Comparison of end-tidal carbon dioxide and arterial blood bicarbonate levels in patients with metabolic acidosis referred to emergencymedicine (original) (raw)
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Pathophysiology, Evaluation and Management of Metabolic Acidosis
Metabolic acidosis is a reduction in blood pH due to a primary reduction in serum bicarbonate (HCO 3 −). It is associated with a secondary reduction in carbon dioxide arterial pressure (P a CO 2). Metabolic acidosis can be acute or chronic. Acute metabolic acidosis results from excess organic acids as in lactic acidosis, while chronic metabolic acidosis reflects reduced renal acidification. Metabolic acidosis is further classified into anion-gap (AG-MA) and hyperchloremic (normal anion-gap [NAG-MA]) based on serum anion gap (AG). Metabolic acidosis has adverse effects on a variety of body functions. Although base administration is helpful in the management of chronic metabolic acidosis, it is controversial in acute metabolic acidosis. Treatment of the underlying cause is the cornerstone of the management of acute metabolic acidosis.
Approach to the patient with metabolic acidosis: Newer concepts
Nephrology, 1996
A new classification for patients with metabolic acidosis is provided: a pathophysiological classification. To recognize an overproduction of acids which results in a hydrogen ion (H') gain the number of new anions retained in the body is added to those excreted in the urine when the cation accompanying them was not H or ammonium (NH,'). The first tools are to recognize new anions that were added during the overproduction of acids. The nature of these anions can be recognized by assessing their fractional excretion. The second set of tools focuses on an assessment of NH,* in the urine using urine anion and osmolar gaps. The clinical approach suggested focuses on detecting an emergency (severity of H accumulation, toxic alcohols and/or dyskalaemias). The second step analyzes the expected responses to acidaemia; here the focus is on the P,,, in vital organs and the rate of excretion of ammonium. The principles used for diagnosis and treatment of metabolic acidosis are illustrated by a case example.
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.]
The aims of this study were to determine whether standard base excess (SBE) is a useful diagnostic tool for metabolic acidosis, whether metabolic acidosis is clinically relevant in daily evaluation of critically ill patients, and to identify the most robust acid-base determinants of SBE. Thirty-one critically ill patients were enrolled. Arterial blood samples were drawn at admission and 24 h later. SBE, as calculated by Van Slyke's (SBE VS) or Wooten's (SBE W) equations, accurately diagnosed metabolic acidosis (AUC = 0.867, 95%CI = 0.690-1.043 and AUC = 0.817, 95%CI = 0.634-0.999, respectively). SBE VS was weakly correlated with total SOFA (r = -0.454, P < 0.001) and was similar to SBE W (r = -0.482, P < 0.001). All acid-base variables were categorized as SBE VS <-2 mEq/L or SBE VS <-5 mEq/L. SBE VS <-2 mEq/L was better able to identify strong ion gap acidosis than SBE VS <-5 mEq/L; there were no significant differences regarding other variables. To demonst...
The patient with a severe degree of metabolic acidosis: a deductive analysis
QJM, 2006
This teaching exercise demonstrates how principles of physiology might help in identifying the cause of a particularly severe case of metabolic acidosis and making appropriate decisions about therapy. The patient's plasma pH was 7.00 and their plasma bicarbonate concentration was 2 mmol/l. Because the time course of the patient's illness was believed to be <24 h, this suggested that a large quantity of acid had been added to the body in this short time period, but the medical team managing the case could not identify any acid that could have been produced rapidly by endogenous processes, or was ingested by the patient. Moreover, there was a question about how such a very low arterial PCO 2 (8 mmHg) could be sustained. Even once the diagnosis was made, there were issues to resolve concerning therapy. These included questions about how much sodium bicarbonate to administer, and what dangers might arise during this therapy. The missing links in this interesting story emerge during a discussion between the medical team and their imaginary mentor, Professor McCance.
Bicarbonate Therapy for Critically Ill Patients with Metabolic Acidosis: A Systematic Review
Cureus, 2019
The management of acid-base disorders always calls for precise diagnosis and treatment of the underlying disease. Sometimes additional means are necessary to combat systemic acidity itself. In this systematic review, we discuss the concept and some specific aspects of bicarbonate therapy for critically ill patients with metabolic acidosis (i.e., patients with blood pH < 7.35). We conducted a systematic literature review of three online databases (PubMed, Google Scholar, and Cochrane) in November 2018 to validate usage of bicarbonate therapy for critically ill patients with metabolic acidosis. Twelve trials and case series were included in the final analysis, from which we assessed population, intervention, comparison, and outcome data. The current literature suggests limited benefit from bicarbonate therapy for patients with severe metabolic acidosis (pH < 7.1 and bicarbonate < 6 mEq/L). However, bicarbonate therapy does yield improvement in survival for patients with accompanying acute kidney injury.
Critical Care, 2021
Background Metabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic acidosis in the ICU are poorly understood. Method This was an international retrospective observational study in 18 ICUs in Australia, Japan, and Taiwan. Adult patients were consecutively screened, and those with early metabolic acidosis (pH < 7.3 and a Base Excess < –4 mEq/L, within 24-h of ICU admission) were included. Screening continued until 10 patients who received and 10 patients who did not receive sodium bicarbonate in the first 24 h (early bicarbonate therapy) were included at each site. The primary outcome was ICU mortality, and the association between sodium bicarbonate and the clinical outcomes were assessed using regression analysis with generalized linear mixed model. Results We screened 9437 patients. Of these, 1292 had early metabolic acidosis (14.0%). Early sodium bicarbonate was give...
International Journal of General Medicine, 2021
Background: Metabolic acidosis is the most frequent medical condition occurring in critically ill renally compromised patients. This study was aimed to determine clinical outcomes of bicarbonate therapy in renally compromised critically ill patients having metabolic acidosis. Methods: A prospective longitudinal cohort study was undertaken in three military hospitals in Rawalpindi, Pakistan. All patients fulfilling the inclusion criteria who were admitted to the ICU of any of the three study hospitals from July 2019 to March 2020 were studied for clinical outcomes of bicarbonate therapy using an evidence-based clinical checklist. Outcome measures include changes in blood pH, serum potassium, and sodium levels, blood pressure and weight, along with other clinically significant laboratory parameters. Results: Eighty-one patients fulfilling the inclusion criteria were evaluated. The mean age of the patients was 55.61±19.5 years, while the mean weight was 63.43±14.19 Kg. A mortality rate of 45.7% was observed. Disease-related complications including hypoxia, cardiac failure, multiple organ failure, elevated blood pressure, and ischemic heart disease (IHD) were found to be associated with a higher mortality rate (P<0.005). Whereas using Fisher's exact test, concomitant administration of sodium chloride, along with bicarbonate therapy was associated with a low mortality rate and had no significant impact on sodium loading or weight gain. Moreover, various drug-drug interactions were found to be associated with a higher mortality rate (P<0.05). Conclusion: Bicarbonate therapy was not found to affect the mortality rate in critically ill renally compromised patients with metabolic acidosis.