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Hypovolemic shock
Specialty Emergency care
Hypovolemic shock is a medical emergency and an advanced form of hypovolemia due to
insufficient amounts of blood and/or fluid inside the human body to let the heart
pump enough blood to the body.[1][2] More specifically, hypovolemic shock occurs
when there is decreased intravascular volume to the point of cardiovascular
compromise. The hypovolemic shock could be due to severe dehydration through a
variety of mechanisms or from blood loss.[3][2]

People 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.[4]

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.[4] Factors to consider
when replacing fluid loss include the rate of fluid replacement and type of fluid
to be used.[4]

Trauma is the most common cause of hemorrhagic shock, but causes can span multiple
systems.[3] Tachycardia is typically the first abnormal vital sign of hemorrhagic
shock.[3] As the body attempts to preserve oxygen delivery to the brain and heart,
blood is shunted away from extremities and nonvital organs.[3] This causes cold and
mottled extremities with delayed capillary refill.[3] This shunting ultimately
leads to worsening acidosis.[3] The "lethal triad" of trauma is acidosis,
hypothermia, and coagulopathy.[3] Trauma-induced coagulopathy can occur in the
absence of the hemodilution of resuscitation.[3] Damage control resuscitation is
based on three principles: permissive hypotension, hemostatic resuscitation, and
damage control surgery.[3] Permissive hypotension targets a systolic blood pressure
of 90 mmHg accepting suboptimal perfusion to end organs for a limited time to
achieve hemostasis.[3]

Contents
1 Signs and symptoms
2 Cause
2.1 Blood loss
2.2 Fluid loss
2.2.1 Gastrointestinal
2.2.2 Kidneys
2.2.3 Skin
2.2.4 Third-spaceing
3 Pathophysiology
3.1 Blood loss
3.2 Fluid loss
4 Diagnosis
4.1 Bleeding
4.2 Non-bleeding
4.3 Differential diagnosis
5 Management
5.1 Bleeding
5.2 Fluid loss
5.3 Monitoring parameters
6 Prognosis
7 Epidemiology
7.1 Blood loss
7.2 Fluid loss
8 See also
9 References
Signs and symptoms
See also: Cardiogenic shock § signs and symptoms, Vasodilatory shock § signs and
symptoms, and Shock (circulatory) § Signs and symptoms
Symptoms of hypovolemic shock can be related to volume depletion, electrolyte
imbalances, or acid-base disorders that accompany hypovolemic shock.[4]

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 characterize brain mal-perfusion.[4]

Dry mucous membranes, decreased skin turgor, low jugular venous distention,
tachycardia, and hypotension can be seen along with decreased urinary output.[4]
Patients in shock can appear cold, clammy, and cyanotic.[4]

Early signs and symptoms comprise tachycardia given rise to by catecholamine

release, skin pallor due to vasoconstriction triggered by catecholamine release,
hypotension followed by hypovolaemia and perhaps come after myocardial
insufficiency, confusion, aggression, drowsiness and coma either caused by cerebral
hypoxia or acidosis.[5] Tachypnoea owing to hypoxia and acidosis, general weakness
caused by hypoxia and acidosis, thirst induced by hypovolaemia and oliguria caused
by reduced perfusion.[5]

Abnormal growing central venous pressure indicates either hypotension or

hypovolemia. Tachycardia accompanied by declined urine outflow implies either
tension pneumothorax, cardiac tamponade or cardiac failure which is thought
secondary to cardiac contusion or ischaemic heart disease.[5] Echocardiography in
such case may be helpful to distinguish cardiac failure from other diseases.[5]
Cardiac failure manifests a weak contractibility myocardium; treatment with an
inotropic drug such as dobutamine may be appropriate.[5]

Cause
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.[4]

Hypovolemic shock occurs as a result of either blood loss or extracellular fluid

loss.[4]

Blood loss
Hemorrhagic shock is hypovolemic shock from blood loss. Traumatic injury is by far
the most common cause of hemorrhagic shock,[4] particularly blunt and penetrating
trauma,[3] followed by upper and lower gastrointestinal sources,[3] such as
gastrointestinal (GI) bleed.[4] Other causes of hemorrhagic shock include bleed
from an ectopic pregnancy, bleeding from surgical intervention, or vaginal
bleeding.[4]
Obstetrical, vascular, iatrogenic, and even urological sources have all been
described.[3] Bleeding may be either external or internal.[3] A substantial amount
of blood loss to the point of hemodynamic compromise may occur in the chest,
abdomen, or the retroperitoneum.[3] The thigh itself can hold up to 1 L to 2 L of
blood.[3]

Localizing and controlling the source of bleeding is of utmost importance to the

treatment of hemorrhagic shock.[3]

The sequence of the most-commonly-seen causes that lead to hemorrhagic type of

hypovolemic shock is given in order of frequencies: blunt or penetrating trauma
including multiple fractures absent from vessel impairment, upper gastrointestinal
bleeding e.g., variceal hemorrhage, peptic ulcer., or lower GI bleeding e.g.,
diverticular, and arteriovenous malformation.[6]

Except for the two most common causes, the less common causes are intra-operative
and post-operative bleeding, abdominal aortic rupture or left ventricle aneurysm
rupture, aortic–enteric fistula, hemorrhagic pancreatitis, iatrogenic e.g.,
inadvertent biopsy of arteriovenous malformation, severed artery., tumors or
abscess erosion into major vessels, post-partum hemorrhage, uterine or vaginal
hemorrhage owing to infection, tumors, lacerations, spontaneous peritoneal
hemorrhage caused by bleeding diathesis, and ruptured hematoma.[7]

Fluid loss
In spite of hemorrhage, the amount of circulating blood in the body may drop as
well when one loses excessive body fluid owing to non-hemorrhagic reasons.[1]
Hypovolemic shock as a result of extracellular fluid loss can be of the 4
etiologies.[4]

Gastrointestinal
Gastrointestinal Losses (GI) losses can occur via many different etiologies. The
gastrointestinal tract usually secretes between 3 and 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.[4]

Kidneys
Renal losses of salt and fluid can lead to hypovolemic shock. The kidneys usually
excrete sodium and water in a manner that matches sodium intake and water intake.
[4]

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.[4]

Skin
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.[4]

Third-spaceing
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, vascular endothelium[8] or any
other pathological condition that results in a massive inflammatory response.[4]
Pathophysiology
Blood loss
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
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]

Further information: Hemodynamic, Vasoconstriction, Peripheral artery disease,

Cardiac output, and Urinary output
Diagnosis
Shock index (SI) has been defined as
heart rate
/
systolic blood pressure
; SI≥0.6 is a clinical shock.

Such ratio value is clinically employed to determine the scope or emergence of

shock.[9] The SI correlates with the extent of hypovolemia and thus may facilitate
the early identification of severely injured patients threatened by complications
due to blood loss and therefore need urgent treatment, i.e. blood transfusion.[10]
[11]

Patients classified by Shock Index: traditional vital signs presented at the

emergency department (ED) admission and at first scene.
Group I (SI <0.6, no shock) Group II (SI ≥0.6 to <1.0, mild shock) Group III
(SI ≥1.0 to <1.4, moderate shock) Group IV (SI ≥1.4, severe shock)
SBP at scene (mmHg)
Mean ± standard deviation 136.8 (32.8) 121.9 (29.4) 105.2 (33.1)
92.9 (34.4)
Median (IQR) 138 (120 to 160) 120 (105 to 140) 100 (90 to 120) 90 (70 to
110)
SBP at ED (mmHg)
Mean ± standard deviation 148.4 (25.6) 124.1 (20.2) 96.9 (16.8) 70.6
(15.7)
Median (IQR) 147 (130 to 160) 120 (110 to 138) 98 (86 to 108) 70 (60 to
80)
HR at scene (beats/minute)
Mean ± standard deviation 83.0 (19.2) 94.0 (20.6) 103.7 (26.6) 110.5 (31.3)
Median (IQR) 80 (70 to 95) 94 (80 to 105) 105 (90 to 120) 115 (100 to
130)
HR at ED (beats/minute)
Mean ± standard deviation 73.7 (13.6) 91.3 (15.1) 109.1 (17.9) 122.7 (19.5)
Median (IQR) 74 (65 to 80) 90 (80 to 100) 110 (100 to 120) 120 (110 to
135)
SI at scene (beats/minute)
Mean ± standard deviation 0.6 (0.2) 0.8 (0.3) 1.1 (0.4) 1.3 (0.5)
Median (IQR) 0.6 (0.5 to 0.7) 0.8 (0.6 to 0.9) 1.0 (1.0 to 1.0) 1.2 (0.9 to
1.6)
Data presented as n (%), mean ± standard deviation or median (interquartile range
(IQR)). n = 21,853; P <0.001 for all parameters. ED Emergency department, GCS
Glasgow coma scale, HR Heart rate, SBP Systolic blood pressure, SI = Shock index.

[11]

Further information: Pre-shock

Bleeding
Recognizing the degree of blood loss via vital sign and mental status abnormalities
is important. The American College of Surgeons Advanced Trauma Life Support (ATLS)
hemorrhagic shock classification links the amount of blood loss to expected
physiologic responses in a healthy 70 kg patient. As total circulating blood volume
accounts for approximately 7% of total body weight, this equals approximately five
liters in the average 70 kg male patient.[3]

Class 1: Volume loss up to 15% of total blood volume, approximately 750 mL. Heart
rate is minimally elevated or normal. Typically, there is no change in blood
pressure, pulse pressure, or respiratory rate.[3]
Class 2: Volume loss from 15% to 30% of total blood volume, from 750 mL to 1500 mL.
Heart rate and respiratory rate become elevated (100 BPM to 120 BPM, 20 RR to 24
RR). Pulse pressure begins to narrow, but systolic blood pressure may be unchanged
to slightly decreased.[3]
Class 3: Volume loss from 30% to 40% of total blood volume, from 1500 mL to 2000
mL. A significant drop in blood pressure and changes in mental status occur.[3]
Heart rate and respiratory rate are significantly elevated (more than 120 BPM).
Urine output declines. Capillary refill is delayed.[3]
Class 4: Volume loss over 40% of total blood volume. Hypotension with narrow pulse
pressure (less than 25 mmHg). Tachycardia becomes more pronounced (more than 120
BPM), and mental status becomes increasingly altered. Urine output is minimal or
absent. Capillary refill is delayed.[3]
Again, the above is outlined for a healthy 70 kg individual. Clinical factors must
be taken into account when assessing patients. For example, elderly patients taking
beta blockers can alter the patient's physiologic response to decreased blood
volume by inhibiting mechanism to increase heart rate. As another, patients with
baseline hypertension may be functionally hypotensive with a systolic blood
pressure of 110 mmHg.[3]

Non-bleeding
Various laboratory values can be abnormal in hypovolemic shock. Patients can have
increased BUN and serum creatinine as a result of pre-renal kidney failure.
Hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia.[4]

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.[4]

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. 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.[4]

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.[4]

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.[4]

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.[4]

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.
[4] 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.[4]

Although relatively nonsensitive and nonspecific, physical exam can be helpful in

determining the presence of hypovolemic shock.[4] 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.[4]

Differential diagnosis
While hemorrhage is the most common cause of shock in the trauma patient, other
causes of shock are to remain on the differential. Obstructive shock can occur in
the setting of tension pneumothorax and cardiac tamponade. These etiologies should
be uncovered in the primary survey.[3] In the setting of head or neck trauma, an
inadequate sympathetic response, or neurogenic shock, is a type of distributive
shock that is caused by a decrease in peripheral vascular resistance.[3] This is
suggested by an inappropriately low heart rate in the setting of hypotension.[3]
Cardiac contusion and infarctions can result in cardiogenic shock.[3] Finally,
other causes should be considered that are not related to trauma or blood loss. In
the undifferentiated patient with shock, septic shock and toxic causes are also on
the differential.[3]

Management
The first step in managing hemorrhagic shock is recognition. Ideally, This should
occur before the development of hypotension. Close attention should be paid to
physiological responses to low-blood volume.[3] Tachycardia, tachypnea, and
narrowing pulse pressure may be the initial signs. Cool extremities and delayed
capillary refill are signs of peripheral vasoconstriction.[3]

Bleeding
In the setting of trauma, an algorithmic approach via the primary and secondary
surveys is suggested by ATLS. Physical exam and radiological evaluations can help
localize sources of bleeding. A trauma ultrasound, or Focused Assessment with
Sonography for Trauma (FAST), has been incorporated in many circumstances into the
initial surveys. The specificity of a FAST scan has been reported above 99%, but a
negative ultrasound does not rule out intra-abdominal pathology.[3]

With a broader understanding of the pathophysiology of hemorrhagic shock, treatment

in trauma has expanded from a simple massive transfusion method to a more
comprehensive management strategy of "damage control resuscitation". The concept of
damage control resuscitation focuses on permissive hypotension, hemostatic
resuscitation, and hemorrhage control to adequately treat the "lethal triad" of
coagulopathy, acidosis, and hypothermia that occurs in trauma.[3]

Hypotensive resuscitation has been suggested for the hemorrhagic shock patient
without head trauma. The aim is to achieve a systolic blood pressure of 90 mmHg in
order to maintain tissue perfusion without inducing re-bleeding from recently
clotted vessels. Permissive hypotension is a means of restricting fluid
administration until hemorrhage is controlled while accepting a short period of
suboptimal end-organ perfusion. Studies regarding permissive hypotension have
yielded conflicting results and must take into account type of injury (penetrating
versus blunt), the likelihood of intracranial injury, the severity of the injury,
as well as proximity to a trauma center and definitive hemorrhage control.[3]

The quantity, type of fluids to be used, and endpoints of resuscitation remain

topics of much study and debate. For crystalloid resuscitation, normal saline and
lactated ringers are the most commonly used fluids. Normal saline has the drawback
of causing a non-anion gap hyperchloremic metabolic acidosis due to the high
chloride content, while lactated ringers can cause a metabolic alkalosis as lactate
metabolism regenerates into bicarbonate.[3]

Recent trends in damage control resuscitation focus on "hemostatic resuscitation"

which pushes for early use of blood products rather than an abundance of
crystalloids in order to minimize the metabolic derangement, resuscitation-induced
coagulopathy, and the hemodilution that occurs with crystalloid resuscitation. The
end goal of resuscitation and the ratios of blood products remain at the center of
much study and debate. A recent study has shown no significant difference in
mortality at 24 hours or 30 days between ratios of 1:1:1 and 1:1:2 of plasma to
platelets to packed RBCs. However, patients that received the more balanced ratio
of 1:1:1 were less likely to die as a result of exsanguination in 24 hours and were
more likely to achieve hemostasis Additionally, reduction in time to first plasma
transfusion has shown a significant reduction in mortality in damage control
resuscitation.[3]

In addition to blood products, products that prevent the breakdown of fibrin in

clots, or antifibrinolytics, have been studied for their utility in the treatment
of hemorrhagic shock in the trauma patient. Several antifibrinolytics have been
shown to be safe and effective in elective surgery. The CRASH-2 study was a
randomized control trial of tranexamic acid versus placebo in trauma has been shown
to decrease overall mortality when given in the first eight hours of injury.[3]
Follow-up analysis shows additional benefit to tranexamic acid when given in the
first three hours after surgery.[3]

Damage control resuscitation is to occur in conjunction with prompt intervention to

control the source of bleeding.[3] Strategies may differ depending on proximity to
definitive treatment.[3]

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.[4]

Fluid loss
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.[4] Vasopressors may
be used if blood pressure does not improve with fluids.

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.[4]

Isotonic saline is hyperchloremic relative to blood plasma, and resuscitation with

large amounts can lead to 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 hyper-oncotic starch leads to increased mortality rate and renal
failure.[4] Patients in shock can appear cold, clammy, and cyanotic.[4]

Hypothermia increases the mortality rate of patients suffering hypovolemic shock.

It is advised to keep the patient warm for the sake of maintaining the temperatures
of all kinds of fluids inside the patient.[5]

Monitoring parameters
Oxygen saturation by pulse oximetry (SpO2).
Respiratory rate.
Pulse rate.
Arterial blood pressure.
Pulse pressure.
Central venous pressure.
Urine output.
Base deficit and/or lactic acid.
Temperature.
Mental state.
Changes in the electrocardiogram.[5]
Prognosis
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 identifying patients who are likely to succumb to
their illness is of utmost importance.[12]

Epidemiology
Blood loss
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
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 a less physiologic reserve.[4]

Hypovolemia secondary to diarrhea/dehydration is thought to be predominant in low-

income countries.[13]

See also
Adipsia
Anemia
Cardiac index
Heart murmur
References
"Hypovolemic shock: MedlinePlus Medical Encyclopedia". MedlinePlus. 2019-01-28.
Retrieved 2019-02-21.
McGee, Steven (2018). Evidence-based physical diagnosis. Philadelphia, PA:
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collectively to two distinct disorders: (1) volume depletion, which describes the
loss of sodium from the extracellular space (i.e., intravascular and interstitial
fluid) that occurs during gastrointestinal hemorrhage, vomiting, diarrhea, and
diuresis; and (2) dehydration, which refers to the loss of intracellular water (and
total body water) that ultimately causes cellular desiccation and elevates the
plasma sodium concentration and osmolality.
Hooper, Nicholas; Armstrong, Tyler J. (2018-10-27). "Shock, Hemorrhagic". NCBI
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Berger, Tony; Green, Jeffrey; Horeczko, Timothy; Hagar, Yolanda; Garg, Nidhi;
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Fröhlich, M; Driessen, A; Böhmer, A; Nienaber, U; Igressa, A; Probst, C; Bouillon,
B; Maegele, M; Mutschler, M (2016-12-12). "Is the shock index based classification
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PMID 27846837.
vte
Shock
Distributive
Septic shockNeurogenic shockAnaphylactic shockToxic shock syndrome
Obstructive
Abdominal compartment syndrome
Low volume
HemorrhageHypovolemia Osmotic shock
Other
Spinal shockCryptic shockVasodilatory shock
Categories: Medical emergencies
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