learning and traumatic events, rather than genetics, is of greater significance.

The inclusion of “blood-injury phobia” within the category of specific or simple phobias in classificatory systems reflects a perception that fear has a primary role in the disorder. Consistent with this assumption, blood-injury phobia appears to share a common etiology with other phobias. Kendler, Neale, Kessler, Heath, and Eaves (1992) have argued from data comparing monozygotic with dizygotic twins that the genetic factor common to all phobias (agoraphobia, social phobia, and specific phobias), strongly predisposes a person to specific phobias.

The recognition of an inherited vulnerability common to all phobias is consistent with the notion that elevated trait anxiety predisposes one to anxiety disorders. Trait anxiety provides a background of affective arousal that permits a more rapid activation of the fight or flight response. With respect to specific activating events, conditioning is one way that stimuli become able to elicit anxiety (Rachman, 1991).

Accordingly, painful experiences can condition fear to blood-injury stimuli. Investigators typically classify around 60% of self-reported onsets of blood-injury phobia as beginning with conditioning experiences (Ost, 1991; Ost,

1992; Ost & Hugdahl, 1985; Thyer et al., 1985). However, examinations of available case-by-case verbal summaries call into question the conclusion that conditioning episodes are as prevalent as reported (see Mattick, Page, & Lampe, in press). For example, Thyer et al. (1985) identified a conditioning episode when a “patient received an injection at age 13 and fainted” (p. 455), and in another person when ‘at age six she heard her elementary school teacher give a talk on the circulatory system. This frightened the patient to the

point of syncope” (Thyer et al., 1988.)

The medication midodrine can benefit people with orthostatic hypotension, The main side-effect is piloerection ("goose bumps"). Fludrocortisone is also used, although based on more limited evidence.

A number of other measures have slight evidence to support their use indomethacin, fluoxetine, dopamine antagonists, metoclopramide, domperidone, monoamine oxidase inhibitors with tyramine (can produce severe hypertension), oxilofrine, potassium chloride, and yohimbine.

Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.

If the condition of the ischemic limb is stabilized with anticoagulation, recently formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.

Direct arteriotomy may be necessary to remove the clot. Surgical revascularization 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 further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.

Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. 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 reduce reperfusion injury.

Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars in the morning. Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to insulin users who experience high blood sugar in the morning as a result of an overabundance of insulin at night.

This theoretical phenomenon was named after Michael Somogyi, a Hungarian-born professor of biochemistry at the Washington University and Jewish Hospital of St. Louis, who prepared the first insulin treatment given to a child with diabetes in the USA in October 1922. Somogyi showed that excessive insulin makes diabetes unstable and first published his findings in 1938.

Compare with the dawn phenomenon, which is a morning rise in blood sugar in response to waning insulin and a growth hormone surge (that further antagonizes insulin).

The causes of nosebleeds can generally be divided into two categories, local and general factors, although a significant number of nosebleeds occur with no obvious cause.

A nosebleed, also known as epistaxis, is the common occurrence of bleeding from the nose. It is usually noticed when the blood drains out through the nostrils.

There are two types: anterior (the most common), and posterior (less common, more likely to require medical attention). Sometimes in more severe cases, the blood can come up the nasolacrimal duct and out from the eye. Fresh blood and clotted blood can also flow down into the stomach and cause nausea and vomiting.

Although the sight of large amounts of blood can be alarming and may warrant medical attention, nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999. About 60% of people have a nosebleed at some point in their life. About 10% of nosebleeds are serious.

The Infarct Combat Project (ICP) is an international nonprofit organization founded in 1998 to fight ischemic heart diseases through education and research.

Reactive hyperaemia or venous hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischaemia. Following ischaemia there will be a shortage of oxygen and a build-up of metabolic waste.

This is commonly tested in the legs using Buerger's test.

Reactive hyperaemia often occurs as a consequence of Raynaud's phenomenon, where the vasospasm in the vasculature leads to ischaemia and necrosis of tissue and thus a subsequent increase in blood flow to remove the waste products and clear up cell debris.

A hematoma (US spelling) or haematoma (UK spelling) is a localized collection of blood outside the blood vessels, due to either disease or trauma including injury or surgery and may involve blood continuing to seep from broken capillaries. A hematoma is initially in liquid form spread among the tissues including in sacs between tissues where it may coagulate and solidify before blood is reabsorbed into blood vessels. An ecchymosis is a hematoma of the skin larger than 10mm.

They may occur among/within many areas such as skin and other organs, connective tissues, bone, joints and muscle.

A collection of blood (or even a hemorrhage) may be aggravated by anticoagulant medication (blood thinner). Blood seepage and collection of blood may occur if heparin is given via an intramuscular route; to avoid this, heparin must be given intravenously or subcutaneously.

It is not to be confused with hemangioma, which is an abnormal buildup/growth of blood vessels in the skin or internal organs.