Approach to Acid-Base Disorders

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Carbon Dioxide Tension ◽  
Anion Gap ◽  
Secondary Response ◽  
Simultaneous Occurrence ◽  
Acid Base ◽  
Respiratory Disorders ◽  
Base Disorder

This review on the approach to acid-base disorders uses the physiologic approach to assessing acid-base status, namely that based on the H2CO3/[HCO3–] buffer pair. A simple acid-base disorder is characterized by a primary abnormality in either carbon dioxide tension (Pco2) or serum [HCO3–] accompanied by the appropriate secondary response in the other component. The four cardinal, simple acid-base disorders are categorized into respiratory disorders and metabolic disorders. Respiratory disorders are expressed as primary changes in Pco2 and include respiratory acidosis or primary hypercapnia (primary increase in Pco2) and respiratory alkalosis or primary hypocapnia (primary decrease in Pco2). Metabolic disorders are expressed as primary changes in serum [HCO3–]) and include metabolic acidosis (primary decrease in serum [HCO3–]) and metabolic alkalosis (primary increase in serum [HCO3–]). A mixed acid-base disorder denotes the simultaneous occurrence of two or more simple acid-base disorders. Arriving at an accurate acid-base diagnosis rests with assessment of the accuracy of the acid-base variables, calculation of the serum anion gap, and identification of the dominant acid-base disorder and whether a simple or mixed disorder is present. Identifying the cause of the acid-base disorder depends on a detailed history and physical examination as well as obtaining additional testing, as appropriate.   Key words: acid-base disorders; simple disorders; mixed disorders; anion gap; physiologic approach; physicochemical approach; base-excess approach

Approach to Acid-Base Disorders

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Carbon Dioxide Tension ◽  
Anion Gap ◽  
Secondary Response ◽  
Simultaneous Occurrence ◽  
Acid Base ◽  
Respiratory Disorders ◽  
Base Disorder

This review on the approach to acid-base disorders uses the physiologic approach to assessing acid-base status, namely that based on the H2CO3/[HCO3–] buffer pair. A simple acid-base disorder is characterized by a primary abnormality in either carbon dioxide tension (Pco2) or serum [HCO3–] accompanied by the appropriate secondary response in the other component. The four cardinal, simple acid-base disorders are categorized into respiratory disorders and metabolic disorders. Respiratory disorders are expressed as primary changes in Pco2 and include respiratory acidosis or primary hypercapnia (primary increase in Pco2) and respiratory alkalosis or primary hypocapnia (primary decrease in Pco2). Metabolic disorders are expressed as primary changes in serum [HCO3–]) and include metabolic acidosis (primary decrease in serum [HCO3–]) and metabolic alkalosis (primary increase in serum [HCO3–]). A mixed acid-base disorder denotes the simultaneous occurrence of two or more simple acid-base disorders. Arriving at an accurate acid-base diagnosis rests with assessment of the accuracy of the acid-base variables, calculation of the serum anion gap, and identification of the dominant acid-base disorder and whether a simple or mixed disorder is present. Identifying the cause of the acid-base disorder depends on a detailed history and physical examination as well as obtaining additional testing, as appropriate.   Key words: acid-base disorders; simple disorders; mixed disorders; anion gap; physiologic approach; physicochemical approach; base-excess approach

Approach to Acid-Base Disorders

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Carbon Dioxide Tension ◽  
Anion Gap ◽  
Secondary Response ◽  
Simultaneous Occurrence ◽  
Acid Base ◽  
Respiratory Disorders ◽  
Base Disorder

This review on the approach to acid-base disorders uses the physiologic approach to assessing acid-base status, namely that based on the H2CO3/[HCO3–] buffer pair. A simple acid-base disorder is characterized by a primary abnormality in either carbon dioxide tension (Pco2) or serum [HCO3–] accompanied by the appropriate secondary response in the other component. The four cardinal, simple acid-base disorders are categorized into respiratory disorders and metabolic disorders. Respiratory disorders are expressed as primary changes in Pco2 and include respiratory acidosis or primary hypercapnia (primary increase in Pco2) and respiratory alkalosis or primary hypocapnia (primary decrease in Pco2). Metabolic disorders are expressed as primary changes in serum [HCO3–]) and include metabolic acidosis (primary decrease in serum [HCO3–]) and metabolic alkalosis (primary increase in serum [HCO3–]). A mixed acid-base disorder denotes the simultaneous occurrence of two or more simple acid-base disorders. Arriving at an accurate acid-base diagnosis rests with assessment of the accuracy of the acid-base variables, calculation of the serum anion gap, and identification of the dominant acid-base disorder and whether a simple or mixed disorder is present. Identifying the cause of the acid-base disorder depends on a detailed history and physical examination as well as obtaining additional testing, as appropriate.   Key words: acid-base disorders; simple disorders; mixed disorders; anion gap; physiologic approach; physicochemical approach; base-excess approach

Influence of chronic respiratory acid-base disorders on acute CO2 titration curve

1985 ◽  
Vol 58 (4) ◽  
pp. 1231-1238 ◽  
Author(s):  
H. J. Adrogue ◽  
N. E. Madias
Keyword(s):  
Titration Curve ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Ion Concentration ◽  
Whole Body ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Base Disorder ◽  
Acid Base Status

We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). Chronic respiratory alkalosis and acidosis, as well as the acute CO2 titrations, were produced in unanesthetized dogs within a large environmental chamber. For comparison with our data on chronic metabolic acidosis and alkalosis, plasma bicarbonate levels, which are secondarily altered in chronic respiratory acid-base disorders, were used as an index of chronic acid-base status of the animals. Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.

Respiratory Acidosis and Alkalosis

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Carbonic Acid ◽  
Clinical Manifestations ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Body Fluids ◽  
The Body ◽  
Acid Base ◽  
Acid Base Equilibrium ◽  
Therapeutic Principles ◽  
The Impact

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis.  This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

Stability of cerebrospinal fluid pH in chronic acid-base disturbances in blood

1965 ◽  
Vol 20 (3) ◽  
pp. 443-452 ◽  
Author(s):  
R. A. Mitchell ◽  
C. T. Carman ◽  
J. W. Severinghaus ◽  
B. W. Richardson ◽  
M. M. Singer ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Active Transport ◽  
Respiratory Acidosis ◽  
Normal Subjects ◽  
Respiratory Alkalosis ◽  
Regulation Of Respiration ◽  
Respiratory Drive ◽  
Acid Base ◽  
Peripheral Chemoreceptors ◽  
Mean Values

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

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.

Effect of systemic acid-base balance on ileal secretion

1987 ◽  
Vol 253 (3) ◽  
pp. G330-G335
Author(s):  
D. S. Goldfarb ◽  
P. M. Ingrassia ◽  
A. N. Charney
Keyword(s):  
Metabolic Acidosis ◽  
Cholera Toxin ◽  
Metabolic Disorders ◽  
Respiratory Acidosis ◽  
Secretory Process ◽  
Sprague Dawley ◽  
Acid Base Balance ◽  
Acid Base ◽  
Ph Change ◽  
Base Balance

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.

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise

2012 ◽  
Vol 112 (4) ◽  
pp. 571-579 ◽  
Author(s):  
M. Hilbert ◽  
V. Shushakov ◽  
N. Maassen
Keyword(s):  
Force Production ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Muscle Performance ◽  
Protective Effects ◽  
Acid Base ◽  
M Wave ◽  
Hand Grip

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO2 rebreathing, alkalosis by hyperventilation, or control. The Pco2, pH, K+ concentration ([K+]), and Na+ concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis ( P < 0.001). The venous [K+] rose to similar maximum values in all conditions (6.2 ± 0.8 mmol/l). The acidification reduced the decline in contraction speed ( P < 0.001) but decreased the M-wave area to 73.4 ± 19.8% ( P < 0.001) of the initial value. After the first exercise cycle, the M-wave area was smaller with acidosis than with alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition ( P < 0.001). The duration of the M-wave was not affected. Acidification diminished the reduction in performance, although the M-wave area during exercise was decreased. Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.

The use of elements of the Stewart model (Strong Ion Approach) for the diagnostics of respiratory acidosis on the basis of the calculation of a value of a modified anion gap (AGm) in brachycephalic dogs

2015 ◽  
Vol 18 (1) ◽  
pp. 217-222 ◽  
Author(s):  
P. Sławuta ◽  
K. Glińska-Suchocka ◽  
A. Cekiera
Keyword(s):  
Reference Values ◽  
Soft Palate ◽  
Respiratory Acidosis ◽  
Anion Gap ◽  
Correction Procedure ◽  
Acid Base Balance ◽  
Acid Base ◽  
Apparent Lack ◽  
Before And After ◽  
Base Balance

AbstractApart from the HH equation, the acid-base balance of an organism is also described by the Stewart model, which assumes that the proper insight into the ABB of the organism is given by an analysis of: pCO2, the difference of concentrations of strong cations and anions in the blood serum – SID, and the total concentration of nonvolatile weak acids – Acid total. The notion of an anion gap (AG), or the apparent lack of ions, is closely related to the acid-base balance described according to the HH equation. Its value mainly consists of negatively charged proteins, phosphates, and sulphates in blood. In the human medicine, a modified anion gap is used, which, including the concentration of the protein buffer of blood, is, in fact, the combination of the apparent lack of ions derived from the classic model and the Stewart model. In brachycephalic dogs, respiratory acidosis often occurs, which is caused by an overgrowth of the soft palate, making it impossible for a free air flow and causing an increase in pCO2– carbonic acid anhydride The aim of the present paper was an attempt to answer the question whether, in the case of systemic respiratory acidosis, changes in the concentration of buffering ions can also be seen. The study was carried out on 60 adult dogs of boxer breed in which, on the basis of the results of endoscopic examination, a strong overgrowth of the soft palate requiring a surgical correction was found. For each dog, the value of the anion gap before and after the palate correction procedure was calculated according to the following equation: AG = ([Na+mmol/l] + [K+mmol/l]) – ([Cl−mmol/l]+[HCO3−mmol/l]) as well as the value of the modified AG – according to the following equation: AGm= calculated AG + 2.5 × (albuminsr– albuminsd). The values of AG calculated for the dogs before and after the procedure fell within the limits of the reference values and did not differ significantly whereas the values of AGmcalculated for the dogs before and after the procedure differed from each other significantly. Conclusions: 1) On the basis of the values of AGmobtained it should be stated that in spite of finding respiratory acidosis in the examined dogs, changes in ion concentration can also be seen, which, according to the Stewart theory, compensate metabolic ABB disorders 2) In spite of the fact that all the values used for calculation of AGmwere within the limits of reference values, the values of AGmin dogs before and after the soft palate correction procedure differed from each other significantly, which proves high sensitivity and usefulness of the AGmcalculation as a diagnostic method.

Teaching acid/base physiology in the laboratory

2010 ◽  
Vol 34 (4) ◽  
pp. 233-238 ◽  
Author(s):  
Ulla G. Friis ◽  
Ronni Plovsing ◽  
Klaus Hansen ◽  
Bent G. Laursen ◽  
Birgitta Wallstedt
Keyword(s):  
Metabolic Acidosis ◽  
Medical Students ◽  
Respiratory Alkalosis ◽  
Theory And Practice ◽  
Single Group ◽  
Acid Base ◽  
Laboratory Exercise ◽  
Base Disorder

Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied.

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