eMedicine Specialties > Emergency Medicine > Cardiovascular

Shock, Hypovolemic

Author: Paul Kolecki, MD, FACEP, Associate Professor, Department of Emergency Medicine, Thomas Jefferson University Hospital, Director of Undergraduate Emergency Medicine Student Education, Jefferson Medical College, Philadelphia, PA, Consultant, Philadelphia Poison Control Center, Philadelphia, PA
Coauthor(s): Carl R Menckhoff, MD, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Medical College of Georgia
Contributor Information and Disclosures

Updated: Mar 24, 2009

Introduction

Background

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.

Pathophysiology

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.

Clinical

History

• 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.
• The classic sign of a thoracic aneurysm is a tearing pain radiating to the back. Abdominal aortic aneurysms usually result in abdominal, back pain, or flank pain.
• 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.

Physical

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.

• 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.
  • A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately 10%.
• 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.
  • The decrease in pulse pressure is a result of increased catecholamine levels, which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.
• 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.
  • In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.
  • Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids.
• Class IV hemorrhage (loss of >40%)
  • Symptoms include the following: 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.
  • The chest should be auscultated for decreased breath sounds, because 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 femoral fracture and bleeding into the thigh).
  • 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.

Causes

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

• Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries that can result in hemorrhagic 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 hemorrhagic shock include the following: bleeding esophageal varices, 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.

• Search for CME/CE on This Topic »

• Shock (Pediatrics: Cardiac Disease and Critical Care Medicine)
• Shock and Hypotension in the Newborn (Pediatrics: Cardiac Disease and Critical Care Medicine)
• Shock, Distributive (Critical Care)
• Shock, Septic (Emergency Medicine)

• Shock Symptoms
• Shock Center
• Shock Overview
• Shock Treatment
• Shock Causes

• New Analysis of Halted Trial of Hypertonic Saline for Patients in Traumatic Shock
• Prolonged Low-Dose Corticosteroids Linked to Lower All-Cause Mortality in Septic Shock
• Rhinosinusitis Can Cause Toxic Shock Syndrome in Children

• Reperfusion Injury After Hemorrhage: A Collective Review
• Managing Situations of Acute Blood Loss With Limited Resources
• Managing Situations of Acute Blood Loss with Limited Resources

• Stone Disease Resource Center
• Sepsis Resource Center