Patients with hypovolemic shock have severe hypovolemia with decreased peripheral perfusion. If left untreated, these patients can develop ischemic injury of vital organs, leading to multi-system organ failure. The first factor to be considered is whether the hypovolemic shock has resulted from hemorrhage or fluid losses, as this will dictate treatment. When etiology of hypovolemic shock has been determined, replacement of blood or fluid loss should be carried out as soon as possible to minimize tissue ischemia. Factors to consider when replacing fluid loss include the rate of fluid replacement and type of fluid to be used. 
The annual incidence of shock of any etiology is 0.3 to 0.7 per 1000, with hemorrhagic shock being most common in the intensive care unit. Hypovolemic shock is the most common type of shock in children, most commonly due to diarrheal illness in the developing world. Hypovolemic shock occurs as a result of either blood loss or extracellular fluid loss. Hemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far the most common cause of hemorrhagic shock. Other causes of hemorrhagic shock include gastrointestinal (GI) bleed, bleed from an ectopic pregnancy, bleeding from surgical intervention, or vaginal bleeding.
Hypovolemic shock as a result of extracellular fluid loss can be of the following etiologies:
GI losses can occur via many different etiologies. The gastrointestinal tract usually secretes between 3 to 6 liters of fluid per day. However, most of this fluid is reabsorbed as only 100 to 200 mL are lost in the stool. Volume depletion occurs when the fluid ordinarily secreted by the GI tract cannot be reabsorbed. This occurs when there is retractable vomiting, diarrhea, or external drainage via stoma or fistulas.
Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually excrete sodium and water in a manner that matches intake. Diuretic therapy and osmotic diuresis from hyperglycemia can lead to excessive renal sodium and volume loss. In addition, there are several tubular and interstitial diseases beyond the scope of this article that cause severe salt-wasting nephropathy.
Fluid loss also can occur from the skin. In a hot and dry climate, skin fluid losses can be as high as 1 to 2 liters/hour. Patients with a skin barrier interrupted by burns or other skin lesions also can experience large fluid losses that lead to hypovolemic shock.
Sequestration of fluid into a third-space also can lead to volume loss and hypovolemic shock. Third-spacing of fluid can occur in intestinal obstruction, pancreatitis, obstruction of a major venous system, or any other pathological condition that results in a massive inflammatory response. 
While the incidence of hypovolemic shock from extracellular fluid loss is difficult to quantify, it is known that hemorrhagic shock is most commonly due to trauma. In one study, 62.2% of massive transfusions at a level 1 trauma center were due to traumatic injury. In this study, 75% of blood products used were related to traumatic injury. Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have a less physiologic reserve.
Hypovolemic shock results from depletion of intravascular volume, whether by extracellular fluid loss or blood loss. The body compensates with increased sympathetic tone resulting in increased heart rate, increased cardiac contractility, and peripheral vasoconstriction. The first changes in vital signs seen in hypovolemic shock include an increase in diastolic blood pressure with narrowed pulse pressure. As volume status continues to decrease, systolic blood pressure drops. As a result, oxygen delivery to vital organs is unable to meet oxygen demand. Cells switch from aerobic metabolism to anaerobic metabolism, resulting in lactic acidosis. As sympathetic drive increases, blood flow is diverted from other organs to preserve blood flow to the heart and brain. This propagates tissue ischemia and worsens lactic acidosis. If not corrected, there will be worsening hemodynamic compromise and, eventually, death. 
History and physical can often make the diagnosis of hypovolemic shock. For patients with hemorrhagic shock, a history of trauma or recent surgery is present. For hypovolemic shock due to fluid losses, history and physical should attempt to identify possible GI, renal, skin, or third-spacing as a cause of extracellular fluid loss. Symptoms of hypovolemic shock can be related to volume depletion, electrolyte imbalances, or acid-base disorders that accompany hypovolemic shock.
Patients with volume depletion may complain of thirst, muscle cramps, and/or orthostatic hypotension. Severe hypovolemic shock can result in mesenteric and coronary ischemia that can cause abdominal or chest pain. Agitation, lethargy, or confusion may result from brain malperfusion.
Although relatively nonsensitive and nonspecific, physical exam can be helpful in determining the presence of hypovolemic shock. Physical findings suggestive of volume depletion include dry mucous membranes, decreased skin turgor, and low jugular venous distention. Tachycardia and hypotension can be seen along with decreased urinary output. Patients in shock can appear cold, clammy, and cyanotic.
Various laboratory values can be abnormal in hypovolemic shock. Patients can have increased BUN and serum creatinine as a result of prerenal kidney failure. Hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia. Lactic acidosis can result from increased anaerobic metabolism. However, the effect of acid-base balance can be variable as patients with large GI losses can become alkalotic. In cases of hemorrhagic shock, hematocrit and hemoglobin can be severely decreased. However, with a reduction in plasma volume, hematocrit and hemoglobin can be increased due to hemoconcentration.
Low urinary sodium is commonly found in hypovolemic patients as the kidneys attempt to conserve sodium and water to expand the extracellular volume. However, sodium urine can be low in a euvolemic patient with heart failure, cirrhosis, or nephrotic syndrome. A fractional excretion of sodium under 1% is also suggestive of volume depletion. Elevated urine osmolality can also suggest hypovolemia. However, this number also can be elevated in the setting of impaired concentrating ability by the kidneys.
Central venous pressure (CVP) is often used to assess volume status. However, its usefulness in determining volume responsiveness has recently come into question. Ventilator settings, chest wall compliance, and right-sided heart failure can compromise CVPs accuracy as a measure of volume status. Measurements of pulse pressure variation via various commercial devices has also been postulated as a measure of volume responsiveness. However, pulse pressure variation as a measure of fluid responsiveness is only valid in patients without spontaneous breaths or arrhythmias. The accuracy of pulse pressure variation also can be compromised in right heart failure, decreased lung or chest wall compliance, and high respiratory rates.
Similar to examining pulse pressure variation, measuring respiratory variation in inferior vena cava diameter as a measure of volume responsiveness has only been validated in patients without spontaneous breaths or arrhythmias. Measuring the effect of passive leg raises on cardiac contractility by echo appears to be the most accurate measurement of volume responsiveness, although it is also subject to limitations. [
For patients in hemorrhagic shock, early use of blood products over crystalloid resuscitation results in better outcomes. Balanced transfusion using 1:1:1 or 1:1:2 of plasma to platelets to packed red blood cells results in better hemostasis. Anti-fibrinolytic administration to patients with severe bleed within 3 hours of traumatic injury appears to decrease death from major bleed as shown in the CRASH-2 trial. Research on oxygen-carrying substitutes as an alternative to packed red blood cells is ongoing, although no blood substitutes have been approved for use in the United States.
For patients in hypovolemic shock due to fluid losses, the exact fluid deficit cannot be determined. Therefore, it is prudent to start with 2 liters of isotonic crystalloid solution infused rapidly as an attempt to quickly restore tissue perfusion. Fluid repletion can be monitored by measuring blood pressure, urine output, mental status, and peripheral edema. Multiple modalities exist for measuring fluid responsiveness such as ultrasound, central venous pressure monitoring, and pulse pressure fluctuation as described above. In general, for hypovolemic shock, vasopressors should not be used because they can worsen tissue perfusion.
Crystalloid fluid resuscitation is preferred over colloid solutions for severe volume depletion not due to bleeding. The type of crystalloid used to resuscitate the patient can be individualized based on the patients’ chemistries, estimated volume of resuscitation, acid/base status, and physician or institutional preferences. Isotonic saline is hyperchloremic relative to blood plasma, and resuscitation with large amounts can lead to a hyperchloremic metabolic acidosis. Several other isotonic fluids with lower chloride concentrations exist, such as lactated Ringer's solution or PlasmaLyte. These solutions are often referred to as buffered or balanced crystalloids. Some evidence suggests that patients who need large volume resuscitation may have a less renal injury with restrictive chloride strategies and use of balanced crystalloids. Crystalloid solutions are equally as effective and much less expensive than colloid. Commonly used colloid solutions include those containing albumin or hyperoncotic starch. Studies examining albumin solutions for resuscitation have not shown improved outcomes, while other studies have shown resuscitation with hyperoncotic starch leads to increased mortality and renal failure. 234234
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