Early Identif ication of Shock in Crit ical ly I l l Patients Matthew

In the eighteenth century the French surgeon Le Dran coined the term choc for soldiers suffering from severe traumatic injuries and heavy blood loss. Shock began appearing in the medical literature in the nineteenth century, and in 1872 the venerated trauma surgeon Samuel D. Gross defined shock as ‘‘the rude unhinging of the machinery of life.’’ Over the centuries the term shock became synonymous with hypotension. The misconception that hypotension is necessary to define shock persists, despite evidence and international consensus recommendations to the contrary. More appropriately, shock is defined as a life-threatening condition characterized by inadequate delivery of oxygen and nutrients to vital organs relative to their metabolic demand. Inadequate oxygen delivery typically results from poor tissue perfusion but occasionally, may also be caused by an increase in metabolic demand. In the setting of persistent inadequate oxygen delivery, cells are unable to produce adenosine triphosphate (ATP) to power vital functions. Cells transition to anaerobic metabolism to continue production of ATP, generating lactic acid, which accumulates in the cell and is transported into the blood. The accumulation of lactic acid in the cell is compounded by an increase in production of its precursor, pyruvate, via the stress response. Increased production of lactate accounts for most elevation in blood levels, but a reduction in lactate metabolism also occurs. Systemically, the stress response is intended to release energy stores and augment perfusion to vital organs. Receptors in large arteries detect a decrease in wall tension, activating a hormonal response via the hypothalamus-pituitary-adrenal axis and a neurogenic response through sympathetic stimulation. The resultant increase in circulating levels of epinephrine, norepinephrine, corticosteroids, renin, and glucagon