Hypovolemic shock
Hypovolemic shock is a form of shock caused by severe hypovolemia (insufficient blood volume or extracellular fluid in the body).[1][2] It can be caused by severe dehydration or blood loss.[3][2] Hypovolemic shock is a medical emergency; if left untreated, the insufficient blood flow can cause damage to organs, leading to multiple organ failure.[4]
Hypovolemic shock
Severe dehydration or blood loss
Replacement of fluids, surgery to repair cause of bleeding
In treating hypovolemic shock, it is important to determine the cause of the underlying hypovolemia, which may be the result of bleeding or other fluid losses. To minimize ischemic damage to tissues, treatment involves quickly replacing lost blood or fluids, with consideration of both rate and the type of fluids used.[4]
Tachycardia, a fast heart rate, is typically the first abnormal vital sign.[3] When resulting from blood loss, trauma is the most common root cause, but severe blood loss can also happen in various body systems without clear traumatic injury.[3] The body in hypovolemic shock prioritizes getting oxygen to the brain and heart, which reduces blood flow to nonvital organs and extremities, causing them to grow cold, look mottled, and exhibit delayed capillary refill.[3] The lack of adequate oxygen delivery ultimately leads to a worsening increase in the acidity of the blood (acidosis).[3] The "lethal triad" of ways trauma can lead to death is acidosis, hypothermia, and coagulopathy.[3] It is possible for trauma to cause clotting problems even without resuscitation efforts.[3]
Damage control resuscitation is based on three principles:
Pathophysiology[edit]
Blood loss[edit]
Hemorrhagic shock is due to the depletion of intravascular volume through blood loss to the point of being unable to match the tissues' demand for oxygen. As a result, mitochondria are no longer able to sustain aerobic metabolism for the production of oxygen and switch to the less efficient anaerobic metabolism to meet the cellular demand for adenosine triphosphate. In the latter process, pyruvate is produced and converted to lactic acid to regenerate nicotinamide adenine dinucleotide (NAD+) to maintain some degree of cellular respiration in the absence of oxygen.[3]
The body compensates for volume loss by increasing heart rate and contractility, followed by baroreceptor activation resulting in sympathetic nervous system activation and peripheral vasoconstriction. Typically, there is a slight increase in the diastolic blood pressure with narrowing of the pulse pressure. As diastolic ventricular filling continues to decline and cardiac output decreases, systolic blood pressure drops.[3]
Due to sympathetic nervous system activation, blood is diverted away from noncritical organs and tissues to preserve blood supply to vital organs such as the heart and brain. While prolonging heart and brain function, this also leads to other tissues being further deprived of oxygen causing more lactic acid production and worsening acidosis. This worsening acidosis along with hypoxemia, if left uncorrected, eventually causes the loss of peripheral vasoconstriction, worsening hemodynamic compromise, and death.[3]
The body's compensation varies by cardiopulmonary comorbidities, age, and vasoactive medications. Due to these factors, heart rate and blood pressure responses are extremely variable and, therefore, cannot be relied upon as the sole means of diagnosis.[3]
A key factor in the pathophysiology of hemorrhagic shock is the development of trauma-induced coagulopathy. Coagulopathy develops as a combination of several processes. The simultaneous loss of coagulation factors via hemorrhage, hemodilution with resuscitation fluids, and coagulation cascade dysfunction secondary to acidosis and hypothermia have been traditionally thought to be the cause of coagulopathy in trauma. However, this traditional model of trauma-induced coagulopathy may be too limited. Further studies have shown that a degree of coagulopathy begins in 25% to 56% of patients before initiation of the resuscitation. This has led to the recognition of trauma-induced coagulopathy as the sum of two distinct processes: acute coagulopathy of trauma and resuscitation-induced coagulopathy.[3]
Trauma-induced coagulopathy is acutely worsened by the presence of acidosis and hypothermia. The activity of coagulation factors, fibrinogen depletion, and platelet quantity are all adversely affected by acidosis. Hypothermia (less than 34 C) compounds coagulopathy by impairing coagulation and is an independent risk factor for death in hemorrhagic shock.[3]
Fluid loss[edit]
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.[4]
As volume status continues to decrease, systolic blood pressure drops. As a result, oxygen delivery to vital organs is unable to meet the oxygen needs of the cells. 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.[4]
Prognosis[edit]
If the vital organs are deprived of perfusion for more than just a short time, the prognosis is generally not good. Shock is still a medical emergency characterized by a high mortality rate. Early identification of patients who are likely to succumb to their illness is of utmost importance.[14]
Epidemiology[edit]
Blood loss[edit]
Trauma remains a leading cause of death worldwide with approximately half of these attributed to hemorrhage. In the United States in 2001, trauma was the third leading cause of death overall, and the leading cause of death in those aged 1 to 44 years. While trauma spans all demographics, it disproportionately affects the young with 40% of injuries occurring in ages 20 to 39 years by one country's account. Of this 40%, the greatest incidence was in the 20 to 24-year-old range.[3]
The preponderance of hemorrhagic shock cases resulting from trauma is high. During one year, one trauma center reported 62.2% of massive transfusions occur in the setting of trauma. The remaining cases are divided among cardiovascular surgery, critical care, cardiology, obstetrics, and general surgery, with trauma utilizing over 75% of the blood products.[3]
As patients age, physiological reserves decrease the likelihood of anticoagulant use increases and the number of comorbidities increases. Due to this, elderly patients are less likely to handle the physiological stresses of hemorrhagic shock and may decompensate more quickly.[3]
Fluid loss[edit]
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 the blood products used were related to traumatic injury. Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have less physiologic reserve.[4]
Hypovolemia secondary to diarrhea and/or dehydration is thought to be predominant in low-income countries.[15]