The type of shock that results from trauma in which there is blood loss is called:

Hypovolemic Shock

Initially popularized during the Vietnam War for rapid transfusion, venous cutdown has since been used for resuscitation of patients with profound hypovolemia.8,9 The flow rate of saline through a standard IV extension set cut to a length of 28 cm (12 inches) and inserted directly into the vein is 15% to 30% greater than through a 5-cm, 14-gauge catheter. This difference is larger if pressure is applied to the system. Moreover, the improvement in flow rate through large-bore lines is greater for blood than for crystalloid solutions because the viscous characteristics of blood impede its passage through small-bore tubing.9 A unit of blood can be transfused in as little as 3 minutes through IV extension tubing inserted directly into the vein. Consequently, large-bore lines placed by venous cutdown are an excellent mechanism for the treatment of severe hypovolemia.

Lung

Hypovolemic shock often induces an increase in ventilatory minute volume, resulting in tachypnea or hyperventilation and a decrease in arterial Pco2.34,50,51,53,172 Unless complicated by pulmonary abnormalities, these changes are, at least initially, not the result of hypoxemia, but an increase in deadspace ventilation after a decrease in pulmonary perfusion, so that a higher minute ventilation is necessary, for a given CO2 production, to eliminate CO2 from the blood and to maintain a normal Pco2 in arterial blood.34,50,51 Minute ventilatory volume may increase further if a decrease in Pco2 is necessary to compensate for metabolic acidosis after accumulation of lactate in the blood.27,33,34,50,51,53,172 The imbalance between increased demands of the diaphragm and reduced blood flow in shock finally may lead to respiratory muscle fatigue and a subsequent decline in ventilatory minute volume.51

Hypovolemic shock caused by trauma and hemorrhage and followed by extensive transfusion therapy of red blood cell concentrates can be complicated by pulmonary edema and impaired gas exchange.52,173–178 In some patients, overtransfusion and an elevated filtration pressure (pulmonary artery occlusion pressure [PAOP]) may be responsible. In others, pulmonary edema may be due to a pulmonary vascular injury, however, and increased vascular permeability, at a relatively low PAOP, indicating ARDS.52,172,175,176 The reaction to diuretics may help to differentiate between hydrostatic and permeability edema of the lungs. The latter seems relatively rare in polytransfused, polytraumatized patients, unless associated with complications, but other studies suggest that about 30% of patients with severe trauma/hemorrhage may develop ARDS.175,176,178,179 As measured by the transvascular albumin flux in the lungs, almost 80% of patients with multiple trauma may show increased pulmonary vascular permeability in the disease course.52 This leak ultimately may contribute to impaired pulmonary mechanics and gas exchange.52

Experimental studies are at variance concerning alterations in capillary permeability of the lungs during pure hypovolemic shock and resuscitation.4,134,172,180,181 According to some investigators, hypovolemic shock following bleeding and transfusion mildly increases transvascular filtration of fluid and proteins and results in accumulation of interstitial fluid, as a consequence of increased permeability,180 but other authors do not observe such changes.132,134,180,182 In other animal studies, however, traumatic/hypovolemic shock resulted in extensive morphologic changes of the lung, with endothelial and interstitial edema, accumulation of degranulated neutrophils, and scattered fat emboli, which may resemble the pulmonary changes after traumatic/hypovolemic shock in humans.172,183–185 As suggested by animal experiments, among others, several factors may play a role, including release of proinflammatory mediators (TNF-α) and priming and activation of blood neutrophils after ischemia-reperfusion, contusion or ischemia-reperfusion of the lungs themselves, pulmonary microemboli of neutrophils, platelets and fat particles from the medulla of fractured long bones, and neutrophilic antibodies or humoral or cellular breakdown products and released cytokines in transfused blood products (“transfusion-related acute lung injury” [TRALI]).52,117,172,173,178,181,183,185–188 Translocated endotoxin (see the following discussion) also may play a role.183 Finally, aspiration of foreign material or gastric contents and posttraumatic pneumonia and sepsis may contribute to the development of ARDS in trauma patients. When pulmonary edema has developed, active resorption by alveolar cells becomes necessary for clearance. This process is cylic AMP–dependent and can be disturbed by iNOS-derived NO and peroxynitrite and enhanced by expression of heme oxygenase, at least in animal models. How this translates clinically is unclear.

Hypovolemic Shock

TABLE 32. Clinical Classification of Severity of Posthemorrhagic Hypovolemic Shock

MI, Myocardial infarction.

From Parrillo JE, Dellinger RP:Critical care medicine: principles of diagnosis and management in the adult, ed 4, Philadelphia, 2014, Elsevier.

Nontraumatic Hypovolemic

Nontraumatic hypovolemic shock occurs as a result of dehydration or hemorrhage, due to decreased fluid volume. Patients with hemorrhage present with bloody stools, hematemesis, hemoptysis, signs of a ruptured aortic aneurysm, or severe epistaxis. An acute ectopic pregnancy should be considered in any female of childbearing years who is hypotensive. Patients with hypovolemia due to dehydration appear very pale and have moist skin as a result of adrenergic stimulation. Patients with traumatic hypovolemic shock present with hypotension or tachycardia that may respond to intravenous fluids and blood.

Other causes of hypovolemic shock are sedatives, anorexia, bulimia, gastrointestinal obstruction, central nervous system abnormalities, overdiuresis, diabetes, diabetic ketoacidosis, and adrenal insufficiency. Pancreatitis, peritonitis, and ascites can cause sequestration of fluids and hypovolemia.

Hypovolemic Shock

Hypovolemic shock is characterized by increased SVR and decreased CO, with the latter being secondary to decreased preload. This is a so-called “cold shock,” meaning the skin is cold and clammy from the vasoconstriction. For hypovolemic shock from dehydration or fluid losses, such as from prolonged physical activity in warm temperatures or excessive gastrointestinal (GI) losses and lack of oral intake, the treatment is relatively straightforward to include fluid resuscitation with crystalloid.

Hypovolemic Shock

Hypovolemic shock, by far the most common type of shock in children, occurs when a decrease in intravascular volume leads to decreased venous return and, subsequently, decreased preload. Decreased preload results in decreased stroke volume. An increase in heart rate often maintains cardiac output initially, but when this compensatory response is inadequate, cardiac output diminishes. The formula that defines this relationship is as follows:

Cardiac output = Heart rate × Stroke volume

Decreased cardiac output results in decreased delivery of oxygen and other substrates to the tissues. The two main categories of hypovolemic shock are hemorrhagic and nonhemorrhagic; examples are provided in Table 37-2.

In the early stage of hypovolemic shock, autoregulatory mechanisms shunt blood flow preferentially to the brain, heart, and adrenal system. Because flow is diverted from less critical organs, patients may present initially with cool or mottled extremities, decreased urine output, and, of note, normal blood pressure. Other signs may include dry mucous membranes, absence of tears, and abnormal skin turgor.

Hemorrhagic shock due to known trauma is typically diagnosed at the initial presentation; however, hemorrhagic shock can present during hospitalization, especially in postoperative patients. Victims of child abuse are also at risk for delayed diagnosis of hemorrhagic shock because the initial history may be incomplete, inaccurate, or misleading, and symptoms may progress over time. Nonhemorrhagic shock may present in patients with ongoing fluid losses (e.g., vomiting, diarrhea, gastric suctioning, burns), especially if there is inadequate replacement.

Hypovolemic Shock

Hypovolemic shock may be related to dehydration, internal or external hemorrhage, gastrointestinal fluid losses (diarrhea or vomiting), urinary losses secondary to either diuretics or kidney dysfunction, or loss of intravascular volume to the interstitium as a result of decrease of vascular permeability (in response to sepsis or trauma). In addition, venodilation secondary to many causes (sepsis, spinal injury, and various drugs and toxins) may result in a relative hypovolemic state (see Box 22-2 and Fig. 22-1). Hemodynamically, hypovolemic shock is characterized by a decrease in ventricular preload resulting in decreased ventricular diastolic pressures and volumes (Table 22-1). Cardiac index (CI) and stroke volume index are typically reduced. In addition to hypotension, a decreased pulse pressure may be noted. Because of a decreased output and unchanged or increased metabolic demand, mixed venous oxygen saturation (S

Numerous factors may influence the development and hemodynamic characteristics of hypovolemic shock in humans. Studies in animals and humans have shown a clear relationship between the degree of circulating blood volume loss and clinical response.45–48 Acute loss of 10% of the circulating blood volume is well tolerated with tachycardia the only obvious sign. CI may be minimally decreased despite a compensatory increase in myocardial contractility. SVR typically increases slightly, particularly if sympathetic stimulation augments MAP. Compensatory mechanisms begin to fail with a 20% to 25% volume loss. Mild-to-moderate hypotension and decreased CI may be present. Orthostasis (with a blood pressure decrease of 10 mm Hg and increased heart rate of 20 to 30 beats per minute) may become apparent. There is a marked elevation in SVR, and serum lactate may begin to increase. With decreases of the circulating volume of 40% or more, marked hypotension with clinical signs of shock is noted. CI and tissue perfusion may decrease to less than half of normal. Lactic acidosis is usually present and predicts a poor outcome.49,50

The rate of loss of intravascular volume and the pre-existing cardiac reserve is of substantial importance in the development of hypovolemic shock. Although an acute blood loss of 1 L in a healthy adult may result in mild-to-moderate hypotension with a reduced pulmonary wedge pressure (PWP) and CVP,46 the same loss over a longer time may be well tolerated because of compensatory responses, such as tachycardia, increased myocardial contractility, increased red blood cell 2,3-diphosphoglycerate, and increased fluid retention. A similar slow blood loss may lead to substantial hemodynamic compromise, however, in an individual with a limited cardiac reserve even while the PWP and CVP remain elevated.

Hypovolemic shock represents more than a simple mechanical response to loss of circulating volume. It is a dynamic process involving competing adaptive (compensatory) and maladaptive responses at each stage of development. Although intravascular volume replacement is always a necessary component of resuscitation from hypovolemia or hypovolemic shock, the biologic responses to the insult may progress to the point where such resuscitation is insufficient to reverse the progression of the shock syndrome. Patients who have sustained a greater than 40% loss of blood volume for 2 hours or more may be unable to be effectively resuscitated.41,45,48 A series of inflammatory mediator, cardiovascular, and organ responses to shock is initiated, which supersede the importance of the initial insult in driving further injury.

Hypovolemic shock

Hypovolemic shock from uncontrolled hemorrhage is the quintessential form of shock among trauma patients. Much work has been done to advance the care of trauma patients, both in the control of hemorrhage (permissive hypotension, fluid restrictive resuscitation, damage control surgery, applications of tourniquets, topical hemostatic agents, endovascular occlusion, etc.) as well as in the replacement of intravascular volume (colloid, isotonic and hypertonic crystalloid, balanced salt solutions, blood products, massive transfusion protocols, etc.). Details of these techniques can be found elsewhere in this volume. Suffice it to say that mastery of hemorrhage control and fluid resuscitation is critical to the cessation and reversal of hemorrhagic shock.

Complications

Hypovolemic shock, hyponatremia, hypokalemia, metabolic acidosis, and occasional hypocalcemia due to acute and huge loss of water and electrolytes are the major complications of cholera.50 If timely intervention is not initiated these all can lead to death. Severe hypoglycemia from inadequate gluconeogenesis and exhaustion of glycogen stores is an uncommon complication seen in pediatric patients who manifest acute convulsions and even coma if serum glucose concentrations fall below 1 mmol/L.51 In patients with severe dehydration and a marked decrease in renal perfusion, acute renal failure can occur. Very rarely, pulmonary edema can ensue if large volumes of intravenous fluids without bicarbonate are rapidly infused in a patient with severe acidosis, but inadequate fluid replacement is much more common. Rarely, septicemia due to V. cholerae has also been reported.

Hypovolemic Shock

Hypovolemic shock arises from reduced circulating blood volume as the result of blood loss caused by hemorrhage or the result of fluid loss secondary to vomiting, diarrhea, or burns. Reduced circulating blood volume leads to decreased vascular pressure and tissue hypoperfusion. Immediate compensatory mechanisms (e.g., peripheral vasoconstriction and fluid movement into the plasma) act to increase vascular pressure and maintain blood flow to critical tissues such as the heart, brain, and kidney. Increased pressure provides an adequate driving force on which local mechanisms can draw to increase blood flow based on their needs. When the insult is mild, compensation is generally successful and the animal returns to homeostasis. Loss of approximately 10% of blood volume can occur without a decrease in blood pressure or cardiac output. However, if greater volumes are lost, adequate pressure and perfusion cannot be maintained and there is insufficient blood flow to meet the needs of the tissues. When blood loss approaches 35% to 45%, blood pressure and cardiac output can fall dramatically.