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 2022/01/23
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).