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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors use the Bain Circuit with spontaneous breathing during head surgery (neurosurgery and ophthalmological procedures). Suitable for both adult and pediatric use, it seems to be, due to its unique characteristics, the choice circuit for all anaesthesia procedures in which the physician does not have direct control over the patient's head. Comparative analysis of blood gas levels is effected, on the one hand in children connected to a Digby-Leigh system and Bain Circuit, and on the other hand in adults, some of whom are connected to a two-way system and the other under a filter circuit; all of the patients are then connected to the Bain Circuit. In children the analysis of results shows that for an identical protocol of anaesthesia the quality of spontaneous breathing obtained using the Bain Circuit is the same as that obtained using the Digby-Leigh. In adults anaesthetized using fluothane and with spontaneous breathing, the average level of hypercapnia under filter circuit and Bain Circuit is identical. Also, the same level of alveolar hypoventilation is obtained under spontaneous breathing with the two-way and Bain Circuit systems when there are properly provisioned. Thus this work confirms other studies by showing that the Bain Circuit is particularly well adapted to head surgery because of its low weight and easy manageability. On the other hand, when using spontaneous breathing the level of alveolar hypoventilation, and thus the degree of hypercapnia, is directly related to the level of anaesthesia and independent of the circuit chosen. Only the setting up of controlled breathing would allow the physician to work under the desired level of normo or hypocapnia.
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PMID:[Blood gas levels using spontaneous breathing and the Bain circuit. Our experience during head surgery (author's transl)]. 680 Feb 85

Experimental data show that elevation of intracellular pH leads to severe lesions of brain cells. Acidification of intracellular fluid by accumulation of lactate may compensate the effect of respiratory alkalosis. Increased serum pH, and low PCO2, associated with hyperlactataemia (sometimes incorrectly called 'acidosis') have been reported in children with Leigh syndrome (LS). The aim of the study was to determine whether respiratory alkalosis is characteristic of patients with LS due to SURF1 mutations. All venous blood gas data (88 samples) of 18 spontaneously breathing LS patients with recently established SURF1 mutations, hospitalized during 1986-2000, were retrospectively reviewed. The data of an affected boy who survived on a respirator for more than 3 months (79 daily samples) were analysed separately. In spontaneously breathing patients, the data indicated that the patients had compensated or partially compensated respiratory alkalosis (pH 7.388+/-0.060, Pco2 29.2+/-5.7 mmHg, HCO3- 17.4+/-3.0 mmol/L, BE -6.7+/-3.2 mmol/L). Bicarbonate excretion was detected in urine of two examined LS cases in spite of decreased serum HCO3-. In the affected child maintained on a respirator, simple manipulation of the inspired CO2 tension to establish a normal pressure of 35-45 mmHg automatically caused an increase of serum HCO3- concentration to a normal value of 26.3+/-2.9 mmol/L (and BE to +2.2+/-3.1 mmol/L), in spite of cytochrome oxidase (COX) deficiency due to a confirmed SURF1 mutation. We suggest that respiratory alkalosis (hypocapnia) of Leigh syndrome patients with SURF1 mutations results from compulsory hyperventilation and speculate that hypocapnia may contribute to Leigh-like brain damage in the SURF1-deficient patients as well as in other patients presenting with Leigh-like syndrome. The supposition that accumulation of lactate may protect the brain of LS patients from alkalosis-related damage requires further study. Avoidance of any factors stimulating hyperventilation of LS patients and caution when attempting to correct low plasma bicarbonate are suggested.
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PMID:Compulsory hyperventilation and hypocapnia of patients with Leigh syndrome associated with SURF1 gene mutations as a cause of low serum bicarbonates. 1180 7

Leigh syndrome (LS) is a neurogenetic disorder of children caused by mutations in at least 75 genes which impair mitochondrial bioenergetics. The changes have typical localization in basal ganglia and brainstem, and typical histological picture of spongiform appearance, vascular proliferation and gliosis. ATP deprivation, free radicals and lactate accumulation are suspected to be the causes. Hypocapnic hypothesis proposed in the paper questions the energy deprivation as the mechanism of LS. We assume that the primary harmful factor is hypocapnia (decrease in pCO2) and respiratory alkalosis (increase in pH) due to hyperventilation, permanent or in response to stress. Inside mitochondria, the pH signal of high pH/low bicarbonate ion (HCO-3) is transmitted by soluble adenyl cyclase (sAC) through cAMP dependent manner. The process can initiate brain lesions (necrosis, apoptosis, hypervascularity) in OXPHOS deficient cells residing at the LS area of the brain. The major message of the article is that it is not the ATP depletion but intracellular alkalization (and/or hyperoxia?) which seem to be the cause of LS. The paper includes suggestions concerning the methodology for further research on the LS mechanism and for therapeutic strategy.
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PMID:Hypocapnic hypothesis of Leigh disease. 2835 84