Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is reported of a 40-year-old woman presenting with cerebral malaria complicated by an adult respiratory distress syndrome (ARDS). The patient was admitted to the intensive care unit in a coma, scored 5 on the Glasgow scale. Plasmodium falciparum parasitaemia was, at the time, 50%. A continuous intravenous quinine infusion (25 mg.kg-1.day-1) was started, together with the required symptomatic treatment. Blood was transfused because of increasing anaemia (haemoglobin 60 g.l-1). After 24 h, parasitaemia was 12%, consumption of clotting factors broke out (prothrombine 43%, fibrin degradation products greater than 40 micrograms.ml-1, platelets 45 G.l-1). Hypoxaemia (PaO2 = 46 mmHg) and hypocapnia (PaCO2 = 32 mmHg) became obvious, together with bilateral diffuse alveolar infiltrates on chest X-ray. Haemodynamic data suggested non cardiogenic oedema: PEEP 20 cm H2O, cardiac output 6.15 l.min-1, mean pulmonary arterial pressure 35 mmHg, pulmonary wedged pressure 15 mmHg. The hypoxia worsened and the patient died on the 15th day after associated with high levels of parasitaemia. Several reports have suggested that it may be related to increased capillary permeability. Initial fluid overload should therefore be avoided. Parenteral quinine remains the mainstay of treatment, because of its rapid schizonticidal activity. Although exchange transfusion seems to be a valuable adjunct to chemotherapy, it requires further assessment.
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PMID:[Fatal pulmonary edema in a pernicious malaria attack]. 227 23

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

Previous investigations have demonstrated a subset of postural tachycardia syndrome (POTS) patients characterized by normal peripheral resistance and blood volume while supine but thoracic hypovolemia and splanchnic blood pooling while upright secondary to splanchnic hyperemia. Such "normal-flow" POTS patients often demonstrate hypocapnia during orthostatic stress. We studied 20 POTS patients (14-23 yr of age) and compared them with 10 comparably aged healthy volunteers. We measured changes in heart rate, blood pressure, heart rate and blood pressure variability, arm and leg strain-gauge occlusion plethysmography, respiratory impedance plethysmography calibrated against pneumotachography, end-tidal partial pressure of carbon dioxide (Pet(CO2)), and impedance plethysmographic indexes of blood volume and blood flow within the thoracic, splanchnic, pelvic (upper leg), and lower leg regional circulations while supine and during upright tilt to 70 degrees. Ten POTS patients demonstrated significant hyperventilation and hypocapnia (POTS(HC)) while 10 were normocapnic with minimal increase in postural ventilation, comparable to control. While relative splanchnic hypervolemia and hyperemia occurred in both POTS groups compared with controls, marked enhancement in peripheral vasoconstriction occurred only in POTS(HC) and was related to thoracic blood flow. Variability indexes suggested enhanced sympathetic activation in POTS(HC) compared with other subjects. The data suggest enhanced cardiac and peripheral sympathetic excitation in POTS(HC).
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PMID:Postural hypocapnic hyperventilation is associated with enhanced peripheral vasoconstriction in postural tachycardia syndrome with normal supine blood flow. 1656