HYPOVOLEMIC SHOCK DefinitionShock is the clinical syndrome that results from inadequate tissue perfusion. Classification

CausesThis most common form of shock results either from the loss of red blood cell mass due to trauma, surgery, or internal hemorrhage and plasma from hemorrhage or from the loss of plasma volume alone due to extravascular fluid sequestration within the body or lost from the body or GI, urinary, and insensible losses. In some cases, such as in postoperative patients, a number of these problems occur at the same time. For example, a patient may have blood loss secondary to trauma or surgery, with additional fluid being third spaced (e.g., as tissue edema in the gastrointestinal tract with a concomitant ileus) and lost through a high-output gastrointestinal fistula postoperatively. As this example of third-spaced fluid indicates, fluid (i.e., plasma) does not have to be lost from the body for a person to develop hypovolemic shock, although the fistula output would clearly aggravate the situation. Approximately 20 L of fluid is secreted and reabsorbed daily in the gastrointestinal tract, so it is not surprising that volume loss could be substantial depending on the location of the fistula and function of the tract preceding the fistula.Dehydration may result from primary water deficiency, usually because of decreased intake, but in some instances (e.g., diabetes insipidus) may result from increased losses of water. With most forms of dehydration, such as those caused by diarrheal disease and heat-related illness, a combination of inadequate intake and higher than normal losses occurs. In general, the term dehydration implies intracellular and interstitial fluid depletion, in contrast to volume depletion, which implies extracellular, and particularly intravascular, sodium and water loss. In the case of primary water deficit, cell dehydration occurs. Initially, the patient may be thirsty and possibly have some mental status changes, such as confusion. If cellular dehydration occurs slowly, intracellular substances, referred to as idiogenic osmols, develop that limit progressive complications (e.g., cerebral edema or coma). Death due to primary water deficit, if it occurs, is usually a result of delayed circulatory failure. With combined water and salt deficiencies, such as might occur with gastrointestinal (e.g., diarrhea) and skin losses (e.g., heat stroke), interstitial and intravascular depletion is an early occurrence. Fortunately, dehydration is relatively easy to prevent with routine vigilance and water replacement compared with some of the other causes of shock.

Signs and symptomsThe signs and symptoms of non-hemorrhagic hypovolemic shock are the same as those of hemorrhagic shock, although they may have a more insidious onset. The normal physiologic response to hypovolemia is to maintain perfusion of the brain and heart while attempting to restore an effective circulating blood volume. There is an increase in sympathetic activity, hyperventilation, collapse of venous capacitance vessels, release of stress hormones, and an attempt to replace the loss of intravascular volume through the recruitment of interstitial and intracellular fluid and by reduction of urine output. Mild hypovolemia (20% of the blood volume) generates mild tachycardia but relatively few external signs, especially in a supine young patient. With moderate hypovolemia (2040% of the blood volume), the patient becomes increasingly anxious and tachycardic; although normal blood pressure may be maintained in the supine position, there may be significant postural hypotension and tachycardia. If hypovolemia is severe (40% of the blood volume), the classic signs of shock appear; the blood pressure declines and becomes unstable even in the supine position, and the patient develops marked tachycardia, oliguria, and agitation or confusion. Perfusion of the central nervous system is well maintained until shock becomes severe. Hence, mental obtundation is an ominous clinical sign.

The initial presentation of patients with suspected volume depletion can vary markedly depending on factors such as age, concomitant disease states and medications, and the etiology and rapidity of depletion. Intravascular depletion as a consequence of blood loss is signified by postural vital sign changes, and such measurements should be performed unless the diagnosis is obvious, as in the case of bleeding associated with trauma. Early signs and symptoms of dehydration and intravascular depletion caused by gastrointestinal or urinary losses often are relatively nonspecific. Plasma volume losses of 100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.The decrease in pulse pressure is a result of increased catecholamine levels, which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.Class III hemorrhage (loss of 30-40%)By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP, oliguria, and significant changes in mental status, such as confusion or agitation.In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids.Class IV hemorrhage (loss of >40%)Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness), and cold and pale skin.

This amount of hemorrhage is immediately life threatening.A recent study found substantial variability between blood loss and clinical signs. This study concluded that it was difficult to establish specific cutoff points for clinical signs that could be used as triggers for clinical interventions.In the patient with trauma, hemorrhage usually is the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits).The 4 areas in which life-threatening hemorrhage can occur are as follows: chest, abdomen, thighs, and outside the body.The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration.The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury.The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh).The patient's entire body should then be checked for other external bleeding.In the patient without trauma, the majority of the hemorrhage is in the abdomen. The abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease, or liver congestion. Also check for other signs of bruising or bleeding.In the pregnant patient, perform a sterile speculum examination. However, with third-trimester bleeding, the examination should be performed as a "double set-up" in the operating room. Check for abdominal, uterine, or adnexal tenderness.After the history is taken and the physical examination is performed, further workup depends on the probable cause of the hypovolemia, as well as on the stability of the patient's condition.Initial laboratory studies should include analysis of the CBC, electrolyte levels (eg, Na, K, Cl, HCO3, BUN, creatinine, glucose levels), lactate, prothrombin time, activated partial thromboplastin time, ABGs, urinalysis (in patients with trauma), and a urine pregnancy test. Blood should be typed and cross-matched.Patients with marked hypotension and/or unstable conditions must first be resuscitated adequately. This treatment takes precedence over imaging studies and may include immediate interventions and immediately taking the patient to the operating room.The workup for the patient with trauma and signs and symptoms of hypovolemia is directed toward finding the source of blood loss.The atraumatic patient with hypovolemic shock requires ultrasonographic examination in the ED if an abdominal aortic aneurysm is suspected. If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage should be performed. An upright chest radiograph should be obtained if a perforated ulcer or Boerhaave syndrome is a possibility. Endoscopy can be performed (usually after the patient has been admitted) to further delineate the source of bleeding.A pregnancy test should be performed in all female patients of childbearing age. If the patient is pregnant and in shock, surgical consultation and the consideration of bedside pelvic ultrasonography should be immediately performed in the ED. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative pregnancy test, although rare, has been reported.If thoracic dissection is suspected because of the mechanism and initial chest radiographic findings, the workup may include transesophageal echocardiography, aortography, or CT scanning of the chest.If a traumatic abdominal injury is suspected, a focused abdominal sonography for trauma (FAST) ultrasonography examination may be performed in the stable or unstable patient. Computed tomography (CT) scanning typically is performed in the stable patient.If long-bone fractures are suspected, radiographs should be obtained.

Pre-hospital careThe treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure should be applied to external bleeding vessels to prevent further blood loss.Prevention of further injury applies mostly to the patient with trauma. The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful.Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.In the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return, diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock.Appropriate treatment usually can be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated. However, procedures in the field that prolong transportation should be delayed. Benefits to giving IV fluids prior to departure from the scene are not clear; however, IV lines and fluid resuscitation should be started and continued once the patient is en route to definitive care.In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal reports of success, their use became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.Goals of treatmentThe desired outcomes of therapy for circulatory insufficiency that has led to hypovolemic shock are to prevent further progression of the disease with subsequent organ damage and, to the extent possible, to reverse organ dysfunction that has already taken place.Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and appropriately determined.TreatmentInitial resuscitation requires rapid reexpansion of the circulating intravascular blood volume along with interventions to control ongoing losses. In accordance with Starlings law, stroke volume and cardiac output rise with the increase in preload. After resuscitation, the compliance of the ventricles may remain reduced due to increased interstitial fluid in the myocardium. Therefore, elevated filling pressures are frequently required to maintain adequate ventricular performance. Volume resuscitation is initiated with the rapid infusion of either isotonic saline (although care must be taken to avoid hyperchloremic acidosis from loss of bicarbonate buffering capacity and replacement with excess chloride) or a balanced salt solution such as Ringers lactate (being cognizant of the presence of potassium and potential renal dysfunction) through large-bore intravenous lines. Data, particularly on severe traumatic brain injury (TBI), regarding benefits of small volumes of hypertonic saline that more rapidly restore blood pressure are variable, but tend to show improved survival thought to be linked to immunomodulation. No distinct benefit from the use of colloid has been demonstrated, and in trauma patients it is associated with a higher mortality, particularly in patients with TBI. The infusion of 23 L of salt solution over 2030 min should restore normal hemodynamic parameters. Continued hemodynamic instability implies that shock has not been reversed and/or there are significant ongoing blood or other volume losses. Continuing acute blood loss, with hemoglobin concentrations declining to 100 g/L (10 g/dL), should initiate blood transfusion, preferably as fully cross-matched recently banked (