HCO3 E BE: ANÁLISE E IMPORTÂNCIA FISIOLÓGICA NA GASOMETRIA ARTERIAL

Introdução: A gasometria arterial é um exame complementar realizado através de coleta de sangue arterial, que visa a análise dos gases (pressão de oxigênio no sangue arterial- paO2, pressão de gás carbônico- paCO2) e dos principais componentes metabólicos do sangue (bicarbonato- HCO3 e Base Excess- Be), além do pH sanguíneo. De grande utilidade para a equipe multiprofissional, a gasometria arterial tem papel essencial para diagnóstico, avaliação terapêutica e tomada de decisões. Objetivo: Demonstrar a importância de dois componentes metabólicos da gasometria arterial, HCO3 e Be, bem como o impacto fisiológico que ambos podem gerar. Material e métodos: Revisão de literatura não sistematizada, nas bases de busca Google Acadêmico, entre os anos de 2018 e 2020. Resultados: A gasometria arterial revela dados fisiológicos que norteiam o diagnóstico e a busca pela melhor proposta terapêutica, como prescrição precisa de oxigenoterapia, correção bioquímica e ajustes ventilatórios, por exemplo. O HCO3 atua no sistema fisiológico auxiliando no transporte de oxigênio pelo organismo, a regulação desse componente no sangue ocorre através dos rins. O bicarbonato atua no sistema tampão buscando a neutralização do sangue em um aspecto mais básico. Na acidose respiratória o HCO3 plasmático normalmente encontra-se aumentado, a fim de combater o distúrbio primário, quanto a atuação na alcalose respiratória ocorre uma diminuição do bicarbonato em busca da compensação também do distúrbio primário. O Be é quando a soma de todas as bases ultrapassa os parâmetros de referência do Buffer Base, o Base Excess permite que haja a determinação da origem do distúrbio em questão, de modo que aponte quem está alterado e quem está apresentando compensação. Conclusão: O HCO3 e o Be são componentes que devem por suas funções fisiológicas serem analisados para a busca da terapêutica ideal aos pacientes, por suas características tornam-se imprescindíveis na gasometria arterial.

P0005TIME-VARYING DIALYSATE BICARBONATE CONCENTRATIONS CAN REDUCE PEAK INTRADIALTIC SERUM BICARBONATE CONCENTRATIONS

Background and Aims Hemodialysis (HD) treatments using bicarbonate-containing dialysis solutions can result in large intradialytic increases in serum bicarbonate concentration, potentially inducing intradialytic alkalemia. It has been suggested that a time-varying, compared with a constant, dialysate bicarbonate concentration may limit the intradialytic increase in serum bicarbonate concentration (Tobvin & Sherman, Semin Dial 2016). We tested this hypothesis using a mathematical model of bicarbonate transport during HD. Method We used the H+ mobilization model describing bicarbonate transport during HD (Sargent et al, Semin Dial 2018) to compare intradialytic serum bicarbonate concentrations when using constant or time-varying dialysate bicarbonate concentrations that deliver the same total amount of buffer base to the patient during the HD treatment. We employed this model to evaluate different time-varying dialysate bicarbonate concentration profiles that started at a high value and then decreased as a step function with a 10-minute timing resolution. Dialysis time was 210 minutes, dialysis solutions were assumed to contain acetate at 3 mEq/L, and all kinetic parameters were assumed to be identical to those reported by Sargent et al (Semin Dial 2018). All results with time-varying dialysate bicarbonate concentrations were compared to a constant dialysate concentration of 32 mEq/L. Results Example results comparing time-varying (36.0 mEq/L for the initial 40 min, 31.2 mEq/L thereafter) and constant (32 mEq/L) dialysate bicarbonate concentrations are shown in the figure. The time-varying dialysate bicarbonate concentration lowered the peak intradialytic serum bicarbonate by 0.4 mEq/L for approximately one-half of the treatment. Similar reductions in the peak intradialytic serum bicarbonate concentration could be achieved if the initial high dialysate bicarbonate concentration was 37.6 mEq/L for 30 min or 40.8 for 20 min. The optimal initial high dialysate bicarbonate concentrations and the reduction in the peak intradialytic serum bicarbonate concentrations were somewhat dependent on the assumed patient-dependent H+ mobilization coefficient. Conclusion We conclude that a time-varying dialysate bicarbonate concentration can lower the peak intradialytic serum bicarbonate concentrations while delivering the same total amount of buffer base to the patient. Whether this approach will yield improved patient outcomes requires further evaluation.

Base-enhanced catalytic water oxidation by a carboxylate–bipyridine Ru(II) complex

In aqueous solution above pH 2.4 with 4% (vol/vol) CH3CN, the complex [RuII(bda)(isoq)2] (bda is 2,2′-bipyridine-6,6′-dicarboxylate; isoq is isoquinoline) exists as the open-arm chelate, [RuII(CO2-bpy-CO2−)(isoq)2(NCCH3)], as shown by 1H and 13C-NMR, X-ray crystallography, and pH titrations. Rates of water oxidation with the open-arm chelate are remarkably enhanced by added proton acceptor bases, as measured by cyclic voltammetry (CV). In 1.0 M PO43–, the calculated half-time for water oxidation is ∼7 μs. The key to the rate accelerations with added bases is direct involvement of the buffer base in either atom–proton transfer (APT) or concerted electron–proton transfer (EPT) pathways.

Stability of the Strong Ion Gap versus the Anion Gap over Extremes of PCO2 and pH

The strong ion gap (SIG) is under evaluation as a scanning tool for unmeasured ions. SIG is calculated by subtracting [buffer base], which is ([A-]+[HCO3-]), from the apparent strong ion difference, which is ([Na+] + [K+]+[Ca++]+[Mg++]-[Cl-]-[L-lactate]). A- is the negative charge on albumin and phosphate. We compared the pH stability of the SIG with that of the anion gap (AG). In normal and hypoalbuminaemic hyperlactaemic blood, PCO2 was reduced stepwise in vitro from >200 mmHg to < 20 mmHg, with serial blood gas and electrolyte analyses, and [albumin] and [phosphate] measurement on completion. Respective [haemoglobin], [albumin], [phosphate] and [lactate] in normal blood were 156 (0.9) g/l, 44 (2) g/l, 1.14 (0.06) mmol/l and 1.7 (0.8) mEq/l, and in hypoalbuminaemic blood 116 (0.9) g/l, 24 (2) g/l, 0.78 (0.06) mmol/l and 8.5 (0.5) mEq/l. pH increased from <6.85 to >7.55, causing significant falls in [Na+] and elevations in [Cl-]. Initial and final SIG values did not differ, showing no correlation with pH. Mean SIG was 0.5±1.5 mEq/l. AG values were directly correlated with pH (normal: R2=0.51, hypoalbuminaemic: R2=0.65). Final AG values significantly exceeded initial values (normal blood: 15.9 (1.7) mEq/l versus 8.9 (1.8) mEq/l, P<0.01; hypoalbuminaemic blood: 16.5 (0.8) mEq/l versus 11.8 (2.0) mEq/l, P<0.05). We conclude that, unlike the AG, the SIG is not affected by severe respiratory acidosis and alkalosis, enhancing its utility in acid-base disturbances.

Carbon dioxide pressure-concentration relationship in arterial and mixed venous blood during exercise

To calculate cardiac output by the indirect Fick principle, CO2 concentrations (Cco 2) of mixed venous (Cv̄CO2 ) and arterial blood are commonly estimated from Pco 2, based on the assumption that the CO2 pressure-concentration relationship (Pco 2-Cco 2) is influenced more by changes in Hb concentration and blood oxyhemoglobin saturation than by changes in pH. The purpose of the study was to measure and assess the relative importance of these variables, both in arterial and mixed venous blood, during rest and increasing levels of exercise to maximum (Max) in five healthy men. Although the mean mixed venous Pco 2 rose from 47 Torr at rest to 59 Torr at the lactic acidosis threshold (LAT) and further to 78 Torr at Max, the Cv̄CO2 rose from 22.8 mM at rest to 25.5 mM at LAT but then fell to 23.9 mM at Max. Meanwhile, the mixed venous pH fell from 7.36 at rest to 7.30 at LAT and to 7.13 at Max. Thus, as work rate increases above the LAT , changes in pH, reflecting changes in buffer base, account for the major changes in the Pco 2-Cco 2relationship, causing Cv̄CO2 to decrease, despite increasing mixed venous Pco 2. Furthermore, whereas the increase in the arteriovenous Cco 2 difference of 2.2 mM below LAT is mainly due to the increase in Cv̄CO2 , the further increase in the arteriovenous Cco 2 difference of 4.6 mM above LAT is due to a striking fall in arterial Cco 2 from 21.4 to 15.2 mM. We conclude that changes in buffer base and pH dominate the Pco 2-Cco 2 relationship during exercise, with changes in Hb and blood oxyhemoglobin saturation exerting much less influence.

Metabolic component of intestinal Pco 2during dysoxia

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O2 supply diminishes with failing blood flow, tissue acid-base changes are first “respiratory,” with CO2 coming from combustion of fuel and stagnating in the decreasing blood flow. When the O2supply decreases to critical, the changes become “metabolic” due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO3 − and noncarbonate buffer anion (A−). During purely respiratory acidosis, buffer base stays constant because HCO3 − cannot buffer its own progenitor, carbonic acid, so that the rise of HCO3 − equals the fall of A−. During anaerobic “metabolism,” however, lactate's H+ is buffered by both A− and HCO3 −, causing buffer base to decrease. We quantified the partitioning of lactate's H+ between HCO3 − and A−buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring Pco 2 and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0.031 min−1 and half time = ∼22 min. Pco 2 vs. lactate relations were linear. Over 3 h, lactate increased by 31 ± 3 mmol/l tissue fluid (mM) and Pco 2 by ∼17 mM, meaning that one-half of lactate's H+ was buffered by tissue HCO3 − and one-half by A−. The data were consistent with a lumped p K a value near 6.1 and total A− concentration of ∼30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and Pco 2.