RT Book, Section
A1 Javaheri, Shahrokh
A1 Pevernagie, Dirk
A1 Javaheri, Ali
A2 Fuster, Valentin
A2 Narula, Jagat
A2 Vaishnava, Prashant
A2 Leon, Martin B.
A2 Callans, David J.
A2 Rumsfeld, John S.
A2 Poppas, Athena
SR Print(0)
ID 1202456660
T1 Sleep-Disordered Breathing
T2 Fuster and Hurst's The Heart, 15e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781264257560
LK accessmedicine.mhmedical.com/content.aspx?aid=1202456660
RD 2024/04/19
AB Chapter  SummaryThis  chapter  explores  the  pathophysiology  of  obstructive  and  central  sleep  apnea,  as  well  as  the  purported  causal  relationship  between  these  and  hypertension,  atherosclerosis,  cardiac  rhythm  disorders,  and  cardiac  failure.  Obstructive  sleep  apnea  (OSA)—involving  cyclic  asphyxia,  microarousals  from  sleep,  and  negative  swings  in  intrathoracic  pressure—induces  adverse  systemic  effects  that  disrupt  normal  cardiovascular  physiology  and  function  (see  Fuster  and  Hurst’s  Central  Illustration).  Notably,  however,  central  sleep  apnea  of  the  Hunter-Cheyne-Stokes  type  is  a  consequence  of  cardiac  failure  rather  than  a  cause.  Treatment  of  sleep-disordered  breathing  with  positive  airway  pressure  devices  and  other  therapeutic  regimens  has  been  shown  to  improve  cardiovascular  outcomes  in  patients  with  OSA.  Randomized  controlled  trials  have  failed  to  show  any  mortality  benefit,  but  this  is  likely  related  to  methodological  issues  with  the  trials.  Treatment  of  central  sleep  apnea  remains  difficult.  Two  randomized,  controlled  trials  are  ongoing:  one  with  low-flow  nocturnal  oxygen  and  another  with  improved  adaptive  servo-ventilation.  Phrenic  nerve  stimulation  has  shown  benefits  in  a  randomized,  controlled  trial.  Finally,  cardiac  transplant  recipients  have  been  of  particular  interest  because  it  was  anticipated  that  preexisting  central  sleep  apnea  might  be  cured;  however,  OSA  is  prevalent  in  this  patient  population  due  to  weight  gain,  potentially  contributing  to  hypertension,  poor  quality  of  life,  and  even  cardiac  rejection.