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10 Things You Need to Know About Hypovolemic Shock to Save Lives

By Pulsara Staff

EDITOR'S NOTE: Thanks to our guest blogger this week, Dean Meenach, MSN, RN, CNL, CEN, CCRN, CPEN, EMT-P. **

The effects of shock due to major blood loss rapidly become irreversible, so quick identification and intervention are critical.

Shock is not a disease, but a clinical manifestation of the body’s inability to perfuse its tissues adequately. [1] Shock is considered a systemic response to an illness or injury resulting in inadequate tissue perfusion and decreased oxygen to the cells.

Hypovolemic shock is the loss of volume, which can include:

  • Loss of blood, internal or external bleeding/hemorrhage.
  • Loss of water, vomiting, diarrhea, perspiration.
  • Movement of cellular fluid from within cells to the space around cells.

The effects of shock are initially reversible, but rapidly become irreversible. For prehospital professionals to improve shock outcomes, these interventions must begin early in the prehospital setting. [2,3] Here are 10 things you need to know to help you identify hypovolemic shock early and manage it effectively to save lives.


Hypovolemic shock is caused by a decrease in the amount of circulating volume (absolute hypovolemia). In trauma patients, one type of hypovolemic shock, this is usually caused by hemorrhage. Volume loss in non-trauma patients, the other type of hypovolemic shock, it can be caused by hemorrhage, vomiting, diarrhea, excessive perspiration, fever, medication induced diuresis, etc. [1,10,18,19]


Available studies suggest that 2% of EMS calls present with traumatic or nontraumatic hypotension and 1-2% with hypovolemic shock.

Hypovolemic is the second leading type of shock experienced. [6] Hemorrhage is the second leading cause of death in trauma patients, making hemorrhagic shock the most common cause of preventable trauma death within 6 hours of admission. [7,8,9] According to the literature, 1.9 million people die per year worldwide due to hemorrhagic shock. [6,10] It is no surprise that trauma is the most frequent condition leading to hemorrhagic shock. [10,11] Finally, patients with trauma-related hemorrhagic shock have better outcomes when transported to specialty trauma centers. [12,44,47]


In the early stages of shock, the body is unable to meet the demand for oxygen and cellular nutrients. To maintain perfusion to the organs, the body reacts by activating various compensatory mechanisms that result in shunting perfusion away from other organs.

If the shock state is unrecognized, prolonged or untreated, it will progress to a terminal stage. The pathophysiologic changes that occur during shock can be divided into three stages: compensated, uncompensated, and irreversible. [1,13]

  • Stage I (compensated): The sympathetic nervous system is selective, shunting blood to the heart, brain and lungs, which decreases perfusion to other organs. During the compensated stage, there is a narrow window of opportunity to rapidly intervene and restore perfusion. [13]
  • Stage II (decompensated or progressive): Decompensated or progressive shock occurs when compensatory mechanisms begin to fail and are unable to restore perfusion. [1,14] This results in hypotension, reduced organ perfusion, impaired oxygen delivery, anaerobic metabolism and lactic acid production. However, shock may still be reversible at this stage with immediate intervention. [13,14,15,16,21]
  • Stage III (irreversible): Irreversible shock occurs when tissues and cells become ischemic and necrotic. This results in hypotension and possible multiple organ dysfunction. [10,17] Despite aggressive resuscitation, interventions may only have minimal results in reducing morbidity and mortality.


Resuscitation-associated coagulopathy in hemorrhagic shock has been recognized as the major cause of the trauma triad of death. [15] These three lethal complications include:

The "Trauma Triad of Death" from severe blood loss involves coagulopathy, acidosis and hypothermia.
Resuscitation-associated coagulopathy in hemorrhagic shock has been recognized as the major cause of the trauma triad of death. At present, this can only be treated with blood product replacement.(image/EMS1)
  • Hypothermia: Hypothermia results in an increase in clot breakdown and bleeding. [14] Prehospital IV fluid warmers, peripheral warming devices and blankets are typically used to reduce this type of hypothermia.
  • Acidosis: Acidosis decreases production of coagulation factors by as much as 40% due to reduced pH, elevated lactic acid production and increasing base deficit. [14,21] EMS agencies can use point-of-care blood gas analyzers to identify acidosis and sodium bicarbonate to treat the metabolic acidosis.
  • Coagulopathy: Blood loss results in a depletion of clotting factors that may be present in up to 25-35% of trauma patients that arrive to the ED. [14] At present, this can only be treated with blood product replacement. This has led to the push by some EMS agencies that serve remote areas or have prolonged transport times to consider carrying blood products such as packed red blood cells, fresh frozen plasma and other components. [48] Just as with IV fluids, all blood products should be administered through a warming infuser.


Vital signs are important indicators of the patient's physiologic status.

  • Temperature: Fever may direct a further search for signs of infection, but a temperature less than 95 degrees may indicate hypothermia in a shock victim. Hypothermia contributes to poor perfusion.
  • Heart rate: Due to compensatory mechanisms, the heart rate is typically elevated in hypotension. In hypovolemic shock, the heart rate will likely be elevated.
  • Blood pressure: Hypotension defined as MAP <65 mm Hg is often a prominent feature of shock.
  • Respiratory rate: Tachypnea is commonly observed in patients with shock. An elevated respiratory rate helps alleviate systemic acidosis by removing excess CO2.
  • Oxygen saturation: This is typically preserved by increasing oxygen extraction when delivery to tissue is diminished. Saturations fall only at very late stages of hypovolemic shock.


The physical examination of the patient presenting in shock can be expedited by applying the ABCDE approach:

  1. Airway: The airway should be assessed for patency. Mental status changes that often accompany severe forms of shock may disrupt the ability of the patient to protect their airway.

  2. Breathing: Breath sounds should be equal on both sides of the chest on auscultation. Increased work of breathing may be observed in hypovolemic shock.

  3. Circulation: Assess for any signs of active bleeding. Also assess the perfusion of the distal extremities to help differentiate the types of shock. Acral cyanosis of the extremities and cold, clammy skin is consistent with hypovolemic shock.
  4. Disability: Complete a focused neurologic exam based on the patient’s presentation. In hypovolemic shock with poor perfusion, the patient’s mental status will deteriorate, risking airway compromise due to loss of the usual reflexes that allow management of secretions and protection from aspiration.
  5. Exposure and secondary evaluation: An exam of the patient’s entire body is important in the suspected shock patient. Provide warming measures after your exam to maintain body temperature.


The evidence-based guidelines for treating all types of shock are constantly evolving as new research is accepted. Management of shock varies greatly due to age, pre-existing conditions, comorbidities, causes and numerous other factors. Here is a summary of some of the recent evidence-based guidelines and recommendations:

For hemorrhagic hypovolemic shock:

  • Treatment of hemorrhagic shock caused by trauma has evolved to a management strategy of damage control resuscitation (DCR). [9,22,23] Damage control resuscitation focuses on bleeding control, permissive hypotension, hemostatic resuscitation and hemorrhage control to adequately treat the lethal triad that occurs in trauma. [49]
  • Current DCR focuses on hemostatic resuscitation, which pushes for early use of blood products rather than an abundance of crystalloids in order to minimalize the metabolic derangement, resuscitation-induced coagulopathy and the hemodilution that occurs with crystalloid resuscitation. [24,25,26,45] Reduction in time to first plasma transfusion has shown a significant reduction in mortality in DCR. [25]
  • In addition to blood products, antifibrinolytics such as tranexamic acid demonstrate additional benefit when started as soon as practical. [27,28,29]
  • Hypotensive resuscitation is recommended for the hemorrhagic shock patient without head trauma. The goal is to achieve permissive hypotension with a systolic blood pressure of 90 mmHg in order to maintain tissue perfusion without inducing re-bleeding from recently clotted vessels. [30,31] Studies regarding permissive hypotension have yielded conflicting results. [25]
  • The quantity, type of fluids to be used and end goals of resuscitation remain topics of ongoing study and debate. [24,46] Normal saline and lactated ringers are the most common crystalloid fluids used. [31]

For nonhemorrhagic hypovolemic shock:

  • In most cases, initiate an initial fluid bolus rapidly with warmed isotonic crystalloid solution. Administer warmed blood products as indicated by the patient’s condition. [32] Although the end points remain somewhat controversial, vasopressors may also be considered as an adjunctive therapy. [33,34,35]


Hemorrhagic shock and head injury remain the leading causes of maternal death. The most common cause of fetal death is maternal death. In the presence of maternal shock, fetal mortality rates may be as high as 80%. [36,37] Therefore, identifying maternal shock early is paramount in improving outcomes.

When pregnancy and shock intersect, there are unique challenges to consider. Normal physiologic changes in pregnancy can make it more difficult to identify the early signs of shock. These include:

  • Blood volume increases by about 45%.
  • Cardiac output increases by 1-1.5 liter/min during the first trimester and 6-7 liters/min by the late second trimester and until delivery.
  • Red blood cells and plasma increases.
  • Blood pressure decreases about 10-15 mm Hg due to a decline in stroke volume.
  • Heart rate increases by 10-15 beats/minute.

These physiologic changes can result in a blood loss of 30-35% (about 1,500 ml) before a significant change in the pregnant patient’s blood pressure is measured. [18] The prehospital professional must remain vigilant in identifying and treating maternal shock early.


In children, differences in total percentage body water, metabolic rate, oxygen consumption and compensatory mechanisms make early identification of shock challenging. The main mechanisms for compensation include significant increases in heart rate and systemic vascular resistance, but minor changes in stroke volume. [38]

Children can appear surprisingly well in early shock with only minimal changes in blood pressure because of their strong compensatory mechanisms. However, when they deteriorate, they do so rapidly.


Many geriatric patients present with comorbidities and pre-existing conditions that impair the ability of compensatory mechanisms to respond to hemorrhage and shock. [39,40]

Congestive heart failure, high blood pressure, coronary artery disease, cirrhosis, malignancy, diabetes, COPD and renal disease all increase mortality risk in older adults. [41,42] In addition, polypharmacy can alter vital signs and mental status, impair compensatory mechanisms to shock, confuse physical exam findings and responses to trauma and alter blood clotting mechanisms. [43] Because of these factors, elderly patients are less likely to handle the physiological stresses of hypovolemic shock and may decompensate more quickly.


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