Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since February 1990, five children, aged 10 days to 6.5 years, were treated with extracorporeal lung support at our hospital for acute, unrelenting pulmonary failure. Two had viral pneumonia: one with respiratory syncytial virus (RSV) bronchiolitis, and one with herpes simplex virus pneumonia, encephalitis, and disseminated intravascular coagulation. One presented with a febrile illness followed by a pulmonary hemorrhage. Two patients had adult respiratory distress syndrome (ARDS) complicating severe systemic illnesses, toxic epidermal necrolysis in one and cat scratch disease with encephalitis in the other. All children had diffuse parenchymal lung disease by chest x-ray. On maximum medical management all patients were developing carbon dioxide retention and progressive hypoxemia, exceeding previously established NIH study criteria for extracorporeal treatment. Three children (10 days, 2 months, 13 months) were placed on venoarterial support and two children (20 months and 6.5 years) were placed on venovenous extracorporeal support (ECCO2R). Three of the five had open lung biopsies performed, which showed findings consistent with a moderate to severe cellular phase of ARDS. No viral inclusions were found in the patient with RSV infection. One hundred percent immediate survival was achieved in this patient population. Average duration of support was 330 hours (range, 89 to 840). Following completion of extracorporeal support, all children were successfully weaned from the ventilator with an average time to extubation of 23.2 days (range, 2 to 58 days). One child died of congestive heart failure following palliative surgery for a complex noncyanotic congenital cardiac lesion 35 days after successfully weaning from extracorporeal support for an acute febrile illness and pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of acute pulmonary failure with extracorporeal support: 100% survival in a pediatric population. 132 87

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68