Hypovolemic Shock



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. Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic 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 many life-threatening injuries experienced during the wars of the 1900s have significantly affected the development of the principles of hemorrhagic shock resuscitation. During World War I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the hemorrhagic shock was repaired surgically. Crystalloids and blood were used extensively during World War II for the treatment of patients in unstable conditions. Experience from the Korean and Vietnam wars revealed that volume resuscitation and early surgical intervention were paramount for surviving traumatic injuries resulting in hemorrhagic shock. These and other principles helped in the development of present guidelines for the treatment of traumatic hemorrhagic shock. However, recent investigators have questioned these guidelines, and today, controversies exist concerning the optimal treatment of hemorrhagic shock.

For more information, see Medscape's Trauma Resource Center.


The human body responds to acute hemorrhage by activating the following major physiologic systems: the hematologic, cardiovascular, renal, and neuroendocrine systems.

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In addition, platelets are activated (also by means of local thromboxane A2 release) 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.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

The pathophysiology of hypovolemic shock is much more involved than what was just listed. To explore the pathophysiology in more detail, references for further reading are provided in the bibliography. These intricate mechanisms list above are effective in maintaining vital organ perfusion in severe blood loss. Without fluid and blood resuscitation and/or correction of the underlying pathology causing the hemorrhage, cardiac perfusion eventually diminishes, and multiple organ failure soon follows.



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 rely 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.


The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related.

Laboratory Studies

Imaging Studies

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.

Emergency Department Care

Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) 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.[2] 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.

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 Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications).

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.

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.

Controlling further blood loss

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 H2 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 (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) 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. If transfer to another hospital is necessary, resources should be mobilized early.

In patients with trauma, if the emergency medical services personnel indicate potential serious injury, the surgeon (or trauma team) should be notified prior to the patient's arrival. In a 55-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,[3] hypertonic saline, albumin, purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70.

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.

Another argument is that less colloid is needed to increase the intravascular volume. Studies have shown this to be true. However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids.

Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, 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.

The European Society of Intensive Care Medicine (ESICM) advises against the use of colloids-hydroxyethyl starches (HES) in patients with severe sepsis or risk of acute kidney injury. Physicians should also avoid using colloids in patients with head injury and refrain from administering gelatins and HES in organ donors.[4]

The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan have failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution. In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost.

Recent literature suggests that the early administration of FFP and platelets improves survival and decreases overall PRBC need in patients undergoing a massive transfusion.[5]

Restoring normal circulating volume and BP prior to definitive control of bleeding

During World War I, Cannon observed and characterized patients in clinical shock. He later suggested a model of permissive hypotension in the treatment of torso wounds, with the intent of minimizing further bleeding.

Findings from early studies showed that animals that were bled had increased survival if they received fluid resuscitation. However, in these studies, bleeding was well controlled with ligation after the animals were bled.

During the Korean and Vietnam wars, much more aggressive fluid resuscitation, as well as rapid access to definitive care, was emphasized. It was noted that patients who were aggressively resuscitated tended to have better outcomes, and in the 1970s, these principles were widely adopted in civilian patients.

Since then, many studies have been conducted to determine if these principles are valid in patients with uncontrolled hemorrhage. Most of these studies revealed increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure causes more bleeding and disrupts initial clots, whereas extreme hypotension may increase the risk of cerebral perfusion.

The questions that have not been answered adequately are as follows: Which mechanisms and injury patterns are more amenable to the restoration of circulating blood volume? What BP is adequate but not excessive?

Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed.

Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Somatostatin (Zecnil)

Clinical Context:  Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric epithelial cells. Diminishes blood flow to portal system because of vasoconstriction. Has similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared from the circulation, with an initial half-life of 1-3 min.

Octreotide (Sandostatin)

Clinical Context:  Synthetic octapeptide. Compared to somatostatin, has similar pharmacological actions with greater potency and longer duration of action.

Used as adjunct to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.

Class Summary

These agents have vasoconstrictive properties and can reduce blood flow to portal systems.




Paul Kolecki, MD, FACEP, Associate Professor, Department of Emergency Medicine, Director of Undergraduate Emergency Medicine Student Education, Thomas Jefferson University Hospital, Jefferson Medical College of Thomas Jefferson University; Consultant, Philadelphia Poison Control Center

Disclosure: Nothing to disclose.


Carl R Menckhoff, MD, FACEP, Associate Professor, Department of Emergency Medicine, Medical College of Georgia; Medical Director and Chairman, Medical Center of Lewisville; Regional Ultrasound Director, Questcare Partners

Disclosure: Nothing to disclose.

Specialty Editors

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

A Antoine Kazzi, MD, Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

Disclosure: Nothing to disclose.

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty


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