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Hypovolemic Shock
Taghavi S, Askari R.

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Introduction
Patients with hypovolemic shock have severe
hypovolemia with decreased peripheral perfusion.
If left untreated, these patients can develop
ischemic injury of vital organs, leading to multi-
system organ failure. The first factor to be
considered is whether the hypovolemic shock has
resulted from hemorrhage or fluid losses, as this
will dictate treatment. When etiology of
hypovolemic shock has been determined,
replacement of blood or fluid loss should be
carried out as soon as possible to minimize tissue
ischemia. Factors to consider when replacing
fluid loss include the rate of fluid replacement
and type of fluid to be used. [1]

Etiology
The annual incidence of shock of any etiology is
0.3 to 0.7 per 1000, with hemorrhagic shock
being most common in the intensive care unit.
Hypovolemic shock is the most common type of
shock in children, most commonly due to
diarrheal illness in the developing world.
Hypovolemic shock occurs as a result of either
blood loss or extracellular fluid loss.
Hemorrhagic shock is hypovolemic shock from
blood loss. Traumatic injury is by far the most
common cause of hemorrhagic shock. Other
causes of hemorrhagic shock include
gastrointestinal (GI) bleed, bleed from an ectopic
pregnancy, bleeding from surgical intervention, or
vaginal bleeding.

Hypovolemic shock as a result of extracellular

fluid loss can be of the following etiologies:

Gastrointestinal Losses

GI losses can occur via many different etiologies.

The gastrointestinal tract usually secretes between
3 to 6 liters of fluid per day. However, most of
this fluid is reabsorbed as only 100 to 200 mL are
lost in the stool. Volume depletion occurs when
the fluid ordinarily secreted by the GI tract cannot
be reabsorbed. This occurs when there is
retractable vomiting, diarrhea, or external
drainage via stoma or fistulas.

Renal Losses

Renal losses of salt and fluid can lead to

hypovolemic shock. The kidneys usually excrete
sodium and water in a manner that matches
intake. Diuretic therapy and osmotic diuresis
from hyperglycemia can lead to excessive renal
sodium and volume loss. In addition, there are
several tubular and interstitial diseases beyond the
scope of this article that cause severe salt-wasting
nephropathy.

Skin Losses

Fluid loss also can occur from the skin. In a hot

and dry climate, skin fluid losses can be as high
as 1 to 2 liters/hour. Patients with a skin barrier
interrupted by burns or other skin lesions also can
experience large fluid losses that lead to
hypovolemic shock.

Third-Space Sequestration

Sequestration of fluid into a third-space also can

lead to volume loss and hypovolemic shock.
Third-spacing of fluid can occur in intestinal
obstruction, pancreatitis, obstruction of a major
venous system, or any other pathological
condition that results in a massive inflammatory
response. [1]

Epidemiology
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 blood
products used were related to traumatic injury.
Elderly patients are more likely to experience
hypovolemic shock due to fluid losses as they
have a less physiologic reserve.[1]

Pathophysiology
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. As
volume status continues to decrease, systolic
blood pressure drops. As a result, oxygen delivery
to vital organs is unable to meet oxygen demand.
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. [2]

History and Physical

History and physical can often make the
diagnosis of hypovolemic shock. For patients
with hemorrhagic shock, a history of trauma or
recent surgery is present. For hypovolemic shock
due to fluid losses, history and physical should
attempt to identify possible GI, renal, skin, or
third-spacing as a cause of extracellular fluid loss.
Symptoms of hypovolemic shock can be related
to volume depletion, electrolyte imbalances, or
acid-base disorders that accompany hypovolemic
shock.

Patients with volume depletion may complain of

thirst, muscle cramps, and/or orthostatic
hypotension. Severe hypovolemic shock can
result in mesenteric and coronary ischemia that
can cause abdominal or chest pain. Agitation,
lethargy, or confusion may result from brain
malperfusion.

Although relatively nonsensitive and nonspecific,

physical exam can be helpful in determining the
presence of hypovolemic shock. Physical findings
suggestive of volume depletion include dry
mucous membranes, decreased skin turgor, and
low jugular venous distention. Tachycardia and
hypotension can be seen along with decreased
urinary output. Patients in shock can appear cold,
clammy, and cyanotic.[3]

Evaluation
Various laboratory values can be abnormal in
hypovolemic shock. Patients can have increased
BUN and serum creatinine as a result of prerenal
kidney failure. Hypernatremia or hyponatremia
can result, as can hyperkalemia or hypokalemia.
Lactic acidosis can result from increased
anaerobic metabolism. However, the effect of
acid-base balance can be variable as patients with
large GI losses can become alkalotic. In cases of
hemorrhagic shock, hematocrit and hemoglobin
can be severely decreased. However, with a
reduction in plasma volume, hematocrit and
hemoglobin can be increased due to
hemoconcentration.

Low urinary sodium is commonly found in

hypovolemic patients as the kidneys attempt to
conserve sodium and water to expand the
extracellular volume. However, sodium urine can
be low in a euvolemic patient with heart failure,
cirrhosis, or nephrotic syndrome. A fractional
excretion of sodium under 1% is also suggestive
of volume depletion. Elevated urine osmolality
can also suggest hypovolemia. However, this
number also can be elevated in the setting of
impaired concentrating ability by the kidneys.

Central venous pressure (CVP) is often used to

assess volume status. However, its usefulness in
determining volume responsiveness has recently
come into question. Ventilator settings, chest wall
compliance, and right-sided heart failure can
compromise CVPs accuracy as a measure of
volume status. Measurements of pulse pressure
variation via various commercial devices has also
been postulated as a measure of volume
responsiveness. However, pulse pressure
variation as a measure of fluid responsiveness is
only valid in patients without spontaneous breaths
or arrhythmias. The accuracy of pulse pressure
variation also can be compromised in right heart
failure, decreased lung or chest wall compliance,
and high respiratory rates.

Similar to examining pulse pressure variation,

measuring respiratory variation in inferior vena
cava diameter as a measure of volume
responsiveness has only been validated in patients
without spontaneous breaths or arrhythmias.
Measuring the effect of passive leg raises on
cardiac contractility by echo appears to be the
most accurate measurement of volume
responsiveness, although it is also subject to
limitations. [3][[4]

Treatment / Management
For patients in hemorrhagic shock, early use of
blood products over crystalloid resuscitation
results in better outcomes. Balanced transfusion
using 1:1:1 or 1:1:2 of plasma to platelets to
packed red blood cells results in better
hemostasis. Anti-fibrinolytic administration to
patients with severe bleed within 3 hours of
traumatic injury appears to decrease death from
major bleed as shown in the CRASH-2 trial.
Research on oxygen-carrying substitutes as an
alternative to packed red blood cells is ongoing,
although no blood substitutes have been approved
for use in the United States.

For patients in hypovolemic shock due to fluid

losses, the exact fluid deficit cannot be
determined. Therefore, it is prudent to start with 2
liters of isotonic crystalloid solution infused
rapidly as an attempt to quickly restore tissue
perfusion. Fluid repletion can be monitored by
measuring blood pressure, urine output, mental
status, and peripheral edema. Multiple modalities
exist for measuring fluid responsiveness such as
ultrasound, central venous pressure monitoring,
and pulse pressure fluctuation as described above.
In general, for hypovolemic shock, vasopressors
should not be used because they can worsen
tissue perfusion.

Crystalloid fluid resuscitation is preferred over

colloid solutions for severe volume depletion not
due to bleeding. The type of crystalloid used to
resuscitate the patient can be individualized based
on the patients’ chemistries, estimated volume of
resuscitation, acid/base status, and physician or
institutional preferences. Isotonic saline is
hyperchloremic relative to blood plasma, and
resuscitation with large amounts can lead to a
hyperchloremic metabolic acidosis. Several other
isotonic fluids with lower chloride concentrations
exist, such as lactated Ringer's solution or
PlasmaLyte. These solutions are often referred to
as buffered or balanced crystalloids. Some
evidence suggests that patients who need large
volume resuscitation may have a less renal injury
with restrictive chloride strategies and use of
balanced crystalloids. Crystalloid solutions are
equally as effective and much less expensive than
colloid. Commonly used colloid solutions include
those containing albumin or hyperoncotic starch.
Studies examining albumin solutions for
resuscitation have not shown improved outcomes,
while other studies have shown resuscitation with
hyperoncotic starch leads to increased mortality
and renal failure.[5][6][7][8][9]

Di!erential Diagnosis
Femoral shaft fractures in emergency
medicine

Gastrointestinal bleeding

Hemorrhagic shock in emergency medicine

Iron toxicity

Pelvic fracture in emergency medicine

Pregnancy trauma

Peptic ulcer disease

Placental previa imaging

Thoracic aneurysm

Pearls and Other Issues

In patients with hypovolemic shock due to
extracellular fluid loss, the etiology of fluid
loss must be identified and treated.
Monitoring electrolytes and acid/base status
in patients in hypovolemic shock is of
utmost importance.
Trauma is the leading cause of hemorrhagic
shock.
The hemorrhagic shock should be treated
with balanced transfusion of packed red
blood cells, plasma, and platelets.
Determining whether patients will be
responsive to volume resuscitation should
not rely on a single modality such as
ultrasound, pulse pressure wave variation,
passive leg raises, or central venous
pressure. The decision for fluid
administration should be based on the entire
clinical presentation, laboratory values, and
the aforementioned modalities.
For patients with hypovolemic shock due to
fluid loss, the crystalloid solution is
preferred over colloid.

Enhancing Healthcare Team

Outcomes
The management of hypovolemic shock requires
an interprofessional team including ICU nurses.
For patients with hypovolemic shock due to fluid
loss, the crystalloid solution is preferred over
colloid.These patients need monitoring of their
fluid input and output and should be in an ICU
setting. The outcomes depend on the cause of
shock, the patient age, comorbidities and presence
of renal failure.

Continuing Education / Review

Questions
Access free multiple choice questions on
this topic.
Earn continuing education credits
(CME/CE) on this topic.
Comment on this article.

References
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Publication Details

Author Information

Authors

Sharven Taghavi1; Reza Askari2.

A"liations

1 Tulane University School of Medicine

2 Harvard Medical School

Publication History

Last Update: July 20, 2020.

Copyright
Copyright © 2020, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative

Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which
permits use, duplication, adaptation, distribution, and
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Publisher

StatPearls Publishing, Treasure Island (FL)

NLM Citation

Taghavi S, Askari R. Hypovolemic Shock. [Updated 2020

Jul 20]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2020 Jan-.