Ramen noodle neuropathy: an atypical case of partial paralysis from malnutrition.

INTRODUCTION: Due to a COVID-related job loss resulting in financial and food insecurity, a 28-year-old woman initiated a diet consisting solely of one cup of ramen noodles daily for twenty-two months, leading to 27 kg of weight loss. Ramen noodles are low in calories and lack key nutrients, including potassium, chloride, and vitamin B12. CASE DESCRIPTION: The patient presented to the emergency department with acute, worsening weakness and paresthesias in her left wrist and hand. Exam revealed no other abnormalities aside from a cachectic appearance. Labs revealed marked hypokalemia, hypochloremia, lactic acidosis, a mixed metabolic alkalosis with respiratory acidosis, and low levels of zinc and copper. An EKG revealed a prolonged QT interval. After a neurology and psychiatry consult, the patient was admitted for failure to thrive with malnutrition, peripheral neuropathy, hypokalemia, and an acid-base disorder. An MRI of the brain was unremarkable. Studies of other nutritional deficiencies, autoimmune conditions, and sexually transmitted infections were unremarkable. The patient received food and vitamin supplementation, was monitored for re-feeding syndrome, and had a significant recovery. DISCUSSION: After stroke, spinal injury, multiple sclerosis, and the most common focal mononeuropathies were ruled out, the clinical focus turned to nutritional deficiencies, the most significant of which was hypokalemia. Prior research has shown that severe hypokalemia can lead to weakness. It has also shown that chronically insufficient dietary intake is a common cause of hypokalemia. This case, with its partial paralysis of a unilateral upper extremity, may add to the known clinical manifestations of hypokalemia. We review the role of hypokalemia and hypochloremia in acid-base dynamics. Etiologies and clinical manifestations of cobalamin, thiamine, pyridoxine, and copper deficiencies, along with lead toxicity, are also discussed. Diagnostic clarity of mononeuropathies in the context of malnutrition and hypokalemia can be aided by urine potassium levels prior to repletion, neuroimaging that includes the cervical spine, and follow-up electromyography.

ClC-K2 Cl- channel allows identification of A- and B-type of intercalated cells in split-opened collecting ducts.

The collecting duct is a highly adaptive terminal part of the nephron, which is essential for maintaining systemic homeostasis. Principal and intercalated cells perform different physiological tasks and exhibit distinctive morphology. However, acid-secreting A- and base secreting B-type of intercalated cells cannot be easily separated in functional studies. We used BCECF-sensitive intracellular pH (pHi ) measurements in split-opened collecting ducts followed by immunofluorescent microscopy in WT and intercalated cell-specific ClC-K2-/- mice to demonstrate that ClC-K2 inhibition enables to distinguish signals from A- and B-intercalated cells. We show that ClC-K2 Cl- channel is expressed on the basolateral side of intercalated cells, where it governs Cl- -dependent H+ /HCO3- transport. ClC-K2 blocker, NPPB, caused acidification or alkalization in different subpopulations of intercalated cells in WT but not ClC-K2-/- mice. Immunofluorescent assessment of the same collecting ducts revealed that NPPB increased pHi in AE1-positive A-type and decreased pHi in pendrin-positive B-type of intercalated cells. Induction of metabolic acidosis led to a significantly augmented abundance and H+ secretion in A-type and decreased proton transport in B-type of intercalated cells, whereas metabolic alkalosis caused the opposite changes in intercalated cell function, but did not substantially change their relative abundance. Overall, we show that inhibition of ClC-K2 can be employed to discriminate between A- and B-type of intercalated cells in split-opened collecting duct preparations. We further demonstrate that this method can be used to independently monitor changes in the functional status and abundance of A- and B-type in response to systemic acid/base stimuli.

Determinants of hypokalemia following hypertonic sodium bicarbonate infusion.

The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, - 0.16 to - 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses.

Acid content and buffer-capacity: a charge-balance perspective.

Rational treatment and thorough diagnostic classification of acid-base disorders requires quantitative understanding of the mechanisms that generate and dissipate loads of acid and base. A natural precondition for this tallying is the ability to quantify the acid content in any specified fluid. Physical chemistry defines the pH-dependent charge on any buffer species, and also on strong ions on which, by definition, the charge is pH-invariant. Based, then, on the requirement of electroneutrality and conservation of mass, it was shown in 1914 that pH can be calculated and understood on the basis of the chemical composition of any fluid. Herein we first show that this specification for [H+] of the charge-balance model directly delivers the pH-dependent buffer-capacity as defined in the literature. Next, we show how the notion of acid transport as proposed in experimental physiology can be understood as a change in strong ion difference, ΔSID. Finally, based on Brønsted-Lowry theory we demonstrate that by defining the acid content as titratable acidity, this is equal to SIDref - SID, where SIDref is SID at pH 7.4. Thereby, any chemical situation is represented as a curve in a novel diagram with titratable acidity = SIDref - SID as a function of pH. For any specification of buffer chemistry, therefore, the change in acid content in the fluid is path invariant. Since constituents of SID and titratable acidity are additive, we thereby, based on first principles, have defined a new framework for modeling acid balance across a cell, a whole organ, or the whole-body.

Comparison of a modified Story approach to traditional evaluation of acid-base disturbances in patients with shock: a cohort study.

To compare whether the diagnostic evaluation of metabolic acidosis can be improved by using a modified Story method compared to the traditional evaluation in a population of critically ill patients with shock. This prospective cohort study included shock patients admitted to the ICU of a tertiary hospital in Brazil between May 2018 and November 2019. We collected laboratory data necessary for traditional evaluation and the simplified Stewart's method. During the study period, 149 patients were included in the final analysis. Of the 17 patients with a normal SBE and AGcorrected, 13 (76.5%) presented with metabolic acidosis according to the modified Story assessment. Therefore, of the 149 patients included in the study, the traditional approach failed to identify metabolic acidosis that was identified by the modified Story assessment in 13 (8.7%) patients. In addition, the determination of the severity of metabolic acidosis also differed between the two methods by a mean of - 7.8 mEq/L. We found that a modified Story method can identify and quantify metabolic acidosis in patients with disorders that were not revealed by the traditional approach.

Arterial Blood Gas and Rotational Thromboelastometry Parameters in Healthy Rescuers Incidentally Exposed to Nitroglycerin, Nitrogen Compounds, and Combustion Products.

INTRODUCTION: Acute exposure to nitrogen compounds combined with a massive inhalation of air pollutants can influence respiratory and cardiovascular symptoms and coagulation abnormalities in accidentally exposed healthy adults during cave detonation operations. METHODS: Italian alpine and cave rescuers widened a cave in the Abisso Luca Kralj in Trieste, Italy. Volunteers inside the cave were accidentally exposed to the fumes from an uncontrolled detonation of blasting gelatin microcharges. We performed a retrospective cohort study on the clinical data, arterial blood gas analysis, and rotational thromboelastometry parameters from the rescuers involved in the accident. RESULTS: Ninety-three healthy rescuers were involved in the uncontrolled detonation: 47 volunteers handled a mixture of nitrogen compounds (blaster group), and 46 volunteers did not (nonblaster group). After the accident, statistically significant differences (P<0.05) in arterial blood gas values were observed between the groups, with a pattern of mild respiratory acidosis with hypercapnia in the nonblaster group and severe mixed acid-base disorder with hypoxia and hypercapnia in the blaster group. Mild hyperfibrinolysis was observed in 44 volunteers in the blaster group, as were associated bleeding symptoms in 34 volunteers; no significant coagulation modifications were recorded in the nonblaster group. CONCLUSIONS: Respiratory acidosis with hypoxia, hypercapnia, a compensatory metabolic response, and mild hyperfibrinolysis were probably related to the combined effect of nitrogen compounds and the inhaled toxic products of detonation. Therefore, each element exerts a determinant effect on promoting the biological toxicity of the others.

Urinary Diversion: Core Curriculum 2021.

Urinary diversion after cystectomy has been a historical standard for the treatment of numerous benign and malignant diseases of the bladder. Since the first published description in the early 1900s, improvements in surgical technique and a better understanding of the metabolic sequelae postoperatively have greatly enhanced patient outcomes. Both continent and incontinent diversions are available to patients after cystectomy. In appropriately selected patients, orthotopic neobladder reconstruction can offer preservation of body image and continence, and continent cutaneous diversions represent a reasonable alternative. Conduit diversion, which remains the most commonly performed diversion technique, is ideal for patients who would benefit from a less morbid surgical procedure that negates the need for self-catheterization. This installment of the Core Curriculum in Nephrology outlines numerous aspects of urinary diversion, in which a multidisciplinary approach to postoperative management at the intersection of nephrology and urology is required to effectively optimize patient outcomes. This article includes a discussion of the various reconstructive options after cystectomy as well as a comprehensive review of frequently encountered short-term and long-term metabolic abnormalities associated with altered electrolyte and acid-base homeostasis.

Approach to Patients With High Anion Gap Metabolic Acidosis: Core Curriculum 2021.

The anion gap (AG) is a mathematical construct that compares the blood sodium concentration with the sum of the chloride and bicarbonate concentrations. It is a helpful calculation that divides the metabolic acidoses into 2 categories: high AG metabolic acidosis (HAGMA) and hyperchloremic metabolic acidosis-and thereby delimits the potential etiologies of the disorder. When the [AG] is compared with changes in the bicarbonate concentration, other occult acid-base disorders can be identified. Furthermore, finding that the AG is very small or negative can suggest several occult clinical disorders or raise the possibility of electrolyte measurement artifacts. In this installment of AJKD's Core Curriculum in Nephrology, we discuss cases that represent several very common and several rare causes of HAGMA. These case scenarios highlight how the AG can provide vital clues that direct the clinician toward the correct diagnosis. We also show how to calculate and, if necessary, correct the AG for hypoalbuminemia and severe hyperglycemia. Plasma osmolality and osmolal gap calculations are described and when used together with the AG guide appropriate clinical decision making.

Tackling acid-base disorders, one Twitter poll at a time.

Understanding and interpretation of acid-base disorders is an important clinical skill that is applicable to the majority of physicians. Although this topic is taught early in medical school, acid-base disturbances have been described as challenging by postgraduate trainees. We describe the use of Twitter, an online microblogging platform, to augment education in acid-base disturbances by using polls in which the user is shown laboratory values and then asked to select the most likely etiology of the disorder. The answer and a brief explanation are then shared in a subsequent tweet. Both polling questions and answers are shared from the account for the online, mobile-optimized, nephrology teaching tool NephSIM (https://www.nephsim.com/). An anonymous survey was administered to assess attitudes toward these polls. Using Twitter as an approach to enhance teaching of acid-base disturbances was both feasible and an engaging way to teach a challenging topic for trainees and physicians. Moreover, the coronavirus disease 2019 (COVID-19) pandemic has demonstrated the importance of incorporating virtual learning opportunities in all levels of medical education.

Acetazolamide Causes Worsening Acidosis in Uncompensated COPD Exacerbations: Increased Awareness Needed for Patient Safety.

BACKGROUND: Acetazolamide has been studied extensively in post-hypercapnic alkalosis as a tool to facilitate ventilator weaning in chronic obstructive pulmonary disease (COPD). It has also been utilized to facilitate respiratory drive in nonmechanically ventilated patients with COPD. Although this is generally a forgiving intervention, providers must carefully select patients for this medication, as it can cause severe acidosis and deterioration of clinical status in severe COPD cases. The present report describes two cases of patients who developed worsening acidosis and hypercapnia after receiving acetazolamide in acute respiratory failure. CASE REPORT: Case 1 was a 72-year-old obese male with COPD who was dependent on supplemental oxygen and presented to the emergency department (ED) with acute on chronic hypercapnic respiratory failure. He was given a one-time dose of acetazolamide in the ED for "respiratory failure made worse by severe metabolic alkalosis." His arterial blood gas (ABG) worsened overnight, accompanied by decreased mental status: pH 7.32, paCO2 82 mm Hg, paO2 50 mm Hg, HCO3 41.7 mmol/L, FiO2 32% to pH 7.21, paCO2 91.7 mm Hg, paO2 59 mm Hg, HCO3 36.6 mmol/L, and FiO2 32%. Case 2 was a 62-year-old male with COPD who was dependent on supplemental oxygen and presented to the ED with acute on chronic hypercapnic respiratory failure. He was given acetazolamide in the ED with similar results: ABG on presentation pH 7.37, paCO2 79.3 mm Hg, paO2 77.6 mm Hg, HCO3 45.5 mmol/L, and FiO2 32%. The next morning, ABG was pH 7.29, paCO2 79 mm Hg, paO2 77 mm Hg, HCO3 45.5 mmol/L, and FiO2 32%. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Acetazolamide given early in the uncompensated setting can worsen acidosis and potentiate clinical deterioration.

Re-Evaluation of Total CO2 Concentration in Apparently Healthy Younger Adults.

The initial assessment of acid-base status is usually based on the measurement of total CO2 concentration ([TCO2]) in venous blood, a surrogate for [HCO3-]. Previously, we posited that the reference limits of serum [TCO2] in current use are too wide. Based on studies on the acid-base composition of normal subjects, we suggested that the reference limits of serum [TCO2] at sea level be set at 23-30 mEq/L. To validate this proposal, we queried the University of California at Los Angeles (UCLA's) Integrated Clinical and Research Data Repository, a database containing information on 4.5 million patients seen at UCLA from 2006 to the present. Criteria for inclusion included adults (18-40 years of age), who were free of disorders that could affect acid-base balance, were not taking medications that could affect acid-base balance, and were seen for a routine medical examination or immunization in the outpatient setting. The number of individuals who met the inclusion criteria (52% female and 48% male) was 28,480, with a mean age of 28.9 ± 5.1 years. The mean serum [TCO2] level was slightly higher in males than females, 26.6 ± 2.16 mEq/L vs. 25.0 ± 2.11 mEq/L (p < 0.05). Ninety-one percent of patient values were within the proposed 23-30 mEq/L range and 61.7% were within the 24-27 mEq/L range. These findings validate our proposal that the reference range of serum [TCO2] in venous blood at sea level be narrowed to 23-30 mEq/L. Subjects with serum [TCO2] outside this range might require assessment with a venous blood gas to exclude the presence of clinically important acid-base disorders.

Acid-base disorders in liver disease.

Alongside the kidneys and lungs, the liver has been recognised as an important regulator of acid-base homeostasis. While respiratory alkalosis is the most common acid-base disorder in chronic liver disease, various complex metabolic acid-base disorders may occur with liver dysfunction. While the standard variables of acid-base equilibrium, such as pH and overall base excess, often fail to unmask the underlying cause of acid-base disorders, the physical-chemical acid-base model provides a more in-depth pathophysiological assessment for clinical judgement of acid-base disorders, in patients with liver diseases. Patients with stable chronic liver disease have several offsetting acidifying and alkalinising metabolic acid-base disorders. Hypoalbuminaemic alkalosis is counteracted by hyperchloraemic and dilutional acidosis, resulting in a normal overall base excess. When patients with liver cirrhosis become critically ill (e.g., because of sepsis or bleeding), this fragile equilibrium often tilts towards metabolic acidosis, which is attributed to lactic acidosis and acidosis due to a rise in unmeasured anions. Interestingly, even though patients with acute liver failure show significantly elevated lactate levels, often, no overt acid-base disorder can be found because of the offsetting hypoalbuminaemic alkalosis. In conclusion, patients with liver diseases may have multiple co-existing metabolic acid-base abnormalities. Thus, knowledge of the pathophysiological and diagnostic concepts of acid-base disturbances in patients with liver disease is critical for therapeutic decision making.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed.

Beyond bicarbonate: complete acid-base assessment in patients receiving intermittent hemodialysis.

Background: Acid-base assessments in hemodialysis patients have been limited almost entirely to measurements of total CO 2 concentration, and assumptions have been made about the presence of acid-base disorders. To gain a fuller understanding of the acid-base status of stable hemodialysis patients, we analyzed measurements of pCO 2 , pH and HCO 3 - obtained in a cohort of chronic stable hemodialysis patients over a 5-year period. Methods: We reviewed acid-base measurements taken pre-dialysis from fistula blood in 53 outpatients receiving hemodialysis thrice weekly between 2008 and 2012. In these patients, pH and pCO 2 were measured using an onsite blood gas analyzer, and HCO 3 - was computed. Relevant clinical and laboratory data were obtained from medical records. Factors affecting serum HCO 3 - were identified. Simple and mixed acid-base disorders were diagnosed using accepted rules. Results: Serum HCO 3 - was affected by age, normalized protein catabolic rate, interdialytic weight gain and length of interval between treatments. As expected, metabolic acidosis was the most common acid-base disorder, but respiratory acid-base disturbances, as simple or complex disorders, were found in 41% of the measurements. Respiratory alkalosis was seen more frequently than respiratory acidosis, but the latter disorder was more commonly associated with serious comorbidities. Conclusions: Respiratory acid-base disorders are an important component of the acid-base abnormalities seen in hemodialysis patients and are not identified by measuring total CO 2 concentration; hence, complete acid-base measurements are needed to determine the components of hemodialysis patients' acid-base status that are contributing to mortality risk.

Assessing Acid-Base Status: Physiologic Versus Physicochemical Approach.

The physiologic approach has long been used in assessing acid-base status. This approach considers acids as hydrogen ion donors and bases as hydrogen ion acceptors and the acid-base status of the organism as reflecting the interaction of net hydrogen ion balance with body buffers. In the physiologic approach, the carbonic acid/bicarbonate buffer pair is used for assessing acid-base status and blood pH is determined by carbonic acid (ie, Paco2) and serum bicarbonate levels. More recently, the physicochemical approach was introduced, which has gained popularity, particularly among intensivists and anesthesiologists. This approach posits that the acid-base status of body fluids is determined by changes in the dissociation of water that are driven by the interplay of 3 independent variables: the sum of strong (fully dissociated) cation concentrations minus the sum of strong anion concentrations (strong ion difference); the total concentration of weak acids; and Paco2. These 3 independent variables mechanistically determine both hydrogen ion concentration and bicarbonate concentration of body fluids, which are considered as dependent variables. Our experience indicates that the average practitioner is familiar with only one of these approaches and knows very little, if any, about the other approach. In the present Acid-Base and Electrolyte Teaching Case, we attempt to bridge this knowledge gap by contrasting the physiologic and physicochemical approaches to assessing acid-base status. We first outline the essential features, advantages, and limitations of each of the 2 approaches and then apply each approach to the same patient presentation. We conclude with our view about the optimal approach.

Hyperchloremic metabolic acidosis following plasma exchange during myasthenia gravis crisis.

BACKGROUND: Therapeutic plasma exchanges are increasingly used, notably during myasthenia gravis crisis. Repeated exchanges may induce severe adverse events. CASE: We reported a case of symptomatic hyperchloremic metabolic acidosis following a therapeutic plasma exchange. Analysis of 4% albumin substitution solution revealed a chloride concentration of 145 mmol/L, which could explain this acidosis. DISCUSSION: Infusion of high volume of 4% albumin during plasma exchanges may produce hyerchloremic metabolic acidosis. CONCLUSION: Special attention should be paid when repeated plasma exchanges are performed. J. Clin. Apheresis 31:479-480, 2016. © 2015 Wiley Periodicals, Inc.

Diabetic ketoacidosis masked by both Euglycemia and a primary metabolic alkalosis.

Diabetic ketoacidosis (DKA) is an acute, life-threatening metabolic complication of diabetes classically associated with hyperglycemia, metabolic acidosis, and ketosis. Though relatively uncommon, patients can also develop DKA with relative euglycemia, further complicating diagnosis. Here, we describe the case of a patient who presented with intractable vomiting secondary to diabetic gastroparesis. He was euglycemic, non-acidemic, and serum bicarbonate was within normal limits. However, labs were significant for ketonuria, an elevated anion gap, and an elevated beta-hydroxybutyrate. Given the high concern for euglycemic DKA in the setting of a competing primary metabolic alkalosis, he was transferred to the intensive care unit for intravenous insulin infusion and fluid resuscitation with significant clinical improvement and normalization of laboratory results. This serves as an important reminder that DKA can be masked by euglycemia as well as additional metabolic derangements, and should be suspected in any diabetic patient with an anion gap and/or ketosis.

Failure to Thrive With Severe Hypokalemia Yields Cystinosis Diagnosis in a 19-Month-Old Female Child: A Case Report.

Cystinosis is a rare, genetically inherited disease that affects lysosomal storage of cysteine. It is the most common cause of Fanconi syndrome. Mutations have led to early-onset end-stage renal disease as well as other systemic organ failures. In this case, we report a 19-month-old female child who presented acutely to the outpatient clinic with nausea, vomiting, and diarrhea. The patient was previously diagnosed with unspecified renal tubular acidosis and treated with oral electrolytes. Early labs during her acute presentation showed severe hypokalemia and electrolyte imbalance, which necessitated a transfer to a pediatric ICU. Through confirmatory testing, a diagnosis of cystinosis was made. This case is an example of the recognition and treatment of a rare inherited disease.

Type B lactic acidosis associated with multiple myeloma.

We present a 58-year-old man with recurrent multiple myeloma treated with 2 autologous stem cell transplantations. He was admitted for dyspnea and found to have severe type B lactic acidosis with serum lactate level of 193.6 mg/dL. This case reviews malignancy-associated type B lactic acidosis and discusses its etiology, pathogenesis, and management.

Comparison of plasma total carbon dioxide and standard hydrogen carbonate in a hospital laboratory setting.

BACKGROUND: Studies comparing venous total carbon dioxide (tCO2) and standard hydrogen carbonate (HCO3-(P,st)) has shown diverse results, and it is debatable whether these two parameters can be used interchangeably for workup of acid-base disorders in a hospital setting. METHOD: All patients with an HCO3-(P,st) requisition from any department at Odense University Hospital between 11th May 2021 and 1st June 2021 had tCO2 and HCO3-(P,st) analysed simultaneously. TCO2 was measured on Cobas® 8000, c702 module, while HCO3-(P,st) was calculated based on measurements on ABL835 Flex. RESULTS: From 1210 patients, mean (standard deviation (SD)) was 22.9 (3.7) mmol/L for tCO2 and 22.5 (2.9) mmol/L for HCO3-(P,st). TCO2 range was 10.1-42.3 mmol/L and 11.7-41.4 mmol/L for HCO3-(P,st). Linear regression showed that tCO2 (mmol/L) = -2.90 + 1.15 × HCO3-(P,st) (mmol/L) with R2 = 0.81. Bias (mean (SD) difference) between tCO2 and HCO3-(P,st)) was 0.4 (1.7) mmol/L with a -5.0-9.6 mmol/L range. Limits of agreement was -2.90-3.70 mmol/L. Comparison of classification within, above or below reference interval for tCO2 and HCO3-(P,st) showed that 984 samples (81%) retained their classification. Only one sample (0.1%) would be severely misclassified (outside the respective reference intervals) if HCO3-(P,st) was considered the gold standard. Of the samples investigated, 46.1% had a mean difference between tCO2 and HCO3-(P,st) of 0-1 mmol/L and 30.3% had 1.1-2.0 mmol/L. CONCLUSIONS: Our results indicate that venous tCO2 and venous HCO3-(P,st) can be used interchangeably in a hospital setting for workup of acid-base disorders.