1.

0 Introduction

Shock is one of the most complex conditions that can be found in critical patients and
is associated with a high mortality distributed in early (hemorrhagic shock), post injury
(trauma brain injury) and late (organ failure) (Sauaia A. et al. 2015) . The term "shock"
encompasses a wide range of pathological processes that may require diametrically opposed
methods of treatment. It is defined as a life-threatening circulatory failure where the oxygen
delivery is not enough to tissue demand (Cecconi M. et al. 2014). The underlying cause may
be easily identified as in the traumatic shock resulting from massive hidden blood loss. Shock
is a microcirculatory derangement associated with hypo perfusion and cellular death.
Multiple organ insufficiency.

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss
results in multiple organ failure due to inadequate circulating volume and subsequent
inadequate perfusion. Endothelium plays a critical role in vascular physiological,
pathophysiological, and reparative processes. The functions of the endothelium are highly
altered following hypovolemic shock due to ischemia of the endothelial cells and by
reperfusion due to resuscitation with fluids. Due to oxygen deprivation, endothelial cell
apoptosis is induced following hypovolemic shock (Gulati A. et al. 2016).Most often;
hypovolemic shock is secondary to rapid blood loss (haemorrhagic). Acute external blood
loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes
of haemorrhagic shock. Haemorrhagic shock can also result from significant acute internal
blood loss into the thoracic and abdominal cavities.

Two common causes of rapid internal blood loss are solid organ injury and rupture of
an abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other
than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include
refractory gastroenteritis and extensive burns. The remainder of this article concentrates
mainly on hypovolemic shock secondary to blood loss and the controversies surrounding the
treatment of this condition. The reader is referred to other articles for discussions of the
pathophysiology and treatment for hypovolemic shock resulting from losses of fluid other
than blood. The prognosis is dependent on the degree of volume loss.
2.0 Pathophysiology
The hematologic system responds to an acute severe blood loss by activating the
coagulation cascade and contracting the bleeding vessels. In addition, platelets are activated
and form an immature clot on the bleeding source. The damaged vessel exposes collagen,
which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24
hours are needed for complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by increasing the

heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. This
response occurs secondary to an increased release of norepinephrine and decreased baseline
vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and
pulmonary vessels). The cardiovascular system also responds by redistributing blood to the
brain, heart, and kidneys and away from skin, muscle, and GI tract.

The renal system responds to hemorrhagic shock by stimulating an increase in renin

secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin
I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has
2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of
arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex.
Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.
3.0 History Taking

In a patient with possible shock secondary to hypovolemia, the history is vital in

determining the possible causes and in directing the workup. Hypovolemic shock secondary
to external blood loss typically is obvious and easily diagnosed. Internal bleeding may not be
as obvious as patients may complain only of weakness, lethargy, or a change in mental status.
Symptoms of shock, such as weakness, lightheadedness, and confusion, should be assessed in
all patients.

In the patient with trauma, determine the mechanism of injury and any information
that may heighten suspicion of certain injuries (eg, steering wheel damage or extensive
passenger compartment intrusion in a motor vehicle accident). If conscious, the patient may
be able to indicate the location of pain. Vital signs, prior to arrival in the ED, should also be
noted. Chest, abdominal, or back pain may indicate a vascular disorder.

In patients with GI bleeding, inquiry about hematemesis, melena, alcohol drinking

history, excessive nonsteroidal anti-inflammatory drug use, and coagulopathies (iatrogenic or
otherwise) is very important. The chronology of vomiting and hematemesis should be
determined. The patient who presents with hematemesis after multiple episodes of forceful
vomiting is more likely to have Boerhaave syndrome or a Mallory-Weiss tear, whereas a
patient with a history of hematemesis from the start is more likely to have peptic ulcer disease
or esophageal varices.

If a gynecologic cause is being considered, gather information about the following:

last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount
and duration), vaginal passage of products of conception, and pain. All women of
childbearing age should undergo a pregnancy test, regardless of whether they believe that
they are pregnant. A negative pregnancy test typically excludes ectopic pregnancy as a
diagnosis.
4.0 Physical Examination

The physical examination should always begin with an assessment of the airway,
breathing, and circulation. Once these have been evaluated and stabilized, the circulatory
system should be evaluated for signs and symptoms of shock.

Do not focus on systolic BP as the main indicator of shock; this practice results in
delayed diagnosis. Compensatory mechanisms prevent a significant decrease in systolic BP
until the patient has lost 30% of the blood volume. More attention should be paid to the pulse,
respiratory rate, and skin perfusion. Also, patients taking beta-blockers may not present with
tachycardia, regardless of the degree of shock.

Classes of hemorrhage have been defined, based on the percentage of blood volume
loss. However, the distinction between these classes in the hypovolemic patient often is less
apparent. Treatment should be aggressive and directed more by response to therapy than by
initial classification.
Class I hemorrhage (loss of 0-15%)
In the absence of complications, only minimal tachycardia is seen. Usually, no changes in
BP, pulse pressure, or respiratory rate occur.
Class II hemorrhage (loss of 15-30%)
Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in
pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.
Class III hemorrhage (loss of 30-40%)
By this point, patients usually have marked tachypnea and tachycardia, decreased systolic
BP, oliguria, and significant changes in mental status, such as confusion or agitation.
Class IV hemorrhage (loss of >40%)
Symptoms is marked tachycardia, decreased systolic BP, narrowed pulse pressure (or
immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed
mental status (or loss of consciousness), and cold and pale skin.
This amount of hemorrhage is immediately life threatening.

In the patient with trauma, hemorrhage usually is the presumed cause of shock.
However, it must be distinguished from other causes of shock. These include cardiac
tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated
trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of
expected tachycardia, neurological deficits).

The 4 areas in which life-threatening hemorrhage can occur are as follows: chest,
abdomen, thighs, and outside the body. Note the following:
1. The chest should be auscultated for decreased breath sounds, because life-threatening
haemorrhage can occur from myocardial, vessel, or lung laceration.
2. The abdomen should be examined for tenderness or distension, which may indicate
intra-abdominal injury.
3. The thighs should be checked for deformities or enlargement (signs of femoral
fracture and bleeding into the thigh).
4. The patient's entire body should then be checked for other external bleeding.

In the patient without trauma, the majority of the hemorrhage is in the abdomen. The
abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an
aortic aneurysm, peptic ulcer disease, or liver congestion. Also check for other signs of
bruising or bleeding.

In the pregnant patient, perform a sterile speculum examination. However, with third-
trimester bleeding, the examination should be performed as a "double set-up" in the operating
room. Check for abdominal, uterine, or adnexal tenderness.

The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related, as
follows:
 Traumatic causes can result from penetrating and blunt trauma. Common traumatic
injuries that can result in haemorrhagic shock include the following: myocardial
laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and
femoral fractures, and scalp lacerations.
 Vascular disorders that can result in significant blood loss include aneurysms,
dissections, and arteriovenous malformations.
 GI disorders that can result in haemorrhagic shock include the following: bleeding
oesophageal varies, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal
fistulas.
  Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa,
and abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy
is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a
negative urine pregnancy test is rare but has been reported.

Diagnostic Considerations
A common error in the management of hypovolemic shock is failure to recognize it
early, often caused by a reliance on BP or initial haematocrit level, rather than signs of
decreased peripheral perfusion, to make the diagnosis. This error leads to delay in diagnosing
the cause and in resuscitating the patient as follow:
 Injuries in patients with trauma can be missed, especially if the examiner focuses on
more obvious injuries. This error can be avoided by completing a full physical
examination, continuously and closely monitoring the patient's status, and performing
serial examinations.
 Elderly individuals have less tolerance for hypovolemic compared with the rest of the
general population. Aggressive therapy should be instituted early to prevent potential
complications, such as myocardial infarction and stroke.
 Patients taking beta-blockers or calcium-channel blockers and those with
pacemakers may not have a tachycardia response to hypovolemic as a lack of response
may lead to a delay in the diagnosis of shock. To minimize this potential delay, history
taking should always include questioning about medications. The examiner should also
rely on signs of decreased peripheral perfusion other than tachycardia.
 Coagulopathies can occur in patients receiving large amounts of volume resuscitation.
This is due to dilution of platelets and clotting factors but is rare within the first hour of
resuscitation. Baseline coagulation studies should be drawn and should guide the
administration of platelets and fresh frozen plasma.
5.0 Investigation

After the history is taken and the physical examination is performed, further workup
depends on the probable cause of the hypovolemia, as well as on the stability of the patient's
condition.

Initial laboratory studies should include analysis of the CBC, electrolyte levels (eg,
Na, K, Cl, HCO3, BUN, creatinine, glucose levels), lactate, prothrombin time, activated
partial thromboplastin time, ABGs, urinalysis (in patients with trauma), and a urine
pregnancy test. Blood should be typed and cross-matched.

Imaging Studies
Patients with marked hypotension and/or unstable conditions must first be resuscitated
adequately. This treatment takes precedence over imaging studies and may include immediate
interventions and immediately taking the patient to the operating room.

The workup for the patient with trauma and signs and symptoms of hypovolemia is
directed toward finding the source of blood loss. The traumatic patient with hypovolemic
shock requires ultrasonographic examination in the ED if an abdominal aortic aneurysm is
suspected. If GI bleeding is suspected, a nasogastric tube should be placed, and gastric lavage
should be performed. An upright chest radiograph should be obtained if a perforated ulcer or
Boerhaave syndrome is a possibility. Endoscopy can be performed (usually after the patient
has been admitted) to further delineate the source of bleeding.

A pregnancy test should be performed in all female patients of childbearing age. If the
patient is pregnant and in shock, surgical consultation and the consideration of bedside pelvic
ultrasonography should be immediately performed in the ED. Hypovolemic shock secondary
to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy
in a patient with a negative pregnancy test, although rare, has been reported.

If thoracic dissection is suspected because of the mechanism and initial chest

radiographic findings, the workup may include transesophageal echocardiography,
aortography, or CT scanning of the chest.
 If a traumatic abdominal injury is suspected, a focused abdominal sonography for
trauma (FAST) ultrasonography examination may be performed in the stable or unstable
patient. Computed tomography (CT) scanning typically is performed in the stable patient.
If long-bone fractures are suspected, radiographs should be obtained.
6.0 Management Prehospital Care

The treatment of patients with hypovolemic shock often begins at an accident scene or
at home. The prehospital care team should work to prevent further injury, transport the
patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field.
Direct pressure should be applied to external bleeding vessels to prevent further blood
loss(Burns B. et al. 2015).

Prevention of further injury applies mostly to the patient with trauma. The cervical
spine must be immobilized, and the patient must be extricated, if applicable, and moved to a
stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.

Although in selected cases stabilization may be beneficial, rapid transport of sick

patients to the hospital remains the most important aspect of prehospital care. Definitive care
of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention.
Any delay in definitive care, eg, such as delayed transport, is potentially harmful.

Most prehospital interventions involve immobilizing the patient (if trauma is

involved), securing an adequate airway, ensuring ventilation, and maximizing circulation. In
the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return,
diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are
necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering
hypovolemic shock.

Appropriate treatment usually can be initiated without delaying transport. Some

procedures, such as starting intravenous (IV) lines or splinting of extremities, can be
performed while a patient is being extricated. However, procedures in the field that prolong
transportation should be delayed. Benefits to giving IV fluids prior to departure from the
scene are not clear; however, IV lines and fluid resuscitation should be started and continued
once the patient is en route to definitive care.
7.0 Management Emergency Department Care

Three goals exist in the emergency department treatment of the patient with
hypovolemic shock. maximize oxygen delivery like a completed by ensuring adequacy of
ventilation, increasing oxygen saturation of the blood, and restoring blood flow, control
further blood loss, and fluid resuscitation. Also, the patient's disposition should be rapidly
and appropriately determined.

Maximizing oxygen delivery

The patient's airway should be assessed immediately upon arrival and stabilized if
necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If
pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found,
it should be addressed immediately. High-flow supplemental oxygen should be administered
to all patients, and ventilatory support should be given, if needed. Excessive positive-pressure
ventilation can be detrimental for a patient suffering hypovolemic shock and should be
avoided.

Two large-bore IV lines should be started. The Poiseuille law states that flow is
inversely related to the length of the IV catheter and directly related to its radius to the fourth
power. Thus, a short large-caliber IV catheter is ideal; the caliber is much more significant
than the length. IV access may be obtained by means of percutaneous access in the
antecubital veins, cutdown of saphenous or arm veins, or access in the central veins by using
the Seldinger technique. If central lines are obtained, a large-bore single-lumen catheter
should be used. Intraosseous access has and continues to be used for hypotensive children
younger than 6 years. Intraosseous access has also been used in hypotensive adults (Sarkar D.
et al. 2016). The most important factor in determining the route of access is the practitioner's
skill and experience.

Placement of an arterial line should be considered for patients with severe

hemorrhage. For these patients, the arterial line will provide continuous blood pressure
monitoring and also ease arterial blood gas testing. Once IV access is obtained, initial fluid
resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or
normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient),
and the patient's response is assessed (Reinhart K. et al. 2015).
 If vital signs return to normal, the patient may be monitored to ensure stability, and
blood should be sent for typed and cross-matched. If vital signs transiently improve,
crystalloid infusion should continue and type-specific blood obtained. If little or no
improvement is seen, crystalloid infusion should continue, and type O blood should be given
(type O -negative blood should be given to female patients of childbearing age to prevent
sensitization and future complications)(Ghafari MH et al. 2016). If a patient is moribund and
markedly hypotensive (class IV shock), both crystalloid and type O blood should be started
initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be
based on the condition of the patient (Pacagnella RC et al. 2016).

The position of the patient can be used to improve circulation; one example is raising
the hypotensive patient's legs while fluid is being given. Another example of useful
positioning is rolling a hypotensive gravid patient with trauma onto her left side, which
displaces the fetus from the inferior vena cava and increases circulation. The Trendelenburg
position is no longer recommended for hypotensive patients, as the patient is predisposed to
aspiration. In addition, the Trendelenburg position does not improve cardiopulmonary
performance and may worsen gas exchange.

Autotransfusion may be a possibility in some patients with trauma. Several devices

that allow for the sterile collection, anticoagulation, filtration, and retransfusion of blood are
available. In the trauma setting, this blood almost always is from a hemothorax collected by
means of tube thoracostomy.

Control of further hemorrhage depends on the source of bleeding and often requires
surgical intervention. In the patient with trauma, external bleeding should be controlled with
direct pressure; internal bleeding requires surgical intervention. Long-bone fractures should
be treated with traction to decrease blood loss.

In the patient whose pulse is lost in the ED or just prior to arrival, an emergency
thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the
brain. This procedure is palliative at best and requires immediate transfer to the operating
room.
 In the patient with GI bleeding, intravenous vasopressin and H 2 blockers have been
used. Vasopressin commonly is associated with adverse reactions, such as hypertension,
arrhythmias, gangrene, and myocardial or splanchnic ischemia. Therefore, it should be
considered secondary to more definitive measures. H2 blockers are relatively safe but have no
proven benefit.

Somatostatin and octreotide infusions have been shown to reduce gastrointestinal

bleeding from varices and peptic ulcer disease. These agents possess the advantages of
vasopressin without the significant side effects.
In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered.
These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated
first, and then the esophageal one is inflated if bleeding continues. The use of this tube has
been associated with severe adverse reactions, such as esophageal rupture, asphyxiation,
aspiration and mucosal ulceration. For this reason, its use should be considered only as a
temporary measure in extreme circumstances.

Virtually all causes of acute gynecological bleeding that cause hypovolemia (ectopic
pregnancy, placenta previa, abruptio placenta, ruptured cyst) require surgical intervention.
Early consultation and definitive care are the keys. The goal in the ED is to stabilize the
hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly
as possible. In a 57-year-old patient with abdominal pain, for example, emergency
ultrasonography of the abdomen may be necessary to identify an abdominal aortic aneurysm
before the vascular surgeon is notified. Every patient should be individually evaluated,
because delaying definitive care can increase morbidity and mortality.

Whether crystalloids or colloids are best for resuscitation continues to be a matter for
discussion and research. Many fluids have been studied for use in resuscitation; these include
isotonic sodium chloride solution, lactated Ringer solution, hypertonic saline, albumin,
purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70 (Han J.
et al. 2015).
Proponents of colloid resuscitation argue that the increased oncotic pressure produced with
these substances decreases pulmonary edema. However, the pulmonary vasculature allows
considerable flow of material, including proteins, between the intravascular space and
interstitium.
 Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to
be a more important factor in preventing pulmonary edema.
Synthetic colloid solutions have some advantages compared with natural colloids such as
purified protein fraction, fresh frozen plasma, and albumin. They have the same volume-
expanding properties, but because of their structures and high molecular weights, they remain
mostly in the intravascular space, reducing the occurrence of interstitial edema. Although
theoretic advantages exist, studies have failed to show a difference in ventilatory parameters,
pulmonary function test results, days using a ventilator, total hospital days, or survival.
8.0 Conclusion

Shock is a clinical syndrome that occurs due to hemodynamic disorders and

metabolism is characterized by a failure of the circulatory system to maintain perfusion that
goes to the body's vital organs, resulting in dysfunction organs in the body. Shock
hypovolemic is a shock that occurs due to reduced plasma volume in intravascular. This
shock can occur due to heavy bleeding (haemorrhagic). Bleeding will reduce the pressure of
filling blood vessels on average and reduce flow blood back to the heart. This is what causes
a decrease in cardiac output (heart pulse rate). When the heart pulse rate drops, systemic
vascular endurance will try to increase systemic pressure to provide adequate perfusion for
the heart and brain outnumber other tissues such as muscles, skin and especially the tract
gastrointestinal.

Clinical symptoms of hypovolemic shock only clearly seen when the lack of
circulation volume more than 30% due to the initial stages of bleeding lack of compensatory
mechanisms of the cardiovascular system and autonomic nerves can still maintain function
circulation in normal state. Clinical symptoms and signs also does not appear at the same
time, like changes in systolic blood pressure occur more slowly from changes in pulse
pressure, frequency heart and decreased urine production. Therefore careful examination and
management must be carried out for proper management, as well immediate response to cases
at risk so as not to fall into shock. Energy requirements for the implementation of metabolism
in the heart and the brain are very high but the two organ cells are unable to store reserves
energy. If this continues then one by one the organs will die and can lead to death.
(3,763 word)

9.0 Reference
1. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma deaths: A
Reassessment. Injury, Infection, and Critical Care. 2015.
2. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and
hemodynamic monitoring. Task force of the European society of intensive care
medicine. Intensive Care Medicine. 2014

3. Gulati A. Vascular endothelium and hypovolemic shock. Curr Vasc Pharmacol. 2016.

4. Burns B, Gentilello L, Elliot A, Shafi S. Prehospital hypotension redefined. J
Trauma-Injury Infection and Crit Care. 2015.
5. Sarkar D, Philbeck T. The use of multiple intraosseous catheters in combat casualty
resuscitation. Mil Med. 2016.
6. Reinhart K, Perner A, Sprung CL, et al. Consensus statement of the ESICM task force
on colloid volume therapy in critically ill patients. Intensive Care Med. 2015.
7. Ghafari MH, Moosavizadeh SA, Moharari RS, Khashayar P. Hypertonic saline 5% vs.
lactated ringer for resuscitating patients in hemorrhagic shock. Middle East J
Anesthesiol. 2016.
8. Pacagnella RC, Souza JP, Durocher J, et al. A systematic review of the relationship
between blood loss and clinical signs. PLoS One. 2016.
9. Han J, Ren HQ, Zhao QB, Wu YL, Qiao ZY. Comparison of 3% and 7.5% hypertonic
saline in resuscitation after traumatic hypovolemic shock. Shock. 2015.
10. Zink KA, Sambasivan CN, Holcomb JB, Chisholm G, Schreiber MA. A high ratio of
plasma and platelets to packed red blood cells in the first 6 hours of massive
transfusion improves outcomes in a large multicenter study. Am J Surg. 2015.
11. Funk DJ, Jacobsohn E, Kumar A. The role of venous return in critical illness and
shock-part I: Physiology. Critical Care Medicine. 2014.
12. Funk DJ, Jacobsohn E, Kumar A. The role of venous return in critical illness and
shock: partII-Shock and mechanical ventilation. Critical Care Medicine. 2014.