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)

A total of 52 patients with myocardial infarction have been examined. The patients have been subjected to HBO procedures. 40-62 min sessions with a working pressure of 0.3-1.1 atm were performed. The optimal pressure during the first days is 0.3 atm with a gradual increase to 0.7 atm. It is important to prepare the patient before the session with the end in view to achieve hemodynamic normalization and pain relief and to ensure a possibility of coronarolytic intake during the session. By session 4-5 hypercapnia and hypoxia, hyperventilation syndrome were eliminated, hemodynamic and respiratory parameters normalized, and immunity recovered. Only in one case a session had to be interrupted because of pulmonary edema recurrence. In 7 patients usual complications which were easily relieved have been observed. HBO shortened the patients' stay in an intensive care unit by 1.6 days and decreased lethality by 9.5%.
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PMID:[Hyperbaric oxygenation in myocardial infarct]. 808 Jan 31

We assessed 12 patients with hyperventilation syndrome (HVS) who had experienced hypoxaemia (PaO2 < 60 Torr or SaO2 < 90%) despite the lack of any other organic disease and variability in their blood gas data. Hypoxic and hypercapnic ventilatory responses were measured in nine. Eight of the 12 patients had been referred from other hospitals to our institution for hypoxaemia of unknown origin. Mean PaO2 (n = 12) at rest (non-attack stage) was 87.3 +/- 7.5 Torr (mean +/- SD). Their (n = 9) hypoxic (-0.53 +/- 0.32 l/min/%; range 0.12-0.99) and hypercapnic (2.01 +/- 0.76 l/min/Torr; range 0.69-3.17) ventilatory responses were both within the normal range in our laboratory. The patients with HVS had variable blood gas data, and some of them also exhibited hypercapnia (PaCO2 > 45 Torr). Clinicians who treat patients with HVS should be aware of the possibility of hypoxaemia, even when ventilatory responses are normal. Physicians should also consider HVS as a diagnosis when treating patients with hypoxaemia of unknown origin.
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PMID:Hypoxaemia in patients with hyperventilation syndrome. 930 32

Central congenital hypoventilation syndrome (CCHS) is a disorder in which affected individuals fail to breathe during sleep despite progressive hypercapnia and hypoxia. Discovery of the genetic link between PHOX2B gene mutations and CCHS represents a breakthrough in the diagnosis of CCHS, identification of patients with late-onset central hyperventilation syndrome (LO-CHS), association of mutated alleles with disease severity, and clues to the pathophysiology responsible for the disorder. CCHS is a neurocristopathy, and affected individuals are more likely to have disorders of the autonomic nervous system, Hirschsprung disease, and neural crest tumors. Most CCHS patients harbor sporadic mutations, but identification of an affected individual should trigger evaluation of family members because inherited mutations are transmitted in an autosomal dominant fashion. Management of CCHS and LO-CHS is primarily directed at optimizing respiratory status, most often with nighttime mechanical ventilatory support and monitoring with polysomnography. Multidisciplinary care is also necessary to promote better outcomes and long-term survival.
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PMID:Central congenital hypoventilation syndrome: changing face of a less mysterious but more complex genetic disorder. 1945 85