0
selected
-
1.
Sodium bicarbonate therapy for acute respiratory acidosis.
Chand, R, Swenson, ER, Goldfarb, DS
Current opinion in nephrology and hypertension. 2021;(2):223-230
Abstract
PURPOSE OF REVIEW Respiratory acidosis is commonly present in patients with respiratory failure. The usual treatment of hypercapnia is to increase ventilation. During the recent surge of COVID-19, respiratory acidosis unresponsive to increased mechanical ventilatory support was common. Increasing mechanical ventilation comes at the expense of barotrauma and hemodynamic compromise from increasing positive end-expiratory pressures or minute ventilation. Treating acute respiratory acidemia with sodium bicarbonate remains controversial. RECENT FINDINGS There are no randomized controlled trials of administration of sodium bicarbonate for respiratory acidemia. A recent review concluded that alkali therapy for mixed respiratory and metabolic acidosis might be useful but was based on the conflicting and not conclusive literature regarding metabolic acidosis. This strategy should not be extrapolated to treatment of respiratory acidemia. Low tidal volume ventilation in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) has beneficial effects associated with permissive hypercapnia. Whether the putative benefits will be negated by administration of alkali is not known. Hypercapnic acidosis is well tolerated, with few adverse effects as long as tissue perfusion and oxygenation are maintained. SUMMARY There is a lack of clinical evidence that administration of sodium bicarbonate for respiratory acidosis has a net benefit; in fact, there are potential risks associated with it.
-
2.
Management of acute metabolic acidosis in the ICU: sodium bicarbonate and renal replacement therapy.
Yagi, K, Fujii, T
Critical care (London, England). 2021;(1):314
Abstract
This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2021. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2021 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from https://link.springer.com/bookseries/8901 .
-
3.
Effects of Combining Caffeine and Sodium Bicarbonate on Exercise Performance: A Review with Suggestions for Future Research.
Grgic, J
Journal of dietary supplements. 2021;(4):444-460
Abstract
This paper aimed to: (a) critically review studies that explored the isolated and combined effects of caffeine and sodium bicarbonate ingestion on exercise performance; (b) discuss some of the possible reasons for the discrepancy in findings; and, (c) provide suggestions for future studies. Out of the eight studies that examined this topic, only one study found that the combined ingestion of both supplements provided additive effects. In other studies, the following findings were observed: (a) only caffeine was ergogenic; (b) isolated and combined ingestion of both supplements was comparably ergogenic; (c) neither isolated nor combined ingestion of caffeine and sodium bicarbonate provided a performance-enhancing effect; and, (d) caffeine and caffeine plus sodium bicarbonate improved performance compared to sodium bicarbonate (but not as compared to placebo). Even though studies used currently recommended protocols of caffeine supplementation and exercise tasks for which the isolated ergogenic effects of caffeine and sodium bicarbonate are already established, the response to sodium bicarbonate supplementation was very variable, which might largely explain the discrepancies in the findings. The protocols of sodium bicarbonate ingestion generally resulted in high incidence and severity of side-effects, which might have had a negative effect on exercise performance. Future studies that optimize protocols of sodium bicarbonate supplementation are needed to fully explore if combining caffeine and sodium bicarbonate indeed provides any additive effects on exercise performance.
-
4.
Sodium Bicarbonate in Different Critically Ill Conditions: From Physiology to Clinical Practice.
Coppola, S, Caccioppola, A, Froio, S, Chiumello, D
Anesthesiology. 2021;(5):774-783
-
5.
Bicarbonate use and mortality outcome among critically ill patients with metabolic acidosis: A meta analysis.
Lo, KB, Garvia, V, Stempel, JM, Ram, P, Rangaswami, J
Heart & lung : the journal of critical care. 2020;(2):167-174
Abstract
BACKGROUND The use of sodium bicarbonate in the treatment of metabolic acidosis in critically ill subjects has long been a subject of debate. Despite empiric use in the setting of severe acidemia in critically ill patients, there is little data looking into the role of sodium bicarbonate in the treatment of severe metabolic acidosis in the intensive care unit (ICU) setting. METHODS We conducted a comprehensive search of Pubmed and Cochrane Central Register of Controlled Trials addressing bicarbonate use in the metabolic acidosis in the intensive care unit (ICU) setting. We examined mortality as end point. Pooled odds ratios (OR) and their 95% confidence intervals (CI) were calculated for all outcomes using a random-effect model. RESULTS The final search yielded 202 articles of which all were screened individually. A total of 11 studies were identified but 6 studies were excluded due to irrelevance in mortality outcome and methodology. Analysis was done separately for observational studies and randomized controlled trials. The pooled OR [95% CI] for mortality with bicarbonate use in the observational studies was 1.5 [0.62-3.67] with heterogeneity of 67%, while pooled OR for mortality in the randomized trials was 0.72 [0.49-1.05] (figure 2). In combining all studies, the pooled odds ratio was 0.93 95% [0.69-1.25] but with heterogeneity of 63%. After sensitivity analysis with removing the study done by Kim et al. 2013, heterogeneity was 0% with OR 0.8 [0.59-1.10]. CONCLUSION There is no significant difference in mortality in the use of bicarbonate among critically ill patients with high anion gap metabolic acidosis predominantly driven by lactic acidosis.
-
6.
Advances in management of chronic metabolic acidosis in chronic kidney disease.
Chen, W, Abramowitz, MK
Current opinion in nephrology and hypertension. 2019;(5):409-416
-
-
Free full text
-
Abstract
PURPOSE OF REVIEW Chronic metabolic acidosis is a common complication of chronic kidney disease (CKD) and is associated with adverse consequences, such as CKD progression and muscle wasting. We review the findings from recent clinical trials that have examined the effects of sodium bicarbonate therapy and veverimer in patients with CKD and chronic metabolic acidosis. RECENT FINDINGS There are four recent clinical trials on chronic metabolic acidosis of CKD. In a pilot, cross-over study, 6 weeks of sodium bicarbonate therapy improved vascular endothelial function, measured by brachial artery flow-mediated dilation. In a single-center, randomized, open-label study, 6 months of sodium bicarbonate therapy increased muscle mass and lean body mass, and preserved kidney function. The other two clinical trials (phase 1/2 and phase 3 studies) examined the effects of veverimer, which is a hydrochloric acid binder. The phase 3 study showed that 12-weeks of veverimer increased serum bicarbonate levels and might improve physical function. The effects of veverimer on CKD progression, physical function and cardiovascular endpoints as well as its long-term safety are yet to be determined. SUMMARY Recent studies suggest that sodium bicarbonate therapy may improve vascular endothelial function and muscle mass, and preserve renal function. Veverimer increases serum bicarbonate level and could be a potential new therapeutic option for treating chronic metabolic acidosis.
-
7.
Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter?
Bushinsky, DA
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2019;(6):858-865
Abstract
Patients with chronic kidney disease (CKD) continue to produce endogenous acids but have a reduction in net acid excretion, resulting in a primary decrease in serum bicarbonate concentration, which is termed chronic metabolic acidosis. Recent prospective studies, along with retrospective cohort analyses, demonstrate a higher risk for CKD progression with untreated metabolic acidosis. To normalize serum bicarbonate levels, acidemic patients are often treated with sodium bicarbonate (NaHCO3) or sodium citrate, which have been shown to slow the progression of CKD. However, studies using this approach have routinely excluded patients with common sodium-sensitive comorbid conditions, such as poorly controlled hypertension, congestive heart failure, volume overload, or edema. This article examines the effect of the anion that accompanies sodium delivered with these therapies. Do the negative effects on blood pressure (BP) and sodium retention, as measured by an increase in edema, weight gain, and congestive heart failure, observed with oral administration of sodium chloride (NaCl) differ when a similar amount of sodium is given with bicarbonate or citrate in this patient population? A review of the literature suggests that NaHCO3 does not increase BP or sodium retention when administered to patients with CKD during a concurrent severe NaCl dietary restriction (∼10 mEq/d). However, this degree of NaCl restriction is feasible only under strict control in clinical research environments. In contrast, when NaHCO3 is given to patients without severe dietary NaCl restriction, there is an increase in BP and sodium retention. Thus, unless patients with CKD can tolerate a diet virtually devoid of NaCl, additional sodium, regardless of the accompanying anion, appears to increase BP and sodium retention.
-
8.
Distal renal tubular acidosis and severe hypokalemia: a case report and review of the literature.
Vasquez-Rios, G, Westrich, DJ, Philip, I, Edwards, JC, Shieh, S
Journal of medical case reports. 2019;(1):103
Abstract
BACKGROUND Distal renal tubular acidosis is a relatively infrequent condition with complex pathophysiology that can present with life-threatening electrolyte abnormalities. CASE PRESENTATION We describe a case of a 57-year-old Caucasian woman with previous episodes of hypokalemia, severe muscle weakness, and fatigue. Upon further questioning, symptoms of dry eye and dry mouth became evident. Initial evaluation revealed hyperchloremic metabolic acidosis, severe hypokalemia, persistent alkaline urine, and a positive urinary anion gap, suggestive of distal renal tubular acidosis. Additional laboratory workup and renal biopsy led to the diagnosis of primary Sjögren's syndrome with associated acute tubulointerstitial nephritis. After potassium and bicarbonate supplementation, immunomodulatory therapy with hydroxychloroquine, azathioprine, and prednisone was started. Nonetheless, her renal function failed to improve and remained steady with an estimated glomerular filtration rate of 42 ml/min/1.73 m2. The literature on this topic was reviewed. CONCLUSIONS Cases of renal tubular acidosis should be carefully evaluated to prevent adverse complications, uncover a potentially treatable condition, and prevent the progression to chronic kidney disease. Repeated episodes of unexplained hypokalemia could be an important clue for diagnosis.
-
9.
Evidence for biofilm acid neutralization by baking soda.
Zero, DT
Journal of the American Dental Association (1939). 2017;(11S):S10-S14
-
-
Free full text
-
Abstract
BACKGROUND The generating of acids from the microbial metabolism of dietary sugars and the subsequent decrease in biofilm pH below the pH at which tooth mineral begins to demineralize (critical pH) are the key elements of the dental caries process. Caries preventive strategies that rapidly neutralize biofilm acids can prevent demineralization and favor remineralization and may help prevent the development of sugar-induced dysbiosis that shifts the biofilm toward increased cariogenic potential. Although the neutralizing ability of sodium bicarbonate (baking soda) has been known for many years, its anticaries potential as an additive to fluoride dentifrice has received only limited investigation. TYPES OF STUDIES REVIEWED There is evidence that baking soda rapidly can reverse the biofilm pH decrease after a sugar challenge; however, the timing of when it is used in relation to a dietary sugar exposure is critical in that the sooner its used the greater the benefit in preventing a sustained biofilm pH decrease and subsequent demineralization. Furthermore, the effectiveness of baking soda in elevating biofilm pH appears to depend on concentration. Thus, the concentration of baking soda in marketed dentifrice products, which ranges from 10% to 65%, may affect their biofilm pH neutralizing performance. People with hyposalivation particularly may benefit from using fluoride dentifrice containing baking soda because of their diminished ability to clear dietary sugars and buffer biofilm acids. CONCLUSIONS Although promising, there is the need for more evidence that strategies that modify the oral ecology, such as baking soda, can alter the cariogenic (acidogenic and aciduric) properties of biofilm microorganisms. PRACTICAL IMPLICATIONS The acid neutralization of dental biofilm by using fluoride dentifrice that contains baking soda has potential for helping counteract modern high-sugar diets by rapidly neutralizing biofilm-generated acid, especially in people with hyposalivation.
-
10.
[Treatment of metabolic acidosis in patients with chronic kidney disease (CKD)].
Dębowska, M, Przedlacki, J
Wiadomosci lekarskie (Warsaw, Poland : 1960). 2017;(6 pt 2):1197-1200
Abstract
Metabolic acidosis becoming clinically apparent when glomerular filtration rate (GFR) decreases <30 ml/min/1,73m2. Although usually mild, it can have substantial adverse effects like: impair albumin biosynthesis and glucose metabolism, increase protein catabolism with a decrease of muscle mass, increase bone resorption and inhibition of its formation with growth retardation in children. At present KDIGO (Kidney Disease: Improving Global Outcomes) recommendations support oral sodium bicarbonate supplementation and maintaining HCO3 - concentration ≥22 mmol/l in all CKD patients.