SlideShare ist ein Scribd-Unternehmen logo
1 von 30
Downloaden Sie, um offline zu lesen
1	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
Dr.	
  Josep	
  Morera	
  
29	
  noviembre	
  2016	
  
2	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
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	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
NEJM	
  26	
  Oct.	
  1923	
  
5	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
6	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
7	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
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	
  
Presentación	
  del	
  Caso	
  Clínico	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
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	
  
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	
  
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	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
Opinión	
  de	
  los	
  Asistentes	
  
14	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
Opinión	
  de	
  los	
  Asistentes	
  
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	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
DiagnósQco	
  
17	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
DiagnósQco	
  
18	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
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	
  
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	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
22	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
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	
  
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	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
26	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
27	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
28	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  
RaQonale	
  y	
  Discusión	
  
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)	
  
	
  	
  
	
  
UN	
  GRITO	
  EN	
  LA	
  NOCHE:	
  
UNA	
  COMPLICACIÓN	
  NO	
  DESCRITA	
  DE	
  SAOS	
  

Weitere ähnliche Inhalte

Ähnlich wie Un grito en la noche: una complicacion no descrita de SAOS

Approach to Chest pain World Heart day 2022.pptx
Approach to Chest pain World Heart day 2022.pptxApproach to Chest pain World Heart day 2022.pptx
Approach to Chest pain World Heart day 2022.pptxBalajiBscRT
 
Dupuytrens disease
Dupuytrens diseaseDupuytrens disease
Dupuytrens diseasepersonalp
 
General examination by md151
General examination by md151General examination by md151
General examination by md151mohaan11
 
Medicine viva ques for 5th year and final prof
Medicine viva ques for  5th year and final profMedicine viva ques for  5th year and final prof
Medicine viva ques for 5th year and final profNajmus Sakib
 
how to identify diagnosis in respiratory system .pptx
how to identify diagnosis in respiratory system .pptxhow to identify diagnosis in respiratory system .pptx
how to identify diagnosis in respiratory system .pptxAbedinegoMaluka2
 
Definition 0 f pericardial diseases
Definition 0 f pericardial diseasesDefinition 0 f pericardial diseases
Definition 0 f pericardial diseasescardilogy
 
Mitralstenosis 130908040300-
Mitralstenosis 130908040300-Mitralstenosis 130908040300-
Mitralstenosis 130908040300-Haitham Mekkawi
 
Case Study - Adult - Dilemma - Emergency Department
Case Study - Adult - Dilemma - Emergency DepartmentCase Study - Adult - Dilemma - Emergency Department
Case Study - Adult - Dilemma - Emergency DepartmentUscom - Case Studies
 
Peripheral-Vascular-Disease-Surgical-Presentation.ppt
Peripheral-Vascular-Disease-Surgical-Presentation.pptPeripheral-Vascular-Disease-Surgical-Presentation.ppt
Peripheral-Vascular-Disease-Surgical-Presentation.pptmussahemed8
 
History & examination of edema
History & examination of edemaHistory & examination of edema
History & examination of edemaAbino David
 
Pulmonary embolism
Pulmonary embolism Pulmonary embolism
Pulmonary embolism MariahNazir
 
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...MUHAMMAD FAROOQUE
 
Clubbing
ClubbingClubbing
Clubbingkhushyy
 

Ähnlich wie Un grito en la noche: una complicacion no descrita de SAOS (20)

Approach to Chest pain World Heart day 2022.pptx
Approach to Chest pain World Heart day 2022.pptxApproach to Chest pain World Heart day 2022.pptx
Approach to Chest pain World Heart day 2022.pptx
 
Dupuytrens disease
Dupuytrens diseaseDupuytrens disease
Dupuytrens disease
 
Dupuytrens disease
Dupuytrens diseaseDupuytrens disease
Dupuytrens disease
 
General examination by md151
General examination by md151General examination by md151
General examination by md151
 
Medicine viva ques for 5th year and final prof
Medicine viva ques for  5th year and final profMedicine viva ques for  5th year and final prof
Medicine viva ques for 5th year and final prof
 
how to identify diagnosis in respiratory system .pptx
how to identify diagnosis in respiratory system .pptxhow to identify diagnosis in respiratory system .pptx
how to identify diagnosis in respiratory system .pptx
 
Cvs examination
Cvs examinationCvs examination
Cvs examination
 
Dr.sudhanshu
Dr.sudhanshuDr.sudhanshu
Dr.sudhanshu
 
Symptomtology of cardiovascular diseases
Symptomtology of cardiovascular diseasesSymptomtology of cardiovascular diseases
Symptomtology of cardiovascular diseases
 
Definition 0 f pericardial diseases
Definition 0 f pericardial diseasesDefinition 0 f pericardial diseases
Definition 0 f pericardial diseases
 
Mitralstenosis 130908040300-
Mitralstenosis 130908040300-Mitralstenosis 130908040300-
Mitralstenosis 130908040300-
 
Case Study - Adult - Dilemma - Emergency Department
Case Study - Adult - Dilemma - Emergency DepartmentCase Study - Adult - Dilemma - Emergency Department
Case Study - Adult - Dilemma - Emergency Department
 
Wg mitchell-7-5-06
Wg mitchell-7-5-06Wg mitchell-7-5-06
Wg mitchell-7-5-06
 
Peripheral-Vascular-Disease-Surgical-Presentation.ppt
Peripheral-Vascular-Disease-Surgical-Presentation.pptPeripheral-Vascular-Disease-Surgical-Presentation.ppt
Peripheral-Vascular-Disease-Surgical-Presentation.ppt
 
Dyspnoea (2)
Dyspnoea (2)Dyspnoea (2)
Dyspnoea (2)
 
History & examination of edema
History & examination of edemaHistory & examination of edema
History & examination of edema
 
Pulmonary embolism
Pulmonary embolism Pulmonary embolism
Pulmonary embolism
 
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...
“Differential diagnosis of chest pain” by Dr Muhammad Farooque presented on 2...
 
Clubbing
ClubbingClubbing
Clubbing
 
Clubbing
ClubbingClubbing
Clubbing
 

Mehr von Dr. Josep Morera Prat

Enfermedades respiratorias relacionadas con la asbestosis (català)
Enfermedades respiratorias relacionadas con la asbestosis (català)Enfermedades respiratorias relacionadas con la asbestosis (català)
Enfermedades respiratorias relacionadas con la asbestosis (català)Dr. Josep Morera Prat
 
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...Dr. Josep Morera Prat
 
Obesidad y Asma (coincidencia o casualidad)
Obesidad y Asma (coincidencia o casualidad)Obesidad y Asma (coincidencia o casualidad)
Obesidad y Asma (coincidencia o casualidad)Dr. Josep Morera Prat
 
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...Dr. Josep Morera Prat
 
Quan la realitat supera la ficció: Anecdotari d'una vida mèdica
Quan la realitat supera la ficció: Anecdotari d'una vida mèdicaQuan la realitat supera la ficció: Anecdotari d'una vida mèdica
Quan la realitat supera la ficció: Anecdotari d'una vida mèdicaDr. Josep Morera Prat
 
Bienal EPOC Zaragoza, Noviembre 2017
Bienal EPOC Zaragoza, Noviembre 2017Bienal EPOC Zaragoza, Noviembre 2017
Bienal EPOC Zaragoza, Noviembre 2017Dr. Josep Morera Prat
 
MPOC i broncodilatació dual: tiotropium /olodaterol
MPOC i broncodilatació dual:  tiotropium /olodaterolMPOC i broncodilatació dual:  tiotropium /olodaterol
MPOC i broncodilatació dual: tiotropium /olodaterolDr. Josep Morera Prat
 
Sleep Apnea y Riesgo Cardiovascular.
Sleep Apnea y Riesgo Cardiovascular.Sleep Apnea y Riesgo Cardiovascular.
Sleep Apnea y Riesgo Cardiovascular.Dr. Josep Morera Prat
 
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)Dr. Josep Morera Prat
 
Cars 2015 classification and staging of lung cancer 1.6
Cars 2015   classification and staging of lung cancer 1.6Cars 2015   classification and staging of lung cancer 1.6
Cars 2015 classification and staging of lung cancer 1.6Dr. Josep Morera Prat
 
Update 2015 CIMA - actualizaciones de neumologia
Update 2015 CIMA - actualizaciones de neumologiaUpdate 2015 CIMA - actualizaciones de neumologia
Update 2015 CIMA - actualizaciones de neumologiaDr. Josep Morera Prat
 
EPOC Deberes Hechos Asignaturas Pendientes
EPOC Deberes Hechos Asignaturas PendientesEPOC Deberes Hechos Asignaturas Pendientes
EPOC Deberes Hechos Asignaturas PendientesDr. Josep Morera Prat
 
Pulmonary review - Chest World Congress Madrid 2014
Pulmonary review - Chest World Congress Madrid 2014Pulmonary review - Chest World Congress Madrid 2014
Pulmonary review - Chest World Congress Madrid 2014Dr. Josep Morera Prat
 
EPOC: perspectivas de futuro (y una mirada al pasado).
EPOC: perspectivas de futuro (y una mirada al pasado).EPOC: perspectivas de futuro (y una mirada al pasado).
EPOC: perspectivas de futuro (y una mirada al pasado).Dr. Josep Morera Prat
 

Mehr von Dr. Josep Morera Prat (20)

Tuberculosis vs covid 19
Tuberculosis vs covid 19 Tuberculosis vs covid 19
Tuberculosis vs covid 19
 
Enfermedades respiratorias relacionadas con la asbestosis (català)
Enfermedades respiratorias relacionadas con la asbestosis (català)Enfermedades respiratorias relacionadas con la asbestosis (català)
Enfermedades respiratorias relacionadas con la asbestosis (català)
 
Higiene hypothesis,
Higiene hypothesis, Higiene hypothesis,
Higiene hypothesis,
 
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...
Obesidad i asma ( coincidència o causalitat) - actualització Novembre 2019 ( ...
 
Obesidad y Asma (coincidencia o casualidad)
Obesidad y Asma (coincidencia o casualidad)Obesidad y Asma (coincidencia o casualidad)
Obesidad y Asma (coincidencia o casualidad)
 
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...
Disfunció cordes vocals. actualitzacio en coneixements en patologia respirat...
 
Quan la realitat supera la ficció: Anecdotari d'una vida mèdica
Quan la realitat supera la ficció: Anecdotari d'una vida mèdicaQuan la realitat supera la ficció: Anecdotari d'una vida mèdica
Quan la realitat supera la ficció: Anecdotari d'una vida mèdica
 
Bienal EPOC Zaragoza, Noviembre 2017
Bienal EPOC Zaragoza, Noviembre 2017Bienal EPOC Zaragoza, Noviembre 2017
Bienal EPOC Zaragoza, Noviembre 2017
 
MPOC i broncodilatació dual: tiotropium /olodaterol
MPOC i broncodilatació dual:  tiotropium /olodaterolMPOC i broncodilatació dual:  tiotropium /olodaterol
MPOC i broncodilatació dual: tiotropium /olodaterol
 
Sleep Apnea y Riesgo Cardiovascular.
Sleep Apnea y Riesgo Cardiovascular.Sleep Apnea y Riesgo Cardiovascular.
Sleep Apnea y Riesgo Cardiovascular.
 
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)
NEUMOLOGIA: UPDATE 2016 (COSECHA DEL 15-­‐16)
 
Asma y ejercicio.
Asma y ejercicio.Asma y ejercicio.
Asma y ejercicio.
 
Via Respiratoria Unica
Via Respiratoria UnicaVia Respiratoria Unica
Via Respiratoria Unica
 
Fenotips de l'asma bronquial.
Fenotips de l'asma bronquial.Fenotips de l'asma bronquial.
Fenotips de l'asma bronquial.
 
Cars 2015 classification and staging of lung cancer 1.6
Cars 2015   classification and staging of lung cancer 1.6Cars 2015   classification and staging of lung cancer 1.6
Cars 2015 classification and staging of lung cancer 1.6
 
Tos de origen profesional
Tos de origen profesionalTos de origen profesional
Tos de origen profesional
 
Update 2015 CIMA - actualizaciones de neumologia
Update 2015 CIMA - actualizaciones de neumologiaUpdate 2015 CIMA - actualizaciones de neumologia
Update 2015 CIMA - actualizaciones de neumologia
 
EPOC Deberes Hechos Asignaturas Pendientes
EPOC Deberes Hechos Asignaturas PendientesEPOC Deberes Hechos Asignaturas Pendientes
EPOC Deberes Hechos Asignaturas Pendientes
 
Pulmonary review - Chest World Congress Madrid 2014
Pulmonary review - Chest World Congress Madrid 2014Pulmonary review - Chest World Congress Madrid 2014
Pulmonary review - Chest World Congress Madrid 2014
 
EPOC: perspectivas de futuro (y una mirada al pasado).
EPOC: perspectivas de futuro (y una mirada al pasado).EPOC: perspectivas de futuro (y una mirada al pasado).
EPOC: perspectivas de futuro (y una mirada al pasado).
 

Kürzlich hochgeladen

Adenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisAdenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisSujoy Dasgupta
 
AORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectionAORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectiondrhanifmohdali
 
Red Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfRed Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfMedicoseAcademics
 
MedMatch: Your Health, Our Mission. Pitch deck.
MedMatch: Your Health, Our Mission. Pitch deck.MedMatch: Your Health, Our Mission. Pitch deck.
MedMatch: Your Health, Our Mission. Pitch deck.whalesdesign
 
Female Reproductive Physiology Before Pregnancy
Female Reproductive Physiology Before PregnancyFemale Reproductive Physiology Before Pregnancy
Female Reproductive Physiology Before PregnancyMedicoseAcademics
 
Role of Soap based and synthetic or syndets bar
Role of  Soap based and synthetic or syndets barRole of  Soap based and synthetic or syndets bar
Role of Soap based and synthetic or syndets barmohitRahangdale
 
"Radical excision of DIE in subferile women with deep infiltrating endometrio...
"Radical excision of DIE in subferile women with deep infiltrating endometrio..."Radical excision of DIE in subferile women with deep infiltrating endometrio...
"Radical excision of DIE in subferile women with deep infiltrating endometrio...Sujoy Dasgupta
 
blood bank management system project report
blood bank management system project reportblood bank management system project report
blood bank management system project reportNARMADAPETROLEUMGAS
 
Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Peter Embi
 
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfPAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfDolisha Warbi
 
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfSGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfHongBiThi1
 
Male Infertility, Antioxidants and Beyond
Male Infertility, Antioxidants and BeyondMale Infertility, Antioxidants and Beyond
Male Infertility, Antioxidants and BeyondSujoy Dasgupta
 
historyofpsychiatryinindia. Senthil Thirusangu
historyofpsychiatryinindia. Senthil Thirusanguhistoryofpsychiatryinindia. Senthil Thirusangu
historyofpsychiatryinindia. Senthil Thirusangu Medical University
 
ayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptPradnya Wadekar
 
EXERCISE PERFORMANCE.pptx, Lung function
EXERCISE PERFORMANCE.pptx, Lung functionEXERCISE PERFORMANCE.pptx, Lung function
EXERCISE PERFORMANCE.pptx, Lung functionkrishnareddy157915
 
Male Infertility Panel Discussion by Dr Sujoy Dasgupta
Male Infertility Panel Discussion by Dr Sujoy DasguptaMale Infertility Panel Discussion by Dr Sujoy Dasgupta
Male Infertility Panel Discussion by Dr Sujoy DasguptaSujoy Dasgupta
 
High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)kishan singh tomar
 
Mental health Team. Dr Senthil Thirusangu
Mental health Team. Dr Senthil ThirusanguMental health Team. Dr Senthil Thirusangu
Mental health Team. Dr Senthil Thirusangu Medical University
 

Kürzlich hochgeladen (20)

Adenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosisAdenomyosis or Fibroid- making right diagnosis
Adenomyosis or Fibroid- making right diagnosis
 
AORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissectionAORTIC DISSECTION and management of aortic dissection
AORTIC DISSECTION and management of aortic dissection
 
Red Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdfRed Blood Cells_anemia & polycythemia.pdf
Red Blood Cells_anemia & polycythemia.pdf
 
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
How to master Steroid (glucocorticoids) prescription, different scenarios, ca...
 
MedMatch: Your Health, Our Mission. Pitch deck.
MedMatch: Your Health, Our Mission. Pitch deck.MedMatch: Your Health, Our Mission. Pitch deck.
MedMatch: Your Health, Our Mission. Pitch deck.
 
Female Reproductive Physiology Before Pregnancy
Female Reproductive Physiology Before PregnancyFemale Reproductive Physiology Before Pregnancy
Female Reproductive Physiology Before Pregnancy
 
Role of Soap based and synthetic or syndets bar
Role of  Soap based and synthetic or syndets barRole of  Soap based and synthetic or syndets bar
Role of Soap based and synthetic or syndets bar
 
"Radical excision of DIE in subferile women with deep infiltrating endometrio...
"Radical excision of DIE in subferile women with deep infiltrating endometrio..."Radical excision of DIE in subferile women with deep infiltrating endometrio...
"Radical excision of DIE in subferile women with deep infiltrating endometrio...
 
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
Immune labs basics part 1 acute phase reactants ESR, CRP Ahmed Yehia Ismaeel,...
 
blood bank management system project report
blood bank management system project reportblood bank management system project report
blood bank management system project report
 
Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024Clinical Research Informatics Year-in-Review 2024
Clinical Research Informatics Year-in-Review 2024
 
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdfPAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
PAIN/CLASSIFICATION AND MANAGEMENT OF PAIN.pdf
 
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdfSGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
SGK RỐI LOẠN KALI MÁU CỰC KỲ QUAN TRỌNG.pdf
 
Male Infertility, Antioxidants and Beyond
Male Infertility, Antioxidants and BeyondMale Infertility, Antioxidants and Beyond
Male Infertility, Antioxidants and Beyond
 
historyofpsychiatryinindia. Senthil Thirusangu
historyofpsychiatryinindia. Senthil Thirusanguhistoryofpsychiatryinindia. Senthil Thirusangu
historyofpsychiatryinindia. Senthil Thirusangu
 
ayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologypptayurvedic formulations herbal drug technologyppt
ayurvedic formulations herbal drug technologyppt
 
EXERCISE PERFORMANCE.pptx, Lung function
EXERCISE PERFORMANCE.pptx, Lung functionEXERCISE PERFORMANCE.pptx, Lung function
EXERCISE PERFORMANCE.pptx, Lung function
 
Male Infertility Panel Discussion by Dr Sujoy Dasgupta
Male Infertility Panel Discussion by Dr Sujoy DasguptaMale Infertility Panel Discussion by Dr Sujoy Dasgupta
Male Infertility Panel Discussion by Dr Sujoy Dasgupta
 
High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)High-Performance Thin-Layer Chromatography (HPTLC)
High-Performance Thin-Layer Chromatography (HPTLC)
 
Mental health Team. Dr Senthil Thirusangu
Mental health Team. Dr Senthil ThirusanguMental health Team. Dr Senthil Thirusangu
Mental health Team. Dr Senthil Thirusangu
 

Un grito en la noche: una complicacion no descrita de SAOS

  • 1. 1   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Dr.  Josep  Morera   29  noviembre  2016  
  • 2. 2   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 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   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   NEJM  26  Oct.  1923  
  • 5. 5   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 6. 6   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 7. 7   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 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   Presentación  del  Caso  Clínico   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 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   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   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   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Opinión  de  los  Asistentes  
  • 14. 14   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   Opinión  de  los  Asistentes  
  • 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   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  
  • 17. 17   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   DiagnósQco  
  • 18. 18   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS  
  • 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   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   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 22. 22   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 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   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   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 26. 26   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 27. 27   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 28. 28   UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS   RaQonale  y  Discusión  
  • 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. UN  GRITO  EN  LA  NOCHE:   UNA  COMPLICACIÓN  NO  DESCRITA  DE  SAOS