Hypovolemic Shock.pdf

11/11/13Hypovolemic Shock Today News Reference Education Log In Register Hypovolemic Shock Author: Paul Kolecki, MD, FACEP; Chief Editor: David FM Brown, MD more... Updated: Mar 21, 2012 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 emedicine.medscape.com/article/760145-overview 1/4 FACEP is a member of the following medical societies: American College of Emergency Physicians Disclosure: Nothing to disclose. and multiple organ failure soon follows. and Association of Military Surgeons of the US Disclosure: Nothing to disclose. American College of Emergency Physicians. muscle. Department of Emergency Medicine. Consultant.11/11/13 Hypovolemic Shock redistributing blood to the brain. Angiotensin II has 2 main effects. The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Associate Professor.medscape. references for further reading are provided in the bibliography. FACEP Associate Professor. Lebanon A Antoine Kazzi. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation. Philadelphia.com/article/760145-overview 2/4 . Renin converts angiotensinogen to angiotensin I. Department of Pediatrics. Specialty Editor Board Daniel J Dire. FACEP. heart. FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology. Director of Undergraduate Emergency Medicine Student Education. Without fluid and blood resuscitation and/or correction of the underlying pathology causing the hemorrhage. Department of Emergency Medicine. FACEP is a member of the following medical societies: Alpha Omega Alpha and American College of Emergency Physicians Disclosure: Nothing to disclose. American Academy of Emergency Medicine. FACEP Associate Professor. MD. Medscape Drug Reference Disclosure: Medscape Salary Employment A Antoine Kazzi. American University of Beirut Medical Center. PharmD. American Academy of Pediatrics. To explore the pathophysiology in more detail. MD. Contributor Information and Disclosures Author Paul Kolecki. University of Texas Health Sciences Center San Antonio Daniel J Dire. Coauthor(s) Carl R Menckhoff. vasoconstriction of arteriolar smooth muscle. the collecting ducts. PA Paul Kolecki. Department of Emergency Medicine. 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). Clinical Professor. and stimulation of aldosterone secretion by the adrenal cortex. both of which help to reverse hemorrhagic shock. Questcare Partners Carl R Menckhoff. ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule. American University of Beirut. University of Nebraska Medical Center College of Pharmacy. The pathophysiology of hypovolemic shock is much more involved than what was just listed. MD. Medical Director and Chairman. Department of Emergency Medicine. These intricate mechanisms list above are effective in maintaining vital organ perfusion in severe blood loss. Medical Center of Lewisville. Medical College of Georgia. cardiac perfusion eventually diminishes. Thomas Jefferson University Hospital. PhD Adjunct Assistant Professor. Regional Ultrasound Director. FAAP. which subsequently is converted to angiotensin II by the lungs and liver. The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). Philadelphia Poison Control Center. MD. University of Texas Medical School at Houston. FACEP. MD Deputy Chief of Staff. Editor-in-Chief. MD. FAAEM Clinical Professor. and the loop of Henle. and kidneys and away from skin. MD. FAAP. PA. MD is a member of the following medical societies: American Academy of Emergency Medicine emedicine. Francisco Talavera. Philadelphia. Jefferson Medical College. and GI tract. Mar 2012. [Medline]. Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or harmful?. Beth Israel Deaconess Medical Center John D Halamka. [Medline]. [Medline]. Hinckley WR. [Medline]. Hypertonic saline 5% vs. Jun 2002. Mackenzie CF. Intraosseous needles: they're not just for kids anymore. [Medline]. Jan 2008. Beth Israel Deaconess Medical Center.11/11/13 Hypovolemic Shock Disclosure: Nothing to disclose. Attending Physician. Khashayar P. 6. Graham CA. Elliot A. Henriksson A. Harvard Medical School. Activated coagulation in patients with shock due to ruptured abdominal aortic aneurysm. and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Deimling DL. Silbergleit R. American Medical Informatics Association. Division of Emergency Medicine.19(6):1337-47. Philbeck T. MS is a member of the following medical societies: American College of Emergency Physicians. MD. 7. MD Associate Professor. [Medline]. Shafi S. Chief Editor David FM Brown.174(2):106-8. Chief Information Officer. Schortgen F. Massachusetts General Hospital David FM Brown. McNamara RM. Critical care in the emergency department: shock and circulatory support. May 2009. Chisholm G. Reinhart K. Gentilello L. case report and review. Moosavizadeh SA. Intensive Care Med. Sprung CL. et al. Vice Chair. MD. Dec 2008. Satz W. Siegbahn A.38(3):368-83. 13. 5. Moharari RS.com/article/760145-overview 3/4 . Emerg Med J . Kohno M. discussion 570. Suzuki K. Effect of permissive hypotension in continuous uncontrolled intra-abdominal hemorrhage. Jan-Feb 2009. et al. Oct 2008. Mil Med. A high ratio of plasma and platelets to packed red blood cells in the first 6 hours of massive transfusion improves outcomes in a large multicenter study. Holcomb JB. MS Associate Professor of Medicine. Hypotensive resuscitation during active hemorrhage: impact on inhospital mortality. Moran M. Perner A. Bergqvist D. Ghafari MH. 3. Zink KA. CareGroup Healthcare System and Harvard Medical School.197(5):565-70. [Medline]. Ogino R. Phi Beta Kappa. 10. [Medline]. Feb 2009. Johan Groeneveld AB. 2. Skagius E. Schreiber MA. Parke TR. J Trauma.52(6):1141-6.35(1):37-40. Jan 1998. John D Halamka. [Medline]. J Emerg Nurs . lactated ringer for resuscitating patients in hemorrhagic shock. 8. 11.34(4):318-9. Department of Emergency Medicine. J Trauma-Injury Infection and Crit Care. Division of Emergency Medicine. Oct 1996.22(1):17-21. Consensus statement of the ESICM task force on colloid volume therapy in critically ill patients. Scalea TM.3(10):922-6. Acad Emerg Med. The use of multiple intraosseous catheters in combat casualty resuscitation. Eur J Vasc Endovasc Surg. 12. Effects of hypertonic saline and dextran 70 on cardiac contractility after hemorrhagic shock.28(1):37-9.44(1):59-69. MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose.medscape. Smith K. Prehospital hypotension redefined. J Trauma. Middle East J Anesthesiol. Dutton RP. References 1. Harvard Medical School. Jan 2005. Burns B. [Medline]. Curr Opin emedicine. Sarkar D. Air Medical J . Transporting the pregnant patient in shock. Langley DM. [Medline]. Stern SA. Am J Surg. et al. Sambasivan CN. 4.65(6):1217-21. Jaeschke R. [Medline]. Aug 2008. 9. LLC emedicine. Yajima D. Sato Y.28(3):212-5. 14.medscape.11/11/13 Hypovolemic Shock Crit Care.com/article/760145-overview 4/4 . [Medline]. Dec 2001. Hayakawa M.7(6):422-30. A fatal case of hypovolemic shock after cesarean section. [Medline]. Am J Forensic Med Pathol. Iwase H. Sep 2007. Medscape Reference © 2011 WebMD. Motani H.