TY  - CHAP
M1  - Book, Section
TI  - Circulatory and Cardiogenic Shock
A1  - Serrao, Gregory
A1  - Bier, Benjamin
A1  - Gidwani,  Umesh
A2  - Fuster, Valentin
A2  - Narula, Jagat
A2  - Vaishnava, Prashant
A2  - Leon, Martin B.
A2  - Callans, David J.
A2  - Rumsfeld, John S.
A2  - Poppas, Athena
PY  - 2022
T2  - Fuster and Hurst's The Heart, 15e
AB  - Chapter  SummaryThis  chapter  describes  the  pathophysiology,  assessment,  classification,  and  management  of  cardiogenic  shock  (see  Fuster  and  Hurst’s  Central  Illustration).  The  pathophysiology  of  cardiogenic  shock  involves  a  maladaptive  compensatory  cycle  triggered  by  acute  reduction  in  cardiac  output.  All  etiologies  initiate  a  physiologic  cascade  rooted  in  three  main  pathways:  (1)  increase  in  left  ventricular  end  diastolic  pressure,  (2)  reduction  of  blood  pressure,  and  (3)  triggering  of  inflammatory  responses.  If  left  uninterrupted,  the  compensatory  cycle  will  lead  to  progressive  cardiac  dysfunction  and  ultimately  death.  A  thorough  assessment  of  the  patient  with  suspected  cardiogenic  shock  is  necessary  to  confirm  diagnosis  and  inform  treatment  decisions,  and  involves  physical  examination,  ultrasonography,  laboratory  studies,  invasive  hemodynamics,  and  coronary  angiography,  as  appropriate.  Cardiogenic  shock  with  predominant  left  ventricular  failure  is  more  common  than  isolated  right  ventricular  failure,  and  etiology  can  be  categorized  as  primary,  obstructive,  or  valvular.  Etiology  of  cardiogenic  shock  with  predominant  right  ventricular  failure  is  usually  primary  or  obstructive,  often  related  to  acute  pulmonary  embolism  of  hemodynamic  significance.  Concurrent  left  ventricular  failure  and  right  ventricular  failure  is  relatively  common  among  causes  of  cardiogenic  shock  and  the  underlying  etiology  is  primary,  obstructive,  electrical,  or  structural.  Treatment  for  cardiogenic  shock  depends  on  etiology,  and  may  involve  a  combination  of  vasoactive  agents  (pressors  and  inotropes),  treatment  of  myocardial  ischemia  and  revascularization  as  appropriate,  and  mechanical  circulatory  support  (e.g.  intra-aortic  balloon  pump  counterpulsation,  percutaneous  left  ventricular  assist  device,  and/or  extracorporal  membrane  oxygenation)  as  needed.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - accessmedicine.mhmedical.com/content.aspx?aid=1202456766
ER  -