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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Primary alveolar hypoventilation is a rare syndrome of unknown origin, characterized by a dysfunction of the automatic respiratory pattern in spite of normal lungs and in the absence of mechanical ventilatory defects. A reduction of the ventilatory response to CO2 is regularly found, and cardiac failure is common. The differential diagnosis mainly concerns the sleep apnoea syndrome. The usual treatments have little effectiveness.
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PMID:[Primary alveolar hypoventilation. Clinical aspects and diagnostic problems. Apropos of a case]. 367 71

Based on results on central chemosensitivity in cats, paired stimuli were applied for therapy to infants with central respiratory insufficiency of various degrees. An unspecific respiratory stimulus, e.g. light for 1 s, was followed by a jet of either O2 or 2% CO2 in O2 for 1.5 s. The unspecific and the chemical stimuli were interspaced by 0.5 s. The combined stimulation was repeated every 10 s. The program was triggered by using threshold values of transcutaneous pO2. In infants with intratrachial tubes or tracheostoma we used the end tidal pCO2 for triggering the stimulation. The method could prevent hypoxemia during sleep in non-ventilated subjects with sleep apnea syndromes or in infants with severe hypoxemia during sleep after being rescued from Sudden Infant Death Syndrome (SIDS). In patients with Ondine's Curse Syndrome (OCS) with its CO2 insensitivity, paired stimuli were used in order to condition the chemical function of the respiratory system. Polysomnograms from 310 clinically healthy infants including healthy siblings of SIDS victims revealed instability of arterial pO2 and low CO2 sensitivity during sleep within the second month and the fourth to ninth month of life, respectively. These data challenge the described method as a potential preventive or therapeutic measure to defeat SIDS and sleep apnea syndromes in conjunction with disturbed chemical regulation of respiration.
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PMID:Transcutaneous monitoring as trigger for therapy of hypoxemia during sleep. 367 92

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A sleep-induced apneic threshold and its consequences. 371 65

Morbid obesity is often associated with severe respiratory insufficiency, commonly known as the pickwickian syndrome. This can be divided into the following two primary breathing disorders which can affect patients alone or in combination: the obstructive sleep apnea syndrome (SAS); and the obesity-hypoventilation syndrome (OHS). Thirty-eight (14 percent) of 263 morbidly obese patients with respiratory insufficiency of obesity underwent gastric surgery for weight reduction. Ten had OHS, nine has SAS, and 19 had both. Of these patients, one died of postoperative complications, one died at five weeks with an inconclusive autopsy, one was lost to follow-up, and the time since surgery was too short (less than three months) in three. A total of 30 patients lost 45 +/- 25 percent (p less than 0.0001) of excess body weight within 3 to 12 months following surgery, when repeat pulmonary studies were done. Most patients continued to lose additional weight until two years, when they had lost 62 +/- 26 percent of excess weight. Nine patients failed initial surgery (gastroplasty); seven of these were successfully converted to gastric bypass. Weight loss was associated with a significant decrease in the percentage of sleep apnea from 44 +/- 15 to 8 +/- 11 (p less than 0.0001). In patients with OHS, the arterial oxygen pressure (PaO2) increased from 53 +/- 9 to 68 +/- 11 mm Hg (p less than 0.0001), and the arterial carbon dioxide tension decreased from 51 +/- 7 to 41 +/- 4 mm Hg (p less than 0.0001). Pulmonary function tests in the patients with OHS revealed significant increases, as a percentage of predicted normal, in the forced vital capacity, forced expiratory volume in one second, expiratory reserve volume, functional residual capacity, and total lung capacity. Secondary polycythemia, defined as a hemoglobin level greater than 16 g/dl associated with a PaO2 less than 60 mm Hg, was noted in 13 of 29 patients with OHS. This fell from 16.9 +/- 1.1 to 14.9 +/- 1.7 g/dl (p less than 0.001) after weight loss and improved pulmonary function.
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PMID:Gastric surgery for respiratory insufficiency of obesity. 372 Mar 90

We examined the clinical and respiratory physiologic characteristics of 18 patients in whom a diagnosis of central sleep apnea syndrome was established by overnight polysomnographic studies. The patients could be readily divided into 2 groups on the basis of physiologic and clinical criteria. Five patients had an awake arterial PCO2 (PaCO2) of 53 +/- 4 (SEM) mmHg in the absence of intrinsic bronchopulmonary disease, a ventilatory response to CO2 of 0.6 +/- 0.2 L/min/mmHg, and a hemoglobin concentration of 180 +/- 6 g/L. Their clinical course was dominated by recurrent episodes of respiratory failure. In contrast, the other 13 patients had an awake PaCO2 of 35 +/- 1 mmHg (p less than 0.001), a CO2 response of 2.9 +/- 0.4 L/min/mmHg (p less than 0.005), and a hemoglobin concentration of 150 +/- 5 g/L (p less than 0.005). Clinically, they presented with features typical of sleep apnea; none had a history of respiratory failure. Despite the clinical and physiologic differences between the 2 groups, there were no differences between them in the frequency or duration of nocturnal apneic events or in sleep architecture. The findings indicate that the central sleep apnea syndrome is not a homogeneous disease entity. Rather, it includes 2 groups of patients that are clinically and physiologically distinct, with 1 group chronically hypoventilating and the other group either chronically hyperventilating or ventilating normally.
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PMID:Clinical and physiologic heterogeneity of the central sleep apnea syndrome. 374 Jun 46

There is increasing evidence that men have higher ventilatory responses to chemical stimuli than age-matched women and that certain disorders of respiratory rhythmicity, particularly sleep apnea, occur more commonly in men. Accordingly, we studied the influence of the male hormone, testosterone, on the control of breathing. Twelve hypogonadal males were studied at least 30 (mean +/- SE: 69.7 +/- 8.9) days after discontinuing testosterone replacement and again following hormone administration. In each subject plasma testosterone concentration, metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)], minute ventilation (VE), and chemosensitivity [hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses] were determined on and off hormone replacement. With testosterone administration VO2 increased from 248 +/- 15 to 276 +/- 18 ml/min (P less than 0.05), with VCO2 showing a similar but nonsignificant trend. This was associated with an increase in VE from 8.41 +/- 0.78 to 9.91 +/- 0.75 l/min (P less than 0.05) but no change in PCO2. The HVR, expressed as A, increased 44% with hormone replacement from a value of 122 +/- 23 to 176 +/- 28 (P less than 0.01), whereas the HCVR was minimally affected by testosterone administration. These findings may in part explain the previously described differences between male and female subjects in hypoxic sensitivity.
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PMID:Influence of testosterone on ventilation and chemosensitivity in male subjects. 406 75

Polygraphic monitoring studies were performed on more than 150 older preterm infants (postconceptional ages of 36 weeks or more) and full-term neonates to evaluate unexplained or persistent apnea. During polygraphic monitoring, 16 infants were observed to have hypoxemia associated with feedings. The feeding hypoxemia was accompanied by irregular respiratory effort and preceded any associated bradycardia. A comparison group of eight infants with similar gestational and postconceptional ages, but without feeding hypoxemia, was selected retrospectively from other infants referred for evaluation of persistent or unexplained apnea. The group with feeding hypoxemia showed evidence of CNS compromise as manifested by significant elevations of the maximum end-tidal carbon dioxide pressure during sleep and abnormal computed tomograms (7/11 v 0/5 in the comparison group). There was no relationship between feeding hypoxemia and sleep apnea or gastroesophageal reflux. Clinical follow-up showed that the feeding hypoxemia resolved with maturation.
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PMID:Hypoxemia associated with feeding in the preterm infant and full-term neonate. 642 17

The responses of common carotid blood flow (CCF), pressure (BP), and resistance (R) to variations in respiratory gases were compared during waking periods in 10 sleep apnea patients (SA) and 10 healthy controls (N) of similar age. Respiratory gases were altered by 3-min CO2 rebreathing (RB), 3-min hyperventilation (HV), and 4-min hypoxia (HYP) procedures. CCF was measured continuously by a 5-MHz pulsed Doppler duplex scanner and R was calculated using brachial BP. During RB, which increased end-tidal PCO2 (PACO2) by 15 mm Hg, SA had a lower CCF and greater BP response and therefore a significantly different (positive) change in R compared with N. The ventilatory responses to CO2 were not significantly different. With HV the PACO2 fell by 13 mm Hg in both groups and CCF fell more markedly in SA than N with the same change in BP; therefore, R was increased significantly more in SA. The HYP results did not demonstrate a difference between groups. These results suggest that abnormal cerebrovascular responses to PACO2, initiated either by unusual vasoactive properties of cerebral resistance vessels or peculiar venous outlow patterns, may initiate or potentiate periodic breathing in SA by prolonging lung-to-brain circulation time.
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PMID:Abnormal cerebrovascular responses to CO2 in sleep apnea patients. 642 11

A new device for non-invasive monitoring of PCO2, the Hewlett Packard cutaneous capnometer, was studied. Seven patients with disordered breathing, three with sleep apnoea syndrome, and four with chronic respiratory insufficiency, underwent polygraphic sleep recording including non-invasive measurement of oxygen saturation and transcutaneous CO2 pressure (PtcCO2). Two of the apnoea patients showed a modest increase in PtcCO2 with sleep. The patients with respiratory insufficiency showed larger increase in PtcCO2 and more profound hypoxemia during sleep. When the patients with respiratory insufficiency received oxygen (0.3-0.5 l/min) via nasal prongs, the sleep induced hypoxemia almost vanished but their PtcoCO2 increased. Nocturnal hypoventilation probably increased the effectiveness of the low oxygen supply, thus counteracting hypoxemia during periods of hypoventilation. The capnometer was easy to apply and the patients felt no discomfort. It promises to be a useful method for detection of hypercapnia indicating hypoventilation in patients with disordered breathing.
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PMID:Transcutaneous CO2 monitoring and disordered breathing during sleep. 643 47


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