Open Access Peer-Reviewed
Review Article

Sodium bicarbonate in the critically Ill patient with metabolic acidosis

Uso de bicarbonato de sódio na acidose metabólica do paciente gravemente enfermo

Paulo Novis Rocha

Abstract:

Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation.

Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock.

Resumo:

A acidose lática é um distúrbio do equilíbrio ácido-base muito frequente em pacientes internados em unidades de terapia intensiva e está associado a um mau prognóstico. Embora exista um acúmulo substancial de evidências de que níveis críticos de acidemia provocam inúmeros efeitos adversos sobre o funcionamento celular, a utilização de bicarbonato de sódio para o tratamento da acidose lática em pacientes gravemente enfermos permanece alvo de controvérsias. Neste artigo, pretendemos: 1) analisar as principais diferenças entre as acidoses hiperclorêmicas e as acidoses orgânicas, com ânion gap (AG) elevado, visando embasar a discussão sobre os fundamentos da terapia com bicarbonato de sódio nas acidoses metabólicas; 2) avaliar os riscos associados à persistência de níveis críticos de acidemia, contrastando-os com os riscos do uso de bicarbonato de sódio; 3) analisar criticamente as evidências da literatura sobre o uso de bicarbonato de sódio no tratamento da acidose lática do paciente crítico, com ênfase em ensaios clínicos randomizados em seres humanos; 4) fornecer um fundamento para a utilização judiciosa de bicarbonato de sódio nesta situação.

Descritores: acidose láctica, cetoacidose diabética, bicarbonato de sódio, choque séptico.

INTRODUCTION

A Metabolic acidosis is an acid-base imbalance frequently found in critically ill patients at intensive care units. The main type of metabolic acidosis found in those patients is lactic acidosis secondary to circulatory shock. Regardless of its etiology - cardiogenic, hypovolemic, or distributive - circulatory shock causes a reduction in oxygen offer to organs and tissues. At cell level, that reduction in oxygen offer hinders NADH oxidation to NAD+ by the mitochondria. The build-up of NADH favors the preferential conversion of the pyruvate originated from glycolysis to lactic acid.Finally, shock reduces lactate use by the liver and kidneys, contributing to its accumulation in circulation and to acidemia.1

Lactic acidosis is associated with high mortality. The prognosis usually depends on the severity of the disease underlying the acid- base imbalance rather than on the severity of the disorder itself.2 However, very extreme levels of acidemia causes several undesirable effects on cell function, resulting in immediate risk of death. Our organism counts on multiple lines of defense against acid overloads, such as bicarbonate extracellular buffering, respiratory buffering due to increased CO2 excretion, bone and intracellular buffering, in addition to increased renal excretion of hydrogen, all aiming at maintaining pH of the inner medium at levels compatible with cell function and life. When the aforementioned lines of defense are insufficient to buffer the significant acid overload found in some patients, some alkalinizing agents, such as sodium bicarbonate, can be used. However, the administration of sodium bicarbonate to attenuate acidemia in lactic acidosis has been controversial for more than 20 years.3-9

This study does not aim at a detailed analysis of lactic acidosis, but at approaching the controversy about the sodium bicarbonate use in that condition. Therefore, the following steps will be taken: 1) analysis of the main differences between hyperchloremic acidosis and organic acidosis, with high anion gap (AG), to serve as basis for the discussion about the rationale of sodium bicarbonate therapy in metabolic acidosis; 2) assessment of the risks associated with persistent critic levels of acidemia, comparing them with the risks of sodium bicarbonate use; 3) critical analysis of the literature evidence about sodium bicarbonate use in the treatment of lactic acidosis in critically ill patients, emphasizing randomized clinical trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation.

Types of metabolic acidosis: therapeutic implications

Metabolic acidoses are pathological processes characterized by an increase in the acid concentration in the extracellular fluid (ECF).1 Clinically, this translates into a decrease in the serum concentration of bicarbonate, in pH, and in pCO2[a]. The main mechanisms producing metabolic acidosis are: 1) loss of bicarbonate through body fluids; 2) a reduction in the renal excretion of acids; and 3) increased production of organic acids. Traditionally, according to the AG, metabolic acidoses are divided into two groups (Table 1)[b].




a) Metabolic acidosis with normal AG: Diarrhea and renal tubular acidosis (RTA) are the major causes of metabolic acidosis with normal AG. In diarrhea, an important loss of bicarbonate through intestinal secretions exists, while in type II RTA that loss occurs through urine, due to defective bicarbonate reabsorption at the level of the proximal tubules. In distal RTAs, types I and IV, a defect in urine acidification leads to a slow and progressive accumulation of non-carbonic acids generated daily through protein metabolism. Both in diarrhea and in RTAs, AG remains normal, because the reduction in the serum concentration of bicarbonate is counterbalanced by an equimolar increase in chlorine concentration. Such acidoses are also known as hyperchloremic. In hyperchloremic metabolic acidosis, a real deficit of bicarbonate in the ECF occurs. This fact has practical therapeutic implications, because it means that the serum concentration of bicarbonate only returns spontaneously to normal if the kidneys can increase their urinary excretion of protons [c] and regenerate bicarbonate. This can happen when hyperchloremic acidosis has a non-renal origin, as in the case of diarrhea. However, it is worth emphasizing that renal correction does not occur immediately, it can take some days. If the hyperchloremic acidosis caused by diarrhea is severe, there is no reason to wait for renal responses, and the acidosis should be pharmacologically corrected. In addition, if diarrhea occurs in patients with nephropathy, that is, with low renal capacity to reverse metabolic acidosis, the use of bicarbonate is also recommended. When the kidneys account for hyperchloremic acidosis, such as in tubular acidosis, no spontaneous correction occurs. In such cases, persistent chronic hyperchloremic metabolic acidosis generates several problems, such as bone demineralization, hypocitraturia, nephrolithiasis, nephrocalcinosis, muscle catabolism, and growth deficit. Pharmacological correction of metabolic acidosis through the administration of alkalinizing agents (sodium bicarbonate, sodium citrate, potassium citrate) is mandatory to prevent those complications.

b) Metabolic acidosis with high AG: Metabolic acidosis with high AG is characterized by an excessive production of organic acids. Two common examples are diabetic ketoacidosis and lactic acidosis. In those situations, the reduction in serum bicarbonate does not reflect a real bicarbonate loss from the ECF, but its combination with those organic acids in reversible chemical buffering reactions. In diabetic ketoacidosis, for example, acetoacetic acid combines with sodium bicarbonate forming sodium acetate. In lactic acidosis, the lactic acid combines with sodium bicarbonate, forming sodium lactate. Because the decrease in serum bicarbonate is not accompanied by an elevation in chlorine, AG increases. The higher the accumulation of organic acids, the greater the decrease in serum bicarbonate and, consequently, the higher the AG[d].10-14 Another example is lactic acidosis that commonly occurs after a convulsive crisis. In such cases, with only support treatment, rapid (within 60 minutes) metabolism of lactate occurs, with resolution of acidemia.15 Therefore, the magnitude of AG elevation reflects the magnitude of accumulation of organic acids. By treating the underlying disease and reversing the metabolic conditions responsible for the excessive production of those organic acids, acetate and lactate are rapidly converted to bicarbonate (being, thus, considered bicarbonate precursors or "potential bicarbonate"). The therapeutic implication is that, in organic acidosis, efforts should be concentrated on the correction of the underlying disease and not on the exogenous administration of bicarbonate. In type I diabetic patients presenting with ketoacidosis, for example, treatment with intravenous saline solution and insulin can rapidly cause the conversion of ketoacids into bicarbonate. In such cases, even when acidemia is severe, the exogenous administration of alkalinizing agents is unnecessary.




Severe lactic acidosis in sepsis: to treat or not to treat?

In view of the foregoing, the following is concluded:

  • hyperchloremic metabolic acidosis is characterized by a real bicarbonate deficit in the ECF and the impossibility of rapid spontaneous correction, and should, thus, be treated with exogenous administration of sodium bicarbonate;
  • organic acidosis is characterized by excessive production of acids that react with bicarbonate, forming compounds that may be rapidly converted into bicarbonate with the resolution of the underlying disease, making the exogenous administration of bicarbonate unnecessary.


  • Although there is consensus that the best way to correct organic acidosis is by reversing the underlying disease (and not by administering bicarbonate), controversy appears when that organic acidosis is severe and the underlying disease is not rapidly reversible. The case of a patient with septic shock and severe lactic acidosis, with bicarbonate < 10 mEq/L, and pH < 7.15, despite the properly reduced pCO2, illustrates an extremely common situation in intensive care units. Treating the underlying disease with volemiresuscitation, antibiotics, hemodynamic and ventilatory support sometimes cannot reverse lactic acidosis in a few hours. What to do? Accept severe acidemia for undetermined time or try to attenuate it with sodium bicarbonate? The remaining of this text will approach that question.

    Risks related to severe acidemia

    In the example above, if we decide to wait for the treatment of the underlying disease to correct lactic acidosis, the patient will be exposed to the adverse consequences of severe acidemia (Chart 1).2 Respiratory: the decrease in pH stimulates the respiratory center to increase alveolar ventilation, reducing pCO2, and attenuating acidemia. Although this is a positive physiological response, maintenance of that hyperventilation for prolonged time generates the sensation of dyspnea, increases the respiratory work and oxygen consumption, and may lead to fatigue of the respiratory muscles. In patients at intensive care units, those adverse effects may be attenuated through sedation and mechanical ventilation.




    Metabolic: maintenance of an adequate concentration of H+ in the ECF is essential for cell function, due to the high reactivity of H+ ions with proteins. During severe acidosis, proteins gain H+, which results in alterations in the distribution of electric charge, molecular configuration, and, consequently, function. As an example, we can cite the inhibition of the glycolytic enzyme 6-phosphofrutokinase activity during severe acidemia,16 an undesirable fact in situations of hypoxia, when the glycolytic metabolism becomes an essential source of energy. Additionally, acidemia increases muscle and protein catabolism and can cause hyperkalemia, a more important effect on hyperchloremic than on organic acidosis.

    Cerebral: regulation of neuronal volume and cerebral metabolism is altere d by severe acidemia. Clinically, the decrease in cerebrospinal fluid pH may cause confusion, lethargy, and coma. Those alterations are more dramatic in respiratory than in metabolic acidosis, maybe due to the greater permeability of the blood-brain barrier to CO2 than to bicarbonate.

    Cardiovascular: the adverse consequences of severe acidemia on the cardiovascular system are undoubtedly the most feared by intensivists and the most used to justify the administration of sodium bicarbonate in that situation. In the presence of severe acidemia, a reduction occurs in the threshold for malignant ventricular arrhythmias, resulting in increased risk for sudden death. Centralization of blood volume also occurs, increasing susceptibility to acute pulmonary edema. Finally, there is a reduction in myocardial contractility and in cardiovascular response to catecholamines, causing a decrease in cardiac output, arterial tension, and renal and liver perfusion, effects that tend to accentuate and perpetrate lactic acidosis. Theoretically, sodium bicarbonate could be beneficial, because it would reduce the risk of sudden death due to malignant ventricular arrhythmias, and would restore cardiovascular response to catecholamines, with consequent improvement in tissue perfusion and in lactic acidosis itself.


    Figure 1. Rationale for the administration of sodium bicarbonate in severe lactic acidosis.



    Risks related to the use of sodium bicarbonate

    When treating a patient with severe lactic acidosis with sodium bicarbonate, the possible risks associated with that therapy should be considered (Chart 2).




    Hypernatremia and hyperosmolarity: sodium bicarbonate is available for parenteral use in the national market in 10 mL ampules containing 10 mEq NaHCO3 (1 mEq/mL). That is an extremely hypertonic solution (8.4%). The non-diluted use of that solution causes a great sodium overload, and may lead to hypernatremia and hyperosmolarity.

    Volume overload: bicarbonate administration implies sodium administration and, consequently, ECF expansion.

    Hypercapnia and intracellular acidosis: the combination of H+ protons with bicarbonate buffer generates carbonic acid, which is later eliminated by the lungs. Thus, hyperventilation secondary to acidemia is necessary to guarantee the efficiency of that mechanism for eliminating acid by the lungs. It is worth emphasizing that, by administering sodium bicarbonate to a patient with metabolic acidosis, CO2 generation is also increased.

    HCO3- + H+ «-» H CO «-» H2O + CO2

    This is especially relevant in patients with respiratory distress syndrome and significant ventilatory difficulties. In such cases, the administration of sodium bicarbonate can aggravate respiratory acidosis. Because cell membranes are more permeable to CO2 than to bicarbonate, intracellular acidosis occurs. At the myocardial cell level, intracellular acidosis can reduce myocardial contractility; at the hepatocyte level, a decrease in lactate use occurs.

    Greater affinity of hemoglobin with O2: one of the advantages of acidemia is the decrease in the affinity of hemoglobin with O2, facilitating its release to the tissues, an important fact in lactic acidosis, in which the genesis of the problem is tissue hypoperfusion, and consequent hypo-oxygenation. Correction of acidemia in that context may eliminate that advantage by hindering the O2 dissociation from hemoglobin, theoretically worsening tissue oxygenation.

    Stimulus of glycolytic enzymes: the elevation of serum pH stimulates glycolytic enzymes, such as 6-phosphofrutokinase, increasing lactate generation.16

    Decrease in ionized calcium: serum pH influences calcium binding to albumin. In the presence of acidemia, calcium binding to albumin decreases, which elevates the biologically active free calcium fraction (ionic calcium). Similarly, the administration of sodium bicarbonate can aggravate a preexisting ionic hypocalcemia - a common fact in critically ill patients4 - causing a reduction in myocardial and vascular contractility.

    Rebound alkalosis: the administration of sodium bicarbonate to patients with organic acidosis increases bicarbonate serum concentration and pH without solving the main problem: the high concentration of organic acids. Once the underlying disease is corrected, the conversion of those organic acids into bicarbonate will cause a new elevation in serum bicarbonate, leading to potentially severe metabolic alkalosis and alkalemia.

    Theoretically, the use of sodium bicarbonate would be harmful because the elevation in pH would increase the activity of glycolytic enzymes and reduce oxygen release from hemoglobin and ionized calcium. Additionally, the administration of sodium bicarbonate would cause an elevation in PCO2 and, consequently, intracellular acidosis. At the cardiac level, intracellular acidosis leads to a decrease in myocardial contractility; at hepatic level, it leads to a reduction in lactate use. Together, those effects would determine an elevation in serum lactate levels.


    Figure 2. Rationale for not administering sodium bicarbonate in severe lactic acidosis



    Assessment of evidence

    As already mentioned, there is rationale - originated mainly from experimental studies - both to defend and to condemn the use of sodium bicarbonate in cases of severe lactic acidosis. But what do the studies in human beings show? Unfortunately, the literature on the use of sodium bicarbonate in lactic acidosis is full of passionate opinions, but lacks evidence. We identified only two prospective, randomized, clinical trials about the subject, both published almost 20 years ago.

    The first was carried out by Cooper et al. in the intensive care unit of a tertiary hospital in Canada, in 1990.4 The inclusion criteria were as follows: use of Swan-Ganz catheter; serum bicarbonate < 17 mmol/L; and arterial lactate > 2.5 mmol/L. Those authors studied 14 patients, whose ages ranged from 26 to 82 years (mean age, 56 years), all requiring mechanical ventilation. The clinical findings were extremely heterogeneous, because the study included a 75-year-old patient with pneumonia, mesenteric infarction, on epinephrine and dobutamine, and a 34-year-old patient with hypovolemic shock, not requiring vasoactive drugs. Lactate levels ranged from 2.5 to 21.0 mmol/L (mean value of 7.8 mmol/L). The outcomes assessed in the study were laboratory and hemodynamic measurements. The protocol was completed in less than two hours and consisted of infusion of 2 mmol/kg of 0.9 M sodium bicarbonate, during 15 minutes, or sodium chlorine (in equal dose, volume, and time). All patients received both therapies, but the order of the interventions was randomized. Laboratory and hemodynamic assessments were conducted immediately before, immediately after, and 30 minutes after the infusion. Between the infusions, there was a 20-minute washout period.

    The results showed that, when compared with the infusion of saline solution, the infusion of sodium bicarbonate caused the following: 1) an increase in serum bicarbonate; 2) an increase in pH; 3) an increase in pCO2; and 4) a decrease in ionic calcium. From the hemodynamic point of view, the infusion of sodium bicarbonate caused a transient elevation in the pulmonary artery occlusion pressure and in cardiac output. However, identical effects were obtained with the administration of saline solution, suggesting that those hemodynamic changes are due to blood volume expansion (by crystalloid solution containing sodium) rather than to the restoration of the cardiovascular response to catecholamines due to the pH elevation. Similar results have been obtained in a subgroup analysis with seven more acidemic patients (mean pH, 7.13; mean lactate, 10.1 mmol/L).


    Figure 3. Experimental design used in the study by Cooper et al.4



    The second study was published by Mathieu et al. in 1991. The experimental design was practically identical, except for the bicarbonate dose (1 mmol/kg). After assessing 10 patients, the authors concluded that the administration of sodium bicarbonate did not improve the hemodynamic variables of patients with lactic acidosis, but it did not worsen tissue oxygenation.17

    Both studies, which represent the best level of evidence available, showed a neutral effect of the infusion of sodium bicarbonate in critically ill patients with lactic acidosis. It was not associated to benefit nor harm. It is worth emphasizing that both studies have a number of limitations, such as the very reduced number of patients, the great heterogeneity of clinical findings and of disease severity, the crossover design, and the rapid administration of a single dose of sodium bicarbonate. Additionally, the most relevant clinical outcomes, such as survival, were not assessed. In conclusion, the experimental design of those studies does not respond several questions of interest to intensivists.

    Approach suggestion

    The 2008 Surviving Sepsis Guidelines are contrary to the use of sodium bicarbonate in patients with lactic acidosis and pH > 7.15, but leaves it up to the assistant physician its use in cases of more severe acidemia.3 Our opinion is that, if, even after starting the treatment with antibiotics and optimization of ventilatory, and hemodynamic support measures, the patient persists with severe metabolic acidosis and pH < 7.15, the careful use of sodium bicarbonate is justified. The objectives of that treatment would be as follows: 1) to reduce the potential adverse effects of severe acidemia on the cardiovascular system, allowing time for the specific measures against septic shock to take effect; and 2) to obtain a safety margin against new acidifying challenges (decreases in bicarbonate or elevations in pCO2). It is worth emphasizing that the treatment with sodium bicarbonate in that situation should never aim at the complete correction of metabolic acidosis, but rather at elevating serum bicarbonate up to 8 to 10 mEq/L and pH to close to 7.20. By only attenuating - and not correcting - acidemia, the adverse effects associated with the sodium bicarbonate use are minimized (Chart 2).


    Figure 4. Flowchart for the use of bicarbonate in metabolic acidosis.



    In order to estimate the amount of sodium bicarbonate to be administered, the following formula can be used: (desired bicarbonate - found bicarbonate) × 0.5 × weight in kg

    In normal situations, the bicarbonate distribution space corresponds to 50% of body weight. However, that distribution space increases in the presence of acidosis, reaching more than 70% of body weight in more severe cases. To avoid excessive use of bicarbonate, we suggest the use of 0.5 × weight. Alternatively, 1-2 mEq/kg of sodium bicarbonate can be simply infused, such as in the studies by Cooper4 and Mathieu17 and coworkers.

    The intravenous infusion of significant amounts of non-diluted 8.4% sodium bicarbonate can cause hypernatremia and hyperosmolarity. Thus, bicarbonate should be diluted in an electrolyte-free solution (distilled water or 5% glucose solution). If the patient is normovolemic or hypovolemic, an isotonic solution of sodium bicarbonate can be prepared and used for ECF expansion and acidosis attenuation. This can be achieved by adding 15 ampules (150 mL) of 8.4% NaHCO3 to 850 mL of distilled water (or 5% glucose solution), resulting in a solution containing 150 mEq/L of NaHCO3 (similar to a solution of 0.9% NaCl, which contains 154 mEq/L of NaCl). Depending on the severity of the acidemia and the patient's volemic needs, the infusion of the solution can take either 30 to 60 minutes or a few hours. If the patient has congestion, bicarbonate dilution in smaller water volumes can be attempted, remembering that it is the sodium content and not the water content of a solution that determines its capacity to expand the ECF. The administration of the sodium bicarbonate hypertonic solution, by elevating the ECF osmolarity, attracts water from the intracellular fluid, increasing blood volume. In those cases, the association of a loop diuretic, such as furosemide, is more indicated. But in the presence of pulmonary congestion and low diuretic response, such as in cases of renal failure, the intravenous use of sodium bicarbonate should be avoided. In such cases, acidemia is best managed through dialytic procedures. It is worth emphasizing that, during dialysis, bicarbonate gain occurs, and, thus, this is an "alternative" way of sodium bicarbonate administration.




    Because there are no formulae to accurately foresee the therapeutic response to the administration of sodium bicarbonate, careful laboratory reassessment is mandatory, approximately 30 minutes after infusion. That assessment should include the measurement of ionized calcium, which may decrease with pH elevation. Adjustments in ventilation should be made as required, aiming at eliminating the excessive CO2 generated after bicarbonate infusion.


    REFERENCES

    1. Rose BD. Metabolic Acidosis. In: Rose BD (ed.). Clinical physiology of acid-base and electrolyte disorders. 4 ed. McGraw-Hill, 1994, pp. 540-603.

    2. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. First of two parts. N Engl J Med 1998;338:26-34.

    3. Boyd JH, Walley KR. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? Curr Opin Crit Care 2008;14:379-83.

    4. Cooper DJ, Walley KR, Wiggs BR, Russell JA. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med 1990;112:492-8.

    5. Cuhaci B, Lee J, Ahmed Z. Sodium bicarbonate and intracellular acidosis: myth or reality? Crit Care Med 2001;29:1088-90.

    6. Rosival V. Evaluating sodium bicarbonate controversy. Chest 2001;119:1622-3.

    7. Cuhaci B, Lee J, Ahmed Z. Sodium bicarbonate controversy in lactic acidosis. Chest 2000;118:882-4.

    8. Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000;117:260-7.

    9. Sing RF, Branas CA, Sing RF. Bicarbonate therapy in the treatment of lactic acidosis: medicine or toxin? J Am Osteopath Assoc 1995;95:52-7.

    10.Gamba G, Oseguera J, Castrejon M, Gomez-Perez FJ. Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial. Rev Invest Clin 1991;43:234-8.

    11. Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed) 1984;289:1035-8.

    12. Okuda Y, Adrogue HJ, Field JB, Nohara H, Yamashita K. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab 1996;81:314-20.

    13. Rosival V. Should sodium bicarbonate be administered in diabetic ketoacidosis? Am J Respir Crit Care Med 2002;166:1290.

    14. Viallon A, Zeni F, Lafond P et al. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med 1999;27:2690-3.

    15. Lipka K, Bulow HH. Lactic acidosis following convulsions. Acta Anaesthesiol Scand 2003;47:616-8.

    16. Halperin ML, Connors HP, Relman AS, Karnovsky ML. Factors that control the effect of pH on glycolysis in leukocytes. J Biol Chem 1969;244:384-90.

    17. Mathieu D, Neviere R, Billard V, Fleyfel M, Wattel F. Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study. Crit Care Med 1991;19:1352-6.







    1. Departamento de Medicina da FMB - UFBA - Salvador, BA, Brasil

    Correspondence to:
    Paulo Novis Rocha
    Av. Reitor Miguel Calmon, s/no, Vale do Canela
    Salvador - BA - Brasil - CEP: 40110-100
    Tel/Fax: (71) 3283-8862/8863/8864
    E-mail: paulonrocha@ufba.br

    The author declares financial support from Fundação ABM de Pesquisa e Extensão na Área da Saúde (FABAMED)

    Submitted on: 09/21/2009
    Approved on: 10/06/2009



    [a] Em geral, a pCO2 cai aproximadamente 1,2 mmHg para cada 1,0 mEq/L de queda no bicarbonato sérico.

    [b] AG = Na+- (HCO3-+Cl-), com valores normais entre 6 e 12 mEq/L. Como a albumina sérica é o principal componente do AG, este deve ser sempre corrigido na vigência de hipoalbuminemia através da fórmula AGcorrigido = AG + [(4,0 - albumina sérica) × 2,5].

    [c] A principal forma de excreção renal de prótons é combinando H+ com NH3 para formar NH4 +. O NH4 + é excretado pelos rins combinado ao Cl-. Por isso, a excreção urinária de Cl- pode ser usada como um marcador da excreção de NH4+ e, consequentemente, da capacidade de acidificação urinária. É com este objetivo que utilizamos a fórmula do AG urinário: (Na++K+)- Cl-. Na vigência de acidose metabólica hiperclorêmica, resultados NEGATIVOS sugerem uma causa não renal (i. e. diarreia), pois os altos níveis de Cl- urinário necessários para um resultado negativo indicam acidificação renal adequada; pelo raciocínio inverso, resultados POSITIVOS sugerem uma causa renal (i. e. ATR distal) de acidose hiperclorêmica.

    [d] Em geral, a relação entre a elevação do AG (ou delta AG) e a queda no bicarbonato (ou delta bicarbonato) é de 1:1 a 2:1. Quando o delta AG/delta bicarbonato for < 1, podemos dizer que a magnitude da queda no bicarbonato não pode ser explicada apenas pela elevação no AG (que representa o acúmulo de ácidos orgânicos), sugerindo a presença de uma acidose metabólica hiperclorêmica associada. Uma relação delta AG/delta bicarbonato > 2 revela que a queda no bicarbonato foi menor que a esperada pelo aumento no AG, revelando assim a presença de uma alcalose metabólica associada.


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