Medscape is available in 5 Language Editions – Choose your Edition here.


Hemorrhagic Shock

  • Author: John Udeani, MD, FAAEM; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
Updated: Mar 27, 2015


Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock.

On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a given clinical disturbance. Clinicians struggle daily to adequately define and monitor oxygen utilization on the cellular level and to correlate this physiology to useful clinical parameters and diagnostic tests.

The 4 classes of shock, as proposed by Alfred Blalock, are as follows[1] :

  • Hypovolemic
  • Vasogenic (septic)
  • Cardiogenic
  • Neurogenic

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms. Modern advances in trauma care allow patients to survive when these adaptive compensatory mechanisms become overwhelmed.



Well-described responses to acute loss of circulating volume exist. Teleologically, these responses act to systematically divert circulating volume away from nonvital organ systems so that blood volume may be conserved for vital organ function. Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart and other organs. The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys.

Concurrently, a multisystem hormonal response to acute hemorrhage occurs. Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Hyperglycemia commonly is associated with acute hemorrhage. This is due to a glucagon and growth hormone–induced increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose.

In addition to these global changes, many organ-specific responses occur. The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total blood flow for short periods of time. With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.




Hemorrhagic shock is tolerated differently, depending on the preexisting physiologic state and, to some extent, the age of the patient. Very young and very old people are more prone to early decompensation after loss of circulating volume.

Pediatric patients have smaller total blood volumes and, therefore, are at risk to lose a proportionately greater percentage of blood on an equivalent-volume basis during exsanguination compared to adults. The kidneys of children younger than 2 years are not mature; they have a blunted ability to concentrate solute. Younger children cannot conserve circulating volume as effectively as older children. Also, the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to coagulopathy.

Elderly people may have both altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood loss. Atherosclerosis and decreased elastin cause arterial vessels to be less compliant, leading to blunted vascular compensation, decreased cardiac arteriolar vasodilation, and angina or infarction when myocardial oxygen demand is increased. Older patients are less able to mount a tachycardia in response to decreased stoke volume because of decreased beta-adrenergic receptors in the heart and a decreased effective volume of pacing myocytes within the sinoatrial node. Also, these patients frequently are treated with a variety of cardiotropic medications that may blunt the normal physiological response to shock. These include beta-adrenergic blockers, nitroglycerin, calcium channel blockers, and antiarrhythmics.

The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine. Concentrating ability may be impaired by a relative insensitivity to antidiuretic hormone. These changes in the heart, vessels, and kidneys can lead to early decompensation after blood loss. All of these factors in concert with comorbid conditions make management of elderly patients with hemorrhage quite challenging.

Contributor Information and Disclosures

John Udeani, MD, FAAEM Assistant Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science, University of California, Los Angeles, David Geffen School of Medicine

John Udeani, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Robert L Sheridan, MD Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School

Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, American College of Surgeons

Disclosure: Received research grant from: Shriners Hospitals for Children; Physical Sciences Inc<br/>Received income in an amount equal to or greater than $250 from: SimQuest Inc -- consultant on burn mapping softwear ($1,500).

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Additional Contributors

Lewis J Kaplan, MD, FACS, FCCM, FCCP Associate Professor of Surgery, Division of Trauma, Surgical Critical Care, and Emergency Surgery, Perelman School of Medicine, University of Pennsylvania; Section Chief, Surgical Critical Care, Philadelphia Veterans Affairs Medical Center

Lewis J Kaplan, MD, FACS, FCCM, FCCP is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Association for Surgical Education, Connecticut State Medical Society, Eastern Association for the Surgery of Trauma, International Trauma Anesthesia and Critical Care Society, Society for the Advancement of Blood Management, Society of Critical Care Medicine, Surgical Infection Society

Disclosure: Nothing to disclose.

  1. Blalock A. Principle of Surgical Care, Shock, and Other Problems. St Louis: Mosby; 1940.

  2. Mitra B, Gabbe BJ, Kaukonen KM, Olaussen A, Cooper DJ, Cameron PA. Long-term outcomes of patients receiving a massive transfusion after trauma. Shock. 2014 Oct. 42(4):307-12. [Medline].

  3. Levi M, Levy JH, Andersen HF, Truloff D. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med. 2010 Nov 4. 363(19):1791-800. [Medline].

  4. Aledort LM. Off-label use of recombinant activated factor VII--safe or not safe?. N Engl J Med. 2010 Nov 4. 363(19):1853-4. [Medline].

  5. Ambrogi MC, Lucchi M, Dini P, et al. Videothoracoscopy for evaluation and treatment of hemothorax. J Cardiovasc Surg (Torino). 2002 Feb. 43(1):109-12. [Medline].

  6. Barber AE, Shires GT. Cell damage after shock. New Horiz. 1996 May. 4(2):161-7. [Medline].

  7. Brown MA, Casola G, Sirlin CB, et al. Blunt abdominal trauma: screening us in 2,693 patients. Radiology. 2001 Feb. 218(2):352-8. [Medline].

  8. Butler K, Winters M. Shock: beyond the "golden hour". Emergency Medicine Reports. 2003. 24:345-356.

  9. Collins JA. The pathophysiology of hemorrhagic shock. Prog Clin Biol Res. 1982. 108:5-29. [Medline].

  10. Dizien O, Held JP, Eyssette M, et al. [Severe cranial trauma in the rehabilitation milieu. Management in the initial phase]. Rev Infirm. 1993 Mar. 43(5):33-8. [Medline].

  11. Domsky MF, Wilson RF. Hemodynamic resuscitation. Crit Care Clin. 1993 Oct. 9(4):715-26. [Medline].

  12. Falk JL, O'Brien JF, Kerr R. Fluid resuscitation in traumatic hemorrhagic shock. Crit Care Clin. 1992 Apr. 8(2):323-40. [Medline].

  13. Hollenberg SM. Cardiogenic shock. Crit Care Clin. 2001 Apr. 17(2):391-410. [Medline].

  14. Kemp SF. Current concepts in pathophysiology, diagnosis, and management of anaphylaxis. Immunol Allergy Clin North Am. 2001. 21:611-634.

  15. Ketcham EM, Cairns CB. Hemoglobin-based oxygen carriers: development and clinical potential. Ann Emerg Med. 1999 Mar. 33(3):326-37. [Medline].

  16. Kramer GC, Kinsky MP, Prough DS, et al. Closed-loop control of fluid therapy for treatment of hypovolemia. J Trauma. 2008 Apr. 64(4 Suppl):S333-41. [Medline].

  17. Krausz MM. Initial resuscitation of hemorrhagic shock. World J Emerg Surg. 2006 Apr 27. 1(1):14.

  18. McCunn M, Karlin A. Nonblood fluid resuscitation: more questions than answers. Anesthesiol Clin North Am. 1999. 17:107-123.

  19. Orlinsky M, Shoemaker W, Reis ED, et al. Current controversies in shock and resuscitation. Surg Clin North Am. 2001 Dec. 81(6):1217-62, xi-xii. [Medline].

  20. Pearl RG. Treatment of shock-1998. Anesthesia and Analgesia. 1998. suppl:75-84.

  21. Peitzman AB, Billiar TR, Harbrecht BG. Hemorrhagic shock. Current Problems in Surgery. 1995. 32:925-1002. [Medline].

  22. Pryor JP, Pryor RJ, Stafford PW. Initial phase of trauma management and fluid resuscitation. Trauma Reports. 2002. 3:1-12.

  23. Schlag G, Krosl P, Redl H. Cardiopulmonary response of the elderly to traumatic and septic shock. Prog Clin Biol Res. 1988. 264:233-42. [Medline].

  24. Shoemaker WC, Peitzman AB, Bellamy R. Resuscitation from severe hemorrhage. Crit Care Med. 1996 Feb. 24(2 Suppl):S12-23. [Medline].

CT scan of a 26-year-old man after a motor vehicle crash shows a significant amount of intra-abdominal bleeding.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.