1. Hypovolemic Shock http://emedicine.medscape.com/article/760145-overview
Author: Paul Kolecki, MD, FACEP; Chief Editor: David FM Brown, MD more...
Updated: Mar 11, 2010
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.
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2. Hypovolemic Shock http://emedicine.medscape.com/article/760145-overview
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.
Contributor Information and Disclosures
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
Paul Kolecki, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha and American
College of Emergency Physicians
Disclosure: Nothing to disclose.
Coauthor(s)
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
Carl R Menckhoff, MD, FACEP is a member of the following medical societies: American Academy of Emergency
Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.
Specialty Editor Board
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, School of Medicine, University of
Texas Health Sciences Center San Antonio
Daniel J Dire, MD is a member of the following medical societies: American Academy of Clinical Toxicology,
American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency
Physicians, and Association of Military Surgeons of the US
Disclosure: Talecris Biotherapeutics Honoraria Speaking and teaching
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 Chair and Medical Director, Department of Emergency Medicine, American University of
Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
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
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency
Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency
Medicine
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3. Hypovolemic Shock http://emedicine.medscape.com/article/760145-overview
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
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians
and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
References
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