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Shock Resuscitation
Authors

Andrew Kowalski1; Dov Brandis2.

Affiliations
1 Mclaren Macomb
2 Temple University

Last Update: December 13, 2021.

Continuing Education Activity

At its most basic definition, the term "shock" means that there is a lack of adequate tissue oxygenation throughout the
body. Typically, this lack of oxygenation is caused by either a lack of circulating blood volume, a decrease in cardiac
function, a decrease in systemic vascular resistance, or some other means by which the body cannot circulate blood
flow to vital organs. Typically associated with this is a sudden drop in blood pressure by which the body cannot
adequately perfuse vital organs. When trying to resuscitate a patient in shock, it is important to keep in mind the
etiology of the patient’s shock, as this will sometimes drastically alter the process of proper resuscitation. This activity
reviews resuscitation of shock, the types of fluids used, and the role of the interprofessional team in the management
of these patients.

Objectives:

Identify the different grades of hemorrhage.

Describe the fluids used for resuscitation patients in shock.

Review the complications of massive transfusions.

Summarize the importance of improving care coordination among the interprofessional team to enhance
resuscitation of patients in shock and improve outcomes.

Access free multiple choice questions on this topic.

Introduction
At its most basic definition, the term “shock” means that there is a lack of adequate tissue oxygenation throughout the
body. Typically, this lack of oxygenation is caused by either a lack of circulating blood volume, a decrease in cardiac
function, a decrease in systemic vascular resistance, or some other means by which the body cannot circulate blood
flow to vital organs. Typically associated with this is a sudden drop in blood pressure by which the body cannot
adequately perfuse vital organs. When trying to resuscitate a patient in shock, it is important to keep in mind the
etiology of the patient’s shock, as this will sometimes drastically alter the process of proper resuscitation.[1]

The most important type of shock that is encountered in resuscitation is a hemorrhagic shock. Closely related to this
would be a more broad category of hypovolemic shock. Aside from acute hemorrhage, cardiogenic shock describes a
cause of shock in which the cardiac output is strictly the component by which the body cannot perfuse the rest of the
body. Neurogenic and septic shock deal with a decrease in systemic vascular resistance which prevents the body from
directing blood to vital organs due to the decreased pressure. The shock from adrenal insufficiency is another cause
that incorporates factors of cardiac output (CO), systemic vascular resistance (SVR), and volume.

Roughly 21 million blood products are transfused every year in the United States. Daily, almost 36000 packed RBCs,
7000 platelets, and 10000 FFP units are transfused in the United States. However, the vast majority of these
transfusions are not due to hemorrhagic shock, but to prepare a patient for elective surgery (55%), or for patients with
some form of chronic anemia (30%). Only 15% of all transfusions in the United States are initiated due to an
emergent need for blood products or trauma. Despite the relative infrequency of hemorrhagic shock, it is important to
understand the current guidelines regarding appropriate fluid resuscitation in this situation.[2]

Anatomy and Physiology

As a means of measuring the physiologic changes during shock, central venous pressure (CVP), pulmonary capillary
wedge pressure (PCWP), CO, SVR, HR, BP, and O2 saturation are used to describe the severity of shock and help to
determine the etiology. Typically, with hemorrhagic shock the CVP and PCWP are noted to decrease, the cardiac
output decreases and the SVR increases due to the body’s attempt to compensate for the loss in volume. In septic
shock, the CVP and PCWP decrease, but the SVR decreases as well due to diffuse vasodilation, as a result the CO
increases as the heart attempts to compensate. In cardiogenic shock, the CVP and PCWP actually increase due to the
drop in cardiac function. In addition, the CO decreases and the SVR increases to maintain perfusion pressures. In
neurogenic the CVP, PCWP, CO, and SVR are all expected to drop due to the body’s lack of any neurologic
stimulation to sustain vasoconstriction or a compensatory increase in CO. Adrenal insufficiency is noted to also
follow the same trends as a neurogenic shock.

Indications
When defining hemorrhagic shock, it is categorized based on the severity of impact on systemic circulation. The
corresponding class of shock then determines appropriate intervention.

Class 1 hemorrhagic shock is defined by a blood loss of up to 750mL (or up to 15%) of total blood volume. At this
stage, the remainder of the patient’s perfusion parameters is still within normal limits. The patient’s heart rate will
typically remain under 100 bpm and their blood pressure and pulse pressure will remain stable if not slightly
increased due to anxiety. The respiratory rate is stable at 14-20 breaths/min, and their urine output remains at greater
than 30 mL/hr.

In Class 2 shock, the patient has lost 750 mL to 1500 mL of blood (between 15% and 30% of total blood volume) and
is beginning to become symptomatic. They may start to appear more pale or diaphoretic, with mild tachycardia (100-
120 bpm), the respiratory rate may increase slightly (20-30 bpm), and their urine output may drop slightly (20-30
mL/hr). It is important to note that even outside the realm of shock management, urine output remains the single most
important indicator for monitoring fluid status in a patient. Additionally, blood pressure cannot be adequately relied
upon to detect the beginning of shock, as the body’s compensatory mechanisms will keep blood pressure typically
within normal limits until up to 30% of total blood volume has already been lost. Finally, the Class 2 shock patient
may demonstrate a slight decrease in pulse pressure, which may be the first sign of the body failing to compensate for
the sudden blood loss.

In Class 3 hemorrhagic shock, the patient has lost 1500-2000 mL of blood (30-40% total blood volume), they will be
clearly symptomatic, confused and will be tachycardic (120-140 bpm), tachypneic (30-40 breaths/min), with blood
pressure and pulse pressure decreased causing a drop in renal perfusion (urine output decreased to 5-15 mL/hr). Class
4 shock is the most severe case with acute blood loss of over 2000 mL (or over 40% total blood volume). The
patient’s heart rate will be tachycardic, over 140 bpm, with nonpalpable or thready peripheral pulses. Their respiratory
rate will have increased to over 35 breaths/min, and their blood pressure and pulse pressure will subsequently be
severely decreased. Urine output will be negligible, and symptomatically they will be more lethargic with a likely
altered mental status.

Equipment
Packed red blood cells are provided in units of roughly 350 cc, and are more concentrated than whole blood with a
hematocrit of 65-75%. The plasma and platelets are removed via centrifuge, and the remaining packed red blood cells
are stored in a saline-based preservative such as citrate phosphate dextrose adenine (CPDA-1) for increased shelf life.
Packed RBCs (pRBCs) can be stored for up to 35 days at 2-4 degrees Celsius. One unit of pRBCs is thought to raise a
patient’s hemoglobin level by 1g/dL. These products must be typed and matched for ABO and Rh compatibility with
patient recipients.

Fresh frozen plasma is given in units of 200-250 cc each and contains all coagulation factors, with no red blood cells
or platelets. For FFP to be therapeutic, it is required to be given at 10-20 cc/kg body weight, which would
theoretically increase the body’s clotting factor levels by 20-30%. For an increased shelf life of up to 2 years, they are
frozen within 8 hours of collection and stored at -40 to -50 degrees Celsius. They are then thawed and must be used
immediately as their thawed shelf life is only 5 days before they begin to degrade. Frozen plasma (FP), which is less
commonly used, and typically frozen within 24 hours of collection (FP24), has slightly reduced levels of factor 5 and
8 as compared to FFP. FFP is particularly useful for certain coagulopathies or in isolated clotting factor deficiencies.
There is some speculation as to the benefit of FFP in patients with multiple clotting factor deficiencies or coumadin
coagulopathy, but its standard use in the hemorrhagic shock patient remains valid.

Platelets are given in high concentration “6 packs” of platelets with one “6 pack” being equal to one apheresis Unit. 1
Unit is typically 250 cc, is stored concentrated in a small volume of plasma, and only has a shelf life of 5 days at 20-
24 degrees Celsius. Unlike pRBCs, platelets lose what little shelf life they have when they are frozen, and so must
remain fresh from collection to administration. One Unit of platelets is thought to increase the body’s platelet count
by 30,000-60,000 platelets/uL. Roughly 20% of patients can develop antiplatelet antibodies after 10-20 transfusions.

Finally, one other commonly used blood product is cryoprecipitate, which is used in a similar fashion to FFP.
Cryoprecipitate, or Cryo, is gathered by centrifuging plasma and gathering the precipitate, which contains large ratios
of vWBF, factor 8, fibrin (factor 13), and fibrinogen. Like plasma, Cryo is frozen and can be stored for up to two
years at -30 degrees Celsius. Cryo is typically provided in 10-15 cc units which are then given in 6-10 unit pooled
increments.

Technique
During the primary survey of the patient in hemorrhagic shock, a circulatory assessment should include the insertion
of two large-bore IVs (16-18 gauge) bilaterally to facilitate the fastest administration of fluids. If this is not available,
then a central venous catheter (CVC) or a standard 7 French triple lumen CVC should be placed. The reason which 2
large-bore peripheral IVs are more successful than a CVC in rapid fluid resuscitation is due to Poiseuille law which
states that fluids passing through a lumen can be transfused most quickly when there is laminar flow (width and
length affect velocity). This law also states that the longer the lumen through which the fluids pass, the less laminar
flow there is. Therefore, two short peripheral IVs of sufficient diameter are more expedient in transfusions than one
large long CVC.

Initial hemorrhagic shock resuscitation begins with the administration of IV fluids, followed by transfusion of blood
products at a 1:1:1 ratio. The initial IV fluids should be a 2 L bolus of 0.9% normal saline or two 20 mL/kg boluses by
patient weight. The patient is then determined to be either a responder, transient responder, or nonresponder to IV
fluids based on their improvement. Typically, patients in Class 1 or 2 can be treated initially with a trial bolus of
crystalloids, but patients in Class 3 or 4 should be getting blood products immediately with the first bolus of
crystalloids. The amount of blood transfused depends on a variety of factors, but is specifically centered around the
concept of “permissive hypotension”. Permissive hypotension is the idea that a patient in active hemorrhagic shock
should be transfused just enough blood products to retain a systolic blood pressure above 70 mmHg. Then, after
hemorrhage is controlled, the patient can be transfused to retain a systolic blood pressure above 90 mmHg.[3] As a
rule of thumb, one can expect roughly a loss of 1 L blood with a femur fracture, and at least 1 L blood loss with a
pelvic fracture. Other long bone fractures such as the humerus, tibia, or fibula can also account for as much as 500 ccs
each of blood loss. As such, a patient with bilateral femur fractures or a pelvic fracture can already be assumed to be
approaching stage 3 or IV of hemorrhagic shock. As the saying goes in accounting for blood loss in hemorrhagic
shock, “blood on the floor, plus four more”. This phrase meaning basically that a life-threatening amount of blood can
be lost as active hemorrhage outside the body, in the thigh compartments of bilateral femur fractures, the pelvis,
abdomen, or chest. It should also be noted that no number of transfusions should be used as a substitute for definitive
control of an active bleed.
Complications
During the transfusion process in hemorrhagic shock, it is common for transfusion requirements to extend past the
initial products given. Most all hospitals incorporate a “massive transfusion protocol” into this process, with a
“massive transfusion” being the replacement of one entire blood volume (or 10 U pRBCs) in 24 hours.[4] A rapid
infuser can be used which warms the products as they are transfused, thus improving their ability to clot appropriately.
As stated previously, the patient’s clinical status and vital signs help to gauge the rate of transfusion, but frequent
checks on the patient’s CBC, PT, PTT, INR, fibrinogen, and ionized Ca be made roughly every 5-10 U pRBCs given.
This is to ensure not only appropriate improvement in measured hemoglobin but that the patient has not developed
dilutional thrombocytopenia or coagulation factor deficiency during massive transfusion. Ionized calcium (iCa) is
monitored as it can be reduced rapidly, causing hypocalcemia in light of a massive transfusion. Citrate circulating in
the bloodstream acts to chelate iCa, thereby inactivating it. A unit of pRBCs contains roughly 3 mg of citrate in the
CPDA-1 used for storage. Typically, this is rapidly cleared by the liver within 5 minutes, but with massive
transfusions it can become overwhelming, causing mass chelation of the body’s iCa.[5] 10-20 cc Ca gluconate or 2-5
cc CaCl should be administered via IV for every 500 cc blood products given.

Clinical Significance
Shock resuscitation remains clinically significant simply due to the life-threatening nature of blood loss. Due to the
body's ability to bleed a significant amount into either the chest, abdomen, pelvis, or thighs, the first signs of
hemorrhagic shock may not always be so easily noticed. In addition, many cases of shock resuscitation are not
prompted by traumatic events, but by other forms of blood loss. Whether it be due to a GI bleed, or hemorrhage due
to coagulopathy, physicians must be mindful of changes in vital signs should they occur in order to recognize shock.
Furthermore, the patients' general appearance may be helpful in determining the diagnosis. If the patient appears
diaphoretic and visibly uncomfortable along with having vital signs suggestive of early stages of hemorrhagic shock,
clinical suspicion for shock should be high.

As previously stated, a common sign of impending shock can be a decrease in pulse pressure, an increased heart rate,
or a slight increase in breathing. Most important of all, the clinical evidence of decreased urine output can indicate
impending shock as kidneys become slightly hypoperfused. A decrease of urine output below 30 ccs/hr, or more
exactly less than 0.5 ccs/kg/hr, suggests renal hypoperfusion and could be the first sign of stage 1 shock. Of course,
there are other reasons which could be causing renal hypoperfusion. It is vital to keep in mind the patient's full history
and physical exam, as these may suggest other etiologies besides blood loss. For example, if a patient has been taking
a new beta-blocker, they may be having decreased blood pressure and renal hypoperfusion unrelated to blood loss.
The physical exam must be used to assess the chest, abdomen, pelvis, and thighs to ensure there is no evidence of
blood loss present. These signs could be as apparent as decreased breath sounds due to blood in the pleural space,
or increased abdominal distention or pain due to blood in the abdomen. Patients with some level of coagulopathy may
also have hematomas that may develop along with the psoas, which may be difficult to diagnose on exam along. Any
new pain in lower extremity flexion/extension should be the reason for concern. A CT of the abdomen/pelvis with
contrast can be helpful in diagnosing a psoas hematoma, or retroperitoneal bleed.

Enhancing Healthcare Team Outcomes

There are a variety of products that can be beneficial in shock resuscitation, but the three typical products used in the
acute care setting are packed red blood cells (pRBCs), fresh frozen plasma (FFP), and platelets. The U.S. military
discovered issues with ARDS and MODS developing in patients with large-volume resuscitation with strict
crystalloids as early as 1996. Then, it was studies of the early 2000’s such as the PROMTT study (2013) and PROPPR
trial (2015) which further refined our resuscitative use of blood products to their current form.[6] The PROMTT study
was a prospective, multicenter observational cohort in which a varying ratio of blood products (1:1:1 vs.
1:1:2) was administered to patients in shock to determine any changes in 6-hour survival rates. It was found that 1:2
ratios or higher had a higher likelihood of dying in the first 6 hours, and that earlier transfusion of blood products and
earlier use of FFP showed to have decreased 24 hours and 30-day mortality. In a similar vein, the PROPPR trial was a
randomized clinical trial where 1:1:1 and 1:1:2 ratios for transfusions were compared specifically for any difference
in mortality at 24 hours and then again at 30 days. While there was no significant difference in mortality rates, the
1:1:1 group did experience lower rates of death from exsanguination at 24 hours as well as fewer instances of ARDS,
MODS, sepsis, infection, or VTE. Today, the concept of “balanced fluid resuscitation” is the standard of care, with the
usual intent of a 1:1:1 ratio of FFP, platelets, and pRBCs to be given. It was discovered that this ratio tended to result
in greater 6-hour survival, fewer morbidities, and fewer deaths from exsanguination within the first 24 hours of injury.

Review Questions
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References
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