TY  - CHAP
M1  - Book, Section
TI  - Mitral Valve Disease
A1  - Wasnick, John D.
A1  - Nicoara, Alina
PY  - 2019
T2  - Cardiac Anesthesia and Transesophageal Echocardiography, 2e
AB  - Whereas  the  aortic  valve  serves  as  the  gateway  to  the  systemic  circulation,  the  mitral  valve  (MV)  is  the  doorway  to  the  left  ventricle  (LV).  Should  the  valve  be  too  tight  as  in  mitral  stenosis  (MS),  the  LV  is  under  loaded  reducing  the  stroke  volume  (SV)  (Video  7–1A,  Video  7–1B,  Video  7–1C).  Moreover,  the  narrowed  MV  prevents  adequate  drainage  of  the  left  atrium  (LA)  and  the  pulmonary  circulation.  With  time,  the  LA  dilates  and  pulmonary  arterial  (PA)  pressures  increase,  leading  to  atrial  fibrillation,  pulmonary  edema,  and  right  ventricular  failure.  Consequently,  these  conditions  make  the  anesthetic  management  of  the  MS  patient  for  MV  replacement  most  challenging.When  the  MV  becomes  incompetent,  it  no  longer  functions  to  ensure  the  one-way,  forward  flow  of  blood  during  each  cardiac  cycle.  As  the  LV  contracts  during  systole,  blood  can  be  ejected  forward  through  the  aortic  valve  (AV)  into  the  systemic  circulation,  or  the  blood  can  flow  backward  into  the  LA  via  the  leaky  MV.  Like  aortic  regurgitation  (AR),  mitral  regurgitation  (MR)  can  develop  both  acutely  or  exist  chronically.  Patients  with  chronic  MR  develop  compensatory  mechanisms,  which  permit  them  to  eject  a  sufficient  SV  into  the  systemic  circulation  to  maintain  circulatory  function.  Conversely,  the  patient  with  acute  MR  lacks  adequate  compensatory  mechanisms.  Acute  MR  frequently  presents  secondary  to  papillary  muscle  dysfunction  or  rupture  following  myocardial  infarction  or  due  to  the  destruction  of  the  valve  by  mechanical  trauma  or  infectious  processes.  As  such,  the  acute  MR  patient  usually  presents  in  cardiogenic  shock  as  the  SV  ejected  into  the  systemic  circulation  is  inadequate  to  meet  the  patient’s  metabolic  demands.  Additionally,  acutely  increased  pulmonary  artery  pressures  contribute  to  the  development  of  pulmonary  edema  in  the  MR  patient.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/23
UR  - accessanesthesiology.mhmedical.com/content.aspx?aid=1166980681
ER  -