Dott. Ciammaichella M. M.
Dirigente Medico
Responsabile UAS “Trombosi Venosa Profonda ed Embolia Polmonare”
Responsabile CDF BLSD IRC “Emersan Lateranum”
U.O.C. Medicina Interna I per l’Urgenza
(Direttore: Dott. G. Cerqua)
ACO S. Giovanni - Addolorata - Roma




KEY-WORDS: Hypovolemic shock





Background: Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion. For the most part, hypovolemic shock will result secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma or severe gastrointestinal bleeding disorders are two common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities.

Solid organ injury and rupture of an abdominal aortic aneurysm are two common causes of rapid internal blood loss. Finally, 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 chapter will concentrate mainly on hypovolemic shock secondary to blood loss and the controversies surrounding the treatment of this disease. The reader is referred to other chapters in this text for discussions of the pathophysiology and treatment for hypovolemic shock resulting from fluid losses other than blood.

The many life-threatening injuries suffered during the wars of the 1900's have significantly impacted the development of the principles of hemorrhagic shock resuscitation. During W.W.I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the hemorrhagic shock was surgically repaired. Crystalloid and blood were used extensively during W.W.II for the treatment of unstable patients.

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 develop the present guidelines for the treatment of traumatic hemorrhagic shock. However, recent research studies have questioned these guidelines and today there exist several controversies concerning the optimal treatment of hemorrhagic shock.

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

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (via local thromboxane A2 release). In addition, platelets are activated (also via local thromboxane A2 release) which 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 increase in release of norepinephrine and a decrease in baseline vagal tone (regulated by the baroreceptors in thecarotid 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 the gastrointestinal tract.

The kidneys respond to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which is subsequently converted to angiotensin II by the lungs and liver. Angiotensin II has two main effects, both of which help 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 blood pressure (as detected by baroreceptors) and a decrease in sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increase in reabsorption of water and salt (NaCl) by the distal tubule, collecting ducts and the loop of Henle.

These intricate mechanisms are very effective in maintaining vital organ perfusion in the face of severe blood loss. Without fluid and blood resuscitation and/or a correction of the underlying pathology causing the hemorrhage, cardiac perfusion eventually suffers and multiple organ failure soon follows.




  • When approaching a patient with possible shock secondary to hypovolemia, the history is vital in determining the possible causes and directing the workup.
  • Symptoms of shock such as weakness, lightheadedness, and confusion should be determined in all patients.
  • In the trauma patient, one should determine the mechanism of injury and any information that may heighten suspicion of certain injuries (e.g., steering wheel damage, 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 should also be noted.
  • Vascular disorders may present with chest, abdominal or back pain.
  • The classic history of a thoracic aneurysm is a tearing pain, radiating through to the back. Abdominal aortic aneurysms usually present with abdominal or back pain.
  • For gastrointestinal (GI) bleeding, one should inquire about hematemesis, melena, any drinking history, excessive NSAID use or any coagulopathies (iatrogenic or otherwise).
    • The chronology of vomiting and hematemesis should also be determined.
    • The patient who presents with hematemesis after multiple episodes of forceful vomiting is more likely to have Boerhaave's syndrome or a Mallory-Weiss tear, whereas a history of hematemesis from the start is more consistent with peptic ulcer disease or esophageal varices.
  • If a gynecologic cause is considered, information that should be obtained includes the last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount and duration), vaginal passage of products of conception and any pain. Note that all women of child-bearing age should have pregnancy ruled out with a pregnancy test, regardless of whether they believe they could be pregnant.


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 looking for signs and symptoms of shock.
The practitioner should be careful not to rely on systolic blood pressure as the main indicator for shock, as this will result in a delayed diagnosis. Remember that compensatory mechanisms will prevent a significant fall in systolic blood pressure until the patient has lost 30% of his blood volume. More attention should be paid to the pulse, respiratory rate and skin perfusion. Also, patients on beta-blockers may not present with tachycardia regardless of the degree of shock.
Classes of hemorrhage have been defined, based on percentage of blood volume loss. The distinction between these classes in the hypovolemic patient, however, is often less apparent. Treatment should be aggressive and be 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 will be seen.
    • There are usually no changes in blood pressure, pulse pressure or respiratory rate.
    • A delay in capillary refill of greater than three seconds corresponds to approximately a 10% volume loss.
  • Class II Hemorrhage (Loss of 15-30%):
    • Clinical symptoms include tachycardia > 100 bpm, tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill and slight anxiety.
    • The decrease in pulse pressure is a result of increased catecholamines causing an increase in peripheral vascular resistance and a subsequent rise in the diastolic blood pressure.
  • Class III Hemorrhage (Loss of 30-40%):
    • By this point, patients usually have marked tachypnea and tachycardia, a fall in systolic blood pressure, oliguria and significant changes in mental status, such as confusion or agitation.
    • In patients without other injuries or fluid losses, this is the smallest amount of blood loss that consistently causes a fall in systolic blood pressure.
    • Most of these patients will require blood transfusions, but this decision should be made based on initial response to fluids.
  • Class IV Hemorrhage (Loss of > 40%):
    • Symptoms include: marked tachycardia, decreased systolic blood pressure, 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 trauma patient, hemorrhage is usually 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, and neurological deficits).
  • There are four areas where one can sustain life-threatening hemorrhage: the chest, the abdomen, the thighs and externally (the floor).
    • The chest should be auscultated for decreased breath sounds, as life-threatening hemorrhage can occur from myocardial, vessel or lung laceration.

      The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury.
    • The thighs should be checked for deformities or enlargement (signs of femur fracture and bleeding into the thigh).

      The entire patient should then be checked for any external bleeding.
  • In the atraumatic patient, the majority of hemorrhage will be 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 the patient for other signs of bruising or bleeding.
  • In the pregnant patient, one should perform a sterile speculum examination. This is with the exception of third trimester bleeding where the examination should be done as a "double set-up" in the operating room. Check for abdominal, uterine or adnexal tenderness


Causes: The causes of hemorrhagic shock fall under four main subsets of causes: 1) traumatic, 2) vascular, 3)gastrointestinal, and 4) pregnancy-related.

  • Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries which can result in hemorrhagic shock include: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femur fractures and scalp lacerations.
  • Vascular disorders, which can result in significant blood loss, include aneurysms, dissections and arteriovenous malformations.
  • Examples of gastrointestinal disorders, which can result in hemorrhagic shock, include: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears and aorto-intestinal fistulas.
  • Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa and abruption of the placenta.


Lab Studies:

  • After the history and physical exam are performed, further work-up depends upon the probable cause of the hypovolemia as well as the stability of the patient.
  • Initial laboratory studies should include a complete blood count (CBC), electrolytes (e.g., Na, K, Cl, HCO3, BUN, creatinine, glucose), prothrombin time (PT), partial thromboplastin time (PTT), type and crossmatch, arterial blood gas (ABG) and a urinalysis (in trauma patients).
Imaging Studies:
  • Markedly hypotensive/unstable patients must be first adequately resuscitated. This takes precedence over imaging studies, and may include immediate interventions and/or being rushed immediately to the operating room.

The work-up of the trauma patient who presents with signs and symptoms of hypovolemia is directed toward finding the source of blood loss.

The atraumatic patient who presents in hypovolemic shock will require an ultrasound in the emergency department if an AAA is suspected. If gastrointestinal bleeding is suspected, the patient will need to have a nasogastric tube placed and gastric lavage performed. Upright CXR should be obtained if a perforated ulcer or Boerhaave's syndrome is a possibility. Endoscopy can be performed to further delineate the source of bleeding (usually after the patient has been admitted).

All female patients of child bearing years should have a pregnancy test done. If the patient is pregnant and in shock, a pelvic US should be performed immediately in the emergency department. A culdocentesis may be performed, although in most places, ultrasound can be done in the ED, and yields more information on the source of bleeding.

    • If thoracic dissection is suspected by mechanism and initial chest x-ray, the work up may include transesophageal echocardiography, aortography or computerized tomography (CT) of the chest.
    • If abdominal injury is suspected, diagnostic peritoneal lavage (DPL) may be performed in the unstable patient or CT scan in the stable patient.
    • An increasing role for ultrasound is emerging, although not yet as sensitive as DPL or CT scan.
    • If long bone fractures are suspected, radiographs should be obtained.



Prehospital Care: Management of patients with hypovolemic shock often begins at an accident scene or at home. The purpose of the prehospital care team is to prevent further injury, transport the patient to the hospital as rapidly as possible and initiate appropriate treatment in the field.

Prevention of further injury refers mostly to the trauma patient. Patients must have their cervical spines immobilized, be extricated, and be 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 getting definitive care by delaying transport is, therefore, potentially harmful.

Most prehospital intervention revolves around immobilizing the patient (if trauma is involved), securing an adequate airway, insuring ventilation, and maximizing circulation. Appropriate treatment can usually be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines, or splinting of extremities, can be done while a patient is being extricated for instance. Procedures in the field that will prolong transportation, however, should be delayed. There is no clear benefit to giving IV fluids prior to scene departure, however, IV lines and fluid resuscitation should be started and continued once in route to definitive care.

There has been considerable debate, in recent years, over the use of military antishock trousers (MAST). MAST were introduced in the 1960's and, based mostly on anecdotal reports of success, they became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970's. By the 1980's the American College of Surgeons Committee on Trauma had made them the standard of care for all trauma patients with signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. Current recommendations by the American College of Surgeons Committee on Trauma call for the use of MAST for 1) the splinting of pelvic fractures in cases of continuing bleeding and hypotension, and 2) for intra-abdominal trauma in patients with severe hypovolemia, who are in route to definitive care. Contraindications include pulmonary edema, diaphragmatic rupture, and uncontrolled hemorrhage outside of the confines of the garment.

Emergency Department Care: There are three goals in the emergency department management of the patient with hypovolemic shock:

(1) Maximize oxygen delivery - done by ensuring adequacy of ventilation, increasing O2 saturation of the blood and restoring blood flow

(2) Control further blood loss

(3) Obtain rapid and appropriate patient disposition

Maximizing Oxygen Delivery: The airway should be assessed immediately upon arrival of the patient and stabilized if necessary. The depth and rate of respirations should be assessed, as well as breath sounds. If pathology is found which interferes with breathing (e.g., pneumothorax, hemothorax, and flail chest), it should be addressed immediately. High flow supplemental oxygen should be administered to all patients and ventilatory support given, if needed.

Two large bore IVs should be started. Poiseuille's 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 is ideal, with caliber being much more significant. IV access may be obtained via percutaneous access of antecubital veins, cutdown of saphenous or arm veins, or access of central veins by the Seldinger technique.

If central lines are obtained, a large bore, single lumen catheter should be used. In children less than six years of age, intraosseus access may also be used. The most important factor in determining the route of access is the practitioner's skill and experience.

Once IV access is obtained, initial fluid resuscitation is with an isotonic crystalloid, such as lactated Ringer's solution (LR) or normal saline (NS). An initial bolus of 1- 2 liters is given for an adult or 20 ml/kg for a pediatric patient, and then the patient's response is assessed.

If the vital signs return to normal, the patient may be monitored to ensure stability and blood should be sent for type and crossmatch. If the vital signs transiently improve, crystalloid infusion should continue and type specific blood obtained. If littleor no improvement is seen, crystalloid infusion should continue and type O blood should be given (type O Rh negative blood should be given to females of childbearing age to avoid sensitization and future complications).

If a patient presents who is moribund and markedly hypotensive (class IV shock), crystalloid and type O blood should both be started initially. Note that these are guidelines for crystalloid and blood infusion and not rules. The emergency physician should select this therapy based on the condition of the patient at hand.

The position of the patient can also be used to improve circulation. The Trendelenburg position will increase blood flow to the brain for instance. Also, in the gravid patient who has been involved in a trauma and comes in hypotensive, rolling the patient onto her left side and displacing the fetus from the inferior vena cava, will increase circulation.

Autotransfusion may be a possibility in some trauma patients. Several devices are available which allow for the sterile collection, anticoagulation, filtration and retransfusion of blood. In the trauma setting this will almost always be from a hemothorax via a tube thoracostomy.

Controlling Further Blood Loss: Control of further hemorrhage depends on the source of bleeding and often requires operative intervention. In the trauma patient, external bleeding should be controlled with direct pressure and internal bleeding requires operative intervention. Long bone fractures should be treated with traction to decrease blood loss.

In the patient who loses his pulse in the emergency department or just prior to arrival, an emergency thoracotomy may be indicated with cross clamping of the aorta, in order 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, IV vasopressin and H-2 blockers have been used. Vasopressin is commonly associated with adverse reactions, such as hypertension, arrhythmias, gangrene, andmyocardial or splanchnic ischemia. It should therefore be considered secondary to more definitive measures. H-2 blockers are relatively safe, but have no proven benefit.

In patients with variceal bleeding, 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 if bleeding continues. Once again, this has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For these reasons, it should be considered only as a temporizing measure in extreme circumstances.

Virtually all causes of acute gynecological bleeding causing hypovolemia (e.g., ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, and miscarriage) will require surgical intervention.

Early consultation and definitive care is the key. The goal in the emergency department is to stabilize the hypovolemic patient, determine the cause of bleeding and get the patient to definitive care as quickly as possible. If transfer to another hospital will be necessary, early mobilization of resources should be initiated.

In the case of the trauma patient, if report from EMS personnel indicates potential serious injury, the surgeon (or trauma team), should be notified prior to the patient's arrival. In the 55 year old with abdominal pain, an emergency ultrasound of the abdomen may be necessary before an abdominal aortic aneurysm is identified and the vascular surgeon is notified. Again, every patient should be evaluated on a case-by-case basis since delay in definitive care can cause increased morbidity and mortality.

  • There has been much discussion and research on whether crystalloids or colloids are best for resuscitation. Many fluids have been studied for resuscitation including NS, LR, hypertonic saline, albumin, purified protein fraction (PPF), fresh frozen plasma (FFP), Hetastarch (HES), Pentastarch (PES) and dextran 70.
    • Proponents of colloid resuscitation argue that the increased oncotic pressure offered by these substances will decrease pulmonary edema. The pulmonary vasculature, however, allows considerable flow between the intravascular space and interstitium (including proteins). Maintenance of pulmonary hydrostatic pressure below 15 mm Hg appears to be a much larger 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 over crystalloids.

    • Synthetic colloid solutions, such as HES, PES and dextran 70, have some advantages over natural colloids such as PPF, FFP 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. Again, although there are theoretical advantages, studies have failed to show a difference in ventilatory parameters, pulmonary function tests, days on a ventilator, total hospital days or survival.
  • The combination of hypertonic saline and dextran (HSD) has also been studied because of some previous evidence that it may improve cardiac contractility and circulation. Studies in the United States and Japan have failed to show any difference when compared with NS or LR.
    • Thus, despite the many types of resuscitation fluid available, current recommendations still advocate the use of NS or LR.
  • Another area of interest with regard to resuscitation is whether or not the goal should be to restore normal circulating volume and blood pressure prior to definitive control of bleeding.
    • Cannon, during World War I, 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.

    The early studies showed that animals who were bled, had increased survival if they were fluid resuscitated. In these studies, however, bleeding was well controlled by ligation after the animals were bled.

    • During the Korean and Vietnam wars, there was a push toward much more aggressive fluid resuscitation as well as rapid access to definitive care. It was noted that patients who were aggressively resuscitated tended to do better and, in the 1970's, these principles were widely adopted for civilian victims.
    • Since then, many studies have been done trying to determine if these principles are valid in patients with uncontrolled hemorrhage. The majority of these studies show increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure will cause more bleeding and disrupt initial clots, whereas extreme hypotension may risk cerebral perfusion.

    The questions which haven't been adequately answered are: 1. Which mechanisms and injury patterns are more amenable to this? 2. What blood pressure is adequate but not too much?

    Although there is limited data indicating that a systolic blood pressure of 80- 90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed.

    • Current recommendations call for aggressive fluid resuscitation with LR or NS in all patients exhibiting signs and symptoms of shock, regardless of underlying cause.




  • Neurologic sequelae
  • Death


  • The prognosis is dependent on the degree of volume loss.




Medical/Legal Pitfalls:

  • A very common error in the management of hypovolemic shock, is failure to recognize it early.
    • This leads to delay in diagnosing the cause and in resuscitating the patient.
    • This often happens due to a reliance on blood pressure or initial hematocrit, rather than signs of decreased peripheral perfusion, in order to make the diagnosis.
    • Missed injuries in trauma patients can occur, especially if the examining physician focuses on more obvious injuries. This can be avoided by being sure to complete the physical examination and by continuing to monitor the patient closely and performing repeated examinations.
    • The elderly tolerates hypovolemia less well. Aggressive therapy should be instituted early to avoid potential complications such as myocardial infarction and stroke.
    • In patients who require large amounts of volume resuscitation, care should be taken to avoid hypothermia as this can contribute to developing an arrhythmia or coagulopathy. This can be avoided by warming the IV fluids prior to administration.
    • Patients on beta blockers, calcium channel blockers, and those with pacemakers may not mount a tachycardic response to hypovolemia leading to a delay in the diagnosis of shock. To minimize this, all patients histories should include medications and the examiner should rely on other signs of decreased peripheral perfusion.
    • 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 (FFP).


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