Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 +/- 7.3 apneas and hypopneas/h on N1 to 5.8 +/- 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 +/- 6.9 apneas and hypopneas/h during room air breathing to 5.9 +/- 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.
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PMID:Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. 907 83

A 57-yr-old man with idiopathic central apnea is reported. He presented at our hospital complaining of excessive daytime sleepiness. Polysomnography, including esophageal pressure monitoring, confirmed central sleep apnea with an apnea index of 27/h. He had mild non-insulin-dependent diabetes mellitus (NIDDM) but no signs of diabetic neuropathy or other background diseases. The ventilatory responses to hypoxia and hypercapnia tested while he was awake indicated increased respiratory chemosensitivity. We applied nasal continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) in an attempt to compare the possible difference in therapeutic efficacy. Although nasal CPAP completely reversed central apnea, nasal BPAP adversely affected both apnea length and frequency in an applied pressure-dependent manner. Arterial blood gas analyses while he was being treated indicted alveolar hypoventilation with CPAP and hyperventilation with BPAP. Additionally, administration of a mixed gas containing 5% CO2 through a face mask had a significant effect on the disappearance of central apnea in this patient. These findings support the theory that the arterial PCO2 level is critical in generating idiopathic central apnea and that nasal CPAP therapy may be effective in eliminating central apnea by raising the PaCO2.
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PMID:Continuous versus bilevel positive airway pressure in a patient with idiopathic central sleep apnea. 910 99

The respiratory control system guarantees acid-base-homeostasis as well as the rhythmic activities of the respiratory motor system in accordance with exercise and behavioural programmes of the human being. Cortical patterns and synchronized respiratory patterns with tracheal flow and pressure variations in the fetus indicate the common network of respiration and sleep-wake mechanisms in an early stage already. During fetal life acid-base-homeostasis is dependent on progesterone controlled mechanisms. CO2 partial pressure of the uterine artery reduces to 32 mmHg. The O2 Partial pressure of the umbilical vein is 25-30 mmHg only. The raise of PCO2 during delivery is accompanied by a shower of sensory input to the reticular formation causing arousal and the opening of the lungs. The continuation of postnatal breathing is the consequence of the integration of the central chemosensitive mechanism and the reticular activating system at an adequate threshold. Perinatal defense reflexes, functional patterns and strategies in early life may outline later pathophysiological mechanisms for sleep apnea, apparently life threatening event (ALTE), sudden infant death, and congenital central hypoventilation syndrome.
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PMID:[Control and development of breathing, pathophysiological aspects]. 924 85

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.
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PMID:Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia. 927 11

Sleep apnea with neuromuscular disorders has been successfully treated with bi-level positive airway pressure ventilation (BiPAP), which, unlike continuous positive airway pressure ventilation (CPAP), creates pressure difference between expiratory and inspiratory phases. Hence if the respiration of patients stops longer than a pre-set duration, BiPAP can automatically force them to breath through a nasal mask. We report a 60-year-old woman with olivo-ponto-cerebellar atrophy (OPCA), whose mixed-type sleep apnea was difficult to treat with conventional CPAP. We therefore tried BiPAP on this patient at night. Nocturnal CO2 retention was nearly resolved, and unexpectedly daytime PaCO2 was also corrected with marked improvement of daytime somnolence. BiPAP is totally non-invasive, and may be one of the most effective treatments in patients with OPCA suffering from sleep apnea.
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PMID:[Efficacy of nasal bi-level positive airway pressure ventilation in a patient with olivo-ponto-cerebellar atrophy suffering from sleep apnea syndrome]. 936 76

There have been very few studies assessing the long-term physiological effects of nasal continuous positive airway pressure (CPAP) for the obstructive sleep apnoea syndrome. We therefore investigated prospectively the evolution of lung function, arterial blood gases and pulmonary haemodynamics in patients with this syndrome treated with CPAP. Sixty five patients were included. The mean duration of home treatment with nasal CPAP was 64+/-6 months. Most of the patients (77%) were smokers at the baseline assessment. We observed a small, but significant, decrease in forced expiratory volume in one second (FEV1) from 80+/-21% at baseline (t0) to 76+/-21% of the predicted value at the follow-up evaluation (t5) (p<0.01). Arterial oxygen tension (P[a,O2]) for the group as a whole remained stable (9.4+/-1.5 kPa (71+/-11 mmHg) versus 9.4+/-1.2 kPa (71+/-9 mmHg)). However, P(a,O2) increased in the subgroup of patients with hypoxaemia at t0 (n=23), from 7.8+/-0.7 kPa (59+/-5 mmHg) to 8.9+/-1.2 kPa (67+/-9 mmHg). Arterial carbon dioxide tension (P[a,CO2]) for the group as a whole increased slightly, but significantly, from 5.2+/-0.7 kPa (39+/-5 mmHg) to 5.4+/-0.5 kPa (41+/-4 mmHg) (p<0.05). Mean pulmonary artery pressure (Ppa) at rest did not change (16+/-5 mmHg versus 17+/-5 mmHg; NS) nor did exercising Ppa. In the 11 patients with pulmonary hypertension at t0, Ppa was 24+/-5 mmHg at t0 versus 20+/-7 mmHg at t5 (NS). We conclude that the significant decrease of forced expiratory volume in one second after 5 yr follow-up was related to a high percentage of smokers and exsmokers in the study population. Daytime arterial oxygen tension and pulmonary artery pressure remained stable in an unselected series of 65 obstructive sleep apnoea syndrome patients treated for 5 yrs with nasal continuous positive airway pressure, unlike arterial carbon dioxide tension, which increased by a small, but significant, amount.
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PMID:Five-year effects of nasal continuous positive airway pressure in obstructive sleep apnoea syndrome. 942 98

Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-microgram i.v. boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 +/- 5 (mean +/- SD) mmHg (range 12-37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20-25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.
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PMID:An induced blood pressure rise does not alter upper airway resistance in sleeping humans. 945 46

We postulated that three extremely obese Yucatan miniature pigs would have more sleep apnea than three nonobese Yucatan miniature pigs. Pigs were studied with the use of electroencephalograms, inductance plethysmography, oximetry, expired nasal CO2, or thermistors. All of the obese pigs, but none of the nonobese pigs, had both sleep apnea (8.5, 10.3, and 97.0 in obese pigs vs. O apnea + hypopnea/h in all nonobese pigs; P < 0.05) and oxyhemoglobin desaturation episodes during sleep [9.4 +/- 3.0 vs. 0 + 0.53 (SD) mean desaturation episodes/h in obese pigs vs. nonobese pigs, respectively; P < 0.05]. Two of the extremely obese pigs had obstructive sleep apnea, whereas the third obese pig had central sleep apnea. We conclude that sleep apnea occurs in extremely obese Yucatan minipigs and suggest that this animal can be used as a model for sleep apnea in obesity.
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PMID:Sleep apnea in obese miniature pigs. 947 62

Noninvasive positive pressure ventilation (NPPV) can improve ventilation in obese subjects during the postoperative period after abdominal surgery. Compared to nasal continuous positive airway pressure (nCPAP), NPPV was superior in correcting blood gas abnormalities both during the night-time and during the daytime in a subgroup of patients with the obesity hypoventilation syndrome (OHS). However, as it is unknown, if and to what extent NPPV can unload the respiratory muscles in the face of the increased impedance of the respiratory system in obesity, this is what was investigated. Eighteen obese subjects with a body mass index > or = 40 kg x m(-2) were investigated during the daytime, which included five healthy controls (simple obesity (SO)), seven patients with obstructive sleep apnoea (OSA) and six patients with the obesity hypoventilation syndrome (OHS). Assisted PPV was performed with bi-level positive airway pressure (BiPAP), applied via a face mask. Inspiratory positive airway pressure (IPAP) was set to 1.2 or 1.6 kPa and expiratory positive airway pressure (EPAP) was set to 0.5 kPa. Inspiratory muscle activity was measured as diaphragmatic pressure time product (PTPdi). Comparison of spontaneous breathing with BiPAP ventilation showed no significant difference in breathing pattern, although there was a tendency towards an increase in tidal volume (VT) in all three groups and a decrease in respiratory frequency (fR) in patients with OSA and OHS. End-tidal carbon dioxide (PET,CO2) with BiPAP was unchanged in SO and OSA, but was decreased in OHS. In contrast, inspiratory muscle activity was reduced by at least 40% in each group. This was indicated by a decrease in PTPdi with BiPAP 1.2/0.5 kPa from mean+/-SD 39+/-5 to 20+/-9 kPa x s (p<0.05) in SO, from 42+/-7 to 21+/-8 kPa x s (p<0.05) in OSA, and from 64+/-20 to 38+/-17 kPa x s (p<0.05) in OHS. With BiPAP 1.6/0.5 kPa, PTPdi was further reduced to 17+/-6 kPa x s in SO, and to 17+/-6 kPa x s in OSA, but not in OHS (40+/-22 kPa x s). We conclude that noninvasive assisted ventilation unloads the inspiratory muscles in patients with gross obesity.
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PMID:Influence of noninvasive positive pressure ventilation on inspiratory muscle activity in obese subjects. 949 72

We evaluated the effect of non-invasive nocturnal ventilation with the bi-level positive airway pressure (BiPAP) ventilator in 12 overweight patients with verified obstructive sleep apnoea syndrome (OSAS) and nocturnal hypercapnia. All patients exhibited subsequently less overnight CO2 accumulation (p < 0.0001), the desaturation event frequency was reduced (p < 0.002), daytime O2 tension rose (p < 0.001), daytime CO2 tension was reduced (p < 0.01), and apnoeas were eliminated. All symptoms characterising the syndrome, when present at the beginning of the therapy, were eliminated during the treatment. Patient compliance was high. This study showed that OSAS patients with hypercapnia can be effectively treated by BiPAP ventilation during sleep.
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PMID:Bi-level positive airway pressure treatment of obstructive sleep apnoea syndrome. 958 Sep 22


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