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At least 19 recordsLinked to original sources
PubMed1978

The obesity-hypoventilation syndrome.

The triad of obesity, hypoventilation and inordinate hypersomnolence characterizes the obesity-hypoventilation syndrome. The reasons for daytime hypoventilation appear related to decreased chemical drives to breathe combined with the added physical impediment of extreme obesity. When the physiology of sleep was investigated in patients with this syndrome, intermittent nocturnal obstructive apneas were documented that produced blood gas abnormalities, arrhythmias and serious elevations of both pulmonary and systemic pressures. The obstructive apneas are due to intermittent loss of muscle tone of the tongue resulting in its prolapse against the posterior pharynx. The special importance of the obesity-hypoventilation syndrome lies in its being an example of a disorder of sleep and breathing that can appear in widely different clinical settings. Therapeutic measures include weight loss, progestational agents or permanent tracheostomy.

Apnea↗
PubMed1975

Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome.

Most patients with extreme obesity do not exhibit alveolar hypoventilation, but an intriguing minority do. The mechanism(s) of this phenomenon remain unknown. A disorder in ventilatory control has been suggested as a major factor in the pathogenesis of the obesity-hypoventilation syndrome. Accordingly, hypoxic and hypercapnic ventilatory drives were measured in 10 patients with the typical symptoms of the syndrome: obesity, hypersomnolence, hypercapnia, hypoxemia, polycythemia and cor pulmonale. Hypoxic ventilatory drive, measured as the shape parameter A, averaged 21.9 +/- 5.35, approximately one-sixth that in normal controls, A = 126 +/- 8.6 (P less than 0.01). The ventilatory response to hypercapnia also was markedly reduced, the slope of the response averaging 0.51 +/- 0.005, or about one-third the normal value of 1.83 +/- 0.13 (P less than 0.01). This decreased responsiveness in hypoxic and hypercapnic ventilatory drive was consistent throughout the group. The depression in ventilatory drive found in the obesity-hypoventilation syndrome may be causally related to the alveolar hypoventilation manifested by these patients.

Adult↗
PubMed1975

Pulmonary shunting during alveolar hypoventilation in the dog.

Pulmonary shunting (Qs/Qt) was measured in 16 anesthetized and paralyzed healthy beagle puppies during a control period when the end-expired CO2 concentration was 5 per cent and during alveolar hypoventilation, when the PaCO2 increased to 100 plus or minus 13 torr (mean plus or minus SE) and the ;Ha vecame 7.04 plus or minus 0.04. A constant tidal volume was maintained throughout each study, and hypoventilation was achieved by slowing only the respiratory rate. During the control period Qs/Qt was 2.9 plus or minus 0.3 per cent; during hypoventilation Qs/Qt was 3.2 plus or minus 0.3 per cent (an insignificant difference). The puppies, therefore, responded to anesthesia and alveolar hypoventilation without development of increased pulmonary shunts.

Anesthesia, Intravenous↗
PubMed1975

Alveolar hypoventilation and hyperosmnia in myotonic dystrophy.

A case of myotonic dystrophy accompanied by alveolar hypoventilation and hypersomnia is presented. Radiological studies and EMG examination of the intercostal muscles demonstrated that the respiratory muscles were affected by the disease, while polygraphic recordings showed that the alveolar hypoventilation and pulmonary hypertension worsened during sleep. The hypersomnia preceded the appearance of clinical signs of the muscular disease by many years and persisted even after treatment when the blood gas analysis values were greatly improved. During both diurnal and nocturnal sleep, the patient frequently fell asleep directly into a REM stage. The possibility is discussed that, concomitant with the respiratory musculature involvement, there is an alteration in the central nervous system in myotonic dystrophy which is at least partially responsible for both the alveolar hypoventilation and the hypersomnia.

Aminobutyrates↗
PubMed1975

Central alveolar hypoventilation in a child: an evaluation using a whole body plethysmograph.

A disorder in the central nervous system control of breathing is thought to be responsible for the clinical syndrome of "primary" or central alveolar hypoventilation. Only 2 of the 7 reported cases in children have included any functional evaluation of this control system disorder. We report the case of a 2-year-old girl with central alveolar hypoventilation attributed to an abnormality in be central nervous system of unknown etiology. In evaluating her ventilatory control system, we used a method (whole body pleildren and small animals but has since received little clinical use. The findings included an irregular respiratory rhythm and a diminished ventilatory response to inhaled CO2, which suggested a functional abnormality of brainstem neurons responsible for rhythmic effective breathing and the CO2 response. A relatively normal change in breathing with sleep and exercise as well as qualitively normal peripheral chemoreceptor function suggested that these aspects of the control system were undisturbed. These findings are contrasted to those in other children; it is suggested that the syndrome of central alveolar hypoventilation may reflect a variety of functional abnormalities in the nervous system control of ventilation.

Brain Diseases↗
PubMed1978

Central hypoventilation syndrome: experience with bilateral phrenic nerve pacing in 3 neonates.

Successful long-term phrenic nerve pacing has been reported in adults with acquired central hypoventilation syndrome. This report summarizes our experience with phrenic nerve pacing in 3 infants with congenital central hypoventilation syndrome. The electrodes were implanted in the lower thoracic portion of each phrenic nerve. In all patients. bilateral simultaneous pacing was required to maintain an adequate arterial PO2, tidal volume, and minute ventilation during quiet sleep. Case 1 died of problems primarily related to the severe cor pulmonale that had been present before pacemaker insertion; at autopsy, the pacemaker system was intact and there were no significant phrenic nerve abnormalities. Case 2 later developed failure of awake ventilatory control and died because of extensive phrenic nerve damage incurred by 19 days of continuous pacing. Case 3 has received quiet sleep pacemaker support since September 1977 and has been able to maintain normal quiet sleep ventilation in this manner. Phrenic nerve pacing can be successful in infants as long as continuous pacing is not required. Bilateral simultaneous pacing appears to be an appropriate alternative to home-based intermittent positive-pressure breathing for long-term management of children with central hypoventilation syndrome.

Electric Stimulation↗
PubMed1976

Diaphragm function and alveolar hypoventilation.

A syndrome of alveolar hypoventilation has been identified in a group of patients with bilateral diaphragm paralysis. Eight patients were studied in whom diaphragm weakness had been suggested by paradoxical (inward) movement of the abdominal wall on inspiration, of whom seven had evidence of a generalized neuromuscular disorder. Diaphragm function was assessed quantitatively by measurement of the change in transdiaphragmatic pressure during a maximum inspiration (deltaPDi). In five patients, deltaPDi was zero and in the others ranged from 2-6 cm H2O (normal greater than 25 cm H2O) indicating paralysis and severe weakness in the respective groups. Fluoroscopy of the diaphragm was found to give misleading results, and the resons for this are considered. Vital capacity ranged from 65-30 per cent of the predicted normal in the upright posture, typically falling by about a half in the supine posture. Alveolar hypoventilation was present in five patients when supine and in six when asleep, the deterioration in blood gases associated with sleep generally being much greater in these patients than in normal subjects. Respiratory rate was significantly greater than age-matched controls. The ventilatory response to CO2 was impaired. The PCO2 could be brought to normal levels by voluntary hyperventilation, and the unreliability of voluntary respiratory manoeuvres of this kind as indices of ventilatory reserve is emphasized. Alveolar hypoventilation was associated with disturbed sleep, morning headache and day-time fatigue. Symptomatic benefit was achieved by the use of a cuirass respirator at night.

Adult↗
PubMed1975

A case of primary alveolar hypoventilation associated with mild proximal myopathy.

A 34-year-old man presented with clinical features of primary alveolar hypoventilation, but was found additionally to have an adult onset myopathy caused by acid maltase deficiency. This was not severe, as judged clinically, and was initially overlooked. His vital capacity and sprint maximal ventilatory volume were only slightly reduced, and the ventilatory response to CO2 was virtually absent. There was, however, a mild impairment in the ability to decrease Pco2 to normal by voluntary hyperventilation. The relation of myopathy and alveolar hypoventilation is discussed, and it is proposed that the primary muscle disease predisposed the patient to the development of the ventilatory abnormality.

Adult↗
PubMed1978

Primary alveolar hypoventilation treated with nocturnal electrophrenic respiration.

A case of primary alveolar hypoventilation is described. Despite characteristic clinical findings, the diagnosis was delayed for 4 years. Alleviation of nocturnal hypoxemia and hypercapnia initially by a rocking bed and subsequently by phrenic nerve stimulation was accompanied by reversal of cor pulmonale and polycythemia. Electrophrenic respiration is an effective form of long-term management in primary alveolar hypoventilation.

Carbon Dioxide↗
PubMed1978

Primary alveolar hypoventilation treated by nocturnal administration of O2.

A case of idiopathic alveolar hypoventilation is described. Although lung function was normal, the alveolar-arterial O2 tension difference was abnormally large for reasons which were unclear. Despite this, the patient's pulmonary hypertension and polycythemia were out of proportion to the relatively mild hypoxemia that he demonstrated while awake. Sleep was associated with severe hypoxemia, and administration of O2 during sleep produced CO2 retention. The patient did well on no treatment for 5 years, until respiratory infection precipitated severe hypoxemia and pulmonary hypertension. He was treated with O2, at first continuously then nocturnally (12 hours per day), with reversal of polycythemia and pulmonary hypertension. He was then treated with nocturnal O2 as an outpatient for 7 months and maintained his improvement. Nocturnal administration of O2 may be an effective treatment of some forms of primary hypoventilation.

Adult↗
PubMed1979

Respiratory and nonrespiratory effects of doxapram in congenital central hypoventilation syndrome.

Doxapram is a respiratory stimulating drug that affects both peripheral chemoreceptors and medullary respiratory and nonrespiratory neurons. We administered doxapram 60 2 infants with congenital central hypoventilation syndrome. In 6 separate trials at a dose range of 0.32 to 2.0 mg per kg of body weight per min, quiet-sleep tidal volume increased from 4.9 +/- 1.0 to 8.5 +/- 0.9 ml per kg of body weight, minute ventilation increased from 140 +/- 38 to 286 +/- 31 ml per kg of body weight per min, and alveolar PCO2 decreased from 60 +/- 5 to 32 +/- 2 mm Hg. In all instances, the maximal quiet-sleep ventilatory response was achieved within 10 min. The ventilatory response to steady-state CO2 breathing was not improved with doxapram. A continuous infusion of doxapram for 5.2 days in one infant successfully maintained normal quiet-sleep ventilation. In both infants, multiple nonrespiratory effects of doxapram occurred; enteral administration was associated only with generalized neuromuscular stimulation, but the 5-day intravenous infusion was also associated with acute hepatotoxicity and a perforated duodenal ulcer. The medullary respiratory neurons in central hypoventilation syndrome may be incapable of responding to doxapram, and the ventilatory responses observed may be due entirely to stimulation of peripheral chemoreceptors. Although quiet-sleep ventilation can be successfully maintained with intravenous and enteral administration of doxapram, and tachyphylaxis has not been observed, we have been unable to avoid at least the neuromuscular manifestations of nonrespiratory medullary stimulation.

Chemical and Drug Induced Liver Injury↗
PubMed1978

Congenital central hypoventilation syndrome: a pathologic study of the neuromuscular system.

An infant with congenital central hypoventilation was managed by bilateral phrenic nerve pacing for 3 months. He died at 8 months of age, following 19 days of continuous bilateral pacing necessitated by the eventual loss of voluntary as well as autonomic ventilatory control. The phrenic nerves showed axonal dystrophy at the site of electrode implantation and more severe distal degeneration. Focal neurogenic atrophy was seen in the diaphragmatic muscle. These changes were attributed to electrical injury resulting from the period of continuous pacing. The most significant neuropathologic finding was a mild generalized decrease in the density of neurons and myelinated nerve fibers in the respiratory centers of the medulla. These morphologic abnormalities were attributed to a sublethal intrauterine lesion that would be the first example of a morphologic correlation with the functional abnormality in congenital central hypoventilation.

Brain↗
PubMed1975

Hypoventilation secondary to chronic upper airway obstruction in childhood.

A 6-year-old child manifested symptoms and signs of alveolar hypoventilation and signs of cor pulmonale caused by obstruction of the upper airway. These symptoms and signs disappeared after tonsillectomy and adenoidectomy. The relationship of upper airway obstruction to hypoventilation and cor pulmonale is discussed in the hope of renewing interest in this problem and alerting physicians to think of this possiblity early in the evaluation of such patients.

Adenoidectomy↗
PubMed1976

Complications of obesity-hypoventilation syndrome in childhood.

The obesity-hypoventilation syndrome is rare in children, but it leads to serious complications and is associated with a high mortality. We report a child with this syndrome whose condition improved after intestinal bypass surgery. Review of the literature indicates that vigorous treatment of this disorder is necessary to prevent fatalities.

Adolescent↗
PubMed1978

Hypoventilation in obstructive lung disease. The role of familial factors.

To determine the role of familial factors in the hypoventilation of chronic obstructive lung disease we measured chemical drives to breathe in normal offspring of two groups of patients with an equal degree of obstruction. One group of five patients had repeatedly normal arterial carbon dioxide tension (PaCO2), whereas PaCO2's were elevated in the other group of six. Two adult offspring of each patient were studied. Drives were measured as the ventilatory response to isocapnic hypoxia, and the slopes of the ventilation/PCO2 relation (the hypercapnic ventilatory response). The mean response to isocapnic hypoxia was lower (P less than 0.01) in offspring of patients with high PaCO2's than in the offspring of patients with normal levels (71 +/- 7.8 [S.E.M.] vs. 113 +/- 10.3); one offspring of each patient with high PaCO2 had a response below the range found in offspring of all patients with normal PaCO2. Lower hypercapnic ventilatory responses (P less than 0.05) were also found in the offspring of patients with high PaCO2. Familial factors in the control of breathing may be an important determinant of ventilation in chronic obstructive lung disease.

Adult↗
PubMed1976

Tonsillar hypertrophy in an adult with obesity-hypoventilation syndrome. The use of the flow-volume loop.

A 29-year-old obese man had marked tonsillar hypertrophy, somnolence, hypoxemia, and hypercapnia. Endotracheal intubation followed by tracheostomy relieved the hypoventilation. Weight loss improved the arterial blood gas levels. Sequential upright and supine flow-volume loops were compatible with a fixed upper-airway obstruction (such as would occur) with enlarged tonsils) prior to tonsillectomy. Following surgery, the expiratory flow-volume curve was abnormal in the supine position, consistent with the additional diagnosis of posterior pharyngeal hypotonia. Thus, in this patient the unique combination of tonsillar hypertrophy, posterior pharyngeal hypotonia, obesity, and a depressed respiratory center led to retention of carbon dioxide.

Adult↗