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Showing papers on "Hypoventilation published in 1995"


Journal ArticleDOI
TL;DR: A model of epileptic sudden death in unanesthetized, chronically instrumented sheep supports a role of central hypoventilation in the etiology of sudden unexpected death and confirms the association with pulmonary edema.
Abstract: Unexpected sudden death is a common event in otherwise healthy epileptics, though its etiology has remained unclear. Many authors have suggested cardiac arrhythmias as the cause, and limited data in humans and animal studies have supported this. However, autopsy series in humans have shown pulmonary edema, a phenomenon not compatible with a sudden arrhythmic death, as a possible cause. We developed a model of status epilepticus in unanesthetized, chronically instrumented sheep in which sudden death and pulmonary edema occur. Catecholamine levels and seizure type and duration did not differ between animals dying suddenly and those surviving. Benign arrhythmias were generated in all animals; in no case did an arrhythmia account for the death of an animal. Striking hypoventilation was demonstrated in the sudden death group but not in the surviving animals. Differences in peak left atrial and pulmonary artery pressures, and in extravascular lung water were also demonstrated; pulmonary edema did not account for the demise of the sudden death animals. Thus, our model of epileptic sudden death supports a role of central hypoventilation in the etiology of sudden unexpected death and confirms the association with pulmonary edema. The importance of arrhythmia in its pathogenesis is not confirmed.

137 citations


Journal ArticleDOI
01 Jun 1995-Chest
TL;DR: The effectiveness of nocturnal NIPPV is dependent in part on central mediated muscular activity, and central nervous system mediated reflex muscular activity occurred to diminish leak and normalize SAT.

114 citations


Journal ArticleDOI
TL;DR: Central sleep apnoea (CSA) occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain and the unmasking of a CO2 threshold.
Abstract: The prevalence of reported sleep disturbances in a general population is high. Many of the complaints are the result of sleep-related breathing disorders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, characterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.

67 citations


Journal ArticleDOI
01 Oct 1995-Sleep
TL;DR: Therapy of chronic alveolar hypoventilation often focuses on elimination of the nocturnal deterioration in gas exchange, and recent applications of noninvasive positive pressure ventilation during sleep have proven useful in the management of individuals with obesity-hypoventilated syndrome, restrictive thoracic disorders, neuromuscular diseases and central causes for hypoventing.
Abstract: Chronic alveolar hypoventilation may present in an insidious fashion with nonspecific manifestations. The clinician should be aware of the potential for developing this condition in patients with certain thoracic and systemic diseases. Once chronic alveolar hypoventilation is confirmed with arterial blood gas analysis, a systematic evaluation can often point to the underlying etiology. As sleep in affected individuals is often associated with marked worsening of gas exchange and may also contribute to worsening daytime cardiopulmonary dysfunction, polysomnography is often indicated to determine the severity of nocturnal aberrations and to look for coexistent obstructive sleep apnea. Therapy of chronic alveolar hypoventilation often focuses on elimination of the nocturnal deterioration in gas exchange, and recent applications of noninvasive positive pressure ventilation during sleep have proven useful in the management of individuals with obesity-hypoventilation syndrome, restrictive thoracic disorders, neuromuscular diseases and central causes for hypoventilation. It is unclear whether wide-spread application of nocturnal ventilatory support to patients with chronic ventilatory failure due to chronic obstructive pulmonary disease is of long-term benefit.

65 citations


Journal ArticleDOI
TL;DR: The alveolar hypoventilation and the hypersomnia in the case may be attributed to these morphological abnormalities, and would appear to be central in nature.

44 citations


Journal ArticleDOI
TL;DR: Neuroblastoma, Hirschsprung's disease, and central hypoventilation (Ondine's curse) are considered aberrations of neural crest cell growth, migration, or differentiation, and as such are considered to be under the general heading of neurocristopathy.

41 citations


Journal ArticleDOI
TL;DR: A review of the factors that cause respiratory depression in anesthetized birds can be found in this article, where anesthetic-induced depression of the central nervous system, muscular relaxation of the muscles of respiration, and effects on central and peripheral chemoreceptors.
Abstract: A number of factors cause respiratory depression in anesthetized birds. Hypoventilation can be due to anesthetic-induced depression of the central nervous system, muscular relaxation of the muscles of respiration, and effects on central and peripheral chemoreceptors. Compared to mammals, respiratory function in birds may be more sensitive to the effects of inhalant anesthetics because of their effect on unique carbon dioxide (CO2)-sensitive intrapulmonary chemoreceptors located within the avian lung. High fractions of inspired oxygen also contribute to hypoventilation, possibly by depressing oxygen-sensitive chemoreceptors. This article is a review of the factors that cause respiratory depression in anesthetized birds.

22 citations


Journal ArticleDOI
TL;DR: Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
Abstract: Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.

21 citations


Journal ArticleDOI
TL;DR: A 39-year-old morbidly obese male presented with severe and poorly controlled diabetes mellitus (DM) and hypertension (HBP) as well as moderately severe obesity hypoventilation syndrome (OHS) that threatened the survival of his cardiac graft which had been transplanted 7 years previously.
Abstract: A 39-year-old morbidly obese male presented with severe and poorly controlled diabetes mellitus (DM) and hypertension (HBP) as well as moderately severe obesity hypoventilation syndrome (OHS) that threatened the survival of his cardiac graft which had been transplanted 7 years previously. A gastric bypass procedure with a 45-cm Roux-limb was performed. His OHS resolved, his DM became undetectable off medication, and his HBP medication was significantly reduced with good control. His maximum excess weight loss was 95%. Importantly, his Cyclosporine and Imuran anti-rejection therapy was maintained without any difficulty attributable to the gastric bypass procedure until his sudden death in late November 1994, 2.75 years following the gastric bypass procedure.

5 citations


Journal ArticleDOI
TL;DR: The implications for anesthesia include atrioventricular node and infranodal conduction abnormalities, hypoventilation secondary to ventdatory drive depression, potential myopathic or neuropathic changes, possible mahgnant hyperthermia susceptibility, and undue sensitwity to anesthetic induction agents.

4 citations



Journal Article
TL;DR: Therapeutic effects of nasal CPAP and BIPAP can replace surgical ENT-Therapy in large extent mainly in ages at 2-5 years, but also in older children is it possible to treat obstructive sleep apnea and hypoventilation neuromuscular diseases by BIP AP.
Abstract: Sleep-apnea in childhood shows a frequency similar to adults but it is caused by many other reasons. Therapeutic effects of nasal CPAP and BIPAP can replace surgical ENT-Therapy in large extent mainly in ages at 2-5 years. But also in older children is it possible to treat obstructive sleep apnea and hypoventilation neuromuscular diseases by BIPAP. Examples for treatment of children by BIPAP who are two years old were given. Other demonstrated cases cover children with stridor congenitus, obstructive sleep apnea, hypoventilation, adenoidal breathing disturbances with primary surgical treated tonsillar hyperplasia and one case of thoracal postobstructive malformation with therapeutic BIPAP options.

Journal Article
TL;DR: The nasal BiPAP-System using the T-mode is a useful device to support ventilation at night and thus it could replace ventilatory support by the IPPV-mode in many patients.
Abstract: The BiPAP-System is a useful ventilatory support for patients with severe sleep apnea and need for high inspiratory pressure. Using the BiPAP as a full ventilatory support is new due to the recent addition of a timed control modus and individual control of inspiratory time. We used the new BiPAP ST-System in one young men with Duchenne-disease, one man with heredo ataxia (Friedreich), one women with spinal muscular atrophy, one man with central sleep apnea due to brainstem infarction as well as two women and one men with severe kyphoscoliosis. All patients had a significant hypoventilation and hypoxemia at night, which was documented by polysomnography. Mechanical ventilation at night with nasal BiPAP increased the baseline oxygen saturation (SaO2) by an average of 11.9% in all seven patients. The frequency of desaturations below 90% diminished by an average of 81%. The lowest SaO2 measured increased by 28% in all seven patients combined. Rhinitis due to the dryness of the inspired air were noticed in only two patients. Two other patients needed adaptation to the customized mask. The nasal BiPAP-System using the T-mode is a useful device to support ventilation at night and thus it could replace ventilatory support by the IPPV-mode in many patients.


01 Jan 1995
TL;DR: Central sleep apnoea (CSA) occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain and the unmasking of a CO 2 threshold.
Abstract: The prevalence of reported sleep disturbances in a general popula- tion is high. Many of the complaints are the result of sleep-related breathing dis- orders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main under- lying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, char- acterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO 2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO 2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with aceta- zolamide, is easier to perform. Stimulation of upper airway reflexes, by less inva- sive methods, seems to be promising for the near future.