scholarly journals Metabolic alkalosis is the most common acid–base disorder in ICU patients

Critical Care ◽  
2014 ◽  
Vol 18 (2) ◽  
pp. 420 ◽  
Author(s):  
Kjersti Mæhle ◽  
Bjørn Haug ◽  
Hans Flaatten ◽  
Erik Nielsen
Keyword(s):  
Metabolic Alkalosis ◽  
Acid Base ◽  
Icu Patients ◽  
Base Disorder

scholarly journals Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat kidney

2011 ◽  
Vol 301 (4) ◽  
pp. F823-F832 ◽  
Author(s):  
Ki-Hwan Han ◽  
Hyun-Wook Lee ◽  
Mary E. Handlogten ◽  
Jesse M. Bishop ◽  
Moshe Levi ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Family Members ◽  
Ammonia Excretion ◽  
Intercalated Cells ◽  
Acid Base ◽  
Ammonia Metabolism ◽  
Transporter Family ◽  
Base Disorder

Hypokalemia is a common electrolyte disorder that increases renal ammonia metabolism and can cause the development of an acid-base disorder, metabolic alkalosis. The ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg), are expressed in the distal nephron and collecting duct and mediate critical roles in acid-base homeostasis by facilitating ammonia secretion. In the current studies, the effect of hypokalemia on renal Rhbg and Rhcg expression was examined. Normal Sprague-Dawley rats received either K+-free or control diets for 2 wk. Rats receiving the K+-deficient diet developed hypokalemia and metabolic alkalosis associated with significant increases in both urinary ammonia excretion and urine pH. Rhcg expression increased in the outer medullary collecting duct (OMCD). In OMCD intercalated cells, hypokalemia resulted in more discrete apical Rhcg expression and a marked increase in apical plasma membrane immunolabel. In principal cells, in the OMCD, hypokalemia increased both apical and basolateral Rhcg immunolabel intensity. Cortical Rhcg expression was not detectably altered by immunohistochemistry, although there was a slight decrease in total expression by immunoblot analysis. Rhbg protein expression was decreased slightly in the cortex and not detectably altered in the outer medulla. We conclude that in rat OMCD, hypokalemia increases Rhcg expression, causes more polarized apical expression in intercalated cells, and increases both apical and basolateral expression in the principal cell. Increased plasma membrane Rhcg expression in response to hypokalemia in the rat, particularly in the OMCD, likely contributes to the increased ammonia excretion and thereby to the development of metabolic alkalosis.

scholarly journals Acid based disorders in intensive care unit: a hospital-based study

2019 ◽  
Vol 6 (1) ◽  
pp. 62 ◽  
Author(s):  
Babu Rajendran ◽  
Seetha Rami Reddy Mallampati ◽  
Sheju Jonathan Jha J.
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Metabolic Acidosis ◽  
Infectious Diseases ◽  
Respiratory Alkalosis ◽  
Simple Type ◽  
Acid Base ◽  
Icu Patients ◽  
Mixed Acid ◽  
Base Disorder

Background: Acid base disorders are common in the ICU patients and pose a great burden in the management of the underlying condition.Methods: Identifying the type of acid-base disorders in ICU patients using arterial blood gas analysis This was a retrospective case-controlled comparative study. 46 patients in intensive care unit of a reputed institution and comparing the type of acid-base disorder amongst infectious (10) and non-infectious (36) diseases.Results: Of the study population, 70% had mixed acid base disorders and 30% had simple type of acid base disorders. It was found that sepsis is associated with mixed type of acid-base disorders with most common being metabolic acidosis with respiratory alkalosis. Non-infectious diseases were mostly associated with metabolic alkalosis with respiratory acidosis. Analysis of individual acid base disorders revealed metabolic acidosis as the most common disturbance.Conclusions: These results projected the probability of acid bases disorders in various conditions and help in the efficient management. Mixed acid base disorders are the most common disturbances in the intensive care setup which is metabolic acidosis with respiratory alkalosis in infectious diseases and metabolic acidosis is the most common simple type of acid base disorder.

scholarly journals Serious acid-base disorder or life-threatening arrhythmia in patients with ABO-incompatible liver transplantation who received therapeutic plasma exchange : A report of two cases

2021 ◽  
Author(s):  
Sangho Lee ◽  
Kyoung-Sun Kim ◽  
Bo-Hyun Sang ◽  
Gyu-Sam Hwang
Keyword(s):  
Plasma Exchange ◽  
Metabolic Alkalosis ◽  
Therapeutic Plasma Exchange ◽  
Acid Base ◽  
Metabolic Derangement ◽  
Surgical Incision ◽  
Electrolyte Disturbance ◽  
Electrolyte Disturbances ◽  
Base Disorder ◽  
Life Threatening

Background: Excessive citrate load during therapeutic plasma exchange (TPE) can cause metabolic alkalosis with compensatory hypercarbia and electrolyte disturbances. If TPE is required immediately before ABO-incompatible (ABOi) liver transplant (LT) surgery, metabolic derangement and severe electrolyte disturbance could worsen during LT anesthesia.Case: We report two ABOi LT cases who received TPE on the day of surgery because isoagglutinin titers did not be dropped below 1:8. One case had a surprisingly high metabolic alkalosis with a pH of 7.73 immediately after tracheal intubation because of hyperventilation during mask bagging. The other experienced sudden ventricular tachycardia and blood pressure drop after surgical incision accompanied with severe hypokalemia of 1.8 mmol/L despite supplementation with potassium.Conclusions: Special attention should be paid to patients who just completed TPE the operative day morning as they are vulnerable to severe acid-base disturbances and life-threatening ventricular arrhythmias in ABOi LT.

scholarly journals Acid-Base Status Disturbances in Patients on Chronic Hemodialysis at High Altitudes

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Javier Enrique Cely ◽  
Oscar G. Rocha ◽  
María J. Vargas ◽  
Rafael M. Sanabria ◽  
Leyder Corzo ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Base Excess ◽  
Chronic Hemodialysis ◽  
High Altitudes ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Disorder ◽  
Acid Base Status ◽  
Normal Acid

Background. Acid-base disorders have been previously described in patients with chronic hemodialysis, with metabolic acidosis being the most important of them; however, little is known about the potential changes in acid-base status of patients on dialysis living at high altitudes. Methods. Cross-sectional study including 93 patients receiving chronic hemodialysis on alternate days and living in Bogotá, Colombia, at an elevation of 2,640 meters (8,661 feet) over sea level (m.o.s.l.). Measurements of pH, PaCO2, HCO3, PO2, and base excess were made on blood samples taken from the arteriovenous fistula (AVF) during the pre- and postdialysis periods in the midweek hemodialysis session. Normal values for the altitude of Bogotá were taken into consideration for the interpretation of the arterial blood gases. Results. 43% (n= 40) of patients showed predialysis normal acid-base status. The most common acid-base disorder in predialysis period was metabolic alkalosis with chronic hydrogen ion deficiency in 19,3% (n=18). Only 9,7% (n=9) had predialysis metabolic acidosis. When comparing pre- and postdialysis blood gas analysis, higher postdialysis levels of pH (7,41 versus 7,50, p<0,01), bicarbonate (21,7mmol/L versus 25,4mmol/L, p<0,01), and base excess (-2,8 versus 2,4, p<0,01) were reported, with lower levels of partial pressure of carbon dioxide (34,9 mmHg versus 32,5 mmHg, p<0,01). Conclusion. At an elevation of 2,640 m.o.s.l., a large percentage of patients are in normal acid-base status prior to the dialysis session (“predialysis period”). Metabolic alkalosis is more common than metabolic acidosis in the predialysis period when compared to previous studies. Paradoxically, despite postdialysis metabolic alkalosis, PaCO2 levels are lower than those found in the predialysis period.

scholarly journals Acid-base status in canine babesiosis caused by Babesia canis

2020 ◽  
Vol 90 (6) ◽  
pp. 603-610
Author(s):  
Marin Torti ◽  
◽  
Josipa Kuleš ◽  
Vesna Matijatko ◽  
Mirna Brkljačić ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Strong Ion Difference ◽  
Canine Babesiosis ◽  
Acid Base ◽  
Mixed Acid ◽  
Naturally Occurring ◽  
Base Disorder ◽  
Acid Base Status ◽  
Healthy Dogs

Acid-base disturbances have been reported in severe canine babesiosis caused by Babesia rossi (B. rossi), but they have not been studied in babesiosis caused by B. canis. The objective of this study was to determine the acid-base status, blood gases and electrolyte concentrations in naturally occurring canine babesiosis caused by B. canis, and to compare the results to those in healthy dogs. Two groups of animals were used: group 1 consisted of 10 healthy dogs, and group 2 consisted of 14 dogs naturally infected with B. canis. The following acid-base disturbances occurred in the dogs with naturally occurring babesiosis: half of the dogs had a mixed acid-base disorder, and the other half a simple acid-base disorder. The most common mixed disorder was metabolic acidosis with metabolic alkalosis. It may be said that a variety of acid-base disorders occurs in canine babesiosis. The dogs in the present study had metabolic acidosis due to hyperlactemia and hyperchloremia, metabolic alkalosis due to hypochloremia and hypoalbuminemia, and respiratory alkalosis due to hypoxemia. With the use of the strong-ion difference approach clearer recognition of mixed acid-base disorders and their better understanding is possible.

scholarly journals Renal ammonia excretion in response to hypokalemia: effect of collecting duct-specific Rh C glycoprotein deletion

2013 ◽  
Vol 304 (4) ◽  
pp. F410-F421 ◽  
Author(s):  
Hyun-Wook Lee ◽  
Jill W. Verlander ◽  
Jesse M. Bishop ◽  
Mary E. Handlogten ◽  
Ki-Hwan Han ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Collecting Duct ◽  
Ammonia Excretion ◽  
Immunogold Electron Microscopy ◽  
Acid Base ◽  
Outer Medulla ◽  
Rhesus Factor ◽  
Base Disorder ◽  
Urine Alkalinization

The Rhesus factor protein, Rh C glycoprotein (Rhcg), is an ammonia transporter whose expression in the collecting duct is necessary for normal ammonia excretion both in basal conditions and in response to metabolic acidosis. Hypokalemia is a common clinical condition associated with increased renal ammonia excretion. In contrast to basal conditions and metabolic acidosis, increased ammonia excretion during hypokalemia can lead to an acid-base disorder, metabolic alkalosis, rather than maintenance of acid-base homeostasis. The purpose of the current studies was to determine Rhcg's role in hypokalemia-stimulated renal ammonia excretion through the use of mice with collecting duct-specific Rhcg deletion (CD-Rhcg-KO). In mice with intact Rhcg expression, a K+-free diet increased urinary ammonia excretion and urine alkalinization and concurrently increased Rhcg expression in the collecting duct in the outer medulla. Immunohistochemistry and immunogold electron microscopy showed hypokalemia increased both apical and basolateral Rhcg expression. In CD-Rhcg-KO, a K+-free diet increased urinary ammonia excretion and caused urine alkalinization, and the magnitude of these changes did not differ from mice with intact Rhcg expression. In mice on a K+-free diet, CD-Rhcg-KO increased phosphate-dependent glutaminase (PDG) expression in the outer medulla. We conclude that hypokalemia increases collecting duct Rhcg expression, that this likely contributes to the hypokalemia-stimulated increase in urinary ammonia excretion, and that adaptive increases in PDG expression can compensate for the absence of collecting duct Rhcg.

scholarly journals Metabolic Alkalosis

2020 ◽  
Vol 15 (12) ◽  
pp. 1848-1856
Author(s):  
Michael Emmett
Keyword(s):  
Metabolic Alkalosis ◽  
Acid Base ◽  
Base Disorder ◽  
Therapeutic Model ◽  
Pathophysiologic Mechanisms

Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms. Multiple mechanisms are also responsible for the persistence, or maintenance, of metabolic alkalosis. Understanding these generation and maintenance mechanisms helps direct appropriate intervention and correction of this disorder. The framework utilized in this review is based on the ECF volume-centered approach popularized by Donald Seldin and Floyd Rector in the 1970s.  Although many subsequent scientific discoveries have advanced our understanding of the pathophysiology of metabolic alkalosis, that framework continues to be a valuable and relatively straightforward diagnostic and therapeutic model.

Metabolic Alkalosis Secondary to Baking Soda Treatment of a Diaper Rash

PEDIATRICS ◽  
1981 ◽  
Vol 67 (6) ◽  
pp. 820-822
Author(s):  
Jose Gonzalez ◽  
Ronald J. Hogg
Keyword(s):  
Case Report ◽  
Side Effects ◽  
Sodium Bicarbonate ◽  
Complete Resolution ◽  
Metabolic Alkalosis ◽  
Acid Base ◽  
Prior Application ◽  
Acid Base Disturbance ◽  
Base Disturbance

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

scholarly journals KIDNEY AND URINARY BLADDER RESPONSES OF FRESHWATER RAINBOW TROUT TO ISOSMOTIC NaCl AND NaHCO3 INFUSION

1992 ◽  
Vol 173 (1) ◽  
pp. 181-203 ◽  
Author(s):  
B. James-Curtis ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Urinary Bladder ◽  
Metabolic Alkalosis ◽  
Bladder Function ◽  
Acid Base ◽  
Burst Frequency ◽  
Arterial Ph ◽  
Acid Base Status ◽  
Nacl Load ◽  
Kidney Functions

The relative roles of the kidney and urinary bladder in ion, fluid and acid-base regulation were examined in freshwater rainbow trout chronically infused with either 140 mmol l-1 NaCl or 140 mmol l-1 NaHCO3 (3 ml kg-1 h-1) for 32 h. NaCl had a negligible effect on blood ionic and acid-base status, whereas NaHCO3 induced a metabolic alkalosis characterized by a rise in arterial pH and [HCO3-] and an equimolar fall in [Cl-]. Urine was collected via either an internal catheter, which bypassed bladder function, or an external urinary catheter, which collected naturally voided urine. As a percentage of the infusion rate, glomerular filtration rate increased by about 135 %, but urine flow rate (UFR) by only 80 %, reflecting increased tubular reabsorption of H2O. During NaCl infusion, virtually all of the extra Na+ and Cl- filtered was reabsorbed by the kidney tubules, resulting in an increased UFR with largely unchanged composition. During NaHCO3 infusion, tubular Na+ and Cl- reabsorption again kept pace with filtration. HCO3- reabsorption also increased, but did not keep pace with filtration; an increased flow of HCO3--rich urine resulted, which excreted about 10 % of the infused base load. At rest, fish fitted with external catheters voided in discrete bursts of about 0.85 ml kg-1 at 25 min intervals. During infusion, burst frequency increased by about 40 % and burst volume by about 20 %. Reabsorption by the bladder reduced UFR by 25 %, the excretion of Na+ and Cl- by 50 %, of K+ by 44 % and of urea by 25 %. These differences persisted on a relative basis during NaCl and NaHCO3 infusion despite the decreased residence time. However, HCO3- was neither secreted nor reabsorbed by the bladder. We conclude that the freshwater kidney functions to remove as much NaCl as possible from the urine, regardless of the NaCl load, and this role is supplemented by bladder function. The bladder plays no role in acid-base regulation during metabolic alkalosis.

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