Hypovolemic shock
Hypovolemic shock: Excerpt from Professional Guide to Diseases (Eighth Edition)
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. (See What happens in hypovolemic shock, page 1116.)
Causes
Hypovolemic shock usually results from acute blood loss — about one-fifth of total volume. Such massive blood loss may result from GI bleeding, internal hemorrhage (hemothorax and hemoperitoneum), 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, or 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 (less than 25 ml/hour); 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.
Diagnosis
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 (more 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, computed tomography scan, and X-rays identify internal bleeding sites; coagulation studies may detect coagulopathy from DIC. Echocardiography or right-heart catheterization can help differentiate between hypovolemic and cardiogenic shock.
Treatment
Emergency treatment measures must include prompt and adequate blood and fluid replacement to restore intravascular volume and raise blood pressure. Saline solution or lactated Ringer’s solution, 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. (See Using a pneumatic antishock garment.) Dopamine, dobutamine, epinephrine, and norepinephrine can help increase blood pressure and cardiac output after fluid resuscitation measures are done. 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.
Special considerations
Management of hypovolemic shock necessitates prompt, aggressive supportive measures and careful assessment and monitoring of vital signs. Follow these priorities:
❑ Check for a patent airway and adequate circulation. If blood pressure and heart rate are absent, start cardiopulmonary resuscitation.
❑ Record blood pressure, pulse rate, peripheral pulses, respiratory rate, and other vital signs every 15 minutes and the electrocardiograph continuously. Systolic blood pressure lower than 80 mm Hg usually results in inadequate coronary artery blood flow, cardiac ischemia, arrhythmias, and further complications of low cardiac output. When blood pressure drops below 80 mm Hg, increase the oxygen flow rate and notify the physician immediately. A progressive drop in blood pressure, accompanied by a thready pulse, generally signals inadequate cardiac output from reduced intravascular volume. Notify the physician and increase the infusion rate.
❑ Start I.V. lines with normal saline or lactated Ringer’s solution, using a large-bore catheter (14G), which allows easier administration of later blood transfusions. (Caution: Don’t start I.V. lines in the legs of a patient in shock who has suffered abdominal trauma, because infused fluid may escape through the ruptured vessel into the abdomen.)
❑ An indwelling urinary catheter may be inserted to measure hourly urine output. If output is less than 30 ml/hour in adults, increase the fluid infusion rate, but watch for signs of fluid overload such as an increase in pulmonary artery wedge pressure (PAWP). Notify the physician if urine output doesn’t improve. An osmotic diuretic such as mannitol may be ordered to increase renal blood flow and urine output. Determine how much fluid to give by checking blood pressure, urine output, central venous pressure (CVP), or PAWP. (To increase accuracy, CVP should be measured at the level of the right atrium, using the same reference point on the chest each time.)
❑ Draw an arterial blood sample to measure blood gas levels. Administer oxygen by face mask or airway to ensure adequate oxygenation of tissues. Adjust the oxygen flow rate to a higher or lower level, as blood gas measurements indicate.
❑ Draw venous blood for complete blood count and electrolyte, type and crossmatch, and coagulation studies.
❑ During therapy, assess skin color and temperature, and note changes. Cold, clammy skin may be a sign of continuing peripheral vascular constriction, indicating progressive shock.
❑ Watch for signs of impending coagulopathy (petechiae, bruising, and bleeding or oozing from gums or venipuncture sites).
❑ Explain procedures and their purpose. Throughout these emergency measures, provide emotional support to the patient and his family.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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