Shock, Shock has long been recognized as a state of extreme pathophysiologic and metabolic derangement. As early as 1800 John Collins referred to it as a “momentary pause in the act of death,” and Samuel Gross later termed it a “rude unhinging of the machinery of life.” Many of the greatest luminaries in medicine were intrigued by shock and investigated it. During World War I Walter Bradford Cannon thought that it was caused primarily by “wound toxins,” and identified acidosis as a key feature. A generation later Alfred Blaylock focused on hypovolemia as a key element of shock, which he characterized in 1937 as “a peripheral circulatory failure resulting from a discrepancy in the size of the vascular bed and volume of the intravascular fluid.” Our current understanding of shock is that of a microcirculatory disorder in which a variety of etiologies result in failure of adequate oxygen delivery or utilization at the cellular level, and which is perpetuated by cellular and humoral responses. Causes may include: • Loss of circulating blood volume due to hemorrhage • Cardiac failure • Lack of vasomotor tone • Obstruction to venous return (e.g., cardiac tamponade, tension pneumothorax) • Impaired cellular utilization of oxygen (e.g., cyanide toxicity) Shock results in a profound physiologic response that may initially compensate for the underlying deficit, but which may also produce adverse systemic effects. Prolonged shock results in a cumulative “oxygen debt,” severe metabolic and physiologic derangement, and ultimately disruption of end-organ integrity and homeostasis. Once the cause of shock is fixed, it is still necessary to correct the associated derangements and restore normal function, which is often referred to as “repaying” the oxygen debt.
|Original language||English (US)|
|Title of host publication||Essentials of Trauma Anesthesia|
|Publisher||Cambridge University Press|
|Number of pages||12|
|State||Published - Jan 1 2012|
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