Ironjustic
Fri, Sep-28-07, 17:16
It seems sleep apnea scores rise AS one ascends to altitude
and actually .. changes .. from one to another ..
coincidentally .. as red blood cell count changes / increases.
-----------------------------------------------------------
Fourteen normal adult volunteers were studied. Thirteen
subjects developed Central and obstructive sleep apnoea .
Central and obstructive sleep apnoea during ascent to high
altitude. BURGESS KR, JOHNSON PL, EDWARDS N. Respirology
2004;9(2):222-9. Peninsula Private Sleep Laboratory, Manly,
New South Wales, Australia Abstract:
Central and obstructive sleep apnoea during ascent to high
altitude BURGESS KR, JOHNSON PL, EDWARDS N. Respirology 2004;
9: 222-229 Objective: The aim of the study was to investigate
the relationship between central sleep apnoea (CSA) at high
altitude and arterial blood gas tensions, and by inference,
ventilatory responsiveness. Methodology: Fourteen normal adult
volunteers were studied by polysomnography during sleep, and
analysis of awake blood gases during ascent over 12 days from
sealevel to 5050 m in the Nepal Himalayas. Results: Thirteen
subjects developed CSA. Linear regression analysis showed
tight negative correlations between mean CSA index and mean
values for sleep SaO(2), PaCO(2) and PaO(2) over the six
altitudes (r(2) >/= 0.74 for all, P < 0.03). Paradoxically
there was poor correlation between the individual data for CSA
index and those parameters at the highest altitude (5050-m)
where CSA was worst (r(2) < 0.12 for all, NS), possibly due to
variation in degree of acclimatization between subjects. In
addition, CSA replaced mild obstructive sleep apnoea during
ascent. Obstructive sleep apnoea index fell from 5.5 +/- 6.9/h
in rapid eye movement sleep at sealevel to 0.1 +/- 0.3/h at
5050 m (P < .001, analysis of variance), while CSA index rose
from 0.1 +/- 0.3/ h to 55.7 +/- 54.4/h (P < 0.001).
Conclusion: There was a general relationship between
decreasing PaCO(2) and CSA, but there were significant effects
from variations in acclimatization that would make hypoxic
ventilatory response an unreliable predictor of CSA in
individuals.
------------------------------------------------
http://www.medical-conditions.org/?q=Sleep+Apnea
Sleep Apnea Disorders characterized by multiple cessations of
respirations during sleep that induce partial arousals and
interfere with the maintenance of sleep. Sleep apnea syndromes
are divided into central (see SLEEP APENA, CENTRAL),
obstructive (see SLEEP APNEA, OBSTRUCTIVE), and mixed
central-obstructive types.
--------------------------------------------------
P473 Hemochromatosis and sleep disturbance
R. F. PERALTA and T. PAIVA EEG/Sleep Laboratory, Molecular
Medicine Institute, Lisbon, Portugal Introduction:
Hereditary hemochromatosis (HH) is a hereditary autosomal
recessive condition, due to mutation of the HFE genotype.
Recent papers have evaluated the relation between HH and
restless legs syndrome (RLS), which occurs in 16.4% of HH
patients. There are no references concerning other sleep
disturbances and HH. We describe five adult male patients
with hereditary hemochromatosis, affected by different
sleep pathologies. Clinical cases: 1-49 years old male
patient, obese, with hemochroma-tosis with regular
phlebotomies, suffered from excessive daytime sleepiness
(EDS). The PSG showed significant obstructive sleep apnea
and snoring, no RLS, no periodic leg movements (PLMs). 2-63
years old man, non-obese with HH and EDS. The PSG
documented significant obstructive sleep apnea, no RLS, no
PLMS. 3-49 years old man with long standing HH treated with
frequent phlebotomies. The patient complained of EDS, he
had no RLS and the PSG documented OSAS with no PLMs. 4-52
years old man with a recent diagnosis of HH treated with
phlebotomies. Subsequently the patient developed severe
insomnia. There were severe RLS and the PSG documented
severe PLMs. 5-70 years old male patient with long standing
refractory insomnia. There were no RLS symptoms or PLMs on
PSG and no history of secondary insomnia. The patient was
subsequently diagnosed hemochromatosis (Ferritin: 438 ng mL
)1 ). Discussion: The presence of OSAS, insomnia and
RLS/PLMs in HH patients does not imply a specific
relationship. These sleep diseases are common pathologies
and this may represent a mere casual relationship. The
rational between RLS and HH is related to iron metabolism
and iron deposits in the brain. Hemochromatosis may however
induce changes in hypothalamic/pituitary structures and
cause changes in sleep/circadian rhythms. Furthermore, OSAS
and HH concur in the development of endocrinologic,
hematologic and cardiovascular morbidity. The correct
diagnosis of sleep disturbances in HH patients is important
and should be broadened to different sleep pathologies.of
choice for revealing regulatory disturbances in
cardiovascular diseases.
--------------------------------------------------------
"iron encrustation of elastica "
Hum Pathol. 1997 Mar;28(3):264-9.Links Comment in: Hum
Pathol. 1997 Mar;28(3):261-3. Hum Pathol. 1997
Nov;28(11):1329-30. Cardiopulmonary pathology in patients
with sleep apnea/obesity hypoventilation syndrome.Ahmed Q,
Chung-Park M, Tomashefski JF Jr. Department of Pathology,
Case Western Reserve University, School of Medicine at
MetroHealth Medical Center, Cleveland, OH 44109, USA.
We reviewed clinical data, autopsy reports, and microscopic
slides on 10 patients with sleep apnea/obesity hypoventilation
syndrome (SA/OHS) to define the cardiopulmonary pathological
features and establish clinicopathologic correlations. Ten
obese (>136 kg) patients without SA/OHS were studied as
controls. Patients with SA/OHS exhibited biventricular cardiac
failure and pulmonary hypertension with a higher prevalence of
moderate/severe pulmonary hemosiderosis (8 v 0 patients),
alveolar hemorrhage (7 v 4 patients), capillary proliferation
(4 v 0 patients), iron encrustation of elastica (1 v 0
patients) and medial hypertrophy of muscular pulmonary
arteries (11.9 +/- 2.4 v 9.7 +/- 1.6%) (P < .05). In two
patients capillary proliferation resembled capillary
hemangiomatosis. Mean right ventricular thickness was higher
in the SA/OHS group (0.71 +/- 0.17 v .42 +/- 0.1 cm) (P <
.01). Four patients with SA/OHS and three controls had
moderate/severe myocardial fibrosis. Biventricular cardiac
failure caused death in seven patients with SA/OHS. Hypoxia is
probably the most important cause of pulmonary hypertension,
arterial muscularization, and right ventricular hypertrophy in
SA/ OHS. Left ventricular failure in some SA/OHS patients may
be the result of hypertensive cardiac disease. In others, the
etiology of left ventricular failure was not determined
morphologically, suggesting functional abnormalities related
to obesity and/or apneic episodes.
PMID: 9042788 [PubMed - indexed for MEDLINE]
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
and actually .. changes .. from one to another ..
coincidentally .. as red blood cell count changes / increases.
-----------------------------------------------------------
Fourteen normal adult volunteers were studied. Thirteen
subjects developed Central and obstructive sleep apnoea .
Central and obstructive sleep apnoea during ascent to high
altitude. BURGESS KR, JOHNSON PL, EDWARDS N. Respirology
2004;9(2):222-9. Peninsula Private Sleep Laboratory, Manly,
New South Wales, Australia Abstract:
Central and obstructive sleep apnoea during ascent to high
altitude BURGESS KR, JOHNSON PL, EDWARDS N. Respirology 2004;
9: 222-229 Objective: The aim of the study was to investigate
the relationship between central sleep apnoea (CSA) at high
altitude and arterial blood gas tensions, and by inference,
ventilatory responsiveness. Methodology: Fourteen normal adult
volunteers were studied by polysomnography during sleep, and
analysis of awake blood gases during ascent over 12 days from
sealevel to 5050 m in the Nepal Himalayas. Results: Thirteen
subjects developed CSA. Linear regression analysis showed
tight negative correlations between mean CSA index and mean
values for sleep SaO(2), PaCO(2) and PaO(2) over the six
altitudes (r(2) >/= 0.74 for all, P < 0.03). Paradoxically
there was poor correlation between the individual data for CSA
index and those parameters at the highest altitude (5050-m)
where CSA was worst (r(2) < 0.12 for all, NS), possibly due to
variation in degree of acclimatization between subjects. In
addition, CSA replaced mild obstructive sleep apnoea during
ascent. Obstructive sleep apnoea index fell from 5.5 +/- 6.9/h
in rapid eye movement sleep at sealevel to 0.1 +/- 0.3/h at
5050 m (P < .001, analysis of variance), while CSA index rose
from 0.1 +/- 0.3/ h to 55.7 +/- 54.4/h (P < 0.001).
Conclusion: There was a general relationship between
decreasing PaCO(2) and CSA, but there were significant effects
from variations in acclimatization that would make hypoxic
ventilatory response an unreliable predictor of CSA in
individuals.
------------------------------------------------
http://www.medical-conditions.org/?q=Sleep+Apnea
Sleep Apnea Disorders characterized by multiple cessations of
respirations during sleep that induce partial arousals and
interfere with the maintenance of sleep. Sleep apnea syndromes
are divided into central (see SLEEP APENA, CENTRAL),
obstructive (see SLEEP APNEA, OBSTRUCTIVE), and mixed
central-obstructive types.
--------------------------------------------------
P473 Hemochromatosis and sleep disturbance
R. F. PERALTA and T. PAIVA EEG/Sleep Laboratory, Molecular
Medicine Institute, Lisbon, Portugal Introduction:
Hereditary hemochromatosis (HH) is a hereditary autosomal
recessive condition, due to mutation of the HFE genotype.
Recent papers have evaluated the relation between HH and
restless legs syndrome (RLS), which occurs in 16.4% of HH
patients. There are no references concerning other sleep
disturbances and HH. We describe five adult male patients
with hereditary hemochromatosis, affected by different
sleep pathologies. Clinical cases: 1-49 years old male
patient, obese, with hemochroma-tosis with regular
phlebotomies, suffered from excessive daytime sleepiness
(EDS). The PSG showed significant obstructive sleep apnea
and snoring, no RLS, no periodic leg movements (PLMs). 2-63
years old man, non-obese with HH and EDS. The PSG
documented significant obstructive sleep apnea, no RLS, no
PLMS. 3-49 years old man with long standing HH treated with
frequent phlebotomies. The patient complained of EDS, he
had no RLS and the PSG documented OSAS with no PLMs. 4-52
years old man with a recent diagnosis of HH treated with
phlebotomies. Subsequently the patient developed severe
insomnia. There were severe RLS and the PSG documented
severe PLMs. 5-70 years old male patient with long standing
refractory insomnia. There were no RLS symptoms or PLMs on
PSG and no history of secondary insomnia. The patient was
subsequently diagnosed hemochromatosis (Ferritin: 438 ng mL
)1 ). Discussion: The presence of OSAS, insomnia and
RLS/PLMs in HH patients does not imply a specific
relationship. These sleep diseases are common pathologies
and this may represent a mere casual relationship. The
rational between RLS and HH is related to iron metabolism
and iron deposits in the brain. Hemochromatosis may however
induce changes in hypothalamic/pituitary structures and
cause changes in sleep/circadian rhythms. Furthermore, OSAS
and HH concur in the development of endocrinologic,
hematologic and cardiovascular morbidity. The correct
diagnosis of sleep disturbances in HH patients is important
and should be broadened to different sleep pathologies.of
choice for revealing regulatory disturbances in
cardiovascular diseases.
--------------------------------------------------------
"iron encrustation of elastica "
Hum Pathol. 1997 Mar;28(3):264-9.Links Comment in: Hum
Pathol. 1997 Mar;28(3):261-3. Hum Pathol. 1997
Nov;28(11):1329-30. Cardiopulmonary pathology in patients
with sleep apnea/obesity hypoventilation syndrome.Ahmed Q,
Chung-Park M, Tomashefski JF Jr. Department of Pathology,
Case Western Reserve University, School of Medicine at
MetroHealth Medical Center, Cleveland, OH 44109, USA.
We reviewed clinical data, autopsy reports, and microscopic
slides on 10 patients with sleep apnea/obesity hypoventilation
syndrome (SA/OHS) to define the cardiopulmonary pathological
features and establish clinicopathologic correlations. Ten
obese (>136 kg) patients without SA/OHS were studied as
controls. Patients with SA/OHS exhibited biventricular cardiac
failure and pulmonary hypertension with a higher prevalence of
moderate/severe pulmonary hemosiderosis (8 v 0 patients),
alveolar hemorrhage (7 v 4 patients), capillary proliferation
(4 v 0 patients), iron encrustation of elastica (1 v 0
patients) and medial hypertrophy of muscular pulmonary
arteries (11.9 +/- 2.4 v 9.7 +/- 1.6%) (P < .05). In two
patients capillary proliferation resembled capillary
hemangiomatosis. Mean right ventricular thickness was higher
in the SA/OHS group (0.71 +/- 0.17 v .42 +/- 0.1 cm) (P <
.01). Four patients with SA/OHS and three controls had
moderate/severe myocardial fibrosis. Biventricular cardiac
failure caused death in seven patients with SA/OHS. Hypoxia is
probably the most important cause of pulmonary hypertension,
arterial muscularization, and right ventricular hypertrophy in
SA/ OHS. Left ventricular failure in some SA/OHS patients may
be the result of hypertensive cardiac disease. In others, the
etiology of left ventricular failure was not determined
morphologically, suggesting functional abnormalities related
to obesity and/or apneic episodes.
PMID: 9042788 [PubMed - indexed for MEDLINE]
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk