Acid-Base Disorders

2017 ◽  
Author(s):  
Herbert Chen ◽  
Jason Primus ◽  
Colin Martin
Keyword(s):  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Proton Donor ◽  
The Body ◽  
Proton Acceptor ◽  
Acid Base ◽  
Mixed Acid ◽  
Organ Systems ◽  
Homeostatic Mechanisms

This review is a summary of the acid-base physiology that is essential to understanding acid-base pathophysiology. An acid is defined as a proton donor; a base is defined as a proton acceptor. The body fluids are composed of acids and bases, which are tightly regulated by our organ systems, specifically the respiratory system and kidneys. Derangements in the body’s acid-base homeostatic mechanisms or overloading the capacity of the body’s ability to respond can lead to acid-base disorders. These include acidosis and alkalosis, which can be further classified into respiratory, metabolic, or mixed disorders. The approach to these disorders is to stabilize the patient, focusing on respiratory and circulatory status and treating the underlying cause of the acid-base derangement. This review contains 4 highly rendered figures, 2 tables, and 26 references. Key words: acid-base disorders, acid-base homeostasis, acid-base physiology, acidemia, alkalemia, metabolic acidosis, metabolic alkalosis, mixed acid-base disorders, respiratory acidosis, respiratory alkalosis 

Acid-Base Disorders

2017 ◽  
Author(s):  
Herbert Chen ◽  
Jason Primus ◽  
Colin Martin
Keyword(s):  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Proton Donor ◽  
The Body ◽  
Proton Acceptor ◽  
Acid Base ◽  
Mixed Acid ◽  
Organ Systems ◽  
Homeostatic Mechanisms

This review is a summary of the acid-base physiology that is essential to understanding acid-base pathophysiology. An acid is defined as a proton donor; a base is defined as a proton acceptor. The body fluids are composed of acids and bases, which are tightly regulated by our organ systems, specifically the respiratory system and kidneys. Derangements in the body’s acid-base homeostatic mechanisms or overloading the capacity of the body’s ability to respond can lead to acid-base disorders. These include acidosis and alkalosis, which can be further classified into respiratory, metabolic, or mixed disorders. The approach to these disorders is to stabilize the patient, focusing on respiratory and circulatory status and treating the underlying cause of the acid-base derangement. This review contains 4 highly rendered figures, 2 tables, and 26 references. Key words: acid-base disorders, acid-base homeostasis, acid-base physiology, acidemia, alkalemia, metabolic acidosis, metabolic alkalosis, mixed acid-base disorders, respiratory acidosis, respiratory alkalosis   

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

scholarly journals Effect of acute acid-base disturbances on ErbB1/2 tyrosine phosphorylation in rabbit renal proximal tubules

2013 ◽  
Vol 305 (12) ◽  
pp. F1747-F1764 ◽  
Author(s):  
Lara A. Skelton ◽  
Walter F. Boron
Keyword(s):  
Metabolic Alkalosis ◽  
Kinase Inhibitor ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Proximal Tubules ◽  
Whole Body ◽  
Ph Homeostasis ◽  
Acid Base ◽  
Major Site ◽  
The Individual

The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing ∼80% of filtered HCO3−, the major plasma buffer, into the blood. The PT adapts its rate of HCO3− reabsorption ( JHCO3−) in response to acute acid-base disturbances. Our laboratory previously showed that single isolated perfused PTs adapt JHCO3− in response to isolated changes in basolateral (i.e., blood side) CO2 and HCO3− concentrations but, surprisingly, not to pH. The response to CO2 concentration can be blocked by the ErbB family tyrosine kinase inhibitor PD-168393. In the present study, we exposed enriched rabbit PT suspensions to five acute acid-base disturbances for 5 and 20 min using a panel of phosphotyrosine (pY)-specific antibodies to determine the influence of each disturbance on pan-pY, ErbB1-specific pY (four sites), and ErbB2-specific pY (two sites). We found that each acid-base treatment generated a distinct temporal pY pattern. For example, the summated responses of the individual ErbB1/2-pY sites to each disturbance showed that metabolic acidosis (normal CO2 concentration and reduced HCO3− concentration) produced a transient summated pY decrease (5 vs. 20 min), whereas metabolic alkalosis produced a transient increase. Respiratory acidosis (normal HCO3− concentration and elevated CO2 concentration) had little effect on summated pY at 5 min but produced an elevation at 20 min, whereas respiratory alkalosis produced a reduction at 20 min. Our data show that ErbB1 and ErbB2 in the PT respond to acute acid-base disturbances, consistent with the hypothesis that they are part of the signaling cascade.

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

Acid-Base Disorders

2018 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

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.

Acid-Base Disorders

2015 ◽  
Author(s):  
Aaron Skolnik ◽  
Jessica Monas
Keyword(s):  
Metabolic Acidosis ◽  
Renal Tubular Acidosis ◽  
Metabolic Alkalosis ◽  
Respiratory Acidosis ◽  
The Body ◽  
Anion Gap ◽  
Hydrogen Ions ◽  
Acid Base Balance ◽  
Acid Base ◽  
Renal Tubular

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.

Relative influence of respiratory and metabolic acid-base changes on renal acid excretion

1960 ◽  
Vol 198 (2) ◽  
pp. 237-243 ◽  
Author(s):  
Daniel H. Simmons ◽  
Nicholas A. Assali ◽  
Melvin Avedon
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Time Lag ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Excretion ◽  
Acid Base ◽  
Urine Ph ◽  
Renal Handling ◽  
Anesthetized Dogs

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.

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.

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.

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