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Common causes of hypovolemia can be dehydration, bleeding, vomiting, severe burns and drugs such as diuretics or vasodilators typically used to treat hypertensive individuals. Rarely, it may occur as a result of a blood donation, sweating, and alcohol consumption.
Severe hypovolemia leads to hypovolemic shock.
A low blood volume can result in multiple organ failure, kidney damage and failure, brain damage, coma and death (desanguination).
This function is accomplished by two sets of receptors; one in the kidneys and the other in the heart.
The kidneys have a specialized set of cells that enable the recognition of changes in blood flow to the kidneys. Naturally, these cells detect the presence of hypovolemia and react accordingly to the loss of blood volume. These cells secrete a hormone called renin when there is a decrease in the flow of blood to the kidneys. Renin flows into the blood and there, initiates the conversion of a protein called angiotensinogen to angiotensin. In order to exert its effects on the body, angiotensin I must be converted by enzymes into its active form, angiotensin II. Physiologically, angiotensin II stimulates the release of hormones by the posterior pituitary gland (ADH, also known as vasopressin) and the adrenal cortex (aldosterone). Aldosterone causes the kidneys to reabsorb sodium, leading to the reabsorption of water. ADH (vasopressin) also causes the kidneys to reabsorb water. Angiotensin II increases blood pressure by contracting arterial muscles.
The next set of receptors responsible for detecting volumetric insufficiency are located in the heart atria. Commonly referred to as stretch receptors, these atrial baroreceptors detect the amount of blood that is being pumped back into the heart from the veins. The body constantly returns blood to the heart through veins. Therefore, when the volume of blood being transported back to the heart is decreased, these receptors detect the change in the amount of blood thereby reducing the release of atrial natriuretic peptide.
Furthermore, as intravascular fluid decreases, blood pressure is reduced and the body attempts to compensate by moving fluid from other cellular compartments into the vasculature. Fluid is transferred from all of the fluid compartments in the body, including intracellular, interstitial and other extravascular compartments.
Clinical symptoms may not present until 10-20% of total whole-blood volume is lost.
Hypovolemia can be recognized by elevated pulse, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.
Note that in children, compensation can result in an artificially high blood pressure despite hypovolemia. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should always be treated aggressively.
Also look for obvious signs of external bleeding while remembering that people can bleed to death internally without any external blood loss.
Also consider possible mechanisms of injury (especially the steering wheel and/or use/non-use of seat belt in motor vehicle accidents) that may have caused internal bleeding such as ruptured or bruised internal organs. If trained to do so and the situation permits, conduct a secondary survey and check the chest and abdominal cavities for pain, deformity, guarding or swelling. (Injuries to the pelvis and bleeding into the thigh from the femoral artery can also be life-threatening.)
Minor hypovolemia from a known cause that has been completely controlled (such as a blood transfusion from a healthy patient who is not anemic) may be countered with initial rest for up to half an hour, oral fluids including moderate sugars (apple juice is good) and rich in electrolytes is needed to replenish the organism of lost sodium ions. Furthermore the advice is to the donor to eat good solid meals with proteins for the next few days. Typically, this would involve a fluid volume of less than one liter (1000 ml), although this is highly dependent on body weight. Larger people can tolerate slightly more blood loss than smaller people.
More serious hypovolemia should be assessed by a nurse or doctor. When in doubt, treat hypovolemia aggressively.
External bleeding should be controlled by direct pressure. If direct pressure fails, other techniques such as elevation and pressure points should be considered. The tourniquet should be used in the case of massive hemorrhage i.e. arterial bleeds, such as the femoral artery. If a first-aider recognizes internal bleeding, the life-saving measure to take is to immediately call for emergency assistance.
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. See also emergency medical services for a discussion of techniques used in IV fluid management of hypovolemia.
If the hypovolemia was caused by medication, the administration of antidotes may be appropriate but should be carefully monitored to avoid shock or the emergence of other pre-existing conditions.
Blood transfusions coupled with surgical repair are the definitive treatment for hypovolemia caused by trauma. See also the discussion of shock and the importance of treating reversible shock while it can still be countered.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Hypovolemia". A list of authors is available in Wikipedia.|