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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six young male patients with grade I (mild) myotonic dystrophy and a complaint of excessive daytime sleepiness were studied during wakefulness and sleep. Pulmonary function tests during wakefulness showed evidence of mild abnormality related to respiratory muscle weakness. During sleep, some patients developed a sleep apnea syndrome with high sleep Apnea Indices. There was no relation between hypoxic and hypercapnic ventilatory responses during wakefulness and sleep Apnea Indices. But hypoxemia and hypercapnia worsened considerably during REM sleep. Myotonic dystrophy patients with sleep apnea presented increased pulmonary and systemic arterial pressures during sleep. It was also during sleep that arrhythmias were observed.
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PMID:Respiratory and hemodynamic study during wakefulness and sleep in myotonic dystrophy. 22 21

A case of cor pulmonale is reported, due to chronic nasopharyngeal obstruction by hypertrophied tonsils and adenoids. This syndrome is characterized by stridor, somnolence, arterial hypoxia and hypercarbia, pulmonary and right heart failure. The pathogenesis of this syndrome is due to pulmonary hypoventilation. After tonsillectomy and adenoidectomy the symptoms disappeared.
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PMID:[Cor pulmonale due to upper airway obstruction by hypertrophied tonsils and adenoids (author's transl)]. 74 83

For over 15 years, upper respiratory tract obstruction due to adenotonsillar hypertrophy has been known to cause hypoxia, hypercapnia, increased pulmonary vascular resistance and thereby cor pulmonale and congestive heart failure. This is now an uncommon but not rare entity and three recent cases prompted this report. The typical patient is dyspneic with retractions, cyanosis, occasional periods of apnea and somnolence. Edema and hepatomegaly and at times splenomegaly are common. X-rays show cardiomegaly, which on electrocardiogram is found to involved mainly the right ventricle. The strict definition of cor pulmonale is right ventricular hypertrophy secondary to lung disease or abnormal pulmonary function, a definition that may logically be stretched to include abnormal respiratory function secondary to upper airway pathology. The mechanisms by which this occurs are generally agreed upon. Hypoxia has been demonstrated to cause pulmonary vasoconstriction. Acidosis and hypercapnia are thought by some to have the same effect. Pressure across the pulmonary vascular bed is also increased, as predicted by Poiseuille's law, by the high rate of blood flow required to maintain tissue oxygenation with poorly oxygenated blood. Conditions producing hypoxia of hypercapnia or both lead to hypertrophy and eventually to dilatation of the right ventricle. Three cases of children who underwent cardiac catheterization while suffering from cor pulmonale due to adenotonsillar hypertrophy are reported. Right ventricular pressure averaged 44/5, PAO2 72, pH 7.32, and PACO2 52. All were clinically improved following adenotonsillectomy. Cardiac catheterization was repeated in one case, with right ventricular pressure dropping from 44/5 to 21/2, pulmonary vascular resistance from eight units to three, and PACO2 from 62 to 44.
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PMID:Cardiac and pulmonary failure secondary to adenotonsillar hypertrophy. 95 48

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.
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PMID:Tonsillar hypertrophy in an adult with obesity-hypoventilation syndrome. The use of the flow-volume loop. 97 91

A 38-year-old patient with effort dyspnea, somnolence, cianosis and cor pulmonale is presented. Chest roentgenograms and lung function studies suggested the diagnosis of pulmonary fibrosis. The patient showed also severe hypercapnia with normal resting ventilation and ventilatory response to exercise lower than usual for this condition. Autopsy confirmed the clinical diagnosis. This subject may belong to the growing group of patients where CO2 retention is not explained by their pulmonary pathology.
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PMID:Idiopathic interstitial pulmonary fibrosis with hypercapnia. 117 39

A 36-year-old woman with myotonic dystrophy presented with generalized weakness and daytime somnolence. Arterial blood gas analysis revealed significant hypoxemia and hypercapnia, and a polysomnogram revealed additional oxygen desaturation during sleep. For nocturnal ventilatory assistance, the patient received positive-pressure ventilation via a nasal mask. This mode of ventilation produced marked improvement in the patient's nocturnal hypoxemia.
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PMID:The use of mechanical ventilation via a nasal mask in myotonic dystrophy. 155 16

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.
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PMID:[Central anticholinergic syndrome during postoperative period]. 219 41

The distribution of symptoms, physiologic responses, and upper airway structure in members of one family with three generations of subjects with sleep apnea (SA) is reported. Questionnaire data were obtained from ten family members (ages 7 to 66 years), overnight sleep studies were performed in nine subjects, and ventilatory responses to hyperoxic hypercapnia and to eucapnic hypoxia and cephalometry were obtained in five subjects. All ten family members reported habitual snoring or nighttime snorting/gasping; five of ten family members also reported excessive daytime sleepiness. All studied subjects except for a pregnant woman had greater than ten apneas/hypopneas per hour. Ventilatory responses to hypoxia were markedly reduced in all five subjects studied (less than or equal to 0.51 L/min/SaO2); hypercapnic responses were reduced in three of five subjects (less than or equal to 0.61 L/min/mm Hg CO2). No subject was morbidly obese (body mass index less than 29 kg/m2) or demonstrated retrognathia. The posterior airway space was reduced in three subjects, and the mandibular to hyoid distance was increased in four subjects. The two subjects with the longest soft palates and the most inferiorly displaced hyoids had the most severe sleep disorder. Sleep apnea was present, albeit less profound, in the one subject with normal anatomy who had an abnormal hypoxic ventilatory response. The distribution of these physiologic and anatomic measurements in this family provides further support for a genetic basis for SA, and suggests that the disorder may occur as a result of interactions between ventilatory control abnormalities and anatomic risk factors.
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PMID:A family study of sleep apnea. Anatomic and physiologic interactions. 239 35

Three patients with respiratory muscle weakness developed sleep fragmentation due to nonobstructive apnea and hypopnea. In two patients in whom inspiratory muscle electromyogram was recorded, the apneas and hypopneas were terminated only by arousal and excessive recruitment of accessory muscles. Nocturnal rocking bed ventilatory support resulted in immediate improvement in sleep fragmentation and inhibited arousal-associated phasic accessory muscle activation, resulting in improvement in daytime hypercapnia and subjective sleepiness. Sleep fragmentation may occur more commonly than generally appreciated in neuromuscular disease patients who are independent of daytime ventilatory support. The use of nocturnal rocking bed is an effective noninvasive method of reversing sleep fragmentation and daytime sequelae when obstructive apnea is absent.
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PMID:Nocturnal rocking bed therapy: improvement in sleep fragmentation in patients with respiratory muscle weakness. 279 14

In December 1986 a 30-month-old female child with morbid obesity and respiratory failure was admitted to the Izaak Walton Killam Hospital for Children in Halifax. The etiology of the obesity was found to be dietary in origin after ruling out genetic, neurological and metabolic causes. This patient exhibited somnolence and cyanosis in association with hypercapnia and right ventricular overload. Her respiratory failure in the presence of a normal upper airway required ventilatory support, first with nasal endotracheal intubation, and then, tracheotomy. Weight reduction normalized her capillary blood gases and her somnolence disappeared. Subglottic stenosis hampered removal of the tracheotomy tube until 9 months after admission. The pathogenesis and management of obese hypoventilation syndrome are reviewed by the authors.
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PMID:Obese hypoventilation syndrome of early childhood requiring ventilatory support. 306 Apr 36


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