Pathophysiology of Hemorrhagic Shock.
- Author:
Wu Seong KANG
1
;
Ji Woong YEOM
;
Young Goun JO
;
Jung Chul KIM
Author Information
- Publication Type:Review
- Keywords: Hemorrhagic shock; Lethal triad; Acidosis; Hypothermia; Consumption coagulopathy
- MeSH: Acidosis; Anoxia; Baroreflex; Blood Pressure; Blood Volume; Cause of Death; Disseminated Intravascular Coagulation; Hemorrhage; Humans; Hypothermia; Lactic Acid; Mortality; Renin-Angiotensin System; Shock, Hemorrhagic*; Vasoconstriction; Vasopressins
- From: Journal of Acute Care Surgery 2016;6(1):2-6
- CountryRepublic of Korea
- Language:Korean
- Abstract: Hemorrhage is a major cause of death in trauma patients. The medical definition of hemorrhagic shock is tissue hypoperfusion resulting from a reduction of blood volume. Decreased blood pressure resulting from acute blood loss induces cardiac stimulation, systemic vasoconstriction, and volume redistribution. These effects are due to the baroreceptor reflex, the humoral compensatory mechanisms including the renin angiotensin system, and the release of catecholamine and vasopressin. Hemorrhagic shock causes acidosis, hypothermia, and coagulopathy, known as ‘the lethal triad.’ Tissue hypoxia induces metabolic acidosis by producing lactic acid. The three components of the lethal triad amplify each other and form a vicious cycle, eventually causing the death of the patient. To reduce the risk of mortality in severely bleeding patients, we need to understand the pathophysiology of hemorrhagic shock and the related complications.
