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)

The modifications of systemic hemodynamics, oxygen transport and tissular oxygenation in mechanically-ventilated critical ARF (acute respiratory failure) patients, after the correction of its hypocapnia by addition of dead space (VD) are determined. The prospective and randomized study was carried out in a multidisciplinary ICU. Fifteen ARF patients were studied within the first 48 hours of evolution. All the patients were intubated and mechanically ventilated. Three stages were delimited: I) 30 min after the beginning of anesthesia; II) 30 min after adding 30 cm of VD; III) 30 min after replacing the previous VD with a VD of 60 cm. Similar steady states had been reached when the measurements were taken. Ventilation parameters and FiO2 were kept stable. In stage I the patients presented a pure respiratory alkalosis and, with respect to hemodynamics, a hyperdynamic situation. In stage II the acid-base balance was normalized with a continuation of the hyperdynamic situation and an increase in mixed venous oxygen tension and saturation (PvO2 and SvO2) (p < 0.001). Stage III was characterized by a pure hypercapnic acidosis and an increase in capillary wedge pressure (CWP) (p < 0.05), right atrial pressure (RAP) (p < 0.001) and cardiac output (Qt) (p < 0.001); simultaneously, the systemic vascular resistances (SVR) decreased (p < 0.01), the PvO2, SvO2 and oxygen delivery (DO2) increased (p < 0.001); oxygen utilization coefficient (OUC) decreased (p < 0.01). The results suggest that the variations in PvO2 and SvO2 are a direct consequence of the modifications in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modifications of tissular oxygenation and systemic hemodynamics after the correction of hypocapnia induced by mechanical ventilation. 799 35

Ten healthy Labrador Retrievers (4 females and 6 males aged 3-6.5 years [mean, 4.5 years]) training with a professional trainer were studied. The dogs were in training during the entire study. Dogs were monitored within 5 minutes after retrieving birds on land and in water on 2 consecutive days during training and on 2 consecutive days at the Atlanta Retriever Club Fall Field Trial. Baseline samples were taken in the morning on a separate day before the dogs were loaded onto a truck. Venous samples were analyzed with a portable blood analyzer. Measurements included hematocrit, sodium, potassium, chloride, blood urea nitrogen (BUN), glucose, lactate, blood pH, Pco2, Po2, HCO3, and TCO2 plus rectal temperature, pulse rate, and respiratory rate. Ambient temperatures were recorded. Distances and times were estimated. Compared to baseline, significant increases occurred in rectal temperature, pulse rate, respiratory rate, chloride, lactate, and pH postexercise (P < .05): sodium, potassium, BUN, Pco2, and TCO2 were significantly decreased postexercise. Blood pH was markedly higher after retrieves on land than after retrieves in water. Estimated mean speeds were 11.4 mph (18.3 km/h) during a triple retrieve on land and 5.6 mph (9.0 km/h) during a retrieve in water. Maximal ambient temperatures were 84-86 degrees F (29-30 degrees C). In summary, Labrador Retrievers training with a professional trainer had evidence of hyperthermia, respiratory alkalosis, hypocapnia, and mild metabolic acidosis monitored within 5 minutes postexercise during training and field trial competition when maximal ambient temperatures were 85 degrees F (29 degrees C). The results provide a baseline against which physiologic responses of dogs with poor performance can be compared.
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PMID:Physiologic responses in healthy Labrador Retrievers during field trial training and competition. 1505 63

* Based on some research evidence, DKA is a significant contributor to morbidity and mortality in children who have type 1 diabetes, and cerebral edema is responsible for most of the deaths during DKA in children. (Dunger, 2004). * Based on strong research evidence, treatment of DKA requires replacement of water and electrolytes and correction of the insulin deficiency. (Dunger, 2004). * Based on some research data and consensus opinion, after providing initial volume expansion (if needed), fluid resuscitation of children who have DKA should be calculated to rehydrate evenly over at least 48 hours. Initial fluid resuscitation should be with an isotonic solution; subsequent fluid management should be with a solution that has a tonicity of at least 0.45% saline. (Dunger, 2004). * Based on strong research evidence, insulin treatment for DKA should begin at a dose of 0.1 units/kg per hour and generally should remain at or above this level until the ketoacidosis is resolved. (Dunger, 2004). * Based on some research evidence, risk factors for the development of cerebral edema during treatment of DKA include the severity of acidosis, greater hypocapnia (after adjusting for the degree of acidosis), higher blood urea nitrogen concentration at presentation, and treatment with bicarbonate. (Dunger, 2004; Glaser, 2002).
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PMID:Management of diabetic ketoacidosis in children and adolescents. 1904 33