Shock

Abstract

Evolving knowledge of critical illness has greatly influenced our understanding of shock and how we define it. The first century Roman savant Aulus Cornelius Celsus made the following observation, “When much blood is lost, the pulse becomes feeble, the skin extremely pale, the body covered with a malodorous sweat, the extremities frigid, and death occurs speedily.” In 1737, French surgeon, Le Dran, introduced the term “choc” to describe a severe impact or jolt, which was later adapted by Clarke, an English physician who used the term “shock” to describe the rapid physiological deterioration of a badly injured trauma victim. Historic advances in medicine, specifically the ability to measure blood pressure, changed the meaning of the term “shock” to denote arterial hypotension associated with hemorrhage. Later in the first part of the twentieth century, great physiologists such as Keith, Cannon, Blalock, and Cournard introduced the notion that tissue hypoperfusion, rather than isolated arterial hypotension, was the key feature of hemorrhagic shock. The contemporary understanding of shock is generally regarded as a syndrome precipitated by a systemic derangement of perfusion (global tissue hypoperfusion) that leads to widespread cellular dysoxia and vital organ dysfunction. Furthermore, by acknowledging that acquired derangements in mitochondrial function can impair cellular energetics, shock can be even more broadly defined as an acute physiological derangement resulting from the inadequate production of adenosine triphosphate (ATP) by cells in many organs of the body.