Adaptação metabólica diante de hipercapnia persistente aguda em pacientes submetidos à ventilação mecânica por síndrome do desconforto respiratório agudo / Metabolic acid-base adaptation triggered by acute persistent hypercapnia in mechanically ventilated patients with acute respiratory distress syndrome

RESUMO Objetivo: A hipercapnia resultante da ventilação protetora na síndrome do desconforto respiratório agudo desencadeia uma compensação metabólica do pH que ainda não foi completamente caracterizada. Nosso objetivo foi descrever esta compensação metabólica. Métodos: Os dados foram recuperados a partir de uma base de dados registrada de forma prospectiva. Foram obtidas as variáveis dos pacientes no momento da admissão e quando da instalação da hipercapnia até o terceiro dia após sua instalação. Analisamos 41 pacientes com síndrome do desconforto respiratório agudo, incluindo 26 com hipercapnia persistente (pressão parcial de gás carbônico acima de 50mmHg por mais de 24 horas) e 15 sem hipercapnia (Grupo Controle). Para a realização da análise, utilizamos uma abordagem físico-química quantitativa do metabolismo acidobásico. Resultados: As médias de idade dos Grupos com Hipercapnia e Controle foram, respectivamente, de 48 ± 18 anos e 44 ± 14 anos. Após a indução da hipercapnia, o pH diminuiu acentuadamente e melhorou gradualmente nas 72 horas seguintes, de forma coerente com os aumentos observados no excesso de base padrão. A adaptação metabólica acidobásica ocorreu em razão de diminuições do lactato sérico e do strong ion gap e de aumentos na diferença aparente de strong ions inorgânicos. Além do mais, a elevação da diferença aparente de strong ions inorgânicos ocorreu por conta de ligeiros aumentos séricos de sódio, magnésio, potássio e cálcio. O cloreto sérico não diminuiu por até 72 horas após o início da hipercapnia. Conclusão: A adaptação metabólica acidobásica, que é desencadeada pela hipercapnia aguda persistente em pacientes com síndrome do desconforto respiratório agudo, foi complexa. Mais ainda, aumentos mais rápidos no excesso de base padrão em pacientes com hipercapnia envolveram diminuições séricas de lactato e íons não medidos, e aumentos na diferença aparente de strong ions inorgânicos, por meio de ligeiros aumentos séricos de sódio, magnésio, cálcio e potássio. Não ocorreu redução do cloreto sérico.

ABSTRACT Objective: Hypercapnia resulting from protective ventilation in acute respiratory distress syndrome triggers metabolic pH compensation, which is not entirely characterized. We aimed to describe this metabolic compensation. Methods: The data were retrieved from a prospective collected database. Variables from patients' admission and from hypercapnia installation until the third day after installation were gathered. Forty-one patients with acute respiratory distress syndrome were analyzed, including twenty-six with persistent hypercapnia (PaCO2 > 50mmHg > 24 hours) and 15 non-hypercapnic (control group). An acid-base quantitative physicochemical approach was used for the analysis. Results: The mean ages in the hypercapnic and control groups were 48 ± 18 years and 44 ± 14 years, respectively. After the induction of hypercapnia, pH markedly decreased and gradually improved in the ensuing 72 hours, consistent with increases in the standard base excess. The metabolic acid-base adaptation occurred because of decreases in the serum lactate and strong ion gap and increases in the inorganic apparent strong ion difference. Furthermore, the elevation in the inorganic apparent strong ion difference occurred due to slight increases in serum sodium, magnesium, potassium and calcium. Serum chloride did not decrease for up to 72 hours after the initiation of hypercapnia. Conclusion: In this explanatory study, the results indicate that metabolic acid-base adaptation, which is triggered by acute persistent hypercapnia in patients with acute respiratory distress syndrome, is complex. Furthermore, further rapid increases in the standard base excess of hypercapnic patients involve decreases in serum lactate and unmeasured anions and increases in the inorganic apparent strong ion difference by means of slight increases in serum sodium, magnesium, calcium, and potassium. Serum chloride is not reduced.

Presentation of an experimental method to induce in vitro ("organ chambers") respiratory acidosis and its effect on vascular reactivity

PURPOSE: To create in vitro a model to generate acidosis by CO2 bubbling "organ chambers", which would be useful for researchers that aim to study the effects of acid-base disturbs on the endothelium-dependent vascular reactivity. METHODS: Eighteen male Wistar rats (230-280g) were housed, before the experiments, under standard laboratory conditions (12h light/dark cycle at 21°C), with free access to food and water. The protocol for promoting in vitro respiratory acidosis was carried out by bubbling increased concentrations of CO2. The target was to achieve an ideal way to decrease the pH gradually to a value of approximately 6.6.It was used, initially, a gas blender varying concentrations of the carbogenic mixture (95% O2 + 5% CO2) and pure CO2. RESULTS: 1) 100% CO2, pH variation very fast, pH minimum 6.0; 2) 90%CO2 pH variation bit slower, pH minimum6.31; 3) 70%CO2, pH variation slower, pH minimum 6.32; 4) 50% CO2, pH variation slower, pH minimum 6:42; 5) 40 %CO2, Adequate record, pH minimum 6.61, and; 6) 30 %CO2 could not reach values below pH minimum 7.03. Based on these data the gas mixture (O2 60% + CO2 40%) was adopted, CONCLUSION: This gas mixture (O2 60% + CO2 40%) was effective in inducing respiratory acidosis at a speed that made, possible the recording of isometric force. .

Does Hypercapnic Acidosis, induced by Adding CO2 to Inspired Gas, Have Protective Effect in a Ventilator-induced Lung Injury?

To investigate whether hypercapnic acidosis, induced by adding CO2 to inspired gas, would be protective effect against ventilator-induced lung injury (VILI), we ventilated 55 normal white rabbits for 6 hr or until PaO2/FIO2 <200 mmHg. Control group (n=15) was ventilated with peak inspiratory pressure (PIP) of 15 cm H2O, positive end-expiratory pressure (PEEP) of 3 cm H2O, an inspiration-to-expiration ratio of 1:2, and an inspired oxygen fraction (FIO2) of 0.40. High pressure hypercapnic group (HPHC; n=20) was ventilated with PIP of 30 cm H2O, PEEP of 0 cm H2O, and FIO2 of 0.40. Carbon dioxide was introduced into the inspiratory limb of the ventilator circuit, as necessary to maintain hypercapnia (PaCO2, 65 to 75 mmHg). High pressure normocapnic group (HPNC; n=20) was ventilated with same setting of HPHC, except normocapnia (PaCO2, 35 to 45 mmHg). Bronchoalveolar lavage fluid (BALF) lactate dehydrogenase, aspartate aminotransferase, interleukin-8 were significantly higher in high pressure ventilator group than control group (p<0.05). Wet weight to dry weight (WW/DW) and histologic scores were significantly higher in high pressure ventilator group than control group (p<0.05). However, there were no significant differences in oxygenation, BALF inflammatory markers, WW/DW and histologic scores between HPHC and HPNC groups. These findings suggest that hypercapnic acidosis at least induced by CO2 insufflation would not be protective effect against VILI in this model.

Effects of fetal anoxia and acidosis on superoxide dismutase / 中华妇产科杂志

Objective To analyze the effects of fetal anoxia, respiratory and metabolic acidosis on the activity of antioxidation in fetal distress Methods Blood samples were taken from umbilical artery in 386 neonates for blood gas analysis and detection of the concentration of superoxide dismutase (SOD) Normal situation, anoxia, acidosis, respiratory acidosis, metabolic acidosis and mixed acidosis were diagnosed in all neonates according to the results of blood gas values, and the neonate asphyxia was diagnosed according to the Apgar scores (one minute) The effect of anoxia and acidosis to SOD were analyzed with multiple factor analysis of variation Results (1) Among the all 386 cases, 317 were normal, 31 with anoxia, 17 with acidosis, and 21 with both anoxia and acidosis Among the total cases of acidosis, 8 respiratory, 21 metabolic, and 9 mixed acidosis (2) The plasma levels of SOD of umbilical artery blood in anoxia, acidosis, both anoxia and acidosis, and normal sitution were (118 5?7 1) mmol/L, (122 0?11 4) mmol/L,(140 0?7 0)mmol/L, and (98 5? 2 6) mmol/L,respectively The results of unvariate analysis of variance showed that anoxia: F =4 999 ( P 0 05) (3) The plasma levels of SOD with respiratory acidosis, metabolic acidosis and mixed acidosis were (127 3?18 4) mmol/L, (126 0?8 1) mmol/L, (150 0?10 4) mmol/L The results of univariate analysis of variance showed that respiratory acidosis: F =4 404 ( P 0 05) Conclusion The superoxidation and antioxidation can be effected by factors like anoxia and acidosis, respiratory acidosis and metabolic acidosis However, the mechanisms of these effects are different. There is additive, but not synergistic effects among them

EXPERIMENTAL STUDY ON H~+/K~+ EXCHANGE FUNCTION AND cH-K-ATPase mRNA EXPRESSION IN RENAL IMCD CELL MONOLAYER UNDER RESPIRATORY ACID-BASE DISORDERS IN RABBIT / 解放军医学杂志

To study the cellular pathophysiological change in kidney IMCD cell under respiratory acid base disorders. 3% or 10% CO 2 was used to initiate chronic respiratory alkalosis(ALG) or chronic respiratory acidosis(ACG) of cultured rabbit IMCD cell. 5% CO 2 was used in control group(CG). Fluorescent probe was used to measure H + /K + exchange function of these cells. In situ hybridization and RT PCR were used to measure cH K ATPase mRNA expression of these cells.The results showed that H + /K + exchange in ACG was significantly higher than that in CG ( P 0 05). It is suggested that chronic respiratory acidosis could induce an increase in H + /K + exchange function and cH K ATPase mRNA expression. However, chronic respiratory alkalosis could induce decreases in H + /K + exchange function and cH K ATPase mRNA expression with no statistical significance, the reason of which calls for further study.