Tuesday, May 16, 2017

Hypovolemic Shock - A Brief Discussion

In hypovolemic shock, reduced intravascular blood volume causes circulatory dysfunction and inadequate tissue perfusion. Without sufficient blood or fluid replacement, hypovolemic shock syndrome may lead to irreversible cerebral and renal damage, cardiac arrest and, ultimately, death. Hypovolemic shock requires early recognition of signs and symptoms and prompt, aggressive treatment to improve the prognosis.


Hypovolemic shock usually results from acute blood loss—about one-fifth of the total volume. Such massive blood loss may result from GI bleeding, internal hemorrhage (hemothorax and hemoperitoneum), or external hemorrhage (accidental or surgical trauma) or from any condition that reduces circulating intravascular plasma volume or other body fluids such as in severe burns. Other underlying causes of hypovolemic shock include intestinal obstruction, peritonitis, acute pancreatitis, ascites and dehydration from excessive perspiration, severe diarrhea or protracted vomiting, diabetes insipidus, diuresis, and inadequate fluid intake.

Signs and symptoms

Hypovolemic shock produces a syndrome of hypotension with narrowing pulse pressure; decreased sensorium; tachycardia; rapid, shallow respirations; reduced urine output; and cold, pale, clammy skin. Metabolic acidosis with an accumulation of lactic acid develops as a result of tissue anoxia as cellular metabolism shifts from aerobic to anaerobic pathways. Disseminated intravascular coagulation (DIC) is a possible complication of hypovolemic shock.


No single symptom or diagnostic test establishes the diagnosis or severity of shock. Characteristic laboratory findings include:
  • elevated potassium, serum lactate, and blood urea nitrogen levels
  • increased urine specific gravity (greater than 1.020) and urine osmolality
  • decreased blood pH and partial pressure of arterial oxygen and increased partial pressure of arterial carbon dioxide.
In addition, gastroscopy, aspiration of gastric contents through a nasogastric tube, and X-rays identify internal bleeding sites; coagulation studies may detect coagulopathy from DIC.

Emergency treatment measures must include prompt and adequate blood and fluid replacement to restore intravascular volume and raise blood pressure. Normal saline solution or lactated Ringer’s solution and then possibly plasma proteins (albumin) or other plasma expanders may produce adequate volume expansion until whole blood can be matched. A rapid solution infusion system can provide these crystalloids or colloids at high flow rates. Application of a pneumatic antishock garment may be helpful. Treatment may also include oxygen administration, identification of bleeding site, control of bleeding by direct measures (such as application of pressure and elevation of an extremity) and, possibly, surgery.

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