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1	
  
UN	
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UNA	
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Dr.	
  Josep	
  Morera...
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NEJM	
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8	
  
Presentación	
  del	
  Caso	
  Clínico	
  
	
  F.H.P.	
  (30-­‐10-­‐2012)	
  
-­‐  Varón	
  de	
  67	
  años	
  
-­‐...
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Presentación	
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  Caso	
  Clínico	
  
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Presentación	
  del	
  Caso	
  Clínico	
  
La	
  exploración	
  en	
  la	
  consulta	
  fue	
  relaQvamente	
  	
  ...
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DiagnósQco	
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DiagnósQco	
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Opinión	
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DiagnósQco	
  
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DiagnósQco	
  
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DiagnósQco	
  
Fisura...
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RaQonale	
  y	
  Disc...
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UN	
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UNA	
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RaQonale	
  y	
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UN	
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UNA	
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RaQonale	
  y	
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UN	
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UNA	
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RaQonale	
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UN	
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UNA	
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RaQonale	
  y	
  Disc...
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UN	
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UNA	
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  DE	
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RaQonale	
  y	
  Disc...
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UN	
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UNA	
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  DE	
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RaQonale	
  y	
  Disc...
27	
  
UN	
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UNA	
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  DE	
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RaQonale	
  y	
  Disc...
28	
  
UN	
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  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
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  DE	
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RaQonale	
  y	
  Disc...
29	
  
UN	
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  NOCHE:	
  
UNA	
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  DE	
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Conclusiones	
  
	
  ...
UN	
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Un grito en la noche: una complicacion no descrita de SAOS

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Presentación de un caso clinico no común, fisuras costales por presión torácica negativa durante una apnea prolongada.

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  • Nothing short of a miracle! I'm writing on behalf of my husband to send you a BIG THANK YOU!! The improvement has been amazing. Peter's sleep apnea was a huge worry for both of us, and it left us both feeling tired and drowsy every morning. What you've discovered here is nothing short of a miracle. God bless you. ●●● http://t.cn/Aigi9dEf
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Un grito en la noche: una complicacion no descrita de SAOS

  1. 1. 1   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Dr.  Josep  Morera   29  noviembre  2016  
  2. 2. 2   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  3. 3. 3   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS                                        GUIÓN   1.-­‐  Introducción   2.-­‐  Presentación  de  Caso  Clínico   3.-­‐  Opinión  de  los  Asistentes   4.-­‐  DiagnósQco   5.-­‐  RaQonale  y  Discusión   6.-­‐  Conclusiones    
  4. 4. 4   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   NEJM  26  Oct.  1923  
  5. 5. 5   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  6. 6. 6   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  7. 7. 7   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  8. 8. 8   Presentación  del  Caso  Clínico    F.H.P.  (30-­‐10-­‐2012)   -­‐  Varón  de  67  años   -­‐  No  fumador   -­‐  Jubilado.  Trabajó  como  comercial  de  una  FARMA  de  veterinaria   -­‐  Sedentario   -­‐  HepaJJs  a  los  4  años   -­‐   Adenoidectomia  a  los  6  años  y  apendicetomía  a  los  22  años   -­‐   Antecedentes  de  algunos  análisis  con  hiperglicemia  sin  diagnósJco  definiJvo  de  diabetes   -­‐  Acudió  a  nuestra  consulta  de  neumología  porque  tres  días  antes,  mientras  dormía,              despertó  por  dolor  torácico  intenso  brusco,  en  hemitórax  I.  Fue  atendido  en  el  Servicio                de  Urgencias  del  Hospital  CIMA.   -­‐  En  Urgencias  las  constantes  fueron  normales,  la  RX  de  tórax  fue  normal,  el  ECG  fue  normal.                La  analíJca  que  incluyó  CPK  y  Troponina  fue  normal.   -­‐  Estuvo  en  observación  durante  unas  horas,  se  le  administró  tratamiento  analgésico.   -­‐        Vista  la  evolución  fue  dado  de  alta  con  el  diagnósJco  de  dolor  torácico  y  la  indicación              de  acudir  a  consultas  externas  de  neumología.     UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  9. 9. 9   Presentación  del  Caso  Clínico   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  10. 10. 10   Presentación  del  Caso  Clínico   La  exploración  en  la  consulta  fue  relaQvamente    anodina:   -­‐  Altura  1.72m   -­‐  Peso  80  Kg   -­‐  IMC  28.39  (sobrepeso)   -­‐  Distribución  troncular  de  la  grasa   -­‐  Auscultación  respiratoria  y  cardíaca  normal   -­‐  Sat.  O2  de  97%.  Fr  cardíaca  72   -­‐  No  edemas   -­‐  Flacidez  palpebral   -­‐  No  adenopagas,  no  organomegálias.     -­‐  Presión  sobre  pared  costal  izquierda  dolorosa     UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  11. 11. 11   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  diferencial  de  dolor  torácico:   Origen  cardio-­‐vascular:                                                                  Ángor/infarto  de  miocardio                                                                Disección  de  aorta                                                                Angina  de  Prinzmetal/  S.  de  Takotsubo                                                                PericardiJs                                                                Necrosis  de  grasa  pericárdica                                                                  Otros   Origen  respiratorio:                                                                  Neumonía/pleuriJs  aguda                                                                  Infarto  pulmonar                                                                  Neumotórax/NeumomediasJno                                                                  Neoplasia  pulmonar                                                                  Mesotelioma  /Tumor  de  Pancoast                                                                  Otros                         Presentación  del  Caso  Clínico  
  12. 12. 12   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  diferencial  de  dolor  torácico:   Origen  pared  torácica:                                                                    Fractura  costal/fisura  costal                                                                    Metástasis    costal/tumores  primiJvos                                                                    Síndrome  de  Tietze                                                                    Enfermedad  de  Mondor                                                                    Roturas  fibrilares  musculares/hematoma                                                                    Herpes  Zoster                                                                    Otros   Origen  otras  localizaciones:                                                                      Meteorismo  abdominal                                                                      Enfermedad  de  Bornholm                                                                      Espasmo  esofágico/Boerhaave                                                                      Hernia  discal  dorsal                                                                      Otros   Presentación  del  Caso  Clínico  
  13. 13. 13   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Opinión  de  los  Asistentes  
  14. 14. 14   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Opinión  de  los  Asistentes  
  15. 15. 15   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Opinión  de  los  Asistentes   1.-­‐  Cuál  cree  que  es  el  diagnósQco  más  probable?       2.-­‐  Qué  dos  exploraciones  pediría?    
  16. 16. 16   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  
  17. 17. 17   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  
  18. 18. 18   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  19. 19. 19   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco   Fisuras/fracturas  costales  por  estrés     secundaria  a  esfuerzos  repeJdos  para“vencer  apnea”durante  la  noche     Síndrome  de  Apnea  ObstrucQva  de  grado  severo    
  20. 20. 20   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión   Pistas:     1.  Episodio  nocturno   2.  Descartados  angor  e  infarto,  pleuriJs  y  pericardiJs   3.  Dolor  a  la  presión  torácica  local   4.  Signo  del  párpado  flácido(floppy  eyelid)   5.  IMC  de  28.39  con  distribución  de  grasa  troncular   6.Conocimiento  del  mecanismo  de  presión  negaJva        intratorácica  en  apnea  prolongada  
  21. 21. 21   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  22. 22. 22   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  23. 23. 23   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión   (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection. (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection. (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection.
  24. 24. 24   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión   (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection. (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection. (24) or other antihypertensive drugs (25). These facts raise the hypothesis that OSAS, besides favoring the presence of arterial hypertension, could be a contributing factor to dissection in some patients through the mechanical stress on the aorta wall caused by repeated episodes of apnea and hypopnea. Inspiratory efforts against an occluded upper airway determine progressively negative intrathoracic pressures, which reach final mean peak values of approximately Ϫ60 cm H2O (8, 26). These negative pressures are transmitted to all intrathoracic structures and have been related to worsening of left ventricle function (27) and gastroesophageal reflux (28). In an animal model, Peters and colleagues (29, 30) observed an increase in systolic and diastolic aortic diameters during obstruc- tive apnea episodes. In parallel to this development of progres- sively negative intrathoracic pressures, a marked increase in sympathetic activity and blood pressure is produced during ap- neas, which at the end of the obstructive event may double the basal systolic values (9, 31, 32). Upper airway obstructive episodes during sleep are known to be frequently asymptomatic (2) and may have been evolving for years before being clinically detected. Thus, it could be speculated that in our patients, the sudden rises in the transmural pressure of the aortic wall, re- cations secondary to OSAS per se, rises in transmural pr during upper airway obstructive episodes may have a partic adverse effect on the recently surgically repaired thoracic Because the anesthetic and postoperative management of patients with OSAS benefits from specific measures (44, 4 believe that the early detection of OSAS could contribute to perioperative management of these patients. Our results indicate the need to assess the presence of toms suggestive of OSAS in patients with thoracic aorta d tion. Given the relative absence of sleepiness detected an lack of specificity of other symptoms such as snoring, we b that their presence should be additionally studied by s screening tests such as nocturnal pulsioxymetry or a limited study and, when the patient is stable, with full polysomnog In summary, in this study, a high mean AHI was fou patients with thoracic aorta dissection. We speculate th coexistence of OSAS may impose an additional risk of dissection in predisposed patients or determine worse evo because of the increase in aortic transmural pressure im Because effective treatment for OSAS is available, we b its diagnosis should be considered in the overall assessm patients with aortic dissection. Otros  efectos  de  la  presión  negaQva  intratorácica:     1.-­‐  Reflujo  esofágico   2.-­‐  Hernia  de  hiato   3.-­‐  Tos  persistente   4.-­‐  Afectación  función  ventricular  izquierda/derecha   5.-­‐  Nicturia   6.-­‐  HTA   7.-­‐  Edema  pulmonar?  
  25. 25. 25   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  26. 26. 26   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  27. 27. 27   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  28. 28. 28   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  29. 29. 29   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Conclusiones     1.-­‐  Los  cambios  de  presión  intratorácicos  en  el  SAOS  son  comunes  y              causan  diferentes  patologías     2.  La  repercusión  sobre  la  Aorta,  sobre  los  receptores  natriuréJcos  de  la  Aurícula  I  y            sobre  ambos  Ventrículos,  contribuye  a  patología  cardiovascular  secundaria  al  SAOS     3.-­‐  No  es  infrecuente  que  los  pacientes  con  SAOS  severo  se  quejen            de  dolores  torácicos  inespecíficos     4.-­‐  Se  ha  presentado  un  caso  no  descrito  de  fracturas  costales              producidas  por  Apneas  durante  el  sueño  (SAOS)        
  30. 30. UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  

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