Acid-Base Disorders

2013 ◽  
Author(s):  
Ann P. O'Rourke ◽  
James Orr ◽  
Suresh Agarwal

Anticipation and early identification of conditions that alter the body's ability to compensate for acid-base disorders are vital in managing surgical patients. This review describes the general principles and classification of acid-base disorders. Metabolic acid-base disorders are presented, including metabolic acidosis and alkalosis. Respiratory acid-base disorders are also presented, including respiratory acidosis and alkalosis. Tables show the differentiation of acid-base disorders, causes of positive–anion gap acidosis, the differential diagnosis for normal–anion gap metabolic acidosis, the mechanisms associated with increased serum lactate concentration, and the differential diagnosis for metabolic alkalosis. This review contains 7 highly rendered figures, 5 tables, and 135 references.

2018 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.


2015 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas

Under physiologic conditions, the acid-base balance of the body is maintained via changes in ventilation that eliminate carbon dioxide, buffering of acid loads, and renal excretion of hydrogen ions. Failure to maintain the pH of the blood between 7.35 and 7.45 can result in life-threatening conditions. This review details the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of acid-base disorders. Figures show the relationship between hydrogen ions and blood pH, proximal tubular bicarbonate reabsorption, the secretion of hydrogen ions, renal ammonia production, ammonium diffusion, metabolic alkalosis, electrocardiographic changes in hypokalemia and hyperkalemia, pseudoinfarction caused by hyperkalemia, and an algorithmic approach to suspected acid-base disorders. Tables list causes of high–anion gap metabolic acidosis, metabolic acidosis with a normal anion gap, type 1 renal tubular acidosis, type 4 renal tubular acidosis and aldosterone resistance, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis; treatment of hyperkalemia; and a stepwise approach for the evaluation of suspected acid-base disorders. This review contains 9 highly rendered figures, 9 tables, 64 references, and a list of pertinent Web sites.


2017 ◽  
Vol 8 (3) ◽  
pp. 60-67
Author(s):  
Prem Amalraj ◽  
Arun Kumar Narayanan ◽  
Satish Balan ◽  
Mathew Thomas

Background: Metabolic acidosis is a common abnormality in the intensive care unit. There has recently been a surge of interest in nontraditional approaches to the analysis of acid base disorders.Aims and Objectives: This study was undertaken to compare the application of the physicochemical method of Stewart and the traditional Henderson-Hasselbach equation withcorrection for albumin in quantification of acid base disorders.Materials and Methods: All patients with metabolic acidosis admitted to the ICU as defined by a base deficit of >2.5 were included in the study. The APACHE II score was calculated at admission and the predicted mortality was defined. The acid base disorders were quantified by the traditional approach with anion gap correction for serum albumin as well as by the Stewart method with calculation of the strong anion gap acidosis.Results: One-hundred forty patients were included in the study of which 58% were males. In 125 subjects (89%) acidosis was discovered by the Stewart method. The traditional method detected increased anion gap in 109 subjects (78%) but this increased to 124 (88.5%) when corrected for albumin. Both the strong ion gap (SIG) and the albumin corrected anion gap correlated strongly. Serum lactate levels and SIG predicted mortality as did albumin corrected anion gap.Conclusion: Albumin correction of the anion gap correlates well with acidosis as discovered by the SIG and therefore should be used in the ICUs rather than the traditional anion gap. With this modification, we can thus depend on the application of the intuitive traditional method rather than the more difficult to apply Stewart method for analysis of the acid base abnormalities in the ICU.Asian Journal of Medical Sciences Vol.8(3) 2017 60-67


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248264
Author(s):  
Sancho Rodríguez-Villar ◽  
Paloma Poza-Hernández ◽  
Sascha Freigang ◽  
Idoia Zubizarreta-Ormazabal ◽  
Daniel Paz-Martín ◽  
...  

Background Point-of-care arterial blood gas (ABG) is a blood measurement test and a useful diagnostic tool that assists with treatment and therefore improves clinical outcomes. However, numerically reported test results make rapid interpretation difficult or open to interpretation. The arterial blood gas algorithm (ABG-a) is a new digital diagnostics solution that can provide clinicians with real-time interpretation of preliminary data on safety features, oxygenation, acid-base disturbances and renal profile. The main aim of this study was to clinically validate the algorithm against senior experienced clinicians, for acid-base interpretation, in a clinical context. Methods We conducted a prospective international multicentre observational cross-sectional study. 346 sample sets and 64 inpatients eligible for ABG met strict sampling criteria. Agreement was evaluated using Cohen’s kappa index, diagnostic accuracy was evaluated with sensitivity, specificity, efficiency or global accuracy and positive predictive values (PPV) and negative predictive values (NPV) for the prevalence in the study population. Results The concordance rates between the interpretations of the clinicians and the ABG-a for acid-base disorders were an observed global agreement of 84,3% with a Cohen’s kappa coefficient 0.81; 95% CI 0.77 to 0.86; p < 0.001. For detecting accuracy normal acid-base status the algorithm has a sensitivity of 90.0% (95% CI 79.9 to 95.3), a specificity 97.2% (95% CI 94.5 to 98.6) and a global accuracy of 95.9% (95% CI 93.3 to 97.6). For the four simple acid-base disorders, respiratory alkalosis: sensitivity of 91.2 (77.0 to 97.0), a specificity 100.0 (98.8 to 100.0) and global accuracy of 99.1 (97.5 to 99.7); respiratory acidosis: sensitivity of 61.1 (38.6 to 79.7), a specificity of 100.0 (98.8 to 100.0) and global accuracy of 98.0 (95.9 to 99.0); metabolic acidosis: sensitivity of 75.8 (59.0 to 87.2), a specificity of 99.7 (98.2 to 99.9) and a global accuracy of 97.4 (95.1 to 98.6); metabolic alkalosis sensitivity of 72.2 (56.0 to 84.2), a specificity of 95.5 (92.5 to 97.3) and a global accuracy of 93.0 (88.8 to 95.3); the four complex acid-base disorders, respiratory and metabolic alkalosis, respiratory and metabolic acidosis, respiratory alkalosis and metabolic acidosis, respiratory acidosis and metabolic alkalosis, the sensitivity, specificity and global accuracy was also high. For normal acid-base status the algorithm has PPV 87.1 (95% CI 76.6 to 93.3) %, and NPV 97.9 (95% CI 95.4 to 99.0) for a prevalence of 17.4 (95% CI 13.8 to 21.8). For the four-simple acid-base disorders and the four complex acid-base disorders the PPV and NPV were also statistically significant. Conclusions The ABG-a showed very high agreement and diagnostic accuracy with experienced senior clinicians in the acid-base disorders in a clinical context. The method also provides refinement and deep complex analysis at the point-of-care that a clinician could have at the bedside on a day-to-day basis. The ABG-a method could also have the potential to reduce human errors by checking for imminent life-threatening situations, analysing the internal consistency of the results, the oxygenation and renal status of the patient.


1978 ◽  
Vol 235 (4) ◽  
pp. F291-F297 ◽  
Author(s):  
H. J. Adrogue ◽  
J. Brensilver ◽  
N. E. Madias

A basic premise in the utilization of the plasma anion gap in the assessment of acid-base disorders is that this parameter remains constant during hyperchloremic metabolic acidosis and metabolic alkalosis. Experimental data under in vitro conditions, however, cast serious doubt on this premise. The purpose of the present study was to characterize the plasma anion gap, estimated as (Na + K) - Cl + HCO3), in two large groups of dogs with graded degrees of chronic, HCl-induced metabolic acidosis or chronic, diuretic-induced metabolic alkalosis. The data indicate that the plasma anion gap decreases significantly in HCl acidosis and increases significantly in metabolic alkalosis; the predicted mean anion gap in animals with a plasma bicarbonate concentration of 10, 21 (normal), and 40 meq/liter approximated 13, 18, and 26 meq/liter, respectively. The observed variation in the plasma anion gap is interpreted as originating mainly from directional changes in the net negative charge of plasma proteins; these changes result from the titration process secondary to the altered plasma acidity and, in the case of metabolic alkalosis, from the additional effect of an increased plasma protein concentration.


2021 ◽  
Vol 2 (5) ◽  
pp. 182-185
Author(s):  
Sanjay Mohan ◽  
David Goldfarb ◽  
Robert Hoffman

Introduction: The term “lactic acidosis” reinforces the misconception that lactate contributes to acidemia. Although it is common to discover an anion gap acidosis with a concomitant elevated lactate concentration, the two are not mutually dependent. Case Report: Here we describe two patients exhibiting high lactate concentrations in the setting of metabolic alkalemia. Conclusion: Lactate is not necessarily the direct cause of acid-base disturbances, and there is no fixed relationship between lactate and the anion gap or between lactate and pH. The term “metabolic acidosis with hyperlactatemia” is more specific than “lactic acidosis” and thus more appropriate.


1960 ◽  
Vol 198 (2) ◽  
pp. 237-243 ◽  
Author(s):  
Daniel H. Simmons ◽  
Nicholas A. Assali ◽  
Melvin Avedon

Arterial pH of anesthetized dogs was maintained constant for 90 minutes during continuous infusion of 0.15 m HCl or NaHCO3 (0.3 cc/kg/min.) by adjusting alveolar ventilation with a respiration pump. This resulted in simultaneous metabolic acidosis and respiratory alkalosis (acid infusion) or metabolic alkalosis and respiratory acidosis (base infusion) equal in degree with respect to their effect on blood pH. Since urine pH dropped and renal acid excretion increased during metabolic acidosis and respiratory alkalosis, while pH rose and acid excretion decreased during metabolic alkalosis and respiratory acidosis, metabolic acid-base disturbances appear to exert more influence on renal acid excretion than do respiratory disturbances comparable in terms of their effect on pH. This difference in response was shown not to be due to a time lag in renal response to respiratory disturbances, nor could it be explained by effects on urine flow, renal hemodynamics or renal handling of sodium.


1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  

In chronic acid-base disturbances, CSF pH was generally within the normal limits (7.30–7.36 units, being the range including two standard deviations of 12 normal subjects). The mean values of CSF and arterial pHH, respectively, were: 1) metabolic alkalosis, 7.337 and 7.523; 2) metabolic acidosis, 7.315 and 7.350; 3) respiratory alkalosis, 7.336 and 7.485; and 4) respiratory acidosis (untreated), 7.314 and 7.382. Other investigators report similar values. The constancy of CSF pH cannot be explained by a poorly permeable blood-CSF barrier in chronic metabolic acidosis and alkalosis, nor can it be explained by respiratory compensation. It cannot be explained by renal compensation in respiratory alkalosis (high altitude for 8 days), although it may be explained by renal compensation in respiratory acidosis. The former three states suggest that active transport regulation of CSF pH is a function of the blood-CSF barrier. Since CSF pH is constant, so also must that portion of the respiratory drive originating in the superficial medullary respiratory chemoreceptors be constant. Ventilation changes in chronic acid-base disturbances thus may result from changes in the activity of peripheral chemoreceptors, in response to changes in arterial pH, arterial PO2, and possibly in neuromuscular receptors. regulation of respiration; medullary respiratory; chemoreceptors; peripheral chemoreceptors; metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; active transport; blood-brain barrier; pregnancy Submitted on July 27, 1964


1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.


CJEM ◽  
2019 ◽  
Vol 21 (3) ◽  
pp. 435-437
Author(s):  
Chelsea R. Beaton ◽  
Clinton Meyer

Learning Points:•Know and identify clinical presentations of toxic alcohols.•Understand the differential diagnosis of high anion gap metabolic acidosis.•Appreciate the importance of history and clinical findings in establishing methanol toxicity diagnoses, especially in centres where laboratory testing is unavailable.•Recognize the value of provincial poison centres in supporting emergency physicians in the diagnosis and management of poisonings and overdoses.


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