RT Book, Section A1 Maier, Ronald V. A2 Kasper, Dennis A2 Fauci, Anthony A2 Hauser, Stephen A2 Longo, Dan A2 Jameson, J. Larry A2 Loscalzo, Joseph SR Print(0) ID 1120808770 T1 Approach to the Patient with Shock T2 Harrison's Principles of Internal Medicine, 19e YR 2014 FD 2014 PB McGraw-Hill Education PP New York, NY SN 9780071802154 LK accessmedicine.mhmedical.com/content.aspx?aid=1120808770 RD 2021/04/16 AB Shock is the clinical syndrome that results from inadequate tissue perfusion. Irrespective of cause, the hypoperfusion-induced imbalance between the delivery of and requirements for oxygen and substrate leads to cellular dysfunction. The cellular injury created by the inadequate delivery of oxygen and substrates also induces the production and release of damage-associated molecular patterns (DAMPs or “danger signals”) and inflammatory mediators that further compromise perfusion through functional and structural changes within the microvasculature. This leads to a vicious cycle in which impaired perfusion is responsible for cellular injury that causes maldistribution of blood flow, further compromising ­cellular perfusion; the latter ultimately causes multiple organ failure (MOF) and, if the process is not interrupted, leads to death. The clinical manifestations of shock are also the result, in part, of autonomic neuroendocrine responses to hypoperfusion as well as the breakdown in organ function induced by severe cellular dysfunction (Fig. 324-1).