RT Book, Section
A1 Rubin, Lewis J.
A2 Fuster, Valentin
A2 Narula, Jagat
A2 Vaishnava, Prashant
A2 Leon, Martin B.
A2 Callans, David J.
A2 Rumsfeld, John
A2 Poppas, Athena
SR Print(0)
ID 1202456471
T1 Cor Pulmonale: The Heart in Structural Lung Disease
T2 Fuster and Hurst's The Heart, 15e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781264257560
LK accesscardiology.mhmedical.com/content.aspx?aid=1202456471
RD 2023/12/06
AB Chapter  SummaryThis  chapter  addresses  the  pathogenesis,  pathophysiology,  and  management  of  pulmonary  hypertension  (PH)  in  the  setting  of  structural  lung  disease,  commonly  referred  to  as  cor  pulmonale.  Airway  obstruction,  lung  fibrosis  with  restriction,  or  a  combination  of  both  factors  causes  a  loss  of  pulmonary  vascular  surface  area  and  impairment  in  intrapulmonary  gas  exchange,  leading  to  hypoxemia  with  or  without  hypercarbia,  which  are  potent  stimuli  for  pulmonary  vasoconstriction  and  vascular  remodeling.  Polycythemia  with  increased  blood  viscosity,  resulting  from  hypoxia-induced  increased  red  blood  cell  production,  may  further  increase  pulmonary  vascular  resistance.  The  subsequent  elevations  in  pulmonary  artery  pressure  result  in  right  ventricular  pressure  and  volume  overload  that  may  ultimately  lead  to  right  heart  failure  and  death  (see  Fuster  and  Hurst’s  Central  Figure).  The  presence  of  cor  pulmonale  may  be  inferred  from  echocardiographic  signs  of  right  ventricular  enlargement  and  hypertrophy,  along  with  measurement  of  an  increased  tricuspid  regurgitant  jet  velocity,  but  the  definitive  diagnosis  requires  the  direct  measurement  of  pulmonary  hemodynamics.  Management  of  cor  pulmonale  is  primarily  directed  at  optimizing  lung  function  and  gas  exchange  with  conventional  medical  therapies  (ie,  bronchodilators,  corticosteroids,  and  other  anti-inflammatory  agents),  minimizing  hypoxemia  with  supplemental  oxygen,  and  identifying  and  treating  comorbid  conditions.  The  role  of  pulmonary  arterial  hypertension–targeted  therapies  in  cor  pulmonale  is  controversial  and  can  result  in  worsening  V/Q  mismatching  and  clinical  deterioration.