scholarly journals The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Dimitrios Velissaris ◽  
Vasilios Karamouzos ◽  
Nikolaos Ktenopoulos ◽  
Charalampos Pierrakos ◽  
Menelaos Karanikolas
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Therapeutic Option ◽  
Ongoing Debate ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Bicarbonate Therapy ◽  
Reasonable Approach

Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option.Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years.Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gaspH>7.15.Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and more studies are required to determine the potential benefit, if any, of bicarbonate therapy in the sepsis patient with acidosis.

scholarly journals Prehospital Diagnosis of Shortness of Breath Caused by Profound Metformin-Associated Metabolic Acidosis

Healthcare ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 74
Author(s):  
Pietro Elias Fubini ◽  
Laurent Suppan
Keyword(s):  
Metabolic Acidosis ◽  
Hospital Setting ◽  
Blood Gases ◽  
Shortness Of Breath ◽  
Potential Harm ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Common Causes ◽  
Prehospital Diagnosis ◽  
Gas Measurement

Shortness of breath is a common complaint among patients in emergency medicine. While most common causes are usually promptly identified, less frequent aetiologies might be challenging to diagnose, especially in the pre-hospital setting. We report a case of prehospital dyspnoea initially ascribed to pulmonary oedema which turned out to be the result of profound metformin-associated metabolic acidosis. This diagnosis was already made during the prehospital phase by virtue of arterial blood gas measurement. Pre-hospital measurement of arterial blood gases is therefore feasible and can improve diagnostic accuracy in the field, thus avoiding unnecessary delay and potential harm to the patient before initiating the appropriate therapeutic actions.

scholarly journals Metabolic Acidosis in Patients with CKD: Epidemiology, Pathogenesis, and Treatment

2021 ◽  
pp. 1-16
Author(s):  
Marcin Adamczak ◽  
Stanisław Surma
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Current Knowledge ◽  
Venous Blood ◽  
The Body ◽  
Hydrogen Ions ◽  
Ckd Progression ◽  
New Drug ◽  
Treatment And Prevention

<b><i>Background:</i></b> Metabolic acidosis in CKD is diagnosed in patients with plasma or venous blood bicarbonate concentration lower than 22 mmol/L. Metabolic acidosis occurs in about 20% of patients with CKD. Metabolic acidosis may lead to dysfunction of many systems and organs as well as CKD progression. Currently, sodium bicarbonate is mainly used for pharmacological treatment of metabolic acidosis in patients with CKD. Veverimer is a new drug dedicated to treatment of metabolic acidosis in patients with CKD. Orally given veverimer binds hydrogen ions in the intestines and subsequently is excreted from the body with feces. Clinical studies have shown that veverimer is effective in increasing serum bicarbonate concentrations in CKD patients with metabolic acidosis. Here, we present review of the epidemiology, pathogenesis, diagnosis, treatment, and prevention of metabolic acidosis in CKD patients. <b><i>Summary:</i></b> Metabolic acidosis is common in patients with CKD and contributes to CKD progression and many complications, which worsen the prognosis in these patients. Currently, sodium bicarbonate is mainly used in metabolic acidosis treatment. The role of the new drug veverimer in the metabolic acidosis therapy needs further studies. <b><i>Key Message:</i></b> The aim of this review article is to summarize the current knowledge concerning the epidemiology, pathogenesis, diagnosis, treatment, and prevention of metabolic acidosis in CKD patients.

Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

1989 ◽  
Vol 256 (5) ◽  
pp. H1316-H1321 ◽  
Author(s):  
J. I. Shapiro ◽  
M. Whalen ◽  
R. Kucera ◽  
N. Kindig ◽  
G. Filley ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Ammonium Chloride ◽  
Respiratory Acidosis ◽  
Arterial Pco2 ◽  
Bicarbonate Therapy ◽  
Brain Ph ◽  
Dose Dependent ◽  
Intracellular Alkalinization

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

scholarly journals Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Sodium Bicarbonate ◽  
Negative Impact ◽  
Qtc Interval ◽  
Bicarbonate Therapy ◽  
Proximal Tubular ◽  
Acute Metabolic Acidosis ◽  
Renal Proximal Tubular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

scholarly journals Long-Term Oxygen Therapy in COPD: evidences and open questions of current indications

2016 ◽  
Vol 73 (1) ◽  
Author(s):  
A. Corrado ◽  
T. Renda ◽  
S. Bertini
Keyword(s):  
Oxygen Therapy ◽  
Supplemental Oxygen ◽  
Future Research ◽  
Chronic Obstructive ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Copd Patients ◽  
Number Of Patients ◽  
Long Term Oxygen Therapy

Long term oxygen therapy (LTOT) has been shown to improve the survival rate in Chronic Obstructive Pulmonary Disease (COPD) patients with severe resting hypoxemia by NOTT and MRC studies, published more than 25 years ago. The improved survival was found in patients who received oxygen for more than 15 hours/day. The effectiveness of LTOT has been documented only in stable COPD patients with severe chronic hypoxemia at rest (PaO255%. In fact no evidence supports the use of LTOT in COPD patients with moderate hypoxemia (55&lt;PaO2&lt;65 mmHg), and in those with decreased oxygen saturation (SO2&lt;90%) during exercise or sleep. Furthermore, it is generally accepted without evidence that LTOT in clinical practice is warranted in other forms of chronic respiratory failure not due to COPD when arterial blood gas criteria match those established for COPD patients. The prescription of oxygen in these circumstances, as for unstable patients, increases the number of patients receiving supplemental oxygen and the related costs. Comorbidities are likely to affect both prognosis and health outcomes in COPD patients, but at the moment we do not know if LTOT in these patients with complex chronic diseases and mild-moderate hypoxemia could be of any use. For these reasons a critical revision of the actual guide lines indications for LTOT in order to optimise effectiveness and costs, and future research in the areas that have not previously been addressed by NOTT and MRC studies, are mandatory.

Role of EP2 and EP3 PGE2receptors in control of murine renal hemodynamics

2001 ◽  
Vol 280 (1) ◽  
pp. H327-H333 ◽  
Author(s):  
Laurent P. Audoly ◽  
Xiaoping Ruan ◽  
Victoria A. Wagner ◽  
Jennifer L. Goulet ◽  
Stephen L. Tilley ◽  
...  
Keyword(s):  
Renal Artery ◽  
Vascular Reactivity ◽  
Renal Hemodynamics ◽  
Receptor Subtypes ◽  
Male Mice ◽  
Unique Role ◽  
Arterial Blood ◽  
Renal Vascular

The kidney plays a central role in long-term regulation of arterial blood pressure and salt and water homeostasis. This is achieved in part by the local actions of paracrine and autacoid mediators such as the arachidonic acid-prostanoid system. The present study tested the role of specific PGE2 E-prostanoid (EP) receptors in the regulation of renal hemodynamics and vascular reactivity to PGE2. Specifically, we determined the extent to which the EP2 and EP3 receptor subtypes mediate the actions of PGE2 on renal vascular tone. Renal blood flow (RBF) was measured by ultrasonic flowmetry, whereas vasoactive agents were injected directly into the renal artery of male mice. Studies were performed on two independent mouse lines lacking either EP2or EP3 (−/−) receptors and the results were compared with wild-type controls (+/+). Our results do not support a unique role of the EP2 receptor in regulating overall renal hemodynamics. Baseline renal hemodynamics in EP2−/− mice [RBF EP2−/−: 5.3 ± 0.8 ml · min−1 · 100 g kidney wt−1; renal vascular resistance (RVR) 19.7 ± 3.6 mmHg · ml−1 · min · g kidney wt] did not differ statistically from control mice (RBF +/+: 4.0 ± 0.5 ml · min−1 · 100 g kidney wt−1; RVR +/+: 25.4 ± 4.9 mmHg · ml−1 · min · 100 g kidney wt−1). This was also the case for the peak RBF increase after local PGE2 (500 ng) injection into the renal artery (EP2−/−: 116 ± 4 vs. +/+: 112 ± 2% baseline RBF). In contrast, we found that the absence of EP3receptors in EP3−/− mice caused a significant increase (43%) in basal RBF (7.9 ± 0.8 ml · min−1 · g kidney wt−1, P < 0.05 vs. +/+) and a significant decrease (41%) in resting RVR (11.6 ± 1.4 mmHg · ml−1 · min · g kidney wt−1, P < 0.05 vs. +/+). Local administration of 500 ng of PGE2 into the renal artery caused more pronounced renal vasodilation in EP3−/− mice (128 ± 2% of basal RBF, P < 0.05 vs. +/+). We conclude that EP3 receptors mediate vasoconstriction in the kidney of male mice and its actions are tonically active in the basal state. Furthermore, EP3receptors are capable of buffering PGE2-mediated renal vasodilation.

scholarly journals Risk Potential for Organ Dysfunction Associated with Sodium Bicarbonate Therapy (SBT) in Critically Ill Patients with Hemodynamic Worsening

2021 ◽  
Author(s):  
Tiehua Wang ◽  
Lingxian Yi ◽  
Hua Zhang ◽  
Tianhao Wang ◽  
Jingjing Xi ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Critically Ill ◽  
Organ Dysfunction ◽  
Critically Ill Patients ◽  
Control Group ◽  
Increased Risk ◽  
Bicarbonate Therapy ◽  
Risk Potential

Abstract Background: The role of sodium bicarbonate therapy (SBT) remains controversial. This study aimed to investigate whether hemodynamic status before SBT contributed to the heterogeneous outcomes associated with SBT in acute critically ill patients.Methods: We obtained data from patients with metabolic acidosis from the Medical Information Mart for Intensive Care (MIMIC)-III database. Propensity score matching (PSM) was applied to match the SBT group with the control group. Logistic regression and Cox regression were used to analyze a composite of newly “developed or exacerbated organ dysfunction” (d/eOD) within 7 days of ICU admission and 28-day mortality associated with SBT for metabolic acidosis.Results: A total of 1765 patients with metabolic acidosis were enrolled, and 332 pairs obtained by PSM were applied to the final analyses in the study. An increased incidence of newly d/eOD was observed in the SB group compared with the control group (54.8% vs 44.6%, p<0.01). Multivariable logistic regression indicated that the adjusted OR of SBT for this composite outcome was no longer significant [OR (95% CI): 1.39 (0.9, 1.85); p=0.164]. This effect of SBT did not change with the quintiles stratified by pH. Interestingly, SBT was associated with an increased risk of the composite of newly d/eOD in the subgroup of patients with worsening hemodynamics before SBT [adjusted OR (95% CI): 3.6 (1.84, 7.22), p< 0.001]. Moreover, the risk potential for this composite of outcomes was significantly increased in patients characterized by both worsening [adjusted OR (95% CI): 2.91 (1.54, 5.47), p< 0.001] and unchanged hemodynamics [adjusted OR (95% CI): 1.94 (1.01, 3.72), p=0.046) compared to patients with improved hemodynamics before SBT. Our study failed to demonstrate an association between SBT and 28-day mortality in acute critically ill patients with metabolic acidosis.Conclusions: Our findings suggested that SBT for metabolic acidosis was associated with an increased risk potential for subsequent d/eOD, while the hemodynamic status remained unstable during the acute phase of critical illness.

Successful Treatment of Experimental Neonatal Respiratory Failure Using Extracorporeal Membrane Lung Assist

1986 ◽  
Vol 9 (6) ◽  
pp. 427-432 ◽  
Author(s):  
R. Fumagalli ◽  
T. Kolobow ◽  
P. Arosio ◽  
V. Chen ◽  
D.K. Buckhold ◽  
...  
Keyword(s):  
Respiratory Failure ◽  
Pulmonary Ventilation ◽  
Blood Gases ◽  
Blood Gas ◽  
Arterial Blood Gases ◽  
Arterial Blood Gas ◽  
Membrane Lung ◽  
Arterial Blood ◽  
Long Term Survivors

A total of 44 preterm fetal lambs at great risk of developing respiratory failure were delivered by Cesarean section, and were then managed on conventional mechanical pulmonary ventilation. Fifteen animals initially fared well, and 14 of these were long term survivors. Twenty-nine other lambs showed a progressive deterioration in arterial blood gases within 30 minutes of delivery, of which 10 lambs were continued on mechanical pulmonary ventilation (20% survival), while the remaining 19 lambs were placed on an extracorporeal membrane lung respiratory assist (79% survival). Extracorporeal membrane lung bypass rapidly corrected arterial blood gas values, and permitted the use of high levels of CPAP instead of the continuation of mechanical pulmonary ventilation at high peak airway pressures. Improvement in lung function was gradual, and predictable. Early institution of extracorporeal respiratory assist using a membrane artificial lung rapidly corrected arterial blood gas values and significantly improved on neonate survival.

Effect of temperature on arterial blood gas tensions and pH during exercise

1964 ◽  
Vol 19 (2) ◽  
pp. 243-245 ◽  
Author(s):  
Alf Holmgren ◽  
Malcolm B. McIlroy
Keyword(s):  
Metabolic Acidosis ◽  
Normal Subjects ◽  
Bicycle Ergometer ◽  
Effect Of Temperature ◽  
Membrane Diffusion ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Capillary Membrane ◽  
Severe Exercise ◽  
Alveolar Capillary

We measured arterial blood Po2, Pco2 and pH at rest and during a standard exercise test on a bicycle ergometer in ten normal subjects. In five we measured esophageal and five arterial blood temperature during the exercise and corrected the arterial blood values to the temperature at the time the samples were collected. We found an average rise in temperature of 1 C (range 0.2–1.6 C) during exercise lasting about 30 min at loads up to an average of 1,200 kg-m/min. At the highest load the average correction for PaOO2 was 5.6 mm Hg, for PaCOCO2 1.6 mm Hg and for pH 0.014 units. Our corrected values showed a fall in PaCOCO2 and pH and a rise in PaOO2 during severe exercise. These findings are compatible with the development of a metabolic acidosis during severe exercise and indicate that our subjects were not limited by diffusion across the alveolar-capillary membrane. metabolic acidosis; alveolar capillary membrane diffusion; hyperventilation; PaOO2 and PaCOCO2 in severe exercise Submitted on June 17, 1963

Ventilatory response to moderate and severe hypoxia in adult dogs: role of endorphins

1988 ◽  
Vol 65 (3) ◽  
pp. 1383-1388 ◽  
Author(s):  
J. I. Schaeffer ◽  
G. G. Haddad
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Before And After ◽  
The Relationship ◽  
Arterial Po2

To determine the role of opioids in modulating the ventilatory response to moderate or severe hypoxia, we studied ventilation in six chronically instrumented awake adult dogs during hypoxia before and after naloxone administration. Parenteral naloxone (200 micrograms/kg) significantly increased instantaneous minute ventilation (VT/TT) during severe hypoxia, (inspired O2 fraction = 0.07, arterial PO2 = 28-35 Torr); however, consistent effects during moderate hypoxia (inspired O2 fraction = 0.12, arterial PO2 = 40-47 Torr) could not be demonstrated. Parenteral naloxone increased O2 consumption (VO2) in severe hypoxia as well. Despite significant increases in ventilation post-naloxone during severe hypoxia, arterial blood gas tensions remained the same. Control studies revealed that neither saline nor naloxone produced a respiratory effect during normoxia; also the preservative vehicle of naloxone induced no change in ventilation during severe hypoxia. These data suggest that, in adult dogs, endorphins are released and act to restrain ventilation during severe hypoxia; the relationship between endorphin release and moderate hypoxia is less consistent. The observed increase in ventilation post-naloxone during severe hypoxia is accompanied by an increase in metabolic rate, explaining the isocapnic response.

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